Manual of Pediatric Cardiac Intensive Care

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Manual of
Pediatric Cardiac
Intensive Care
Manual of
Pediatric Cardiac
Intensive Care
Pre- and Postoperative Guidelines
Manoj Luthra
MS, DNB, MCh (Cardiothoracic Surgery), FIACS
Professor of Cardiothoracic Surgery and Dean
Armed Forces Medical College
Pune, Maharashtra, India
ERRNVPHGLFRVRUJ
ELSEVIER
A division of
Reed Elsevier India Private Limited
Manual of Pediatric Cardiac Intensive Care
Luthra
ELSEVIER
A division of
Reed Elsevier India Private Limited
Mosby, Saunders, Churchill Livingstone, Butterworth-Heinemann and
Hanley & Belfus are the Health Science imprints of Elsevier.
2012 Elsevier
All rights are reserved. No part of this publication may be reproduced, stored
in a retrieval system, or transmitted in any form or by any means, electronic,
mechanical, photocopying, recording or otherwise, without the prior written
permission of the publisher.
ISBN: 978-81-312-3050-3
Medical knowledge is constantly changing. As new information becomes avail-
able, changes in treatment, procedures, equipment and the use of drugs become
necessary. The authors, editors, contributors and the publisher have, as far as it
is possible, taken care to ensure that the information given in this text is accu-
rate and up-to-date. However, readers are strongly advised to confirm that the
information, especially with regard to drug dose/usage, complies with current
legislation and standards of practice. Please consult full prescribing information
before issuing prescriptions for any product mentioned in this publication.
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While it is human to err, it is inhuman not to try, if possible,
to protect those who entrust their lives into our hands
from avoidable failures and danger
Max Thorek (18801960)
Foreword
The ability to escort the cardiac patient through the pre- and post-
interventional or operative period in the intensive cardiac care unit suc-
cessfully is the most important part of a clinicians commitment. A pediatric
cardiac patient requires to be handled by an integrated group of specialists
that may include not only the surgeon, cardiologist and intensivist but a
host of other related specialities. Given this complexity, there is a need for
guidelines and protocols to be laid down and a common approach to be
followed at any institution.
There is an exhaustive amount written on cardiac intensive care as the
subject is vast and varied, but not always readily accessible. This book is a
practical reference guide with a balanced perspective that can be consulted
when faced with a challenging pediatric cardiac case or read otherwise.
It is never easy to remember pediatric doses of even common drugs and
this manual would serve as a useful aid. Newer techniques and consensus
statements have been incorporated. A number of related aspects and com-
plications have been covered which of course is highly relevant as we are
dealing with situations where in a large number of drugs are being used on
a sick child often in a background of altered milieu interior.
Writing a foreword for this book has brought to the forefront, my own
involvement of over three decades, in the surgical treatment of children
with heart disease. There have been exciting new developments occurring
in the field of intensive care all the time, however, the fundamental issues
in management have not changed greatly. Often variations in manage-
ment amongst the treating specialists are more variations in style rather
than substance, and accepted institutional norms of treatment will be of
immense benefit to our junior colleagues.
Despite the explosive growth of digital technologies, residents and fel-
lows still need that manual which is a concise and readable summary of
established clinical methods and protocols. I believe this book can stand
as one of those cornerstones of intensive care therapy of a child.
Graham Nunn FRACS

Consultant Pediatric Cardiothoracic Surgeon
Formerly, Director of Pediatric Cardiac Surgery,
Mater Childrens Hospital, Brisbane, Australia
Preface
The ability to manage a pediatric cardiac surgical patient in the pre- and
postoperative period is as important as the surgery itself. Undoubtedly, the
continued improvement in monitors, ventilators, and analyzers has made
the task easier, and the results today are better than ever before. Despite
the advancement, the precision of a medical device can only compli-
ment a clinicians knowledge and his practical abilities, and is not going
to prevent complications and errors in medical or surgical management.
So much has been written about the prevention and management of com-
plications and errors, yet there is no substitute for simple protocols, check
lists, and guidelines.
This book is an effort in that direction. It summarizes and reiterates the
accepted pre- and postoperative guidelines in the intensive care of pediat-
ric cardiac surgery patients. It has been my endeavor to prepare a practi-
cal sort of a book that can be easily read at leisure and referred to at the
bedside and provide relevant information with drug doses and protocols.
I have aimed to keep the chapters short and highly relevant thereby pro-
viding simple solutions and explanations to clinical problems rather than
offering detailed physiological explanations. Drugs relevant to the system
under consideration have been given in tables so that these can be easily
referred to at the point of care.
Drug doses have been quoted primarily from two sources, the online
pharmaceutical reference drugs.com web site (http://www.drugs.com/) and
Martindale: The Complete Drug Reference (Pharmaceautical Press, Great
Britain). Wherever applicable, the current international guidelines on the
topic under consideration have been quoted. In several of the chapters,
I have taken the liberty of mentioning a relevant quotation at the begin-
ning to provide the reader something to think about!
Even though this book is specifically written for the perioperative man-
agement of the child undergoing cardiac surgery, it will be equally useful
to physicians and nursing staff who are actively involved in the bedside
management of any acutely ill child. This book targets cardiac surgery, pedi-
atric and critical care residents working in cardiac intensive care units and
junior cardiac surgery consultants. It will address the need of a reference
x Preface
manual for general surgery and medicine residents too, while on rotation
in the cardiac care unit.
In the end, I do sincerely hope that I have been able to write something
worthwhile for the new cardiac surgeon in the making, which will in some
small way contribute to his ascent to the pinnacle of his profession. I am
sanguine that this book will also prove adequate for others involved in the
intensive care of children.
Acknowledgments
In the preparation of this manual I owe a deep debt of gratitude to many
of my colleagues from various departments at the college who spared
their valuable time to review the chapters in their areas of specialization
Drs. JK Kairi and Sharmila Sinha from the Department of Pharmacology,
Drs. Mukti Sharma and Daljit Singh from Pediatrics and Neonatogy, Drs.
Ravi Chaturvedi and Vipul Sharma from Anesthesiology, Dr. Velu Nair from
Medicine, Dr. Jyoti Kotwal from Hematology, Dr. Subroto Dutta from
Cardiology, and Dr. Gaurav Kumar from my Department of Cardiothoracic
Surgery. I am grateful to Dr. Prabel Deb for verifying the bibliography and
sources. I had the opportunity to interact with some very fine people of
the editorial staff of Elsevier, the publishers of this book, and in particular
wish to express my gratitude to Mr. Shravan Kumar, Ms. Shabina Nasim,
and Ms. Shukti Mukherjee for their professional attitude and support for
this project. I would like to thank Mr. Benjamin Jacob who was involved
with the initial conception of the book and provided the time and encour-
agement. The excellent line diagrams and ECGs were made by Mr. Nishant
Shinde from the Medical Arts Department. I guess the maximum contribu-
tion to any medical text is none other than the patient himself. He pro-
vides us not only the purpose of the text but the practical experience to go
with it. Even though I mention them last, I owe my wife and daughters so
much more than patience, cheer, and sound judgment.
Manoj Luthra
Contents
Foreword vii
Preface ix
Acknowledgments x
1 Hemodynamic Monitoring 1
2 Low Cardiac Output 15
3 Inotropes and Other Vasoactive Drugs 24
4 Congestive Heart Failure 32
5 Cardiac Tachyarrhythmias 37
6 Bradyarrhythmias and Pacemakers 63
7 Hypertensive Emergencies 78
8 Pulmonary Hypertension 83
9 Cyanotic Spells 87
10 Pediatric Resuscitation 89
11 Fluid and Electrolytes 100
12 Arterial Blood Gas Analysis 112
13 Parenteral Nutrition 124
14 Enteral Feeding 130
15 Gastrointestinal Drugs 136
16 Postoperative Respiratory Complications 140
17 Acute Respiratory Distress Syndrome 146

xii Contents
18 Postoperative Bronchospasm 150
19 Ventilation 156
20 Ventilator Associated Pneumonia 176
21 Antibiotics 182
22 Sepsis and Multiorgan Dysfunction 202
23 Systemic Antifungal Agents 211
24 Sedatives, Analgesics, and Muscle Relaxants 217
25 Seizures 227
26 Management of the Comatose Child 233
27 Acute Kidney Injury 241
28 Coagulation Disorders in the Postoperative Period 256
29 Antithrombotic Agents 267
30 Management of Anaphylaxis 273
Appendices
A International System of Units (SI Units) and Conversion Factors 277
B Vital Signs 280
C Anthropometric Measurements and Major Motor Milestones 281
D Hematological Parameters 283
E Normal Laboratory Values for Children 285
F Composition of Frequently Used Parenteral Fluids 287
G Size and Length of Pediatric Endotracheal Tubes and Suction
Catheters 289
H Postoperative Checklist on Arrival in ICU 290
I Postoperative Instructions 291
J Fluid Prescription after Open Heart Surgery 295
K Calculations of Drug Infusions 297
L Preparation of Various Concentrations of Solutions 299
M Cries Pain Scale 301
N Drug Prescription in Renal Failure 302
O Pediatric Blood Levels of Commonly Used Drugs 306
Index 307
Hemodynamic Monitoring
Everything that can be counted does not necessarily count;
everything that counts cannot necessarily be counted
Albert Einstein (1879 1955)
Isovolumic
relaxation
Isovolumic Diastasis
contraction Rapid
Ejection inflow Atrial systole
Aortic valve
opens
120 Aortic
Aortic
Pressure (mmHg)
100 valve closes

pressure
80
60 A-V valve Atrial
closes A-V valve
40 pressure
opens
20 a c v
0
Ventricular
R
P pressure
T
ECG
Q S
Fig. 1: Cardiac cycle.
Mean Arterial Pressure
The mean arterial pressure (MAP) determines the volume of blood ow to

various organs of the body. It is dependent upon the cardiac output (CO),
systemic vascular resistance (SVR), and central venous pressure (CVP)
based on the following relationship:
MAP = (CO SVR) + CVP

At normal resting heart rates, MAP can be approximately calculated by
adding one-third of the pulse pressure to the diastolic pressure:
MAP = DBP + 1 3 (SBP DBP)
(SBP: systolic blood pressure, DBP: diastolic blood pressure)
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2 Manual of Pediatric Cardiac Intensive Care
However, at higher heart rates, because of the altered shape of the arterial
pressure waveform, the MAP is approximated more closely by the arithme-
tic mean of systolic and diastolic pressures.
The 5th percentile systolic and 5th and 50th percentile mean arterial
pressure in normal children can be estimated by the following clinical
formulae:
SBP (5th percentile at 50th height percentile) = (2 age in years) + 65
MAP (5th percentile at 50th height percentile) = (1.5 age in years) + 40
MAP (50th percentile at 50th height percentile) = (1.5 age in years) + 55.
The 5th percentile SBP values have been used to dene hypotension in
various age groups.
Pulse Pressure
Systolic
120 pressure
Pulse pressure (mmHg)
Dicrotic notch
Diastolic
pressure
80
Fig. 2: Normal arterial pressure waveform.
The pulse pressure is the difference between the systolic and diastolic pres-
sures. An increase in stroke volume or vasodilatation causes widening of
the pulse pressure; examples of causes include, anemia, fever, aortic regur-
gitation, and AV malformation. A decrease in stroke volume or vasocon-
striction results in narrowing of the pulse pressure as in hypovolemia,
congestive cardiac failure, aortic stenosis, and cardiac tamponade.
Analysis of the Arterial Pressure Waveform
The arterial pressure waveform consists of an upstroke to the level of the

peak systolic pressure, and then a decline to the level of the end diastolic
pressure. The down slope is interrupted by the dicrotic notch, which is a
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Hemodynamic Monitoring 3
150
mmHg
100
Normal
50
150
mmHg
100
Overshoot
50
150
mmHg
100
Damped trace
50
Fig. 3: Systolic overshoot and damped arterial waveforms.
reection of the closure of the aortic valve. The characteristics of the pres-
sure recordings depend upon various factors:
Systolic overshoot is a false higher blood pressure reading than
the actual pressure because of the dynamic response characteristics of the
monitoring system. This may happen when there is a sudden rise in the
pressure upstroke of the wave form, as in the pressure recordings in hyper-
tension or rapid heart rates.
Damping of the blood pressure tracing abnormally narrows the pulse
pressure and should be suspected when the dicrotic notch is not visible
on the recording. Damping can be caused by air bubbles or blood in the
monitoring lines or kinking of the arterial cannula.
The level of the transducer has an effect on the blood pressure record-
ing. Transducer level above the actual level of the left atrium results in
under-estimation of the blood pressure and vice versa. (1 cm difference in
transducer level causes a 0.74 mmHg variation in the measured pressure,
i.e., a level 10 cm below will result in an overestimation of 7.4 mmHg).
Correct transducer level is more important for recording CVP and PA
pressures, since these pressures are much lower with a smaller range of
variation.
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Ascending aorta
Abdominal aorta
Radial artery
Fig. 4: Change in the arterial waveform as the arterial pulse travels peripherally.
Site of recording: The arterial pressure waveform also changes as it

travels from the central aorta to the periphery, the systolic pressure rises
and the diastolic pressure falls (i.e., the pulse pressure widens) and in
addition the dicrotic notch appears later. The MAP in the aorta is slightly
higher than in the radial artery.
Cardiac lesions: Various pathological conditions of the heart also result
in alteration of the morphology of the arterial pressure waveform:
Pulsus tardus et parvus occurs in aortic stenosis, the upstroke of the
pulse rises slowly and peaks late (tardus), the pulse amplitude is small
(parvus) with an anacrotic notch on the upstroke and an absent dicrotic
notch.
In a collapsing pulse, a large stroke volume causes the arterial pulse to
rise rapidly and an increased runoff results in a lower diastolic pressure
with a wide pulse pressure, e.g., aortic regurgitation and patent ductus
arteriosus.
In a bisferiens pulse, the arterial pressure pulse has two systolic peaks
because of the large stroke volume and a wave of reection. The
bisferiens pulse may be present in aortic regurgitation, in patients
with mixed aortic regurgitation and stenosis, and in hypertrophic
cardiomyopathy.
Pulsus alternans is recognized by the presence of alternating large
and small systolic peaks. It is a sign of severe left ventricular systolic
dysfunction and may become evident during general anesthesia.
Ventricular bigeminy also creates alternating pressure peaks in the
arterial pressure waveform, but the ECG rhythm reveals bigeminy.
In pulsus alternans, the ECG is regular with a normal QRS conguration.
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Normal pulse
Pulses tardus et parvus
Collapsing pulse
Bisferiens pulse
Pulsus alternans
Fig. 5: Different arterial waveforms in diseased conditions of the heart.
Pulsus paradoxus is an exaggeration of the inspiratory fall in systolic

arterial pressure (more than 10 mmHg) noted during spontaneous
respiration. Some inspiratory reduction of blood pressure is normal,
and pulsus paradoxus is an exaggeration of this normal phenomenon.
It is found in cardiac tamponade, constrictive pericarditis, and in
patients with airway obstruction or bronchospasm.
Baseline pressure
110
mmHg
70
0
Inspiration Expiration Inspiration
Fig. 6: Pressure variation during intermittent positive pressure ventilation.
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Blood pressure variation during positive pressure ventilation: A phe-

nomenon that is reverse of pulsus paradoxus is seen during positive
pressure ventilation due to changes in systemic venous return. During
inspiration, there is an augmentation of systolic pressure and a later
decrease in pressure during expiration (in an adult patient, up to a 5 mm
increase followed by a 5 mm fall below the baseline measured at end expi-
ration). Hypovolemia results in an increase in this variation, especially
downwards even if the systolic pressure is normal.
Analysis of the Central Venous Pressure
P T
Q S ECG
a v
c
x y
Normal JVP
a
c v
x y Cannon a wave
Giant v wave
Fig. 7: CVP waveforms and its correlation with the ECG.
The central venous pressure (CVP) is a measure of the mean right atrial
pressure, and the waveform reects the events of cardiac contraction. There
are three positive waves (a, c, and v) and two negative descents (x and y),
and these correlate with different phases of the cardiac cycle and ECG.
a wave: This wave is a reection of right atrial contraction and
immediately follows P wave on ECG.
c wave: During early ventricular contraction, there is a slight elevation
of the tricuspid valve into the right atrium resulting in the c wave. It
therefore correlates with the end of the QRS segment on ECG.
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x descent: The x descent is caused by the downward movement of the

ventricle during systole.
v wave: Right atrial lling results in the v wave.
y descent: The y descent is produced by blood ow into the right
ventricle in diastole. It therefore precedes P wave on ECG.
Central venous pressure falls slightly with spontaneous inspiration, and
increases marginally with positive pressure inspiration and forced exhala-
tion. Addition of positive end expiratory pressure (PEEP) further increases
the CVP, though this may not be signicant. (A PEEP of 10 cm H2O is
likely to increase the CVP by less than 3 mmHg).
The CVP falls because of hypovolemia, shock, and vasodilatation. It is
elevated in case of hypervolemia, increased pulmonary vascular resistance,
or right ventricular failure.
Abnormal CVP Waveforms
Trace Lesion
Cannon a waves Complete heart block, tricuspid stenosis, pulmonary hypertension,
pulmonary stenosis
Absent a waves Atrial fibrillation
Giant v waves Tricuspid regurgitation
Canon a waves are produced in AV dissociation because of contraction of

the atrium against a closed tricuspid valve. These may also be seen in tri-
cuspid stenosis, pulmonary hypertension, and pulmonary stenosis due to
resistance to RV lling.
In tricuspid regurgitation, the c wave and x descent are replaced by giant
v waves because of the regurgitation of blood into the right atrium during
ventricular contraction. This can cause a false elevation in the mean CVP.
In cardiac tamponade, the CVP is elevated and the y descent is absent.
Normal Pressures and Saturations in Pediatric Heart
Chamber Pressure (mmHg) O2 saturation (%)

Right atrium (mean) 26 6080
Right ventricle 30/3 6080
Pulmonary artery (systolic) 1525
Pulmonary artery (diastolic) 612
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Chamber Pressure (mmHg) O2 saturation (%)

Pulmonary artery (mean) 15
Left atrium (mean) 612 97100
Left ventricle 100/6 97100
Aorta 100/60 97100
Left ventricular end diastolic pressure (LVEDP) is a reection of LV function,

and in the absence of mitral valve disease the LVEDP is equal to the left
atrial pressure (LAP). Further, if there is no obstruction in the pulmonary
venous or capillary blood circulation, the LAP will equal the pulmonary
capillary wedge pressure (PCWP). Therefore, the LAP or PCWP is used to
monitor left heart function in addition to the volume status of the patient.
The LAP can be measured by a direct LA line placed at surgery, and the
PCWP can be measured by a pediatric Swan Ganz catheter (4-5 F).
Right ventricle Pulmonary artery

25
20
mmHg
15 Wedge
10
Right atrium
5
0
Fig. 8: Pressure trace in various locations on the right side of the heart.
Central venous pressure is equal to the right atrial pressure and right
ventricular end diastolic pressure (RVEDP) provided there is no obstruc-
tion to central venous return (e.g., SVC syndrome, IPPV with high airway
pressures) or tricuspid valve disease and is a reection of the RV function
and the volume status of the patient.
Pulmonary artery pressure provides objective evaluation of pulmonary
hypertension and can be measured by a thermistor PA catheter or a Swan
Ganz placed via a large vein or by a direct PA catheter placed at surgery.
A continuous postoperative recording is useful in the management of
children with pulmonary artery hypertension.
Systemic Arterial Oxygen Saturations
In normal individuals, systemic arterial oxygen saturation (SpO2) is

97100% and systemic venous oxygen saturation (SvO2) is 6080%. The
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100
98
100 97
91
90 90
80
70
60
SpO2 (%)
50
40
30
20
10
27
0
0 10 20 30 40 50 60 70 80 90 100
PaO2 (mmHg)
Fig. 9: Normal oxygen dissociation curve (Centre graph) with shift to the left and right.
SpO2 varies with the partial pressure of oxygen, but the relationship is not
linear and is described by the oxygen dissociation curve. The implication
of the sigmoid shape of the oxygen dissociation curve is that at the lower
and upper end of the curve, i.e., at PaO2 of less than 20 mmHg and more
than 60 mmHg, a signicantly large change in PaO2 results in little change
in SpO2. At PaO2 range of 2060 mmHg, a small change in PaO2 results in
a marked change in SpO2.
Provided the patients pH is normal, one can approximately estimate
the PaO2 from the recorded SpO2 by the rule of 4-5-6, 7-8-9.
1. SpO2 of 90% : 60 mmHg PaO2
However, with a shift of the oxygen dissociation curve to the left
( pH, temperature, PaCO2) there is an increased afnity of hemo-
globin for oxygen and the same O2 saturation implies a lower PaO2. With
a shift of the curve to the right ( pH, temperature, PaCO2), there is a
decreased afnity for oxygen and with the same O2 saturation, the PaO2 is
higher.
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Systemic Venous Oxygen Saturation
Causes Remark
Decreased SvO2 Decreased oxygen supply Hypoventilation, pulmonary edema,
atelectasis, anemia, residual intracardiac
RL shunt.
Increased oxygen demand Fever, pain, shivering, arrhythmia, cardiac
failure.
Decreased cardiac output
Increased SvO2 Increased oxygen supply Mechanical ventilation, PEEP, sedation,
anesthesia.
Decreased oxygen demand Inotropic support, tachycardia.
Increased cardiac output
Systemic venous oxygen saturation (SvO2, normal range: 6080%) can be

monitored continuously with a specialized PA catheter or in vitro, with
blood samples obtained from the right atrium or superior vena cava.
SvO2 monitoring provides assessment of tissue oxygenation. It shows
whether the oxygen supply is adequate to meet the tissue demands and is
thus a non-specic indicator of the cardiac output.
Hemodynamic Calculations
Calculation Child normal Adult normal

values values
Cardiac output (CO) CO = Stroke volume At birth: 56 L/min
heart rate 300400 mL/kg/min
Cardiac index (CI) Cardiac output 3.04.5 L/min/m2 2.74.3 L/min/m2
CI =
BSA
Systemic vascular MAP CVP 12002800 10001300
SVR = 80
resistance (SVR: CO dynes-sec-cm5 dynes-sec-cm5
dynes-sec-cm5)
Pulmonary vascular MPA PCWP 40320 150250
PVR = 80
resistance (PVR: CO dynes-sec-cm5 dynes-sec-cm5
dynes-sec-cm5)
MAP: mean arterial pressure, CVP: central venous pressure, MPA: mean pulmonary artery pressure, PCWP: pulmonary
capillary wedge pressure, BSA: body surface area.
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Cardiac Output
Cardiac output (liters/minute) is dened as the amount of blood ejected
from the left ventricle in 1 minute. Stroke volume (SV) is the amount of
blood ejected from the left ventricle with each beat.
CO = Stroke volume (SV) Heart rate (HR)
Stroke volume = End diastolic volume (EDV)
End systolic volume (ESV)
Ejection fraction (EF) = (SV/EDV) 100%
The average cardiac output for an adult is about 56 liters per minute at
rest and the stroke volume 5080 mL per beat.
Cardiac output can be measured by a number of clinical methods
ranging from intracardiac catheterization to non-invasive assessment
of the arterial pulse. The standard method of measuring CO used in the
laboratory is by the Ficks oxygen consumption method, which requires
measurement of:
1. O2 consumption per minute using a spirometer,
2. The arterial O2 content of peripheral arterial blood,
3. The mixed venous O2 content from a sample of blood taken from the
pulmonary artery.
Then,
O2 consumption
CO =
(Arterial O2 content Venous O2 content)
Arterial O2 content Venous O2 content is also known as the arterio-venous

oxygen difference. The arterial and venous oxygen content of the blood
can be calculated from the fact that the oxygen in the blood is bound to
hemoglobin and that one gram of hemoglobin can carry 1.34 mL of O2
and a small amount of oxygen is in a dissolved state.
O2 content of blood = [Hb (g/dL) 1.34 % saturation of blood] +
[0.0032 Partial pressure of O2 (mmHg)]
At the bedside, the cardiac output can be calculated by the thermodilution
technique, using a cardiac output computer after placing a thermistor PA
catheter or a pediatric Swan Ganz catheter (4-5 F).
Systemic Vascular Resistance

An abnormally high SVR indicates peripheral vasoconstriction (e.g., in
response to hypovolemia or inotropes). An abnormally low SVR reects
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peripheral vasodilation (e.g., in septic shock or as a result of administra-

tion of vasodilator drugs).
Pulmonary Vascular Resistance

Normal PVR is approximately one-sixth of the SVR. PVR may be abnor-
mally high in cardiac disease associated with pulmonary hypertension, in
lung disease, pulmonary embolism, acidosis or hypoxia.
Calculation of Shunts
BODY BODY
AO SVC/IVC AO SVC/IVC
LR
LV RA LV RA
LA RV LA RV
PV PA PV PA
LUNGS LUNGS
Fig. 10: Line diagram of normal circulation (L); Circulation in LR shunt (R). AO: aorta,
SVC: superior vena cava, IVC: inferior vena cava, RA: right atrium, RV: right ventricle,
PA: pulmonary artery, PV: pulmonary veins, LA: left atrium, LV: left ventricle.
Qp (SpO2 MVO2 )
=
Qs (PVO2 PAO2 )
Qp: pulmonary blood ow, Qs: systemic blood ow, SpO2: systemic arterial
O2 saturation, MVO2: mixed venous O2 saturation (MVO2 is the average of
SVC, IVC, and RA saturation and the average of SVC and IVC saturations, in
case of VSD), PVO2: pulmonary venous O2 saturation (assumed 98% if not
measured), PAO2: pulmonary artery O2 saturation.
The ratio of pulmonary to systemic blood ow (Qp/Qs) is used to

quantify the shunt. Oxygen saturation of blood samples obtained from
various cardiac chambers are used to calculate pulmonary and systemic
blood ow as noted in the formula above. The shunt can also be calculated
ERRNVPHGLFRVRUJ
more accurately by obtaining systemic and pulmonary blood ows by the

Ficks method. Qp/Qs > 1.5:1.0 is a signicant shunt.
In the normal circulation, the systemic and the pulmonary circulation
are in series. The blood which is ejected into the aorta, returns to the right
heart via the SVC/IVC and then is pumped into the pulmonary circulation.
Thus, the pulmonary blood ow is equal to the systemic blood ow.
In LR shunt, part of the systemic blood ow bypasses the systemic
circulation and ows directly into the pulmonary part of the circulation
with every cycle, so that the systemic circulation is depleted of this blood
and the pulmonary circulation has this additional amount of blood ow.
Therefore, the effective pulmonary blood ow in:
Left-to-right shunt = Systemic blood ow + Shunt ow
Right-to-left shunt = Systemic blood ow Shunt ow.
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[Updated: 2005 Apr 21; cited: 2011 Oct 15] Available at: http://www.healthsystem.virginia.
edu/internet/anesthesiology-elective/cardiac/cvpwave.cfm.
9. Lpez-Herce J, Bustinza A, Sancho L, et al. Cardiac output and blood volume parameters
using femoral arterial thermodilution. Pediatr Int 2009;51:5965.
10. Mark JB, Slaughter TF, Reeves JG. Cardiovascular monitoring. Practice Guidelines for
Perioperative Transesophageal Echocardiography and Practice Guidelines for Pulmonary
Artery Catheterization. Churchill Livingstoine. 1979 [Updated: 2000; cited: 2011 Feb 22]
Available at: http://web.squ.edu.om/med-Lib/MED_CD/E_CDs/anesthesia/site/content/v03/
030267r00.HTM
11. McGhee BH, Bridges EJ. Monitoring arterial blood pressure: what you may not know. Crit Care
Nurse 2002;22:604, 6670, 73 passim.
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tation. In: Fuster V, Alexander RW, ORourke RA eds. Hursts The Heart Vol 1. The McGraw-Hill
Companies Inc; 2004:21794.
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13. Powell FL Jr. Oxygen and carbon dioxide transport in the blood. In: Johnson LR ed. Essential
Medical Physiology 3rd ed. California, USA: Academic Press. An Imprint of Elsevier; 2003:28998.
14. Salyer JW. Neonatal and pediatric pulse oximetry. Respir Care 2003;48(4):38696.
15. Schlame M, Blanck TJJ. Cardiovascular system. In: Gabrielli A, Layen AJ, Yu M eds. Civetta,
Taylor & Kirbys Critical Care 4th ed. Philadelphia: Lippincott Williams and Wilkins; 2009:68299.
16. Tamer DM, Watson DD, Kenny PP, et al. Noninvasive detection and quantification of left-to-
right shunts in children using oxygen-15 labeled carbon dioxide. Circulation 1977;56:62631.
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Low
Cardiac Output
The heart is the chief mansion of the soul, the organ of vital capacity,
the beginning of life, the foundation of the vital spirits the rst to live,
the last to die
Ambroise Par (15101590)*
Clinical Evaluation of Low Cardiac Output
Parameter Normal perfusion Low cardiac output

Skin Warm, brisk capillary fill Sluggish capillary refill (>34 sec),
mottled appearance, peripheral
cyanosis
Color of mucous membranes Pink Pallor
Temperature Normal Cool periphery, core
temperature >39C
Heart rate As per age Tachycardia
Blood pressure As per age BP, narrow pulse pressure
respiratory variation of BP in
hypovolemia
Urine output Normal Oliguria, anuria
Neurological status Age appropriate activity Irritable, lethargic
Feeding Eats well/strong sucking Weak sucking reflex, tires during
reflex feeding
GIT Normal gastric tube aspirate, abdominal
distension, later jaundice, liver
enzymes
Hydration Normal Sunken fontanelle, poor skin
turgor, dry mucous membranes in
prolonged hypovolemia
CVP/LAP 26 mmHg/612 mmHg in hypovolemia, CVP in
RV failure
Mixed venous saturation 6080% <60%
Serum electrolytes Normal Metabolic acidosis
BP: blood pressure, CVP: central venous pressure, LAP: left atrial pressure, RV: right ventricle.
*Ambroise Par was the official surgeon to four French kings. He is known as the father of
modern surgery for his numerous innovations in operative methods.
ERRNVPHGLFRVRUJ
Skin, Temperature, and Peripheral Pulses

Early signs of low cardiac output include tachycardia, peripheral cooling,
and prolonged capillary rell times (>34 sec). Absent pulses, mottling of
the skin, and peripheral cyanosis are late signs.
Blood Pressure
In the initial phases of low cardiac output, the blood pressure may be well
maintained by vasoconstriction. In hypovolemia, even though the blood
pressure is normal, a narrow arterial pulse pressure (<15 mmHg in small
children)which is associated with an increased variation of the systolic
blood pressure with respirationis an early sign. Hypotension becomes
evident when the loss in the circulating volume can no longer be compen-
sated by tachycardia and vasoconstriction (decompensated shock).
Urine Output
Urine output gradually diminishes, and oliguria (urine output <0.51 mL/kg/h)
progresses to anuria.
CNS Manifestations
Neurological deterioration becomes apparent with low cardiac output;
the child initially becomes irritable, then lethargic, and subsequently
unresponsive.
GIT
Impaired gastrointestinal perfusion causes feeding intolerance, abdominal
distension, and increased feeding tube aspirate because of paralytic ileus.
Over a period of time, there may be mild jaundice with elevation of hepatic
enzymes.
Dehydration
Signs of dehydration eventually become apparent in children in whom the
cause of low cardiac output is hypovolemia.
ERRNVPHGLFRVRUJ
Low Cardiac Output 17
Filling Pressures
CVP and LAP levels depend on the cause of the low cardiac output. Both
are low in a volume depleted patient (hemorrhage, vasodilatation).
Mixed Venous Saturation

Mixed venous saturation is low due to excessive oxygen extraction (i.e.,
<60%).
Biochemistry
Biochemical parameters reveal metabolic acidosis and elevation of serum
lactate levels (normal 12 mmol/L).
Septic Shock
The clinical manifestations are different in patients with vasodilatory

shock (sepsis or anaphylaxis). These patients initially have a normal or
high cardiac output and low systemic vascular resistance. They present with
brisk capillary rell, bounding pulses, and a warm periphery. The classical
signs of low cardiac output appear subsequently.
Factors Controlling Cardiac Output
Parameter Factors increasing CO Factors decreasing CO

Heart rate HR results in CO within a range / HR beyond a point
Preload High (to a limit) Low
Atrial kick Present Absent (e.g., atrial fibrillation)
Afterload Low High
Myocardial contractility Inotropes Ischemic/non-compliant
myocardium
CO: cardiac output, HR: heart rate.
Heart Rate
In general, the heart rate (HR) and cardiac output (CO) have a direct relation-
ship up to a maximum heart rate. As the HR increases, so does CO up to a
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point, depending upon the age of the patient and the state of the myocardium.
Beyond this point, a rise in HR results in a fall in CO because of increased
myocardial oxygen consumption and a shorter ventricular lling time. With
a diseased myocardium, the ability to increase CO with an increasing HR
is restricted compared to the normal myocardium. On the other hand, in
such a ventricle, the cardiac output also falls more rapidly with a decrease
in HR. The non-compliant ventricle is unable to compensate for changes
in preload associated with changes in heart rate.
Cardiac output
0 50 100 200 250

Heart rate
Fig. 1: Relationship of heart rate and cardiac output.
Stroke Volume
Stroke volume is dependent on the preload, afterload, and myocardial
contractility.
FrankStarling Law
Cardiac output
End diastolic volume

Fig. 2: FrankStarling law. Relationship of cardiac output and end diastolic volume.
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The FrankStarling law of the heart states that the more the myocardial mus-
cle ber is stretched in diastole, the more forceful will be the next systolic
contraction. In other words, an increase in the end diastolic volume or
preload results in an increase in the stroke volume. This is sustained only
until a physiological limit has been reached thereafter any further increase
in ber length will cause the force of contraction to decline.
Preload
Normal
heart
Contractility
Diseased
heart
12
Left ventricular end diastolic pressure (mmHg)
Fig. 3: Relationship of contractility and left ventricular end
diastolic pressure.
The stroke volume generated by the heart varies with the end diastolic vol-
ume or preload of the heart (FrankStarling law). At the bedside, it is not
feasible to measure the ventricular end diastolic volume hence the end
diastolic pressure is used as a measure of the preload.
The actual relationship between end diastolic volume and end diastolic
pressure is however not linear and is dependent upon the compliance of the
cardiac muscle. With normal compliance, relatively large increase in vol-
ume causes only a small elevation in pressure. Whereas in a non-compliant
ventricle, a small increase in volume causes a greater rise in pressure.
Thus, when one compares the left ventricular end diastolic pressure/
contractility curves of the diseased heart with that of the healthy heart, it is
noted that the diseased heart requires higher pressures to achieve the same
preload and contractility.
Also note that the atrial kick contributes up to 35% of the preload, espe-
cially in children. Atrial brillation can reduce cardiac output by the loss of
this atrial contribution.
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Afterload
60 Normal
Stroke volume (mL)
40 Increased
afterload
20
0
0 5 10 15 20 25
Left ventricular end diastolic pressure
Fig. 4: Relationship of stroke volume and left ventricular end diastolic pressure.
Afterload refers to the pressure that the ventricle must overcome to eject its
blood volume. Afterload is determined by a number of factors, including
the wall thickness of the ventricle, the diastolic blood pressure, and the sys-
temic vascular resistance or the pulmonary vascular resistance in the case of
the right ventricle. Afterload has an inverse relationship with the stroke
volume. As resistance increases, the force of contraction and stroke volume
decreases and this is more evident when there is myocardial dysfunction.
Causes of Low Cardiac Output in the Postoperative Period
1. Rhythm disorders
Severe bradycardia/tachycardia
Arrhythmias, e.g., AF, heart block, ventricular arrhythmias
2. Decreased LV preload
Hypovolemia/vasodilatation
Cardiac tamponade
RV dysfunction/pulmonary hypertension/high PEEP/tension
pneumothorax
3. Increased afterloadacidosis/hypothermia/-adrenergic agents
4. Poor myocardial contractility
Cardiac failure
Myocardial stunning
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Electrolyte/acidbase disorder, e.g., acidosis, hypokalemia,

hypocalcemia, hypoxia
Sepsis
Diagnosis
CVP LAP SVR CI

Hypovolemia
Cardiac failure LAP is low in isolated right heart failure
Septic shock Initially increases CO initially maintained by increased
then falls heart rate
Tamponade Equalization of diastolic pressure in all
chambers
CVP: central venous pressure, LAP: left atrial pressure, SVR: systemic venous resistance, CI: cardiac index,
LAP: left atrial pressure, CO: cardiac output.
An elevated CVP suggests RV dysfunction, increased pulmonary vascular

resistance, or cardiac tamponade; in the absence of any of these disorders,
the CVP is a reection of the volume status of the patient.
An increased LAP shows left ventricular dysfunction and is normal in
isolated right heart failure. Like the CVP is used to assess the volume status
of the patient, the LAP is the appropriate monitor of the LV preload pro-
vided the LV function is normal (or adequate allowance needs to be given
for a raised LAP because of LV dysfunction).
In hypovolemia both the CVP and LAP are low and are associated with
other features of low cardiac output.
Pulmonary hypertension may cause low cardiac output by affecting left-
sided preload. When severe pulmonary hypertension or right ventricular failure
is the cause of low cardiac output, the CVP will be raised, while the LAP is
low/normal.
In cardiac tamponade, there is equalization of the CVP, LAP, and diastolic
pressures of the LV and RV. Oliguria, peripheral cooling, and other signs of
low cardiac output become evident. If the tamponade is caused by a collection
of blood in the pericardium, there is also a fall in the hematocrit. ECG,
x-ray chest, and 2-D echocardiography will conrm the diagnosis.
Management
Transient postoperative cardiac dysfunction and low CO after cardiopul-

monary bypass (CPB) is not unexpected. Typically, cardiac output is ade-
quate immediately after surgery and then gradually declines to reach its nadir
ERRNVPHGLFRVRUJ
812 hours after surgery. With appropriate management, the CO recovers

in the next 24 hours or so.
Cardiac output is monitored by an assessment of the clinical signs, urinary
output, acidbase status, and mixed venous saturations. Blood pressure
may not be a true reection of CO if it is being maintained by an increased
SVR. Invasive monitoring (Swan Ganz/pulmonary artery catheters) of CO
may not be feasible in small children.
1. Optimize Preload
LAP is a reection of LV contractility and preload. The early phase
after CPB is associated with a decrease in compliance of the ventricles,
which may require a higher LA pressure for adequate preload to be
maintained. The optimum LA pressure that augments the CO may
therefore be higher than normal. Raising the LA pressure beyond this
point may however, decrease the CO (FrankStarling law) and also
cause pulmonary edema. In the absence of an LA line, CVP is used as a
guide to uid therapy.
Preload is optimized by repeated uid boluses of 510 mL/kg based
on the LAP/CVP and the clinical parameters. Fluid administered may
consist of FFP, 5% albumin, or crystalloids. There is no evidence-based
support for one type of uid over another.
2. Inotrope and Vasodilator Agents
Blood pressure SVR Indicated drugs
Low Low Adrenaline/dopamine (in a dose
>5 mcg/kg/min)/noradrenaline
Low Normal/high Dopamine (in a dose <5 mcg/kg/min)
Dopamine + milrinone
Adrenaline + milrinone
Normal Low/normal/high Dobutamine/milrinone
High High NTG (labetalol/esmolol in severe
hypertension)
SVR: systemic vascular resistance, NTG: nitroglycerin.
After the LA pressure has been optimized, the need for inotrope/
vasodilator therapy is dictated by the blood pressure and SVR. Poor
capillary rell, acidosis, and a cool periphery are signs of peripheral
vasoconstriction. A core temperature over 39C is also a reection of
high SVR, because of the inability of the vasoconstricted periphery to
dissipate heat. In the presence of a low blood pressure and a high SVR,
in addition to a -1 agonist (dopamine, adrenaline), a vasodilator
is indicated (milrinone, dobutamine, NTG). A low blood pressure
associated with a low SVR requires therapy with a drug with -1,
-1 action (adrenaline, noradrenaline, dopamine).
ERRNVPHGLFRVRUJ
Various institutions have different inotrope preferences. In the

immediate postoperative period, some degree of cardiac dysfunction
is anticipated and the SVR is also likely to be increased secondary
to a number of factors including hypothermia, pain, and drugs.
Therefore, the heart is supported with a predominantly -1 agent
(low dose dopamine or adrenaline.) and the after load is reduced by
a vasodilator (milrinone/NTG). Alternatively, dobutamine (which has
-1 and -2 activity) may be used alone to support the heart.
Bibliography
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Rev Hosp Clin Fac Med S Paulo 2002;57(3):11523.
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2002;25(3):6371.
3. Doyle AR, Dhir AK, Moors AH, et al. Treatment of perioperative low cardiac output syndrome.
Ann Thorac Surg 1995;59:S311.
4. Haque IU, Zaritsky AL. Analysis of the evidence for the lower limit of systolic and mean arterial
pressure in children. Pediatr Crit Care Med 2007;8(2):13844.
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cardiac output syndrome in infants and children after corrective surgery for congenital heart
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2003;79(Suppl 2):S213S22.
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poreal life support: What is feasible? Ann Pediatr Cardiol 2010;3(2):14758.
8. Mass L, Antonacci M. Low cardiac output syndrome: identification and management. Crit
Care Nurs Clin North Am 2005;17(4):37583.
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artery bypass. J Thorac Cardiovasc Surg 1996;112:3851.
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Yamashiroya VK, eds. Case Based Pediatrics for Medical Students and Residents. Department of
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Inotropes and
Other Vasoactive Drugs
Life is short and art is long; the crises is eeting, experience risky, decision dicult
Hippocrates (460377 BC)
Adrenergic Receptors
Receptor Tissue Action of agonist Agonists/antagonists

1 Heart Heart rate, contractility Agonists: noradrenaline,
and A-V conduction adrenaline, isoprenaline,
Cardiac output dobutamine
Antagonists: metoprolol,
atenolol
2 Blood vessels of Vasodilatation Agonists: salbutamol,
skeletal muscles and Bronchodilation isoprenaline, levalbuterol,
liver. Smaller coronary terbutaline
vessels Antagonists: propranolol
Smooth muscle of Relaxation of intestine,

bronchi, bladder, uterus, bladder
uterus, intestine
1 Blood vessels of skin, Vasoconstriction Agonists: noradrenaline,
GIT, kidney adrenaline, phenylephrine
Contraction
Antagonists:
Smooth muscle (Contraction of ciliary
phenoxybenzamine,
of ureter, uterus, body causes mydriasis)
phentolamine
bronchioles, ciliary body
2 Sphincters of the Contraction of the Agonists: clonidine,
gastrointestinal tract, sphincters of the GIT dexmedetomidine
bladder and bladder Antagonist: phentolamine
The actions of adrenergic drugs are based on the type of receptors the
drugs act upon. The clinically relevant types of receptors are 1, 2, 1, 2,
and dopaminergic () receptors.
Myocardial adrenergic receptors are of 1 type, and stimulation of these
leads to increased heart rate, AV conduction, myocardial contractility, and
cardiac output.
ERRNVPHGLFRVRUJ
Inotropes and Other Vasoactive Drugs 25
Blood vessels supplying the skin, GIT, and kidneys have 1 receptors,
while skeletal, hepatic, and smaller coronary vessels predominantly pos-
sess 2 receptors. Stimulation of 1 receptors causes vasoconstriction and
increase in venous return, while 2 stimulation results in vasodilatation
and a decrease in venous return.
During adrenergic stimulation, both and receptors are activated
leading to decreased blood supply to skin, GIT, and kidneys and increased
blood to the skeletal and cardiac musculature. 2 stimulation also causes
bronchodilatation. This constitutes the ght and ight reaction, which
diverts blood to the organs important in such a response.
Vasoactive Agents: Dose and Hemodynamic Actions
Agent Dose Site of action Effect

Dopamine 0.52.5 mcg/kg/min IV infusion RBF
2.57.5 mcg/kg/min IV infusion , 1 CO, HR
7.520 mcg/kg/min IV infusion 1, 1 CO, HR, SVR,
MAP, RBF
Dobutamine 120 mcg/kg/min IV infusion 1, 2 CO, HR, SVR,
MAP, RBF
Isoproterenol 0.052 mcg/kg/min IV infusion 1, 2 CO, HR, SVR,
MAP
Adrenaline <0.025 mcg/kg/min IV infusion 1, 2 CO, HR, SVR
0.0251 mcg/kg/min IV 1, 1 CO, HR, SVR,
infusion MAP, RBF
Noradrenaline 0.051 mcg/kg/min IV infusion 1, 2, 1 CO, HR, SVR,
MAP, RBF
Phenylephrine Children: 520 mcg/kg/dose 1, 2 HR, SVR, PVR,
slow IV bolus, can be repeated MAP
every 1015 min
Alternatively, 100 mcg/kg/dose
IM/SC can be repeated every
12 h up to a max of 5 mg
Adults: 100500 mcg slow
IV bolus
Sodium 0.510 mcg/kg/min IV infusion Nitric oxide SVR, CO, MAP
nitroprusside mediated vasodilator
(arterial > venous)
Nitroglycerin 120 mcg/kg/min IV infusion Nitric oxide SVR, CO, MAP
(NTG) mediated vasodilator
(venous > arterial)
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Agent Dose Site of action Effect

Milrinone 2550 mcg/kg bolus over Phosphodiesterase-3 CO, HR, SVR
10 min, infusion 0.250.75 mcg/ inhibitor
kg/min
Vasopressin 0.00030.006 units/kg/min Vasoconstrictor and SVR, MAP
antidiuretic effect
Alprostadil 0.052 mcg/kg/min IV infusion Prostanoid receptors SVR, maintains
(PgE1) patency of ductus
arteriosus
Epoprostenol 0.516 ng/kg/min Causes vasodilatation SVR and PVR,
(PgI2, and inhibits platelet CO
prostacyclin) aggregation
RBF: renal blood flow, CO: cardiac output, HR: heart rate, SVR: systemic vascular resistance, MAP: mean arterial
pressure, PVR: pulmonary vascular resistance.
Dopamine, in a dose of less than 2.5 mcg/kg/min, has a selective

dopaminergic effect on the renal blood ow, which increases urine output.
In doses of 2.57.5 mcg/kg/min, dopamine also acts on 1 receptors to
increase the cardiac output. It may, however, cause unpredictable tachycar-
dia. In higher doses, in addition to 1 effects, it has an effect on 1 recep-
tors, which causes an increase in SVR and afterload.
Dobutamine is a selective agent (1 action > 2), it therefore increases
the cardiac contractility, heart rate, and cardiac output with some decrease
in SVR. The degree of tachycardia is variable. The reduction in SVR may
rarely cause hypotension, and thus dobutamine is not indicated by itself in
a hypotensive patient.
In patients with poor LV function but without signicant hypotension,
dobutamine (1, 2 action) is superior to dopamine (1, 1 action) as dob-
utamine decreases the afterload and preload, and results in an improvement
in myocardial function. However, in patients with poor LV, severe hypotension
and high SVR, dopamine or adrenaline used in combination with a vasodila-
tor (NTG/nitroprusside/milrinone/dobutamine) may be more appropriate.
Isoproterenol acts on 1 and 2 receptors. It causes signicant increase in
heart rate in addition to increasing the force of contraction and bronchodila-
tion. It is therefore used in complete heart block to increase the ventricular rate,
overdose of beta-blocker, or severe bradycardia unresponsive to atropine. It is
administered in a dose of 0.052 mcg/kg/min by IV infusion or as 520 mcg IV
bolus (Adult dose: 220 mcg/min IV infusion; 2060 mcg IV bolus).
Adrenaline in low doses (<0.025 mcg/kg/min) stimulates the 1 and 2
receptors. The 1 action increases the heart rate, force of contraction, and
cardiac output. 2 stimulation results in a fall in SVR, but the mean arterial
pressure is maintained or increased due to the increase in cardiac output. As
the dose is increased, 1 receptors are stimulated causing vasoconstriction
of the vascular beds increasing the SVR and the blood pressure signicantly.
ERRNVPHGLFRVRUJ
The 2 properties of adrenaline produce bronchodilatation and an eleva-

tion in the blood sugar level because of glycogenolysis.
Noradrenaline is a potent 1 stimulant, which causes increased SVR
with the smallest dose. The moderate 1 action increases the heart rate,
force of contraction, and cardiac output. However, it is less likely to
cause tachycardia than adrenaline. It is indicated in systemic hypotension
because of vasodilatory shock (sepsis, trauma, cardiopulmonary bypass, or
spinal block), which does not respond to volume expansion and adrena-
line or dopamine. Since it acts by increasing the afterload, it may not be
appropriate for use in patients with poor LV function. Blood supply to
kidneys and periphery may be reduced.
Phenylephrine is a selective -receptor (1 and 2) agonist and results
in increased SVR and increased BP without any direct action on the
myocardium. The heart rate may decrease because of reex action.
Sodium nitroprusside is a direct acting vasodilator of both arteries
and veins (arteries > veins). The arterial vasodilator effects are prompt and
manifest at low doses. It causes fall in blood pressure, but the cardiac out-
put is increased due to afterload reduction. The pulmonary artery pressure
falls but may show a rebound increase when treatment is withdrawn. High
doses or prolonged use can result in cyanide or thiocyanate toxicity.
Cyanide toxicity and thiocyanate toxicity are breakdown products of
sodium nitroprusside (SNP) metabolism in the body. Cyanide in excess
interferes with cellular oxygen utilization, and clinical features of toxic-
ity are known to occur with cumulative doses of SNP of >0.5 mg/kg/h.
Cyanide toxicity is more likely if hepatic dysfunction is present; thiocy-
anate is cleared by the kidney and toxicity is more likely if there is renal
dysfunction or with prolonged infusion.
An early sign of cyanide toxicity is increasing resistance to doses of
nitroprusside (tachyphylaxis). Subsequent clinical features include meta-
bolic acidosis, tachycardia, hypertension, cardiac arrhythmias, CNS dys-
function, metabolic acidosis, and increased mixed oxygen saturation (as a
result of the inability to utilize oxygen). Treatment consists of mechanical
ventilation with 100% oxygen and administration of sodium thiosulfate
(150 mg/kg over 15 min) or 3% sodium nitrite (5 mg/kg over 5 min).
Manifestations of thiocyanate toxicity include abdominal pain, vomit-
ing, weakness, tinnitus, tremor, agitation, progressing to lethargy, seizures
and coma. Treatment requires clearance of excess thiocyanate by dialysis.
NTG causes venodilatation more than arteriolar dilatation. This results
in a decrease in LV lling pressure (preload) relatively more than systemic
vascular resistance (afterload). As low-dose infusions are titrated upward,
the earliest response is a decrease in cardiac lling pressures (i.e., CVP
and LAP) with little or no change in cardiac output. As the dose rate is
increased further, the cardiac output begins to rise as a result of progressive
arterial vasodilatation. Further increases in the dose rate will eventually
produce a drop in blood pressure.
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Milrinone is an inodilator and has an inotropic effect on the heart, and

a dilator effect on the circulation, which signicantly decreases the SVR and
PVR. It increases the CO with little effect on HR and myocardial oxygen
demand. Milrinone has a longer half-life than dobutamine and is very use-
ful in pulmonary HTN. It is administered with a loading dose followed by a
continuous infusion. Reductions in infusion rate may be necessary in patients
with renal impairment and should not be used in patients with a creati-
nine >2.5. It has a long half-life and if not excreted by the kidneys can cause
severe hypotension and right sided heart failure. Milrinone in combination
with adrenaline or dopamine is advocated in the management of low cardiac
output in the postoperative cardiac patient with pulmonary hypertension.
Vasopressin is a potent vasopressor that may be used in several forms
of shock, notably septic shock. The vasoconstrictive action of vasopressin
is mediated through V1 receptors in the vessels of the skin, skeletal mus-
cle, and small intestines. In recommended doses, blood ow to the coro-
naries, cerebral, pulmonary, and renal vascular beds, is preserved. It leads
to increase in blood pressure, decrease in heart rate, and reduction in the
dose requirements of other catecholamines. It has an antidiuretic effect,
which is mediated through V2 receptors in the capillaries at the renal distal
tubules and collecting ducts, which causes increased reabsorption of water
to augment systemic blood volume.
High doses of vasopressin cause intense vasoconstriction, which can
result in gangrene of the tips of ngers and toes, and ischemia of other
organs, including the gastrointestinal tract and kidneys. Extravasation
may result in tissue necrosis. Other complications include arrhythmias,
hyponatremia, thrombocytopenia and bronchial constriction. The half-
life of vasopressin is 1035 minutes, and its vasoconstrictive effect can be
counteracted by vasodilators, such as nitroglycerin or nitroprusside.
Alprostadil (PgE1) is indicated in infants with congenital heart defects and
a duct dependant pulmonary or systemic circulation to keep the ductus tem-
porarily open. Infants with decreased pulmonary blood ow will respond with
an increase in PaO2, and infants with diminished systemic blood ow will
show an improvement in the blood pressure and a decrease in the acidosis.
Alprostadil injection should be infused for the shortest time and at the
lowest dose that produces the desired result. Apnea has been reported in
about 12% of the neonates on alprostadil infusion. Other adverse reac-
tions include fever, irritability, seizures, hypotension, thrombocytopenia,
cerebral bleeding, and gastric outlet obstruction when the duration of
infusion has exceeded 120 hours.
Infusion is started at 0.050.1 mcg/kg/min. It may be necessary to
increase the dose to obtain a therapeutic response. After an adequate
response, the infusion rate is reduced to provide the lowest possible dos-
age (0.010.025 mcg/kg/min) to maintain the response. (500 mcg of
alprostadil is added to 50 mL saline/dextrose for infusion).
ERRNVPHGLFRVRUJ
Epoprostenol (PgI2, prostacyclin) is a prostaglandin that causes

vasodilatation of the vascular beds, including the pulmonary and cerebral
circulation, and is a potent inhibitor of platelet aggregation. There is a fall
in the mean systemic and pulmonary artery pressures and a decrease in the
SVR and PVR. Indications for its use include long-term intravenous treat-
ment of primary pulmonary hypertension and for the management of pul-
monary hypertension secondary to congenital heart diseases and congenital
diaphragmatic hernia. It is initiated at the rate of 0.52 ng/kg/min and
increased by 0.51 ng/kg/min every 3060 min until dose limiting clinical
effects are noted or to a maximum of 16 ng/kg/min. Symptoms of over-
dose include ushing, headache, hypotension, tachycardia, nausea, vom-
iting, and diarrhea, which require the dose to be reduced. Epoprostenol
enhances the hypotensive effects of other vasodilators and increases risk of
bleeding with anticoagulants and other antiplatelet agents.
Method of Preparation of Infusion and Dose Calculation
Two alternative methods of drug formulation that allow for ease of cal-
culations are described below. Various formulas for dose calculation are
given in Appendix K.
Method 1
Drug Formulation Method of dose calculation
Dopamine/dobutamine 3 mg/kg in 50 mL 1 mL/h = 1 mcg/kg/min
15 mg/kg in 50 mL 1 mL/h = 5 mcg/kg/min
Adrenaline/noradrenaline/ 0.3 mg/kg in 50 mL 1 mL/h = 0.1 mcg/kg/min
isoprenaline
NTG/sodium nitroprusside 3 mg/kg in 50 mL 1 mL/h = 1 mcg/kg/min
Milrinone 0.75 mg/kg in 50 mL 1 mL/h = 0.25 mcg/kg/min
Method 2
Drug Formulation Method of dose calculation
Dopamine/dobutamine 50 mg in 50 mL 0.3 body wt (mL/h) = 5 mcg/kg/min
(1000 mcg/mL)
Sodium nitroprusside/NTG/ 5 mg in 50 mL 0.3 body wt (mL/h) = 0.5 mcg/kg/min
milrinone (100 mcg/mL)
Adrenaline/isoprenaline/ 0.5 mg in 50 mL 0.3 body wt (mL/h) = 0.05 mcg/kg/min
noradrenaline (10 mcg/mL)
Vasopressin 5 units in 50 mL 0.3 body wt (mL/h) = 0.0005 unit/kg/min
(0.1 unit/mL)
ERRNVPHGLFRVRUJ
In children, to decrease the uid intake, usually 2 the above strength of

solutions are prepared (dopamine/dobutamine: 100 mg in 50 mL; milrinone/NTG/
sodium nitroprusside: 10 mg in 50 mL; adrenaline/noradrenaline/isoprenaline:
1 mg in 50 mL and vasopressin 10 units in 50 mL), so that 0.3 body wt 2
in mL/h would then provide the doses noted in the Method 2 table above.
In a 12 kg child, dopamine prepared in a concentration of 100 mg in
50 mL of 5% dextrose administered at a rate of 1.8 mL will give a dose of
5 mcg/kg/min (0.3 12 2 in mL/h = 5 mcg/kg/min).
Similarly, in adults 4 strength may be prepared, then 0.3 body wt 4
in mL/h would give the above doses, e.g., for dopamine, 200 mg in 50 mL
in a 50 kg adult, 3.75 mL/h would give 5 mcg/kg/min (0.3 50 4 in
mL/h = 5 mcg/kg/min).
Diluents: Diluents may be 5% dextrose in water, 5% dextrose in half-
normal saline, normal saline, or Ringers lactate. SNP and NTG are prepared
in dextrose only.
Bibliography
1. Alprostadil injection. Available at: dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=14726
2. Aung K, Htay T. Vasopressin for cardiac arrest: a systematic review and meta-analysis. Arch
Intern Med 2005;165(1):1724.
3. Bellomo R, Giantomasso DD. Noradrenaline and the kidney: friends or foes? Crit Care
2001;5:2948.
4. Biaggioni I, Robertson D. Adrenoceptor agonists & sympathomimetic drugs. In: Katzung BG,
Masters SB, Trevor AJ, eds. Basic and Clinical Pharmacology 11th ed. USA: McGraw Hill Inc.;
2009:12748.
5. Buck ML. Low-dose vasopressin infusions for vasodilatory shock: adverse effects. Pediatr
Pharm 2003;9(9) [Updated: 2003 Sep 10; cited: 2011 Sep 28]. Available at: http://www.med-
scape.com/viewarticle/462394.
6. Choudhury M, Saxena N. Inotropic agents in pediatric cardiac surgery patients: current prac-
tice, concerns, and controversies. Indian J Anaesth 2003;47:246.
7. Esoprostenol. Available at: http://nursing.ucsfmedicalcenter.org/NursingDept/AdultProcedures/
PDFsafter12-29-2003/FlolanInfusionforPulmonaryHypertensionAdult.pdf
8. Epoprostenol. Package insert: information for healthcare professionals flolan 1.5. Available at:
www.medicines.ie/pdfviewer.aspx?isattachment=true...9841.
9. Gilmore K. Pharmacology of vasopressors and inotropes. Pharmacology 1999;10:4. [Cited:
2011 Dec 17] Available at: http://www.nda.ox.ac.uk/wfsa/html/u10/u1004_01.htm.
10. Gomersall C. Nitroprusside. The Chinese University of Hong Kong. [Updated: 1999 Dec; cited:
2011 Sep 28]. Available at: http://www.aic.cuhk.edu.hk/web8/sodium_nitroprusside.htm.
11. Helfaer MA, Wilson MD, Nichols DG. Pharmacology of cardiovascular drugs. In: Nichols DG,
Cameron DE, Greeley WJ, Lappe DG, Ungerleider RM, Wetzel RC, eds. Critical Heart Disease in
Infants and Children. St Louis: Mosby; 1995:185213.
12. Hill NS, Antman EM, Green LH, Alpert JS. Intravenous nitroglycerin. A review of pharmacol-
ogy, indications, therapeutic effects and complications. Chest 1981;79(1):6976.
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13. Ilbawi MN, Idriss FS, DeLeon SY, Berry TE, Duffy CE, Paul MH. Hemodynamic effects of
intravenous nitroglycerin in pediatric patients after heart surgery. Circulation 1985;72(3 Pt 2):
II1017.
14. Infusions. In: Alder Hey Book of Childrens Doses 6th ed. Liverpool: Royal Liverpool Childrens
Hospital (Alder Hey); 1994:2545.
15. McAuley DF. What are the current recommendations regarding the use of vasopressin in
the treatment of shock? [Cited: 2011 Apr 14]. Available at: http://www.globalrph.com/vaso-
pressin_shock.htm.
16. Milrinone. South Thames retrieval service. 2008 Jan [Cited: 2011 Sep 28]. Available at: http://
www.strs.nhs.uk/resources/pdf/guidelines/milrinone.pdf.
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Nitroprusside_toxicity.
18. Patel BM, Chittock DR, Russell JA, Walley KR. Beneficial effects of short-term vasopressin
infusion during severe septic shock. Anesthesiology 2002;96:57682.
19. Sodium nitroprusside. In: Sweetman SC, ed. In Martindale The Complete Drug Reference
36th ed. IL, USA: Pharmaceutical Press 2009:13978.
20. Vasopressin. In: USP Drug Dispensing Information Vol I. Massachusetts: Drug Information of the
Health Care Professional. Thompson Micromedex; 2004:28167.
21. Westfall TC, Westfall DP. Neurotransmission: the autonomic and somatic motor ner-
vous systems. In: Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilmans The
Pharmacological Basic of Therapeutics 12th ed. USA: McGraw Hill Inc.; 2011:171218.
ERRNVPHGLFRVRUJ
Congestive
Heart Failure
For suddenly a grievous sickness took him, that makes him gasp and stare
and catch the air
King Henry VI; Part II - William Shakespeare (15641616)
Clinical Manifestations
Low cardiac output Left heart failure Right heart failure

Failure to thrive Respiratory distress (tachypnea, Raised jugular venous pulse
Sweating during feeding chest retractions) Hepatomegaly
Tachycardia Rales/crepitations Edema
Cool periphery Pulmonary edema Pleural effusion
Oliguria Ascites
In general, heart failure results either from an excessive volume overload

(left-to-right shunts, regurgitant lesions), pressure overload (aortic steno-
sis, coarctation), or from a primary myocardial abnormality (myocarditis,
cardiomyopathy). Other lesions that can result in congestive heart failure
(CHF) are arrhythmias, pericardial diseases, and a combination of various
factors.
Clinical manifestations of CHF are a combination of features of low car-
diac output, left heart failure, and right heart failure. The decrease in cardiac
output because of CHF triggers a compensatory sympathetic response result-
ing in tachycardia, vasoconstriction, and reninangiotensin mediated uid
retention. Fluid retention initially increases the cardiac output by increasing
the end diastolic volume (preload) but eventually results in renal and other
organ dysfunction.
Left-sided heart failure is associated with signs of pulmonary venous
congestion (tachypnea, chest retractions, rales, pulmonary edema), whereas
right-sided heart failure is associated with signs of systemic venous con-
gestion (raised jugular venous hepatomegaly, edema, ascites, pleural effu-
sion). In pediatric patients, failure of one ventricle invariably affects the
other ventricle and children usually present with signs of biventricular
failure. CHF with normal cardiac output is called compensated CHF, and
CHF with inadequate cardiac output is called decompensated failure.
ERRNVPHGLFRVRUJ
Congestive Heart Failure 33
Signs of CHF vary with the age of the child. Infants have sweating
during feeding, inability to complete feeding (taking <90100 mL/feed or
>40 min/feed), and failure to thrive. Pulsus alternans (alternate strong and
weak pulse) or pulsus paradoxus (an inspiratory fall in systolic pressure
of >10 mmHg) are observed in infants with severe CHF. A gallop rhythm
may be present. Signs of pulmonary venous congestion include tachypnea
(sleeping respiratory rate of >50/min) and chest retractions. Right-sided
venous congestion is characterized by hepatosplenomegaly and, less fre-
quently, edema, ascites, and a distended jugular venous pulse. In severe cases,
persistent low cardiac output may result in signs of renal and hepatic fail-
ure. Chest X-ray shows cardiac enlargement, i.e., a cardiothoracic ratio of
>60% in the newborn and >55% in older infants. However, it is well to
note that an expiratory lm can often be misinterpreted as showing cardiac
enlargement.
Older children may have fatigue or sometimes syncopy. Clinical nd-
ings include hypotension, cool extremities with poor peripheral perfusion,
a low volume pulse, and decreased urine output. Left-sided venous con-
gestion causes tachypnea and wheezing. Right-sided congestion results
in hepatosplenomegaly, raised jugular venous pulse, edema, ascites, and
pleural effusion. Renal and liver function tests may be deranged.
Drugs Used in the Treatment of Heart Failure
Drug Dosage Remarks and side effects

Digoxin Children Approx time to steady state is
Digitalizing dose 510 days and the therapeutic
Preterm: PO 20 mcg/kg/day, IV 15 mcg/kg/day range is 0.81.2 ng/mL (sample
Term: PO 30 mcg/kg/day, IV 20 mcg/kg/day is taken 6 h after oral/IV dose).
< 2 yr: PO 4050 mcg/kg/day, The bioavailability of the tablet
IV 3040 mcg/kg/day is 70%, and syrup 80% of the
210 yr: PO 3040 mcg/kg/day, IV dose.
IV 2030 mcg/kg/day
>10 yr: PO 1015 mcg/kg/day, Digoxin is potentiated by
IV 812 mcg/kg/day amiodarone, diltiazem,
50% dose is given initially, 25% at 8 h, and verapamil, and quinidine; the
25% at 16 h. Maintenance dose is started 24 h maintenance dose should be
after loading. halved if any of these are also
Maintenance dose given.
Preterm: PO 2.5 mcg/kg q12h
Neonate10 yr: PO 5 mcg/kg q12h
>10 yr: PO 2.5 mcg/kg q12h
IV: 75% of oral dose is given.
ERRNVPHGLFRVRUJ
Adults Digoxin toxicity is enhanced by

Digitalizing dose hypokalemia (administration of
IV 0.51 mg diuretics or amphotericin) and
PO 0.751.5 mg hypercalcemia.
50% of total dose is given initially, then 25% dose
in each of 2 subsequent doses at 812 h intervals. Toxic effects
Maintenance dose Cardiac arrhythmias (esp
IV 0.10.4 mg q24h bradycardia and bigeminy);
PO 0.1250.5 mg q24h Gastrointestinal (nausea and
Renal failure vomiting is the most common);
Crcl 1015 mL/minreduce dose by 50%; Ocular (aberrant color
Crcl <10 mL/minreduce dose by 75% perception).
Digoxin is not cleared by dialysis.
Digoxin is administered IV over 10 min diluted with
NS, 5% D or IGS. Digitalization dose is given over
30 min.
Diuretics
Furosemide Children Hyponatremia, hypokalemia, chloride
PO: 12 mg/kg q612h depletion, metabolic alkalosis,
(max 4 mg/kg/day) hyperuricemia, hyperglycemia, LDH,
IV: 0.51 mg/kg q612h triglycerides, ototoxicity may occur.
IV infusion: 0.052 mg/kg/h Nephrocalcinosis is possible due to
increased calcium excretion.
Adults
PO: 2080 mg q624h
IV: 1080 mg q624h
IV infusion: 0.1 mg/kg stat,
followed by 0.10.4 mg/kg/h
Hydrochlorothiazide Children Electrolyte imbalance may occur.
24 mg/kg/day in divided
doses q12h PO
Adults
25100 mg/day in divided
doses q1224h PO
Metolazone Children Electrolyte imbalance may occur.
0.20.4 mg/kg/day in divided
doses q1224h PO
Used with loop diuretics
Adults
2.55 mg/day in divided
doses q1224h PO
ERRNVPHGLFRVRUJ
Congestive Heart Failure 35
Spironolactone Neonates Hyperkalemia, anorexia, gastritis,

13 mg/kg/day in divided gastric bleeding, diarrhea,
doses q1224h PO gynecomastia, hirsutism, and
Children menstrual irregularities may occur
1.53.5 mg/kg/day in divided as adverse effects.
doses q624h PO
Adults
doses q1224h PO
Vasodilators
Captopril Neonates Start with lowest dose and increase
(ACE inhibitor) 0.41.6 mg/kg/day in divided every 4th5th dose. Monitor BP, and
doses q8h PO renal parameters to titrate the dose.
Children Hypotension with the first dose
0.33.0 mg/kg/day in divided may occur, especially if a diuretic
doses q8h PO has been administered at the same
Adults time. Hyperkalemia (avoid ACEI with
6.2550 mg q812h PO spironolactone). Dry cough due to
increased levels of bradykinin, altered
taste, and rashes.
Enalapril Children Start with lowest dose and increase
(ACE inhibitor) 0.10.5 mg/kg/day in divided dose daily. Monitor BP, and renal
doses q1224h PO. Avoid in parameters to titrate the dose.
neonates. Hypotension, hyperkalemia (avoid
Adults ACEI with spironolactone). Dry cough
2.55 mg/day in divided doses due to increased levels of bradykinin.
q1224h PO. Can be increased
to a max of 20 mg/day.
Losartan Children Monitor BP, and renal parameters to
(Angiotensin 0.50.75 mg/kg q24h PO titrate the dose. Hypotension may
receptor blocker) Adults occur.
50100 mg q24h PO
Beta-blockers
Metoprolol Children Efficacy and safety not established
0.10.5 mg/kg q12h PO in children. Indicated in mild/
moderate heart failure associated with
ventricular dysfunction. Start with
lowest dose and gradually increase
the dose over weeks to achieve the
desired dose. Modest 1 selectivity.
Bronchospasm, bradycardia, heart
block may take place.
ERRNVPHGLFRVRUJ
Adults
12.525 mg q24h PO may
be increased to a max of
200 mg/day in divided doses
q1224h
Carvedilol Children Non-selective -blocker and some
Start with 0.05 mg/kg q12h -blocking activity.
and increase to a max of Watch for bronchospasm, bradycardia,
0.5 mg/kg q12h. heart block, hyperglycemia in patients
Adults who are at risk.
Start with 3.125 mg q12h
PO and increase to a dose of
12.525 mg q12h PO
Bibliography
1. Bernstein D, Fajardo G, Zhao M. The role of B-adrenergic receptors in heart failure: differential
regulation of cardiotoxicity and cardioprotection. Prog Pediatr Cardiol 2011;31(1):358.
2. Bruns LA, Chrisant MK, Lamour JM, et al. Carvedilol as therapy in pediatric heart failure:
an initial multicenter experience. J Pediatr 2001;138:50511.
3. Heart Failure Society of America. Executive summary: HFSA 2006 Comprehensive Heart
Failure Practice Guideline. J Card Fail 2006;12:1038.
4. Hsu DT, Pearson GD. Heart failure in children: Part I: history, etiology, and pathophysiology.
Circ Heart Fail 2009;2:6370.
5. Hsu DT, Pearson GD. Heart failure in children: part II: diagnosis, treatment, and future directions.
Circ Heart Fail 2009;2(5):4908.
6. Jong P, Demers C, McKelvie RS, Liu PP. Angiotensin receptor blockers in heart failure: meta-
analysis of randomized controlled trials. J Am Coll Cardiol 2002;39:46370.
7. Khan MG. Management of heart failure. In: Khan MG, ed. Cardiac Drug Therapy 5th ed. London:
W.B. Saunders Company Ltd; 1999:20946.
8. Malcolm J, Arnold O. Heart failure. The Merck Manuals: online medical library. [Updated:
2009 Dec; cited: 2011 Sep 21] Available at: http://www.merckmanuals.com/professional/
cardiovascular_disorders/heart_failure/heart_failure_hf.html?qt=&sc=&alt=
9. Margossian R. Contemporary management of pediatric heart failure. Expert Rev Cardiovasc
Ther 2008;6:18797.
10. Park MK. Use of digoxin in infants and children with specific emphasis on dosage. J Pediatr
1986;108:8718.
11. Prescription Drug Information, Interactions & Side Effects. [Cited: July 2012] Available at:
http://www.drugs.com/
12. Satou GM, Halnon NJ. Pediatric congestive heart failure. [Updated: 2009 Mar 19; cited: 2011
Feb 21] Available at: http://emedicine.medscape.com/article/901307-overview.
13. Saxena A, Juneja R, Ramakrishnan S. Drug therapy of cardiac diseases in children. Working
Group on Management of Congenital Heart Diseases in India. Indian Pediatr 2009;46(4):31038.
14. Shaddy RE, Penny D. Chronic cardiac failure: physiology and treatment. In: Enderson RH,
Baker EJ, Penny DJ, et al. eds. Paediatric Cardiology 3rd ed. USA: Churchill Livingstone, an imprint
of Elsevier Ltd; 2010:25768.
15. Tweddell JS, Hoffman GM. Postoperative management in patients with complex congenital
heart disease. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 2002;5:187205.
ERRNVPHGLFRVRUJ
Cardiac
Tachyarrhythmias
The heart has its reasons of which reason knows nothing:
we know this in countless ways
Blaise Pascal (16231662)*
Normal ECG
QRS
ST
T
P
PR Q
S
QT
Fig. 1: Components of a normal ECG complex.
The P wave represents atrial depolarization. Normal P duration is age

dependant (<0.08 sec in infants, <0.10 sec in children, and <0.12 sec in
adults) with an amplitude of not >0.25 mV (2 and small squares). The
axis of the P wave is +0 to +90, and thus the P wave is positive in lead I, II,
and aVF and negative in lead aVR. Retrogradely conducted impulses origi-
nating in the AV node produce inverted P waves in lead II and upright in
aVR. However, if atrial and ventricular depolarization occurs simultaneously,
the P waves may be obscured in the QRS complexes.
The PR interval (from the beginning of the P wave to the beginning of
the QRS complex) is the time from the onset of atrial activation to the
*Blaise Pascal was a French mathematician, physicist, author, and philosopher. He is the
inventor of the mechanical calculator.
start of ventricular activation (upper limit of normal in infants <0.14 sec;

812 yr <0.18 sec; adults <0.21 sec).
The QRS complex represents ventricular depolarization, and the T wave
represents ventricular repolarization. The normal QRS duration is shorter
in childhood (birth 2 yr: 0.030.08 sec; 315 yr: 0.040.09 sec; adult:
0.060.10 sec) and with fast ventricular rates.
The QT interval (from the beginning of the QRS complex to the end of
the T wave) represents the duration of ventricular depolarization and repo-
larization. Normal values for the QT interval are longer in females and are
also prolonged with a slower heart rate. The QT interval is corrected for
inuence of heart rate by Bazetts formula.
QT interval
Corrected QT (QTC ) = ,
(RR interval)
where RR interval = 60/HR.

Normal QTC in children is <0.44 sec, in adults <0.425 sec.
ECG Recording
The normal speed of an ECG recording is 25 mm/sec. The width of
each small square (1 mm 1 mm) at this speed represents 0.04 sec and
the height 0.1 mv (each large square is 5 5 mm and is equivalent of
0.20 sec 0.5 mv).
At this speed, 300 large squares (or 1500 small squares) are covered in
a minute. The heart rate can therefore be calculated by dividing 300 by
the number of large squares between two RR complexes (or 1500 by the
number of small squares).
Atrial Electrocardiograms (AEG)

An AEG is useful to determine the position of the P wave relative to the
QRS complex in the diagnosis of various types of arrhythmias and heart
blocks, when P waves are not visible on the surface ECG. The AEG can be
recorded on a rhythm strip of a bedside monitor or as a standard 12-lead
ECG. Simultaneous recording of the AEG and a surface ECG lead allows com-
parison of the two recordings. The AEG recording is done by attaching one
atrial pacing wire to the right upper limb electrode and the second atrial wire
to the left upper limb electrode. The leg electrode is attached as for a normal
ECG. Lead I then records a bipolar AEG, and leads II and III record a unipo-
lar AEG. If only one atrial lead is present, unipolar AEG can be recorded by
attaching the wire to the left upper limb electrode and normal electrodes to
the right upper limb and lower limb and recording either lead I or II.
ERRNVPHGLFRVRUJ
Cardiac Tachyarrhythmias 39
In the absence of postoperative atrial pacing wires, a transvenous elec-

trode placed in the right atrium or an esophageal electrode can be used to
record a unipolar AEG.
In the unipolar AEG, P waves are recorded as large complexes and the
QRS as a small deection; while in a bipolar AEG, generally, only P waves
are recorded and QRS complexes are not visible. The relationship between
atrial and ventricular complexes will help differentiate sinus tachycardia,
and supraventricular arrhythmias. In sinus tachycardia, the P waves are in
the normal position (PR interval < RP interval); while in reentrant tachyar-
rhythmias, the P waves may either precede or fall within the QRS complex
or follow it (PR interval > RP interval). In junctional ectopic tachycardia,
either the P waves fall within the QRS complex or there is AV dissociation
with the P waves occurring at a slower rate than the R waves.
The AEG can also be utilized in the diagnosis of wide complex tachy-
cardias to differentiate ventricular tachycardia from SVT with aberrant con-
duction (bundle branch block), by identication of a P wave with each
QRS complex in SVT and AV dissociation in VT.
Normal Sinus Rhythm
Fig. 2: Normal sinus rhythm at the rate of 120/min, in a 6-month-old child.
A normal sinus rhythm implies a heart rate appropriate for age, with a
regular rhythm, P waves of normal morphology, with an axis from +0
to +90, which are followed by a normal PR interval and QRS complex.
Rhythm Disorders
Site of origin of arrhythmia Arrhythmia

Sinoatrial node Sinus tachycardia
Sinus bradycardia
Sinus arrhythmia
Sinus arrest
ERRNVPHGLFRVRUJ
Atrium Atrial ectopics

Wandering pacemaker
Atrial ectopic tachycardia
Multifocal atrial tachycardia
Atrial flutter
Atrial fibrillation
A-V junction Atrioventricular reentrant tachycardia
Atrioventricular nodal reentrant tachycardia
Junctional ectopics
Junctional rhythm
Junctional ectopic tachycardia
Ventricles Ventricular ectopics
Ventricular tachycardia
Ventricular fibrillation
Pulseless electrical activity
Sinus Node Arrhythmias
Sinus Tachycardia
Fig. 3: Sinus tachycardia at the rate of 160/min with a simultaneous recording of a

unipolar AEG. The larger atrial and the smaller ventricular recordings on the
AEG coincide respectively with the P waves and the R waves on the normal ECG.
Heart rate is faster than the normal for age. The impulse originates in the
sinoatrial (SA) node with a normal P wave morphology, PR interval, and
QRS complex.
Sinus Bradycardia
The heart rate is slower than the normal for age. The impulse originates in the
SA node with normal P wave morphology, PR interval, and QRS complex.
ERRNVPHGLFRVRUJ
Fig. 4: Sinus bradycardia at the rate of 60/min.
Sinus Arrhythmia
Fig. 5: Sinus arrhythmia.
ECG of sinus arrhythmia shows a varying RR interval, which has no rela-

tionship to respiration. The P wave and QRS complex are normal. An
increase in RR interval with inspiration and a decrease with expiration may
be a normal nding (respiratory sinus arrhythmia).
Sinus Arrest
Fig. 6: Sinus arrest with junctional escape beats (marked by arrows).
When SA pacemaker activity is absent and a subsidiary pacemaker takes

over either in the atrium, A-V junction, or ventricle. Atrial escape beats are
similar in conguration to atrial ectopics, morphologically abnormal
P waves precede normal QRS complexes. With junctional escape beats, nor-
mal QRS complexes are preceded or followed by retrogradely conducted
ERRNVPHGLFRVRUJ
P waves (negative in lead II and positive in aVR) or the P waves may not
be discernible. A ventricular escape beat is evident by its wide QRS complex.
Sinus arrest may occur with increased vagal tone, hypoxia, hypothermia,
digitalis toxicity, or sick sinus syndrome.
Atrial Arrhythmias
Atrial Ectopics
a b c d e
Fig. 7: Atrial ectopics (marked by arrows).
The P wave impulse does not generate in the SA node but elsewhere in the
atrium and thus has a different morphology. It is followed by a normal
QRS complex (except in aberrant conduction). The ectopic comes early in
the cardiac cycle and is followed by an incomplete compensatory pause
(in Fig. 7, interval ab + bc > cd + de).
Atrial ectopics may occur with digoxin toxicity, anxiety, drugs, heart fail-
ure, atrial hypertrophy, electrolyte disorders, post cardiac surgery, and may
sometimes be a normal benign nding.
Wandering Pacemaker
Fig. 8: Wandering pacemaker.
When there are three or more pacemakers beating at a rate faster than the
sinus node but <100/min. In such a situation, the rhythm will be irregular,
ERRNVPHGLFRVRUJ
P wave morphology and the PR interval will keep varying from beat to
beat, but the QRS will be normal. It may be a precursor to multifocal atrial
tachycardia (when rate >100/min).
Occurs with hypoxia, digoxin toxicity, sick sinus syndrome, and some-
times in otherwise healthy children.
Atrial Ectopic Tachycardia (AET)
Fig. 9: Atrial ectopic tachycardia.
AET is caused by a single ectopic focus within the atria, resulting in a

P wave of abnormal (positive or negative axis) but uniform morphol-
ogy, which falls before a narrow, regular QRS complex (in the absence of
aberrancy).
The rate ranges from 120 to 300 beats per minute (typically >200)
and commonly with an associated rst or second degree AV block. The
tachycardia may exhibit a warming up (i.e., a progressively shorten-
ing PP interval for the rst few beats) and a cooling down period at its
termination.
Multifocal Atrial Tachycardia (MAT)
Fig. 10: Multifocal atrial tachycardia.
MAT is a tachycardia resulting from at least three ectopic foci within the
atria, distinguished by P waves of at least three different morphologies;
ERRNVPHGLFRVRUJ
the rhythm is irregular and the PR interval varies from beat to beat, but the
QRS complex is normal. It is in fact akin to a wandering pacemaker with
a heart rate >100 beats/min. Can be confused with AF, however, MAT has
discernible P waves and similar QRS complexes.
Occurs in patients with a structural heart disorder, pericarditis, and dig-
oxin toxicity.
Atrial Flutter
Fig. 11: Atrial flutter with 4:1 AV block with a simultaneous recording of a unipolar AEG.
The P waves have a saw tooth conguration and a rate >300/min with
24:1 AV block. The QRS complexes are normal (except in aberrant
conduction).
Atrial utter may occur after atrial surgery, in atrial enlargement, digoxin
toxicity, or myocarditis.
Atrial Fibrillation (AF)
Fig. 12: Atrial fibrillation.
There are no discernible P waves (atrial rate >350/min). The rhythm is

irregular, and the RR interval and the size of the QRS complex vary from
beat to beat.
AF is seen after atrial surgery, in atrial enlargement, digoxin toxicity,
myocarditis, etc.
ERRNVPHGLFRVRUJ
Rhythm Disorders Arising from the AV Node
Atrioventricular Reentrant (or Reciprocating)

Tachycardia (AVRT)
Fig. 13: Atrioventricular reentrant tachycardia.
There is an extra-nodal accessory conduction pathway (AP) between the

atria and ventricle, in addition to the normal AV conduction system. In
orthodromic AVRT, the impulse originates in the AV node and travels down
the normal pathway to rst activate the ventricles and up the AP to acti-
vate the atria. The impulse then returns back to the AV node by the normal
pathway forming a reentry circuit.
The rhythm is regular, rate 150250/min, and the QRS complex is nar-
row with a retrograde P wave (negative in lead II and positive in aVR),
which may not be discernible within the QRS complex (Fig. 13) or may
follow the QRS.
In antidromic AVRT (in <5%), the reentry circuit occurs in the oppo-
site direction, the impulse from the AV node rst activates the atrium ret-
rogradely via the normal pathway and then the ventricle via the AP. The
rhythm is regular, but the QRS complex is wide because of its abnor-
mal activation and looks exactly like ventricular tachycardia. Retrograde
P waves precede the wide QRS complex.
AVRT is more common in infants and children than is AVNRT.
WolfeParkinsonWhite (WPW) Syndrome
Fig. 14: WolfeParkinsonWhite syndrome (delta waves are marked by arrows).
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The ECG pattern of this condition is produced by the presence of an

extranodal AP. In normal sinus rhythm, initial antegrade activation of the
ventricle via this AP results in a delta wave (Fig. 14) on ECG. This is then
followed by normal antegrade pathway activation of the ventricles result-
ing in a normal QRS complex.
Patients with WPW syndrome are susceptible to both orthodromic and
antidromic AVRT.
AV Nodal Reentrant Tachycardia (AVNRT)

AVNRT has also been called junctional reciprocating tachycardia. In
addition to the normal pathway, there is an accessory pathway within the
node itself. In 90% cases, the impulse stimulates the ventricle through the
normal pathway and then retrogradely the atria via AP (similar to ortho-
dromic AVRT). The ECG recording of the arrhythmia is similar to AVRT.
AVNRT is the most common recurrent SVT in adults.
Junctional Ectopics
Fig. 15: Junctional ectopics (marked by arrows).
A premature beat arising from the AV node will have a QRS complex with
normal conguration. There may be no P wave or a retrograde P wave
(negative in lead II and positive in aVR) because of reverse activation of
the atria, which may follow or precede the QRS complex. The compensa-
tory pause is complete.
Junctional Rhythm
Enhanced automaticity of the AV node, faster than the SA node, will result
in a junctional rhythm (Fig. 16).
Junctional Ectopic Tachycardia

JET is caused by increased automaticity of the AV node with a ventricu-
lar rate of 180200/min and regular, narrow QRS complexes. JET may be
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Fig. 16: Junctional rhythm.
Fig. 17: Junctional ectopic tachycardia at the rate of 200/min. In the bipolar AEG recorded
at the same time, atrial complexes also occur at the rate of 200/min, indicating
1:1 AV conduction. The retrogradely conducted P waves on the AEG are noted to occur
almost at the same time as the QRS complexes on the normal ECG because of simultaneous
activation of the atria and ventricles.
associated with atrioventricular dissociation and slower atrial than ven-

tricular rate. When JET manifests as 1:1 atrioventricular conduction, almost
simultaneous activation of the atria and ventricles takes place. The atrial
impulse is conducted retrogradely, and the P wave (axis 120) falls any-
where in relation to the QRS complex.
JET is poorly tolerated hemodynamically because of loss of atrial con-
tribution, which usually adds 2030% to the cardiac output. It is an
incessant tachycardia, which shows no response to -blockers or calcium
channel blockers. A child who has undergone surgical manipulation in the
close vicinity of the AV node is more likely to have this supraventricular
arrhythmia in the immediate postoperative period.
Ventricular Arrhythmias
Ventricular Ectopics
The premature ventricular contraction (PVC) originates in the ventricle
and is not preceded by a P wave. The QRS complex is wide (>0.09 sec in
children) with a T wave pointing in the opposite direction to the QRS.
ERRNVPHGLFRVRUJ
a b c d e
Fig. 18: Unifocal ventricular ectopics (marked by arrows).
Fig. 19: Multifocal ventricular ectopics.
Fig. 20: Bigeminy.
A complete compensatory pause is present, i.e., the interval between the

preceding and subsequent QRS waves is the same as between two normal
adjacent RR intervals (Fig. 18, interval ab + bc = cd + de). PVCs can be dis-
tinguished from atrial ectopics, because the compensatory pause is shorter
(i.e., incomplete) with atrial ectopics.
Multiple ventricular ectopics of the same morphology are referred to as
unifocal, whereas those with different morphologies are called multifo-
cal. This may be due to ectopics arising from different foci or progressing
through the ventricular myocardium in different ways.
PVCs occurring after every normal beat are called ventricular bigeminy.
PVCs that occur at intervals of two normal beats are termed trigeminy.
Runs of three or more beats constitute ventricular tachycardia.
Causes of PVCs include hypokalemia, hypomagnesemia, digoxin toxicity,
and catecholamine administration.
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Ventricular Tachycardia (VT)
Fig. 21: Monomorphic ventricular tachycardia at the rate of 160/min. Simultaneous

recording of a bipolar AEG shows AV dissociation with a slower atrial rate of 120/min.
Monomorphic VT is a regular rhythm originating from a single focus with

identical wide, bizarre QRS complexes at a rate more than 100 per minute
(usually 150200). There is usually atrioventricular dissociation but ven-
triculoatrial conduction may be present. Ventricular tachycardia usually
causes severe hemodynamic compromise and may progress rapidly to ven-
tricular brillation but may also occur without hemodynamic deterioration.
Fig. 22: Polymorphic ventricular tachycardia.
Polymorphic VT is an irregular rhythm of wide bizarre QRS complexes of var-

ying conguration at a rate of more than 100 per minute (usually 150200).
Fig. 23: Torsades de pointes.
Torsades de pointes is a variant of polymorphic VT where the QRS axis

keeps shifting as if the heart is rotating and the ECG shows a spindle effect.
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Nonsustained VT is dened as a run of tachycardia of <30 seconds duration.

Sustained VT is of a longer duration than 30 seconds.
Fig. 24: Idioventricular rhythm.
Idioventricular rhythm: QRS complexes are wide and bizarre (>0.10 sec)
occurring at a rate of <60/min, in regular rhythm. P waves are absent or, if
visible, have no consistent relationship to the QRS complex. It invariably
causes hemodynamic instability.
Fig. 25: Accelerated idioventricular rhythm.
Accelerated idioventricular rhythm is similar to idioventricular rhythm

but with a rate of 60100/min and is usually not associated with hemody-
namic compromise.
Pulseless VT: When there is no effective cardiac output and there is no pulse
because of a rapid ventricular rate of contraction. It is treated like a VF.
Ventricular Fibrillation
Fig. 26: Ventricular fibrillation.
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VF presents as a rapid, irregular rhythm with low amplitude QRS complexes

and no cardiac output. It may result from degeneration of SVT or VT.
Pulseless Electrical Activity (PEA)

PEA (formerly known as electromechanical dissociation) is recognized by
slow, wide QRS complexes without palpable pulses; at other times, the ECG
may be relatively normal but the pulses are absent. True PEA is dened as the
total absence of myocardial contraction, while pseudo PEA is characterized
by weak myocardial contractions that do not produce a measurable aortic
pressure. PEA encompasses various rhythms (V-brillation or V-tachycardia)
that do not produce a pulse including junctional and idioventricular or escape
ventricular rhythms. Three sets of conditions will result in PEA: (i) poor
intrinsic myocardial contractility caused by a severe cardiovascular insult (e.g.,
prolonged hypoxia, acidosis, hyperkalemia or hypokalemia, hypoglycemia
and hypothermia); (ii) hypovolemia; and (iii) obstruction to the circulation
(e.g., massive pulmonary embolus, tension pneumothorax, and cardiac tam-
ponade). Patients with prolonged VF are sometimes debrillated to a state of
PEA with slow broad QRS complexes.
Clinical Classification of Tachyarrhythmias
Supraventricular tachycardias (SVT): Three types of tachycardias are gener-

ally included in this term(i) atrial ectopic tachycardia, (ii) AV reentrant
tachycardias (AVRT and AVNRT), and (iii) junctional ectopic tachycardia.
By convention, atrial brillation and atrial utter are often categorized sep-
arately even though they are supraventricular in origin.
A tachyarrhythmia with a narrow QRS complex (0.09 sec in children
and 0.12 sec in adults) indicates a supraventricular origin, while a wide
QRS complex (>0.09 sec in children and >0.12 sec in adults) indicates a
ventricular arrhythmia. However, a supraventricular arrhythmia with an
aberrant conduction also presents as a wide complex arrhythmia. In chil-
dren, almost all wide complex arrhythmias are VT.
Tachyarrhythmias may be divided into four groups:
1. Narrow QRS complex, irregular tachycardias are atrial brillation, atrial

utter with varying AV block or multifocal atrial tachycardia.
2. Narrow QRS complex, regular tachycardias include sinus tachycardia,
atrial utter, AET, reentrant tachycardias (AVNRT, AVRT) and JET.
3. Wide QRS complex, irregular tachycardias include polymorphic VT and
the irregular atrial tachyarrhythmias with aberrant conduction.
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4. Wide QRS complex, regular tachycardias include monomorphic VT and

the regular atrial tachyarrhythmias with aberrant conduction.
Differential Diagnosis of Narrow QRS Complex

Arrhythmias
Sinus tachycardia AVRT/AVNRT AET

P waves present and normal P waves absent or retrograde P waves present
(P ve in lead II) may precede, (positive or negative in
follow or distort the QRS. lead II).
(Pseudo RBBB in V1).
Gradual onset and Sudden onset and Gradually increases (warm up),
termination, compatible with termination. Rate does and may gradually end. Rate
known cause (e.g., fever, pain, not vary. may vary.
volume loss etc.)
Infant HR <220 bpm Infant HR >220 bpm Infant HR >220 bpm
Child HR <180 bpm Child HR >180 bpm Child HR >180 bpm
PR interval normal, PR < RP P absent or PR >RP Normal (PR < RP) or
1/2 block
Antiarrhythmic Drugs
Drug IV dose Oral dose Indication

Adenosine Children Effective in reentrant
100 mcg/kg rapid IV bolus SVT (AVRT, AVNRT) and
(max 6 mg) followed by a rarely in some forms
5 mL saline flush. of VT.
If required, repeat 200 May transiently
mcg/kg IV (max 12 mg). decrease the rate but
This dose can be repeated does not convert other
twice. types of SVT.
Adults
Initial dose: 6 mg rapid IV May cause
bolus (administered in bronchospasm and
12 seconds), followed a feeling of chest
by a 5 mL saline constriction as an
flush. adverse effect.
If required a12 mg IV dose

can be repeated twice.
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Amiodarone Children Children Effective in all
Loading 5 mg/kg IV infusion Calculate doses for supraventricular
over 3060 minutes. children <1 year and ventricular
Maintenance 510 mcg/kg/ on body surface tachyarrhythmias.
min IV infusion (max total area. Loading dose: Amiodarone IV may
dose 15 mg/day). 1015 mg/kg/day (or cause bradycardia and
600800 mg/1.73 m2/ severe hypotension.
Adults
day) in divided doses It has an extensive
150 mg IV over 10 minutes,
q1224h for 414 adverse effect profile
followed by 360 mg
days or until adequate on prolonged use.
(1 mg/min) for 6 hour, then
control of arrhythmia. No dose alteration is
540 mg (0.5 mg/min) for
Then 5 mg/kg/day (or required in peritoneal
18 hour. Alternatively 300
200400 mg/1.73 m2/ or hemodialysis.
mg IV is given over 3060
day) q24h for several After 4 weeks of
minutes followed by 900
weeks. Reduce to a therapy, optimum
mg over 23 hour. In case of
maintenance dose serum level each
recurrence of arrhythmia,
of 2.5 mg/kg/day; of amiodarone and
a supplemental dose of
maintenance doses desethyl amiodarone
150 mg over 10 minutes is
may be given for 5 of should be 12.5
given. Infusion at 0.5
7 days/week. mcg/mL.
mg/min is continued until
oral therapy is initiated. Adults
Ventricular arrhythmias:
8001600 mg/day
in 12 doses for 13
weeks, then decrease
to 600800 mg/day in
12 doses for
4 weeks; maintenance:
200400 mg/day in
12 doses. Lower doses
are recommended
for supraventricular
arrhythmias.
Conversion to initial oral
therapyIf duration of
IV infusion was <1 week,
oral dose should be
8001600 mg/day; IV
infusion of 13 wk, oral
dose 600800 mg/day;
IV infusion of >3 wk,
oral dose 400 mg/day.
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Diltiazem Children Children May terminate
0.250.35 mg/kg IV bolus 1.52 mg/kg/day in reentrant SVT.
over 2 minutes. It can be divided doses q68h. Useful for rate control
repeated after 10 and 30 of atrial fibrillation,
Adults
minutes. atrial flutter, and atrial
3060 mg q68h;
tachycardias.
Adults increase to a
Adverse effects are
Initial dose 0.25 mg/kg maintenance dose of
AV block and asystole,
(usually 20 mg) IV 180360 mg/day in
which requires reversal
bolus over 2 minutes. If divided doses q68h.
with 10% Inj. calcium
necessary, a second bolus SR dose: 60120 mg
gluconate 0.20.3
of 0.35 mg/kg (usually q12h; increase to a
mL/kg IV.
25 mg) IV may be given. maintenance dose of
An infusion of diltiazem 180360 mg/day in
5 mg/h may be started, divided doses q12h.
and advanced in 5 mg/h
increments to 15 mg/h for
up to 24 hour.
Esmolol Children and adults May terminate reentrant
500 mcg/kg IV bolus over SVT and catecholamine
12 minutes. This may be sensitive VT.
followed by 50300 Useful for rate control
mcg/kg/min IV infusion. of atrial fibrillation,
atrial flutter, and atrial
tachycardias.
Lignocaine Children Indicated in acute
1 mg/kg IV bolus, may be management of VT
repeated in 5 minutes. (including torsades),
Maintenance 2050 mcg/ and multiple
kg/min IV infusion. ventricular ectopics.
Adults
50100 mg IV bolus. May
be repeated if required.
Maintenance 14 mg/min
IV infusion.
Magnesium Children Antiarrhythmic
sulfate 2550 mg/kg IV/IO over indicated in ventricular
1020 minutes. Faster in ectopics and VT,
torsades (max 2 g). especially torsades.
Adults
12 g IV over 1020
minutes. May be repeated
in 15 minutes and 12 g
continued as an IV
infusion for 2448 hour.
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Metoprolol Children Children Efficacy and safety
0.1 mg/kg slow IV (over 117 years: 12 mg/kg/ of IV metoprolol in
5 minutes). May be day in divided doses children has not been
repeated every 5 minutes q12h; increase to a max established.
for a max of 3 doses. 6 mg/kg/day.
Can be followed by
infusion 12 mcg/kg/min. Adults
Adults doses q1224h;
5 mg IV repeated for a max increase to max
of 3 doses at 2 minutes 450 mg/day.
intervals.
Procainamide Infants Children Indicated in
710 mg/kg IV 40100 mg/kg/day in stable, regular VT.
Children divided doses q46h Contraindicated in
1015 mg/kg IV torsades.
Administer loading dose Adults 2nd line therapy in atrial
over 3045 minutes. 500 mg q6h fibrillation, atrial flutter,
Maintenance 4050 and reentrant SVTs.
mcg/kg/min IV infusion.
Adults
Loading dose 500 mg
is administered over 20
minutes. Maintenance
2 mg/kg/h IV infusion.
Verapamil Children (>1 year age) 36 mg/kg/day in Adverse effects include
0.10.3 mg/kg/dose (max divided doses q8h. AV block and asystole,
5 mg) IV over 10 minutes. which requires reversal
Repeat dose after Adults with 10% Inj. calcium
30 minutes if required 240320 mg/day in gluconate 0.20.3
(max 10 mg). divided doses q68h mL/kg IV (alternatively
Adults (digitalized patient); administer calcium
2.55 mg IV. Repeat 240480 mg/day (non- gluconate IV
510 mg every 1530 digitalized patient). prophylactically prior
minutes if required to a to verapamil).
max 20 mg.
IV: intravenous, IO: intra osseous, ET: via endotracheal tube. Drug requires to be flushed with 5 mL normal saline,
followed by 5 ventilations.
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Flowchart for the Management of Tachyarrhythmias
Evaluate patient
Monitor blood pressure

Monitor rhythm
Stable Unstable
12 lead ECG
Synchronized DC
shock (14 J/kg)
Narrow complex Wide complex IV analgesia
Regular Irregular
Monomorphic recurrent VT SVT with aberrant Polymorphic recurrent VT

Sustained monomorphic VT conduction Sustained polymorphic VT
Amiodarone Adenosine Cardioversion
Lignocaine Diltiazem (sustained VT)
Procainamide -blocker Follow-up with amiodarone
Cardioversion Amiodarone or -blocker
(sustained VT) Magnesium sulfate
for torsades
Regular
Irregular
Vagal maneuvers
Adenosine
Rhythm converted Rhythm not converted Atrial fibrillation

Atrial flutter with
variable block
Re-entry SVT AET MAT
Prevent recurrence Atrial flutter Diltiazem/-blocker/
with diltiazem or JET amiodarone
-blocker Re-entry SVT
Diltiazem/-blocker/
amiodarone
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Management of Narrow QRS Complex Tachycardias
DC Cardioversion
Cardioversion is used as the rst line of therapy in the hemodynamically
unstable patient with an atrial arrhythmia or VT.
The dose of the initial shock for cardioversion in children is 0.51 J/kg,
which is increased to 2 J/kg if there is no response to this shock. (In the
adult, the shock sequence is an initial shock of 120 J followed by 200 J
when a biphasic debrillator is used. With a monophasic waveform, an
initial shock of 200 J is followed by 360 J.) For cardioversion (atrial or ven-
tricular), the DC shock must be synchronized to the QRS complex because
a shock that falls on the T wave can induce VF. The initial dose for de-
brillation in children in VF or pulseless VT is 2 J/kg, which is increased to
4 J/kg in subsequent shocks. (The default initial energy dose with a bipha-
sic debrillator recommended for debrillation in adults is 120 or 200 J. If
a monophasic debrillator is used, the recommended initial dose is 360 J.)
Debrillation does not require synchronization.
IV analgesia and sedation is necessary prior to cardioversion in all
awake patients, e.g., fentanyl 1 mcg/kg + midazolam 0.050.1 mg/kg IV
can be given. Midazolam may be repeated 0.05 mg/kg at 23 minutes
intervals up to a total of 0.2 mg/kg. Alternatively, ketamine 12 mg/kg IV
provides 510 minutes of surgical anesthesia.
Vagal Maneuvers
In a hemodynamically stable patient with a regular rhythm, rst vagotonic
maneuvers can be tried. These vagotonic maneuvers include the Valsalva
maneuver, unilateral carotid sinus massage, or application of an ice pack
to the face. One method of Valsalva maneuver is to have the child blow
through an obstructed straw.
This may terminate the arrhythmia (AVRT, AVNRT) or transiently slow the
ventricular rate so that the relationship of the P waves with the QRS com-
plexes becomes evident and it becomes possible to diagnose the rhythm dis-
order. Normal P waves are present in sinus tachycardia and retrograde P waves
(negative in lead II, positive in aVR.) may be apparent in reentrant tachycardias.
P waves outnumber the QRS complexes in atrial utter or AET with a block.
Vagal maneuvers and adenosine are ineffective in atrial brillation.
Adenosine
The action of adenosine is similar to vagotonic maneuvers and acts by
slowing AV nodal conduction. It may terminate reentrant tachycardias or
ERRNVPHGLFRVRUJ
cause transient slowing of the ventricular rate. It acts in 1020 seconds

and causes a brief (23 seconds) period of cardiac standstill, which is fol-
lowed by return of normal sinus rhythm or a recurrence of the arrhythmia.
Its advantages are the short half-life (<2 seconds), no negative inotropic
effects, and it has no adverse effects in wide QRS complex tachycardias.
It can be repeated in up to 3 incremental doses.
Thereafter, a number of alternative treatment options are available,
which will control the fast ventricular rate or convert the arrhythmia to
sinus rhythm viz. calcium channel blockers (e.g., diltiazem), -blockers
(e.g., esmolol), or Inj. amiodarone. Calcium channel blockers and -blockers
must not be combined because of the severe negative inotropic effect.
Calcium Channel Blockers

IV diltiazem or verapamil can be given. Calcium channel blockers are con-
traindicated in infants (high risk of electromechanical dissociation) and
in patients with wide QRS-complex tachycardias or with signicant hemo-
dynamic compromise. Side effects include hypotension, congestive heart
failure, AV block, and asystole. These effects can however be managed with
adrenergic agents and IV calcium gluconate.
Beta-Blockers
Esmolol may effectively control the heart rate in narrow complex tachycar-
dias. IV metoprolol needs to be used with caution in children as its efcacy
and safety is yet to be established.
Amiodarone
Amiodarone may cause cardioversion of both supraventricular and ven-
tricular arrhythmias and has minimal negative inotropic effects. It however,
often causes severe bradycardia and must be used with caution following
-blockers or calcium channel blockers. Its other cardiovascular adverse
effects include hypotension, congestive heart failure, VT, AV blocks, and car-
diac arrest.
Digoxin
Digoxin may be given to patients of all forms of tachyarrhythmias with
poor LV function as an adjunct to amiodarone, calcium channel blockers,
or -blockers, except in preexcitation syndrome (WPW).
ERRNVPHGLFRVRUJ
Therapeutic Overdrive Pacing

Temporary atrial overdrive pacing (transthoracic or transvenous) may be
attempted in narrow complex tachycardias. Pacemaker rates 1020 beats faster
than the tachycardia, with adequate pacing output may result in pacing the
myocardium. Progressively faster rates are tried till pacing takes place and the
pacemaker is then suddenly stopped, in an effort to terminate the arrhythmia.
In AET, overdrive atrial pacing may result in a 2:1 AV block, thus
decreasing the ventricular rate. Similarly, by increasing the degree of block,
atrial pacing at rates faster than the atrial rate (not ventricular rate) may
be effective in atrial utter. In junctional ectopic tachycardia, it may some-
times be possible to establish AV synchrony by pacing the atrium at rates
faster than the junctional rate.
Treat Possible Causes

Possible causes of arrhythmias include hypoxia, acidosis, hypothermia,
hypovolemia, hyperkalemia, hypokalemia, cardiac tamponade, tension
pneumothorax, and various drugs.
Management of Atrial Fibrillation
1. Inj. amiodarone promotes cardioversion and controls the ventricular

rate and may be preferable in the hemodynamically stable patient.
2. IV calcium channel blockers (diltiazem or verapamil) or -blockers
(esmolol) are alternatives to amiodarone and are indicated when
a faster action is needed, e.g., when arrhythmia is the cause of
hemodynamic instability. -blockers and Ca channel blockers must
not be combined and must be used with caution with amiodarone.
3. Digoxin can be used as adjunctive therapy to -blockers, calcium channel
blockers, or amiodarone in patients with heart failure or poor LV function.
4. Synchronized cardioversion 0.52 J/kg is indicated in the hemodynamically
unstable patient either as rst line of therapy, or in patients who do not
respond to IV calcium channel blockers (or -blockers).
Management of JET
The problem with JET is that it is unresponsive to DC cardioversion, cal-

cium channel blockers, and -blockers. The patients are hemodynamically
ERRNVPHGLFRVRUJ
compromised, and its management may need to be prolonged for days

before the arrhythmia settles down.
1. Chronotropic agents are withdrawn; electrolyte disturbances and all
uid decits are corrected.
2. Induced hypothermia is usually very effective in slowing the
arrhythmia rate. The patient is placed on a cooling blanket and ice
packs utilized to bring down the core temperature by 12C.
3. The patient needs to be ventilated, with full neuromuscular paralysis
and sedation to decrease the basal metabolic rate.
4. Intravenous amiodarone: Loading 5 mg/kg (over 30 minutes) is
followed by a maintenance 35 mcg/kg/min infusion.
5. The use of xed-rate atrial pacing at a rate higher than the tachycardia
rate may restore AV synchrony and improve hemodynamics in some
patients.
Differential Diagnosis of Broad QRS Complex

Tachycardias
Ventricular tachycardia Supraventricular tachycardia with

bundle branch block or accessory
pathway
Atrioventricular dissociation. Ventriculoatrial 1:1 AV conduction
conduction may be present. Presence of
capture beats and fusion beats are
supportive evidence.
QRS >160 msec. (VT from the conduction QRS <160 msec. (SVT with accessory
system has QRS <140 msec) pathway QRS >160 msec)
Left axis deviation > 30. (Not valid Right axis (posterolateral accessory pathway
in presence of left bundle branch will have left axis deviation).
block)
Occasionally concordant pattern in Concordant pattern is absent in precordial
precordial leads. (Entirely +ve or leads. (Left posterolateral AP has concordant
ve QRS complexes in all precordial pattern)
leads)
Wide complex tachycardia has several potential causes, which include (i)
VT; (ii) SVT with aberrant interventricular conduction (bundle branch
ERRNVPHGLFRVRUJ
blocks) or atrioventricular conduction over an accessory pathway (Wolff-

Parkinson-White); and (iii) QRS widening due to drugs, electrolyte abnor-
malities, or ventricular pacing.
Management of Broad QRS Complex Tachycardia

(>0.09 Second)
1. Drugs
In patients with VT, even though DC cardioversion is the most
effective treatment, it requires systemic analgesia and sedation,
thus monomorphic VT with adequate vital end-organ perfusion
and no signs of hemodynamic compromise can initially be treated
with intravenous amiodarone, lignocaine, or procainamide. As
hypomagnesemia is a cause of VT, especially torsades, a stat dose
magnesium sulfate (50 mg/kg over 20 minutes) can also be given.
Any electrolyte abnormalities are corrected.
2. Cardioversion
If medical therapy fails to correct the rhythm or the patient is unstable,
synchronized cardioversion is given in increments (children 0.52 J/kg,
adults 120 J initially, then 200 J if unsuccessful). Amiodarone is also
indicated after electric cardioversion to prevent further episodes of VT.
3. Adenosine
When it is not possible to differentiate VT from a supraventricular
arrhythmia with aberrant conduction,the options available are:
(i) Inj. adenosine (0.1 mg/kg IV) may be considered in a
hemodynamically stable patient in regular rhythm with a
monomorphic QRS. It may convert the supraventricular
arrhythmia to sinus rhythm.
(ii) IV amiodarone.
(iii) Alternatively, synchronized cardioversion (0.52 J/kg in children,
120200 J in adults) may be attempted in the rst place.
Cardiac Arrest
Cardiac arrest is classied into (i) shockable rhythm and (ii) non-shockable
rhythm, based upon whether the particular arrhythmia responds to de-
brillation or not. The two shockable rhythms are ventricular brillation and
pulseless ventricular tachycardia, while the two non-shockable rhythms are
ERRNVPHGLFRVRUJ
asystole and pulseless electrical activity. These patients require emergency man-
agement as per the PALS protocols (see chapter on Pediatric Resuscitation).
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cited: 2011 Sep 21] Available at: http://www.merckmanuals.com/professional/cardiovascu-
lar_disorders/arrhythmias_and_conduction_disorders/overview_of_arrhythmias.html
10. Penny-Peterson ED, Naccarelli GV. Supraventricular tachycardia. In: Yusuf S, Cairns JA,
Camm AJ, Fallen EL, Gersh BJ, ed. Evidence Based Cardiology 3rd ed. Blackwell Publishing;
2010:60618.
12. Reentrant Supraventricular Tachycardias (SVT, PSVT). The Merck Manuals: online medical
library. [Updated: 2010 Jan; cited: 2011 Sep 21] Available at: http://www.merckmanuals.com/
professional/cardiovascular_disorders/arrhythmias_and_conduction_disorders/reentrant_
supraventricular_tachycardias_svt_psvt.html
13. Robida A. Early arrhythmias in children after cardiac surgery. Heart Views 1999;1:2238.
Available at: http://www.hmc.org.qa/heartviews/VOL1NO6/07CONGENITAL_HEART_DISEASE.
htm
14. Rosenthal L, McManus DD. Atrial Fibrillation. [Updated: 2010 Jun 1; cited: 2011 Sep 21].
Available at: http://emedicine.medscape.com/article/151066-overview.
15. Sanatani S, Hamilton RM. Supraventricular Tachycardia, Atrial Ectopic Tachycardia.
[Updated: 2011 Sep 12; cited: 2011 Sep 21]. Available at: http://emedicine.medscape.com/
article/898784.
16. Saxena A, Juneja R, Ramakrishnan S. Working Group on Management of Congenital Heart
Diseases in India. Drug therapy of cardiac diseases in children. Indian Pediatr 2009;46:31038.
17. Schlechte EA, Boramanand N, Funk M. Supraventricular tachycardia in the primary care
setting: age-related presentation, diagnosis, and management. J Pediatr Health Care 2008;
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18. Valsangiacomo E, Schmid ER, Schpbach RW, et al. Early postoperative arrhythmias after
cardiac operation in children. Ann Thorac Surg 2002;74:7926.
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Bradyarrhythmias
and Pacemakers
I seriously doubt if anything I ever do will ever give me the elation
I felt that day when my own two cubic inch piece of
electronic design controlled a living heart
Wilson Greatbatch (19192011)*
Heart Blocks
Fig. 1: First-degree heart block.
Fig. 2: Mobitz type 1 second-degree heart block.
Fig. 3: Mobitz type 2 second-degree heart block.
*Wilson Greatbatch was the inventor of implantable cardiac pacemaker. He is credited with
320 inventions and more than 150 patents.
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Fig. 4: Complete heart block.
Types of Heart Block

Type ECG findings Comments
First-degree AV PR interval is prolonged above the PR prolongation may be
block upper limit of normal for age. All QRS caused by drugs such as
complexes are preceded by a P wave. digoxin, -blockers, or
calcium channel blockers
and also occurs in a
variety of cardiac
diseases.
Second-degree AV In Mobitz type 1, second-degree AV Drugs or disease processes
block block, the PR interval is progressively that affect the AV node
Mobitz type 1 (also prolonged with each beat, until a P produce this type of block,
called Wenckebach wave is not followed by a QRS complex. e.g., digoxin or an inferior
block) The cycle is constantly repeated. infarction.
Mobitz type 2 In Mobitz type 2, second-degree AV Mobitz type 2 block is usually
block, after a number of normal beats caused by an organic lesion
a QRS complex is blocked (2:1 block, in the conduction pathway
3:1 block). The PR interval does not and is not the effect of drugs.
lengthen before a dropped beat. More It may progress to complete
than one dropped beat may occur in heart block and is an
succession. indication for a pacemaker
implantation.
Third-degree AV No conduction between the atria and Complete heart block can
block (complete ventricles takes place and both function be congenital and also
heart block) independently at different rates. caused by injury to the
Normal P waves may be present or there conduction pathway during
may be an atrial arrhythmia. Alternatively, surgery or as a side effect of
there may be no atrial activity. drug toxicity.
With associated junctional escape

rhythm, the QRS complexes have
a normal configuration; while with
ventricular escape rhythm, the QRS has
a wide abnormal configuration.
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Bradyarrhythmias and Pacemakers 65
NASPE/BPEG Generic Code for Pacemakers
1. Chamber(s) 2. Chamber(s) 3. Response to 4. Rate 5. Multisite

paced sensed sensing modulation pacing
O None O None O None O None O None
A Atrium T Triggered R Rate modulation A Atrium
V Ventricle V Ventricle I Inhibited V Ventricle
D Dual (A + V) D Dual (A + V) D Dual (T + I) D Dual (A + V)
The North American Society of Pacing and Electrophysiology (NASPE) and

the British Pacing and Electrophysiology Group (BPEG) have devised a
generic letter code to describe the types and functions of pacemakers. The
rst three letters are used to describe pacing functions in bradycardia and
heart blocks.
1. The letter in the rst position identies the chamber paced (O, none;
A, atrium; V, ventricle; D, dual chamber [A + V]).
2. The second is the chamber sensed (O, none; A, atrium; V, ventricle;
D, dual).
3. The third letter corresponds to the response of the pacemaker to an
intrinsic cardiac event (O, none; I, inhibited; T, triggered; D, dual [I + T]).
4. The fourth letter indicates both programmability and rate modulation.
5. The fth position of the code is used to indicate whether multisite
pacing is present.
Pacing Modes
Parameters to be set in various modes

Parameters AAI VVI DVI VDD DDD
Rate + + + + +
Upper rate + +
A sense + + +
A output + + +
V sense + + + +
V output + + + +
PVARP + +
AV interval + + +
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External (or temporary) pacemakers may be single chamber or dual cham-

ber pacemakers. Single chamber pacemakers are capable of pacing only the
atria or ventricle at one time and can be programmed in the VVI, VOO,
AAI, or AOO mode. Dual chamber pacemakers are capable of synchro-
nously pacing the atria and the ventricle.
Demand pacemakers are pacemakers with single and double chamber
pacing modes with a sensing function, which causes triggering or inhibi-
tion of a paced event (AAI, VVI, DVI, VDD, DDD).
1. In AOO mode, the atria is paced at a xed rate with no atrial or
ventricular sensing. AOO pacing may be used for overdrive pacing in
atrial arrhythmias.
2. In VOO pacing, the ventricles are paced at a xed rate with no atrial or
ventricular sensing. This type of pacing can be used in an emergency
and also during surgery when electrocautery causes interference with
demand pacing.
3. In AAI mode, the atria are paced and sensed. Intrinsic atrial activity
inhibits the paced atrial impulse, otherwise the atria is paced at a set
rate. This type of pacing is commonly used in sinus node dysfunction
with intact AV conduction.
4. In VVI pacing, the ventricle is paced and sensed. If an intrinsic
ventricular beat is sensed the paced impulse is inhibited, otherwise,
the ventricle is paced at the set rate. In VVI pacing, there is no AV
synchrony. This type of pacing may be used for episodic AV block or
bradycardia in small infants.
5. In DVI pacing, both the atrium and ventricle are paced but only
the ventricle is sensed. It allows AV sequential pacing, if after an
atrial stimulus, AV conduction takes place, ventricular pacing is
inhibited; otherwise, ventricular pacing occurs. Competing atrial
rhythm may precipitate atrial utter or brillation, since atria is
not sensed.
6. In VDD mode, the ventricle is paced but both atrium and ventricle
are sensed. Provided the intrinsic atrial rate is higher than the set
atrial rate, sequential pacing will occur. In other circumstances when
there is no atrial activity or the intrinsic atrial rate is slow, VDD mode
functions like VVI.
7. A DDD device is a dual-chamber pacemaker, which is capable of
sensing both atria and ventricles, and then triggering or inhibiting
the paced output in either chamber. A sensed atrial impulse will
inhibit the atrial pacing impulse and after the programmed AV delay,
it will initiate a ventricular paced event. In case it senses an intrinsic
ventricular impulse, ventricular pacing is inhibited.
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Access Sites for Pacing
Site Indication
Epicardial Postoperatively
Transcutaneous In an emergency till another method of pacing can be initiated
Transvenous Used in the absence of epicardial pacing wires
Esophageal Management of atrial arrhythmias by overdrive pacing
Epicardial pacing is used postoperatively after cardiac surgery. In the bipolar

system of wire placement, two wires each are sutured to the right atrium
and right ventricle, while in the unipolar system one negative electrode
is attached to the RA and one to the RV and the two positive electrodes are
attached to the subcutaneous tissue. The advantage of the bipolar system
for temporary postoperative pacing is that lower pacing outputs and sens-
ing thresholds are needed for pacing. Single or double chamber pacing is
instituted by the appropriate set of wires. By convention, atrial wires are
made to exit on the right of the sternum and the ventricular wires to the left
of the sternum.
Transcutaneous asynchronous ventricular pacing can be initiated in an
emergency by an external pacing device or pacing capable debrillator unit
through skin electrodes. This method of pacing requires high energy for
capture and is used only as a bridge for a couple of hours till pacing can be
established by another method.
Transvenous pacing is instituted via a lead inserted under uoroscopic
guidance to pace the RV (VVI/VOO).
Transesophageal pacing can only be used to pace the atria so it is not
useful in AV dissociation. Its main use is in the treatment of atrial arrhyth-
mias for overdrive pacing using a specialized generator. High pacing out-
put over a long period can cause esophageal perforation.
Pacemaker Parameters
Pacemaker Output
The lowest output (dened in mV or mA) that will result in contraction
of atrium or ventricle is called the capture threshold. The duration of the
pacing impulse (dened in milliseconds) is known as the pulse width. In
temporary pacemakers, the pacing output can be set but the pulse width is
a xed parameter.
To establish the pacemaker output required for capture of the atria, the
following method is used. The pacing rate is set to 10 beats/min above the
ERRNVPHGLFRVRUJ
patients intrinsic heart rate and if the AV conduction is intact, the AV inter-
val is kept less than the intrinsic AV interval. Starting with an atrial output
of 5 mV, the output is decreased till capture is lost or increased till capture
occurs. Capture is indicated by the presence of an atrial pacing spike fol-
lowed by a P wave. For safety reasons, the pacing output is kept at twice the
value which was required for capture.
The output required for pacing the ventricle is similarly determined
(start with 5 mV). Capture is indicated by the presence of a ventricular pac-
ing spike followed by a wide pacing complex. The pacing output is again
kept at twice the value determined for capture.
If the AV conduction is intact, increasing the AV interval to more than
the patients AV interval will allow conducted ventricular beats.
Sensing
The sensing threshold is the highest voltage set on the pacemaker at
which the pacemaker can still detect the intrinsic atrial or ventricular
electrical impulse. Setting the threshold too high will cause failure of sens-
ing (undersensing) leading to xed-rate pacing (AOO/VOO), and setting
it too low will result in sensing of other activity (oversensing) and loss of
pacing.
The optimal atrial sensing threshold is established by keeping the pac-
ing rate to 10 beats/min below the patients intrinsic atrial rate and the
pacing output set to a minimum. Starting with the maximum atrial sens-
ing threshold, which results in xed rate pacing, the sensing threshold
is slowly reduced till the pacemaker starts to sense. The sensing thresh-
old is set to half this value, but if muscle activity is sensed, this setting is
increased. This is repeated for ventricular threshold.
Pacing Rate
Single chamber pacing modes require a single rate setting. In AAI and
VVI modes, the pacemaker will pace at the set rate unless exceeded by the
intrinsic rate.
Dual chamber pacing modes require a lower rate setting and an
upper tracking rate setting. The upper rate is the maximum rate at which
the pacemaker will pace the ventricle even if the sensed intrinsic atrial
rate becomes higher than this set rate. At intrinsic atrial rates above the
upper tracking rate, the ventricular response results in a second-degree AV
block (Wenckebach response). This is a safety measure, which prevents
pacemaker mediated tachycardia resulting from tracking of high atrial
rates.
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Refractory Periods
P P
AVI
PVARP
Fig. 5: Refractory periods. AVI: atrioventricular interval, PVARP: post ventricular atrial refractory period.
Total atrial refractory period (TARP) is the combination of the atrioventricular

interval (AVI) (which is analogous to the PR interval) and the post ventricu-
lar atrial refractory period (PVARP) (which is the period beyond the ventricu-
lar sensed or paced impulse during which also the atria are refractory). The
purpose of the refractory period is to prevent the atrial channel of the pace-
maker from sensing the output impulse of the ventricular lead (cross talk),
retrograde P waves, or the QRS complex (far eld R waves) as atrial signals.
Ventricular refractory period (VRP) follows the ventricular paced or
sensed impulse and prevents the ventricular channel of the pacemaker
from sensing of the pacing stimulus and the R waves. VRP is not program-
mable on temporary pacemakers (typical values for VRP are 200350 msec).
DDD pacemakers have settings for upper tracking rates, AVI, and PVARP.
Higher tracking rates in children require shorter PVARP or/and AVI. Too
short an AV interval may not allow adequate ventricular lling (generally
set between 100140 msec for children and 150200 msec in adults when
paced at 80110/min) and too short a PVARP may result in oversensing or
pacemaker-mediated tachycardia.
Initial Pacemaker Settings
Atrial and ventricular output Typical atrial: 5 mA/mV

Typical ventricular: 810 mA/mV
AV interval (same as PR interval) In children 100140 msec. Sets automatically with the set rate
Atrial and ventricular sensing Typical atrial: 0.4 mV (<1 mV)
threshold Typical ventricular: 2.0 mV (25 mV)
Atrial/ventricular rate Set at physiologic rate for individual patient
Upper rate Automatically adjusts to 30 bpm higher than the set rate
Refractory period PVARP (post ventricular atrial refractory period) sets
automatically depending on the set rate
mA: milliamperes, mV: millivolts, PVARP: post ventricular atrial refractory period.
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Setting the Pacemaker in a Postoperative Patient
AV Sequential Pacing
Fig. 6: AV sequential pacing: atrial and ventricular pacing spikes are followed by atrial and
ventricular complexes. However, note that the P waves are often barely discernable between
the pacing spikes, and ventricular pacing produces wide QRS complexes.
Sinus bradycardia with AV block requires sequential pacing of the atria and
ventricles. The pacing rate is set at the normal rate for the patients age (to
pace, the set rate must be higher than the intrinsic atrial rate), and the
atrial and ventricular pacing outputs are set at 2 the minimum required
for capture. The atrial and ventricular sensing is appropriately set at half
the noted sensing threshold. In temporary pacemakers, the AV interval,
upper rate, and PVARP change automatically with set rate, however, can
also be manually altered to ensure the best hemodynamics.
Synchronized Ventricular Pacing
Fig. 7: Synchronized ventricular pacing. Ventricle pacing follows P waves at the atrial rate of
140 beats/min.
Normal sinus rhythm with AV dissociation requires tracking of P waves with

synchronized ventricular pacing. This needs the atrial pacing rate to be
kept less than the intrinsic atrial rate. If it is more than the intrinsic atrial
rate, the atria will also be paced in addition to the ventricle. This will also
happen if the atrial P wave is not sensed for any reason.
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Single Chamber Atrial Demand Pacing
Fig. 8: Atrial pacing. Atrial pacing spikes are followed by P waves and normal QRS complexes.
In sinus bradycardia without AV block, single chamber pacing of the atria

alone is required. With appropriate atrial sensing, pacing of the atria will
take place as long as the set rate is higher than the intrinsic rate.
Troubleshooting Pacemakers
Problem Causes Solutions

Failure to (1) Pacing output inadequate (1) Increase the pacing output
capture (2) Dislodged or fractured lead, low (2) Try with reversing the wires
(pacing battery connected to the pacemaker
spikes not (3) Electrolyte abnormalities (acidosis, cable (reverse polarity) or convert
followed by hypokalemia) a bipolar system to a unipolar
P waves/QRS system or change battery, cables,
complexes) pacemaker
(3) Correct electrolytes
Failure to (1) Sensitivity threshold set too high (1) Sensitivity threshold ( mV)
sense (atrial/ (2) Dislodged or fractured lead, low (2) Try with reverse polarity or
ventricular battery convert bipolar system to unipolar
pacing spikes (3) Electrolyte abnormalities (acidosis, system or change battery, cables,
not related to hypokalemia) pacemaker
P/QRS) (3) Correct electrolytes
Failure to pace (1) Sensitivity threshold set too (1) Increase sensitivity threshold
(pacing spikes low or PVARP too short causing ( mV) or increase duration of
absent) oversensing PVARP
(2) Dislodged or fractured lead, low (2) Try with reverse polarity or
battery convert bipolar system to unipolar
(3) Electrolyte abnormalities (acidosis, system or change cables, battery,
hypokalemia) pacemaker
(3) Correct electrolytes
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Problem Causes Solutions

Competition Set pacemaker and patients intrinsic (1) Increase rate of pacing
rates are similar and there is failure to (2) Troubleshoot as for failure to
sense or asynchronous pacing sense (decrease sensitivity
threshold by mV)
Wenckebach (1) May occur with sinus tachycardia, (1) Treat cause of tachycardia:
response atrial fibrillation and flutter fever, pain, hypovolemia,
(2) Upper rate limit may be set antiarrhythmic drugs
inappropriately low (2) Adjust pacemaker upper rate
limit as appropriate
Pacemaker In DDD, a reentrant tachycardia Increase PVARP setting or convert to
mediated caused by retrograde conduction atrial nonsensing mode (DVI)
tachycardia of P wave
Failure to Capture
Fig. 9: Atrial non-capture. Note that atrial pacing spikes are not followed by P waves.
Fig. 10: Ventricular non-capture. Note that some ventricular pacing spikes are not followed by
QRS complexes.
Failure of atrial capture is evident by presence of atrial pacing spikes that

are not followed by P waves, and similarly failure of ventricular capture is
shown by ventricular pacing spikes not followed by QRS complexes. In a
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critical setting, inappropriate pacing may result in bradycardia, low cardiac

output, or cardiac arrest.
In case of failure of capture, the rst step is to conrm that the pacing
output is adequate. Reversing lead polarity or conversion of a bipolar sys-
tem to a unipolar system may resolve the problem. The integrity of the
pacemaker leads and the battery is checked.
Failure to Sense
Fig. 11: Atrial undersensing. Atrial pacing spikes occur regardless of P waves, and the ventricular
pacing is not synchronized to the normal P waves.
a a b a b a
Fig. 12: Ventricular undersensing; ventricular pacing spikes occur at a fixed

rate since intrinsic activity is not sensed. Pacing rate 110/min, intrinsic rate 150/min.
a: Ventricular paced beats are noted whenever pacing take place during the
non-refractory phases of the ventricle (Crest of preceding T wave to onset of next QRS),
b: Fusion beats result with simultaneous occurrence of intrinsic and paced beats.
In atrial undersensing, atrial pacing spikes occur irrespective of inherent

P waves; similarly in ventricular undersensing, ventricular pacing spikes
occur regardless of QRS complexes. The pacemaker will continue to pace
with no regard to the patients inherent rhythm. With undersensing, there
is potential danger of a paced ventricular beat falling on the T wave and
causing ventricular brillation.
The sensitivity threshold is checked to conrm if it has not been set too
high. Reversing lead polarity or conversion of a bipolar system to a unipolar
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system may correct the problem. The pacemaker leads and the battery may
require replacement.
Failure to Pace
a b
Fig. 13: The pacemaker is inhibited by a T wave (arrow a). Similarly artifacts may inhibit the
pacemaker (arrow b).
During the period when the pacemaker fails to pace, there is no pacing
spike and no paced P or QRS complex is seen. Causes of failure of pacing
include oversensing, dislodged or fractured leads, low battery, and electro-
lyte abnormalities (acidosis, hypokalemia).
Oversensing occurs when the pacemaker sensing threshold has been set
too low and the pacemaker senses other signals, e.g., skeletal muscle con-
traction, electromagnetic interference, etc. This is corrected by increasing the
sensitivity threshold (i.e., decreasing the sensitivity). Increasing the thresh-
old too high will convert demand pacing to asynchronous VOO pacing.
The pacemaker is checked to conrm the function of the pacemaker,
leads, and battery. Pacing is tried with the polarity of the leads reversed
and if required, the bipolar system is converted to a unipolar system.
Competition
Fig. 14: Competitive pacing. The pacing rate is 136/min and the intrinsic rate 124/min. The
intrinsic rhythm is not sensed resulting in unrelated ventricular pacing spikes to the QRS
complexes, paced beats, and fusion beats (arrow).
In demand pacemakers, competition between the intrinsic cardiac rhythm

and the pacemaker rhythm occurs when two things happen(i) the intrinsic
ERRNVPHGLFRVRUJ
heart rate is similar to the paced rate and (ii) xed rate pacing occurs
because of failure of sensing of the intrinsic rhythm or alternatively if
xed rate pacing is being used. The ECG shows unrelated pacer spikes to
P waves and QRS complexes, multiple paced beats and fusion beats. There
is danger that the pacemaker spike can fall on the intrinsic T wave and
cause ventricular brillation.
To prevent competition, the pacing rate is increased and the sensitiv-
ity threshold of the pacemaker is reduced ( mV) to ensure sensing of the
atrial impulses.
Wenckebach Response
In case of a fast atrial rate, which rises above the upper tracking rate, a fast
ventricular response is prevented by the occurrence of a second-degree AV
block (Wenckebach block response). This is a safety measure, which prevents
pacemaker mediated tachycardia resulting from tracking of high atrial rates.
Treatment involves the control of tachycardia and increasing the pace-
maker upper tracking rate limit in case it had been set inappropriately low.
Pacemaker Mediated Tachycardia

During synchronous AV pacing (DDD, VDD), a ventricular extrasystole
may result in retrograde VA conduction and a retrograde P wave. If this
retrograde P wave is sensed by the atrial electrode, it will initiate a paced
ventricular complex. This can again result in a retrograde P wave and a
reentrant tachyarrhythmia will be established. This is prevented by setting
a PVARP long enough to prevent the sensing of retrograde P waves or con-
version to a P wave nonsensing mode (DVI).
Therapeutic Overdrive Pacing
Temporary overdrive pacing may be effective as a means of terminating

paroxysmal supraventricular tachycardias, atrial utter, and JET. Pacing
at rates 1020 beats faster than the tachycardia may capture the myocar-
dium, which is indicated by a change in the morphology of the P wave, or
a change in the conducted RR interval. Adequate pacing output is required
and progressively faster rates are tried till capture is conrmed, the pacing
is then stopped abruptly to terminate the arrhythmia.
In SVTs and atrial utter, pacing is done at rates faster than the atrial
rate and not the ventricular rate. In junctional ectopic tachycardia, it may
be possible to establish AV synchrony by temporary dual chamber pacing
at a faster rate than the junctional rate.
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Removal of Pacing Wires
Once it is conrmed that the coagulation prole is normal, temporary epi-

cardial pacing leads can be removed by gentle traction. The ECG is moni-
tored for arrhythmias during the removal, and the patient is clinically
observed for a few hours for any signs of cardiac tamponade. Occasionally,
it may not be possible to remove the wires without use of force, in which
case the wires are pulled only as far as possible and then cut close to the
skin. This permits the wires to retract under the skin.
MRI in Patients with Pacing Wires
MRI is avoided in patients with temporary epicardial pacing wires because

of the risk of causing an arrhythmia or injury from excessive heat at the
electrode tip. An MRI may however be performed in patients with retained
epicardial wires, which are not exposed at the skin as these do not concen-
trate energy.
Bibliography
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Pediatr Cardiol 2008;1:1205.
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Hypertensive
Emergencies
All the causes of things cannot be seen, because they appear to depend on
circumstances which are unknown, or appear to be accidental
John Hunter (17281793)*
Parenteral Antihypertensive Agents
Drug Remarks
Diazoxide An arteriolar vasodilator with onset of action in
Children/Adults: 13 mg/kg 35 minutes and duration of action of 212 hours.
(max 150 mg) is given every Hyperglycemia, persistent hypotension, and salt and
515 minutes till optimal control water retention are adverse effects.
of blood pressure. Dose may be
repeated q424h.
Alternatively, 35 mg/kg infused
over 30 minutes may result in less
hyperglycemia and a controlled fall
in BP.
Enalapril IV enalapril is of variable effectiveness, with an onset of
Children: 510 mcg/kg q68h IV action of 3060 minutes. These factors limit its use in
over 5 minutes. hypertensive emergencies.
Adults: 1.252.5 mg q6h IV.
Esmolol Selective 1blocker; has a rapid onset of action and a
Children and adults: Bolus 500 mcg/ short half-life of a couple of minutes.
kg IV over 12 minutes, followed by
an IV infusion of 50300 mcg/kg/min.
Dilute to a concentration of 10 mg/mL
in 5% dextrose or normal saline for
infusion.
Hydralazine Directly acting arteriolar vasodilator. Onset of action is
Children: 100500 mcg/kg IM/IV within 520 minutes and duration of action is about
infusion over 20 min; repeat 26 hours. Prolonged hypotension and reflex
every 46 hours if required. tachycardia are important adverse effects.
Alternatively, IV infusion
12.550 mcg/kg/h may be given.
Adults: 510 mg IV, repeat q46h if
required. Alternatively, IV infusion
39 mg/h.
*John Hunter is regarded as one of the most distinguished anatomists and surgeons of his day.
The Hunterian oration of the Royal College of Surgeons of England is delivered in his honor.
ERRNVPHGLFRVRUJ
Hypertensive Emergencies 79
Drug Remarks
Labetalol Predominant -blocker with some -blocking action.
Children: Initially 250 mcg/kg is Onset of action is 510 minutes and action lasts
administered over 2 minutes. 36 hours after discontinuation of the drug. Its use
250500 mcg/kg may be repeated is limited in cardiac failure and is to be used with
every 10 minutes until the desired caution in patients with asthma. No change in dosing
BP is reached. Max dose 1 mg/kg. is required in renal failure. It is the drug of choice in
If required, this is followed by an hypertensive encephalopathy.
infusion of 0.251.5 mg/kg/h titrated
to blood pressure.
Adults: Initially 20 mg IV is
administered over 2 minutes.
2080 mg may be repeated every
10 minutes up to a max dose of
300 mg.
If required, this is followed by an
infusion of 13 mg/min titrated to
blood pressure.
Nicardipine IV calcium channel blocker with onset of action in 1015
Children: 0.53 mcg/kg/min IV minutes and a half life of 40 minutes. Advantages over
infusion. nitroprusside include the ability to use it for more than
a few days, as it does not produce toxic metabolites. It is
Adults: 5 mg/h initially, increase dose
used in a gradually increasing dose up to 3 mcg/kg/min.
by 2.5 mg/h every 1015 minutes
Unwarranted hypotension is treated with 10% calcium
up to a max of 15 mg/h; then reduce
gluconate 0.2 mL/kg IV over 5 minutes.
to 13 mg/h.
Sodium nitroprusside Arteriolar and venous vasodilator with immediate onset
0.510 mcg/kg/min IV infusion. of action and a short half-life of a few minutes. Dose is
titrated to achieve effect.
Oral Antihypertensive Agents
Drug Remarks
Amlodipine A 12 hours dose may provide better efficacy in
Children (>6 years): 2.55 mg q24h children. It has a gradual onset of action and may take
or in divided doses q12h. 57 days for full effect thus dose adjustments should
be made only after this period.
Adults: 510 mg q24h.
Atenolol Cardio-selective -blocker. Contraindicated in
Children: 11.2 mg/kg q24h; increase pulmonary edema and cardiogenic shock. May cause
to a max 2 mg/kg q24 h. bradycardia, hypotension, second or third degree
Adults: 25100 mg/kg q24h; increase AV block. Exercise caution in diabetes and asthma.
to a max 200 mg q24h.
ERRNVPHGLFRVRUJ
Drug Remarks
Captopril Onset of action in 1530 minutes and duration of
Children: 0.36 mg/kg/day in divided action 812 hours. Starting with a lower dose, the
doses q8h. dose is increased over 12 weeks.
Adults: 6.2512.5 mg q812h; increase
to a max 50 mg q8h.
Diltiazem Maximum antihypertensive effect is seen within
Children: 1.52 mg/kg/day in divided 2 weeks.
doses q68h; increase to a max
3.5 mg/kg/day.
Adults: 3060 mg q68h; increased
to a maintenance of 180360 mg/day
in divided doses q68h. (Diltiazem
SR 60120 mg q12h; increased to a
maintenance of 180360 mg/day in
divided doses q12h)
Enalapril Starting with a lower dose, the dose is gradually
Children: 0.10.5 mg/kg/day divided increased over a period of 2 weeks. Cough is a
q1224h. common reported side effect.
Adults: PO 2.55 mg/day divided
q1224h; increase to a max 20 mg/day.
Hydralazine Directly acting arteriolar vasodilator. May induce
Children: 0.751 mg/kg/day in divided reflex tachycardia and increased cardiac output,
doses q6h; increase to a max which can blunt its hypotensive effect. After an oral
8 mg/kg/day. dose, it has an effect in 2030 minutes that lasts 24 h
Adults: 1050 mg q6h. (less than IV).
Labetalol Predominant -blocker with some -blocking
Children: 13 mg/kg/day in divided action. Peak plasma levels occur 12 hours after oral
doses q12h PO; increase to a max administration with a half life of 68h. Steady state is
10 mg/kg/day. achieved on the third day of dosing.
Adults: 100400 mg q12h.
Metoprolol Modest 1 selectivity.
Children (117 yr): 12 mg/kg/day in Bronchospasm, bradycardia, heart block may take
divided doses q12h; increase to a max place.
6 mg/kg/day.
Adults: 100 mg/day in divided doses
q1224h; increase to a max 450 mg/day.
Nifedipine Calcium channel blocker that reduces blood pressure
Children: Hypertensive urgency: within 520 minutes, with maximum effects in
0.250.5 mg/kg q46h PRN 6090 minutes. Available for oral/sublingual use and
(max 10 mg/dose or 3 mg/kg/day). is recommended only for children with hypertensive
Hypertension: SR tablets 0.250.5 urgency.
mg/kg/day in divided doses q1224h;
increase to a max 3 mg/kg/day.
ERRNVPHGLFRVRUJ
Hypertensive Emergencies 81
Drug Remarks
Adults: Hypertension: 10 mg q8h;
increase to max 180 mg/day in
divided doses q68h.
SR tablet 3060 mg q24h; increase to
max 120 mg q24h.
Propranolol Non-selective -blocker. Contraindicated in bronchial
Children: 0.51 mg/kg/day in divided asthma, heart failure, and heart block. Starting with
doses q612h; increase to a max a lower dose, the dose is increased every 35 days till
8 mg/kg/day. the desired effect.
Adults: 40 mg/dose q12h; increase to
a max 640 mg/day.
A hypertensive crisis is an extreme elevation of blood pressure that may

be life-threatening or likely to result in signicant morbidity if untreated.
It occurs infrequently in children but may be associated with renovascular
hypertension, head injury, in the postoperative period following cardiopul-
monary bypass, repair of coarctation of the aorta and supra-aortic stenosis.
Hypertensive crisis is classied as either a hypertensive emergency or
a hypertensive urgency. Hypertensive emergency is said to be present
when the blood pressure is extremely high (1.31.5 times 95th percen-
tile) and end-organ damage (cardiac, CNS, renal, lung, or eye) is evident.
Hypertensive encephalopathy is an example of a hypertensive emergency
and is suggested by the presence of vomiting, fever, ataxia, stupor, and sei-
zures. Hypertensive urgency is present when the blood pressure is signi-
cantly high, but end-organ damage is not present.
In response to a hypertensive crisis, it is important to select an agent
with a rapid and controlled action and to carefully monitor the reduc-
tion of blood pressure. In hypertensive emergencies, the aim is to lower the
mean arterial pressure by a maximum of 25% in a period of minutes by
the use of IV antihypertensives and then gradually to normal over the next
48 hours. In hypertensive urgencies, the blood pressure is gradually reduced
to normal in 48 hours with either IV or oral medication. There is a risk of
cerebral and renal hypoperfusion if reduction of blood pressure is done at
a rate faster than this.
Vasodilators (sodium nitroprusside or nicardipine) may rst be given
to control the hypertension. In case optimum control of hypertension is
not achieved by IV vasodilators, a -blocker (esmolol or labetalol) can be
added to the vasodilator or used in its place.
Intravenous labetalol is the drug of choice in a hypertensive encepha-
lopathy, where vasodilators may increase the cerebral blood ow and
increase brain damage. Labetalol blocks both - and -adrenergic receptors
and a controlled reduction of blood pressure can be achieved.
ERRNVPHGLFRVRUJ
IV/IM diazoxide, hydralazine, or oral nifedipine are other alternative

drugs, especially in hypertensive urgencies. Sublingual administration of
nifedipine is no longer recommended.
Hypertensive crises may be associated with sodium and volume deple-
tion, and volume expansion with isotonic sodium chloride must also be
considered. Urine output requires diligent monitoring.
A number of drugs, used alone or in combination, are available for the
subsequent management of persistent hypertension. These include (i) cal-
cium channel blockersnifedipine, diltiazem, amlodipine; (ii) ACE inhibitors
captopril, enalapril; (iii) diureticsfurosemide, thiazides, K+ sparing diuretics; and
(iv) -blockerspropranolol, nadolol, metoprolol, atenolol.
Bibliography
1. Aggarwal M, Khan IA. Hypertensive crisis: hypertensive emergencies and urgencies.
Cardiology Clin 2006;24:13546.
2. Flanigan JS, Vitberg D. Hypertensive emergency and severe hypertension: what to treat, who
to treat, how to treat. Med Clin North Am 2006;90:43951.
3. Hari P, Sinha A. Hypertensive emergencies in children. Indian J Pediatr 2011;78(5):56975.
4. Houtman P. Management of hypertensive emergencies in children. Paediatr Perinat Drug Ther
2003;5(3):10710.
5. Hypertension in Children and Adolescents. The Seventh Report of the Joint National
Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. U.S.
Department Of Health And Human Services. National Institutes of Health National Heart,
Lung, and Blood Institute. National High Blood Pressure Education Program NIH Publication
No. 04-5230. August 2004.
6. Perez MI, Musini VM, Wright JM. Pharmacological interventions for hypertensive emergen-
cies. Cochrane Database of Systematic Reviews 2008;1: CD003653. DOI: 10.1002/14651858.
CD003653.pub3.
8. Robertson J, Shilkofski N. Drug doses. The Harriet Lane Handbook 17 ed. Philadelphia: Mosby;
2005:105368.
9. Temple ME, Nahata MC. Treatment of pediatric hypertension. Pharmacotherapy 2000;20(2):
14050.
10. Varon J, Marik PE. The diagnosis and management of hypertensive crises. Chest 2000;118:
21427.
ERRNVPHGLFRVRUJ
Pulmonary
Hypertension
All we know is still innitely less than all that remains unknown
William Harvey (15781657)*
Factors Controlling Pulmonary Circulation
Parameter Pulmonary vasoconstrictors Pulmonary vasodilators

pH Acidosis Alkalosis
Oxygenation Hypoxia Oxygen
Temperature Hypothermia Normothermia
Stimulation Pain, agitation Sedation, analgesia
Ventilation Hypoventilation, Mild hyperventilation
alveolar hyperinflation
The parameters for pulmonary arterial hypertension in children are the same
as for adult patients. It is dened as a mean pulmonary artery (PA) pressure
of more than 25 mmHg at rest (or more than 30 mmHg during exercise),
with a pulmonary vascular resistance of more than 3 Woods units/m2 in
the presence of a normal left atrial pressure (i.e., <15 mmHg). In the fetus,
pulmonary vascular resistance (PVR) is high because the lungs are lled
with uid. PVR begins to fall immediately after birth and reaches adult
levels within the rst few weeks of life.
In children with congenital heart disease with pulmonary hypertension or
even with normal PA pressure, the pulmonary arteries may undergo intense
vasoconstriction in response to various stimuli, such as hypoxia or acidosis.
PA constriction then results in further increase in PA pressure, which may
cause acute RV dysfunction. Such episodes of elevation of PA pressure may
occur in infants in the immediate postoperative period, after repair of con-
genital heart diseases like large VSDs, TAPVCs, and AV canal defects. An
acute rise in PA pressure that causes desaturation, tachycardia, hypotension,
or hemodynamic deterioration is called a pulmonary hypertensive crisis.
*William Harvey was an English physician who was the first to accurately describe circulation
of blood in his treatise Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus
[An Anatomical Exercise on the Motion of the Heart and Blood in Living Beings] (1628).
ERRNVPHGLFRVRUJ
Postoperative Measures to Optimize Hemodynamics in

Pulmonary Hypertension
Parameter Treatment
Sedation and analgesia Administer adequate sedation + analgesia (fentanyl or morphine
IV infusion).
Paralysis Paralyse if necessary (vecuronium or pancuronium) ET tube
suctioning is done with extreme caution.
Mechanical ventilation Hyperventilate to PaCO2 30, pH 7.50
Optimize PEEP to a minimum (05 mmHg) and maintain low peak
airway pressures (< 2530 mmHg).
Fluid electrolyte balance Correct electrolyte disturbances. Maintain alkalosis (administer
inj. sodium bicarbonate 8.4% IV if required). Correct anemia.
Inotropic support Minimize the use of pulmonary vasoconstrictors, e.g., dopamine.
Administer pulmonary vasodilators milrinone, dobutamine,
nitroprusside or isoprenaline.
Pulmonary vasodilator Phenoxybenzamine 0.250.5 mg/kg PO q12h (maximum
drugs dose <10 mg/day). Dose may be titrated upwards gradually.
Epoprostenol (PgI2) 0.516 ng/kg/min IV infusion.
Nitric oxide (580 ppm) is administered through the ventilator.
Sildenafil: Children 1 month: 0.252 mg/kg/dose PO q46h;
titrate dose upwards gradually.
An FiO2 of 1.0 is established on return from the operation theater, which

is gradually reduced according to the blood gases such that the arterial
PaO2 is maintained above 100 mmHg. Physiotherapy and tracheal suction
should be gentle and preceded by a bolus of sedative plus analgesic and
preoxygenation by hand bagging. Phenoxybenzamine (alpha block) 1 mg/kg
can be given before CPB and again during rewarming. It is continued post-
operatively in a dose of 0.250.5 mg/kg/dose every 12 hours.
Management of a Pulmonary Hypertensive Crisis
In a pulmonary hypertensive crisis, sedation is increased and the child is

paralysed (fentanyl 210 mcg/kg/h, vecuronium 0.1 mg/kg/h). Hand bag-
ging with 100% oxygen improves the oxygen levels and at the same time
increases respiratory alkalosis by elimination of carbon dioxide. Additional
sodium bicarbonate is given to maintain metabolic alkalosis. The aim
is to reduce the PaCO2 to less than 30 mmHg and pH to more than 7.5.
Alkalosis, not hypocarbia, reduces PVR.
ERRNVPHGLFRVRUJ
Pulmonary Hypertension 85
If possible, the doses of catecholamines should be reduced and of pul-

monary vasodilators increased to the maximum tolerated levels. Nitric
oxide inhalation is commenced or increased. Extracorporeal membrane
oxygenation may be considered in the child who remains unresponsive to
the above therapeutic measures.
Weaning
If the child is stable for a period of 24 hours, weaning of support should

be attempted very slowly over at least 2448 hours. Inotropes are gradually
reduced. PaCO2 is allowed to rise to 3035 mmHg, while a PaO2 of over
95 mmHg is maintained. Paralysis is discontinued and sedation reduced.
The child is extubated and only then are pulmonary vasodilators gradually
withdrawn. Recurrence of crisis would require reinstitution of measures for
the control of PA pressure.
Management of Excessive Pulmonary Blood Flow
In a child on ventilator support, when pulmonary blood ow is excessive

(e.g., in single ventricles, transposition of the great arteries, and postop-
eratively in a large BT shunt), factors that cause pulmonary vasoconstriction
need to be initiated to optimize the pulmonary blood ow. Such a strategy
will improve systemic blood ow and decrease the ventilation-perfusion mis-
match, and permit extubation. Promoting hypercarbia and a reduction in the
FiO2 even down to 20% will increase PVR and improve the systemic blood
ow. However, an arterial saturation of at least 80% should be maintained.
Bibliography
1. Balser JR, Butterworth J. Cardiovascular drugs. In: Hensley FA, Martin DE, Gravlee GEP, eds.
A Practical Approach to Cardiac Anesthesia 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins;
2003:46.
2. Beghetti M, Tissot C. Pulmonary hypertension in congenital shunts. Rev Esp Cardiol 2010;
63(10):117993.
3. Fischer LG, Van Aken H, Brkle H. Management of pulmonary hypertension: physiological and
pharmacological considerations for anesthesiologists. Anesth Analg 2003;96:160316.
4. Gorenflo M, Gu H, Xu Z. Peri-operative pulmonary hypertension in paediatric patients: current
strategies in children with congenital heart disease. Cardiology 2010;116(1):107.
5. Huddleston AJ, Knoderer CA, Morris JL, Ebenroth ES. Sildenafil for the treatment of pulmo-
nary hypertension in pediatric patients. Pediatr Cardiol 2009;30(7):87182.
6. Lovell AT. Anaesthetic implications of grown-up congenital heart disease. Br J Anaesth
2004;93:12939.
ERRNVPHGLFRVRUJ
7. Mossad E, Motta P, Sehmbey K, Toscana D. The hemodynamic effects of phenoxybenzamine

in neonates, infants, and children. J Clin Anesth 2008;20(2):948.
8. Palma G, Giordano R, Russolillo V, et al. Sildenafil therapy for pulmonary hypertension before
and after pediatric congenital heart surgery. Tex Heart Inst J 2011;38(3):23842.
9. Peiravian F, Amirghofran AA, Borzouee M, et al. Oral sildenafil to control pulmonary hyperten-
sion after congenital heart surgery. Asian Cardiovasc Thorac Ann 2007;15(2):1137.
10. Rich GF, Murphy GD Jr., Roos CM, Johns RA. Inhaled nitric oxide. Selective pulmonary vasodi-
lation in cardiac surgical patients. Anesthesiology 1993;78(6):102835.
11. Rosenzweig EB, Widlitz AC, Barst RJ. Pulmonary arterial hypertension in children. Pediatr
Pulmonol 2004;38:222.
12. Shiyanagi S, Okazaki T, Shoji H, et al. Management of pulmonary hypertension in congeni-
tal diaphragmatic hernia: nitric oxide with prostaglandin-E1 versus nitric oxide alone. Pediatr
Surg Int 2008;24(10):11014.
13. Taylor MB, Laussen PC. Fundamentals of management of acute postoperative pulmonary
hypertension. Pediatr Crit Care Med 2010;11(2 Suppl):S279.
14. Vlahakes GJ. Management of pulmonary hypertension and right ventricular failure: another
step forward. Ann Thorac Surg 1996;61:10512.
ERRNVPHGLFRVRUJ
Cyanotic Spells
Management
Drug/maneuver Remarks
Oxygen is administered by face mask at Oxygen is a potent pulmonary vasodilator and
6 L/min. systemic vasoconstrictor.
Knee-chest position The knee-chest position increases the systemic
vascular resistance and improves pulmonary
blood flow.
Inj. sodium bicarbonate 8.4%, 1 mL/kg Sodium bicarbonate corrects the acidosis.
diluted in an equal quantity of sterile H2O,
is given slow IV over 510 minutes. May be
repeated after 10 minutes.
Inj. morphine 0.10.2 mg/kg IM or Sedation decreases irritability and controls
0.050.1 mg/kg slow IV over 510 minutes. hyperpnea. Possibly decreases infundibular
Alternative sedatives that can be given spasm and increases pulmonary blood flow.
include:
Inj. midazolam 0.050.1 mg/kg IV
Inj. fentanyl 12 mcg/kg IV
Inj. ketamine 12 mg/kg IV
Inj. esmolol 0.5 mg/kg IV over 12 minutes, Esmolol is a short-acting -blocker and
this may be followed by an IV infusion decreases the heart rate and relieves
50300 mcg/kg/min up to 48 hours. infundibular spasm.
Alternative -blockers that can be given are: The heart rate, blood pressure, and saturation
Inj. metoprolol 0.1 mg/kg slow IV (over is monitored. The aim is to maintain the heart
5 minutes). May be repeated every 5 minutes rate below 100/min.
for a maximum of 3 doses. Can be followed
by infusion 12 mcg/kg/min.
Inj. propranolol 0.10.2 mg/kg IV. Can be
repeated if required up to 34 times/day.
ERRNVPHGLFRVRUJ
Drug/maneuver Remarks
Phenylephrine 520 mcg/kg/dose slow IV -adrenergic agents increase the systemic
bolus; can be repeated every 1015 minutes vascular resistance and thus increase
(or noradrenaline 0.010.02 mcg/kg/min IV pulmonary blood flow.
infusion).
IV Normal saline/Ringers lactate 1020 mL/kg Isotonic IV fluids improve pulmonary blood
bolus followed by maintenance fluids. flow by increasing venous return and reducing
hyperviscosity.
Cyanotic spells occur in cyanotic children of 2 months2 years age who

have a congenital heart defect with associated subpulmonic obstruction,
(tetralogy of Fallot, tricuspid atresia, transposition of the great arteries or
single ventricle when associated with pulmonary stenosis). The spell may
be initiated by crying, feeding, hypoxia, or any other stimulus. It is char-
acterized by irritability and prolonged crying, which progresses to rapid
and deep respiration (hyperpnea), an increase in the cyanosis, and on aus-
cultation, a decrease in the intensity of the pulmonary outow murmur. A
cyanotic spell may result in seizures, coma, and death. Emergency manage-
ment aims to improve pulmonary blood ow and correction of the acido-
sis. Continuous ECG, oxygen saturation, and blood pressure monitoring
are initiated. In addition to the management listed above, any underlying
cause such as arrhythmia, hypothermia, and hypoglycemia are corrected.
In refractory spells, the child may need to be paralysed and ventilated.
Tab propranolol 0.251 mg/kg/dose q68h PO may be given to prevent
recurrences.
Bibliography
1. Bernstein D. Cyanotic congenital heart disease lesions: Lesions associated with decreased
pulmonary blood flow. Chapter 423. In: Behrman, Kleigmen and Jenson eds. Nelsons Textbook
of Pediatrics 17th ed. Elsevier; 2004.
2. Kothari SS. Mechanism of cyanotic spells in tetralogy of Fallotthe missing link? Intl J Cardiol
1992;37(1):15.
3. Park M. Pathophysiology of cyanotic congenital heart disease. In: Park M, ed. Pediatric
Cardiology for Practitioners 4th ed. Mosby; 2002:11326.
4. Saxena A, Juneja R, Ramakrishnan S; Working Group on Management of Congenital Heart
Diseases in India. Drug therapy of cardiac diseases in children. Indian Pediatr 2009;46:31038.
5. Wood P. Attack of deeper cyanosis and loss of consciousness (syncope) in Fallots tetralogy.
Br Heart J 1958;20:282.
ERRNVPHGLFRVRUJ
Pediatric
Resuscitation
I made use of the opportunities that life oered to do some good
Peter J Safar (19242003)*
Medications Used in Pediatric Resuscitation
Drug IV dose Remarks

Adenosine 100 mcg/kg (maximum 6 mg); Monitor ECG. Rapid IV/IO bolus
second dose: 200 mcg/kg followed by 5 mL saline flush.
(maximum 12 mg).
Adrenaline 10 mcg/kg (0.1 mL/kg, 1:10,000*) Indicated in asystole, pulseless
IV/IO. Max 1 mg. tachycardia, and severe
100 mcg/kg (0.1 mL/kg, 1:1000*) ET. bradycardia.
Max 2.5 mg.
Amiodarone 5 mg/kg IV/IO; may repeat twice up Adjust administration rate to
to 15 mg/kg. Maximum single dose urgency (IV push over several
300 mg. minutes during cardiac arrest;
more slowly, over 2060
minutes, with perfusing
rhythm). Monitor ECG and
blood pressure.
Atropine 0.02 mg/kg IV/IO Indicated in bradycardia.
0.040.06 mg/kg ET (minimum
dose IV/IO/ET 0.1 mg, maximum
single dose in a child 0.5 mg,
adolescent 1 mg).
May be repeated once if needed
10% Calcium gluconate 2030 mg/kg (0.20.3 mL/kg) slow Correction of hypocalcemia.
IV/IO (adult 510 mL)
Dextrose 0.51 g/kg, i.e., Correction of hypoglycemia.
dextrose 10%: 510 mL/kg
Lignocaine Bolus: 1 mg/kg IV/IO
Infusion: 2050 mcg/kg/min
*Peter J Safar was the pioneer of cardiopulmonary resuscitation, author of ABC of Resuscitation.
ERRNVPHGLFRVRUJ
Drug IV dose Remarks

Magnesium sulfate 2550 mg/kg IV/IO over 1020
minutes, faster in torsades de
pointes. Maximum dose 2 g.
Naloxone Initial dose 10 mcg/kg. Then: < 5 yr Indicated for respiratory
or 20 kg: 100 mcg/kg IV/IO/ET. depression because of opioids.
5 yr or > 20 kg: 2 mg IV/IO/ET. Use lower dose initially
May be repeated PRN every 23 followed by a higher dose if
minutes to maintain opioid reversal. there is no response.
If required start an IV infusion
520 mcg/kg/h.
Sodium bicarbonate 1 mmol/kg slow IV/IO (8.4% Correction of acidosis.
sodium bicarbonate
1 mL = 1 mmol; max 50 mL)
IV: intravenous, IO: intraosseous, ET: via endotracheal tube. Drug requires to be flushed with 5 mL normal saline,
followed by 5 ventilations.
*Adrenaline 1:10,000 implies 1 g in 10,000 mL, i.e., 10 mcg in 0.1mL; 1:1000 implies 1 g in 1000 mL, i.e., 100 mcg in 0.1 mL.
The following protocols are based on the American Heart Association

guidelines for Pediatric cardiopulmonary resuscitation 2010.
Pediatric Basic Life Support
The sequence of cardiopulmonary resuscitation (CPR) has previously

been known by the initials ABC, i.e., Airway, Breathing, and Chest com-
pressions (or Circulation). The 2010 AHA Guidelines for CPR and External
Cardiac Compression now recommends a CAB sequence (chest compres-
sions, airway, breathing) instead of ABC.
For a single person available for rescue, a compression-ventilation ratio
of 30:2 is recommended. Chest compressions are commenced rst and
after 30 compressions, two breaths are given.
When two individuals are available for CPR, a ratio of 15:2 is recom-
mended. One person performs chest compressions at a rate of 100120/min,
while the other provides 2 breaths after every 15 compressions.
Chest Compressions
External chest compressions (ECC) for a newborn or infant can be per-
formed with two ngers placed just below the intermammary line, alter-
natively, the chest is encircled with both hands, compressing the sternum
anteriorly with the thumbs while stabilizing the vertebral column poste-
riorly with the ngers. The hands must encircle the chest freely and not
restrict chest expansion.
ERRNVPHGLFRVRUJ
Pediatric Resuscitation 91
ECC for a child is performed with the heel of one or two hands com-
pressing the lower half of the sternum. A cycle should allow complete
chest recoil after each compression.
Sufcient force is used to depress the chest at least one-third the anterior-
posterior (AP) diameter (approximately 1 inches/4 cm in infants and
2 inches/5 cm in children).
Airway and Breathing

For the provision of effective ventilation during CPR, bag-mask ventila-
tion with 100% supplemental O2 is needed. Two persons are required for
bag-mask ventilation, and it is not recommended for a single individual
providing CPR. The single person can possibly only use mouth-to-barrier
device techniques (if available), mouth-to-mouth ventilation, or chest
compressions alone (no ventilation).
A self-inating bag-mask is available in appropriate sizes for infants,
children, and adults for ventilation. To deliver high oxygen concentrations
(6095%), an oxygen reservoir is attached to the self-inating bag.
Pediatric Advanced Life Support (PALS)
The term ALS covers various aspects of resuscitation including endotracheal

intubation and mechanical ventilation, management of cardiac arrhythmias,
and treatment of cardiorespiratory arrest and its complications.
Endotracheal Intubation and Ventilation
Recommended endotracheal (ET) tube sizes for different age groups

Age (years) Internal diameter of uncuffed Internal diameter of cuffed
ET tube (in mm) ET tube (in mm)
Infant 3.5 3
12 4 3.5
>2 4 + (age 4) 3.5 + (age 4)
A patent airway is established with endotracheal (ET) intubation. This

facilitates mechanical ventilation with 100% oxygen, minimizes pulmonary
aspiration, and enables suctioning of the trachea.
The position of the ET tube is conrmed clinically by bilateral chest
movement and breath sounds and the absence of gastric insufation sounds
over the stomach. The position is subsequently assessed radiologically. End-
tidal CO2 and pulse oximetry are additional monitoring aids.
ERRNVPHGLFRVRUJ
Cuffed ET tubes decrease the risk of aspiration and may be preferable.

When a cuffed tube is used, an optimal cuff pressure is needed to be main-
tained (2030 cm H2O).
Laryngeal mask airway is an alternative to bag-mask ventilation when
endotracheal intubation is not feasible.
Routes of Drug Administration

IV access is secured with a peripheral venous, external jugular, or femoral vein
cannulation. If cannulation is not immediately successful (>90 seconds),
the intraosseous (IO) route or ET tube is utilized in an emergency for drug
administration and later an IV cannula is placed. All drugs and resuscitative
uids may be given via the IO route, but only lignocaine, adrenaline, atro-
pine, and naloxone (mnemonic LEAN) can be given via the ET tube.
When drugs need to be administered via the ET tube, chest compressions
are stopped briey, medications are given into the ET tube and followed
with a ush of at least 5 mL of normal saline and 5 consecutive positive-
pressure ventilations. Optimal endotracheal doses of medications are in gen-
eral double or triple the IV doses for lidocaine, atropine, and naloxone.
Defibrillation
The doses of drugs and DC shock are based on the patients body weight,
which may be estimated from the age if the weight is unknown:
Age Estimated body weight

Newborn 3.5 kg
1 year 10 kg
110 years (age in years + 4) 2
Debrillation is equally effective with manual or self adhesive pads. Adult

size (810 cm) paddles or adhesive pads are used for children more than
10 kg weight and infant size (4.5 cm) for children under 10 kg. One paddle
is rmly placed over the right side of the upper chest and the second on
the left of the nipple over the lower ribs (cardiac apex), with preferably at
least a 3 cm gap between the paddles. In infants and small children, pad-
dles or pads may alternately be applied to the front and back of the chest.
The initial dose in ventricular brillation (VF) or pulseless ventricular
tachycardia (VT) is 2 or 4 J/kg, but the subsequent shocks recommended
are 4 J/kg. Higher energy levels may be considered, not exceeding 10 J/kg
in refractory cases. No synchronization with the ECG is required, and IV
sedation or analgesia are not indicated.
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The initial adult dose (with a biphasic debrillator) for VF is 120200 J

and subsequent shocks 200360 J, depending upon the manufacturers
recommendations.
Monitoring
Arterial Pressure Line

If the patient has an arterial monitoring line in place, the amplitude of the
arterial pressure trace on the monitor can be used to evaluate the efcacy of
the chest compressions and the return of spontaneous circulation (ROSC).
End Tidal Carbon Dioxide Monitoring (ETCO2)

ETCO2 monitoring (capnography or colorimetry) is recommended to conrm
tracheal tube position and to help guide therapy, especially the effective-
ness of chest compressions during CPR.
Pulse Oximetry
The systemic arterial oxygen saturation can only be recorded once a perfus-
ing rhythm is present.
Drugs
Adrenaline
Adrenaline is a potent , 1, and 2 agent and causes vasoconstriction in
the dose recommended in CPR. It enhances the coronary perfusion pres-
sure, stimulates spontaneous contractions, and increases the intensity of
VF so increasing the likelihood of successful debrillation.
Amiodarone
Amiodarone is a membrane stabilizing antiarrhythmic drug. It causes
bradycardia and also has a mild negative inotropic effect. Hypotension
is related to the rate of administration of the drug and is because of an
-blocking effect as well as a consequence of the histamine released by the
solvent used (polysorbate 80 and benzyl alcohol). Amiodarone is prefer-
ably administered in a central line as it can cause thrombophlebitis when
injected into a peripheral vein.
Atropine
Atropine is not a routine part of ALS algorithms as it has not shown improve-
ment in the outcome of cardiac arrest. Atropine may increase myocardial
oxygen demand and have its associated side effects. It is indicated when
bradycardia is unresponsive to improved ventilation and circulatory support.
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The dose of atropine is 0.02 mg/kg, however, a minimum dose of 0.1 mg

is given to avoid paradoxical bradycardia because of its central effect at low
doses.
Calcium
Calcium administration is not recommended for administration dur-
ing CPR and should only be given when specically indicated, e.g., for
hypocalcemia, calcium channel blocker overdose, hypermagnesemia, or
hyperkalemia.
Sodium Bicarbonate
Acidosis during cardiac arrest is best corrected by effective CPR.
Administration of sodium bicarbonate increases CO2 production and intra-
cellular acidosis. It has a negative inotropic effect, increases the sodium
load and shifts the oxygen dissociation curve to the left impairing oxygen
release to the tissues.
Sodium bicarbonate administration may however be considered in
special circumstances such as hyperkalemic cardiac arrest or in prolonged
arrest. Catecholamines and sodium bicarbonate should not be adminis-
tered through the same IV line simultaneously because alkaline solutions
inactivate catecholamines.
Magnesium
Administration of magnesium is indicated in children only if there is known
hypomagnesemia or for treatment of torsades de pointes.
Lignocaine
Lignocaine may be given in the acute management of ventricular tachy-
cardia (including torsades) and multiple ventricular ectopics but is a less
effective alternative to amiodarone. Toxic effects of lignocaine include
myocardial depression, drowsiness, and seizures.
PALS Protocols
Abnormal cardiac rhythms, which do not produce a cardiac output (i.e.,

cardiac arrest), can be categorized into (i) shockable rhythms (ii) non-
shockable rhythms based upon whether the particular arrhythmia responds
to debrillation or not. The two shockable rhythms are ventricular bril-
lation (VF) and pulseless ventricular tachycardia (VT), while the two non-
shockable rhythms are asystole and pulseless electrical activity (PEA).
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Protocol for shockable rhythm

Cardiac arrest
Bag-mask ventilation
(15:2; compressions:breaths)
Chest compression rate 100120/min
Monitor cardiac rhythm (rhythmshockable)
Tracheal intubation (ventilation rate 810/min)
Monitor ETCO2
Establish vascular access (IV/IO)
DC shock 2 J/kg
CPR 2 minutes
Check rhythm
DC shock 4 J/kg
Resume CPR Resume CPR

Amiodarone 5 mg/kg Adrenaline 10 mcg/kg, IV/IO
(after 3rd & 5th shock only) CPR 2 minutes
CPR 2 minutes Check rhythm
DC shock 4 J/kg
During CPR
Adrenaline is administered after every alternate DC shock.
Reversible causes are corrected.
At any stage, if on rhythm check there is asystole, non shockable protocol
is commenced instead.
At any stage, when there is ROSC, post resuscitation care is instituted.
Ventricular Fibrillation and Pulseless Ventricular Tachycardia

The only effective treatment of VF or pulseless VT is DC shock:
1. CPR
ECC is started at a rate of 100120/min and with bag-mask
ventilation, 2 breaths are given after every 15 chest compressions.
The child is intubated as soon as feasible with minimal interruption
to CPR, and chest compressions are then given continuously at a rate
of 100120/min and ventilation at 810 breaths/min. On return of
spontaneous circulation, chest compressions are stopped and the
ventilation rate is adjusted to 1220/min (depending on the age of
the patient).
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2. Debrillation
As soon as the debrillator is ready and it is conrmed that the
rhythm is shockable, an initial DC shock of 2 J/kg is given and the
CPR is resumed without reassessing the rhythm.
After every 2 minutes of CPR, the rhythm is assessed and if it
remains shockable, a DC shock of 4 J/kg is repeated.
3. Adrenaline
Inj. adrenaline 10 mcg/kg IV (0.1 mL of 1:10,000 solution)
is administered after the 2nd shock and repeated after the 4th and
6th shocks (i.e., after every 2 shocks).
In the Resuscitation Council, UK guidelines 2010, adrenaline is
given rst after 3 shocks and then after every 2 shocks.
4. Amiodarone
Refractory VF or VT is treated with amiodarone 5 mg/kg (or lignocaine
1 mg/kg IV, if amiodarone is NA) after the 3rd shock and if required
after the 5th shock.
5. Asystole/PEA
If asystole or PEA is noted anytime on rhythm assessment prior to
giving a shock, non-shockable protocol is instituted.
6. Return of spontaneous circulation
If there is ROSC, CPR is discontinued and post-resuscitation care is
commenced.
If VF/VT recurs after successful debrillation, resumption of CPR
sequence and debrillation is indicated. Amiodarone bolus is
given (unless 2 doses have previously been administered) and a
continuous infusion is started.
Asystole and Pulseless Electrical Activity

PEA (formerly known as electromechanical dissociation) is recognized by
slow, wide QRS complexes, but there is no cardiac output; at times, the
ECG is relatively normal but the pulses are absent.
1. CPR
ECC is initiated at a rate of 100120/min, and a compression:ventilation
ratio of 15:2 is provided with bag-mask ventilation. The child is
intubated with minimal interruption to CPR and then continuous
chest compressions are given at a rate of 100120/min and ventilation
at 810 breaths/min. The chest compressions are discontinued only on
ROSC and the ventilation rate is adjusted to 1220/min (depending
on the age of the patient).
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Protocol for non-shockable rhythm
Cardiac arrest
Bag-mask ventilation
(15:2; compressions:breaths)
Chest compression rate 100120/min
Monitor cardiac rhythm (rhythm non-shockable)
Tracheal intubation (ventilation rate 810/min)
Monitor ETCO2
Establish vascular access (IV/IO)
Adrenaline 10 mcg/kg IV
CPR 2 minutes
Check rhythm
CPR 2 minutes
Check rhythm
During CPR
Adrenaline is administered after every alternate loop of CPR (i.e., every 35 minutes).
Reversible causes are corrected.
At any stage, if on rhythm check the rhythm becomes shockable, shockable
protocol is commenced instead.
At any stage, when there is ROSC, post resuscitation care is instituted.
2. Adrenaline
Inj. adrenaline 10 mcg/kg IV (0.1 mL/kg of 1:10,000 solution) is
administered as soon as it is conrmed that the rhythm is non-
shockable and CPR is continued. The rhythm is checked after every
2 minutes of CPR. Adrenaline is repeated after every two such cycles of
CPR and cardiac rhythm check (i.e., every 35 minutes).
3. DC shock
Whenever the rhythm converts to VF, a DC shock of 4 J/kg is
administered and the shockable rhythm protocol followed.
4. Correct reversible causes
Any evident cause of arrhythmia or associated metabolic disorder is
treated. Hypovolemia is corrected with a bolus of 20 mL/kg of crystalloid.
5. Discontinuing CPR
CPR is discontinued only when there is ROSC or it is decided to
terminate the effort.
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Torsades de Pointes
Torsades is a variant of polymorphic VT and deteriorates rapidly to VF or
pulseless VT, so CPR is initiated as soon as possible. An IV infusion of mag-
nesium sulfate (2550 mg/kg; maximum single dose 2 g) is administered
over several minutes and the heart is debrillated.
Bradycardia
If the heart rate is less than 60/min and is associated with signs of poor
peripheral perfusion, CPR is urgently needed.
1. CPR
All inotrope lines, stopcocks, and infusion pumps are checked
to conrm these are functioning, and adequate oxygenation and
ventilation is ensured. If bradycardia with signs of poor perfusion
persists, CPR with ECC at the rate of 100120/min is instituted.
2. Adrenaline
Adrenaline 10 mcg/kg (0.1 mL/kg of 1:10,000 solution) IV bolus can
be given to increase the HR. If IV/IO access not available, it may be
administered via the ET tube in a dose of 100 mcg/kg (0.1 mL/kg of
1:1000 solution).
3. Atropine
In bradycardia due to increased vagal tone or primary AV conduction
block, atropine 0.02 mg/kg IV/IO bolus or an endotracheal dose of
0.040.06 mg/kg may be effective.
4. Cardiac pacing
In complete heart block or sinus node dysfunction unresponsive to
ventilation, chest compressions, or medications, some form of cardiac
pacing will be needed.
Management After Resuscitation
1. Oxygen
100% oxygen is used for initial resuscitation. After ROSC, the FiO2 is
reduced to achieve an oxygen saturation of 9498%. However, in the
single ventricle patient, who has undergone a bidirectional superior
cavopulmonary shunt or a systemic to pulmonary artery shunt,
following resuscitation from cardiac arrest, FiO2 should be adjusted
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to optimize the systemic and pulmonary blood ow and the arterial

oxygen saturation maintained at around 80%.
2. Hypothermia
Mild hypothermia may improve neurological outcomes, whereas fever
may be detrimental following ROSC. A child who remains in coma
following successful resuscitation may benet from core cooling to
3234C for at least 24 hours. Following a period of hypothermia, the
child is rewarmed slowly (0.250.50C/h).
3. Blood glucose control
Hypo- and hyperglycemia are avoided following resuscitation. Moderate
glucose control (as against tight glucose control) has been advocated.
Bibliography
1. Biarent D, Bingham R, Eich C, et al. European Resuscitation Council Guidelines for
Resuscitation 2010 Section 6. Paediatric life support. Resuscitation 2010;81:136488.
2. Kleinman ME, Chameides L, Schexnayder SM, et al. American Heart Association. Pediatric
advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Pediatrics 2010;126:e136199.
3. Kleinman ME, de Caen AR, Chameides L, et al. Pediatric Basic and Advanced Life Support
Chapter Collaborators. Pediatric basic and advanced life support: 2010 International Consensus
on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment
Recommendations. Pediatrics 2010;126:e1261318.
4. Kotur PF. An update on pediatric resuscitation. Indian J Anaesth 2004;48:330.
5. Part 12: Pediatric Advanced Life Support. Circulation 2005;112:IV-167IV-187. Resuscitation
Council (UK). [Updated: 2010 Dec; cited: 2011 Feb 22] Available at: http://www.resus.org.uk/
pages/pals.pdf
6. Burke DP, Bowden BF. Modified paediatric resuscitation chart. BMJ 1993;306:10968.
7. Pediatric Drug Lookup. CPR Pediatric Drug Dosages. Pediatriccareonline. [Updated: 2011
Mar 21; cited: 2011 Apr 29] Available at: http://www.pediatriccareonline.org/pco/ub/view/
Pediatric-Drug-Lookup/153899/all/cpr_pediatric_drug_dosages
8. Madden SCV. Paediatric drug doses. University Hospitals Coventry and Warwickshire N.H.S.
Trust. [Updated: 2011 Mar 21; cited: 2011 Apr 29] Available at: http://www.esculape.com/
pediatrie/medicament_dose.html#index.
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Fluid and
Electrolytes
A good heart and kidneys can survive all but the most willfully
incompetent uid regimen
Mark M Ravitich (19101989)*
Fluid and electrolyte management can be divided into two components:

(i) maintenance therapy and (ii) decit therapy.
Maintenance therapy comprises of replacement of the ongoing physi-
ological losses of water and electrolytes, which occur in urine, sweat, res-
piration, and stool. Maintenance uid requirements need to be increased
if there are additional losses, as with fever, surgical drainage or ongoing
gastrointestinal losses. The requirements are decreased in oliguric renal
failure, edematous states and in the syndrome of inappropriate ADH
secretion.
Decit therapy comprises of existing water and electrolyte decits, which
may be present as a result of gastrointestinal, urinary, skin or blood loss
and third-space sequestration.
Maintenance Therapy
Daily electrolyte requirements in children

Electrolytes Daily requirement (mmol/kg) Normal blood levels
Sodium (Na) 24 mmol/kg 136145 mmol/L
Potassium (K) 23 mmol/kg 3.55.0 mmol/L
Calcium (Ca) 0.20.4 mmol/kg Total Ca: 2.22.8 mmol/L
(8.811.2 mg/dL)
Ionized Ca: 1.11.4 mmol/L
(4.45.4 mg/dL)
Magnesium (Mg) 0.150.25 mmol/kg 1.83.0 mg/dL (1.52.5
meq/L or 0.751.25 mmol/L)
Chloride (Cl) 3 mmol/kg 95105 mmol/L
*Mark M Ravitich was a renowned pediatric surgeon, teacher, author of medical textbooks, and
editor of several medical journals.
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Fluid and Electrolytes 101
Daily maintenance fluid requirements in a newborn

Age (days) Daily requirement Hourly requirement Type of fluid
(mL/kg/day) (mL/kg/h)
1 2040 23 10% Dextrose
2 4060 34 1/5 Saline + 10% dextrose
3 6080 46 1/5 Saline + 10% dextrose
4 80100 68 1/5 Saline + 10% dextrose
Daily maintenance fluid requirements in infants and children

Weight (kg) Daily requirement Hourly requirement Type of fluid
010 100 mL/kg 4 mL/kg Saline in 10% dextrose
1120 1000 mL (for 10 kg) 40 mL (for 10 kg) Saline in 5% dextrose
+ 50 mL/kg (for wt + 2 mL/kg (for wt
>10 kg) >10 kg)
2130 1500 mL (for 20 kg) 60 mL (for 20 kg) + Saline in 5% dextrose
+ 20 mL/kg (for wt 1 mL/kg (for wt > 20 kg)
>20 kg)
Maintenance Fluid Requirement

Maintenance uid requirements in infants and children can be calcu-
lated based on body weight or surface area. By the body weight method,
100 mL/kg is the requirement for the rst 10 kg, 50 mL/kg for the next
10 kg, and 20 mL/kg for the remaining weight. By the surface area method
(applicable to children >10 kg), the requirement is 15002000 mL/m2/day.
Type of Fluid
The type of IV uid required to be given is dependent on the electrolyte
requirement of the child. One liter of normal saline (NS) contains 154 mmol
of Na and an equal concentration of chloride. One liter of NS will contain
about 38 mmol of sodium, which will meet the daily sodium requirement
of children up to 20 kg. The maintenance regimen is changed to a more con-
centrated saline solution (e.g., NS instead of NS) if the serum sodium
drops, or to a more dilute solution if the serum sodium starts to rise.
The daily potassium requirement calculated as per body weight is added
to the days IV uid unless the patient is hyperkalemic or in renal failure.
2 mmol of potassium added to every 100 mL of maintenance uid will
approximately provide the daily potassium requirement of 2 mmol/kg/day.
The calcium requirement can be given as 12 mL/kg/day of 10% calcium
gluconate by continuous IV infusion.
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Daily maintenance requirements of adult patients with normal renal

function are met with two liters of half isotonic ( N) saline, to which
20 mmol of potassium chloride (KCl) is added per liter. Patients with
ongoing gastrointestinal or third-space losses may require a higher rate
of saline (or blood) administration to maintain volume balance. Gastric
aspiration uids are replaced by N/2 saline and intestinal losses by NS.
Guidelines for fluid therapy in postoperative open heart patients

Post Op day Hourly fluid maintenance requirement
Day of operation 1 mL/kg/h (for first 10 kg) + 0.5 mL/kg (for next 10 kg) + 0.25 mL
(for remaining weight)
Day 1 Post Op 2 mL/kg/h (for first 10 kg) + 1 mL/kg/h (for next 10 kg) + 0.5 mL/kg/h
Day 2 Post Op 3 mL/kg/h (first 10 kg) + 1.5 mL/kg/h (for next 10 kg) + 0.75 mL/kg/h
Day 3 Post Op Normal maintenance, i.e., 4 mL/kg/h (first 10 kg) + 2 mL/kg/h
(for next 10 kg) + 1 mL/kg/h (for remaining weight)
In the immediate postoperative period following cardiac surgery, there is

a need for uid restriction because of cardiac dysfunction and uid retention
caused by cardiopulmonary bypass. The general guidelines for uid admin-
istration following open heart surgery are enumerated in the table. The total
uid intake is restricted to 2550% of normal maintenance on the day of
surgery and increased each morning by 2025% (provided systemic or pul-
monary edema is not present) until normal requirement is reached. (Based
on these guidelines, the calculated daily requirement in the immediate post-
operative period for an open heart surgery patient is given in Appendix J.)
After closed heart surgery one can commence with a higher intake, 50%
of the normal daily requirement is given on the day of surgery and normal
requirements can be given the following day or on day 2.
Deficit Therapy
Analysis of the severity of dehydration by physical signs

Clinical sign Mild Moderate Severe
Pre-illness body wt <5% loss 510% loss >10% loss
Skin color Pale Ashen Mottled
Skin turgor Tented Tented
Dryness of mucous + ++ ++
membranes
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Clinical sign Mild Moderate Severe

Heart rate Normal/
Blood pressure Normal Normal/ Shock
Urine output Azotemic
Fontanelle (<7 months) Flat Soft Sunken
CNS Consolable Irritable Lethargic/coma
In adults and older children (post pubertal), same symptoms and signs are present in mild, moderate, and severe
dehydration with 3%, 6%, and 9% loss of body weight, respectively.
In isotonic dehydration, volume decit (mL) = % Dehydration Wt (kg)

1000 (g/kg) 100
The goal of decit therapy is to correct existing abnormalities in volume

status and serum electrolytes in 2448 hours. The total uid decit can
be estimated from pre- and post-decit body weight and other clinical
parameters. The rate of correction of volume depletion depends upon its
severity. In children with severe volume depletion or hypovolemic shock
(estimated 1015% dehydration), initially uid bolus of 20 mL/kg of
crystalloid (e.g., normal saline) or 10 mL/kg colloid (e.g., 5% albumin) is
administered rapidly and repeated until the circulation improves (warm
skin, decreased heart rate, improved capillary rell time, increased urine
output).
Hyper-/hyponatremia should be corrected slowly, since overly rapid cor-
rection can be potentially harmful. The addition of sodium bicarbonate
may be required in patients with metabolic acidosis.
Hypokalemia
Hypokalemia (serum K+ <3.5 mmol/L) can be caused by:

GI losses, i.e., vomiting, nasogastric aspiration, and diarrhea.
Renal losses: Excessive diuretics lead to loss of both K+ and acid resulting
in hypokalemia and metabolic alkalosis. Hypomagnesemia itself
promotes urinary K+ loss and hypomagnesemia is therefore, often
associated with hypokalemia.
Transcellular shifts of potassium into the cells occur with respiratory
or metabolic alkalosis, hypothermia, insulin therapy and other drugs
(e.g., -agonist bronchodilators). In general, for every 0.1 unit change in
pH, the serum K+ level changes in the opposite direction by a value of
0.30.6 mmol/L.
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Clinical Features
Hypokalemia may result in paresthesias, skeletal muscle weakness, hypo-
ventilation, and ileus. It promotes rhythm disturbances (ventricular ectop-
ics, bigeminy, supraventricular tachyarrhythmias, and atrial brillation)
when associated with some electrolyte abnormalities (e.g., magnesium
depletion) and administered drugs (e.g., digoxin). There is therefore an
increased risk of digoxin toxicity with hypokalemia.
ECG changes: Hypokalemia causes ST depression, shallow, at or inverted
T waves and prominent U waves. Cardiac arrhythmias (atrial and ventricu-
lar ectopics, tachycardia and brillation), prolongation of the QRS and
increased P wave amplitude and duration occur less frequently.
Management
1. If serum K+ falls to <3.4 mmol/L, potassium chloride is given in a
dose of 0.51 mmol/kg, at a rate of 0.5 mmol/kg/h. Higher rates up to
2 mmol/kg/h may be given in arrhythmia. It is administered in saline
or dextrose in a maximum concentration of 20 mmol/100 mL for
a central line and 4 mmol/100 mL for a peripheral line. K+ level is
checked after the infusion, and the dose of potassium is repeated if
required. (1 g KCl = 13.3 mmol K+; 7.5% KCl = 1 mmol/mL)
2. Associated conditions that cause transcellular K+ shift (e.g., alkalosis)
are treated.
3. If the signs of hypokalemia or arrhythmias do not respond to
potassium chloride, consider associated magnesium depletion.
Check the blood level of magnesium.
Hyperkalemia
Hyperkalemia (Se K >5 mmol/L) can be caused by:

Impaired renal excretion. Low cardiac output states and renal failure
cause decreased renal excretion of potassium because of reduced urinary
output. In addition, the associated acidosis induces a transcellular shift
of K+ out of the cells. Hyperkalemia also occurs with various drugs that
prevent renal elimination of K+, e.g., potassium sparing diuretics, ACE
inhibitors, etc.
Transcellular shift of potassium out of the cells as seen with acidosis,
myonecrosis, and drugs (e.g., -blockers, NSAIDs, digoxin, etc.).
Hemolytic reactions and massive blood transfusions may be a cause of
hyperkalemia.
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Clinical Features
Clinical features include CNS features (irritability, paresthesias, and muscle
weakness especially of the legs), GI symptoms (nausea, abdominal cramps,
and diarrhea), and hypotension.
ECG Changes
The rst changes on the ECG are tall T waves, most evident in leads V2 and
V3. These are followed by PR prolongation with decreasing P wave ampli-
tude. Eventually, prolongation of QRS, ventricular brillation, and asystole
occurs.
Management
Treatment Remark
10% Calcium gluconate 0.5 mL/kg (max dose Response lasts 2030 minutes
10 mL) over 10 minutes Dose can be repeated Contraindicated if the child is on
in 5 minutes. digoxin.
Frusemide 1 mg/kg IV stat The dose may be repeated in
IV infusion 0.11 mg/kg/h. 3060 minutes or an infusion
started.
Insulin 0.1 U/kg IV with 0.5 g/kg dextrose Insulin-dextrose should drop Se
(2 mL/kg of 25% D) over 30 minutes. K+ by 1 mmol/L for 12 hour.
Sodium bicarbonate 12 mmol/kg IV given Duration of action 2 h. Use
over 510 minutes (8.4% sodium bicarbonate controversial in the absence of
1 mL = 1 mmol). acidosis. Sodium bicarbonate is
not to be given immediately after
calcium.
Kayexalate sodium or calcium resonium is Indicated after management of
given 1 g/kg PR as a retention enema or via the acute phase or only if no ECG
an NG tube q46h. It is administered mixed changes are present.
with 20% sorbitol to prevent concretion.
Hemodialysis or peritoneal dialysis. Hemodialysis is the most effective
method of controlling serum K+.
Hypocalcemia
Calcium is present in the blood in two forms: (i) Bound to the plasma
proteins (mainly albumin) and plasma anions (sulfates and phosphates)
constitutes 5060%; and (ii) Free ionized fraction, 4050%. The ionized
ERRNVPHGLFRVRUJ
fraction constitutes the physiologically active form. A decrease in the

serum albumin level results in a decrease in the bound form, but the ion-
ized active fraction may remain unchanged.
Total serum calcium level is 2.22.8 mmol/L (8.811.2 mg/dL), and the
range of ionized calcium is 1.11.4 mmol/L (4.45.4 mg/dL). Hypocalcemia
requires treatment if ionized serum calcium level is <1.0 mmol/L.
Causes of Hypocalcemia
Increased calcium binding to albumin, as occurs in alkalosis and sepsis,
decreases the active ionized fraction.
Binding of the ionized fraction to drugs. Infusion of sodium bicarbonate
can result in hypocalcemia because of calcium binding to the
bicarbonate. Other drugs that bind ionized calcium include heparin
and aminoglycosides.
Citrate in multiple blood transfusions chelates calcium and causes
hypocalcemia.
Magnesium depletion inhibits parathormone secretion and thus
promotes hypocalcemia. Hypocalcemia caused by hypomagnesemia
is refractory to calcium therapy alone, and magnesium replacement is
required in addition.
Renal failure causes hypocalcemia because of two reasons: conversion
of Vitamin D to its active form needed for calcium absorption from the
gut is impaired, and there is an increase in the level of serum phosphate
which binds additional calcium.
Clinical Features
Clinical features are related to enhanced neuromuscular irritability (hyper-
reexia, seizures, and tetany) and cardiac depression (hypotension, decreased
cardiac output, ventricular ectopics, and tachycardia).
ECG changes: Hypocalcemia results in prolongation of the QT interval
because of lengthening of the ST segment, which is directly proportional
to the degree of hypocalcemia. T wave attening and inversion are late
changes and heart blocks and VF may rarely occur.
Management
Symptomatic hypocalcemia requires urgent management. 10% Calcium
gluconate (i.e., 100 mg/mL or 0.23 mmol Ca/mL) is given in a dose of
1020 mg/kg (0.10.2 mL/kg) slow IV bolus. Dilute to at least 1 in 5
with 5% dextrose or isotonic saline.
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Daily maintenance IV dose of calcium is 0.20.4 mmol/kg/day

(100200 mg/kg/day or 12 mL/kg/day) of 10% calcium gluconate.
To counteract citrate in transfused blood, 10% calcium gluconate is
recommended in a dose of 50 mg (0.5 mL) per 50 mL of transfused blood.
Calcium gluconate is used as an inotrope in the dose of 1040 mg/kg/h
(0.10.4 mL/kg/h).
10% Calcium chloride (i.e., 100 mg/mL) has three times the content of calcium
(0.68 mmol Ca/mL) compared to 10% calcium gluconate. It is therefore given
in 1/3rd the dose of 10% calcium gluconate.
Hypomagnesemia
Magnesium is largely an intracellular cation, like potassium. It is present

in the plasma in a bound and a free ionic form. The physiologically active
form is the ionic form but since the total plasma levels are low, the dif-
ference between the bound and ionic forms is not clinically relevant and
generally total serum magnesium levels are measured. Normal total serum
magnesium level is 1.83.0 mg/dL (1.52.5 meq/L or 0.751.25 mmol/L).
Causes of hypomagnesemia are as follows:
Dietary deciency or malabsorption are the commonest causes of
hypomagnesemia.
Renal losses of magnesium are associated with diuretics and antibiotics
like aminoglycosides and amphotericin.
Transcellular shift of magnesium into the cells, which promotes
hypomagnesemia, is seen with a variety of drugs (e.g., digoxin,
adrenergic agents, etc.).
Clinical Features
The clinical features of hypomagnesemia are not specic but involve
the following systems: CNS (altered level of consciousness, confusion);
neuromuscular (muscular weakness, lower limb cramps, exaggerated reexes
and tetany); cardiovascular (tachycardia, hypertension), and GIT (dysphagia,
anorexia, nausea, and vomiting).
ECG changes: may be similar to the ndings in hypokalemia, i.e., ST seg-
ment depression; at or inverted T waves in the precordial leads and prom-
inent U waves; other infrequent presentations include PR prolongation,
widened QRS, torsades de pointes, and refractory atrial brillation.
Since hypomagnesemia and hypokalemia occur from similar causes
and hypomagnesemia promotes urinary potassium excretion, over 40%
of patients with hypokalemia have associated hypomagnesemia. Patients
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with hypokalemia with rhythm disorders who do not respond to potas-

sium administration require magnesium in addition.
Magnesium depletion inhibits parathormone secretion and thus pro-
motes hypocalcemia. Hypomagnesemia should therefore be suspected
when tetany does not respond to calcium infusion.
In hypomagnesemia, since most magnesium is intracellular, a total
body decit can be present with a normal plasma level. A nding of
hypocalcemia, hypokalemia, and ECG changes is suggestive of associated
hypomagnesemia.
Management
Hypomagnesemia is treated with parenteral therapy. Inj. magnesium sul-
fate 50% (i.e., 500 mg/mL or 2 mmol mg/mL) is given in a dose of 2550
mg/kg/dose (0.050.1 mL/kg/dose) IM/slow IV. (Max single dose 2 g). It
is diluted to a concentration 1 in 10 with 0.9% saline or 5% dextrose for
IV (1 in 5 with 0.9% saline for IM) and administered over 10 minutes.
Hyponatremia
In hyponatremia, serum Na is <135 mmol/L, and in severe cases it is

<120 mmol/L. Hyponatremia may be caused by:
Sodium loss more than water loss: As occurs in excessive use of diuretics,
vomiting, diarrhea, and post cardiopulmonary bypass capillary leak
syndrome (Hypovolemic hyponatremia).
Water retention: As in rapid infusion of hypotonic uids and in
postoperative syndrome of inappropriate antidiuretic hormone secretion
(SIADH), which cause water retention (Isovolemic hyponatremia/Dilutional
hyponatremia).
Water retention more than sodium retention: In congestive cardiac failure
and renal failure, both water and sodium are retained but water gain is
greater than sodium gain; edema occurs and the hyponatremia is mild
(Hypervolemic hyponatremia).
Clinical Features
The clinical features of hyponatremia are primarily neurological, because
severe hyponatremia causes cerebral edema as a result of movement of
water from hypo-osmolar plasma into the brain cells. Headache, vomit-
ing, lethargy, seizure, and coma occur depending on the rate and severity
of hyponatremia.
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Associated hypovolemia causes poor skin turgor, tachycardia, and hypo-

tension, while hypervolemia is associated with edema, weight gain, tachy-
cardia, and hypertension.
Management
In hypovolemic hyponatremia, adequate volume and Na replacement is
needed. In patients with neurological signs (seizure, coma), initially 23
mL/kg of 3% NaCl (contains 51.3 mmol of sodium per 100 mL) is given
over 3060 minutes. The increase in serum osmolality will reverse the
cerebral edema. Thereafter, the serum sodium is corrected gradually over
4872 hours by an infusion of appropriate maintenance uid based on
the sodium decit. Rapid correction (an increase in serum Na level at a
rate faster than 810 mmol/L/day) carries the risk of iatrogenic osmotic
demyelination. The sodium decit is determined by:
Na decit (mmol) = (Desired Na Present Na) Wt 0.6
The management of dilutional hyponatremia is by uid restriction. In

SIADH, uids are restricted to two-thirds the normal daily maintenance.
Administration of full volumes of maintenance uids (esp. hypotonic u-
ids e.g., or NS) will exacerbate the hyponatremia. Additionally, a loop
diuretic may be combined with IV 0.9% saline.
Hypervolemic hyponatremia is managed with uid restriction, diuretics,
and treatment of the underlying disorder.
Hypernatremia
In hypernatremia, serum Na is more than 145 mmol/L, and in severe cases

it is more than 160 mmol/L. Hypernatremia is caused by:
Water loss more than Na loss, e.g., in vomiting, diarrhea. Pure water loss
can occur secondary to nephrogenic diabetes insipidus. (Hypovolemic
hypernatremia, hypernatremic dehydration.)
Sodium excess is unusual; it may be iatrogenic from excess bicarbonate or
sodium chloride administration. (Hypervolemic hypernatremia.)
Clinical Features
Hypernatremia causes CNS dysfunction by the movement of uid from the
brain to the ECF, resulting in lethargy, exaggerated reexes, seizures, and
coma. Rarely, intracerebral hemorrhage and central pontine myelinolysis
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(though classically associated with rapid correction) may occur. Volume

loss of more than 10% will result in shock.
Management
A patient with hypovolemic hypernatremia, who is in shock, is initially treated
with repeated boluses of isotonic saline or Ringers solution 1020 mL/kg IV
over 20 minutes. Up to 60100 mL/kg may need to be given before heart
rate normalizes and urine output, capillary rell, and mental status improve.
Then the remaining volume decit is replaced by or normal saline
over 4872 hours. Rapid correction (a fall in serum Na level at a rate faster
than 810 mmol/L/day) can cause cerebral edema and central pontine
myelinolysis because of movement of ECF water into the relatively hyper-
tonic brain cells. The volume decit is calculated by the following formula:
Volume decit (L) = 0.6 Body weight (kg) [1 (140/serum Na)]
In hypervolemic hypernatremia, 5% dextrose or hypotonic solutions are
used as maintenance uid. In addition, sodium excretion may be increased
with a diuretic (e.g., furosemide). The diuresis will however aggravate the
hypernatremia unless hypotonic solutions are used as maintenance uid.
Blood Sugar
Glucose homeostasis is frequently altered in infants and children during

the postoperative period following cardiopulmonary bypass and circu-
latory arrest. Hyperglycemia may lead to osmotic diuresis, dehydration,
and cerebral hemorrhage. Hypoglycemia manifests with seizures, gener-
ally when the blood sugar level falls to <30 mg%. The normal blood sugar
level range in children is 70150 mg/dL. However, in children undergoing
complex congenital heart surgery, the suggested optimal postoperative glu-
cose range is 110126 mg/dL.
Management
Hypoglycemia is treated with dextrose 0.51 g/kg (i.e., dextrose 10%: 510
mL/kg; dextrose 25%: 24 mL/kg; dextrose 50%: 12 mL/kg). If required, the
maintenance uid is changed to 10% dextrose IV to keep the blood sugar
level in normal range.
Hyperglycemia is treated with regular insulin 0.10.2 U/kg IV. The
blood sugar level is checked (q612h), and the dose repeated as required.
Alternatively, insulin 0.1 unit/kg/h IV infusion in 0.9% sodium chloride
ERRNVPHGLFRVRUJ
(prepared to a concentration of 1 unit/mL) is administered. The rate of

infusion is adjusted according to the response.
Bibliography
1. Adrogu HJ, Madias NE. Changes in plasma potassium concentration during acute acid-base
disturbances. Am J Med 1981;71:45667.
2. Ambalavanan N. Fluid, electrolyte, and nutrition management of the newborn. [Updated:
2010 Jun 29; cited: 2012 Jan 4] Available at: http://emedicine.medscape.com/article/
976386-overview.
3. Davis ID, Avner ED. Fluid, electrolytes, and acid-base homeostasis. In: Fanaroff AA, Martin RJ
eds. NeonatalPerinatal Medicine 7th ed. Mosby, St. Louis; 2002:619.
4. Elenberg E. Hypernatremia. [Updated: 2009 Nov 2; cited: 2011 Apr 11] Available at: http://
emedicine.medscape.com/article/907653-overview.
5. Fluid and electrolyte requirements in children. [Updated: 2011 Feb 16; cited: 2011 Apr 11]
Available at: http://www.pediatriccareonline.org/pco/ub/view/Pediatric-Drug-Lookup/153910/0/
ub?cmd=cookiep.
6. Friis-Hansen B. Body water compartments in children: changes during growth and related
changes in body composition. Pediatrics 1961;28:16981.
7. Hypomagnesemia. [Updated: 2011 Mar 11; cited: 2011 Apr 11] Available at: http://
en.wikipedia.org/wiki/Hypomagnesemia.
8. Intravenous fluids. Clinical practice guideline: The Royal Childrens Hospital, Melbourne.
[Updated: 2009 Oct 8; cited: 2011 Feb 22] Available at: http://www.rch.org.au/clinicalguide/
cpg.cfm?doc_id=5203.
9. James MB, Mario FV, Ben TU, Belding HS. The effect in humans of extracellular pH change on
the relationship between serum potassium concentration and intracellular potassium. J Clin
Invest 1956;35(9):9359.
10. Marino PL. Fluid and electrolyte disorders. In: Marino PL ed. The ICU Book 2nd ed. Hong Kong:
Williams & Wilkins Asia Pacific Ltd; 1997:63172.
11. Nair SG, Balachandran R. Perioperative fluid and electrolyte management in pediatric patients.
Indian J Anaesth 2008;48:35564.
12. Polito A, Thiagarajan RR, Laussen PC, et al. Association between intraoperative and early
postoperative glucose levels and adverse outcomes after complex congenital heart surgery.
Circulation 2008;118:223542.
13. Reynolds RM, Padfield PL, Seckl JR. Disorders of sodium balance. BMJ 2006;332:7025.
14. Roberts KB. Fluid and electrolytes: parenteral fluid therapy. Pediatr Rev 2001;22:3806.
15. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders 5th ed. New York:
McGraw-Hill; 2001:2857, 441.
16. RuDusky BM. ECG abnormalities associated with hypocalcemia. Chest 2001;119(2):6689.
17. Shafiee MA, Bohn D, Hoorn EJ, Halperin ML. How to select optimal maintenance intravenous
fluid therapy. QJM 2003;96:60110.
18. Tam M. Maintenance IV fluids in euvolaemic children. [Updated: 2006 June 19;
cited: 2011 Feb 25]. Available at: http://vitualis.wordpress.com/2006/05/02/maintenance-iv-
fluids-in-euvolaemic-children/.
19. Wiederseiner JM, Muser J, Lutz T, et al. Acute metabolic acidosis: characterization and diagno-
sis of the disorder and the plasma potassium response. J Am Soc Nephrol 2004;15:158996.
20. Yamamoto LG. Fluids and electrolytes. Case Based Pediatrics For Medical Students and
Residents. University of Hawaii, Department of Pediatrics [Updated: 2003 March; cited: 2011
Feb 25]. Available at: http://www.hawaii.edu/medicine/pediatrics/pedtext/s02c04.html.
21. Yeates KE, Singer M, Morton AR. Salt and water: a simple approach to hyponatremia. CMAJ
2004;170(3):36570.
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Arterial
Blood Gas Analysis
Life is a struggle, not against sin, not against the money power, not against
malicious animal magnetism, but against hydrogen ions
HL Mencken (18801956)*
Normal Values
Parameter Normal range

pH 7.357.45
H+ 3545 nmol/L
PaO2 80100 mmHg or 9.313.3 kPa
SpO2 97100%
tO2 1622 mL O2/dL
PaCO2 3545 mmHg or 4.76.0 kPa
AaDO2 <10 mmHg
2226 mmol/L
HCO3
SBC 2127 mmol/L
Base excess 3 to +3 mmol/L
tCO2 2530 mmol/L
pH
The pH indicates if a patient is acidotic (pH <7.35) or alkalemic
(pH >7.45). The concentration of hydrogen ions in the blood determines
the pH of the blood.
Hydrogen Ion
The hydrogen ion (H+) concentration in the extracellular uid is a direct
measure of acidosis (H+ >45 nmol/L) or alkalosis (H+ <35 nmol/L).
*Henry Louis Mencken was an American author, journalist, magazine editor, and critic. He was
known for his satirical writings on social and other controversial issues.
ERRNVPHGLFRVRUJ
Arterial Blood Gas Analysis 113
Partial Pressure of Oxygen

Oxygen is transported in the blood in the freely dissolved form and bound
to the hemoglobin. The partial pressure of oxygen (PaO2) reects only the
free oxygen molecules dissolved in plasma and not which is bound to the
hemoglobin. The PaO2 is determined by the partial pressure of alveolar
oxygen and the state of the alveolar membrane. It is decreased in ventila-
tion perfusion mismatch and right to left shunt. It is not affected by the
hemoglobin level.
Systemic Arterial Oxygen Saturation

The arterial oxygen saturation (SpO2) is the percentage of hemoglobin
saturated with oxygen. The more the PaO2, the higher is the SpO2, but the
relationship is not linear and is described by the sigmoid shape of oxygen
dissociation curve (see Fig. 9 of Chapter 1). At the upper and lower end
of the curve, signicant changes in PaO2 cause little change in the SpO2,
but in the steep part of the curve, changes in PaO2 are reected by equiva-
lent alterations in SpO2. The SpO2 depends not only on the PaO2 but also
on the pH, PaCO2, and temperature. A rise in the pH, a fall in PaCO2 or
a decrease in the temperature shifts the curve to the left increasing the
afnity of hemoglobin for oxygen, and the same hemoglobin saturation
implies a lower PaO2. A fall in pH and a rise in PaCO2 and temperature
shifts the curve to the right. The afnity of hemoglobin for O2 is decreased,
and with the same hemoglobin O2 saturation, the PaO2 is higher.
Oxygen Content
The oxygen content (tO2) is the sum of the dissolved oxygen and the oxy-
gen bound to hemoglobin. The dissolved fraction constitutes 0.003 mL per
mmHg (PaO2) per dL, and each gram of hemoglobin (Hb) binds to 1.34 mL
of oxygen.
tO2 = (Hb in g/dL 1.34 SpO2) + (PaO2 0.003)
Normal tO2 ranges from 16 to 22 mL O2/dL.
Partial Pressure of Carbon Dioxide

Carbon dioxide is transported from the body cells back to the lungs in
three forms(i) dissolved in the plasma (10%); (ii) as carbohemoglobin
(30%); and (iii) as bicarbonate (60%). Only a small amount of carbon
dioxide that enters the blood remains in the dissolved form, the rest enters
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the RBCs. Some of the carbon dioxide combines with desaturated hemo-
globin to form carbohemoglobin. In the RBCs, the remaining carbon
dioxide is converted to carbonic acid, which dissociates into hydrogen ion
and bicarbonate. This bicarbonate then diffuses back into the plasma and
is transported to the lungs. On reaching the lungs, the bicarbonate and
hydrogen ion combine to form CO2 and H2O, and the CO2 is exhaled.
Hb CO2 Hb
CO2 (Carbohemoglobin)
CO2 CO2 H2CO3 HCO3
Carbonic
unhydrase H+
H2O
Fig. 1: CO2 metabolism in RBC.
The partial pressure of carbon dioxide reects the dissolved form. A normal
PaCO2 of 3742 mmHg indicates normal alveolar ventilation. Values above
normal indicate respiratory acidosis and are present with hypoventilation.
Values below normal are evidence of respiratory alkalosis and are present
with hyperventilation.
AlveolarArterial Oxygen Gradient

The alveolararterial oxygen gradient (AaDO2) depends on the state of the
alveolar membrane. In cases with hypoxemia where the lungs are normal,
the AaDO2 will be normal (e.g., low FiO2, right to left shunts, and central
respiratory depression). In patients with parenchymal lung disease with
impaired oxygen diffusion, hypoxemia will be associated with an increase
in AaDO2.
Bicarbonate (HCO3-) Level

Bicarbonate level reects the metabolic component of an acidbase distur-
bance. A low HCO3 reects metabolic acidosis and a high HCO3 meta-
bolic alkalosis.
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HCO3 level, however, is varied by both components, respiratory and

metabolic, since carbon dioxide itself is transported in the blood as sodium
bicarbonate. However, in a patient with no respiratory abnormality, the
bicarbonate will reect the metabolic disturbance.
Standard Bicarbonate (SBC)

It is dened as the bicarbonate concentration under standard conditions
of PCO2 40 mmHg, temperature 37C, and oxygen saturation 100%. It is
a more accurate measure of the metabolic component of an acidbase dis-
order than the nonstandardized (actual) bicarbonate. The respiratory frac-
tion of the sodium bicarbonate level in the blood is converted to a similar
value in all samples by the standardized conditions.
Base Excess
Base excess is a measure of all metabolites (not only HCO3), which will
alter the acidbase status. A base decit indicates metabolic acidosis, and
base excess indicates metabolic alkalosis.
Total CO2 Content (tCO2)

Total CO2 content is the sum of the blood bicarbonate level and the dis-
solved carbon dioxide present in the blood.
tCO2 = (HCO3) + ( PaCO2),
[where = 0.226 mM/kPa, HCO3 is expressed in (mmol/L) and PaCO2
in kPa]
AcidBase Balance
Acidbase disorder Primary disorder Compensatory response

Respiratory acidosis PaCO2 HCO3
Respiratory alkalosis PaCO2 HCO3
Metabolic acidosis HCO3 PaCO2
Metabolic alkalosis HCO3 PaCO2
Same direction rule: A low PaCO2 is compensated by a low HCO3 and a high PaCO2 by a high HCO3. Similarly,
a low HCO3 is compensated by a low PaCO2 and a high HCO3 is by a high PaCO2.
In acidosis, the pH of the blood is <7.35 and in alkalosis it is more

than 7.45. pH is a measure of hydrogen ion concentration of the blood.
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Furthermore, the concentration of the H+ is determined by the ratio of the

partial pressure of carbon dioxide and the blood bicarbonate level.
H+ (nmol/L) = 24 PaCO2/HCO3
An alteration of this ratio results in an acidbase disorder.
Respiratory acidosis results from an increase in the PaCO2 level (i.e.,
accumulation of carbonic acid) and alkalosis by a fall of the PaCO2 level.
Metabolic acidosis is caused by an accumulation of acids or by a loss
of bases and is reected by a low bicarbonate level. Metabolic alkalosis is
caused by accumulation of bases or a loss of acids and is reected by a
high bicarbonate level.
When either component (PaCO2 or HCO3) is altered, the other compo-
nent is accordingly changed as a compensatory mechanism, in an attempt
to keep the ratio constant. Thus, when a primary disorder is metabolic, the
response is respiratory compensation; the lungs provide compensation by
altering the rate of respiration by either retaining or washing off the car-
bon dioxide. When the primary disorder is respiratory, the response is
metabolic compensation. The kidneys provide compensation for respira-
tory acidbase disorders by increasing or decreasing the reabsorption and
production of bicarbonate. However, the adjustment by the kidneys is slow
and takes 612 hours to start and increases over days.
Specimen Care
Samples should be analyzed within 30 minutes of withdrawal (samples
drawn in glass syringes can be kept longer in ice baths). Delay in analysis
leads to inaccurately low PaO2 and high PaCO2 levels as a result of ongo-
ing cellular respiration. Similarly, air bubbles that exceed 12% of the
blood volume can cause a falsely high PaO2 and a falsely low PaCO2.
The amount of heparin solution used should be minimized and at least
2 mL of blood should be obtained to ensure accuracy.
Interpretation of Blood Gas Analysis
Interpretation of blood gases involves systematically checking the various

parameters:
Step 1pH
pH <7.35 = acidosis; pH >7.45 = alkalosis.
Step 2CO2
PaCO2 gives information about the respiratory component of acidbase
balance.
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In respiratory acidosis, PaCO2 increases; in respiratory alkalosis, the

PaCO2 decreases.
Respiratory acidbase disorders have been classied as acute or chronic
depending upon whether renal compensation has taken place or not.
For acute disturbances, a PaCO2 variation from normal by 10 mmHg
is accompanied by a pH shift of approximately 0.08 units and in a
chronic respiratory acidbase disorder by 0.03 units. A PaCO2 change
of <10 mmHg will be associated with a smaller pH shift.
Step 3HCO3-, SBC, and base excess

These parameters provide information about the metabolic component of
the acidbase disorder.
In metabolic acidosis, the pH is low, the HCO3 (and SBC) is low, and
there is base decit.
In metabolic alkalosis, the pH is high, the HCO3 (and SBC) is high,
and there is base excess.
Step 4Compensation
If a change is seen in both, PaCO2 and bicarbonate, the disorder consistent
with the direction of change of pH, indicates the primary disorder and the
disorder which is reversing this change in pH, is the compensatory disor-
der. Compensation does not return pH completely to normal (and never
overshoots). Thus in:
Primary respiratory alkalosis and compensatory metabolic acidosis:
pH , PaCO2 , HCO3
Primary respiratory acidosis and compensatory metabolic alkalosis:
pH , PaCO2 , HCO3
Primary metabolic alkalosis and compensatory respiratory acidosis:
pH , HCO3 , PaCO2
Primary metabolic acidosis and compensatory respiratory alkalosis:
pH , HCO3 , PaCO2
A mixed disorder is suspected if the compensatory change in pH is more
than expected or returns the pH to normal.
Step 5PaO2 and SaO2

PaO2 reects ability of the lungs to oxygenate the blood. A low PaO2 and
SaO2 (<95%) indicates inadequate oxygenation.
Step 6For metabolic acidosis, determine whether anion gap is present

The anion gap is the calculated difference between the positively charged
(cation) electrolytes (i.e., Na) and the negatively charged (anion) electro-
lytes (i.e., HCO3 and Cl) in the blood.
Anion gap = Na+ (Cl + HCO3)
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The normal anion gap is 312 mmol/L.

Anion gap acidosis (Gap >12 mmol/L) results from the accumulation
of anions other than Cl and HCO3 (organic acids, phosphates, sulfates,
albumin, etc.) and these decrease the HCO3 level, thus increasing the gap.
Causes of anion gap acidosis include uremia, diabetic ketoacidosis, and
lactic acidosis.
Non-anion gap acidosis (Gap <12 mmol/L), also called hyperchloremic
acidosis, results from loss of HCO3, and causes include diarrhea, renal tubu-
lar acidosis, hyperalimentation, compensation for respiratory alkalosis, etc.
Respiratory Acidosis
A decrease in the respiratory rate or tidal volume can result in accumula-

tion of CO2 and respiratory acidosis. It occurs in brain stem lesions, air-
way obstruction, pulmonary disease, inadequate mechanical ventilation,
splinting of the chest wall following surgery, drugs, etc.
Clinical Features
It is manifested by restlessness, tremors, diaphoresis, dyspnea, tachycardia,
a warm ushed skin, and decreased reexes.
Blood Gas Analysis

Uncompensated respiratory acidosis: pH <7.35, PaCO2 >45 mmHg,
and a normal HCO3.
Compensated respiratory acidosis: pH <7.35 but approaching normal,
PaCO2 >45 mmHg, and HCO3 >26 mmol/L.
Treatment
In the ventilated patient, tracheal suctioning and increasing the respiratory
rate and/or tidal volume may correct the disorder. The unventilated patient
may need bronchodilators, chest physiotherapy to remove secretions and
supplemental oxygen. Associated hyperkalemia needs to be corrected.
Respiratory Alkalosis
Respiratory alkalosis results from hyperventilation, which may be because of

pain, drugs (e.g., overdose of salicylate or aminophylline), hypermetabolic
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states, excessive mechanical ventilation or acute hypoxia (this may cause

stimulation of the respiratory center).
Clinical Features
The clinical features of respiratory alkalosis are restlessness, diaphoresis,
dyspnea, tachycardia, exaggerated reexes, paresthesias, tetany, and ECG
changes of hypokalemia.
Blood Gas Analysis

Uncompensated respiratory alkalosis: pH >7.45, PaCO2 <35 mmHg, and
a normal HCO3.
Compensated respiratory alkalosis: pH >7.45 but approaching normal,
PaCO2 <35 mmHg, and HCO3 <22 mmol/L.
Treatment
In the ventilated patient, the ventilator rate and/or tidal volume is reduced.
The non-ventilated patient may require sedation and oxygen for associated
hypoxemia. Rebreathing into a paper bag will increase the PaCO2.
Metabolic Acidosis
Metabolic acidosis is characterized by accumulation of acid or loss of

bicarbonate and has been classied into two types(i) anion gap acidosis
and (ii) non-anion gap acidosis.
Anion gap acidosis can be because of (a) accumulation of lactic acid,
which occurs secondary to shock, dehydration, low cardiac output, hypoxia,
infection, seizures, renal failure, and hepatic failure or (b) formation of
Ketone bodies, as in diabetes mellitus and starvation.
Non-anion gap acidosis occurs in renal tubular acidosis from loss of
bicarbonate, as a response to hyperkalemia and as a compensatory mecha-
nism in respiratory alkalosis.
Clinical Features
Clinical features of metabolic acidosis include confusion, lethargy, and
headache. The skin is warm and dry. In later stages, there is hypotension,
Kussmauls respiration (a deep and labored breathing pattern), and sluggish
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reexes. There may be signs of hyperkalemia (abdominal cramps, diarrhea,

muscle weakness, and ECG changes).
Blood Gas Analysis

Uncompensated metabolic acidosis: pH <7.35, PaCO2 normal, HCO3
<22 mmol/L.
Compensated metabolic acidosis: pH <7.35 but approaching normal,
PaCO2 <35 mmHg, HCO3 <22 mmol/L.
Treatment
IV sodium bicarbonate (NaHCO3) is given for rapid correction (sodium
bicarbonate 8.4% : 1 mL = 1 mmol).
Dose of NaHCO3 (in mL of 8.4% solution) = Base decit 0.3 body wt.
50% of the amount is given initially, and the base excess is checked after
1 hour. Further correction is done if required. Fluid losses are corrected.
Dialysis may be needed in extreme cases.
Metabolic Alkalosis
Metabolic alkalosis is the more commonly encountered disorder in the

intensive care unit and has also been classied into two types(i) chloride-
responsive metabolic alkalosis and (ii) chloride-resistant metabolic
alkalosis.
Chloride-responsive metabolic alkalosis is caused by loss of hydrogen ions
through the GI tract by vomiting or nasogastric suctioning. Excessive diu-
retic therapy results in renal losses of chloride, potassium and magnesium
ions, which promote bicarbonate reabsorption and metabolic alkalosis. It
can also be caused by excessive administration of organic anions such as
HCO3 or because of citrate in multiple blood transfusions. It occurs as a
compensatory response to respiratory acidosis and hypokalemia.
Chloride-responsive metabolic alkalosis is characterized by urine chloride
levels of <10 mmol/L, low serum chloride levels, and a decrease in the ECF
volume. This type responds to administration of IV saline.
Chloride-resistant metabolic alkalosis occurs in primary aldosteronism
or with excessive corticosteroid therapy and is characterized by urine chlo-
ride levels of more than 20 mmol/L and an increased ECF volume rather
than volume depletion. It is resistant to treatment by administration of IV
sodium chloride.
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Clinical Features
In the non-ventilated patient, metabolic alkalosis results in anorexia, nau-
sea, apathy, and confusion. There is muscle weakness and loss of reexes.
It impairs myocardial contractility, reduces cardiac output, and causes
hypotension. In the ventilated patient, it can be a cause of failed weaning
and decreased tissue oxygenation.
Blood Gas Analysis

Uncompensated metabolic alkalosis: pH >7.45, PaCO2 normal, HCO3
>26 mmol/L.
Compensated metabolic alkalosis: pH >7.45 but approaching normal,
PaCO2 >45 mmHg, HCO3 >26 mmol/L.
Treatment
Chloride-Responsive Metabolic Alkalosis

Administration of isotonic saline
Metabolic alkalosis is commonly associated with depletion of chloride
and extracellular uid volume, which are corrected by administration of
isotonic saline. Chloride decit and the volume of isotonic saline required
can be calculated by the following formulae:
Chloride decit (mmol) = 0.3 Wt (kg) (100 plasma Cl)
Volume of isotonic saline (L) = Chloride decit 154
With correction of the chloride decit, a brisk alkaline diuresis is initiated,
which returns the plasma bicarbonate level towards normal. (Normal serum
chloride level is 95105 mmol/L and bicarbonate level 2226 mmol/L).
Correction of hypokalemia
Hypokalemia is corrected by concomitant potassium repletion. Potassium
can be provided by adding KCl 12 mmol/kg to the uid regimen.
Hydrochloric acid
Intravenous HCl is indicated in severe cases (pH > 7.55) when admin-
istration of NaCl or KCl is contraindicated (e.g., in hypervolemia, CCF,
hyperkalemia). The volume of HCL to be given can be calculated by the
following formula:
H+ decit (mmol) = 0.3 Weight (kg) (measured HCO3
desired HCO3 [mmol/L])
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Volume of 0.1 N HCl (L) = H+ decit (mmol) 100

(0.1 N HCl contains 100 mmol/L of H+)
Rate of H+ replacement: 0.10.2 mmol/kg/h (i.e., 12 mL/kg/h of 0.1 N
HCl).
Ammonium chloride
Ammonium chloride (NH4Cl) is an alternative to IV HCl. The recom-
mended dose for children is 75 g/kg/day in divided doses q6h PO or IV
(max 6g/day) and for adults is 1.5 g q6h IV (max 6 g/day) or 23 g q6h
PO (max 12 g/day). It is diluted to a concentration <12% and given at
the rate of <50 mg/kg/h. NH4Cl is contraindicated in the presence of renal
or hepatic insufciency.
Dialysis
Hemodialysis or peritoneal dialysis will effectively correct metabolic alka-
losis in unresponsive patients and in renal failure. The normal dialysis
uid for peritoneal or hemodialysis, which contains bicarbonate or its
metabolic precursors, will however require to be modied. In an emer-
gency, peritoneal dialysis can be performed using isotonic saline with
appropriate maintenance of plasma potassium, calcium, and magnesium
concentrations by intravenous infusion.
Chloride-Resistant Metabolic Alkalosis

It is associated with uid retention and hypokalemia. The management
involves correcting the potassium deciency and appropriate diuretic ther-
apy. Acetazolamide is a carbonic anhydrase inhibitor and promotes bicar-
bonate excretion. It is administered in a dose of 5 mg/kg/day in divided
doses q8h.
Bibliography
1. Acid-Base Regulation and Disorders. The Merck Manuals 19th ed. Accessed 2011 Oct 26.
Available at: http://www.merckmanuals.com/professional/endocrine_and_metabolic_disorders/
acid-base_regulation_and_disorders/acid-base_regulation.html.
2. Atkins EL. Assessment of acid-base disorders. A practical approach and review. Canad Med Ass
1969;100:9926.
3. Baillie JK. Simple, easily memorised rules of thumb for the rapid assessment of physiological
compensation for acid-base disorders. Thorax 2008;63:28990.
4. Brackett NC Jr. An approach to clinical disorders of acid-base balance. South Med J 1974;
67(9):1084101.
5. Breen PH. Arterial blood gas and pH analysis. Clinical approach and interpretation. Anesthesiol
Clin North America 2001;19(4):885906.
6. Doyle DJ. Synopsis of acid base analysis. [Updated: 2006 Jan; cited: 2011 Feb 25]. Available at:
http://acidbase.homestead.com/ABG_Analysis_Rev_2.0.pdf
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7. DuBose TD Jr. Acidosis and alkalosis. In: Fauci AS, Braunwald E, Kasper DL, et al. eds. Harrisons
Principles of Internal Medicine 17th ed. Vol I. McGraw-Hill Companies Inc.; 2008:28796.
8. Galla JH. Metabolic alkalosis. JASN 2000;11(2):36975.
9. Huang LH, Priestly LA. Pediatric metabolic alkalosis. [Updated: 2010 May 5; cited: 2011 Feb
25]. Available at: http://emedicine.medscape.com/article/906819-diagnosis.
10. Kaehny WD. Respiratory acid-base disorders. Med Clin North Am 1983;67(4):91528.
11. Lynch F. Arterial blood gas analysis: implications for nursing. Paediatr Nurs 2009;21(1):414.
12. Marino PL. Acid base disorders. In: Marino PL, ed. The ICU Book 2nd ed. Hong Kong: Williams &
Wilkins Asia Pacific Ltd; 1997:581616.
13. Reddy P, Mooradian AD. Clinical utility of anion gap in deciphering acid`base disorders. Int J
Clin Pract 2009;63(10):151625.
14. Rowlands BJ, Tindall SF, Elliott DJ. The use of dilute hydrochloric acid and cimetidine to
reverse severe metabolic alkalosis. Postgrad Med J 1978;54(628):11823.
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Parenteral Nutrition
Manual skill has not appreciably improved in the last 50 years, and cannot
improve much further. But manual skill is not the whole of surgery
Sir William Heneage Ogilvie (18871971)*
Daily Nutritional Requirements (Based on Body Weight)
310 kg 1030 kg >30 kg

st
Fluids/day 100120 mL/kg 1000 mL (1 10 kg)
+ 50 mL/kg (2nd 10 kg)
+ 20 mL/kg (3rd 10 kg)
Fluids (mL/m2/day) 15001800 1500
Caloric requirement (kcal/kg/day) 90150 6090 4060
Ratio non-protein calories: Nitrogen 150200:1 150200:1 150200:1
Carbohydrates (g/kg/day) 1530 1525 1020
Proteins (mg/kg/day) 2.53.0 1.52.5 1.01.5
Fats (g/kg/day) 24 24 23
Sodium (mmol/kg/day) 24 24 23
Potassium (mmol/kg/day) 23 23 1.53
Calcium (mmol/kg/day) 0.20.4 0.20.4 0.20.4
Magnesium (mmol/kg/day) 0.150.25 0.150.25 0.15
Phosphorus (mmol/kg/day) 0.52.0 0.52.0 1.01.5
Guidelines for Initiation and Maintenance of Parenteral

Nutrition
Substrate Initiation Advancement Goals

Amino acids 0.51 g/kg/day 0.51 g/kg/day 23 g/kg/day
20% Lipids 0.51 g/kg/day 0.51 g/kg/day 23 g/kg/day
Dextrose 6 mg/kg/min 2 mg/kg/min 1012 mg/kg/min
89 g/kg/day 23 g/kg/day 1418 g/kg/day
g/kg/day = mg/kg/min 24 60 1000.
*Sir William Heneage Ogilvie was a renowned British surgeon, who described the syndrome
of acute colonic pseudo-obstruction (Ogilvies syndrome). He was appointed Knight of the
British Empire in 1946 for his extra-ordinary military service.
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Parenteral Nutrition 125
Parenteral Nutrition (PN) in Children
The provision of nutrition to infants and children following surgery

remains one of the most important aspects of postoperative care. IV nutri-
tional therapy is indicated as a replacement for enteral nutrition when oral
intake is not feasible or as a supplement to enteral feeding.
Caloric Requirements
Caloric requirements of children are noted in the table above. In children aged
6 months15 years, caloric requirements may also be estimated by the formula:
kcal/kg/day = 95 [3 age (yr)]
Small children (<3 kg) require 90 kcal/kg/day for growth, but 40 kcal/kg/day
will prevent catabolism. Fever increases the requirement by 1012% for
every degree rise, surgery by 2030%, and sepsis up to 50%. Caloric
requirements are reduced in sedated ventilated patients.
Amino Acids
Neonates and children are given only pediatric formulations due to the
requirement of essential amino acids, cysteine, taurine, tyrosine, and histi-
dine, which are added to these formulations.
Amino acids are available in 6% and 10% concentration (Aminoven,
Primene). These are started in a dose of 0.51 g/kg/day and increased up
to 3 g/kg/day with daily increments of 0.51 g/kg/day. For efcient protein
utilization for tissue building, 1 g nitrogen (1g N = 6.25 g protein) requires
150200 non-protein calories (nPC), i.e., calories from carbohydrates and
fats. The ratio of nPC:N in the PN is calculated by the formula:
CHO (kcal) + Fat (kcal) 6.25
nPC:N =
Protein (g)
1 g of protein provides 4 kcal; 1 g dextrose: 3.4 kcal; and 1g fat: 9 kcal. Thus,
the amount of amino acids that can be given is restricted by the non-
protein calories being administered. Grams of nitrogen that can be given are
calculated by the kcal provided by Carbohydrate (kcal) + Fat (kcal) 150.
In other words, to prevent catabolism, calories from non-protein and
protein sources are maintained at a ratio of more than 6:1.
Fat
Fat is available as 10% and 20% intralipid. 20% lipid is preferable as it
is isotonic, besides the higher phospholipid content of the 10% solution
impedes plasma triglyceride clearance.
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Fats are started on day 2 or 3 in a dose of 0.51 g/kg/day and increased by

0.5 g/kg/day up to 3 g/kg/day. The dose of lipids needs to be reduced follow-
ing sepsis, respiratory distress, thrombocytopenia, or hyperbilirubinemia.
To maintain its stability, the intralipid is given as a separate infusion
from other solutions, and is covered from light. The solution can, however,
be joined with the amino acid containing solution with a Y-connector near
the infusion point. The lipid infusion for the day is generally given over
20 hours to allow for blood sampling 4 hours after stopping lipid, prior to
starting the next days requirement.
Dextrose
The daily dextrose volume (in mL) is estimated by: Total uid requirement
(Amino acid + Lipid + Supplements). The percentage of dextrose to be admin-
istered is tailored according to the calculated requirement. It is started at
6 mg/kg/min on day 1 and increased by 2 mg/kg/min daily to reach a tar-
get of 1012 mg/kg/min.
Maximum concentration of dextrose that can be given via peripheral
line is 12.5%. Higher concentrations need to be given via a central line.
Blood sugar level is monitored and maintained between 70 and 150 mg/dL.
The intake of dextrose may need to be decreased to control the blood
sugar level. In case the child still has persistent hyperglycemia, glycosuria,
and osmotic diuresis, insulin is given as a continuous infusion starting at a
rate of 0.05 units/kg/h, and increasing the dose as required.
To calculate the rate of glucose administration, the following formula
can be used:
%Glucose mL/kg/day
Glucose infusion rate (mg/kg/min) =
144
Electrolytes
Electrolyte Daily requirement Supplement in PN providing Strength

(mmol/kg/day) daily requirement (mmol/mL)
Sodium 24 mmol/kg/day 0.9% saline or 0.9% saline:
3% saline 1mL = 0.154 mmol
3% saline:
1mL = 0.5 mmol
Potassium 23 mmol/kg/day 15% potassium chloride 1 mL = 2 mmol
Calcium 0.20.4 mmol/kg/day 10% calcium gluconate 1 mL = 0.23 mmol
Magnesium 0.150.25 mmol/kg/day 50% magnesium sulfate 1 mL = 2 mmol
ERRNVPHGLFRVRUJ
Isotonic saline is used to provide the daily sodium requirement. In case

of volume restriction, 3% NaCl may be used instead of 0.9% saline to
provide the daily sodium requirement.
Trace Elements
Trace elements (Zn, Cu, Min, Se, etc.) are provided by giving 10 mL/kg of
plasma over 4 hours every third day.
Vitamins
Add MVI (multivitamin intravenous) 1 mL/kg/day to the TPN solution.
Also give weekly doses of injection vitamin K (0.51 mg) and injection
vitcofol (5 mcg vit B12 and 500 mcg folic acid).
Heparin
Inj. heparin is indicated for central lines in a dose of 0.51 unit/mL of TPN.
Complications
Complications as related to various aspects of PN are as follows:

1. Dextrose: Hypoglycemia, hyperglycemia, hyperosmolality, and
dehydration.
2. Amino acids: Metabolic acidosis, azotemia, cholestatic jaundice.
3. Lipids: Hyperlipidemia, platelet dysfunction, abnormalities in
pulmonary gas diffusion.
4. Mechanical: Thrombosis, embolism.
5. Sepsis: S. epidermidis, Candida.
Laboratory Monitoring
All blood sampling should be done after 4 hours of stopping lipid infusion.
1. Urine specic gravity, glucose and proteindaily.
2. Blood glucoseinitially 6 hourly; once glucose infusion rate is stable,
12 hourly.
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3. Serum Na+/K+daily for 34 days, then twice weekly.

4. Blood pHinitially daily; once protein intake is stable, twice
weekly.
5. Blood Hb and PCVinitially daily, later twice weekly.
6. Blood urea, serum creatinine, serum proteins, LFT, serum
triglyceridesweekly.
Steps for Calculation of Parenteral Nutrition
1. The rst step is to calculate the daily caloric requirement.

2. Note the daily uid requirement, e.g., 100120 mL/kg/day for a child
310 kg weight.
3. Volume of PN = Daily uid requirement minus volume of other
infusions (inotropes, blood products).
4. Volumes of lipid, amino acids, and supplements (saline, potassium
chloride, calcium gluconate, magnesium sulfate, and vitamins)
required is calculated.
Volume of each Daily requirement (mg or mmol/kg) body wt

=
PN component Strength of solution (mg or mmol/mL)
5. Volume of dextrose that can be given = Volume of PN (Volume of

lipids + amino acids + supplements). Calculate the percentage of
dextrose that will provide the daily requirement in this volume.
6. Calculate the non-protein:protein calorie ratio.
Example (10 kg child on day 2)

Component Calculation Amount
Total fluid requirement 110 mL/kg 10 1100 mL
Volume of PN (total fluid requirement 1100100 1000 mL
other infusions)
Fats (20% intralipid) (1 g/kg 10)/0.2 50 mL
Amino acids (6%) (1 g/kg 10)/0.06 167 mL
Sodium (0.9% saline), i.e., 0.154 mmol/mL (3 mmol/kg 10)/0.15 200 mL
KCl 15% (2 mmol/mL) (2 mmol/kg 10)/2 10 mL
Calcium (10% calcium gluconate), i.e., (0.3 mmol/kg 10)/0.23 13 mL
0.23 mmol/mL
ERRNVPHGLFRVRUJ
Component Calculation Amount

Magnesium (MgSO4 50%), i.e., 2 mmol/mL (0.20 mmol/kg 10)/2 1.0 mL
Multivitamins 1.5 mL
Lipid + amino acids + supplements (LAsp) 443 mL
Dextrose Total volume of PN LAsp = 557 mL
(1000 443)
Percentage of dextrose: 20% (8 mg/kg/min = 115 g/day; 115 g/day 557 mL 100).
Ratio of non-protein calories:N = 300:1 [CHO kcal (115 3.4) + Fat kcal (10 9)] 6.25 Protein g (10).
Classically, amino acids, dextrose, and other supplements are mixed together
under aseptic conditions and given via the central line. Lipids can be given
through a peripheral line or via a Y connection in the central line.
Bibliography
1. Acra SA, Rollins C. Principles and guidelines for parenteral nutrition in children. Pediatr Ann
1999;28:13120.
2. Chaudhari S, Kadam S. Total parenteral nutrition in neonates. Indian Pediatr 2006;43:95364.
3. Fusch C, Bauer K, Bhles HJ, et al. Neonatology/Paediatrics Guidelines on Parenteral
Nutrition, Chapter 13. GMS Ger Med Sci 2009;7.
4. Herman R, Btaiche I, Teitelbaum DH. Nutrition support in the pediatric surgical patient. Surg
Clin North Am 2011;91(3):51141.
5. Intravenous fluids. Clinical practice guideline: The Royal Childrens Hospital, Melbourne.
[Updated: 2009 Oct 8; cited: 2011 Oct 29] Available at: http://www.rch.org.au/clinicalguide/
cpg.cfm?doc_id=5203
6. Kraus DM. Pediatrics nutrition. PMPR 652 Pharmacotherapeutics. [Updated: 1997 Dec 19;
cited: 2011 Oct 29]. Available at: http://www.uic.edu/classes/pmpr/pmpr652/Final/krauss/
pedsnutrition.html
7. Krohn K, Babl J, Reiter K, Koletzko B. Parenteral nutrition with standard solutions in paediatric
intensive care patients. Clin Nutr 2005;24:27480.
8. Kurkchubasche AG. Nutritional requirements. Pediatric Surgery Handbook: The Hasbro
Childrens Hospital. [Cited: 2011 Oct 29]. Available at: http://med.brown.edu/pedisurg/Brown/
Handbook/Nutrition.html
9. Math Homepage. Pharmacy Tech Study. [Updated: 1997 Dec 19; cited: 2011 Oct 29]. Available
at: http://www.pharmacy-tech-study.com/math.html
10. Mohandas KM, Shastri YM, Shirodkar M. Total parenteral nutrition. Natl Med J India 2003;
16:2933.
11. Owens JL, Musa N. Nutrition support after neonatal cardiac surgery. Nutr Clin Pract 2009;
24(2):2429.
12. Reimer SL, Michener WM, Steiger E. Nutritional support of the critically ill child. Pediatr Clin
North Am 1980;27(3):64760.
13. TPN solution requirements. [Cited: 2011 Apr11]. Available at: http://www.rxkinetics.com/
tpntutorial/3_1.html
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Enteral Feeding
The doctor of the future will no longer treat the human frame with drugs,
but rather will cure and prevent disease with nutrition
Thomas Edison (18471931)*
Indications for Enteral Tube Feeding
Enteral tube feeding is indicated in children who have been on the ventila-
tor for 35 days and may be started within 48 hours of surgery if a delay in
weaning from ventilator and extubation is anticipated. It is, however, pos-
sible only in patients with stable hemodynamics and a functional gastroin-
testinal tract. It is not advised when high doses of adrenergic drugs and
neuromuscular blockers are being used. Enteral feeding is well tolerated in
critically ill children and is preferable to parenteral nutrition as it prevents
intestinal atrophy and is not associated with the risk of infection and other
complications.
It is also indicated in patients after extubation who are malnourished
and require additional caloric intake or whose documented energy intake
is less than the required levels.
Route
Nasogastric (NG) or orogastric (OG) tubes are usually placed for short-
term enteral feeding. Long-term use of NG or OG tubes is associated
with esophagitis and gastroesophageal reux (GER) and if tube feeding is
required for >812 weeks, gastrostomy or gastrojejunostomy tube place-
ment should be considered.
Fluid and Nutritional Requirements
Daily uid and nutritional requirements have been discussed earlier in the
chapter on parenteral nutrition.
*Thomas Edison was the inventor of the phonograph, motion picture camera, and electric
light bulb.
ERRNVPHGLFRVRUJ
Enteral Feeding 131
Daily maintenance uid requirements based on the body weight are as follows:
<10 kg: 100 mL/kg
1020 kg: 1000 mL + 50 mL for each kg >10 kg
>20 kg: 1500 mL + 20 mL for each kg >20 kg
Method of Administration
Tube feeding can be instituted by either of the following methods:

(i) Bolus feedings are given using a syringe or gravity ow over a
relatively short period of time at regular intervals during the day.
Feeds are generally delivered 68 times per day; each feeding lasting
about 515 minutes.
(ii) Continuous feedings are given using an infusion pump over
a number of hours. It may be a continuous infusion over 24 hours or
as a cyclical infusion for a period of 820 hour per day. Continuous
feeding is usually preferred for small bowel feedings and may be better
tolerated for NG/OG feedings in critically ill patients, because of
a slower infusion rate and volumes.
Types of Feed
Infants should receive expressed breast milk (EBM) or standard infant

formula feeds (e.g., Lactogen). For older children, standard pediatric for-
mulas (which are an appropriate combination of proteins, carbohydrates,
fats, vitamins, and minerals) are designed specically to meet their nutrient
Table 1: Composition of human milk fortifier (per 2 g sachet)

Protein (g) 0.2
Fat (g) 0.1
Carbohydrate (g) 1.2
Calcium (mg) 50
Phosphate (mg) 25
Sodium (mg) 1.75
Vitamin A (IU) 730
Vitamin D (IU) 250
Vitamin E (IU) 1.25
Energy (kcal) 6.5
ERRNVPHGLFRVRUJ
requirements. These formulae are isotonic with osmolality similar to vari-

ous body uids (300 mOsm/L). Diets for adult use have a higher osmolar-
ity and concentration of electrolytes and are therefore not recommended in
children, owing to the inherent risk of diarrhea and hypertonic dehydration.
Supplements may be added to the EBM or to various formula feeds to
increase the caloric content and provide additional nutrients, e.g., human
milk fortier (HMF) powder sachet of 2 g is added to 50 mL EBM to pro-
vide additional proteins, minerals, and vitamins.
Elemental formulas (monomeric formulas) are made from amino acids
or hydrolyzed proteins, carbohydrate, fat in the form of medium-chain
triglycerides plus essential fatty acids and also contain appropriate vita-
mins and minerals. These diets are readily digestible, cause less stimulation
of bile and pancreatic secretions, and result in a smaller amount of stool
formation. Elemental diets are, however, hyperosmolar and need careful
monitoring because of the risk of hyperosmolar dehydration. Indications
for administration include various malabsorption disorders.
Modular formulas provide carbohydrates, proteins, or fats, separately
(as modules) for addition to diets and other formulas for specic nutrition
needs (e.g., medium chain triglycerides in management of chylothorax).
Kitchen Based Feeds

Kitchen based feeds may be used in older children, however, require care
in preparation to prevent contamination and are likely to be thick and
unsuitable for delivery through narrow NG tubes. The following feeds pro-
vide approximately 100 kcal/100 mL:
Milk (100 mL) + Sugar (1 tsp) + Oil ( tsp)
Milk (100 mL) + Sugar (1 tsp) + Cereal our (1 tsp)
Curd (100 mL) + Sugar (2 tsp)
Orange (1) + Sugar (2 tsp) + Water (100 mL)
Egg (1) + Milk (150 mL) + Sugar (2 tsp)
Initiation and Progression
Table 2: Guidelines for enteral feeding in neonates

Weight (g) Starting volume Increased by Full feed (mL/kg/day)
15002000 23 mL q3h 2 mL q6h 160180
20002500 45 mL q3h 3 mL q6h 160180
>2500 510 mL q4h 48 mL q8h 160180
q24h if demand fed
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Enteral Feeding 133
Table 3: Guidelines for 4 hourly bolus tube feeding in children

Weight (kg) Starting volume/ Starting volume of Increase in volume Final volume
day (mL/day) each feed (mL/4h) of each feed q24h of each feed
(mL/4h) (mL/4h)
35 72120 1220 1220 4880
610 145240 2440 2440 96160
1120 278360 4660 4660 185240
2130 365420 6070 6070 240280
Table 4: Guidelines for continuous tube feeding in children

Weight (kg) Starting volume/ Starting rate of Rate of increase Goal (mL/h)
day (mL/day) infusion (mL/h) q824h (mL/h)
35 72120 35 35 1220
610 145240 610 610 2440
1120 278480 1120 1120 4660
2130 500720 2030 2030 6070
Tube feedings are initiated in low volumes, and if tolerated, the volume
is increased every 824 hour to meet the childs daily uid requirements.
While isotonic formulas are started at full strength, hypertonic formulas
are initially given at half strength and subsequently increased in steps to
full strength. Either the volume or the concentration is increased at any
one time, so that the effect of the change can be monitored.
Bolus feedings may be administered starting with 25% of the daily
uid requirement divided equally into the number of daily feedings. One
method is to increase the administered volume every 24 hour by 25% of
the daily requirement. Faster increments may be given if tolerated and full
feeding is instituted in 4872 hour.
To prevent the feeding tube from becoming blocked, the tube may require
to be ushed with water after every feed but not >35 mL water should be
used, as infants may not tolerate large amounts of calorie-free uid.
Continuous feeding can be started at 12 mL/kg/h and advanced by
0.51 mL/kg/h every 824 hour until the goal volume is achieved. Preterm,
critically ill children may require a lower initial volume of 0.51 mL/kg/h.
Complications of Tube Feeding
Complication Cause and possible intervention

Nausea/vomiting/large gastric Rapid administration of feeding
residuals Hyperosmolar formula
gastric motility: consider prokinetic and acid inhibitory
medication
ERRNVPHGLFRVRUJ
Complication Cause and possible intervention

Medication, e.g., antibiotics
Gastric air collection: position child 30 head up.
Vent NG tube
High fat content of formula
Diarrhea Medication, e.g., antibiotics
Lactose intolerance
Nutrient malabsorption
Bacterial infection; check stools for Rotavirus, Lorovirus,
C. difficile
Inadequate fiber
Rapid infusion
Hyperosmolar formula
Constipation Dehydration
Fecal impaction: laxative, stool softner
Inadequate fiber
Electrolyte abnormalities
Medications (narcotics, codeine)
Metabolic disorders: dehydration, Inadequate fluid intake/excessive fluid loss
dyselectrolytemia, hyper/ High/low electrolyte content of formula
hypoglycemia Excess glucose intake/prolonged feeding interval
Drug therapy
Mechanical problems: blocked Excessive residue in formula
tube, tube displacement Inappropriate mixing of medication if administered via
the tube
Tube displacement: verify position by auscultation and
pH testing of tube aspirate
Gastric Residue
Abdominal girth and gastric residue are recorded before every bolus
feed (or every 4 hours if continuous feeding is being given). In case of
abdominal distension or if gastric residue is >50% of previous bolus feed
(or >2 times the hourly volume for continuous drip feeding), either the
volume or the strength of the next feed is reduced by one or two steps. The
aspirated contents are returned and the feeds advanced more slowly. In
severe cases of feed intolerance, the feeding is stopped and recommenced
when the distension or vomiting settles down and the residue is no more
than a few mL.
Feeding the child in a 2030 head up tilt and placing the child in the
right lateral decubitus position after feeding has been helpful in prevent-
ing gastroesophageal reux and decreasing the amount of gastric residue.
If high residuals persist without associated clinical signs and symptoms,
a promotility agent (e.g., erythromycin, metoclopramide) may be tried.
ERRNVPHGLFRVRUJ
Enteral Feeding 135
Bibliography
1. Aquilina A, Kelly J, Bisson R, et al. Guidelines for the administration of enteral and parenteral
nutrition in paediatrics. SickKids, Toronto, Ontario, Canada [Cited: 2012 May 22]. Available at:
www.sickkids.ca/pdfs/.../19499-Enteral_Parenteral_Nutrition.pdf
2. Elizabeth KE. Nutrition in health and illness. In: Gupte S. Textbook of Pediatric Nutrition
New Delhi: Peepee; 2006:3545.
3. Kurkchubasche AG. Nutritional requirements. Pediatric Surgery Handbook: The Hasbro
Childrens Hospital. [Cited: 2011 Feb 22]. Available at: http://bms.brown.edu/pedisurg/Brown/
Handbook/Nutrition.html
4. Seashore JH. Nutritional support of children in the intensive care unit. Yale J Biol Med 1984;
57(2):11134.
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Gastrointestinal Drugs
Anti-emetics
Name Dose Remarks
Domperidone Children: 250500 mcg/kg q68h PO Side effects include
(max 2.4 mg/kg/day which should not extrapyramidal symptoms
exceed 80 mg) (anxiety, distress, slurred
Adults: 1020 mg q68h PO (max 80 mg/ speech, tremor and various
day) movement disorders).
Metoclopramide Children Side effects include
Anti-emetic and GE reflux0.10.2 mg/ extrapyramidal symptoms.
kg/dose q68h PO/IM/IV
>14 yr and adults
Anti-emetic dose10 mg q68h IV
GE reflux1015 mg 30 min before meals
and HS PO/IM/IV (4 doses)
Ondansetron Children Indicated in chemotherapy
hydrochloride IV: 212 yr: 0.1 mg/kg/dose and radiotherapy induced
(max 4 mg). emesis. Single dose used for
PO: 411 yr: 4 mg q8h the prevention and treatment
>12 yr and adults of postoperative nausea and
8 mg q8h PO/IV vomiting. Repeated after
4 hours if required.
Cisapride Children Indicated for GE reflux.
>1 year0.20.3 mg/kg/dose q68h PO
Adults
1020 mg 15 min before meals and HS
(4 doses) PO
Prochlorperazine Children Side effects include
>10 kg: PO0.4 mg/kg/day in divided extrapyramidal symptoms.
doses q68h or alternatively: 1013 kg:
2.5 mg q1224h (max 7.5 mg/day);
1417 kg: 2.5 mg q812h (max 10 mg/
day); 1839 kg: 2.5 mg q8h or 5 mg q12h
(max 15 mg/day)
IM0.13 mg/kg single dose
Adults
PO: 510 mg q68h
IM: 510 mg q34h (max 40 mg/day)
ERRNVPHGLFRVRUJ
Gastrointestinal Drugs 137
Name Dose Remarks

Triflupromazine Children Side effects include
PO: 0.5 mg/kg q8h. extrapyramidal symptoms.
IM: 0.20.25 mg/kg (max 10 mg/day). Safety and efficacy not
Adults established for children
IM: 515 mg q4h (max 60 mg/day). <2.5 years of age
IV: 1 mg (max 3 mg/day).
PO: 1025 mg q12h.
Prophylactic agents for GI hemorrhage

Name Dose Remarks
Ranitidine 1 month16 yr: 24 mg/kg in
(150/300 mg Tab) divided doses q12h PO. (For
treatment max 300 mg/day;
maintenance max 150 mg/day)
Adult: 150 mg q12h or 300 mg HS
PO; maintenance 150 mg HS.
Inj. ranitidine 1 month12 yr: 3 mg/kg/day in Dilute 10 times with 0.9%
(25 mg/mL amp) divided doses q8h IV. saline (over 25 minutes) or
>12 yr: 150 mg/day in divided doses inject into running infusion.
q8h IV. Use dose in severe renal
impairment and liver disease.
Omeprazole 1 month12 yr: 1020 mg/day in Reduce dose in severe liver
(20 mg capsule) divided doses q1224h PO. disease.
>12 yr: 2040 mg/day in divided
doses q1224h PO.
Sucralfate 01 yr: 6 mL/day in divided doses Contraindicated in severe
suspension q4h PO. renal impairment.
(1 g in 5 mL) 26 yr: 12 mL/day in divided doses
q4h PO.
712 yr: 18 mL/day in divided doses
q4h PO.
>12 yr: 30 mL/day in divided doses
q4h PO.
Stress Ulceration and Upper GI Bleeding
Stress ulceration and upper gastrointestinal bleeding are well-known com-

plications in the postoperative period in children operated for heart dis-
ease. Some of the factors which increase the risk of stress ulceration are
as follows:
Children on ventilator for >48 hours
Coagulopathy
ERRNVPHGLFRVRUJ
Unstable hemodynamic condition requiring high doses of intravenous

catecholamines
Re-thoracotomy
Multiorgan dysfunction or sepsis
Steroids
Various available prophylactic agents include H2-receptor blocking agents,
proton pump inhibitors (PPIs), sucralfate, and antacids.
H2-receptor antagonists (ranitidine, famotidine) decrease the acid secre-
tion in the stomach and lower the incidence of stress ulceration and the
occurrence of GI bleeding. PPIs however, provide a higher level of stomach
pH control and are therefore more effective therapy for prophylaxis. At the
same time, this elevation in the level of gastric pH has been implicated in
an increase in bacterial colonization of the gut promoting bacterial trans-
location and an increased incidence of blood-borne sepsis and also an
increased incidence of aspiration and ventilator-associated pneumonias.
H2 blocking agents and PPIs are therefore not generally used for routine
postoperative prophylaxis but in patients who are at a higher risk for GI
bleeding and in the treatment of GI bleeding.
Sucralfate has not been shown to be as effective as H2 blockers and PPIs
in the control of stress ulceration but since it does not increase the gastric
pH, it may be safer and has been recommended for routine use in post-
operative protocols. It may also be used in combination with H2-receptor
blocking agents, and PPIs in the treatment of GI bleeding.
Antacids are associated with diarrhea and electrolyte disturbances and
have not proven to be of any benet in GI prophylaxis.
Bibliography
1. Allen ME, Kopp BJ, Erstad BL. Stress ulcer prophylaxis in the postoperative period. American
Journal of Health-System Pharmacy 2004;61(6). Medscape. [Updated: 2004 Apr 16; cited: 2011
Apr 26] Available at: http://www.medscape.com/viewarticle/472701.
2. Araujo TE, Vieira SM, Carvalho PR. Stress ulcer prophylaxis in pediatric intensive care units.
J Pediatr (Rio J) 2010;86(6):52530.
3. Arora NK, Ganguly S, Mathur P, Ahuja A, Patwari A. Upper gastrointestinal bleeding: etiology
and management. Indian J Pediatr 2002;69(2):15568.
4. Behrens R, Hofbeck M, Singer H, Scharf J, Rupprecht T. Frequency of stress lesions of the
upper gastrointestinal tract in paediatric patients after cardiac surgery: effects of prophylaxis.
Br Heart J 1994;72:1869.
5. Cook D, Guyatt G, Marshall J, et al. A comparison of sucralfate and ranitidine for the preven-
tion of upper gastrointestinal bleeding in patients requiring mechanical ventilation. Canadian
Critical Care Trials Group. N Engl J Med 1998;338(12):7917.
6. Cook DJ, Fuller HD, Guyatt GH, et al. Risk factors for gastrointestinal bleeding in critically ill
patients. Canadian Critical Care Trials Group. N Engl J Med 1994;330:37781.
7. Deorari AK. Rational drug therapy. In: Ghai OP, Paul VK, Bagga A, ed. Essential Paediatrics
7th ed. New Delhi: CBS Publishers & Distributors Pvt Ltd; 2009:72930.
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Gastrointestinal Drugs 139
8. Elliot MJ, Delius RE. Renal issues. In: Chang AC, Hanley FI, Wernovsky GU, Wessei DL, ed.
Pediatric Cardiac Intensive Care Pennsylvania: Williams and Wilkins; 1998:388.
9. Ephgrave KS, Kleiman-Wexler R, Pfaller M, et al. Effects of sucralfate vs antacids on gastric
pathogens: results of a double-blind clinical trial. Arch Surg 1998;133(3):2517.
10. Fennerty MB. Pathophysiology of the upper gastrointestinal tract in the critically ill patient:
rationale for the therapeutic benefits of acid suppression. Crit Care Med 2002;30:S3515.
12. Reveiz L, Guerrero-Lozano R, Camacho A, Yara L, Mosquera PA. Stress ulcer, gastritis, and
gastrointestinal bleeding prophylaxis in critically ill pediatric patients: a systematic review.
Pediatr Crit Care Med 2010;11:12432.
13. Sean C. Sweetman. Gastrointestinal drugs. Martindale: The Complete Drug Reference 36th ed.
2009:1693778.
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Postoperative
Respiratory Complications
It is unsettling to nd how little it takes to defeat success in medicine
Atul Gawande* (In: Better: A Surgeons Notes on Performance)
Pulmonary Dysfunction
Postoperative pulmonary dysfunction (PPD) refers to an impairment of

blood gases and alteration of lung mechanics in the immediate post surgi-
cal period. The cause of the dysfunction is primarily because of the inam-
matory response and microatelectasis initiated by cardiopulmonary bypass
(CPB) resulting in abnormalities of oxygen and carbon dioxide transfer
across the alveolar membrane. The AaDO2 is signicantly higher, and there
is a decrease in the vital capacity, functional residual capacity, and lung
compliance following CPB.
In the extubated patient, this may be clinically evident by tachypnea,
respiratory distress, and tachycardia. The severity of dysfunction may range
from hypoxemia (which is present to a variable degree in all patients fol-
lowing CPB) to acute respiratory distress syndrome (ARDS) (0.42%).
Recovery from PPD requires a variable period of postoperative mechan-
ical ventilation. Appropriate mode of ventilation, moderate PEEP, and
repeated endotracheal suctioning gradually improves the oxygenation
and increases the functional residual capacity permitting extubation.
Thereafter, positioning, pain management, and chest physiotherapy further
improves alveolar recruitment. Postoperative pain is certainly an important
consideration in patient recovery, and failure to control postoperative pain
may itself result in inadequate tidal volume with increasing areas of lung
collapse and poor blood gases.
Pleural Effusion
Causes of pleural effusion in the postoperative period include right heart

failure, uid overload, pulmonary edema, and extravasation from extracardiac
*Atul Gawande is a practicing general surgeon and author of three best sellers, Complications,
Better and The Checklist Manifesto which are based on his personal experience of surgical
triumphs, errors, and controversies.
ERRNVPHGLFRVRUJ
Postoperative Respiratory Complications 141
shunts. The inammatory response to CPB may also itself result in small,
transient effusions. Small effusions will resolve with treatment of the
cause, however, large effusions will require chest tube drainage. The most
appropriate position for chest drains for uid collections is the 5th or 6th
intercostal space in the posterior axillary line.
Chylothorax
Chylothorax may occur after injury to the thoracic duct or its tributaries
either within the pericardium or more often after extrapericardial opera-
tions, e.g., BlalockTaussig shunt or coarctation repair. It may also be seen
after open heart procedures associated with high systemic venous pressure,
especially the Fontan operation. Often, a chylothorax becomes evident
only after 27 days of surgery. The reason for this is that lymph initially
accumulates in the posterior mediastinum until the mediastinal pleura
gives way, usually into the right pleural cavity.
Diagnosis
Presence of a milky white effusion, which increases with the intake of die-
tary fat, is an indication of a chylothorax. Chyle is sterile and can be distin-
guished from other opalescent collections by the presence of chylomicrons,
which are stained with Sudan III and estimation of the triglyceride content
(>110 mg/dL). Chyle has a protein concentration of 2.26 g/dL and has
a white blood cell count >1000/mL with a lymphocyte fraction >80%.
Management
As a rst step, conservative management is initiated with chest tube drain-
age and a fat-free formula consisting of only proteins and starch or a die-
tary intake of medium chain triglycerides instead of normal fats. Medium
chain triglycerides are absorbed directly into the portal venous system and
allow healing of the injured duct. Alternatively, the child is placed on IV
hyperalimentation at the time of diagnosis or later after a trial of the above
management.
Inj. somatostatin (or its synthetic analog octreotide) has been effectively
used to treat chylothorax in various dosing schedules. One recommended
dose is 80100 mcg/kg/day, which can be given in divided doses 8 hourly
either IM or IV. An alternative dose protocol is 14 mcg/kg/h as a continuous
infusion. It is tapered after cure and may need to be given up to 3 weeks.
If the drainage persists, recommendations about the length of conserva-
tive management vary considerably. One opinion is to continue aggressive
ERRNVPHGLFRVRUJ
nonoperative management for 4 weeks before surgical intervention. Other

authors have advocated surgical intervention at 12 weeks if there is no
signicant improvement in the drainage.
Operative procedures include surgical ligation of the injured duct at the
site of operation or above the right diaphragm. Alternatively, a pleurodesis
or a pleuroperitoneal shunt may be performed.
Diaphragmatic Paralysis
Phrenic nerve injury can occur during surgery, along the course of the
nerve in the mediastinal pleura either by cold cardioplegia solution, dia-
thermy, or direct surgical trauma. It is a cause of failure to wean from the
ventilator. It may be difcult to diagnose, and an abnormal abdominal
breathing pattern in the extubated child may be the pointer. Respiratory dis-
tress and CO2 retention after extubation may require that the child be put
back on the ventilator. X-ray chest after extubation reveals a raised dome
of diaphragm with atelectasis, which was not evident during ventilation.
Ultrasound examination or uoroscopy conrms the paradoxical diaphrag-
matic movements (upward diaphragmatic movement during inspiration).
Plication of the affected diaphragm may be needed before the child can
eventually be extubated.
Pneumothorax
Intermittent positive pressure ventilation (IPPV) or vigorous hand bagging

may result in barotrauma and pneumothorax. Entry of air from around a
loosely tting chest drain can also be a cause.
Pneumothorax is suspected in the ventilated patient, if there is an
increase in the peak inspiratory pressure, a fall in the oxygen saturation,
and a decrease of breath sounds on the affected side. In the extubated
patient, there may be tachypnea, cyanosis, tracheal deviation away from
the affected side, and reduced respiratory breath sounds. In tension pneu-
mothorax, there is in addition, sudden hemodynamic decompensation
manifested by hypotension and bradycardia or tachycardia.
X-ray chest will show pneumothorax. In the unstable patient, rather
than waiting for the X-ray, the diagnosis can be conrmed with a needle
and syringe aspiration, and the pneumothorax relieved by the introduction
of a 20 gauge needle. A chest tube is inserted subsequently. For a pneumo-
thorax, the appropriate position for the chest tube is the third intercostal
space in the anterior axillary line.
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Atelectasis
Atelectasis produces tachypnea, tachycardia, and impairment of blood

gases, depending upon the extent of collapse. In case of a large collapse,
there is a decrease in chest expansion, a mediastinal shift towards the
affected side, and diminished breath sounds over the corresponding area
of the chest. The patient may have fever 4872 hours after a persistent col-
lapse lung. Radiological ndings show inltration of the collapsed seg-
ment or lobe. Typically, the right upper or middle lobe collapse obscures
the right heart border, left upper lobe atelectasis may be evident by a tri-
angular inltrate extending to the upper mediastinum, and a left lower
collapse causes an increased density of the cardiac silhouette.
Causes
Collapse of the lung may be caused by obstruction of the endotracheal
tube, or bronchial airway with blood clot or secretions. Vascular structures
such as dilated pulmonary arteries or enlarged cardiac chambers, because
of their close association with the respiratory tract, can cause extrinsic
compression of the airways. The trachea, the left bronchus, and the origin
of the right middle lobe bronchus are the more common sites of compres-
sion. Signicant airway compression presents with pulmonary collapse or
persistent wheezing or rarely it is a cause of failure of extubation of the
ventilated patient.
Management
Postoperative management involves measures to assist complete lung
expansion and prevention of atelectasis. The ventilated child needs humid-
ication of inspired gases, institution of adequate PEEP (or CPAP) and reg-
ular endotracheal suction. Minimal negative pressure (80 to 120 mmHg)
is utilized to aspirate endotracheal secretions so as not to cause epithelial
damage. After the child is extubated, chest physiotherapy and adequate
analgesia prevents pain and splinting of the chest.
A collapse segment or lobe may re-expand with chest physiotherapy
alone. More often it may require tracheal aspiration with a exible bron-
choscope. Alternatively, endotracheal intubation is done to allow tra-
cheal suctioning. This is followed by short-term IPPV with PEEP before
extubation.
Atelectasis may be difcult to distinguish from pneumonia and non-
resolving atelectasis may progress to pneumonia. Endotracheal secretions
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should be Gram stained and cultured, and appropriate prophylactic antibi-

otics should be started in non-resolving atelectasis.
Aspiration Pneumonitis
Aspiration pneumonitis (Mendelson syndrome) is caused by an episode

of vomiting or reux, with aspiration of the gastric contents. This can
possibly occur in a sedated or neurologically obtundated child or in a ven-
tilated child in whom a non-cuffed endotracheal tube has been used. The
aspiration causes a chemical pneumonitis, which may be followed subse-
quently by a bacterial infection. The extent of damage to the tracheobron-
chial tree depends upon the amount and acidity of the material aspirated,
and the pathological lesions can vary from mild bronchiolitis to acute
pulmonary edema.
Clinical Features
The child usually presents with clinical features of mild to severe respira-
tory distress 25 hours after the episode of aspiration. Severe cases may
progress to ARDS. Radiological ndings vary from segmental or lobar con-
solidation to bilateral perihilar or multifocal opacities. In the recumbent
child, the posterior segments of the upper lobes and the superior segments
of the lower lobes are more likely to be involved.
Treatment
Oropharyngeal and tracheal suctioning is urgently required in a child who
has aspirated following vomiting. Pulse oximetry is monitored and sup-
plemental oxygenation is provided. The need for intubation is assessed
depending on the oxygenation and the patients neurological status.
Antibiotics are indicated if aspiration pneumonitis fails to resolve
within 48 hours; Pseudomonas aeruginosa, Klebsiella pneumoniae, and
methicillin-resistant Staphylococcus aureus must be covered.
Bibliography
1. Apostolakis EE, Koletsis EN, Baikoussis NG, Siminelakis SN, Papadopoulos GS. Strategies to
prevent intraoperative lung injury during cardiopulmonary bypass. J Cardiothorac Surg 2010;
5:1. [Cited: 2011 Oct 8] Available at: http://www.cardiothoracicsurgery.org/content/5/1/1.
2. Bandla HPR, Hopkins RL, Beckerman RC, Gozal D. Pulmonary risk factors compromising post-
operative recovery after surgical repair for congenital heart disease. Chest 1999;116:7407.
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3. Bennet NR. Paediatric intensive care. Br J Anaesth 1999;83:13956.

4. Bttiker V, Fanconi S, Burger R. Chylothorax in children: guidelines for diagnosis and manage-
ment. Chest 1999;116:6827.
5. Chakrabarti B, Calverley PMA. Management of acute ventilatory failure. Postgrad Med J
2006;82:43845. doi: 10.1136/pgmj.2005.043208.
6. Engelherdt T, Webster NR. Pulmonary aspiration of gastric contents in anaesthesia. Br J
Anaesth 1999;83:45360.
7. Helin RD, Angeles STV, Bhat R. Octreotide therapy for chylothorax in infants and children:
a brief review. Paediatr Crit Care Med 2006;7(6):5769.
8. Nair SK, Petko M, Hayward MP. Aetiology and management of chylothorax in adults. Eur J
Cardiothorac Surg 2007;32:3629.
9. Ng CS, Wan S, Yim AP, Arifi AA. Pulmonary dysfunction after cardiac surgery. Chest 2002;
121:126977.
10. Oster JB, Sladen RN, Berkowitz DE. Cardiopulmonary bypass and the lung. In: Gravlee GP,
Davis RF, Kurusz M, Utley JR, eds. Cardiopulmonary Bypass: 2nd ed. Philadelphia: Lippincott
Williams & Wilkins; 2000:367.
11. Pratap U, Slavik Z, Ofoe VD, Onuzo O, Franklin RCG. Octreotide to treat postoperative chylo-
thorax after cardiac operations in children. Ann Thorac Surg 2001;72:17402.
12. Sandora TJ, Harper MB. Pneumonia in hospitalized children. Pediatr Clin N Am 2005;52:
105981.
13. Wynne R, Botti M. Postoperative pulmonary dysfunction in adults after cardiac surgery with
cardiopulmonary bypass: clinical significance and implications for practice. Am J Crit Care
2004;13:38493.
ERRNVPHGLFRVRUJ
Acute Respiratory
Distress Syndrome
Diagnosis
Parameter ARDS
Onset Acute
Clinical setting Predisposing condition exists
Gas exchange PaO2/FiO2 <200 mmHg regardless of PEEP level
Chest X-ray Bilateral infiltrates
Wedge pressure 18 mmHg
Acute respiratory distress syndrome (ARDS) has been dened as a syndrome

characterized by an acute onset of dyspnea, severe hypoxemia, bilateral lung
inltrates on X-ray chest, and a decreased compliance of the respiratory
system in the absence of congestive cardiac failure.
It is a complication that arises when other disease processes produce a
diffuse inammatory injury of the lungs. Predisposing conditions in the
postoperative cardiac patient include sepsis, multiple transfusions, ventilator-
associated pulmonary contusion, aspiration pneumonia, and cardiopulmo-
nary bypass itself.
The term acute lung injury (ALI) has been used in order to identify
patients who have not yet progressed to ARDS or have a milder form of ARDS
and the ratio of PaO2:FiO2 denes the degree of severity of hypoxemia.
The criteria for diagnosis that have been proposed by American-European
Consensus Conference (1993) for ARDS and ALI are as follows:
Acute bilateral inltrates on chest X-ray.
Ratio of the partial pressure of oxygen to the fraction of inspired oxygen
(PaO2/FiO2): in ARDS is 200 and for ALI from 200300.
A pulmonary artery wedge pressure of <18 mmHg, as evidence that
the cause of the pulmonary edema is non-cardiogenic. In children, an
echocardiogram may instead be used to assess the LA pressure.
ERRNVPHGLFRVRUJ
Acute Respiratory Distress Syndrome 147
Presentation
The clinical features of ARDS may develop over hours or days after the
predisposing event. The rst sign is tachypnea with associated hypoxemia,
which shows no response to O2 therapy. The patient has progressive respi-
ratory distress and may develop cyanosis and eventually require mechani-
cal ventilation. In severe cases, in spite of IPPV, the clinical condition may
continue to worsen and there may be an outpouring of intra-alveolar uid
of high protein content from the endotracheal tube. The peak inspiratory
pressure is increased, and there may be a further deterioration in the oxy-
gen saturation. Pneumothorax as a result of barotrauma is a frequent com-
plication of ARDS because of high peak inspiratory pressures generated with
mechanical ventilation.
Blood gas analysis reveals a low PaO2 because of severe intrapulmonary
shunting, and a high alveolar-arterial oxygen gradient (AaDO2). The left
atrial pressure is normal and excludes cardiogenic pulmonary edema.
Differential Diagnosis
Signs ARDS Left heart failure Aspiration pneumonia

Fever and Yes Absent Yes
leukocytosis
Hypoxemia Hypoxemia is more Chest X-ray findings Chest X-ray findings
pronounced than more pronounced more pronounced
X-ray findings
Chest X-ray Diffuse bilateral Bilateral hilar infiltrates Infiltrate usually involves
infiltrates, white superior segments of
out in severe cases lower lobes or posterior
segments of upper lobes
Pleural effusion Absent Present May be present
Wedge pressure <18 mmHg >18 mmHg <18 mmHg
Predisposing cause Present Associated cardiac defect Sepsis
Bronchoalveolar Polymorphonuclear Polymorphonuclear Polymorphonuclear
lavage cells (>18%) cells <5% cells (>18%)
X-ray chest shows bilateral, diffuse pulmonary inltrates but is not specic
for ARDS. Air bronchograms may be present but Kirley B lines, peribron-
chial cufng and pleural effusions are uncommon.
In left ventricular failure (cardiogenic pulmonary edema), there is a
conuent alveolar shadowing spreading out from the hilum giving a bats
wing appearance. Presence of Kirley B lines, pleural effusion, uid in the
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ssures, and peribronchial cufng is more common while air broncho-

grams are unusual. Kirley B lines are caused by edema of the interlobular
septa and are seen perpendicular to the pleural surface at the lung bases.
In the upright lm, the upper lobe blood vessels may be wider than the
lower lobe vessels. This upper lobar diversion occurs because of lower
zone arteriolar vasoconstriction secondary to alveolar hypoxia. Upper lobe
diversion is however, normal in the supine lm. Associated LV enlarge-
ment may be additional evidence of LV failure.
Management
Management strategy Comments

Ventilation
1. Tidal volume 57 mL/kg. The plateau pressure is maintained 30 cm H2O. CO2
retention (permissive hypercapnia) because of low TV is accepted.
2. PEEP 510 cm is added to prevent atelectasis.
3. FiO2 5060% to minimize O2 toxicity. An arterial oxygen saturation
of >90% is acceptable.
Diuretics Diuretic may be used to reduce fluid overload but does not
decrease the inflammation.
Volume infusion Large amounts of colloid/crystalloid infusions may be required to
maintain the CVP because of the capillary leak syndrome.
Dobutamine Dobutamine cardiac output. Dobutamine is preferable to
dopamine since dopamine in higher doses acts as a pulmonary
vasoconstrictor. Pulmonary vasodilators are also avoided as they
may increase the intrapulmonary shunting.
Blood products Packed RBCs are given to maintain Hb >10 g%.
Steroids Steroids have no specific role.
Surfactant Aerosolized surfactant may be of benefit in neonates.
Various ventilatory strategies in the management of ARDS have been advo-

cated with debatable outcomes. One of the prevalent methods (ARDS net-
work trial 2000) aims at ventilatory settings that prevent any further lung
injury by achieving the lowest peak inspiratory pressures (PIP) and tidal
volumes (TV) that will allow gas exchange. Some degree of CO2 retention
(permissive hypercapnia) because of low TV is accepted. End expiratory
atelectasis is prevented by appropriate levels of PEEP.
Volume or pressure preset ventilation can be used. The following proto-
col is appropriate in volume assist control mode:
1. The initial TV is set at 57 mL/kg.
2. A plateau pressure of 30 cm H2O is maintained by reducing the TV to
5 or 4 mL/kg if necessary.
ERRNVPHGLFRVRUJ
Acute Respiratory Distress Syndrome 149
3. The ventilator rate is set at 1235 breaths/min to provide appropriate

minute ventilation. Hypercapnea is accepted as a protective
lung strategy and an increase in PCO2 (pH >7.10 and PCO2
4090 mmHg) is allowed to the extent that it does not result in
signicant hemodynamic instability.
4. A moderate prolongation of inspiratory time (IT) is used to improve
oxygenation (1:1 to 1:3). Excessive IT (which shortens the expiratory
time) is avoided as this can cause intrinsic PEEP and lung injury.
5. One method recommended for setting the appropriate PEEP and FiO2
is to titrate levels of PEEP and FiO2 combinations against increasing
oxygen saturations. The following combinations of FiO2/PEEP are
stepped up to achieve an oxygenation goal of PaO2 5580 mmHg
(SaO2 8895%):
FiO2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0

PEEP (cm H2O) 5 8 810 10 1014 14 1418 1822
6. Attempts to wean by pressure support are indicated when

FiO2/PEEP 0.40/8.
Bibliography
1. Corne J, Carrol M, Brown I, Delany D, eds. Chest X-ray Made Easy 2nd ed. Churchill Livingston;
2002:5663.
2. Christie JD, Lanken PN. Acute lung injury and acute respiratory distress syndrome. In: Hall JB,
Schmidt GA, Wood LDH, eds. Principles of Critical Care 3rd ed. New Delhi: McGraw-Hill
2005:51547.
3. Feng AK, Steele DW. Pediatrics, respiratory distress syndrome: treatment and medication.
[Updated: 2009 Sep 18; cited; 2011 Feb 22]. Available at: http://emedicine.medscape.com/
article/803573.
4. Fiore ML, Lieh-Lai MW. Acute respiratory distress syndrome [Cited: 2011 Feb 22]. Available at:
http://www.scribd.com/doc/24857688/ARDS-Lecture.
5. Hess D. Mechanical ventilation of patients with ARDS [Cited: 2011 Feb 22]. Available at:
http://www.rcsw.org/Download/2004_RCSW_conf/ARDS%20Dean%20Hess.pdf
6. OCroinin D, Chonghaile MN, Higgins B, Laffey JG. Bench-to-bedside review: permissive
hypercapnia. Crit Care 2005;9(1):519.
7. Prodhan P, Noviski N. Pediatric acute hypoxemic respiratory failure: management of oxygena-
tion. J Intensive Care Med 2004;19:14053.
8. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes
as compared with traditional tidal volumes for acute lung injury and the acute respiratory dis-
tress syndrome. N Engl J Med 2000;342:13018.
9. Varon J, Wenker OC. The acute respiratory distress syndrome: myths and controversies. The
Internet Journal of Emergency and Intensive Care Medicine 1997;1(1). [Updated: 2009 Feb 13;
cited: 2011 Feb 22]. Available at: http://www.ispub.com/ostia/index.php?xmlFilePath=journals/
ijeicm/vol1n1/ards.xml.
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Postoperative
Bronchospasm
Postoperative Causes
Bronchospasm or respiratory wheeze in the immediate postoperative

period is not uncommon and may be caused by a number of potential
factors:
1. Primarily, it may be a manifestation of preexisting bronchial asthma
or airway hypersensitivity. Bronchial irritation by the endotracheal
tube, anesthetic gases, or secretions in predisposed individuals may
precipitate an acute episode.
2. Hypersensitivity reactions to various drugs, in particular protamine,
-adrenergic blockers, and drugs that cause histamine release
(e.g., morphine or atracurium), may induce bronchospasm. Activation
of inammatory factors by the CPB (e.g., C5a anaphylatoxin) may
itself be the cause.
3. Bronchospasm may be a manifestation of pulmonary edema, possibly
the result of over transfusion in a child with poor LV function.
4. Other postoperative respiratory complications (e.g., respiratory
infection, pneumothorax, or atelectasis) may present with
bronchospasm.
Assessment of Severity of Acute Bronchial Asthma
Clinical feature Mild Moderate Severe

Breathlessness Only on activity, Becomes breathless Is breathless even
e.g., walking on talking. In infants, on rest, inability
cry is softer and to feed
shorter; difficulty in
feeding
ERRNVPHGLFRVRUJ
Postoperative Bronchospasm 151
Clinical feature Mild Moderate Severe

Ability to talk Is able to talk in Talks in phrases or Drowsy/confused
sentences words
Use of accessory Not in evidence Evident Evident.
muscles of respiration/ Breathing may be
suprasternal retraction thoracoabdominal
Wheeze Moderate, may be Loud Loud/may be
only end expiratory inaudible
Pulsus paradoxus Absent <10 mmHg May be present Often present
1025 mmHg 2040 mmHg
PaO2 on air Normal >60 mmHg <60 mmHg,
possible cyanosis
PaCO2 <45 mmHg >45 mmHg >45 mmHg
SaO2% >95% 9195% <90%
PEF after >80% 6080% <60% or response
bronchodilator lasts <2 h
therapy; % of
predicted
The respiratory rate and the heart rate are increased in proportion to the severity of bronchospasm
(Normal heart rates2 mths1 yr: <160/min, 12 yr: <120/min, 28 yr: <110/min; Normal respiratory rates
up to 2 mths: <60/min, 2 mths1 yr: <50/min, 15 yr: <40/min, 68 yr: <30/min).
Drug Therapy in Acute Bronchial Asthma
Drugs given by nebulization

Drugs Dose Comments
Salbutamol Adults and children: Inhaled short-acting 2-
(albuterol) 100200 mcg/kg/dose every agonists used in the treatment
46 h. (Max dose <20 kg: of acute bronchospasm
2.5 mg q6h; >20 kg: 5 mg include salbutamol,
q46h) Initially, the dose can terbutaline, levalbuterol, and
be repeated every 20 min pirbuterol. Salbutamol can
3 times. cause tachycardia and severe
electrolyte disturbances.
Inhaled, long-acting 2-
agonist salmeterol and
formoterol are used for
maintenance therapy,
typically with inhaled
corticosteroids.
ERRNVPHGLFRVRUJ
Drugs Dose Comments

Ipratropium 15 yr: 125250 mcg/dose Ipratropium is an inhaled
q46h anticholinergic bronchodilator,
>5 yr: 250500 mcg/dose chemically related to atropine.
q46h It has a delayed onset of action
(20 minutes) and is used
as adjuvant therapy in
combination with salbutamol
for acute episodes of
bronchospasm.
Budesonide >3 mo: 0.51 mg q12h Inhaled corticosteroids
(maintenance 0.250.5 mg are used for their anti-
q12h) inflammatory effects, primarily
Adults: 12 mg q12h for maintenance therapy in
Maintenance: 0.51 mg q12h. persistent asthma. Alternative
drugs include beclomethasone,
fluticasone, and triamcinolone.
L-adrenaline 1:1000 0. 5 mL/kg with 3 mL saline May be tried in severe
(1000 mcg/mL) (max dose <4 yr: 2.5 mL; bronchospasm not responding
>4 yr: 5 mL) to other drugs.
Drugs given IV
Drug Dose Comments
Methylprednisolone Children Systemic steroid is indicated in severe cases
12 mg/kg/day divided not responding to nebulization therapy
q612h alone. Parenteral corticosteroids that may
Adults be given include methylprednisolone,
60500 mg/day divided hydrocortisone, or prednisone.
q612h. (High dose is
given for a few days and
then tapered.)
Hydrocortisone Children In severe bronchospasm, Inj.
5 mg/kg q6h. hydrocortisone may be used instead of
Adults methylprednisolone.
100500 mg q6h.
Theophylline Children and adults May be given in addition to nebulization
Loading dose: therapy in severe cases. Used with caution
45 mg/kg IV over in infants as theophylline acts as a central
2030 minutes. stimulant and is metabolized slowly.
Then Theophylline can cause tachycardia and
19 yr: 800 mcg/kg/h. tremors and has a narrow therapeutic index
912 yr: 600700 mcg/ (therapeutic serum levels: 1020 mcg/mL).
kg/h. Children have a more rapid theophylline
Adults: 400600 mcg/ clearance rate, thus the maintenance doses
kg/h. in them are higher than in adults.
ERRNVPHGLFRVRUJ
Drug Dose Comments

Terbutaline Children >2 yr Terbutaline is an IV short-acting 2-
10 mcg/kg (max agonist, which may be used in patients
300 mcg) SC/IM/IV, unresponsive to conventional therapy.
followed by an infusion Adverse effects include headache, tremor,
of 0.14 mcg/kg/min. tachycardia, hypertension, hyperglycemia,
Adults and hypokalemia.
250500 mcg q6h
SC/IM/IV.
Management of Acute Bronchial Asthma
Oxygen
Oxygen is administered by face mask at ow rates of 68 L/min to main-
tain oxygen saturation above 95%.
Salbutamol
Salbutamol nebulization (0.15 mg/kg) is administered every 20 minutes
for the initial 1 hour. Thereafter, it is continued every 46 hourly, and once
there is improvement in the bronchospasm, the interval is increased to
68 hourly and further 12 hourly before discontinuation. Ideally, nebuli-
zation should be followed by chest physiotherapy.
Salbutamol may also be given in a dose of 0.51 mg/kg/h diluted to a
minimum of 4 mL by continuous inhalation for the rst hour along with
the oxygen. Monitoring of the heart rate is required with continuous neb-
ulization because of the possibility of severe tachycardia.
Ipratropium
In a patient with moderately severe bronchospasm or if the response to
the above therapy is inadequate, inhaled ipratropium is administered in
addition to the salbutamol. In case of severe bronchospasm, initially ipra-
tropium nebulization is given every 20 minutes following each salbuta-
mol nebulization by 510 minutes to maximize airway deposition. After
1 hour of therapy, salbutamol and ipratropium can be mixed in the recom-
mended doses and nebulized 46 hourly.
Systemic corticosteroids
Systemic corticosteroids are indicated in all patients who do not respond
promptly and completely to the initial bronchodilator therapy. Steroids
also diminish the frequency and intensity of exacerbations. IV methyl-
prednisolone is given in a dose of 1 mg/kg every 6 hourly for 2448 hours
before decreasing the dose.
ERRNVPHGLFRVRUJ
Oral corticosteroids are apparently equally effective, however, intrave-

nous administration ensures optimal drug levels in severe cases and is also
preferable because of the risk of intubation in these patients. Oral pred-
nisolone may be given in a dose of 12 mg/kg/day in 13 divided doses
for 5 days.
Inhaled corticosteroids are not generally used in the management
of acute bronchospasm but mainly for maintenance therapy. These are
administered in daily 24 doses in addition to the -agonist.
Other drugs
In case of severe bronchospasm which is refractory to conventional ther-
apy, other drugs that may be tried include Inj. adrenaline, theophylline,
terbutaline or magnesium sulfate.
Inj. adrenaline is administered in a dose of 10 mcg/kg (i.e., 0.1 mL/kg
of 1:10000) IM or SC. Dose may be repeated twice at an interval of 2030
minutes.
Ventilation
Intubation and IPPV are indicated in unresponsive severe bronchospasm
associated with a silent chest, drowsiness or confusion, and elevated PCO2
and hypoxemia.
Inj. ketamine 13 mg/kg IV or vecuronium 0.10.3 mg/kg may be used
for intubation. A volume preset mode is recommended with low set res-
piratory rate (812 per minute) and long expiratory time (I:E ratio of 1:4
or 1:3). A tidal volume of 1012 mL/kg is set with plateau airway pres-
sure limited to 30 cm H2O and PIP to < 45 cm H2O. If required, the TV
is reduced to limit the PIP, and a high level of PCO2 is allowed. PEEP is
not advocated or kept at a minimal to prevent further gas trapping. High
inspiratory ow rates are achieved with sedation and muscle relaxants and
help improve gas exchange. During the period of ventilation, 2-agonists
are nebulized into the inspiratory circuit of ventilator.
Management of Bronchospasm in a Ventilated Patient
1. The cause of acute bronchospasm is conrmed as bronchial asthma

or airway hypersensitivity. Other potential causes are excluded.
Mechanical obstruction of the endotracheal tube is identied by
endotracheal suction and if required by bronchoscopy. A chest
X-ray is obtained to diagnose atelectasis, pneumothorax, or
pulmonary edema.
2. The bronchospasm is managed with bronchodilators. Inhaled
salbutamol is administered directly into the endotracheal tube either
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by a dose inhaler or by nebulization. Alternatively, an IV infusion

of epinephrine or IV theophylline may relieve the bronchospasm.
Systemic IV steroids are also indicated; however, these have a slow
onset of action and do not immediately relieve acute bronchospasm.
3. In patients not responding to the above measures, bronchospasm
can be treated by increasing the depth of anesthesia. Ketamine
IV, isourane, sevourane, and halothane gas anesthesia, all have
bronchodilator properties.
4. In a known case of bronchial asthma, Inj. hydrocortisone can be
started prophylactically at the onset of surgery and tapered in
2448 hours.
Bibliography
1. Herner SJ, Seaton TL, Mertens MK. Combined ipratropium and beta 2-adrenergic receptor
agonist in acute asthma. J Am Board Fam Med 2000;13(1):5565.
2. Mehta P. Asthma controller drugs. [Updated: 2010 Jul 30; cited: 2011 Feb 22]. Available at:
http://www.mehtachildcare.com/asthma/controllers.htm#can.
3. New asthma management guidelines. Health Central: Myasthmacentral.com. [Updated: 2008
Mar 18; cited: 2011 Feb 22]. Available at: http://www.healthcentral.com/asthma/introduction-
000005_7-145.html?ic=506019.
4. Robinson P, Chang A. Differential diagnosis. Acute asthma exacerbation in children. [Updated:
2009 Nov 30; cited: 2011 Feb 22] Available at: https://online.epocrates.com/noFrame/show-
Page.domethod=diseases&MonographId=1098&ActiveSectionId=35.
5. Rudra A, Sengupta S, Chatterjee S, Ghosh S, Ahmed S, Sirohia S. Paediatric asthma and anaes-
thesia. Indian J Anaesth 2008;52(Suppl 5):71324.
6. Sethi GR, Bajaj M, Sehgal V. Management of acute asthma. Indian Pediatr 1998;35:74562.
7. Siwik JP, Nowak RM, Zoratti EM. The evaluation and management of acute, severe asthma.
Med Clin N Am 2002;86:104971.
8. Sweetman SC, Blake S. Bronchodilators and anti-asthma drugs. In: Martindale: The Complete
Drug Reference 34th ed. 2005:777808.
9. Woods BD, Sladen RN. Perioperative considerations for the patient with asthma and bron-
chospasm. Br J Anaesth 2009;103 (Suppl 1):i57i65.
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Ventilation
Nature healsassist it
Hippocrates (460 BC370 BC)
Normal Breathing
Inspiration
Expiration
30
Airway pressure (cm H2O)
20
10
Time (sec)
10
Fig. 1: Airway pressure changes during normal breathing.
Spontaneous breathing is initiated by outward movement of the rib cage

and lowering of the diaphragm. This results in generation of a negative
intrathoracic pressure (4 to 7 cm H2O), relative to the atmospheric pres-
sure and ow of air into the lungs (for the purpose of discussion, atmos-
pheric pressure is taken as 0 cm H2O). Expiration is a passive phenomenon
initiated by elastic recoil of the chest wall and upward movement of the
diaphragm resulting in reversal of the pressure gradient and ow of air out
of the lungs. In the graphical display of spontaneous breathing (Figs. 1 and
2), the negative pressure tracing of airway pressure is that of inspiration
and the positive tracing of expiration. However, in positive pressure venti-
lation as gas is delivered under pressure, the airway and alveolar pressures
are positive during inspiration and fall to zero (or the set PEEP value) dur-
ing expiration (Fig. 3).
ERRNVPHGLFRVRUJ
Ventilation 157
Inspiration
Expiration
Flow
(L/min)
Pressure
(cm H2O)
Volume
(mL)
Time (sec)
Fig. 2: Relationship of air flow and lung volume with pressure changes during
spontaneous breathing.
Ventilatory Modes
Ventilatory modes can primarily be classied on the basis of the method

used to provide ventilation.
Volume preset ventilation: When the tidal volume (TV) delivered
to the patient is decided by the set value of the TV and is constant
with every breath. The alveolar pressure generated is variable and
depends upon the lung compliance, resistance, and other ventilatory
parameters.
Pressure preset ventilation: When the TV delivered to the patient is
decided by the set peak inspiratory pressure (PIP) and may not be
constant with every breath. The TV varies with the change in resistance
and compliance of the lungs and other ventilatory parameters.
Combination or dual modes: Two or more modes are combined to
provide ventilation.
Various modes of ventilation can be further dened by the method used

for triggering, i.e., initiation of ventilation (time/pressure/ow triggered),
the parameter which is limited in inspiration from rising beyond the set
value (pressure/volume/ow limited) and the method used for cycling, i.e.,
changing over from inspiration to expiration (pressure/volume/ow/time
cycled).
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Volume Preset Modes
Controlled Mechanical Ventilation (CMV)
60
40
20
0
Time (sec)
20
Fig. 3: Controlled mechanical ventilation. Set tidal volume is given at a regular rate.
Flow
(L/min)
Pressure
(cm H2O)
Volume
(mL)
Time (sec)
Fig. 4: Controlled mechanical ventilation (CMV). Relationship of air flow and lung volume with
pressure changes. CMV is time triggered, flow limited, volume cycled.
The patient is given a set tidal volume at a set rate (the PIP generated may
be variable) and he or she is not allowed to breath between ventilator
breaths. The advantage of CMV is the ability to precisely manipulate ven-
tilation and the partial pressure of carbon dioxide (PaCO2). It is used only
when the patient is deeply sedated and paralyzed, as during surgery or at
the time of initiation of ventilation.
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Ventilation 159
Intermittent Mandatory Ventilation (IMV)

The patient is given a set tidal volume at a set rate but can also initiate
his own spontaneous breaths. The ventilator breaths are not synchronized
with the patients breaths, and the ventilator may deliver a breath even
when the patient is exhaling. Since the patient does not interact with the
ventilator, there is an increased incidence of barotrauma and a greater
need for sedatives. Other complications include low cardiac output and
increased work of breathing. In order to make the mode more patient
friendly and decrease the complication rate, synchronized IMV was intro-
duced. The mechanical cycles, which were time controlled in IMV, are
triggered by the patients inspiratory effort in SIMV, thus allowing for syn-
chronization of the ventilated and patient breaths.
40
20
0
20 Time (sec)
Fig. 5: Intermittent mandatory ventilation. Mandatory breaths are delivered at a set rate
with no co-ordination with the patients breathing.
Synchronized Intermittent Mandatory Ventilation (SIMV)

40
20
0
20 Time (sec)
Fig. 6: Synchronized intermittent mandatory ventilation. A set number of patient breaths are
supplemented by the ventilator.
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Flow
(L/min)
Pressure
(cm H2O)
Volume
(mL)
Time (sec)
Fig. 7: Volume preset, SIMV. Relationship of flow, pressure, and volume. The first breath
is ventilator initiated, the second, third, and fifth breaths are patient breaths, and the
fourth is a patient initiated ventilated breath (note the negative deflection in the
pressure trace of the patient initiated ventilated breath).
The patient is given a set tidal volume at a set rate (the PIP generated may
be variable) but the ventilator waits for the patients spontaneous breaths,
which it uses as a trigger to deliver the machine set tidal volume.
If the patient breathes at a rate faster than the machine set rate, only
the set number of breaths every minute will be supplemented. If the
patient breathes at a slower rate, all patient breaths are supplemented, and
in addition, the patient receives machine breaths, so that the set number
of breaths are delivered. The ventilator delivers a breath at the end of a
time cycle, if there was no spontaneous breath during this period. The time
cycle depends on the set rate.
In SIMV mode, since all spontaneous breaths do not trigger a machine
breath, the risk of respiratory alkalosis and hyperination is less than in
other modes and changes in the patients spontaneous respiratory rate do
not cause a large alteration in minute ventilation. The disadvantages of
SIMV remain an increase in the work of breathing and a possible reduction
in cardiac output. Spontaneous breathing during SIMV requires a venti-
lator valve to be opened and breathing through a high resistance ventila-
tor circuit, which increases the work of breathing and respiratory muscle
fatigue. Pressure support may be added to overcome this increase in res-
piratory work of spontaneous breaths. SIMV is the most commonly used
mode of ventilation and is also utilized as a weaning mode. The mechani-
cal breaths are gradually reduced in frequency until weaning is complete
and the patient can be extubated.
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Ventilation 161
Assist Control (AC)
60
40
20
0
10 Time (sec)
Fig. 8: Assist control mode. Every patient breath initiates a mechanical breath (note the negative
deflection of the patient initiated ventilated breaths). Also in case, the patient fails to breathe in
the set time period, a mechanical breath is given (breath 1 and 4).
Flow
(L/min)
Pressure
(cm H2O)
Preset volume
Volume
(mL)
Time (sec)
Fig. 9: Assist control ventilation. Note the preset volume delivered to each breath.
Unlike SIMV, in this mode, the set tidal volume is delivered to all patient
breaths even if the patient is breathing faster than the machine set rate. If
the ventilator senses a patient respiratory effort, it will deliver the machine
set tidal volume. But if the patient is breathing at a rate less than the set
ventilator rate, the ventilator will deliver additional breaths so that the set
number of breaths/min are given (as in SIMV).
Thus, if the patient is breathing at a fast rate, the minute ventilation is
likely to be large, since all breaths are being supplemented. A doubling of
the patient respiratory rate will double the minute ventilation. This could
cause hyperventilation and also generate high intrathoracic pressures, a
decrease in venous return and hypotension.
AC is used in patients with very weak respiratory effort. This mode is also
selected in crises situations, e.g., cardiac arrest or early phases of resuscitation
and in patients with high minute ventilation requirements (sepsis/ARDS).
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Pressure Preset Modes
Pressure Controlled Ventilation (PCV)
Flow
(L/min)
Pressure limit
Pressure
(cm H2O)
Volume
(mL)
Time (sec)
Fig. 10: Pressure controlled ventilation (PCV). Figure depicts time triggered, pressure limited,
time cycled PCV.
Flow
(L/min)
Pressure
(cm H2O)
Volume
(mL)
Time (sec)
Fig. 11: Pressure preset, SIMV. Relationship of flow, pressure, and volume. The first breath is
ventilator initiated, the second, third, and fifth breaths are patient breaths, and the fourth is a
patient initiated ventilated breath.
PCV is similar to CMV, a set number of breaths/min are delivered at a xed

interval but the difference is that the PIP setting controls the TV delivered
to the patient and the TV is not set directly. (Technically, the term for this
mode should be pressure preset CMV.)
PCV may be pressure limited and time cycled or pressure cycled.
Pressure limited, time cycled implies that once the pressure reaches the set
ERRNVPHGLFRVRUJ
Ventilation 163
value, it is maintained at this value for the specied inspiratory time, at the
end of which the inspiration cycles to expiration. In pressure cycled venti-
lation, inspiration cycles to expiration, once PIP is reached.
Limiting the rise of pressure decreases the risk of barotrauma. PCV is
used in neonates, or in patients with high airway pressures (such as ARDS)
to avoid barotrauma.
Pressure Preset SIMV

Pressure preset SIMV is similar to volume preset SIMV except that the
setting of PIP controls the TV delivered to the patient rather than the TV
setting itself. If the patients respiratory rate is higher than the ventilator set
rate, only the set number of patient breaths are supported. On the other
hand if the patients respiratory rate is less than the ventilator set rate, addi-
tional breaths are delivered to achieve the set rate.
Pressure Assist Control

Pressure assist control mode is the counterpart of the volume assist con-
trol mode. Irrespective of the patient respiratory rate, all patient breaths
are supported. If the ventilator senses a patient respiratory effort, it will
deliver the machine set breath. In case, the patients respiratory rate is less
than the set ventilator rate, additional ventilator breaths will be given to
achieve the set rate.
Pressure Support Ventilation (PSV)
Flow
(L/min)
Pressure support level
Pressure
(cm H2O)
Volume
(mL)
Time (sec)
Fig. 12: Pressure support ventilation. Spontaneously breathing patient; supplemental flow
maintains set inspiratory pressure.
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The ventilator supports all spontaneous patient breaths with supplemen-

tal ow to achieve a set inspiratory pressure. Increasing the pressure sup-
port increases the tidal volume of the patients spontaneous breaths. This
may be useful in patients who have an adequate spontaneous rate but a
low TV.
PSV may be used alone in intubated, spontaneously breathing patients
with an adequate respiratory rate and used together with other volume-
preset modes (e.g., SIMV + PS) to provide pressure support to the sponta-
neous breaths.
A level of 520 cm is recommended depending upon the need of the
patient.
Positive End-Expiratory Pressure (PEEP)

PEEP is not a stand-alone mode but is applied in combination with other
modes. During intermittent positive pressure ventilation, the airway pres-
sure falls to 0 cm H2O (actually atmospheric pressure) at the end of expira-
tion. With the application of PEEP, the baseline end expiratory pressure is
not allowed to fall to zero and at the end of expiration, the patient exhales
against this pressure.
Application of PEEP prevents alveolar collapse at the end of expiration,
thus increasing the functional residual capacity. Since more alveoli remain
open, the V/Q mismatch and intrapulmonary shunting are decreased and
oxygenation is improved. However, PEEP results in an increase of both PIP
and mean airway pressure, and high values of PEEP may decrease venous
return and cardiac output. In addition, a PEEP of >10 cm H2O is associated
with a higher incidence of barotrauma, increased intracranial pressure, and
decreased urine output.
CPAP
It is the equivalent of the application of constant PEEP during all phases
of respiration and is applicable only to patients with spontaneous respira-
tion. It can be administered either through a tight tting mask, nasopha-
ryngeal catheter, nasal prongs, or through an endotracheal tube. CPAP is
utilized either as a part of weaning protocols or as a modality to improve
oxygenation in a conscious patient with hypoxemia or respiratory acidosis.
It can be used in conjunction with bronchodilators and steroids in patients
with bronchospasm to avoid intubation.
CPAP may be started at 5 cm water and increased in increments of
23 cm up to 1012 cm.
ERRNVPHGLFRVRUJ
Ventilation 165
With improvement in the blood gases, CPAP is gradually reduced in

steps of 23 cm. A PaO2 of <50 mmHg, despite a FiO2 100% and a CPAP
of 1012 cm is an indication for assisted ventilation.
Flow
(L/min)
CPAP
Pressure
(cm H2O)
Volume
(mL)
Time (sec)
Fig. 13: Spontaneously breathing patient. Application of CPAP. Relationship of flow, pressure,
and volume.
BIPAP
Flow
(L/min)
Pressure CPAP
(cm H2O)
Volume
(mL)
Time (sec)
Fig. 14: Spontaneously breathing patient; application of CPAP + pressure
support. All patient breaths receive supplemental flow to achieve a set inspiratory
pressure.
BIPAP is a noninvasive mode and is a combination of CPAP along with

PS (520 cm H2O). It is used in spontaneously breathing adult patients in
respiratory failure to improve oxygenation and avoid intubation.
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Dual/Combination Modes
SIMV + PS
Flow
(L/min)

Pressure
(cm H2O)
Volume
(mL)
Time (sec)
Fig. 15: Volume preset SIMV + PS. Breaths one, three, and four are patient initiated ventilated
breaths; breath two is a pressure supported patient breath.
Flow
(L/min)
Pressure support
level
Pressure
(cm H2O)
Volume
(mL)
Time (sec)
Fig. 16: Pressure preset SIMV + PS. Breaths one, three, and four are patient initiated ventilated
breaths; breath two is a pressure supported patient breath.
In SIMV mode, if the patient breathes at a rate faster than the set rate, only
the machine set number of breaths are supplemented with additional TV.
In SIMV + PS, the extra breaths, which did not receive supplementation
with additional TV, are provided pressure support.
SIMV + PS thus allows machine synchronization with the patients
breathing and at the same time reduces the work of breathing.
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Ventilation 167
Pressure Regulated Volume Control (PRVC)

It is a volume assist control mode, with an additional parameter setting
for limiting maximum pressure. PRVC has a decelerating ow pattern, and
the ow rates are adjusted by the ventilator to deliver the set tidal volume,
below the set maximum pressure. PRVC is particularly suitable in patients
with high airway pressures and is more friendly in awake patients.
Ventilator Settings
Initially when the child is paralyzed or deeply sedated and has no respira-
tory effort, ventilation is started with 100% oxygen in the control mode
(controlled mechanical ventilation). Once the child begins to breathe spon-
taneously, a suitable mode is selected (e.g., SIMV, SIMV with PS, etc). The
initial settings primarily depend on the diagnosis and age of the patient.
Positive pressure mechanical ventilation is produced through an inter-
action of ve primary variablesrespiratory rate (RR), tidal volume, peak
inspiratory pressure, inspiratoryexpiratory ratio (I:E ratio), and inspiratory ow
ratewhich are set differently in various modes and ventilators. Additional
manually set or machine preset variables further dene the type of venti-
lated breath that the patient receives.
Ventilator Settings in Volume Preset Modes
Initial Ventilator Settings in SIMV Mode
Neonate Child Adult

FiO2 1.0 1.0 1.0
TV 1012 mL/kg 1012 mL/kg 810 mL/kg
RR 2030 1525 1014
IT 0.51.0 sec 0.51.0 sec 1.01.5 sec
PEEP 35 cm H2O 5 cm H2O 5 cm H2O
RR: respiratory rate, IT: inspiratory time.
The different parameters, which are required to be set directly or moni-

tored, in different ventilators are somewhat variable.
Tidal Volume
In volume preset ventilation, the ventilator delivers a set TV regardless
of PIP generated. In children, a TV of 1012 mL/kg is adjusted to achieve
ERRNVPHGLFRVRUJ
visible chest excursion and audible air entry. The lowest TV, which allows a
SpO2 of >90% and PaO2 >60 mmHg, is set since lower tidal volumes avoid
barotrauma. The goal is to adjust the TV so that plateau pressures are less
than 30 cm H2O.
Some ventilators may require the minute volume to be set instead of the TV.
Respiratory Rate
Total respiratory rate is the sum of the patients respiratory rate and venti-
lator rate. Ideally, this combined rate should be 2025 per minute for chil-
dren under 2 years and 1520 per minute for older children.
PaCO2 has an inverse relationship with the minute ventilation (MV =
TV RR). In hypercarbia, since increasing the TV will result in a higher air-
way pressure, the minute ventilation can be increased by increasing the RR.
I:E Ratio
The I:E ratio is usually kept in the range of 1:21:4. Incomplete exhalation
because of a short expiratory time will result in auto PEEP. When the end
expiratory pressure does not return to 0 cm H2O or the PEEP level, it is an
indication of auto PEEP.
Depending on the ventilator in use, the I:E ratio may be preset or deter-
mined by the ventilator from a combination of other controls:
1. Flow rate: Increasing the ow rate, shortens the inspiratory time (IT)
and prolongs the expiratory time (ET).
2. Inspiratory time: Optimal inspiratory time is between 0.51.5 sec.
3. Respiratory rate: An increase in the respiratory rate has minimal effect
on the inspiratory time but results in a decrease in the expiratory time.
4. Minute volume/tidal volume: An increase in the TV results in an
increase in the inspiratory time and a decrease in the expiratory time.
Flow Rate
The inspiratory ow rate is equal to the TV divided by the inspiratory time
and may be controlled internally by the ventilator via the settings of TV, I:E
ratio, and the respiratory rate. As an approximation, 34 times the minute
ventilation is the ow rate required to be set on the ventilator to achieve the
parameters of TV, I:E ratio, and respiratory rate (6080 L/min in the adult).
At lower ows, a longer inspiratory time is required for the TV to be
delivered, which may result in inadequate expiratory time and auto PEEP.
With higher ows, the tidal volume is delivered in shorter inspiratory time
and expiratory time is longer.
ERRNVPHGLFRVRUJ
Ventilation 169
The set inspiratory ow rate also determines the level of peak inspira-
tory pressure, and higher ow rates result in higher PIP.
FiO2
FiO2 is initially kept at 0.91. It is gradually reduced to 0.5 provided a
SaO2 of >90% can be maintained. FiO2 >60% for over 24 hours has been
associated with oxygen toxicity.
PEEP
PEEP increases functional residual capacity and decreases intrapulmonary
shunting. It is initially set at 35 cm water and any subsequent increase
is based on the patients PaO2 and FiO2 requirement. The need for a high
FiO2 to maintain an adequate PO2 requires an increment in the level of
PEEP. High levels of PEEP (>1020 cm H2O) may, however, cause baro-
trauma and hypotension by a decrease in the cardiac preload.
Sensitivity
This setting is provided on some ventilators for triggering a ventilator
breath by a pressure change or ow alteration caused by the patients res-
piratory effort. It is usually adjusted by trial and error to the degree of the
patients effort (in pressure triggered ventilators, 0.5 to 2.5 cm H2O). If
the sensitivity is too high, the patients work of breathing is increased but
too low a setting will allow the ventilator to initiate breaths spontaneously.
Sigh
A sigh is a ventilator breath with a larger volume than the tidal volume.
The hyperination caused was used to prevent atelectasis but currently
considered of doubtful value. The usual sigh volume is 1.52 times the TV
at a rate of 48 times/h.
Inspiratory pause
Pressure (cm H2O)
PIP
Plateau
pressure
Time (sec)
Fig. 17: Controlled mechanical ventilation with inspiratory pause. Note PIP and plateau pressure.
ERRNVPHGLFRVRUJ
Pressure Limit and Inspiratory Pause

The pressure limit setting does not allow the peak pressure to rise beyond
the set limit. If the pressure limit is reached, inspiration will be terminated,
and a TV less than the set volume is then delivered to the patient.
In volume preset ventilation, an inspiratory pause (usually 0.51 sec)
may also be set to allow measurement of plateau pressure. Plateau pressure
is the pressure recorded at the end of inspiratory ow and at the begin-
ning of expiratory ow during the phase when there is no air ow taking
place.
Monitoring of pressures (PIP and plateau pressure) is essential in vol-
ume preset ventilation. PIP is a reection of the airway pressure, while
plateau pressure is the pressure at the alveolar level. Without lung disease,
PIP is only slightly above the plateau pressure. The PIP and plateau pres-
sures rise proportionately with an increase in TV or a decrease in pulmo-
nary compliance. The peak pressure increases with no signicant change
in plateau pressure when the inspiratory gas ow rates or airway resistance
is raised (e.g., obstruction to the ventilator tubing, airway secretions, bron-
chospasm, etc.).
In children and adults, PIP should ideally be maintained under 2530
cm H2O. Patients with lung disease may require a PIP of more than 30 cm
for adequate TV to be delivered. PIP of more than 40 cm H2O and a pla-
teau pressure of more than 30 cm H2O increase the risk of barotrauma and
an alternative mode of ventilation should be considered.
Flow Waveforms
Ventilators may allow four different types of ow waveforms to be set.
Flow (L/min)
Square Decelerating Accelerating Sine
Fig. 18: Flow waveforms.
Square waveform: The square ow waveform delivers a set ow rate

(peak ow rate) through the entire inspiratory phase.
Decelerating waveform: The peak ow is delivered at the start of
inspiration and decreases gradually until a percentage of the peak
inspiratory ow rate is reached.
ERRNVPHGLFRVRUJ
Ventilation 171
Accelerating waveform: A fraction of the peak inspiratory ow is

initially delivered and gradually increases until the peak ow is
reached.
Sine/sinusoidal waveform: The waveform resembles a sinusoidal curve
similar to the normal breathing pattern.
Ventilator Settings in Pressure Control Ventilation
In PCV, instead of the tidal volume the PIP is set and the ventilator delivers
gas at the set pressure for the duration of inspiration. The resulting tidal
volume is variable, and the patient receives smaller tidal volumes when the
compliance is low or the airway resistance is high.
In children, the PIP may initially be set at 1620 cm H2O (above PEEP)
and adjusted to provide desirable TV. One guideline is starting with two-
thirds the PIP that was generated during the original CMV.
In addition to the PIP, the RR, and IT or I:E ratio requires to be set.
In PCV, the ow rate is determined by the patients airway resistance,
compliance, inspiratory effort, and PIP. On some machines, the time taken
for the PIP to be reached can be adjusted by altering the initial ow rate or
rise time. On other ventilators, it is possible to manipulate the maximum
ow rate allowing greater ow rates to be set when needed, e.g., during
suctioning.
Alarm Settings
1. Volume alarm: Low volume alarm is set about 100 mL less than the
expired TV. It detects circuit leaks or disconnection.
2. Pressure alarms: Low inspiratory pressure alarm is set 1015 cm H2O
below the PIP. This alarm also detects circuit leaks or disconnection.
The high inspiratory pressure alarm is set 1015 cm above the
observed PIP. Causes of high PIP include airway obstruction,
pneumothorax, and poor lung compliance.
3. Apnea alarm: This can be set at a delay of 1020 sec or less depending
on the respiratory rate.
4. Respiratory rate alarm: This may be set at 1012 breaths above the
observed respiratory rate. An increased rate may be indication of
respiratory distress.
5. FiO2 alarm is set at 510% more and less than the set FiO2.
ERRNVPHGLFRVRUJ
Monitoring
Oxygenation
Cause of fall in O2 saturation Treatment If no improvement

Right-to-left intracardiac shunt Improve oxygen delivery and
pulmonary blood flow:
Hemoglobin
Cardiac output
PVR
RV function
Alveolar hypoventilation/ FiO2 Change to pressure control
intrapulmonary shunt PEEP ventilation.
VT or PIP Consider high frequency jet
Inspiratory time ventilation (HFJV),
Rate ECMO
Inadequate oxygenation (SaO2 < 85% or inability to decrease FiO2 to <60%)

may be either because of alveolar hypoventilation or an R-L intracardiac shunt.
In alveolar hypoventilation, oxygenation may be improved by increasing
the level of PEEP, the TV or PIP depending on the mode of ventilation in
use. Changes in TV or PIP affect both PaO2 and PaCO2. An increase will
improve oxygenation and decrease PaCO2. However, a high TV or PIP is
associated with an increased risk of barotrauma.
Improvement in PaO2 may also be achieved by increasing the inspiratory
time. The I:E ratio is altered to 1:1 or even 2:1. Changes in the I:E ratio do
not affect the TV but may result in auto PEEP because of a short expiratory
time. Higher frequency, with smaller TV (68 mL/kg) may be tried if other
methods are ineffective.
Hypercarbia
Cause Treatment If no improvement

Bronchospasm Inspiratory time
Expiratory time
RR
VT
Bronchodilator therapy sedation/paralysis
Inadequate alveolar RR Change to PCV
ventilation Increase sedation, add paralysis (to Consider HFJV
decrease CO2 production)
VT until PIP 3540 cm
Expiratory time
ERRNVPHGLFRVRUJ
Ventilation 173
Hypercarbia (PaCO2 >4550 mmHg) is caused by inadequate ventilation

or sometimes bronchospasm. Hypercarbia causes the inadequately sedated
patient to hyperventilate. In addition there may be tachycardia, hyperten-
sion, and sweating. The PCO2 is corrected by increasing the minute ventila-
tion either by increasing the tidal volume or the respiratory rate.
Peak Airway Pressure

As noted above, the PIP generated depends upon the preset TV and is more
with high ow rates, high airway resistance caused by obstruction to the ven-
tilator tubing or airway, and with pulmonary pathology affecting pulmonary
compliance (pulmonary edema, pneumothorax, pulmonary collapse, etc.).
If the PIP is persistently high in spite of adequate sedation, analgesia, and
bronchodilators, it may be necessary to change to pressure control ventilation.
Asynchrony
The patient is unable to breathe in synchrony with the ventilator, the air-
way resistance rises and inadequate TV is delivered, the PO2 falls and the
PCO2 rises. The causes include:
1. Discomfort because of pain, coughing, full bladder, etc.
2. Decreased pulmonary compliancepneumothorax, pulmonary
edema, collapse, etc.
3. Increased airway resistancebronchospasm, secretions, etc.
4. Hypoxia/hypotension itself may be the cause.
Once the above causes have been ruled out, manual ventilation with 100%
O2 is started for a while before putting the patient back on ventilator.
Adequate chest expansion and bilateral air entry are conrmed. If required
the mode of ventilation is changed to a better tolerated mode, e.g., SIMV,
PSV. If all these measures fail, the patient is sedated and paralyzed.
Weaning
Weaning from SIMV
Parameter Initial setting Extubate when

FIO2 <0.60 <0.50
PEEP <5 cm H2O
SIMV rate 20 breaths per min <510 breaths per min
ERRNVPHGLFRVRUJ
Parameter Initial setting Extubate when

Pressure support 1015 cm H2O 510 cm H2O
PIP <25 cm H2O
Tidal volume 15 mL/kg 46 mL/kg
SIMV Weaning
The SIMV rate and TV is gradually decreased as the patient takes over more
of the respiratory work. The patient is extubated when hemodynamically
stable and is able to maintain normal blood gas values at an SIMV rate of
<510 breaths/min with minimal TV.
Pressure Support Weaning

The level of pressure support is gradually reduced to minimal levels
(510 cm H2O above PEEP). The patient can then be extubated or CPAP
instituted till he can maintain acceptable blood gas values (PaCO2 <45
and SaO2 >92%).
If at any stage, there are signs of respiratory distress (increasing respi-
ratory rate, use of accessory muscles of respiration, etc.) or deterioration
of blood gases or evidence of hemodynamic compromise (in particular
tachycardia and hypertension), then weaning is stopped and ventilation is
returned to a higher level of support.
Bibliography
1. Abdallah A. Mechanical ventilation. [Cited: 2011 Jul 11] Available at: www.alexaic.com/alexai-
cfiles/presentation2010/day3/035002.pdf.
2. Amitai A, Kulkarni R. Ventilator management: introduction to ventilator management.
[Updated: 2009 May 17; cited: 2011 Jul 11] Available at: http://emedicine.medscape.com/
article/810126-overview#aw2aab6b2.
3. Batiha A. Mechanical ventilation: critical care nursing theory. [Updated: 2004 Mar; cited: 2011
Jul 11] Available at: http://www.philadelphia.edu.jo/academics/abatiha/uploads/Mechanical%
20ventilation.doc.
4. Butcher R, Boyle M. Mechanical ventilation learning package. [Cited: 2011 Jul 11] Available at:
http://update.anesthesiologists.org/wp-content/uploads/2009/09/Mechanical-Ventilation-in-
the-ICU.pdf
5. Cantwell S, Hopkins F, Totaro R. Intensive care service: nursing policy and procedures.
Royal Prince Alfred Hospital Intensive Care Service. [Updated: 2004 Mar; cited: 2011 Jul 11]
Available at: http://intensivecare.hsnet.nsw.gov.au/five/doc/ventilation_modes_V_rpa.pdf.
6. Chang DW, Hiers JH. Operating modes of mechanical ventilation. In: Chang DW, ed. Clinical
Application of Mechanical Ventilation New Delhi: Delmar Learning; 2006:80122.
ERRNVPHGLFRVRUJ
Ventilation 175
7. Evans N. How to determine the initial settings for mechanical ventilation. [Updated: 2010
Jan 30; cited: 2011 Feb 22] Available at: http://www.helium.com/items/1726975-initial-
settings-mechanical-ventilator-icu-patient.
8. Kuschel C. Basic principles of ventilation. Auckland district health board: Neborn services clin-
ical guideline. [Updated: 2003 Dec; cited: 2011 Feb 22] Available at: http://www.adhb.govt.nz/
newborn/TeachingResources/ventilation/VentilationBasics.htm#BasicPrinciples.
9. Lumb AB. Elastic forces and lung volumes. Nunns Applied Respiratory Physiology 6th ed.
Philadelphia: Elsevier; 2005:289.
10. Mariani GL, Carlo WA. Ventilatory management in neonates. Science or art? Clin Perinatol
1998;25:3348.
11. Schmidt GA, Hall JB. Management of the ventilated patient. In: Hall JB, Schmidt GA, Wood
LDH, eds. Principles of Critical Care 3rd ed. New Delhi: McGraw-Hill; 2005:48198.
12. Stoelting RK, Hillier SC. The lung. Pharmacology & Physiology in Anaesthetic Practice 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2006:7712.
ERRNVPHGLFRVRUJ
Ventilator
Associated Pneumonia
Every operation in surgery is an experiment in bacteriology
Sir Berkeley Moynihan (18651936)*
Definition
Ventilator associated pneumonia (VAP) is dened as pneumonia occur-

ring more than 48 hours after a patient has been placed on ventilator.
It has been further classied as early-onset VAP when it occurs between
24 days of ventilation and late-onset VAP, occurring more than 4 days
after ventilation.
Pathogenesis
Pneumonia can result from inhalation of small amounts of infected oropha-

ryngeal contents, either by endotracheal aspiration or by passage around
the endotracheal tube. Bacterial translocation from the GIT by reux or
hematogenous spread from various sites in the body may also be a pos-
sible means of bacterial spread to the lungs. Increased incidence of VAP
has been correlated with a number of factors, which include duration of
mechanical ventilation, re-intubation, frequency of endotracheal suctioning,
depth of sedation, use of H2-receptor antagonists, and various interven-
tions like placement of multiple central venous catheters, bronchoscopy,
and thoracocentesis.
Late-onset VAP is considered to be hospital acquired and in all prob-
ability caused by nosocomial strains of organisms including Pseudomonas
aeruginosa, Staphylococcus aureus, and Acinetobacter baumannii. Early onset
VAP is more likely to be the result of infection with community-acquired
pathogensStreptococcus pneumoniae, Staphylococcus aureus, Haemophilus
inuenzae, and gram-negative enteric bacilli.
*Sir Berkeley Moynihan was a noted British surgeon. He was a recipient of numerous awards,
and his book Abdominal Operations earned him international reputation.
ERRNVPHGLFRVRUJ
Ventilator Associated Pneumonia 177
Diagnosis of VAP in Children
Denitive diagnosis of VAP in children requires clinical, radiological, and

microbiological evidence. The clinical features of VAP, other than respira-
tory signs, will be those of generalized sepsis.
Radiological criteria include development of pulmonary inltration,
consolidation, or cavitation. X-ray features are however not specic for VAP
and may well be difcult to differentiate from atelectasis, ARDS, or conges-
tive cardiac failure.
Microbiological evidence of pathogenic bacteria can help establish the
diagnosis, and culture can guide antibiotic therapy. A number of different
methods are available to obtain specimens from the lower respiratory tract.
Bronchoscopic bronchoalveolar lavage (BAL) can obtain specimens from
the infected area with the least chance of contamination but may
cause hypoxia. A small volume of saline (quantity of saline injection
is not standardizedin children <20 kg, 1 mL/kg; >20 kg, 20 mL;
repeated 3 times is one recommendation) is injected and aspirated
for culture. Quantitative bacterial cultures (>104 or 105 cfu/mL) are used
to distinguish colonization from infection. Sensitivity of obtaining
quantitative BAL uid cultures ranges from about 40% to 90% and
specicity varies from 45% to 100%. These techniques, however, require
large endotracheal tubes and may not be routinely feasible in children.
Non-bronchoscopic bronchoalveolar lavage (NBL): In NBL, a suction catheter
is inserted into the endotracheal tube and advanced until resistance is

encountered. Warm sterile saline in a volume similar to BAL (<20 kg,
1 mL/kg; >20 kg, 20 mL; repeated 3 times) is then injected and
aspirated. Sensitivity and specicity are nearly the same as BAL.
Tracheal aspiration (TA) involves obtaining secretions by suctioning of
the endotracheal tube and using these for Gram stain examination and
culture. Even though the technique is sensitive, specimens obtained by
TA have low specicity because of likelihood of contamination from
upper respiratory tract and oropharyngeal ora.
Initial antibiotic therapy can be guided by Gram stain of specimens obtained
by either of the above procedures. Evidence of infection includes presence of
polymorphonuclear and other inammatory cells, and intracellular organisms.
Center for Disease Control and Prevention (USA) has suggested clinical
criteria for the diagnosis of VAP for various age groups of patients as refer-
ence standards to enable incidence and results of intervention and therapy
to be compared between institutions.
Clinical criteria for VAP in infants <12 months of age: Worsening gas
exchange (e.g., SpO2 <94%, increased FiO2 requirement) with at least three
of the following:
Temperature instability with no other recognized cause
White blood cell count <4000/mm3 or >15000/mm3 and band forms >10%
ERRNVPHGLFRVRUJ
New-onset or change in character of sputum or increased respiratory

secretions
Apnea, tachypnea, increased work of breathing, grunting
Wheezing, rales, or rhonchi
Cough
Heart rate <100 beats/min or >170 beats/min
Clinical criteria for VAP in children between 1 and 12 years of age: At least
three of the following:
Temperature >38.4C or <37C with no other recognized cause
White blood cell count <4000/mm3 or >15000/mm3
New-onset or change in character of sputum or increased respiratory
secretions
New-onset or worsening of cough, dyspnea, or tachypnea
Rales or bronchial breath sounds
Worsening gas exchange (e.g., SpO2 <94%, increased FiO2 requirement)
In addition to the clinical criteria, the following radiological criteria must
be met for any age group: Two or more serial chest X-rays showing at least
one of the following: new or progressive inltrates, consolidation, or cavita-
tion. In patients without underlying pulmonary or cardiac disease (e.g., res-
piratory distress syndrome, bronchopulmonary dysplasia, pulmonary edema,
or chronic obstructive pulmonary disease), one denitive chest radiograph is
acceptable.
Care of the Ventilated Patient
Various clinical guidelines (including the recommendations in the Pediatric

Supplement of Institute for Healthcare Improvements VAP bundle: 2008)
for the optimum care of a ventilated patient are as follows:
Hand hygiene: Frequent and meticulous hand washing by all care givers is
perhaps the most signicant factor in reducing the incidence of VAP.
Elevation of the head end: Patients should be nursed in the head up pos-
ition at an angle of 3045 degree to prevent aspiration of secretions. In
neonates, the incubator or radiant warmer is positioned in the reverse
Trendelenburg position (legs raised) by 1530 degrees. Incidence of VAP
in neonates has also been reported to be less in the neonates nursed in lat-
eral position than in the supine position.
Endotracheal tube: Use of a sterile endotracheal tube is recommended for
each intubation attempt. Adequate cuff pressure (2030 cm H2O) must
be maintained in cuffed endotracheal tubes to prevent passage of secre-
tions alongside the tube. Endotracheal suction to aspirate secretions is
done utilizing minimal negative pressure (6080 mmHg in neonates and
ERRNVPHGLFRVRUJ
<120 mmHg in older children). It is preferable to use an in-line, closed

ET tube suction system. Open suction catheters, if used, are disposed after
single use.
Oropharyngeal suction: Regular intermittent or continuous suction must

be used to aspirate collected oropharyngeal secretions. The mouth should
be suctioned before the nose, using an uncontaminated suction catheter.
Multiuse oral and nasal suction catheters are stored in a clean non-sealed
plastic bag when not in use.
Oral hygiene: Oral care of the patient reduces the colonization of oral
cavity with pathogenic bacteria. At least twice a day brushing of teeth and
alcohol-free oral rinses (e.g., chlorhexidine in children >2 months of age)
are advisable. Two hourly frequency of oral care for children at higher risk
for VAP is recommended (IHIs VAP prevention pediatric supplement).
Level of sedation: The child should be permitted to breathe spontane-

ously rather than receive heavy sedation or paralysis. Increased sedatives
and paralytic agents depress the cough reex, prolong weaning, and pre-
dispose to aspiration of oropharyngeal secretions. Daily sedation vaca-
tion, which has been recommended for adults, is not recommended in
children due to high risk of unplanned extubation, however, daily assess-
ment of readiness to extubate is included.
Care of ventilator: The ventilator circuit should be cleared of the condensed

water on a regular basis every 24 hours, and every time the patient is repo-
sitioned to prevent the condensed water from passing into the patients air-
way. The circuit is changed only when it is visibly soiled or mechanically
malfunctioning.
Peptic ulcer prophylaxis: Peptic ulcer disease prophylaxis is recommended

for all ventilated patients as appropriate for the age and condition of the
child. Children at high risk for stress ulceration (ventilation >48 h, coagu-
lopathy, unstable hemodynamics, sepsis, steroids, and following a rethora-
cotomy) should receive H2 blockers or proton pump inhibitors rather than
sucralfate, as these drugs are more effective in decreasing the gastric pH.
Feeding: Early enteral feeding preserves the integrity of the gut mucosa,
promotes establishment of gut motility, and reduces bacterial transloca-
tion. Gastric residues and abdominal distension are monitored before
every feed and 4 hourly to prevent aspiration.
Educational interventions: Effective implementation of VAP preventive

measures in a clinical setting is possible only by adequate education of
healthcare staff.
ERRNVPHGLFRVRUJ
Treatment
Hospital-Acquired and Ventilator Associated Pneumonia

(HAP and VAP)
1. In HAP and VAP, a combination of drugs of different classes is
initially indicated to provide coverage against Pseudomonas and
multidrug-resistant gram ve infections. A -lactam (piperacillin/
tazobactam, ceftazidime, cefuroxime, or a carbapenem) with an
aminoglycoside or uoroquinolone is recommended.
2. In addition, a glycopeptide (vancomycin or tiecoplanin) or linezolid is
added if the risk of MRSA is high.
3. Once the causative organism is isolated, antibiotic therapy is
appropriately tailored. Combination therapy or single drug therapy to
which the organism is sensitive is equally effective, and the decision is
based on the clinical status of the patient.
Duration of Treatment
In general, antibiotics are continued for a minimum of 714 days or for
3 days after resolution of clinical signs and ndings of laboratory tests.
If there is inadequate response after 4872 hours of therapy, patients
should be re-assessed for nosocomial organisms.
Bibliography
1. Aka O, Koltka K, Uzel S, et al. Risk factors for early-onset, ventilator-associated pneumonia
in critical care patients: selected multiresistant versus nonresistant bacteria. Anesthesiology
2000;93:63845.
2. Babcock HM, Zack JE, Garrison T, et al. An educational intervention to reduce ventilator-
associated pneumonia in an integrated health system: a comparison of effects. Chest 2004;
125:222431.
3. Centers for Disease Control and Prevention. Guidelines for preventing health-care-associated
pneumonia, 2003: recommendations of CDC and the Healthcare Infection Control Practices
Advisory Committee. MMWR 2004;53 (No. RR-3). [Updated: June 2011; cited: 2012 Jan 17]
Available at: www.cdc.gov/nhsn/PDFs/pscManual/6pscVAPcurrent.pdf.
4. Foglia E, Meier MD, Elward A. Ventilator-associated pneumonia in neonatal and pediatric
intensive care unit patients. Clin Microbiol Rev 2007;20:40925.
5. Gillespie R. Prevention and management of ventilator-associated pneumonia the Care
Bundle approach. SAJCC 2009;25:4451.
6. How-to Guide: Prevent ventilator-associated pneumonia (Pediatric Supplement). [Accessed:
Jul 2012] Available at: http://www.ihi.org/knowledge/Pages/Tools/HowtoGuidePreventVAP
PediatricSupplement.aspx
ERRNVPHGLFRVRUJ
7. Institute for Healthcare Improvement. Getting started kit: prevent ventilator-associated pneu-
monia. How-to guide. 2008. [Accessed: July 2012] Available at: http://www.premierinc.com/
safety/topics/bundling/downloads/03-vap-how-to-guide.pdf.
8. Morrow BM, Argent AC, Jeena PM, Green RJ. Guideline for the diagnosis, prevention and
treatment of paediatric ventilator-associated pneumonia. S Afr Med J 2009;99:25567.
9. Newburger JW, Takahashi M, Gerber MA, et al. Diagnosis, treatment, and long-term man-
agement of Kawasaki disease: a statement for health professionals from the Committee on
Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in
the Young, American Heart Association. Pediatrics 2004;114:170833.
10. Ratjen F, Bredendiek M, Brendel M, Meltzer J. Costabel JU. Differential cytology of bronchoal-
veolar lavage fluid in normal children. Eur Respir J 1994;7:186570.
11. Srinivasan R, Asselin J, Gildengorin G, Wiener-Kronish J, Flora HR. A prospective study of
ventilator-associated pneumonia in children. Pediatrics 2009;123:110815.
12. Venkatachalam V, Hendley JO, Willson DF. The diagnostic dilemma of ventilator-associated
pneumonia in critically ill children. Pediatr Crit Care Med 2011;12:28696.
13. Wright ML, Romano MJ. Ventilator-associated pneumonia in children. Semin Pediatr Infect Dis
2006;17:5864.
ERRNVPHGLFRVRUJ
Antibiotics
Even diseases have lost their prestige, there arent so many of them left.
Think it over no more syphilis, no more clap, no more typhoid
antibiotics have taken half the tragedy out of medicine
Louis-Ferdinand Celine (18941961)*
Microbiology
Gram-Positive Cocci
Staphylococci are broadly divided into two groups based on the production
of the enzyme coagulase. Clinically, the most signicant coagulase-positive
Staphylococcus is Staph. aureus, which is frequently part of the skin and
nasal ora and causes a range of severe infectionsskin, soft tissue, respi-
ratory, bone, joint, endovascular, and wound infections.
Coagulase-negative Staphylococcus are Staph. epidermidis and Staph.
saprophyticus. Staph. epidermidis is a skin commensal in human beings. It
becomes potentially pathogenic in the immune compromised individuals
and is a cause of intravascular catheter related infections. Staph. saprophyti-
cus causes urinary tract infection in women.
All classes of staphylococci can produce an enzyme penicillinase
(a type of -lactamase), making them resistant to the antibiotics that have
a susceptible -lactam ring in their structure. The -lactam ring has been
modied in some synthetic antibiotics to make them effective against
penicillinase-producing Staph. In other -lactam antibiotics, the spec-
trum has been extended to include penicillinase-producing Staphylococcus
by a combination with the -lactamase inhibitors clavulanate, sulbactam,
or tazobactam. (Note: the following antibiotics have a b-lactam ring in their
structure and constitute the b-lactam group of antibioticspenicillins, cepha-
losporins, carbapenems, and monobactams.)
Currently, antibiotics that are specically given for penicillinase-producing
staphylococci infection include cloxacillin, piperacillintazobactam, rst- and
fourth-generation cephalosporins (e.g., cefazolin, cefpirome), glycopeptides
(vancomycin and teicoplanin), linezolid, clindamycin, quinupristindalfo-
pristin, daptomycin, and tigecycline (safety and effectiveness of daptomycin,
and tigecycline has not been established in patients under 18 years of age).
*Louis-Ferdinand Celine was a French physician and controversial author who became
famous with his rst novel Voyage au bout de la nuit (Journey to the End of the Night), 1932.
ERRNVPHGLFRVRUJ
Antibiotics 183
Methicillin-resistant Staph. aureus (MRSA): Staph. aureus can also

acquire resistance against methicillin, and are designated methicillin-
resistant Staph. aureus (MRSA). MRSA are invariably also resistant to cloxa-
cillin, cephalosporins (cephalexin, cefazolin), and the macrolide group
(erythromycin, clarithromycin and azithromycin) of antibiotics. MRSA
infections are susceptible to vancomycin and teicoplanin, but several
strains of MRSA are now showing resistance even to vancomycin and teico-
planin (VRSA) and require linezolid, quinupristindalfopristin, daptomycin,
or tigecycline for management.
Streptococci are classied based on their hemolytic properties. -hemo-
lytic streptococci cause partial hemolysis with a green coloration on blood
agar plates, -hemolytic streptococci cause clear areas because of complete
hemolysis, while other streptococci are labeled as gamma-hemolytic, when
no hemolysis takes place. The two -hemolytic streptococci are S. pneumo-
niae and S. viridans. S. pneumoniae causes bacterial pneumonia and occa-
sionally otitis media, sinusitis, meningitis, and peritonitis. S. viridans is a
group of streptococcal species found in the oral ora and can rarely cause
endocarditis after release into the blood stream. -hemolytic streptococci
are further characterized by Lanceeld serotyping, based on surface anti-
gens. Clinically signicant are group A and B.
S. pyogenes is a Group A streptococci and causes streptococcal pharyn-
gitis, acute rheumatic fever, scarlet fever, acute glomerulonephritis, and
necrotizing fasciitis. Other organisms of group A do not cause human
infections. S. agalactiae is a group B streptococci, which causes pneumo-
nia and meningitis in neonates and the elderly, with occasional systemic
bacteremia.
Enterococci (E. faecalis, E. faecium) was previously part of streptococci
(Group D) but now a separate genus, it causes urinary tract infection,
intraabdominal infection, and septicemia.
Gram-Negative Bacilli
The Enterobacteriaceae (Klebsiella, Proteus, E. coli, Enterobacter, Serratia, etc.)
are a group of organisms that are primarily found in the colon and cause
GIT infections, urinary tract infections, septicemia, and are associated with
hospital-acquired pneumonias.
H. inuenzae is community acquired and is a causative agent for otitis
media, conjunctivitis, meningitis, pneumonia, and sepsis.
Pseudomonas is primarily an opportunistic organism causing nosocomial
infection in the immunocompromised. In the treatment of Pseudomonas
aeruginosa infections, a combination of two drugs from different chemical
classes, -lactam antibiotics (such as piperacillin, meropenem, ceftazidime,
aztreonam) plus an aminoglycoside (such as amikacin) or uoroquinolone
is advocated to prevent emergence of resistance.
ERRNVPHGLFRVRUJ
Acinetobacters are environmental organisms that are present in the ICU

premises on fomites and other equipment. The main species associated
with human infection is Acinetobacter baumannii, which can cause wound
infections, nosocomial pneumonia, and urinary infection in the immune
suppressed patient and may be resistant to available antibiotics used to
treat gram-negative infections.
In general, for the treatment of severe gram-negative sepsis, because of
the morbidity associated with endotoxin production, empirical coverage
using two antibiotics of different classes effective against gram-negative
organisms is initially recommended.
Anaerobic Pathogens
The principal anaerobic gram-positive cocci that cause disease are pep-
tococci and peptostreptococci and are part of the normal ora of the
mouth, upper respiratory tract, and large intestine. The anaerobic gram-
negative bacilli include Bacteroides fragilis, Prevotella, and Fusobacterium sp.
The B. fragilis group is part of the normal bowel ora and is most fre-
quently isolated from intra-abdominal infections, while the Prevotella and
Fusobacterium sp. are part of the normal oral ora.
The following drugs are effective against anaerobic organisms: metroni-
dazole, carbapenems (imipenem, meropenem), combinations of -lactam
and -lactamase-inhibiting agents (piperacillintazobactam, ampicillin
sulbactam, amoxicillinclavulanate, ticarcillinclavulanate), cephalosporins
(e.g., cefotaxime), and clindamycin. GI or pelvic infections are likely to con-
tain mixed infections, enterobacilli (e.g., E. coli) and anaerobes (e.g., B. fragilis),
thus antibiotic regimens active against both must be used. All the above
drugs (except clindamycin and metronidazole) have good activity against
enterobacilli and can be used as monotherapy.
Antibacterial Spectrum of Various Antibiotics
Natural penicillins
Antibiotics Penicillin G, benzathine penicillin, procaine penicillin
Gram +ve cocci Staph. aureus, Strep. pneumoniae, Strep. pyogenes, Strep. viridans
Gram +ve bacilli B. anthracis, C. diphtheriae, C. perfringens, Listeria monocytogenes,
Treponema pallidum, Leptospira
Gram ve cocci Gram ve cocci: N. gonorrhoeae, N. meningitidis
Comments These penicillins have no effect on penicillinase-producing
Staphylococcus, enterococci, and majority of gram ve bacilli. B. fragilis
is also resistant.
ERRNVPHGLFRVRUJ
Antibiotics 185
Penicillinase-resistant penicillins (anti-Staph. penicillins)

Antibiotics Methicillin (not used clinically), cloxacillin
Gram +ve cocci Staph. aureus, Staph. epidermidis, Strep. pneumoniae
Gram ve
Comments Even though cloxacillin is active against penicillinase-producing
staphylococci, some staphylococci are resistant (so called methicillin-
resistant Staph. aureus [MRSA] and methicillin-resistant Staph. epidermidis
[MRSE]). These penicillins have no effect against gram ve bacteria,
enterococci, and B. fragilis.
The penicillinase-resistant penicillins are used primarily for penicillinase-
producing staphylococci.
Aminopenicillins (extended-spectrum penicillins)

Antibiotics Ampicillinsulbactam, amoxicillinclavulanate
Gram +ve cocci Gram +ve cocci: Strep. pneumoniae, Strep. pyogenes, Strep. viridans,
enterococci
Gram +ve bacilli Listeria monocytogenes
Gram ve bacilli Enterobacilli (E. coli, Proteus, Salmonella, and Shigella)
Other (H. influenzae)
Comments The aminopenicillins, ampicillin, and amoxicillin alone are effective
against nonlactamase-producing enterobacilli, some gram +ve cocci,
and Listeria. The aminopenicillins are not effective against
Staph. aureus, Klebsiella, Serratia, Acinetobacter, Pseudomonas,
and B. fragilis.
The addition of -lactamase inhibitors, ampicillinsulbactam, and
amoxicillinclavulanate extends the spectrum to include methicillin-
sensitive staphylococci (but not MRSA) and some gram ve organisms
such as Serratia, Acinetobacter, and B. fragilis.
Ureidopenicillins (antipseudomonal penicillin)

Antibiotics Piperacillintazobactam
Gram +ve cocci Staph. aureus (MSSA), Strep. pneumoniae, enterococci
Gram ve bacilli Enterobacilli (E. coli, Proteus, Klebsiella, Serratia, Enterobacter)
Pseudomonas, anaerobic bacteria
Comments Piperacillin is active against major gram ve, some gram +ve
(streptococci and enterococci), and anaerobic bacteria. Tazobactam
adds to the activity by including -lactamase producing Staph. aureus
(MSSA) and additional strains of E. coli and Klebsiella.
Piperacillintazobactam has largely supplanted the use of ampicillin
sulbactam, and amoxicillinclavulanate because of its wider spectrum
of activity. It is also more effective than ticarcillinclavulanate for the
treatment of Pseudomonas infection.
ERRNVPHGLFRVRUJ
Carboxypenicillin (antipseudomonal penicillins)

Antibiotics Ticarcillinclavulanate
Gram +ve cocci Staph. aureus (MSSA)
Gram ve bacilli Enterobacilli (E. coli, Proteus, Klebsiella, Serratia, Enterobacter),
Pseudomonas, H. influenzae, B. fragilis
Comments Clavulanic acid enhances the activity of ticarcillin against beta-lactamase
producing bacteria. These include strains of Staph. aureus,
enterobacilli (E. coli, Klebsiella, Proteus), H. influenzae, N. gonorrhoeae,
and B. fragilis.
The activity of ticarcillin against enteric aerobic gram-negative bacilli
is similar to ampicillin and inferior to piperacillin, and in addition it
may interfere more with platelet function. Piperacillintazobactam is
preferable for gram-negative infections unless ticarcillinclavulanate is
specifically indicated.
Cephalosporins (first generation)

Antibiotics Cefazolin, cephalexin
Gram +ve cocci Staph. aureus (MSSA), Strep. pneumoniae, Strep. viridans, Strep. pyogenes
Gram ve bacilli Enterobacilli (E. coli, Klebsiella), H. influenzae
Comments Cefazolin is the only parenteral preparation still in use. Oral preparations are
used in minor infections. It is effective against anaerobes (but not B. fragilis).
Not active against MRSA, Proteus, Enterobacter, Serratia or Pseudomonas.
Cephalosporins (second generation)

Antibiotics Cefuroxime, cefaclor, cefoxitin
Gram +ve cocci Staph. aureus (MSSA), Strep. pneumoniae
Gram ve bacilli Enterobacilli (E. coli, Klebsiella), H. influenzae, anaerobes including B. fragilis.
Comments Less activity against gram +ve and better activity against -lactamase
producing gram ve organisms compared to first generation.
Cephalosporins (third generation)

Antibiotics Ceftriaxone, cefotaxime, ceftazidime, cefoperazone
Gram +ve cocci Staph. aureus (MSSA), Strep pneumoniae
Gram ve bacilli Enterobacilli (E. coli, Klebsiella, Proteus, Serratia, Enterobacter)
H. influenzae
Comments Third generation cephalosporins are mainly used for gram ve infections.
Gram +ve activity is variable.
Ceftazidime and cefoperazone have additional anti-Pseudomonal and
anaerobe coverage but are not effective against Staph. aureus.
ERRNVPHGLFRVRUJ
Antibiotics 187
Cephalosporins (fourth generation)

Antibiotics Cefepime, cefpirome
Gram +ve cocci Staph. aureus (MSSA), Strep. pneumoniae
Gram ve bacilli Enterobacilli (E. coli, Klebsiella, and Proteus). Others (H. influenzae,
Pseudomonas)
Comments Similar to third generation but with activity against Staph. and also
Pseudomonas.
Aminoglycosides
Antibiotics Gentamicin, tobramycin, amikacin, netilmicin
Gram +ve cocci Staph. epidermidis, Staph. saprophyticus, Strep. pneumoniae, Strep. viridans,
enterococci
Pseudomonas, V. cholerae
Comments Broad spectrum of gram ve coverage. Gram +ve organisms are resistant
to gentamicin. No activity against anaerobes.
Fluoroquinolones
Antibiotics Ciprofloxacin, ofloxacin, levofloxacin
Gram +ve cocci Staph. epidermidis, Staph. saprophyticus, Strep. pneumoniae,
enterococci
Gram ve bacilli Enterobacilli (E. coli, Proteus, Klebsiella, Serratia, Enterobacter and Shigella),
Pseudomonas, H. influenzae, Legionella
Gram ve cocci N. gonorrhoeae
Comments Lack of activity against gram +ve organisms though levofloxacin has some
activity against Strep. pneumoniae and Strep. pyogenes. Also effective
against Chlamydia and Mycoplasma.
Ofloxacin and levofloxacin (but not ciprofloxacin) have moderate activity
against anaerobes.
Carbapenems
Antibiotics Imipenemcilastatin, meropenem, ertapenem
Gram +ve cocci Staph. aureus (MSSA), Strep. viridans, Strep. pyogenes, enterococci
Pseudomonas, H. influenzae, anaerobes including B. fragilis
Comments Has one of the broadest spectrums. Meropenem is slightly more effective
against gram ve infections. Anaerobic organisms are very susceptible.
Indicated as a second-line drug in severe infections and sepsis of
unknown cause.
ERRNVPHGLFRVRUJ
Monobactams
Antibiotics Aztreonam
Gram +ve
Gram ve bacilli Enterobacilli (E. coli, Proteus, Klebsiella, Serratia, Enterobacter),
Pseudomonas
Comments It is an option for gram ve coverage in penicillin allergic patients.
Glycopeptides
Antibiotics Vancomycin, teicoplanin
Gram +ve cocci Methicillin-resistant Staph. aureus (MRSA), Staph. epidermidis, Strep. viridans,
enterococci, C. diphtheriae
Gram ve bacilli Anaerobes
Comments Vancomycin is used orally in pseudomembranous colitis caused by
C. difficile and in enterocolitis caused by Staph. aureus. Teicoplanin has
a spectrum similar to vancomycin but has a longer half life, so OD dose
suffices. Teicoplanin can also be injected by the IM route.
Oxazolidinones
Antibiotics Linezolid
Gram +ve cocci Staph. aureus (MRSA), Strep. pneumoniae, Strep. agalactiae, Strep. pyogenes,
Strep. viridans, enterococci
Gram +ve bacilli Listeria monocytogenes, Corynebacterium, Clostridia
Gram ve bacilli Anaerobes
Comments Linezolid has no significant gram ve activity, Pseudomonas and
enterobacilli are not susceptible. The main indications of linezolid are
gram +ve infections of the skin, soft tissues, osteomyelitis, pneumonia
(particularly hospital-acquired), endophthalmitis, and infective
endocarditis.
Lincosamides
Antibiotics Clindamycin
Gram +ve cocci Active against most gram-positive cocci except enterococci and
nosocomially-acquired MRSA. Active against most community-acquired
MRSA, anaerobic bacilli and cocci
Gram ve bacilli Gram ve anaerobic bacilli
Comments No gram ve activity other than anaerobes
ERRNVPHGLFRVRUJ
Antibiotics 189
Macrolides
Antibiotics Erythromycin, clarithromycin, azithromycin
Gram +ve cocci Gram +ve cocci: Staph. aureus (MSSA), Strep. pyogenes, Strep. pneumoniae
Gram +ve bacilli C. diphtheriae
Gram ve bacilli H. influenzae
Comments Macrolides are also active against Chlamydia, Mycoplasma, and Treponema.
Clarithromycin is more effective against gram +ve cocci, H. influenzae,
and Chlamydia compared to erythromycin, while azithromycin is not as
effective against gram +ve cocci.
Sensitivity Summary of Commonly Used IV Antibiotics
Staph. Staph. Enterococcus Enteric gram Pseudomonas B. fragilis

aureus aureus faecalis ve bacilli aeruginosa
(MSSA) (MRSA)
Cloxacillin +++
Amoxicillin + ++ +++ +
clavulanate
Piperacillin + +++ +++ ++ +
tazobactam
Cefotaxime/ ++ +++ +
ceftriaxone
Ceftazidime +++ +++
Cefpirome ++ +++ ++
Imipenem/ +++ ++ +++ +++ +++
meropenem
Vancomycin/ +++ +++ ++
teicoplanin
Aminoglycoside ++ +++ +++
Fluoroquinolones +++ +++ +++
Linezolid +++ +++ +++ ++
Clindamycin +++ + ++
MSSA: methicillin-susceptible Staph. aureus, MRSA: methicillin-resistant Staph. aureus.
ERRNVPHGLFRVRUJ
Antibiotic Doses
Amikacin
Oral dose Parenteral dose

Adult NA 15 mg/kg q24h or 7.5 mg/kg q12h
Pediatric NA 57.5 mg/kg q12h
Neonatal 15 mg/kg q24h. Administer over 30 minutes
Blood levelspeak (30 minutes after dose) 2030 mcg/mL, trough (1224
hours after dose) 25 mcg/mL. In renal failure, increase interval between
doses (creatinine clearance [CrCl] 1050 mL/min: q1218h, CrCl <10 mL/min:
q2448h). Supplemental doses are required for hemodialysis (HD) and
peritoneal dialysis (PD). Aminoglycoside administration is associated with
nephrotoxicity, ototoxicity, and neurotoxicity.
Amoxicillin

Adult 0.250.5 g q8h 500 mg q8h
Pediatric 22.545 mg/kg q12h 50100 mg/kg/day in divided doses q8h
Or 80 mg/kg/day in divided doses q8h
Neonatal Not indicated
In renal failure, increase interval between doses (CrCl 1050 mL/min:

q812h, CrCl <10 mL/min: q1224h). Supplemental dose is required for
HD but not for PD.
Side effects include diarrhea and rashes. Amoxicillin and ampicillin
have a common spectrum, but amoxicillin is better absorbed so diarrhea
is less. Adverse effects of all penicillins include hypersensitivity and local
irritation at the site of injection.
AmoxicillinClavulanate
(1.2 g vial contains Amoxicillin 1 g + Clavulanate 200 mg)
ERRNVPHGLFRVRUJ
Antibiotics 191

Adult 0.250.5 g q8h or 0.875 g q12h 1.2 g vial q68h
(amoxicillin content)
Pediatric 22.545 mg/kg/day in divided doses q8h 30 mg/kg/day in divided doses
(amoxicillin content) q8h (amoxicillin content)

HD and PD.
Ampicillin

Adult 250 mg1g q6h 0.52.0 g q46h
Pediatric 2550 mg/kg/day in divided doses q6h 2550 mg/kg/day in divided doses q6h
Neonatal 07 days: 550 mg/kg q12h
>7 days: 2550 mg/kg q8h

HD but not PD.
AmpicillinSulbactam
(1.5 g vial contains Ampicillin 1 g + Sulbactam 0.5 g)
Adult NA 1.53.0 g vial q68h
Pediatric NA 2550 mg/kg q6h (ampicillin content)

q12h, CrCl <10 mL/min: q24h). Supplemental dose is required for HD but
not PD.
ERRNVPHGLFRVRUJ
Aztreonam

Adult NA 1 g q8h or 2 g q12h
Pediatric NA 30 mg/kg q68h
In renal failure, reduce the dose (CrCl 1050 mL/min: to 50%, CrCl
<10 mL/min: to 25%). Supplemental dose is required in HD. Toxic effects
are phlebitis, rash, and elevated liver function tests.
Cefaclor

Adult 0.250.5 g q8h NA
Pediatric 1020 mg/kg/day in divided doses q12h NA
Or 6.613.3 mg/kg q8h (in more severe infections)
Neonatal NA
In severe renal failure (CrCl <10 mL/min), reduce dose by 50%. In mild/
moderate renal failure (CrCl >10 mL/min), no dose reduction is required.
Supplemental dose is needed in HD and PD. All cephalosporins can cause
allergic reactions.
Cefazolin

Adult NA 12 g q8h
Pediatric NA 25100 mg/kg/day in divided doses q8h

q12h, CrCl <10 mL/min: q24h). Supplemental dose is required for HD but
not PD.
ERRNVPHGLFRVRUJ
Antibiotics 193
Cefepime

Adult NA 12 g q812h
Neonatal 50 mg/kg q812h
In renal failure, the interval between doses is increased and the dose of the
drug is also reduced. (In children, CrCl 1050 mL/min: 25 mg/kg q12h,
CrCl <10 mL/min: 12.5 mg/kg q24h). Supplementary dose is required in
HD and PD.
Cefoperazone

Adult NA 13 g/day in divided doses q812h
Neonatal NA
No change in dosing is required in renal failure.
Cefotaxime

Adult NA 1 g q12h to 2 g q4h (higher dose for life-threatening infections)
In creatinine clearance <20 mL/min, reduce dose by 50%. Supplemental

dose is required for HD but not PD.
Ceftazidime

Adult NA 1 g q12h to 2 g q8h (higher dose for life-threatening infections)
ERRNVPHGLFRVRUJ

HD and PD.
Ceftriaxone

Adult NA 12 g q24h
Or 2537.5 mg/kg q12h
No dose adjustment is required in mild/moderate renal failure.
Cefuroxime

Adult 0.1250.5 g q12h 0.751.5 g q68h
Pediatric 1015 mg/kg suspension q12h; 2550 mg/kg q8h
older children, 125250 mg q12h
Neonatal 50100 mg/kg/day in divided doses q812h

q812h, CrCl <10 mL/min: q24h). Supplemental dose is required for HD
but not PD.
Cephalexin

Adult 0.250.5 g q6h NA
Pediatric 6.2512.5 mg/kg q6h or 8.016 mg/kg q8h NA
Neonatal NA

HD but not PD.
ERRNVPHGLFRVRUJ
Antibiotics 195
Ciprofloxacin

Adult 0.50.75 g q12h 0.20.4 g q812h
Pediatric 1015 mg/kg q12h 1015 mg/kg q12h
(in select circumstances) (in select circumstances)
In renal failure, reduce dose (CrCl 1050 mL/min: to 5075%, in

CrCl <10 mL/min: to 50%). Supplementary dose is indicated in HD and
PD. Adverse reactions of uoroquinolones include nausea, dizziness, pho-
totoxicity, and arthropathy.
Clarithromycin

Adult 0.250.5 g q12h; 500 mg q12h
Extended release 1 g q24h
Pediatric 7.5 mg/kg q12h NA
Neonatal NA
CrCl <30 mL/min reduce dose by 50% and administer q12h24h.
Clindamycin

Adult 150300 mg q6h 200600 mg q8h
Pediatric 1030 mg/kg/day divided q68h 510 mg/kg q68h
Neonatal 07 days: 57.5 mg q8h 07 days: 57.5 mg q8h
>7 days: 57.5 mg q6h >7 days: 57.5 mg q6h
No change of dosing is required in renal failure. Adverse effects include

allergic rashes, neutropenia, thrombocytopenia, and anaphylaxis. Pseudo-
membranous colitis is caused by overgrowth of C. difcile, which responds
to oral metronidazole or vancomycin.
ERRNVPHGLFRVRUJ
Erythromycin

Adult 0.250.5 g q6h 50 mg/kg/day in divided doses q6h
Pediatric 1016.6 mg/kg q8h 50 mg/kg/day in divided doses q6h
or 7.512.5 mg/kg q6h
Neonatal NA
Reduce dose with CrCl <10 mL/min to 5075%. No change of dosing is

indicated in CrCl >10 mL/min. Supplemental dose is not required in HD.
Gentamicin/Tobramycin

Adult NA 57 mg/kg q24h or 12 mg/kg q8h
or 67.5 mg/kg q24h
Neonatal <1.5 kg: 3 mg/kg q18h
>1.5 kg: 3 mg/kg q12h infuse over 30 minutes
Blood levelspeak: 512 mcg/mL (30 minutes after dose), trough: 0.51
mcg/mL (1224 hours after dose). Once-daily dosing for aminoglycosides
is now well accepted in children and adults. Treatment in patients with
renal failure may be best continued with non-aminoglycoside antimicrobi-
als. If an aminoglycoside is strongly indicated, careful monitoring of blood
levels is required to determine frequency or dose of subsequent administra-
tion. (Empirically with a CrCl 1050 mL/min: q1218h; CrCl <10 mL/min:
q2448h). Supplemental dose is required in HD and PD.
ImipenemCilastatin

Adult NA 0.51.0 g q6h
Pediatric NA Infants 4 week to 3 months: 25 mg/kg q6h; children >3 months:
1525 mg/kg q6h or 2040 mg/kg q8h
In renal failure, both dose and interval between dosing are altered
(CrCl >50 mL/min: 50100% of dose q68h; CrCl 1050 mL/min: 2550%
q8h; CrCl <10 mL/min: 25% q12h). Supplemental dose is required in HD.
ERRNVPHGLFRVRUJ
Antibiotics 197
Adverse effects include nausea, vomiting, diarrhea, eosinophilia, neutro-

penia, and lowering of the seizure threshold. Imipenem is nephrotoxic.
Levofloxacin

Adult 0.250.75 g q24h 0.250.75 g q24h
Pediatric 5 years: 10 mg/kg q24h 5 years: 10 mg/kg q24h
6 months to <5 years: 10 mg/kg q12h 6 months to <5 years: 10 mg/kg q12h
Neonatal NA NA
Use of levooxacin in children is controversial because of the high inci-

dence of arthralgia, tendinopathy, or arthritis.
Linezolid

Adult 600 mg q12h 600 mg q12h
Neonatal Neonates <7 days: 10 mg/kg q12h
No change in dosing is required in renal failure. Common adverse effects

of short-term use include headache, diarrhea, and nausea. Long-term use
can cause bone marrow suppression, thrombocytopenia, peripheral neu-
ropathy, optic nerve damage, and lactic acidosis.
Meropenem

Adult NA 0.52 g q8h
In renal failure, the dosing interval is increased and the dose reduced. (In
children, CrCl 1050 mL/min: 50100% of dose q12h; CrCl <10 mL/min:
50% of dose q24h.) Supplementary dose is required in HD and PD.
ERRNVPHGLFRVRUJ
Metronidazole (For Anaerobic Infection)

Adult 7.5 mg/kg (250750 mg) q6h 7.5 mg/kg q6h
(not to exceed 4 g/day) (not to exceed 4 g/day)
Pediatric 7.5 mg/kg q8h 7.5 mg/kg q6h
(1st dose 15 mg/kg may be given)
Neonatal 1st dose 15 mg/kg, then 7.5 mg/kg/dose
07 days: q24h
>7 days: q12h
No change in dosing is required in mild/moderate renal failure. With a

CrCl <10 mL/min, dose is reduced to 50%. Supplemental dose is required
in hemodialysis but not peritoneal dialysis.
Piperacillin

Adult 100150 mg/kg/day in divided doses q8h

but not PD.
PiperacillinTazobactam

Adult 3.375 g (3 g of piperacillin and 0.375 g of tazobactam) q6h.
Pediatric NA 100 mg/kg of piperacillin and 12.5 mg/kg of tazobactam
given every 8 hours.
Pediatric patients 29 months of age should receive 80 mg/kg
of piperacillin and 10 mg/kg of tazobactam every 8 hours.
In renal failure, the interval between doses is increased and the dose of
drug is reduced. (In children, CrCl 1050 mL/min: 70% of dose q68h;
CrCl <10 mL/min: 70% of dose q8h.) Supplementary dose is required in
HD but not PD.
ERRNVPHGLFRVRUJ
Antibiotics 199
QuinupristinDalfopristin

Adult NA 7.5 mg/kg q8h
Neonatal NA NA
Quinupristindalfopristin is a combination injectable streptogramin anti-

biotic that is active against most strains of VRSA. No dosing recommenda-
tions are available in pediatric patients less than 12 years of age. No dosage
adjustment is required for use in patients with renal impairment.
Rifampin

Adult 0.3 g q8h 0.3 g q8h
Or 0.60.9 g q24h Or 0.60.9 g q24h
Pediatric 20 mg/kg q24h or 10 mg/kg q12h 1020 mg/kg q1224h
(Oral 1020 mg/kg q24h)
In renal failure, CrCl 1050 mL/min administer 50100% dose, CrCl <10
mL/min administer 50% of dose. Supplementary dose is not indicated in
HD or PD. Indicated for staphylococcal infections (in combination with
a penicillin, cephalosporin, or vancomycin).
Ticarcillin (5.2 mEq Na/g)

Adult NA 3 g q46h

but not PD.
ERRNVPHGLFRVRUJ
TicarcillinClavulanate
(3.1 g vial containing 3 g Ticarcillin and 100 mg Clavulanic acid)

Adult NA 3.1 g vial q46h
Pediatric NA 2575 mg/kg (ticarcillin dose) q6h

HD but not PD.
Teicoplanin

Adult NA 400 mg q12h for 3 doses then 200400 mg q24h.
Pediatric NA 10 mg/kg q12h for 3 doses, then 610 mg/kg q24h.
Administer IV bolus over 35 minutes
Neonatal Loading dose 16 mg/kg, then 8 mg/kg q24h.
Administer IV over 30 minutes
In renal failure, CrCl 1050 mL/min reduce dose to 33% on 4th day;
CrCl <10 mL/min, administer 50% of dose. Adverse effects include
increased risk of ototoxicity and nephrotoxicity when given along with
aminoglycosides; increased ototoxicity with loop diuretics.
Vancomycin

Adult 125 mg q6h (only effective for C. difficile colitis) 15 mg/kg q12h
(often 11.5 g q12h)
Administer over 1 hour

HD but not PD.
ERRNVPHGLFRVRUJ
Antibiotics 201
Rapid IV infusion can cause severe hypotension (including shock, car-

diac arrest), wheezing, dyspnea, urticaria, pruritus, ushing (Red man
syndrome). Vancomycin has been associated with ototoxicity and nephro-
toxicity, primarily when used in combination with an aminoglycoside.
Bibliography
1. Aoki FY. Principles of antimicrobial therapy and the clinical pharmacology of antimicro-
bial drugs. In: Hall JB, Schmidt GA, Woods LDH, eds. Principles of Critical Care McGraw-Hill;
2005:64197.
2. Approach to infectious diseases. In: Apostolakas MJ, Papadakos PJ, eds. The Intensive Care
Manual McGraw-Hill; 2001:15665.
3. Beta-lactamase. [Updated: 2009 Jul; cited: 2011 Feb 26] Available at: http://www.medic8.
com/medicines/Penicillinase.html.
4. Binkley S. Antibiotic dosing in renal impairment. University of Pennsylvania Medical Center
Guidelines for Antibiotic Use. [Updated: 2008 Sep 23; cited: 2011 Feb 26] Available at: http://
www.uphs.upenn.edu/bugdrug/antibiotic_manual/renal.htm.
5. Bradley JS, Arguedas A, Blumer JL, et al. Comparative study of levofloxacin in the treatment of
children with community-acquired pneumonia. Pediatr Infect Dis J 2007;26:86878.
6. Chien S, Wells TG, Blumer JL, et al. Levofloxacin pharmacokinetics in children. J Clin Pharmacol
2005;45:15360.
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USA November 2010 (1004-11). [Updated: 2000 Jul 25; cited: 2011 Feb 26] Available at: http://
www.cubicin.com/pdf/PrescribingInformation.pdf.
8. Heritage J. The classification and identification of bacteria of medical importance. [Updated:
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Sepsis and
Multiorgan Dysfunction
I do not expect my contemporaries to accept all my doctrines,
but I look to the coming generation to adopt and perfect them
Joseph Lister (18271912)*
Systemic inammatory response syndrome (SIRS) is a non-specic, wide-

spread inammatory reaction, which takes place in response to a patho-
logical event (ischemia, trauma, infection, etc.). This inammatory process
results in disorders of microcirculation, a decrease in organ perfusion, and
nally organ dysfunction.
In general, Sepsis is dened as SIRS caused by infection, and Severe sepsis
is sepsis with evidence of organ dysfunction. Septic shock is sepsis associ-
ated with hypotension unresponsive to uids or requires inotropes for its
management.
To make it possible to compare the results of various clinical trials in
pediatric sepsis, the International Pediatric Sepsis Consensus conference
(2005) has dened infection, SIRS, sepsis, severe sepsis, and septic shock
in pediatrics.
Definitions
Infection A suspected or proven infection caused by any patho-

gen, or a clinical syndrome associated with a high
probability of infection.
SIRS The presence of at least two of the following four cri-
teria, one of which must be abnormal temperature or
leukocyte count:
Core temperature of >38.5C or <36C. (>101F
or <97F).
Tachycardia (dened as a mean heart rate >2 SD above
normal) or for children <1 year old, bradycardia
(dened as a mean heart rate <10th percentile for age).
Mean respiratory rate >2 SD above normal for age or
mechanical ventilation.
*Joseph Lister was the pioneer of antiseptic surgery. He introduced carbolic acid to sterilize
surgical instruments and clean wounds.
ERRNVPHGLFRVRUJ
Sepsis and Multiorgan Dysfunction 203
Leukocyte count elevated or depressed for age

or >10% immature neutrophils.
Sepsis SIRS in the presence of or as a result of suspected or
proven infection.
Severe Sepsis Sepsis plus one of the following: (i) cardiovascular organ
dysfunction or (ii) acute respiratory distress syndrome
(ARDS) or (iii) at least two other organ dysfunction.
Septic Shock Sepsis and cardiovascular organ dysfunction.
Organ Dysfunction Criteria

Cardiovascular Despite administration of isotonic intravenous uid
bolus 40 mL/kg in 1 hour:
Hypotension, i.e., blood pressure <5th percentile for
age or systolic BP >2 SD below normal for age or
Need for vasoactive drug to maintain BP or
Two of the following signs of inadequate organ
perfusion:
metabolic acidosis with a base decit >5.0 mmol/L
increased arterial lactate >2 times upper normal limit
urine output <0.5 mL/kg/h
prolonged capillary rell >5 sec
core to peripheral temperature gap >3C (>5.4F)
Respiratory PaO2/FiO2 ratio 300 or
PaCO2 >65 mmHg or 20 mmHg over baseline PaCO2 or
requirement of >50% FiO2 to maintain saturation >92%
CNS Glasgow coma score <11 or a decrease in Glasgow coma
score 3 points from abnormal baseline.
Hematology Platelet count <80,000/mm3 or a decline of 50% in
platelet count from highest value recorded over the past
3 days (for chronic hematology/oncology patients) or
an international normalized ratio >2.
Renal Serum creatinine 2 times upper normal limit for age
or two-fold increase in baseline creatinine.
Hepatic Total bilirubin 4 mg/dL (not applicable for newborn) or
ALT (alanine transaminase) two times upper normal
limit for age.
ERRNVPHGLFRVRUJ
Sources of Sepsis in the Postoperative Period
Wound infection
Urinary tract infection
Ventilator associated pneumonia (VAP)
Intravenous line related infection
Gastrointestinal infection
Sinusitis
Prosthesis infection
Clinical Manifestations of Sepsis
Features of Organ System Dysfunction
Organ system Features of dysfunction

Cardiovascular Hypotension, poor peripheral perfusion, capillary leak syndrome,
metabolic acidosis
Pulmonary Hypoxia, hypercarbia, ARDS
CNS Altered sensorium, coma
Hematology Fall in platelet count, abnormal INR, DIC
Renal Oliguria, increasing Se/creatinine
Hepatic Abnormal LFT, jaundice
Gastrointestinal Abdominal distension, intolerance to feeds, stress ulceration
Peripheral nervous system Sensory neuropathy or neuropathy
Cutaneous manifestations Petechiae, diffuse erythema, ecchymoses, ecthyma gangrenosum,
and symmetric peripheral gangrene
Early clinical features of sepsis include tachycardia (newborns may have

bradycardia) and tachypnea associated with temperature abnormalities
(fever or hypothermia). The initial phases of septic shock are associated
with vasodilation and capillary leak, and an elevated cardiac output. This
is evident by the presence of strong pulses, warm extremities, good capil-
lary rell, and tachycardia (warm/vasodilatory shock).
Relative or absolute hypovolemia and impaired cardiac function ulti-
mately result in poor cardiac output and vasoconstriction. This is clinically
manifested by delayed capillary rell, diminished peripheral pulses, cool
extremities, and decreased urine output (cold shock).
ERRNVPHGLFRVRUJ
Vasoconstriction maintains the blood pressure for a while, and hypoten-

sion may be a late sign in infants and children and is therefore not a crite-
rion for the diagnosis of shock. Clinical manifestations of various organ
dysfunction progressively appear (multiple organ dysfunction).
Investigations of Suspected Sepsis
Investigation Remark
Hematology Hemoglobin To assess the need for blood transfusion
Platelet count Decreases with persistent sepsis
WBC count WBC >15000 cells/dL or polymorphonuclear
cells >1500 cells/dL is highly significant
Prothrombin time To assess coagulation status
aPTT To assess coagulation status
INR To assess coagulation status
Biochemistry CRP Raised
Glucose Hyperglycemia/hypoglycemia
Serum lactate Raised in severe sepsis
Serum electrolytes Electrolyte abnormalities are common in sepsis
Microbiology Culture of catheter tips
Blood culture
Urine culture
Throat swab
Other investigations X-ray chest
Blood gases
Other imaging; Echo/
CT/ultrasound/MRI
Diagnosis
The diagnosis of sepsis requires SIRS in the presence of proven infection or

a clinical picture consistent with infection. Methods to identify the source
of infection include physical examination, imaging (chest radiograph etc.),
and cytology and culture of clinically appropriate specimens.
Hematologic investigations may show anemia, thrombocytopenia, elevated
neutrophils, and increased immature forms (bands, myelocytes, promyelo-
cytes), vacuolation of neutrophils, and toxic granulations. Neutropenia is
sometimes present in overwhelming sepsis. The erythrocyte sedimentation
ERRNVPHGLFRVRUJ
rate is increased. The coagulation prole may be abnormal with prolonged

prothrombin and partial thromboplastin times, reduced serum brino-
gen levels, and elevated brin degradation products. Metabolic abnormali-
ties include hyperglycemia as a stress response or hypoglycemia if glycogen
reserves are exhausted. Electrolyte abnormalities such as hypocalcemia and
metabolic acidosis may be present. Lactic acidosis can occur if there is sig-
nicant anaerobic metabolism. Elevated C-reactive protein, interleukin-6,
and procalcitonin levels have been reported as potential biochemical
markers of sepsis.
Renal and liver function tests are abnormal in the presence of renal and
liver dysfunction. Patients with acute respiratory distress syndrome or pneu-
monia will have impaired oxygenation (decreased PaO2) and ventilation
(increased PaCO2).
Management of Sepsis
Antimicrobial therapy Appropriate antibiotics

Volume resuscitation Crystalloids/colloids 1020 mL/kg IV boluses, up to
60 mL/kg or more may need to be given in 3060
minutes in children presenting with septic shock.
CVP is monitored, and an arterial line is placed.
Inotropes In case of inadequate response to fluids, dopamine
1020 mcg/kg/min is commenced.
Children who are unresponsive to volume
infusion and dopamine are given epinephrine
0.051 mcg/kg/min if they are vasoconstricted,
or norepinephrine 0.052 mcg/kg/min if they are
vasodilated.
In patients on epinephrine, a vasodilator
(nitroglycerin/dobutamine/milrinone) may also be
required.
In children unresponsive to norepinephrine,
vasopressin may be effective.
Corticosteroids In catecholamine-resistant shock, hydrocortisone is
given in a dose of 50 mg/kg.
Glycemic control Hypoglycemia is treated with 0.51 mg/kg of
dextrose. Blood sugar levels are maintained
between 70 and 110 g/dL.
Calcium gluconate Hypocalcemia is corrected.
Supportive therapy Ventilation, nutrition, and control of fever
(antipyretic drugs and cold sponge/cooling blanket).
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Choice of Antibiotics
Empirical antibiotic therapy based on site of infection

Site of infection Usual pathogens Alternate drug combinations
Intraabdominal Enterobacteriaceae Metronidazole + fluoroquinolone
sepsis (Klebsiella, Proteus, E. coli, (ciprofloxacin).
Enterobacter, Serratia) Metronidazole + 3rd/4th-generation
Enterococci (E. faecalis), cephalosporin.
B. fragilis Carbapenem (imipenem/meropenem)
Piperacillintazobactam
Ventilator P. aeruginosa, S. aureus. -lactam (piperacillintazobactam/
associated Enterobacteriaceae ceftazidime/cefuroxime/
pneumonia (E. coli, K. pneumoniae), carbapenem) + aminoglycoside or
Acinetobacter. fluoroquinolone.
In addition, a glycopeptide (vancomycin/
teicoplanin) or linezolid is added if the
risk of MRSA is high.
IV line sepsis S. aureus, S. epidermidis, Cloxacillin for MSSA or glycopeptide
enterococci, (vancomycin/teicoplanin) for suspected
Candida species. MRSA.
Add 3rd/4th generation cephalosporin/
aminoglycoside/carbapenem for gram
ve organisms in immunocompromised
patients.
Add amphotericin/fluconazole for
suspected fungal infection.
Urosepsis P. aeruginosa, enterobacilli -lactam (piperacillintazobactam/
(Enterobacter, Klebsiella, ceftazidime/cefuroxime/
Serratia) carbapenem) + aminoglycoside or
fluoroquinolone.
Published consensus statements can provide a broad basis for empiri-

cal antibiotic therapy. Initial antibiotic therapy should include agents
from different classes in order to increase the likelihood of coverage of
multidrug-resistant organisms.
Gram-negative organisms are covered with two antibiotics from either
of these groups: -lactams, uoroquinolones, or aminoglycosides. There
is evidence supporting increased survival with aminoglycoside-containing
regimens and therefore an aminoglycoside is generally included.
Nosocomial sepsis or an immunocompromised patient should empirically
be treated with either an extended-spectrum penicillin (e.g., piperacillin
tazobactam), carbapenem (imipenem, meropenem), or cephalosporin which
is effective against pseudomonas (e.g., ceftazidime, cefpirome) plus an
aminoglycoside.
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If MRSA is suspected or the patient has an indwelling medical device, in

addition to the drug combinations noted above, a glycopeptide (vancomy-
cin or teicoplanin) or linezolid is also indicated.
Antifungal therapy: Empirical use of amphotericin B to treat fungal infec-
tions should be considered for selected immunocompromised patients.
Combination versus monotherapy: Once the microbial agent has been
isolated and the antibiotic sensitivity is known, the antibiotics can be
appropriately modied. There is no consensus on efcacy of combination
therapy versus monotherapy. Synergy of drug actions increasing effective-
ness against pseudomonas or any other gram-negative organism has not
been conclusively demonstrated. Drug toxicity and cost of treatment are
less with monotherapy. In view of this, consideration of continuing man-
agement with a combination of drugs as against monotherapy must be
based on clinical judgement.
Fluid Resuscitation
Rapid, aggressive resuscitation with uids (crystalloids or colloids) is ini-
tially required. Fluid boluses of 1020 mL/kg are titrated to normalize
heart rate, urine output (to at least 1 mL/kg/h), capillary rell (<2 sec),
and mental status. Fluid resuscitation may sometimes require as much
as 100120 mL/kg over 3060 minutes. Since hypotension may be a late
sign of shock in children, it is not a reliable end-point for assessing resus-
citation. There is no clearly dened end point in uid resuscitation other
than measurement of CVP (812 mmHg) or signs of uid overload. Blood
transfusion is needed to maintain hemoglobin of 10 g/dL. Coagulopathy is
corrected with fresh frozen plasma and cryoprecipitate, and if the patient
has active bleeding, platelet transfusions may also be needed.
Inotropes
In infants and children, management of sepsis often requires use of ino-
tropic agents to maintain a normal cardiac output. Dopamine (1020
mcg/kg/min) is the initial choice for uid-refractory shock. In dopamine-
resistant shock, epinephrine (in the patient with high systemic vascular
resistance) or norepinephrine (in the patient with low systemic vascu-
lar resistance) is started and the dopamine gradually weaned. Further, in
patients with high systemic vascular resistance with a normal BP but supe-
rior vena cava oxygen saturation (SvO2) of <70%, the addition of a vasodi-
lator such as nitroprusside, nitroglycerin, or milrinone may help reverse
the shock.
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In patients who do not respond to norepinephrine (norepinephrine-

resistant shock), vasopressin may be a useful alternative, as its mechanism
of action is not mediated through -receptors.
Electrolytes
Electrolytes are corrected as needed. Hypoglycemia is treated with 0.51.0 g/kg
of glucose. Hypocalcemia, which can contribute to cardiac dysfunction, is
corrected with 10% calcium gluconate 1020 mg/kg.
Steroids
Up to 50% of children have a relative or absolute adrenal insufciency,
thus if shock is not responsive to catecholamines and uid resuscitation,
IV hydrocortisone 50 mg/kg bolus should be considered (the normal stress
dose of hydrocortisone is 2 mg/kg).
Ventilation
Children requiring ventilation are managed as for acute respiratory distress
syndrome, with low tidal volume ventilation (57 mL/kg), plateau pres-
sures of <30 cm of water, FiO2 of <60%, and a PEEP of 510 cm.
Renal Replacement Therapy

Renal replacement therapy is indicated in children with anuria or oliguria
and a severe uid overload. Extracorporeal membrane oxygenation may be
considered in selected patients with refractory septic shock.
Monitoring
Monitoring patients with septic shock should ideally include central
venous pressure, continuous invasive arterial blood pressure, pulse oxime-
try, systemic venous oxygen saturation and hourly urine output in addition
to heart rate, capillary rell, and mental status. Resuscitation goals include
capillary rell <2 sec, normal pulses, warm extremities, urine output of
>1 mL/kg/h, normal mental status, and normal blood pressure for age.
ERRNVPHGLFRVRUJ
Bibliography
1. Al-Khafaji AH, Sharma S. Multisystem organ failure of sepsis. [Updated: 2010 Jan 29; cited:
2011 Nov 02] Available at: http://emedicine.medscape.com/article/169640-overview.
2. Bugano DD, Camargo LF, Bastos JF, Silva E. Antibiotic management of sepsis: current con-
cepts. Expert Opin Pharmacother 2008;9:281728.
3. Cunha BA, Nicols RL, Rex JH. Sepsis, septic shock and febrile neutropenia. In: Cunha BA, ed.
Antibiotic Essential Michigan: Physicians Press; 2005:11722.
4. Davidson JE, Powers K, Hedayat KM, et al; American College of Critical Care Medicine Task
Force 2004-2005, Society of Critical Care Medicine. Clinical practice guidelines for support
of the family in the patient-centered intensive care unit: American College of Critical Care
Medicine Task Force 2004-2005. Crit Care Med 2007;35:60522.
5. Empiric antibiotic use in critically ill patients. [Update: 2007 August; Accessed: 2012 Jan 17]
Available at: http://www.surgicalcriticalcare.net/Guidelines/empiric_antibiotics.pdf.
6. International Liaison Committee on Resuscitation. The International Liaison Committee on
Resuscitation (ILCOR) consensus on science with treatment recommendations for pediatric
and neonatal patients: pediatric basic and advanced life support. Pediatrics 2006;117(5):
e95577.
7. Khilnani P, Deopujari S, Carcillo J. Recent advances in sepsis and septic shock. Indian J Pediatr
2008;75(8):82130.
8. Lentino JR. Mixed anaerobic infection. The Merck Manuals: Online medical library. [Updated:
2009 Aug; cited: 2011 Feb 22] Available at: http://www.merckmanuals.com/professional/
infectious_diseases/anaerobic_bacteria/mixed_anaerobic_infections.html?qt=&sc=&alt=.
9. Maccioli GA, Dorman T, Brown BR, et al. American College of Critical Care Medicine, Society
of Critical Care Medicine. Clinical practice guidelines for the maintenance of patient physical
safety in the intensive care unit: use of restraining therapiesAmerican College of Critical
Care Medicine Task Force 2001-2002. Crit Care Med 2003;31(11):266576.
10. Management for suspected sepsis for children receiving Parenteral Nutrition (PN) via a central
venous catheter (Hickman type). The Newcastle Upon Tyne Hospitals: NHS Foundation Trust
[Updated: 2008 Nov; cited: 2011 Feb 22]. Available at: http://www.newcastle-hospitals.org.uk/
downloads/clinical-guidelines/Childrens%20Services/CVC_infection_management.pdf.
11. Munford RS. Severe sepsis and septic shock. In: Longo DL, Kasper DL, Jameson JL, et al., eds.
Harrisons Principles of Internal Medicine 18th ed. McGraw-Hill Companies, Inc.; 2012:222332.
12. Russel JA. The current management of septic shock. Minerva Med 2008;99:43158.
13. Silva E, Passos Rda H, Ferri MB, de Figueiredo LF. Sepsis: from bench to bedside. Clinics
(Sao Paulo) 2008;63:10920.
14. Skippen P, Kissoon N, Waller D, Northway T, Krahn G. Sepsis and septic shock: progress and
future considerations. Indian J Pediatr 2008;75:599607.
15. Tantalen JA, Len RJ, Santos AA, Snchez E. Multiple organ dysfunction syndrome in chil-
dren. Pediatr Crit Care Med 2003;4:1815.
16. Watson NA, Denton M, Antibiotic prescribing in critical care: specific indications. JICS 2008;
9:306.
17. Weber DJ, Rutala WA. Central line-associated bloodstream infections: prevention and
management. Infect Dis Clin North Am 2011;25(1):77102.
ERRNVPHGLFRVRUJ
Systemic
Antifungal Agents
Systemic Fungal Infections
Patients who are immunocompromised or have undergone surgery are sus-

ceptible to opportunistic fungal infections; the more common ones being
candidiasis (50%), aspergillosis, and cryptococcosis, with the organism
gaining entry through the lungs, gastrointestinal tract, or through intrave-
nous lines. Infection occurring in previously healthy persons usually arises
through the respiratory route, and examples include histoplasmosis, blas-
tomycosis, and coccidiomycosis.
Candidiasis: C. albicans is part of the normal oral ora and is the most
common cause of disseminated fungal infection in the immunocompro-
mised patient.
Aspergillosis: A. fumigatus can infect the lungs, inner ear, sinuses,
and eyes of previously healthy persons. In the immunosuppressed host,
Aspergillus can cause disseminated infection.
Cryptococcosis: This is a systemic infection caused by Cryptococcus neo-
formans. The commonest manifestation is a subacute or chronic form of
meningitis resulting from the inhalation of the organism. Pulmonary
infection can also occur. The disease affects both healthy and immunosup-
pressed individuals.
Histoplasmosis: This is caused by Histoplasma capsulatum. The lungs are
the main site of infection with symptoms resembling tuberculosis but dis-
semination to the liver, heart, and central nervous system can also occur.
Drug Doses
Amphotericin B deoxycholate
Route IV
Dose Children and adults:
0.51.5 mg/kg/day infused as a single dose over 26 hours for
1014 days. (Total dose for disseminated mycosis is 14 g.)
ERRNVPHGLFRVRUJ
Dose for empiric therapy: 0.5 mg/kg/day.

Dose for invasive candidiasis or aspergillosis: 1 mg/kg/day.
Dose for pulmonary coccidiomycosis: 1.5 mg/kg/day.
A dose reduction is required with a serum creatinine of >3 mg%.
No change in dosing is indicated in hemodialysis or liver failure.
Adverse reactions Amphotericin B is highly nephrotoxic, and up to 80% of patients
will have an increase in serum creatinine within 2 weeks of
therapy. Other adverse effects include hypotension, chills, nausea,
vomiting, drug fever, hypokalemia, musculoskeletal adverse
effects (myalgia, arthralgia), blood disorders (anemia, leukopenia,
thrombocytopenia) and various neurological disorders (hearing
loss, diplopia, convulsions).
To minimize nephrotoxicity, 1015 mL/kg of normal saline is
infused IV before amphotericin administration. In addition,
premedication with antihistaminics (chlorpheniramine 200 mcg/kg)
and corticosteroids (hydrocortisone 4 mg/kg) given 30 min before
may decrease adverse effects. Amphotericin 0.1 mg/kg (max 1 mg)
is first administered as a test dose over 1 hour followed by the
remaining dose.
Amphotericin B lipid complex

Route IV
2.55 mg/kg/day administered q24h, infused over 2 hours for at least
14 days.
Adverse reactions Drug reactions and adverse effects are similar to amphotericin B
deoxycholate but less nephrotoxic.
Amphotericin B liposomal
Route IV
35 mg/kg/day repeat q24h infused over 12 hours.
Adverse reactions Drug reactions and adverse effects are similar to amphotericin B
deoxycholate but less nephrotoxic.
Anidulafungin
Route IV
Dose Children: 1.53 mg/kg loading dose, then 0.751.5 mg/kg/day.
Adults: 100200 mg loading dose, then 50100 mg q24h.
Adverse reactions Fever, headache, nausea, vomiting, diarrhea, hypokalemia, leukopenia,
hepatotoxicity, and phlebitis. Rarely bronchospasm and hypotension.
ERRNVPHGLFRVRUJ
Systemic Antifungal Agents 213
Caspofungin
Route IV
Dose Children: 70 mg/m2 loading dose, then 50 mg/m2 q24h is infused over 1h.
Adults: 70 mg loading dose, then 50 mg q24h infused over 1h.
Adverse reactions Adverse reactions are mild and transient. Fever, rash, pruritus, phlebitis,
headache, gastrointestinal tract symptoms, anemia.
Fluconazole
Route IV/PO
Dose Neonate:
<2 weeks: 3 mg/kg q72h.
24 weeks: 3 mg/kg q48h.
Children:
Prophylaxis and oropharyngeal or esophageal candidiasis: 6 mg/kg once, then
3 mg/kg/day.
Invasive fungal infections: 612 mg/kg/day.
Adults:
Prophylaxis and oropharyngeal or esophageal candidiasis: 200 mg once, then
100 mg/day.
Other invasive fungal infections: 400800 mg/day.
Though not nephrotoxic, the drug dose is reduced in renal dysfunction (50% if
CrCl 2150 mL/min and 25% of dose in CrCl <20 mL/min) because it is cleared
unchanged by renal excretion.
Adverse Rash, gastrointestinal tract symptoms, hepatotoxicity, StevensJohnson
reactions syndrome, anaphylaxis, alopecia, leukopenia, and thrombocytopenia.
Fluconazole is generally well-tolerated with few GIT effects (vomiting) and rashes.
Micafungin
Route IV
Dose Children: 412 mg/kg/day administered q24h (higher dose needed for
patients <8 years of age)
Adults: 50150 mg once daily.
Adverse reactions Fever, headache, nausea, vomiting, diarrhea, leukopenia,
hepatotoxicity, and phlebitis.
Posaconazole
Route PO
Dose Children: Not recommended (Off label use in 313 yr:
300800 mg/day in divided doses q812h).
Children 13 yr and Adults: 400 mg q12h with meals (or liquid
nutritional supplement). Prophylaxis: 200 mg q8h.
Adverse reactions Gastrointestinal tract symptoms, rash, edema, headache, anemia,
neutropenia, thrombocytopenia, fatigue, arthralgia, myalgia, fever,
and visual changes.
ERRNVPHGLFRVRUJ
Voriconazole
Route IV/PO
Dose IV Children and adults: 6 mg/kg q12h for first 24 hours, then
4 mg/kg q12h.
Given IV over 12 h (max rate 3 mg/kg/h and concentration
<5 mg/mL).
Dose PO Children: 10 mg/kg q12h for first 24 hours, then 7 mg/kg q12h.
Adults: <40 kg: 200 mg q12h for first 24 hours, then 100 mg q12h;
>40 kg: 400 mg q12h for first 24 hours, then 200 mg q12h.
Adverse reactions Visual disturbance, photosensitive rash, hepatotoxicity, and GI
symptoms.
Treatment Options
Clinical condition Drug of choice Alternative drug

Prophylactic therapy Caspofungin Voriconazole
Neutropenic/
post transplant patient
Oropharyngeal/ Fluconazole Caspofungin, amphotericin B,
esophageal candidiasis voriconazole
Invasive candidiasis Fluconazole, caspofungin Amphotericin B, voriconazole
Aspergillosis Voriconazole Amphotericin B, caspofungin
Cryptococcal meningitis Liposomal amphotericin B Fluconazole
(can be combined with
flucytosine in severe cases)
Mucormycosis Posaconazole Amphotericin B
Fungal infection should be suspected in seriously ill patients who have

been receiving antibiotics for a prolonged period of time and have per-
sistent fever and elevated WBC. Voriconazole or caspofungin (caspofungin
is preferable in the presence of neutropenia) can be started empirically in
such patients even though fungal serologic studies are negative.
Amphotericin B
Amphotericin B is effective against most systemic fungal infections and
penetrates the CNS; however, it is one of the most toxic antifungals and is
therefore not the rst choice except in cryptococcal meningitis. Liposomal
amphotericin B is preferable to amphotericin B deoxycholate because of
less nephrotoxicity.
ERRNVPHGLFRVRUJ
Systemic Antifungal Agents 215
Fluconazole
Fluconazole is effective against Candida but not Aspergillus. It enters the
CSF and is effective against Cryptococcus and is used as chronic suppressive
therapy of cryptococcal infections after these have been initially treated
with liposomal amphotericin B or voriconazole.
Voriconazole
Voriconazole is effective against aspergillosis and candidiasis. It has a wide
antifungal spectrum but does not enter the CSF.
Caspofungin
Caspofungin is used for antifungal prophylaxis in febrile neutropenic
patients or in patients with invasive candidiasis or aspergillosis who have
not responded to other drugs. It has no effect against Cryptococcus and so is
not used for CNS infections.
Posaconazole
Posaconazole is the drug of choice for mucormycosis. Even though posa-
conazole has not been widely used in children younger than 13 years of
age, it is considered safe and effective.
Other Antifungal Drugs

Itraconazole is a systemic antifungal agent, not generally used because of its
highly variable bioavailability, and Anidulafungin and Micafungin are active
only against Candida.
Griseofulvin and Terbinane are drugs used for dermatophytosis.
Clotrimazole and Ketoconazole are now mainly used in topical preparations,
and Nystatin is used as lozenges, mouth paints, or as vaginal tablets (vagi-
nal candidiasis).
Bibliography
1. Ananthanarayan R, Paniker CKJ. Medical Mycology. In: Textbook of Microbiology 8th ed.
Hyderabad, India: University Press (India) Pvt Ltd; 2009:60017.
2. Bennett JE. Antifungal agents. In: Brunton LL, Chabner BA, Knollmann BC, eds. Goodman &
Gilmans. The Pharmacological Basic of Therapeutics 12th ed. USA: McGraw Hill Inc; 2011:
157191.
ERRNVPHGLFRVRUJ
3. Blyth CC, Palasanthiran P, OBrien TA. Antifungal therapy in children with invasive fungal infec-
tions: a systematic review. Pediatrics 2007;119:77284.
4. British National Formulary. Antifungal drugs 2009:3329.
5. Das S, Shivaprakash MR, Chakrabarti A. New antifungal agents in pediatric practice. Indian
Pediatr 2009;46:22531.
6. Galgiani JN, Ampel NM, Catanzaro A, Johnson RH, Stevens DA, Williams PL. Practice guide-
lines for the treatment of coccidioidomycosis. Clin Infect Dis 2000;30:65861.
7. Mitchell TG. Medical mycology. In: Brooks GF, Carroll KC, Butel JS, et al, eds. Jawetz, Melnick &
Adelbergs Medical Microbiology 25th ed. USA: McGraw Hill Inc; 2010:62544.
8. Sheppard D, Lampiris HW. Antifungal agents. In: Katzung BG, Masters SB, Trevor AJ, eds. Basic
and Clinical Pharmacology 11th ed. USA: McGraw Hill Inc; 2009:83544.
9. Systemic anti-infectives. In: Kastrup EK, Meives CA, et al, eds. Drug Facts and Comparisons.
Missouri, USA: Wolters Kluwer Health; 2010;2096150.
10. Wolkowiez MC, Moran C, Daniel K, Benjamin Jr, Smith PB. Pediatric antifungal agents. Curr
Opin Infect Dis 2009;22:5538.
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Sedatives, Analgesics,
and Muscle Relaxants
A man who cannot work without his hypodermic needle is a poor doctor.
The amount of narcotic you use is inversely proportional to your skill
Martin H Fischer (18791962)*
Sedatives
Drug Dose Onset Duration
of action
Chloral hydrate Children: 1530 min 60120
Sedation: 8 mg/kg or 250 mg/m2 q8h PO min
(max 500 mg q8h).
Sedation for procedures: 2550mg/kg PO.
Adult:
Sedation: 250 mg q8h PO;
hypnotic dose: 0.51 g PO.
Dexmedetomidine Children: Loading dose of 0.250.5 mcg/
kg over 10 min, followed by IV infusion of
0.250.5 mcg/kg/h, titrated to response
Adults: Loading dose of 1mcg/kg over
10 min, followed by IV infusion of 0.20.7
mcg/kg/h
Diazepam Children: 25 min 60120
PO: 0.120.8 mg/kg/day in divided doses (IV dose) min
q68h PRN.
IM/IV: 0.040.3 mg/kg/dose q24h PRN
(max of 0.6 mg/kg in an 8 h period).
Adults:
PO: 210 mg/dose q612h PRN.
IM/IV: 210 mg/dose q34h PRN.
Lorazepam Children: PO: 2030 min 68 h
PO/IM/IV: 0.05 mg/kg/dose q48h (range: IM: 3060 min
0.020.1 mg/kg/dose; max 2 mg/dose). IV: 15 min
Adults:
PO: 12 mg/dose q812h (up to a max of
10 mg/day).
IV: 2 mg (or 0.044 mg/kg, whichever is less)
single dose.
*Martin H Fischer was a German physiologist, chemist, and author.
ERRNVPHGLFRVRUJ
Drug Dose Onset Duration

of action
Midazolam Sedation with mechanical ventilation: 23 min 4560
Children: 0.050.2 mg/kg IV bolus followed min
by 0.060.12 mg/kg/h IV infusion
Adults: 0.150.35 mg/kg IV bolus followed
by 0.020.10 mg/kg/h IV infusion
Conscious sedation:
Children:
IV: < 6 mo: titrate in small increments
6 mo5 yr: 0.05 to 0.1 mg/kg IV (may
increase up to 0.6 mg/kg; max dose
6 mg).
612 yr: 0.0250.05 mg/kg IV (may
increase up to 0.4 mg/kg; max dose
10 mg).
IM: 0.1 to 0.15 mg/kg IM (may increase
up to 0.5 mg/kg; max dose 10 mg)
Adults IV: 12.5 mg. (May increase up to
5 mg)
Triclofos Children: 2530 mg/kg PO (15 yr: 250 3045 min 46 h
500 mg PO; >5 yr: 500 mg1 g PO)
Adults: 12 g PO
Sedation and analgesia are separate entities; although some agents (e.g.,
morphine, ketamine) have both sedative and analgesic properties, others
are almost exclusively analgesics (e.g., fentanyl, paracetamol) or sedatives
(e.g., benzodiazepines, propofol, chloral hydrate).
Dexmedetomidine is an a2-agonist with both sedative and analge-
sic properties. It is used as an IV infusion for ventilated and nonventi-
lated patients and provides a moderate level of sedation without causing
notable respiratory depression. It, however, can cause clinically signi-
cant bradycardia and hypotension because of peripheral a2-receptor
stimulation.
Midazolam is a benzodiazepine derivative. It is a sedative and an anxi-
olytic agent with a short duration of action. May cause hypotension espe-
cially if the patient has hypovolemia. Tolerance and dependence are known
to occur after prolonged use of morphine, fentanyl, or midazolam. Abrupt
discontinuation of these drugs may precipitate withdrawal syndrome.
Clinical features of withdrawal usually occur within a few hours of stop-
ping the drug and include manifestations associated with the following
systems: (i) CNS (e.g., agitation, seizures, hallucinations, and psychosis),
ERRNVPHGLFRVRUJ
Sedatives, Analgesics, and Muscle Relaxants 219
(ii) autonomic system (e.g., vomiting, tachycardia, hypertension, and

fever), and (iii) CVS (e.g., arterial desaturation).
Narcotic analgesics
Drug Dose Onset Duration of action
Fentanyl Children: 12 mcg/kg IV bolus; may be 1 min 1560 min
repeated q30 min1 h or followed by IV
infusion 410 mcg/kg/h
Adults: 50100 mcg IV q12h or
0.51.5 mcg/kg/h IV infusion
Morphine Children 23 min 3060 min
IV
13 mo: 25 mcg/kg; may be repeated q6h
>1 yr: 100200 mcg/kg may be repeated q4h
Followed by IV infusion
16 mo: 5 mcg/kg/h
612 mo: 10 mcg/kg/h
>1 yr: 1050 mcg/kg/h
IM
612 mo: 150 mcg/kg
>1 yr: 250 mcg/kg
Adult
IV2.510 mg; may be repeated q4h,
followed by IV infusion 0.880 mg/h
IM520 mg q4h
Fentanyl is a synthetic opioid, having a relatively short half-life of 3060

minutes and causes less histamine release than morphine, and therefore
less hypotension. Like morphine, it can also cause nausea, constipation,
and respiratory depression. A reduction in dose is required in renal failure.
Respiratory depression caused by an overdose of morphine or fentanyl is
counteracted by Inj. naloxone 10 mcg/kg IV bolus (can be given IM/SC/IO).
This is followed by a higher dose if there is no response (<20 kg: 100 mcg/
kg, >20 kg: 2 mg). The dose may be repeated if required to maintain opioid
reversal or administered as an IV infusion in a dose of 520 mcg/kg/h in a
concentration of 4 mcg/mL.
Morphine is a strong opioid analgesic administered for relief of severe
pain and sedation. It may cause hypotension, because of histamine release,
particularly after bolus administration. Its other adverse effects include res-
piratory depression, nausea, and constipation. Dose reduction (by 2550%)
is required in moderate renal failure.
ERRNVPHGLFRVRUJ
IV anesthetic agents
Drug Dose Onset Duration of action
Etomidate Children >10 yr and adults: 0.20.6 1 min 35 min
mg/kg IV.
Ketamine Children 35 min 15150 min
IV: 1.02.75 mg/kg. (2 mg/kg provides
IM: 34 mg/kg. 510 min of surgical
IV infusion: 520 mcg/kg/min. anesthesia and
Adults analgesia)
IV: 14.5 mg/kg; repeat 50% of
induction dose as required.
IM: 6.513 mg/kg.
IV infusion: 0.10.5 mg/min.
Propofol Dose for GA: 1 min 10 min
Children: Induction2.53.5 mg/kg;
maintenance125300 mcg/kg/min.
Adult: Induction22.5 mg/kg;
maintenance100200 mcg/kg/min.
ICU sedation 550 mcg/kg/min (0.33
mg/kg/h).
Thiopental Children: 26 mg/kg IV (12 mg/kg IV 3060 530 min
sodium in hemodynamic instability). seconds
Adults: 100150 mg IV (can be repeated
if required), maximum dose 500 mg.
Etomidate has a rapid onset and short duration of anesthetic action with-
out analgesia. It may be used for short interventional procedures and
induction of anesthesia. The drug is useful in patients with hemodynamic
instability as it has no effect on the myocardium, peripheral circulation, or
the pulmonary circulation. IV injection causes transient pain and may be
associated with skeletal muscle movements, including myoclonus.
Ketamine in lower doses primarily causes anxiolytic and analgesic
effects. With higher doses, it produces sedation and dissociative anesthesia
and is used as an anesthetic agent for short painful procedures. Recovery
from ketamine anesthesia may be associated with restlessness, agitation,
and disorientation.
Propofol is a short-acting IV anesthetic agent with no analgesic activ-
ity and can be used as an IV infusion for sedation. It has a rapid onset of
action, and the effect lasts for 1015 minutes. Propofol is a negative ino-
trope, vasodilator and a potent respiratory depressant. It can cause hypoten-
sion, respiratory acidosis and apnea.
Thiopental sodium is a short-acting barbiturate, which induces hypnosis
and anesthesia but not analgesia. It has been used for induction of anesthe-
sia, control of status epilepticus, and to reduce increased intracranial
ERRNVPHGLFRVRUJ
pressure in neurosurgical patients. Its adverse effects include pulmonary

(apnea, laryngospasm, coughing), cardiovascular (hypotension progressing
to shock), and CNS (muscle twitching) manifestations.
Muscle relaxants
Drug IV dose Duration of action
Atracurium Children (>1 mo) and adults: 300600 mcg/kg 2030 min
IV followed by 100200 mcg/kg as required
q1525min or 510 mcg/kg/min IV infusion
Pancuronium Neonates: 3040 mcg/kg IV bolus, then 5060 min
1020 mcg/kg as required q11.5h
Adults and children >1 month: 50100 mcg/kg
IV bolus, then 1020 mcg/kg as required q11.5h
Rocuronium Children and adults: 0.61.2 mg/kg IV bolus 3050 min
followed by 150 mcg/kg as required.
IV infusion: 712 mcg/kg/min.
Succinylcholine Children: 12 mg/kg IV bolus (35 mg/kg IM). 35 min (IV onset
(suxamethonium Repeat 0.30.6 mg/kg IV as required q510min. of action: 30 sec;
chloride) Adults: 0.31.1 mg/kg (average 0.6 mg/kg) IV IM: 23 min).
bolus (35 mg/kg IM). Repeat 0.040.07 mg/kg IV
as required q510min.
IV infusion: 2.54.3 mg/min.
Vecuronium <1 mo: 50100 mcg/kg IV bolus 2535 min
>1 mo and adults: 100150 mcg/kg IV bolus,
repeat as required
IV infusion: 5080 mcg/kg/h
Pancuronium produces pharmacologic effects similar to those of other

non-depolarizing neuromuscular blocking agents. In pharmacological doses,
it has a duration of action of 5060 minutes. The drug may produce an
increase in heart rate as a result of its blocking effect on the acetylcholine
receptors of the heart. It does not cause hypotension or bronchospasm.
Rocuronium is an analogue of vecuronium with a rapid onset and inter-
mediate duration of action. It is used as an adjunct to general anesthesia to
facilitate both rapid sequence and routine tracheal intubation and to pro-
vide skeletal muscle relaxation during surgery or mechanical ventilation. The
most common adverse reactions are transient hypotension or hypertension
(in 2%) and rarely, nausea, vomiting, arrhythmias, and bronchospasm may
occur.
Succinylcholine is a short-acting depolarizing muscle relaxant, which
is used in general anesthesia to facilitate tracheal intubation and to pro-
vide a short period of skeletal muscle relaxation during surgery. Its depo-
larizing action is observed as muscle fasciculations, which can be a cause
ERRNVPHGLFRVRUJ
of hyperkalemia and postoperative myalgia. Injection may result in brady-

cardia especially in children. This may be prevented by giving atropine
20 mcg/kg (minimum dose, 0.1 mg) or glycopyrrolate 10 mcg/kg preceding
the dose of succinylcholine. Despite its adverse effects, this agent remains
the drug of choice in an emergency or in patients with anticipated difcult
airway because of its rapid onset and short duration of action.
Vecuronium is a non-depolarizing muscle relaxant indicated in gen-
eral anesthesia to facilitate endotracheal intubation and to provide skel-
etal muscle relaxation during surgery or mechanical ventilation. The drug
does not alter the level of consciousness or provide analgesia or amnesia.
Its advantage is that it has no clinically signicant effects on hemodynamic
parameters. Non-depolarizing neuromuscular blockade is readily reversed
with neostigmine (5070 mcg/kg; in age >12 yr: 5 mg) which is given in
conjunction with an anticholinergic agent (atropine 1020 mcg/kg or glyco-
pyrrolate 10 mcg/kg).
Nonsteroidal anti-inflammatory drugs

Drug Dose Remarks
Aspirin Children: 3060 mg/kg/day divided q46h PO Should be avoided in
Adult: 300900 mg q46h PO (maximum children <12 years due to
4 g/day) risk of Reye syndrome
Ibuprofen Children: 2030 mg/kg/day divided q46h PO Avoid in infants <6 months
Adults: 1.22.4 g/day divided q46h PO
Nimesulide Children: 5 mg/kg/day divided q812h PO Banned in many countries,
Adults: 100200 mg q12h PO but available in India
Paracetamol Children: 4060 mg/kg q46h PO or 5 mg/kg
q46h IV (maximum 30 mg/kg/day IV)
Adult: 0.51g q46h PO (maximum 4 g/day)
Sedation and Analgesia on Ventilator
Muscle Relaxants
At the commencement of ventilation, the patient receives muscle relaxants,
sedation and analgesia. Whenever muscle relaxants are used, sedation and
analgesia must invariably be given. Once the patient has been stabilized,
muscle relaxants may be discontinued because of the risks and complica-
tions associated with their prolonged use. Ventilation is then maintained
with optimum levels of sedation and analgesia. Muscle relaxants may
however, be continued in children who are hemodynamically unstable or
when it is difcult to achieve compliance with the ventilator.
ERRNVPHGLFRVRUJ
Analgesics
Analgesia should be administered to any child who has undergone a sur-
gical procedure and is likely to have some degree of pain or discomfort.
Adequacy of analgesia may be assessed by noting pain related behav-
ior and physiological responses to pain. The use of a pain scoring system
appropriate to the age of the child is advocated for accurate assessment
and pain management (Appendix M).
Morphine or fentanyl administered as a continuous IV infusion have
been the drugs of choice for relief of severe postoperative pain. NSAIDs
are used as adjuncts to opioids in certain patients and have been shown to
reduce opioid requirements by around 1530%. Local/regional anesthetic
techniques (e.g., epidural) are also benecial for the relief of pain.
Sedatives
Modified Ramsay sedation scale
Level response
1 - Awake and anxious, agitated, or restless.
2 - Awake, cooperative, and settled on minimal ventilation.
3 - Awake; responds to commands. Moves spontaneously.
4 - Asleep; brisk response to light glabellar tap or loud noise. No spontaneous movement.
5 - Asleep; sluggish response to light glabellar tap or loud noise stimulus.
6 - Asleep; no response to light glabellar tap or loud noise.
The Ramsay is a simple scale, scored from 1 to 6 for assessment of the level of sedation.
Sedation is given in order to reduce anxiety and stress responses and main-
tain secure placement of tubes and lines in the postoperative patient.
All sedation can cause some degree of hypotension, and reduction in
the ability to clear secretions. There may also be paradoxical agitation,
dependence, and a withdrawal phenomenon. In addition, opiates cause
impaired gastric emptying and constipation. All sedatives therefore need
to be reviewed periodically and administered in the lowest effective doses.
The level of sedation should be regularly assessed and documented against
a scale, such as the Ramsay sedation scale, and doses of sedative agents
titrated to produce the desired level of sedation (a score of 24 is appropri-
ate in most situations).
Before increasing the degree of sedation in an agitated child, one needs
to exclude all irritant factors viz. pain, hypoxia, hypercarbia, secretions, full
bladder, hunger, thirst, ambient temperature too hot/cold, noise, lighting,
position, nausea, constipation, colic, soiled nappy, pruritus, or inappro-
priate ventilator settings. After exclusion of irritant factors in the unsettled
ERRNVPHGLFRVRUJ
child, methods of restraint such as swaddling, arm splinting, and wrist and
ankle ties may be effectively employed so that the lowest required doses
of sedation are administered. Sedation is gradually terminated when the
blood gases are normal, and the patient is hemodynamically stable on
minimal inotropes and ready for extubation.
Midazolam or dexmedetomidine given by continuous IV infusion are
recommended agents of choice for the majority of critically ill children
requiring intravenous sedation. Children may be changed over to enteral
sedation (e.g., chloral hydrate) once enteral (nasogastric or nasojejunal)
feeding is established.
Sedation for Short Procedures

Children on IV sedation can have a bolus (up to 1 hour of infusion given
as a bolus) a couple of minutes prior to physiotherapy, chest tube removal,
catheterization, etc.
More painful procedures can be done under ketamine (IV or IM) alone or
a combination of propofol or midazolam plus an analgesic agent (ketamine/
fentanyl). Propofol alone may be used for nonpainful procedures.
Rapid Sequence Intubation
Normal induction of general anesthesia involves administration of a short-

acting opioid analgesic agent (fentanyl/morphine) followed by a slow injec-
tion of an intravenous anesthetic agent (thiopentone/propofol/etomidate)
with simultaneous assessment of the patients verbal response or eyelash
reex. Once the patient is unconscious, a muscle relaxant (succinyl choline/
rocuronium/vecuronium) is administered and the patient is intubated.
In rapid sequence intubation (RSI), a predetermined dose of intravenous
anesthetic agent or sedative (thiopentone/propofol/etomidate/ketamine/
midazolam) is rst given and this is immediately followed by a quick acting
muscle relaxant (succinyl choline/rocuronium) to allow tracheal intuba-
tion. RSI may be indicated in the cardiac surgical patient because of sud-
den cardiac arrest, hemodynamic instability with impending arrest, or loss
of airway due to dislodgement or obstruction of endotracheal tube.
Step wise approach to RSI is as follows:
(i) Assist spontaneous ventilation with bag mask ventilation and
pre-oxygenate with 100% oxygen.
(ii) Routine use of anticholinergics is not necessary but atropine
1020 mcg/kg or glycopyrrolate 10 mcg/kg may be administered
in presence of bradycardia.
ERRNVPHGLFRVRUJ
(iii) To prevent aspiration, consider cricoid pressure till airway is denitely

secured.
(iv) If the patient is awake and hemodynamic parameters permit,
an induction agent or sedative is administered to prevent recall.
Etomidate (0.20.3 mg/kg) is the drug of choice as it provides
maximum hemodynamic stability and has minimal direct cardiac
depressant action. Ketamine (12 mg/kg), midazolam (0.20.3 mg/kg),
thiopentone (26 mg/kg), or propofol (23 mg/kg) are other
alternative drugs. In severe hemodynamic compromise, an induction
agent is avoided for fear of cardiovascular collapse though a muscle
relaxant may be given. No induction agent or muscle relaxant is
required in case of cardiac arrest.
(v) IV muscle relaxant is next given to assist intubation and maintain
ventilation. Succinylcholine (12 mg/kg) is indicated in difcult
airway as it has a rapid onset and short duration of action. It
may cause bradycardia and is contraindicated in hyperkalemia.
Rocuronium bromide (0.61.2 mg/kg) is an alternative with equally
rapid onset but prolonged duration of action.
(vi) In case intubation is not accomplished, the patient is managed with
an appropriate size supraglottic device (laryngeal mask airway or
cuffed oropharyngeal airway).
Preparation and Administration
Midazolam
2.5 mg/kg made up to 50 mL with 5% dextrose or 0.9% saline.
With this concentration, 1 mL/h = 50 mcg/kg/h.
Morphine
1 mg/kg made up to 50 mL with 5% dextrose.
Fentanyl
0.25 mg/kg made up to 50 mL with 5% dextrose.
Dexmedetomidine
10 mcg/kg made up to 50 mL with 5% dextrose.
With this concentration, 1 mL/h = 0.2 mcg/kg/h.
ERRNVPHGLFRVRUJ
Bibliography
1. Arnold HM, Hollands JM, Skrupky LP, Mice ST. Optimizing sustained use of sedation in
mechanically ventilated patients: focus on safety. Curr Drug Saf 2010;5:612.
2. Buck ML. Dexmedetomidine for sedation in the pediatric intensive care setting. Pediatric
Pharmacotherapy 2006;12(1). 2006 Childrens Medical Center, University of Virginia. Last
accessed on 31th Jul 2011. Available at: http://www.medscape.com/viewarticle/524752.
3. Chrysostomou C, Di Filippo S, Manrique AM, et al. Use of dexmedetomidine in children after
cardiac and thoracic surgery. Pediatr Crit Care Med 2006;7:12631.
4. Darowski M. Sedation for ventilated children. [Updated: 2009 Aug; cited: 2011 Apr 26].
Available at: http://www.leedspicu.org/Documents/Mark%20D%20-%20Sedation%20for%20
Ventilated%20Children7.09%282%29.pdf
5. Deorari AK. Rational drug therapy. In: Ghai OP, Paul VK, Bagga A, ed. Essential Paediatrics
7thed. New Delhi, India: CBS Publishers & Distributors Pvt Ltd; 2009:7212.
6. Guinter JR, Kristeller JL. Prolonged infusions of dexmedetomidine in critically ill patients. Am J
Health Syst Pharm 2010;67(15):124653.
7. Hall RI, Sandham D, Cardinal P, et al; Study Investigators. Propofol vs midazolam for ICU seda-
tion: a Canadian multicenter randomized trial. Chest 2001;119:11519.
8. Khilnani P, Kaur J. Sedation and analgesia in pediatric intensive care unit. Indian J Crit Care
Med 2003;7:429.
9. Newth CJ, Venkataraman S, Willson DF, et al; Eunice Shriver Kennedy National Institute
of Child Health and Human Development Collaborative Pediatric Critical Care Research
Network. Weaning and extubation readiness in pediatric patients. Pediatr Crit Care Med
2009;10:111.
10. Playfor SD. Analgesia and sedation in critically ill children. Cont Educ Anaesth Crit Care Pain
2008;8:904.
11. Precedex (dexmedetomidine hydrochloride) [package insert]. Lake Forest, IL: Hospira, Inc;
2008. Revised September 2010.
http://www.drugs.com.
13. Ramsay MA, Savege TM, Simpson BR, Goodwin R. Controlled sedation with alphaxalone-
alphadolone. Br Med J 1974;2:6569.
14. Ranjit S. Pharmacology of sedative and analgesic agents. In: Ranjit S, ed. Manual of Pediatric
Emergencies and Critical Care Hyderabad, AP, India: Paras Medical Publisher; 2010:43843.
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PastIssues/March2011/PediatricProceduralSedationandAnalgesia2011/tabid/3691/Default.
aspx.
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18. Sweetman SC, Blake S. Anxiolytic sedatives hypnotics and antipsychotics. In: Martindale: The
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Seizures
Drugs for Rapid Control of Seizures
Drug Initial dose (mg/kg) Onset of action Remarks

Diazepam 0.10.3 mg/kg Immediate Dose is repeated after 10 minutes if
slow IV. seizure continues.
0.20.5 mg/kg Must be followed by an immediate

rectal. loading dose of phenytoin, as the
duration of action of diazepam is
Adults: 20 minutes.
510 mg IV.
0.20.5 mg/kg Rectal dose may be repeated after
rectal. 412 hours.
Lorazepam 0.050.1 mg/kg Immediate Dose is repeated after 10 minutes if
slow IV (max 2 mg) seizure continues.
0.10.4 mg/kg rectal Has a longer duration of

action (68 hours), and is less
Adults: 4 mg IV stat respiratory depressant than
diazepam.
Midazolam Dose for sedation: Immediate
6 mo5 yr: 0.050.1
mg/kg slow IV/IM.
Repeat in increments
q2min till effect (up to
0.6 mg/kg; max 6 mg).
612 yr: 0.0250.05
mg/kg. Repeat
q2min PRN (up to 0.4
mg/kg; max 10 mg).
Adult: 12.5 mg.
Repeat in increments
q2min PRN (max
5 mg).
ERRNVPHGLFRVRUJ
Subsequent Therapy
Drug Initial dose Maintenance dose Remarks

Phenytoin Children: 1520 510 mg/kg/day It is infused at not
mg/kg slow IV over in divided doses >1 mg/kg/min at a maximum
2030 minutes. q812h PO/IV. concentration of 10 mg/mL
in normal saline only.
Adults: 1015 mg/kg Adults: 100 mg Extravasation causes tissue
slow IV infusion over q68h PO/IV. necrosis. Therapeutic levels
2030 minutes. are reached in 2030 min.
Phenytoin causes minimal

sedation. Immediate side-
effects are hypotension,
arrhythmia, and phlebitis.
Long-term side effects
include gingival hyperplasia,
ataxia, and megaloblastic
anemia.
Fosphenytoin Children and adults: 45 PE/kg/day The advantages over
(Fosphenytoin 1015 phenytoin in divided doses phenytoin are: it can be
sodium injection equivalent units q1224h PO/IV. administered rapidly IV/
is dispensed in (PE)/kg IV; it is IM, in saline or dextrose,
phenytoin sodium administered at and therapeutic levels are
equivalent a rate of achieved faster. Produces less
units [PE]) 100150 PE/min. venous irritation.
Arrhythmias and hypotension

can occur as with phenytoin.
Phenobarbitone Children: 1020 510 mg/kg/day Immediate side effects include
mg/kg slow IV. repeated q24h hypotension, respiratory
PO/IV. depression, and sedation.
Adults: 10 mg/kg Adults: 60180 Long-term side effects

slow IV (max 1 g). mg/day q24h include drowsiness and
PO HS (may be hyperkinesias.
increased to
300 mg). If seizures are refractory to
phenytoin, phenobarbitone is
given in addition. It is the drug
of first choice in neonates, but
not in older children.
ERRNVPHGLFRVRUJ
Seizures 229

Sodium valproate Children: 2050 mg/kg/day Side effects include nausea,
PO10 mg/kg in in divided doses vomiting, impaired liver
divided doses q12h PO/IV. function, increased appetite,
q12h. and weight gain. Less
IV10 mg/kg bolus Adults: commonly, tremors and motor
over 35 minutes. 2050 mg/kg/day in-coordination, pancreatitis,
The dose is in divided doses and blood disorders.
increased weekly q12h PO/IV
to maintenance (max 2.5 g/day).
level.
Adults:
PO600 mg in
divided doses q12h.
IV10 mg/kg bolus
over 35 minutes.
Carbamazepine Children: 510 mg/ 1030 mg/kg/day Adverse effects include
kg/day q24h PO (at divided q812h PO. drowsiness, headaches, motor
night) and increased in-coordination, and GIT
weekly by 2.55 mg/ Adults: 8001200 symptoms.
kg/day to 1030 mg/ mg/day in divided
kg/day in divided doses q812h PO. Less common side effects
doses q812h PO. are cardiac arrhythmias,
diplopia, aplastic anemia,
Adults: 100200 mg thrombocytopenia, and
q24h PO (at night) dermatological reactions.
increased weekly
by 100200 mg/day
to 8001200 mg/
day in divided doses
q812h PO.
Levetiracetam 20 mg/kg/day 60 mg/kg/day in Indicated as adjunctive
in divided doses divided doses q12h therapy in adults and children
q12h PO, double PO. over 4 years age.
every 2 weeks to
60 mg/kg/day in Adults: 3 g/day in May cause sleepiness,
divided doses q12h divided doses q12h weakness, and dizziness. In
PO. PO. children, the most common
side effects are sleepiness,
Adults: 1 g/day in hostility, irritability, and
divided doses q12h weakness.
PO double every 2
weeks to a max of
3 g/day in divided
doses q12h PO.
ERRNVPHGLFRVRUJ
Control of Refractory Seizures

Midazolam 0.050.1 mg/kg IV Children: 60120 Titrate drip to control seizures.
bolus. May repeat mcg/kg/h IV
dose q23 min up infusion. Monitor respiration and
to max 6 mg ventilation.
(6 mo5 yr) and Adults: 20100
10 mg (>5 yr). mcg/kg/h.
Adults: 12.5 dose

over 2 minutes.
Repeat q23 min
until desired effect
(max 10 mg).
Thiopental 26 mg/kg IV 0.55 mg/kg/h IV Titrate drip to control
sodium (12 mg/kg IV in infusion. seizures.
hemodynamic
instability). Monitor respiration and
ventilation.
Adults: 100150 mg
IV (can be repeated
if required, to a max
of 500 mg).
Propofol Dose for sedation: 2575 mcg/kg/min Titrate drip to control seizures.
Children and adults: (1.54.5 mg/kg/h)
0.51 mg/kg IV infusion. Monitor respiration and
IV bolus then ventilation. Keep for 12 hours
0.10.5 mg/kg after seizure activity.
IV every
310 minutes for
maintenance.
Diazepam 0.10.3 mg/kg IV. 100400 mcg/kg/h Titrate drip to control
IV infusion. seizures.
Adults: 1020 mg IV.
Monitor respiration and
ventilation.
Management of Acute Seizures
Airway, breathing and circulation

In a child having seizures, the airway needs to be rst secured by correct posi-
tioning of the head and neck. Oxygen is administered by a nasal cannula, face-
mask, or endotracheal intubation. Heart rate and respiration are monitored.
ERRNVPHGLFRVRUJ
Seizures 231
IV dextrose
Blood sugar and serum electrolytes are checked. 0.250.5 g/kg of dextrose
may be given empirically (i.e., 2.55 mL/kg of 10% dextrose or 12 mL/kg
of 25% dextrose).
IV sedation
Rapid control of seizures is obtained by any one of the following injec-
tions: diazepam, lorazepam, or midazolam.
Anti-epileptic drug therapy
A loading dose of phenytoin or fosphenytoin is administered to prevent
subsequent seizures. Because of the risk of hypotension and arrhythmias,
phenytoin and fosphenytoin are administered slowly with continuous
ECG, blood pressure, and respiratory monitoring. Ideally if 2 hours after
administration, the plasma level of phenytoin is <10 mg/L, an additional
IV dose of 5 mg/kg is administered. The full anti-epileptic effect of pheny-
toin, or fosphenytoin, is not immediate, and adjunctive benzodiazepines
may be needed to interrupt convulsions if they occur during phenytoin
infusion. Oral or parenteral phenytoin for long-term maintenance medi-
cation is started 12 hours after the loading dose. In case seizures recur
despite single drug therapy, a combination of anti-epileptic drugs may be
required.
Paralysis and Intermittent positive pressure ventilation
Refractory seizures (status) that do not respond to repeated doses of
diazepam, lorazepam, or midazolam are managed by intubation, ven-
tilation, and an infusion of short-acting muscle relaxants or complete
paralysis.
Causes of Postoperative Seizures
Disorder Causes Comment

Drugs Lignocaine, tranexamic acid High doses of Inj.
lignocaine or tranexamic
acid given in the
cardiopulmonary bypass
(CPB) may be a cause.
Hypoxia Hypoxic brain injury may
follow total circulatory arrest,
cardiac arrest, or prolonged
hypotension
Embolization Gaseous and particulate
embolization
Cerebral hemorrhage Anticoagulation, hypertension
ERRNVPHGLFRVRUJ
Disorder Causes Comment

Metabolic disturbances Commonly, hypocalcemia, Less commonly,
hypoglycemia, hyponatremia aminoacidurias, hepatic or
uremic encephalopathy,
hyperglycemia,
hypomagnesemia,
hypernatremia.
In neonates, vitamin B6
(pyridoxine) deficiency.
Febrile convulsion
Neurological injury may result from ischemia, cerebral hemorrhage,

hypoxia, or embolization. Under deep hypothermia, a duration of circula-
tory arrest of >40 minutes is associated with an increased risk of neurologic
injury. Other variables that may inuence the risk of brain injury include
the duration of CPB, depth of hypothermia, the rate and duration of core
cooling, and the degree of hemodilution. Dissemination of both macro-
emboli and microemboli (gaseous or particulate) during cardiopulmonary
bypass may also cause brain injury.
Febrile seizures usually occur in children between the ages of 3 months
and 5 years, and are associated with a rise in the body temperature to
>38C (100.4F). It is a generalized tonic-clonic seizure lasting between a
few seconds to 15 minutes, followed by a brief period of drowsiness and
is diagnosed when no other cause of the convulsion can be identied.
Complex febrile seizures are dened as febrile seizures that are multiple,
focal and last >15 minutes or have postfocal paresis.
In general, treatment of a febrile convulsion is supportive (cold sponge,
antipyretic agents) while seizures of longer duration are treated with IV
diazepam, lorazepam, or midazolam. Prophylaxis by means of medica-
tions is controversial. Prompt treatment of fever alone has been shown to
be effective in preventing recurrences of febrile convulsions.
Bibliography
1. Drislane FW. Status epilepticus. In: Schachter SC, Schomer DL, eds. The Comprehensive
Evaluation and Treatment of Epilepsy San Diego, CA: Academic Press; 1997:14972. [Cited:
2011 Feb 22] Available at: http://professionals.epilepsy.com/page/managing_phenfos.html.
2. Kalra V. Central nervous system. In: Ghai OP, Paul VK, Bagga A, ed. Essential Paediatrics 7th ed.
New Delhi, India: CBS Publishers & Distributors Pvt Ltd; 2009:52333.
3. Kutty MN, Kumar S. Seizures and epilepsy. Journal of Postgraduate Medical Education, Training &
Research 2008;3:912.
http://www.drugs.com.
5. Saleh F. Al-Ajlouni, Kodah I. Febrile convulsions in children. Neurosciences 2000;5:1515.
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Management
of the Comatose Child
I am a brain, Watson. The rest of me is a mere appendix
Arthur Conan Doyle (18591930)*
Assessment of the Level of Consciousness
Glasgow Coma Scale (GCS)

Eye opening
Response Score
Spontaneously 4
To verbal stimuli (command, speech, or shout) 3
To pain 2
No response 1
Best verbal response

Adult response Equivalent response in Score
non-verbal children
Oriented and converses Smiles, oriented to sounds. Older 5
children use appropriate words
Disoriented, but able to answer questions Cries and consolable 4
Inappropriate words Persistent inappropriate crying or 3
screaming
Incomprehensible speech Grunts or is agitated or restless 2
No response No response 1
Best motor response

Response Score
Obeys commands 6
Purposeful movement to painful stimulus 5
Flexion/withdrawal to painful stimulus 4
Abnormal flexion, decorticate posture 3
Extensor response, decerebrate rigidity 2
No response 1
*Excerpt from The Adventure of the Mazarin Stone by Sir Arthur Ignatius Conan Doylea
Scottish physician, novelist, short story writer and poet. He became famous for the character
of detective Sherlock Holmes in his stories.
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The best verbal response category of the adult Glasgow coma scale has
been modied so that the scale becomes applicable to children who are as
yet not of the age to be able to speak (Adelaide coma scale). The total score
is the sum of the scores of three categories. The score may range from 3 to 15.
Patients with scores of 38 are said to be in coma.
AVPU Scale
AVPU scale is another simple method of recording the level of consciousness.
A Alert
V Responds to verbal commands
P Responds only to pain
U Unresponsive
Descriptive Terms that Define Levels of Consciousness
Delirium: Delirium is characterized by a state of uctuating consciousness

associated with agitation, drowsiness, incoherent speech, and disorientation.
Stupor is a state of unawareness in which the patient responds only to
shouts or painful stimuli.
Coma: The comatose patient is unresponsive to ordinary stimuli and
may have a non-purposeful response to painful stimuli. The Glasgow
coma scale is generally <8.
Vegetative state: The patient is awake, eyes are open, and give the
appearance of wakefulness but does not respond to command. Yawning,
grunting, swallowing, as well as limb and head movements may be present.
Brain death: Brain death represents a complete and irreversible loss of
brain and brainstem function. It is recognized clinically by absence of
consciousness, cranial nerve function, motor reexes, and spontaneous
breathing. EEG shows no activity. Patients who are brain dead and
maintained on mechanical ventilation and other life support systems may
continue to have cardiovascular, renal, hepatic, and respiratory functions.
Causes
The causes of coma in the postoperative period can broadly be classied

into two groups:
1. Coma with no focal neurological decit
Hypoxic encephalopathy
Drugs: sedatives, anesthetics, opioids, etc.
ERRNVPHGLFRVRUJ
Management of the Comatose Child 235
Epilepsy: status epilepticus, post-ictal states.

Metabolic derangements: hypoglycemia, hyperglycemia, hypoxemia,
hypercarbia, hyponatremia, hypernatremia, hypercalcemia,
hypothermia, hyperpyrexia, uremia, etc.
Infection: meningitis, encephalitis.
2. Coma with focal neurological decit
Particulate/air embolism
Vascular: embolism, hemorrhage (extradural, subdural,
subarachnoid, intracerebral)
Infection: brain abscess, subdural empyema
Herniation syndromes
Neurological Examination
Clinical signs of transtentorial herniation

Coma
Pupils dilated/constricted/unequal
Lateral gaze palsy
Hemiparesis
Decerebrate posture
Hypertension, bradycardia, CheyneStokes
respiration (Cushings triad)
Neurological examination of a comatose patient involves the examination

of the following:
1. State of consciousness: The level of consciousness is recorded after
evaluation by the GCS.
2. Respiratory pattern: CheyneStokes respiration is present in
lesions involving bilateral cerebral hemispheres (metabolic
disorders, hypoxia, etc.), midbrain or upper pons (as in impending
transtentorial herniation). Cushings triad is a late feature of cerebral
injury and occurs when transtentorial herniation and brain stem
compression take place. The components of the triad are (i) increased
systolic blood pressure, (ii) bradycardia, and (iii) CheyneStokes
respiration.
3. Pupillary size and reactivity: Pupils are pinpoint (<2 mm) and
non-reactive in pontine lesions, and small (23 mm) and reactive with
an overdose of some drugs (opiates, barbiturates, phenothiazines).
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Bilateral dilated and non-reactive pupils are seen after atropine use,
hypothermia and central herniation. A unilateral dilated non-reactive
pupil is caused by compression of the oculomotor nerve and is seen in
uncal herniation and lesions affecting the coronary sinus.
4. Ocular motility and papilledema: Normally, the eyes at rest are in mid
position and looking ahead. Conjugate deviation of the eyes suggests
either an ipsilateral cerebral hemispheric lesion or a contralateral
pontine lesion.
5. Ocular reexes: The oculocephalic reex (Dolls eyes movement)
is present when the eyes do not follow the movements of the head
and move in the direction opposite to head movement. It indicates
an intact brain stem. The reex is absent when the eyes follow the
direction of head movement, and is an indication of a brain stem
lesion. The oculovestibular reex is elicited by injecting cold or warm
saline (30 mL in the adult) into the external auditory meatus. If the
brain stem is intact, both eyes deviate towards the irrigated ear. This
movement is lost if the brain stem is damaged.
6. Papilledema: Raised intracranial pressure over a period of hours results
in papilledema with or without hemorrhages.
7. Motor response: The motor system is evaluated by noting the childs
posture and response to painful stimuli. The muscle tone and reexes
are evaluated. Purposeful withdrawal from painful stimuli is a sign of
cortical function and hence cortical preservation. Hemiparesis may
occur in internal capsule lesions and midbrain compression due to
uncal herniation. Decorticate posturing signies diffuse damage to the
cerebral cortex or basal ganglia, and decerebrate rigidity is a sign of
more extensive damage to the midbrain. Decorticate posture consists
of exion at the elbows and wrists with shoulder adduction and
internal rotation. The lower limbs are extended. Decerebrate rigidity
is characterized by bilateral extension of the elbows with shoulder
adduction and internal rotation and extension of the lower limbs.
Flaccidity and the absence of any motor response are suggestive of
a severe brainstem lesion.
8. Involuntary movements: Hypoxic brain damage may be a cause
of epilepsy or myoclonus. Myoclonus is sudden, brief and jerky,
involuntary movements which may be triggered by attempts at
voluntary movement, sensory stimulation, or startle in a child.
It occurs because of sudden contraction or relaxation of a muscle
group and may be associated with hypoxic brain injury and
various other neurological disorders (infection, injury, tumor,
epilepsy, etc.).
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Investigations
Investigations should include evaluation of blood gases, serum electro-

lytes, blood glucose, liver enzymes, complete and differential blood cell
count, and peripheral blood smear. Prothrombin time, INR, and activated
partial thromboplastin time are used to assess coagulation abnormalities.
Fundoscopy detects papilledema and hemorrhages.
CT Scan
A CT scan is often needed as an emergency investigation, particularly in
children with signs of raised intracranial pressure or focal neurological def-
icits. CT has high sensitivity for diagnosis of acute intracranial hemorrhage,
cerebral edema, and hydrocephalus; and moderate sensitivity for abscess
or tumor. CT may not demonstrate any ndings in hypoxic encephalopa-
thy, ischemic stroke, or a metabolic disorder.
MRI
Patients with equivocal CT ndings should undergo MRI. MRI is more
likely to detect diffuse hypoxic injury and acute ischemic stroke in addi-
tion to cerebral edema, tumor, abscess, and other inammatory processes.
MRI has a higher sensitivity for lesions not diagnosed clinically or by
CT scan.
Lumbar Puncture
Lumbar puncture (LP) is rarely indicated in the postoperative patient. It is
needed to make an early diagnosis of CNS infection and identication of
the pathogen or in suspected subarachnoid hemorrhage. Contraindications
for LP include a low GCS, focal neurological signs, presence of signs of
cerebral herniation or cardiorespiratory compromise.
Care of a Child in Coma
Cerebral perfusion pressure (CPP) is the pressure at which the brain tissue is
perfused and is denoted by the difference between the mean arterial pres-
sure (MAP) and the intracranial pressure (ICP), i.e., CPP = MAP ICP.
Normal value of CPP in adults is >70 mmHg; children >5060 mmHg;
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and infants >4050 mmHg. The normal ICP values are estimated in adults
<20 mmHg; children <18 mmHg; and infants <15 mmHg. Hypoxia, hyper-
carbia, lactic acidosis, or cerebral edema from any cause results in elevation
of ICP. ICP normally also increases with activities such as suctioning,
painful stimuli, and coughing, but returns to baseline values in a couple
of minutes. The primary goal of treatment in adult patients is to maintain
CPP >70 mmHg (or age appropriate in children) and ICP <20 mmHg (or
age appropriate in children).
Various devices that allow continuous intracranial pressure monitoring
and therapeutic CSF drainage for control of ICP are available (intraven-
tricular, subarachnoid, epidural and intraparenchymal devices).
Airway, Breathing, and Circulation

The patient is ventilated if the GCS is <8 or if there is respiratory failure.
A PaO2 >60 mmHg (oxygen saturation >90%) is maintained and mild
hyperventilation (PaCO2 3035 mmHg) is used to decrease the intrac-
ranial pressure by causing vasoconstriction and a decrease in cerebral
blood ow. Excessive hyperventilation (PaCO2 <30 mmHg) is not advis-
able as it may cause severe vasoconstriction and exacerbation of the cer-
ebral ischemia. It may however be utilized as a therapeutic measure in
case of refractory intracranial hypertension or impending herniation. Age-
appropriate blood pressure must is maintained with vasodilators/vasopres-
sors so that the CPP is adequate and further ischemia is avoided.
Positioning
The head end of the bed is elevated 15 to 30 degrees to encourage jugu-
lar venous drainage. Flexion, extension or rotation of the head and neck
are avoided as these increase the ICP. Passive limb exercises and frequent
change of position to relieve pressure areas are instituted.
Analgesia and Sedation

Children in coma who are mechanically ventilated should receive appro-
priate analgesia and sedation to prevent pain and anxiety, which will
increase the ICP. Additional sedation and analgesia is administered prior
to any procedure (e.g., endotracheal suction) that may cause stimulation.
If the child presents with a seizure, initial treatment with a benzodiazepine
(e.g., lorazepam) should be followed by appropriate antiepileptic medica-
tion (e.g., phenytoin, fosphenytoin).
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Fluids, Electrolytes, and Nutrition

The aims of uid therapy are to maintain euvolemia and normoglycemia,
and prevent hyponatremia. Maintenance uid consists of normal saline
with the addition of the daily requirement of potassium chloride based on
body weight. All uids administered must be isotonic. Hypotonic uids
and hyponatremia will cause uid shifts into the brain and worsen the cer-
ebral edema. Dextrose is not administered for the rst 4872 hours unless
the patient is hypoglycemic, due to the increased risk of lactic acidosis.
Hyperglycemia is treated with insulin therapy, and early nasogastric enteral
feeding is started.
Osmotic Diuresis
Mannitol decreases ICP by two mechanisms; rstly, it decreases blood vis-
cosity thus increasing cerebral blood ow, and secondly, by increasing the
osmolality of blood it draws uid from the brain tissue into the vascular
space, to be excreted by diuresis. Mannitol is administered in a dose of
0.250.5 g/kg IV over 20 minutes and is repeated every 26 hours. A higher
initial dose (0.51 g/kg) may be administered for a more rapid reduction
of ICP. Its onset of action is after 1530 minutes, and the effect lasts 46
hours. CVP, serum electrolytes, and osmolality are monitored during ther-
apy, and IV maintenance uids are administered to maintain CVP and pre-
vent a rise in serum osmolality to unacceptable levels (<320 mOsm/L for
mannitol). Mannitol is discontinued after a period of 4872 hours and
on termination of therapy, the dose is gradually reduced because of the
inherent danger of rebound rise of ICP. Other complications of mannitol
include hypotension, hypokalemia, hemolysis, and renal failure.
3% hypertonic saline (HS) has been used as an alternative to mannitol
for osmotic therapy in children. It is administered as a continuous infu-
sion, in a dose of 0.11.0 mL/kg/h. The dose is titrated to achieve a serum
sodium level of 145155 mmol/L. Serum sodium and serum osmolality
are monitored q24h till target sodium level is reached and then q12h. The
maximum acceptable level of serum osmolality for HS is 360 mOsm/L.
Hypertonic saline has been continued for up to 7 days, and therapy is dis-
continued gradually so that the rate of decrease of serum sodium level is
<0.5 mmol/h because of the danger of pontine demyelination. Other com-
plications of hypertonic saline include volume overload and pulmonary
edema, cardiac failure, renal failure, hypokalemia, hyperchloremic acidosis
and rebound increase in ICP.
Other agents:
Inj. furosemide (1 mg/kg q8h) has sometimes been administered
empirically by itself or in combination with mannitol.
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Steroids are not indicated in ischemic and hemorrhagic brain lesions,

and its use remains debatable in head injury. Dexamethasone is
administered in meningitis, brain tumors, and following neurosurgery
to reduce cerebral edema. It is the preferred steroid due to its low
mineralocorticoid activity. (Dose: 1 mg single dose is followed by
11.5 mg/kg/day in divided doses q6h IV/IM/PO (max 16 mg/day) for
5 days and then tapered over a period of 5 days).
Supportive Care
Fever is associated with a rise in ICP and is managed with antipyretics and
cooling. Regular eye and oral care is instituted.
Bibliography
1. Hopp RL, Ford WJA, OConnor SJ. The care and nutrition of patient in prolonged coma. Am J
Clin Nutr 1956;4:625.
2. James H, Trauner D. The Glasgow coma scale. In: James H, Anas N, Perkin R, eds. Brain Insults
in Infants and Children: Pathophysiology and Management Orlando: Grune and Stratton;
1985:17982.
3. Khanna S, Davis D, Peterson B, et al. Use of hypertonic saline in the treatment of severe refrac-
tory posttraumatic intracranial hypertension in pediatric traumatic brain injury. Crit Care Med
2000;28:114451.
4. Maiese K. Stupor and coma. The Merck Manuals: Online medical library. [Updated: 2008 Feb;
cited: 2011 Apr 29] Available at: http://www.merckmanuals.com/home/au/sec06/ch084/
ch084a.html#
5. Marcoux KK, LeFlore J. Management of increased intracranial pressure in the critically ill child
with an acute neurological injury. AACN Advanced Critical Care 2005;16:21231. Available at:
http://www.nursingcenter.com/library/JournalArticle.asp?Article_ID=594176.
6. Ramesh S. Paediatric intensive care update. Indian J Anaesth 2003;47:33844.
7. Sankhyan N, Vykunta Raju KN, Sharma S, Gulati S. Management of raised intracranial pressure.
Indian J Pediatr 2010;77:140916.
8. Tang A. Approach to a child with altered consciousness. [Cited: 2011 Apr 29] Available at:
http://www.kairos2.com/50_Child%20with%20altered%20consciousness.pdf.
9. Yildizdas D, Altunbasak S, Celik U, Herguner O. Hypertonic saline treatment in children with
cerebral edema. Indian Pediatr 2006;43:7719.
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Acute
Kidney Injury
These circumstances are wholly exceptional.
Desperate diseases, they say, call for desperate remedies
Anthony Wynne (18821963)*
The term acute renal failure (ARF) has now been replaced by the term
acute kidney injury (AKI) and involves the entire spectrum of renal dis-
ease associated with decreasing renal function. The spectrum extends from
less severe forms of injury to the point of renal failure when the patient
requires renal replacement therapy.
Predisposing Factors
Low cardiac output is the foremost predisposing cause. In the event of

systemic hypotension, children on drug therapy with ACE inhibitors,
indomethacin, aminoglycosides, and NSAIDs are more susceptible to AKI.
Hypoxemia, acidosis, sepsis, and hypothermia are all associated with
renal vasoconstriction, a decrease in the glomerular ltration rate (GFR),
and a fall in urine output.
Additional risk factors include young age, complex cardiac lesions, and
prolonged cardiopulmonary bypass and circulatory arrest times.
The mechanism of AKI because of ischemia comprises of two phases: (i) prere-
nal failure when the GFR is depressed by renal vasoconstriction but the tubular
structure is normal and restoration of renal blood ow will return renal func-
tion to normal, and (ii) the stage of acute tubular necrosis (ATN).
Urinary Indices to Distinguish Established ARF from

Prerenal Azotemia
Laboratory test Prerenal azotemia ARF

Urinary osmolality (mosm/kg) >500 <400
Urinary sodium level (mmol/L) <20 >40
*Anthony Wynne was an English physician and author. This excerpt is taken from his Toll
House Murder, published by J. B. Lippincott Company (1935).
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Laboratory test Prerenal azotemia ARF

Urine/serum creatinine ratio >40 <20
BUN/serum creatinine ratio >20 <10
Fractional excretion of sodium (FENa) <1% >2%
Fractional excretion of urea (FEUN) <35% >35%
Urinary sediment Normal occasional hyaline Renal tubular epithelial
or fine granular casts cells, granular and
muddy brown casts.
FENa is calculated as: [(urine sodium/plasma sodium)/(urine creatinine/plasma creatinine)] 100.
FEUN is calculated as: [(urine urea nitrogen/blood urea nitrogen)/(urine creatinine/plasma creatinine)] 100.
ARF (AKI) Biomarkers
Currently, a number of urinary and serum biomarkers that reect AKI are
under investigation. These predict the onset of AKI 2448 hours before the
elevation of serum creatinine becomes evident. Increased levels of cystatin C
(normal blood level in age >1 yr: 0.81 mg/L) are present in serum; ele-
vated levels of interleukin-18 (IL-18) and kidney injury molecule-1 (KIM-1)
are found in the urine; and elevated levels of neutrophil gelatinase associated
lipocalin (NGAL) are present in the serum and urine of patients with AKI.
Estimation of Glomerular Filtration Rate in Children
Glomerular ltration rate is the amount of water ltered by the kidney

every minute and is the most physiological indicator of renal function. It is
estimated by the fact that if a substance x is removed from the blood only
by renal ltration and is neither secreted nor reabsorbed then the volume
of blood plasma that is cleared of this substance x per minute is a reec-
tion of the GFR. A number of substances have been used to measure the
GFR, viz. inulin, creatinine, iohexol, cystatin C, etc.
Creatinine clearance is the volume of blood plasma that is cleared of
creatinine per minute. It is about 1015% more than inulin clearance
because creatinine is ltered and secreted in the urinary tubules unlike
inulin, which is only ltered.
Cx = Ux V/Px
Cx is the renal clearance (mL/min) of substance x,
V is the rate of urine ow (mL/min),
Ux is the concentration of substance x in urine, and
Px is the concentration of substance x in plasma.
ERRNVPHGLFRVRUJ
Acute Kidney Injury 243
Normal range of creatinine clearance in males is 90130 mL/min/1.73 m2;

in females it is 80125 mL/min/1.73 m2. (Adult values of GFR are reached
by about 2 years of age and decrease by 6.5 mL/min for every 10 years after
the age of 20).
Since these methods for the measurement of GFR are not clinically fea-
sible, various formulae based on the serum creatinine levels are utilized to
give an estimate of the GFR.
As an approximation, changes in serum creatinine (Se creatinine) level
correlate with changes in GFR as follows:
Se creatinine of 1 mg/dL is normal for an individual with a GFR of
100 mL/min.
Se creatinine of 2 mg/dL reects a 50% reduction in GFR (50 mL/min).
Se creatinine of 4 mg/dL reects a 75% reduction in GFR (25 mL/min).
Se creatinine of 8 mg/dL reects a 9095% reduction in GFR
(12.5 mL/min).
Various formulae based on serum creatinine levels have been devised to
estimate the GFR. The Schwartz and CounahanBarratt formula for esti-
mating the GFR in children use height in the estimate, as height is propor-
tional to muscle mass.
(a) Schwartz equation (Patient population: 1 week to 18 year old):
CrCl (mL/min/1.73 m2) = [Height (cm) K]/Se creatinine
K = 0.45 for infants 152 weeks old;
K = 0.55 for infants 113 year old;
K = 0.55 for adolescent females 1318 year old;
K = 0.70 for adolescent males 1318 year old.
(b) CounahanBarratt equation:
GFR (mL/min/1.73 m2) = [0.43 Length (cm)]/Se creatinine
(c) CockcroftGault equation (Applicable to adult patients):
GFR (mL/min) = (140 Age [yr]) (Weight [kg])/(72 Se creatinine
[mmol/L])
(For female patients, the calculated GFR is multiplied by a factor of 0.85).
Stratification of AKI
International consensus panel described the RIFLE criteria for AKI in 2002,
which were later modied in 2007 using the Acute Kidney Injury Network
(AKIN) criteria. RIFLE criteria dened three levels of increasing severity
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(Risk, Injury, and Failure) and two outcomes (Loss and End-stage kidney disease
based on changes in serum creatinine or urine output).
RIFLE Creatinine criteria Urine output criteria

R - Risk Creat >1.5 or GFR loss >25% <0.5 mL/kg/h for 6 hours
I - Injury Creat >2 or GFR loss >50% <0.5 mL/kg/h for 12 hours
F - Failure Creat >3 or GFR loss >75% <0.3 mL/kg/h for 24 hours or anuria
Creat >4 mg/dL for 12 hours
L - Loss Persistent failure >4 weeks
E - End stage Persistent failure >3 months
p RIFLE*
R - Risk eCCl loss >25% <0.5 mL/kg/h for 8 hours
I - Injury eCCl loss >50% <0.5 mL/kg/h for 16 hours
F - Failure eCCl loss >75% or <0.3 mL/kg/h for 24 hours or anuria
eCCl <35 mL/min/1.73 m2 for 12 hours
L - Loss Persistent failure >4 weeks
E - End stage Persistent failure >3 months
AKIN
modification
Stage 1 Creat >1.5 or >0.3 mg/dL <0.5 mL/kg/h for 6 hours
from baseline
Stage 2 Creat >2 <0.5 mL/kg/h for 12 hours
Stage 3 Creat >3 or <0.3 mL/kg/h for 24 hours or anuria
Creat >4 mg/dL with an acute for 12 hours
>0.5 mg/dL
*pRIFLE: pediatric RIFLE criteria.
GFR: glomerular filtration rate, Creat: serum creatinine, eCCl: estimated creatinine clearance by the Schwartz formula.
Presentation
Acute kidney injury may present as either one of these two types: (i) olig-
uric form when there is an increasing blood urea nitrogen (BUN) and
serum creatinine with oliguria (urine output <0.5 mL/kg/h); or (ii) non-
oliguric form where the rise in BUN and serum creatinine is not associated
with a fall in urine output. With an increasing BUN, symptoms of uremia
become evident, viz., anorexia, nausea, vomiting, confusion, lethargy,
somnolence, seizures, and pruritus.
Fluid overload and electrolyte abnormalities make these AKI patients
more susceptible to cardiovascular (e.g., CHF, arrhythmias, cardiac arrest)
and pulmonary (pulmonary edema and hypoxia) complications. Other
complications that may occur include GI bleeding, jaundice, coagulopa-
thies, and sepsis.
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Laboratory Investigations in AKI
Urinalysis
Microscopic examination of urine is essential in the differential diagnosis
of AKI. Normal urinary sediment without casts or cells is generally consis-
tent with prerenal and postrenal causes of AKI. Granular casts are present
in ATN, glomerulonephritis, and interstitial nephritis, while RBC casts are
present in glomerulonephritis, and WBC casts indicate pyelonephritis.
BUN
The normal level of BUN in children and adults is in the range of 520
mg/dL (<2 yr, 415 mg/dL). BUN correlates poorly with the GFR. In prere-
nal conditions (e.g., low cardiac output), low urine ow rates allow increased
BUN reabsorption, which results in a disproportionate rise of BUN relative
to creatinine, resulting in a serum BUN/creatinine ratio >20. Plasma BUN/
creatinine ratio <1015 is suggestive of ATN (normal BUN:creatinine ratio
1020:1). BUN may also rise signicantly as a result of increase in urea pro-
duction with steroids, trauma, or GI bleeding.
Serum Creatinine
Serum creatinine reects the creatinine clearance and is a good measure for
approximating the GFR. Normal serum creatinine level is 0.51.5 mg/dL
(children and adults). Creatinine levels are lower in young children and
the elderly because of less muscle mass.
Serum Electrolytes
The electrolyte ndings that may be present in AKI include metabolic
acidosis, hyperkalemia, hyperphosphatemia, hypocalcemia, hypermag-
nesemia, and hyperurecemia.
Hematology
AKI may be associated with anemia and abnormal coagulation studies.
Imaging
Renal ultrasound in established ATN shows increased echotexture and loss
of corticomedullary differentiation.
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Treatment of Prerenal Failure
Accurate measurement of volume state with CVP monitoring is mandatory.

During the stage of prerenal failure, i.e., prior to the onset of ATN, urine
output may be restored by correction of the volume status and administra-
tion of diuretics.
Fluid challenge: 510 mL/kg of colloid or crystalloid is given over
3060 minutes to correct the CVP. Careful monitoring is mandatory
as administration of excessive volume in a patient who is unable to
excrete the extra uid may result in volume overload and pulmonary
edema.
Frusemide: Inj. frusemide 13 mg/kg IV stat is administered and can
be repeated after 24 hours to a maximum dose of 510 mg/kg. A
continuous frusemide infusion (0.10.2 mg/kg/h) may be preferred as
an alternative to the bolus injection.
Dopamine: A dopamine infusion may be started in a low dose
primarily for its dopaminergic effect or in higher doses as an inotrope
(510 mcg/kg/min) to increase the mean arterial pressure.
Mannitol: Mannitol causes an osmotic diuresis and is also capable of
scavenging free radicals. It is administered in a dose of 0.5 g/kg
(2 mL/kg of 25% solution) over 2030 minutes (adult dose: 100 mL
of 25% mannitol). Mannitol needs to be administered with caution as it
can precipitate pulmonary edema in a patient with established ATN.
Peritoneal Dialysis and Renal Replacement Therapy
Indications
Peritoneal dialysis (PD) or renal replacement therapy (RRT) is required
in patients with severe kidney injury to remove excess uid and correct
or prevent various associated electrolyte and metabolic abnormalities.
Indications include the following:
1. Increasing Se creatinine levels with clinical signs of uid overload,
hyperkalemia (serum potassium >5.5 meq/L), persistent metabolic
acidosis or low cardiac output syndrome.
2. Prophylactic peritoneal dialysis has been used as a measure to prevent
uid overload in postoperative children with oliguria (e.g., urine
output <1 mL/kg/h for a couple of hours). It may also be considered
with long CPB (>90 min) or circulatory arrest time (>60 min) or if
there has been a persistent intraoperative oliguria/anuria.
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Peritoneal Dialysis
Initial PD Prescription
Parameter Recommended Remarks

prescription
Dextrose 1.7% Increasing dextrose concentration increases ultrafiltration
concentration of fluids and clearance of urea and creatinine.
Volume 10 mL/kg Increasing fill volumes also improves ultrafiltration and
(1030 mL/kg) clearance of urea and creatinine.
Dwell time 45 minutes Decreasing the dwell time (rapid cycles) improves
potassium removal, while longer dwell times improve urea
and creatinine clearance.
The advantages of PD compared to various modalities of RRT include ease

of application, avoidance of anticoagulation, and there is no requirement
of vascular access for administration.
Initial Prescription
Peritoneal dialysis is commenced with a dextrose concentration of 1.7%
(standard dialysis uid), dwell volume 10 mL/kg and continuous 1 hour
cycles (inow time: 5 minutes, dwell time: 45 minutes, and outow time:
10 minutes). To start with, three or more rapid in and out runs are car-
ried out to establish a free ow in the catheter and to clear the dialysate of
any blood. If the drain is still blood stained, 500 U/L of heparin is added
to the dialysis uid to prevent clotting till the drain clears. Potassium is
also added to the PD uid (24 meq/L) once hyperkalemia has been
corrected.
Dextrose Concentration
To improve uid output, the dextrose concentration of the dialysis
uid may be increased. Initially, alternate hypertonic glucose exchanges
(1.7% and 3%) can be used and then if required a higher concentration
of dextrose is used for all exchanges. A 3% dialysis solution is prepared
by adding 26 mL of 50% dextrose to 1 liter of 1.7% dextrose. The general
principle is to start with the lowest concentration of glucose with stepwise
increments if required.
Dwell Time
Short dwell time cycles remove electrolytes (K, Na, etc.) more rapidly.
Short cycles (30 minutes) are considered initially if hyperkalemia needs
ERRNVPHGLFRVRUJ
urgent treatment. Longer dwell times (up to 2 hours) improve clearance of

urea and creatinine.
Volume
Higher inow volumes increase the amount of uid removed and also the
clearance of urea and creatinine. Larger volumes may, however, cause res-
piratory distress by pushing the diaphragm up and also alter the cardiac
lling pressures resulting in hemodynamic compromise. PD is initially
started with an inow volume of 10 mL/kg, which is increased only if this
is well tolerated and there is need to remove higher volumes.
Hyperglycemia
Frequent cycles of 3% solution or presence of sepsis may cause hyperglyc-
emia leading to hyperosmolarity and loss of effective ultraltration. An ele-
vated BSL should be treated with IV insulin (0.10.2 U/kg IV). The blood
sugar level is checked regularly (q612h), and the dose repeated as required.
Feeding
Patients on dialysis can continue with oral or nasogastric tube feeding. If
enteral feeding is not tolerated, TPN is employed and a nasogastric tube is
left in situ to prevent vomiting.
Monitoring
Peritoneal dialysis is generally discontinued after 4572 cycles and if
indicated, it is restarted after 48 hours. Adequacy of PD is assessed by the
clinical status of the patient, the uid output achieved (a net output of 50
mL/kg/day may be adequate), and regular monitoring of the urea, creati-
nine, and bicarbonate levels. Low cardiac output states and oxygenation
needs to be managed appropriately as commercially available dialysis u-
ids contain lactate, and hypoxic babies may be unable to metabolize lactate
resulting in a worsening of the acidosis.
Renal Replacement Therapy
Renal replacement therapy is a more efcient method of uid removal and

urea and creatinine clearance compared to PD. Intermittent or continuous
methods of RRT may be employed.
Intermittent Hemodialysis
Intermittent hemodialysis is the standard form of intermittent renal
replacement therapy. Solute removal in dialysis is by process of diffusion
ERRNVPHGLFRVRUJ
of solutes from blood to dialysis uid across a semipermeable membrane

of a low permeability dialysis lter. This effectively removes small (e.g.,
electrolytes) and small to mid size molecular weight solutes (e.g., glucose,
urea, creatinine). The pore size limits the ability to diffuse larger mol-
ecules. The major disadvantage of the procedure in the cardiac patient is
the associated hemodynamic instability because of rapid uid shifts over a
short period of time.
Continuous Renal Replacement Therapy

Continuous renal replacement therapy (CRRT) is thought to be more
physiological and allows greater control over the amount of uid or elec-
trolytes to be removed. There are a number of modalities of instituting
continuous renal replacement therapy, which include (i) arterio-venous or
veno-venous SCUF (slow continuous ultraltration), (ii) CAVH (continuous
arterio-venous hemoltration), (iii) CVVH (continuous veno-venous hemo-
ltration), (iv) CVVHD (continuous veno-venous hemodialysis), (v) CVVHDF
(continuous veno-venous hemodialtration).
Replacement
Access Return
Hemofilter
Pump
Effluent
Fig. 1: Circuit for CAVH.
ERRNVPHGLFRVRUJ
When arterio-venous cannulation is used (arterio-venous SCUF, CAVH),

the mean arterial pressure provides the pressure for the blood to be driven
through the lter, and no external pump is required. In a veno-venous cir-
cuit (veno-venous SCUF, CVVH, CVVHD, CVVHDF), an external pump is
required to drive the blood through the lter. A controlled veno-venous
circuit permits better control of blood ow and allows more hemody-
namic stability.
CAVH (Fig. 1)
CAVH is a form of CRRT in which an extracorporeal circuit originates
from an artery and terminates in a vein, and the arterial pressure drives the
blood through a highly permeable lter. A pump in the efuent line of the
circuit is used to control the amount of uid removal. High rate of uid
removal permits removal of solutes by the associated process of convec-
tion. The ultraltrate produced is replaced in part or completely with an
appropriate replacement solution to achieve the optimum quantity of uid
and solute removal.
Replacement
Access Return
Hemofilter
Effluent
Fig. 2: Circuit in CVVH.
ERRNVPHGLFRVRUJ
CVVH (Fig. 2)
In CVVH, the extracorporeal circuit originates from a vein and terminates in
a vein, and the blood is driven through a highly permeable lter by means
of a pump on the inow side of the lter, which permits ltration of high
uid volumes. In CVVH, like in CAVH, solutes are removed by the process
of convection, associated with high rate of uid removal. The ultraltrate
produced is replaced in part or completely with an appropriate replacement
solution in order to maintain hemodynamics and electrolyte balance.
SCUF (Fig. 3)
SCUF is a form of CAVH or CVVH in which a very slow rate of uid
removal is permitted, and this process removes only excess water.
Slow ultraltration in SCUF does not result in removal of solutes and
no replacement of uid is done as in CAVH or CVVH. SCUF is often used
in the management of refractory edema with or without renal failure.
CVVHD (Fig. 4)
In CVVHD, the extracorporeal circuit originates in a vein and terminates in
a vein and is driven by a pump. The assembly utilizes a low permeability
dialyzer with a countercurrent dialyzer ow, which results in clearance of
Access Return
Hemofilter
Pump
Effluent
Fig. 3: Circuit for arterio-venous SCUF. Veno-venous SCUF requires a pump in the
inflow limb of the filter.
ERRNVPHGLFRVRUJ
Dialysate
Access Return
Hemofilter
Effluent
Fig. 4: Circuit in CVVHD.
solute by diffusion as in intermittent hemodialysis. No uid replacement

is done.
CVVHDF (Fig. 5)
CVVHDF is a form of CRRT in which the CVVH circuit is modied by
the addition of slow, countercurrent dialysate ow into the ultraltrate-
dialysate compartment of the hemolter. The high permeability lter
results in the removal of high volumes of uids by ltration and elimina-
tion of solutes by convection and diffusion. Fluid replacement is adminis-
tered as clinically indicated in part or completely to replace uid losses.
The modalities of CRRT most frequently used in infants and children
with post heart surgery AKI are CVVH and CVVHDF.
Guidelines for CVVH

<10 kg 1020 kg >20 kg
Blood flow (mL/min) 50 80 150
Predilution flow 200400 300650 6001000
(mL/h)*
Maximum ultrafiltrate 750 1200 2250
removal (mL/h)
*Replacement fluid administered in the inflow limb of the filter.
ERRNVPHGLFRVRUJ
Replacement Dialysate
Access Return
Hemofilter
Effluent
Fig. 5: Circuit for CVVHDF.
The extracorporeal circuit requires adequate central venous access (femoral,

internal jugular, subclavian), usually via a double lumen catheter, to allow
high blood ows. Recommended catheter sizes in French gauge (F) are:
Patient size (kg) Vascular access (double lumen)

Neonate 5F
2.510 6.5 F (10 cm)
1020 8 F (15 cm)
>20 10.8 F or larger (20 cm)
Blood is removed from the patient through the distal port of a double
lumen venous catheter and returned through the proximal port.
Depending upon the negative balance required and at the same time to
prevent sudden volume depletion, the ltration rate is controlled and
some uid is replaced. The replacement uid is isotonic, and bicarbonate
or potassium may be added depending on the biochemical prole of the
patient. To decrease blood viscosity and prevent the lter from blocking,
replacement uids are generally infused on the inow side of the lter
(predilution ow).
Heparinization is needed and is infused into the inow port of the
lter. The recommended dose of non-fractioned heparin is 3050 U/kg
ERRNVPHGLFRVRUJ
(0.30.5 mg/kg) bolus followed by continuous infusion of 1020 U/kg/h

(0.10.2 mg/kg/h). Activated coagulation time is maintained in a range of
170200 s.
In patients at the risk of bleeding, the heparinization should be reduced
or omitted. Platelet count needs to be monitored twice a day because of
the high risk of thrombocytopenia in patients on CVVH, and the electro-
lyte status is monitored 46 hourly.
Bibliography
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ERRNVPHGLFRVRUJ
Coagulation Disorders
in the Postoperative Period
The only weapon with which the unconscious patient can
immediately retaliate upon the incompetent surgeon is hemorrhage
William Stewart Halsted (18521922)*
Normal Hemostasis
Intrinsic pathway
Factor XII XIIa
Factor XI XIa
Extrinsic pathway
Factor VII + tissue factor

Factor IX IXa
Factor VIIIa
Phospholipid
Calcium ions
Factor X Xa Factor X
Factor Va
Phospholipid
Calcium ions
Prothrombin Thrombin
Fibrinogen Fibrin
Fig. 1: Coagulation pathway.
The mechanism of normal coagulation involves three processes:

1. Primary hemostasis: When a vessel is injured, platelets aggregate at the
injured site to form a platelet plug.
2. Secondary hemostasis: During secondary hemostasis, a brin clot
forms and stabilizes the platelet plug. This brin clot is formed via two
*William Stewart Halsted was an American surgeon, and an early advocate of aseptic surgical
technique. He introduced several new operations in surgery, including radical mastectomy for
breast cancer.
ERRNVPHGLFRVRUJ
Coagulation Disorders in the Postoperative Period 257
concurrent pathways, which converge into a common pathway that

leads to the formation of the brin clot.
(a) The intrinsic coagulation pathway involves sequential activation of
factors XII, XI, IX and VIII.
(b) The extrinsic coagulation pathway requires the interaction of factor
VII and tissue factor released from injured endothelial tissues,
which in turn activate factor X in the common pathway.
(c) Common pathway: The intrinsic and the extrinsic pathways
converge into a common pathway of factors X, V and II
(prothrombin), which leads to the formation of factor IIa
(thrombin). This thrombin then cleaves brinogen (factor I) to
form brin monomers, which get cross-linked via the action of
factor XIIa to bind into a brin clot.
3. Fibrinolysis (degradation of the brin clot and restoration of normal
blood ow): The role of the brinolytic system is to restore blood ow
through the healed vessel by lyses of the brin clot. Plasminogen is
activated to plasmin by (i) kallikrein generated by the intrinsic coagulation
pathway, (ii) tissue plasminogen activator released from the injured
endothelial cells, and (iii) urokinase produced by kidney endothelial
cells. Plasmin then degrades the brin clot and brinogen into brinogen
degradation products (FDPs). Whether brin or brinogen is degraded by
plasmin, the FDPs are the same, with the exception of D-dimer, which is
produced only with the degradation of brin.
Coagulation Studies
Activated Partial Thromboplastin Time

Activated partial thromboplastin time (APTT) identies abnormalities of
the intrinsic system and the common pathway and is utilized to moni-
tor the level of anticoagulation in patients on heparin. Prothrombin time
detects abnormalities of the extrinsic and common pathway and is used to
monitor the effect of oral anticoagulants. In normal doses, heparin causes
a prolongation of the APTT because of its action on the intrinsic pathway,
but has no signicant effect on the prothrombin time (PT). In larger doses,
heparin however, does cause a prolongation of the PT by its effect on the
common and extrinsic pathways. When a patient receives heparin, the tar-
get APTT is generally kept 1.52.5 times the control APTT. During initia-
tion of anticoagulation, when the patient is concurrently receiving heparin
and warfarin, the effect of heparin can be monitored with APTT and that
of warfarin by PT.
ERRNVPHGLFRVRUJ
Prothrombin Time
Prothrombin time detects abnormalities of the extrinsic and common
pathways (factors VII, X, V, II and I). It is used to monitor the level of anti-
coagulation in patients prescribed warfarin for anticoagulation. Warfarin
initiates anticoagulation by inhibition of vitamin K dependent clotting
factors (factors II, VII, IX, and X) by its action on vitamin K. Warfarin
also prolongs the APTT in higher doses, but in patients stabilized on
long-term warfarin therapy, the APTT may be prolonged only by a few
seconds.
International Normalized Ratio

International normalized ratio (INR) is the ratio of patients PT divided
by control PT to which a correction factor called International Sensitivity
Index (ISI) has been applied. The ISI is supplied with each batch of rea-
gent for doing the PT, as the sensitivity of different batches of commercial
thromboplastin reagents is variable and the PT value changes with every
batch of reagent used for the test. The INR overcomes this problem and
allows comparison of the level of anticoagulation irrespective of the per-
formance of the reagent used.
INR = (PT patient/PT normal)ISI

PT patient = patients prothrombin time (seconds)
PT normal = mean value for normal patients (seconds)
ISI = International Sensitivity Index
An INR of 1 implies normal clotting, and an INR of 3 means the blood

takes about three times as long to clot compared to the control. An INR
of 2.53.5 is recommended for normal mechanical valves. The therapeu-
tic range of INR for various disorders represents the level at which therapy
should be effective with the least risk of bleeding.
Thrombin Time
The thrombin time (TT) tests the ability of thrombin to convert brinogen
to brin. A prolonged TT is caused by hypobrinogenemia, accumulation
of FDPs, or the presence of heparin. However, it is a relatively insensi-
tive test (detectable prolongation requires brinogen level <75 mg/dL or
FDPs >200 mcg/mL), and with availability of other tests to measure FDPs
and D-Dimer, this test is of little practical utility.
ERRNVPHGLFRVRUJ
Platelet Count
Normal platelet count in children is 150,000450,000/mm3. Thrombo-
cytopenia is dened as a platelet count of <150,000/mm3. With normal
platelet function, thrombocytopenia is unlikely to cause bleeding unless
the count is <50,000/mm3.
A number of drugs cause platelet dysfunction and include aspirin,
clopidogrel, non-steroidal anti-inammatory drugs, and IIb/IIIa inhibi-
tors. Aspirin needs to be discontinued for 57 days for recovery of normal
platelet function.
Bleeding Time
Bleeding time checks the efciency of the vascular and platelet phases of
hemostasis. The normal bleeding time is 19 minutes depending on the
method used (13 minutes with Dukes needle prick method on the nger-
tip or earlobe). Prolongation of bleeding time occurs in severe thrombocy-
topenia or in functional platelet disorders.
Fibrinogen Degradation Products

Fibrinogen degradation products are the breakdown fragments of brin
and brinogen by the action of plasmin on the blood clot. Normal serum
level of FDPs is 2.12.7 mcg/mL and values of >10 mcg/mL are signicant.
False positives are observed after exercise, in individuals under stress, in
patients with liver disease or infection, and during pregnancy.
D-dimer
D-dimer is the breakdown fragment of brin by the action of plasmin.
Normal values are <0.5 mcg/mL, and a positive D-dimer (values >1.0 mcg/mL)
can be seen in patients with DIC, deep venous thrombosis, pulmonary
embolism, neoplasms, liver disease, inammatory disorders, as well as
after surgery.
Fibrinogen
Normal blood brinogen level is 200400 mg/dL. Patients who have dys-
brinogenemia or hypobrinogenemia (<150 mg/dL) with active bleeding
require cryoprecipitate to restore the brinogen level.
ERRNVPHGLFRVRUJ
Activated Clotting Time

The activated clotting time (ACT) is a modication of the whole blood
coagulation time. It qualitatively assesses the anticoagulation effect of
heparin and is used to titrate the dose of heparin on cardiopulmonary
bypass (CPB). The normal ACT value is 100140s and increases in a lin-
ear fashion with increasing heparin concentration. ACT is also inuenced
by many other factors besides heparin, such as hypothermia, hemodilu-
tion, thrombocytopenia, aprotinin, and depletion of coagulation factors
(especially brinogen). Thus, additional protamine to reverse the effect of
heparin may not necessarily return the ACT to its baseline value. The ini-
tial heparin dose for bypass is 300400 U/kg body wt, and the ACT target
value is 480s. The ACT is checked every half hour and maintained between
450s and 500s by repeated doses of heparin.
Causes of Post CPB Bleeding
Postoperative bleeding following CPB can be a result of a number of

hemostatic derangements. The important causes of this bleeding are:
Inadequate heparin reversal

Thrombocytopenia or platelet dysfunction because of hemodilution,
activation by the CPB surfaces, or hypothermia
Decrease in plasma coagulation factors
Isolated primary brinolysis
Disseminated intravascular coagulation.
Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC) is an uncontrolled acti-
vation of the coagulation system with widespread formation of micro-
thrombi. This is associated with an accelerated plasmin degradation of
brin clots and circulating brinogen. The consumption of the coagu-
lation factors and platelets results in generalized bleeding from nee-
dle puncture, surgical and wound sites. In addition to the bleeding, the
patient presents with acute features of various organ dysfunction including
fever, hypoxia, hypotension, acidosis, and acute kidney injury because of
thrombi formation in the microvascular circulation.
The most common cause of DIC is sepsis, but it can be triggered by a mul-
titude of factors including prolonged CPB and massive blood transfusion.
ERRNVPHGLFRVRUJ
A slow chronic form of DIC can also occur and is associated with micro-
thrombi formation but not generalized bleeding, as there is time for regen-
eration of coagulation factors.
Investigations
The recommended coagulation prole of patients with DIC includes
D-dimer (ELISA), antithrombin III, and alpha-2-plasmin inhibitor levels.
These tests are early indicators of consumption and increased brinolysis,
while PT, APTT, and brinogen levels usually change more slowly:
The PT, APTT, and TT will all be prolonged.
The platelet count is low.
Fibrinogen level is decreased and FDPs and D-dimer are elevated
because of increased brinolysis and brinogenlysis.
Plasma level of antithrombin III and 2-antiplasmin are decreased.
Plasma levels of thrombin-antithrombin complexes (TAT) and plasmin-
antiplasmin complexes (PAP) are increased. Elevated TAT levels are a
marker of increased thrombin formation and PAP levels of brinolysis.
Schistocytes and microspherocytes may be present in the peripheral
blood due to microangiopathic hemolysis in 1020% of patients with
DIC.
Serial results of coagulation studies more reliably indicate a consumptive
process than does a random result.
Management
Patients are treated with appropriate antibiotic therapy for sepsis or man-
aged for any other precipitating event. Replacement therapy is required
for coagulation factors (fresh frozen plasma or cryoprecipitate), platelets
(platelet concentrate), and red cells (packed cells) to restore all consumed
blood components.
The use of heparin therapy remains controversial. Low-dose subcutane-
ous or IV heparin (510 U/kg/h) is indicated in the more chronic form
of DIC where clinical features of thrombosis predominate and generalized
bleeding is not a feature.
Primary Fibrinolysis
Primary brinolysis has a clinical presentation similar to acute DIC, but
the pathophysiology is different. Primary brinolysis results from primary
activation of the brinolytic pathway and formation of plasmin, while DIC
is associated with intravascular coagulation and secondary brinolysis.
ERRNVPHGLFRVRUJ
A number of pathological conditions including cardiopulmonary bypass,

liver disease, and disseminated malignancy result in the release of prote-
olytic enzymes (tissue plasminogen activator and urokinase), which acti-
vate plasminogen to form plasmin. This circulating plasmin then degrades
brinogen, brin, and factors V and VIII causing multiple coagulation
factor deciencies and bleeding.
Investigations
The coagulation proles in patients with primary brinolysis shows:
PT and APTT are normal or slightly prolonged.
Platelet count is normal since platelets are not being consumed in
primary brinolysis.
Fibrinogen levels are decreased and plasma level of FDP is increased
with normal level of D-dimer.
The plasma level of antithrombin III is normal and of 2-antiplasmin is
decreased.
Levels of TAT complexes are within normal limits, but the levels of PAP
complexes are increased.
Peripheral blood smear shows normal erythrocyte morphology, as no
microvascular hemolysis occurs.
Management
In addition to blood component replacement therapy, antibrinolytic
drugs (such as aprotinin, aminocaproic acid, or tranexamic acid) are used
to treat primary brinolysis. The diagnosis of DIC should be conclusively
ruled out before administration of antibrinolytic drugs.
Therapeutic Approach in Postoperative Bleeding
Cause PT PTTK TT Platelet Fibrinogen FDP Treatment

count
Heparin excess N N N Protamine
titrated
with ACT
Thrombocytopenia N N N /N N N Platelet
or platelet transfusion
dysfunction*
Coagulation N (except in marked N N N FFP/Cryo
factor deficiency hypofibrinogenemia)
ERRNVPHGLFRVRUJ
Cause PT PTTK TT Platelet Fibrinogen FDP Treatment

count
Primary N EACA/FFP
fibrinolysis
DIC** ++ FFP, Cryo,
platelets
*Platelet dysfunction is suggested by a normal platelet count but a prolonged bleeding time.
**D-dimers are increased only in DIC and are normal in all the above bleeding disorders.
N: normal, : increased, : decreased, FFP: fresh frozen plasma, Cryo: cryoprecipitate, DIC: disseminated
intravascular coagulation, EACA: epsilon-aminocaproic acid.
Indications for Re-exploration

In children, general guidelines for re-exploration for excessive blood loss
can be based on the total blood volume. If after neutralization of heparin,
blood loss exceeds 5% of estimated blood volume per hour for 3 con-
secutive hours or 10% in any hour, it is an indication for re-exploration.
Coagulation tests are not as valuable in children as in adults for guiding
transfusion therapy. (Blood volume: Neonates 8590 mL/kg, children
80 mL/kg, adults 70 mL/kg).
Packed RBCs
Packed red cells are indicated in anemia and hemorrhage to maintain an
optimum hemoglobin level (1214 g% in cyanotics and 1012 g% in
non-cyanotics).
Fresh Frozen Plasma

Fresh frozen plasma (FFP) contains approximately 1 unit of each coagula-
tion factor per mL, and is given prophylactically as part of colloid replace-
ment. Thereafter, if bleeding is continuing, it is given in aliquots of 10 mL/kg
so that it does not cause volume overload.
Platelet Transfusion
It is the rst blood fraction indicated for postoperative bleeding follow-
ing CPB, since CPB causes platelet dysfunction. Platelet transfusion is also
considered under the following circumstances:
(i) Prophylactically post CPB in cyanotic children undergoing open heart
surgery;
ERRNVPHGLFRVRUJ
(ii) In all cases when the duration of CPB is prolonged; and

(iii) Following deep hypothermic circulatory arrest.
510 mL/kg of single donor platelets are recommended. Subsequent
transfusions are given if bleeding is continuing and the platelet count
<100,000/mm3.
Cryoprecipitate
If bleeding persists, deciency of clotting factors is the next consideration.
Cryoprecipitate contains high levels of brinogen (1 unit of cryoprecipi-
tate is 1020 mL and contains about 150 mg of brinogen) and factor VIII.
Cryoprecipitate is given in an amount that will restore plasma brinogen
levels to >100 mg/dL.
Recombinant Factor VII

Generates thrombin at the bleeding sites with the aid of tissue factor, and
factors IX and X. It also activates platelets and stabilizes the clot. It is rec-
ommended in persistent life-threatening bleeding in intravenous doses of
6090 mcg/kg every 23 hours until hemostasis is achieved.
Antifibrinolytic Agents
The antibrinolytic agents, epsilon-aminocaproic acid (EACA), tranexamic
acid, and aprotinin have been used intraoperatively and postoperatively to
reduce bleeding following cardiac surgery. EACA and tranexamic acid have
lesser adverse effects and are currently preferred alternatives to aprotinin,
which has been associated with an increased risk of renal failure, cardiac
failure, and encephalopathy.
Dose
EACA has been recommended as an IV infusion in a loading dose of
75150 mg/kg given at induction followed by an infusion of 1530 mg/
kg/h or alternatively, as an intermittent therapy in a dose of 100 mg/kg each
given at induction, in the CPB prime and at the time of weaning from CPB.
Tranexamic acid is administered in a dose of 10 mg/kg IV after induc-
tion followed by an infusion of 1 mg/kg/h for 10 hours or alternatively as
three intermittent doses of 10 mg/kg each as was given for EACA.
Complications of anti-brinolytic therapy include thrombosis, pulmo-
nary embolism, bradycardia, hypotension, and hypersensitivity reactions.
ERRNVPHGLFRVRUJ
Contents of Blood Components
Blood components Contents Volume Shelf life

Whole blood Content is RBC and 450 mL 10% 35 days at 16C
plasma. WBC and in CPDA-1
platelets are not viable
after 24 hours, and factors
V and VIII are significantly
decreased after 48 hours.
1 unit of 450 mL blood
contains 63 mL of the
anticoagulant CPDA-1
(citrate, phosphate,
dextrose, adenine) and
has a hematocrit (Hct) of
35% (depending on the
donor).
Packed Red cells Content is RBC with 280 50 mL 42 days at
(PRBC) about 25 mL of plasma. 16C in bags
In addition, the containing SAGM.
preservative SAGM (35 days at 16C
(saline, adenine, glucose, in bags without
mannitol) may be added SAGM)
to the PRBC to increase its
shelf life. 1 unit of 280 mL
of PRBC contains 100 mL
of SAGM and has an Hct of
6575%.
Platelet concentrates Platelets 5.5 1010. One 5070 mL 5 days at
from Whole Blood unit gives an increment of 2024C, in a
Random Donor 5,00010,000/L in a platelet agitator
Platelets (RDP) 70 kg adult or 150/L/kg
in pediatric patients.
Single donor platelet Platelets 3 1011. One 200250 mL 5 days at 2024oC,
(SDP) (obtained by unit gives an increment of in a platelet
apheresis) 30,00060,000/L in a agitator
70 kg adult or 700/L/kg
in pediatric patients.
Fresh frozen plasma 1 unit contains factor VIII 150250 mL 1 year at 18C &
(FFP) 0.7 IU/mL, Fibrinogen 7 years at 65C
200400 mg, 200 units
of each of the other
coagulation factors,
plasma proteins, and
complement.
ERRNVPHGLFRVRUJ
Blood components Contents Volume Shelf life

Cryoprecipitate 150 mg of fibrinogen, 1020 mL 1 year at 18C
at least 80 IU of factor
VIII, IX (von Willebrand
factor), factor XIII, and
fibronectin.
Bibliography
1. Cherian MN, Emmanuel JC. Clinical use of blood. World anaesthesia 2002;14:1. [Updated: 2002;
accessed: 31 Jan 2012]. Available at: http://www.nda.ox.ac.uk/wfsa/html/u14/u1406_01.htm.
2. Cunnigham VL. A review of disseminated intravascular coagulation: presentation, laboratory
diagnosis and treatment. Medical Laboratory Observer. [Updated: Jul 1999; cited: 2011 Feb
21] Available at: http://findarticles.com/p/articles/mi_m3230/is_7_31/ai_55343376/?tag=
content;col1.
3. DeLoughery TG. Blood component therapy. Multiprofessional Critical Care Rev 2007:37992. [Cited:
2011 Feb 21]. Available at: www.ohsu.edu/xd/health/services/.../Blood-component-therapy.doc.
4. Despotis GJ, Goodnough LT. Management approaches to platelet-related microvascular
bleeding in cardiothoracic surgery. Ann Thorac Surg 2000;70:S2032.
5. Despotis GJ, Joist JH, Goodnough LT. Monitoring of hemostasis in cardiac surgical patients:
impact of point-of-care testing on blood loss and transfusion outcomes. Clin Chem 1997;43:
168496.
6. Hartstein G, Janssens M. Treatment of excessive mediastinal bleeding after cardiopulmonary
bypass. Ann Thorac Surg 1996;62:19514.
7. Harvey GK, David JA. Immunology of leucocytes, platelets, plasma components. In: Klein HG,
Mollison PL, Anstee DJ, eds. Mollisons Blood Transfusion in Clinical Medicine11th ed.
Massachussettes: Wiley-Blackwell; 2005:547611.
8. Kusuma B, Schulz TK. Acute disseminated intravascular coagulation. Hospital Physician
2009;45:3540.
9. Laffan MA, Manning RA. Investigation of hemostatsis. In: Lewis SM, Bains BJ, Bates I, ed. Dacie
and Lewis: Practical Haematology 9th ed. Philadelphia: Churchill Livingstone; 2001:33990.
10. Novoseven RT: highlights of prescribing information. [Update: 2010 Jan; Accessed: 2012 Jan
31]. Available at: http://www.fda.gov/downloads/biologicsbloodvaccines/bloodbloodprod-
ucts/approvedproducts/licensedproductsblas/fractionatedplasmaproducts/ucm056954.pdf.
11. Roback JD, Grossman BJ, Harris T, Hillyer CD. Technical Manual 17th ed. Bethesda, MD:
American Association of Blood Banks; 2011:21721.
12. Ross F, Luban NL. Blood component therapy. Pediatr Clin N Am 2008;55:42145.
13. Saba HI, Morelli GA. The pathogenesis and management of disseminated intravascular coag-
ulation. Clin Adv Hematol Oncol 2006;4:91926.
14. Salenger RI, Gammie JS, Vander Salm TJ. Postoperative care of cardiac surgical patients.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult 3rd ed. New York: McGraw-Hill;
2003:43969.
ERRNVPHGLFRVRUJ
Antithrombotic Agents
Drug Dose Remarks

Aspirin Antiplatelet dose: Nonopioid analgesic,
Children: 510 mg/kg/day q24h PO anti-inflammatory and
or for under 10 kg: 37.5 mg q24h PO. antipyretic. Increased risk of
Over 10 kg: 75 mg q24h PO. bleeding with anticoagulants.
Adults: 2050 mg/kg/day or Enhances effect of phenytoin
150300 mg/day PO. sodium and sodium valproate.
Anti-inflammatory dose: Risk of Reyes syndrome*
Children: 3060 mg/kg/day divided in children under 12 years
q46h PO of age.
Adult: 300900 mg q46h PO
(max 4 g/day)
Dipyridamole Children: 25 mg/kg/day in divided Enhances the effects of
doses q8h PO. adenosine and anticoagulants.
Adult: 300600 mg/day in divided
doses q8h PO.
Clopidogrel Children: 0.21 mg/kg q24h PO. A pediatric dose of 0.20.3
Adult: 300 mg initially, then mg/kg/day has an equivalent
75 mg q24h PO. antiplatelet effect of an adult
dose of 75 mg/day.
Warfarin Children: An initial loading dose Monitor INR and adjust dose to
of 200 mcg/kg PO can be given nearest 500 mcg (0.5 mg).
on day 1, which can be repeated The goal is to maintain the INR
on day 2 if the INR is between between 2 and 3. Young children
1 and 1.3, then maintenance need more oral anticoagulation
dose 50200 mcg/kg q24h PO per kg body wt than do older
(depending on INR). children and adults.
Adults: 510 mg on day 1, then 39
mg q24h PO (depending on INR).
Unfractionated Children and adults: Monitor APTT q4h till therapeutic
heparin Loading dose: 50100 units/kg range is achieved (22.5
IV/SC followed by an IV infusion of control), thereafter q12h.
1025 units/kg/h. Infused in 5% Alternatively, target is to achieve
dextrose or isotonic saline. anti-Xa assay activity of 0.350.7
Or 50100 units/kg IV/SC q4h. U/mL.
ERRNVPHGLFRVRUJ
Drug Dose Remarks

Low-molecular- Children: LMWH has the advantages of
weight heparin <2 mo: 1.5 mg/kg (150 U/kg) q12h subcutaneous administration,
(LMWH): SC. less frequent monitoring, and
enoxaparin >2 mo: 1 mg/kg (100 U/kg) q12h predictable pharmacokinetics.
SC. Target is to achieve an anti-Xa
Adults: assay activity of 0.51.0 U/mL.
40 mg (4000 U) q24h or 30 mg
(3000 U) q12h SC.
Tissue 0.030.5 mg/kg/h IV infusion. Lower doses 0.030.1 mg/kg/h
plasminogen are associated with a lower
activator (tPA) incidence of bleeding.
Streptokinase Children: 25004000 units/kg
loading dose over 3060 minutes
then 5001000 units/kg/h IV
infusion for 1224 hours.
Adults: 250,000 U/kg IV then
100,000 U/h IV infusion for
2472 hours.
*Reyes syndrome: The classic features are a rash, vomiting, liver derangement, and encephalopathy. It has been
associated with aspirin consumption in children with a viral illness.
There are three primary classes of medications that may be used in the
treatment of patients with a thrombophilic disorder: (i) antiplatelet drugs,
(ii) anticoagulants, and (iii) thrombolytic agents. With all these drugs,
bleeding is a possible side effect. The risk of bleeding is increased when
two of these drugs are given at the same time.
Antiplatelet therapy or anticoagulation is needed in pediatric surgi-
cal patients to either prevent or treat a thrombotic episode. Prophylactic
therapy is indicated during cardiac catheterization and after the placement
of endovascular stents or in patients in atrial brillation. Surgical proce-
dures that require prophylaxis include prosthetic valve replacements, the
BlalockTaussig shunt and the Glen and Fontan operations. Conditions
where denitive treatment is required are venous or arterial thromboem-
bolism and their complications.
Aspirin is the most commonly used antiplatelet agent in children.
Dipyridamole or clopidogrel are adjuncts that may be recommended to be
given in addition to aspirin or warfarin.
When there is need for immediate anticoagulation, therapy with unfrac-
tionated heparin or low-molecular-weight heparin (LMWH) is initiated
till the desired effect of warfarin is apparent (INR 23). Treatment with
LMWH rather than warfarin is preferable in infants under 1 year of age
because of a variable effect of heparin at this age.
ERRNVPHGLFRVRUJ
Antithrombotic Agents 269
Antiplatelet Agents
Aspirin and NSAIDs

Aspirin inhibits the enzyme COX1 present in platelets. COX1 is
involved in platelet aggregation, and its inhibition results in a decreased
ability of the platelets to form clots. Once aspirin is discontinued, it
takes 57 days for normal platelets to replace the affected platelets.
Other nonsteroidal anti-inammatory drugs (NSAIDs), such as ibupro-
fen, similarly inhibit platelet aggregation, but the effect is not of the same
duration.
NSAIDs may also cause thrombocytopenia in addition to platelet dys-
function and increase the susceptibility for acute kidney injury during an
episode of hypotension.
Dipyridamole
Dipyridamole is an antiplatelet agent and a vasodilator. It inhibits plate-
let aggregation by increasing platelet cAMP. This drug has primarily been
used in combination with aspirin for anticoagulation prophylaxis for vas-
cular grafts or an intravascular device and in combination with warfarin in
patients with prosthetic heart valves.
Side effects of dipyridamole, besides the increased risk of bleeding,
include dizziness, hypotension, headache, nausea, abdominal discomfort,
and rashes.
Clopidogrel
The mechanism by which clopidogrel works is different from that of aspi-
rin and other NSAIDs. Platelets require adenosine diphosphate (ADP)
binding to platelet receptor sites to facilitate aggregation and clopidogrel
inhibits this ADP binding.
Clopidogrel is indicated for antithrombotic prophylaxis as an adjunct
to therapy with either aspirin, warfarin, heparin, or low-molecular-weight
heparin.
Side effects of clopidogrel include bleeding, dyspepsia and diarrhea,
rash, fatigue, headache, dizziness, and u-like symptoms. Rarely, throm-
botic thrombocytopenic purpura can occur.
ERRNVPHGLFRVRUJ
Anticoagulants
Warfarin
Warfarin is a vitamin K antagonist and provides anticoagulation by inhib-
iting the effects of vitamin K on clotting factors II, VII, IX, and X. In gen-
eral, after administration, warfarin takes about 48 hours before it has a
measurable effect on coagulation.
Side effects of warfarin include rash, dyspepsia, diarrhea, alopecia, and
hepatitis. Warfarin interacts with a large number of medications including
many antibiotics. Dietary intake of vitamin K (e.g., spinach) can lower the
anticoagulant effect of warfarin.
Bleeding or a raised INR beyond the therapeutic range as a result of war-
farin is managed by administration of fresh frozen plasma (FFP) and Inj.
vitamin K. (Inj. vit K dose: 300 mcg/kg is given as IV bolus over 1530
minutes q24h. It is diluted in 5% dextrose to a concentration of 0.2 mg/mL
for administration. Dose in >12 yr age and adults,: 10 mg IV q24h. An IM
preparation is also available.)
Unfractionated Heparin
The main anticoagulant action of heparin is mediated through its interac-
tion with antithrombin. The heparinantithrombin complex inactivates
factor IIa (thrombin), Xa, IXa, XIa, and XIIa. Of these, thrombin and fac-
tor Xa are most responsive to inhibition. Heparin reduces the procoagulant
activity of factor VIIa and tissue factor and also interacts with platelets to
cause bleeding by a mechanism independent of its anticoagulant effect.
Upon initiating heparin, APTT monitoring is required every 4 hours and
generally maintained at 22.5 control values. Once the proper dose has
been established, sampling is reduced to once or twice a day. APTT is sen-
sitive to the inhibitory effects of heparin on thrombin, factor Xa, and IXa.
Monitoring of therapy may be more accurately done by anti-Xa assay (tar-
get 0.350.7 control).
Side effects of heparin include irritation at the site of infusion,
fever, chills, nasal congestion, osteoporosis (with prolonged use), and
thrombocytopenia.
Low-Molecular-Weight Heparin
LMWH (e.g., enoxaparin, dalteparin) enhances the inhibition of factor Xa,
but not IIa and has actions similar to heparin on tissue factor, factor VIIa,
and platelets.
ERRNVPHGLFRVRUJ
Antithrombotic Agents 271
The anticoagulant effect of LMWH varies in direct proportion to the

dose calculated by body weight. Dose alteration is required in renal dis-
ease. Its dose effect does not correlate with the APTT but can be monitored
by anti-Xa assay (target value 0.51.0 U/mL; sample is collected 4 h after
administration of dose).
Side effects for the low-molecular-weight heparins are similar to those
of heparin including the ability of LMWH to cause thrombocytopenia.
Thrombolytic Therapy
Systemic thrombolytic therapy may be considered for arterial occlusions,

venous thrombosis, pulmonary embolism not responding to heparin ther-
apy, clotted valves, or blocked BT shunts.
Tissue plasminogen activator (tPA) has been the recommended throm-
bolytic agent of choice in children because of higher brin specicity and
lower antigenicity. It acts on circulating plasminogen to generate plasmin,
which cause clot lyses. It is administered as in the following guidelines
(Thrombosis Interest Group):
1. Baseline blood count, platelet count, PT, APTT, and brinogen levels
are done prior to initiation of thrombolytic therapy.
2. FFP 1020 mL/kg IV is administered q812h. It is a plasminogen
source and is commenced either before starting thrombolytic therapy
or simultaneously.
3. tPA is administered at the rate of 0.30.5 mg/kg/h IV initially for
6 hours (dose varies from 0.39 mg/kg/h in various reports). If required,
tPA therapy may be repeated again after 24 hours along with FFP.
4. Unfractionated heparin is started at the same time as the tPA in a
dose of 10 units/kg/h without an initial bolus dose. It is continued in
therapeutic doses (2030 U/kg/h), monitored by APTT for a period of
24 h, even after tPA has been discontinued.
Monitoring
The PT, APTT, and brinogen levels are monitored at 4 hours and every
68 hours thereafter. The brinogen concentration is likely to drop by
2050%. If the brinogen concentration falls to <100 mg/dL, tPA is
discontinued till the brinogen level is restored by the administration
of cryoprecipitate (1U/510 kg). A platelet count >100 109/L is also
maintained.
ERRNVPHGLFRVRUJ
Contraindications
Active bleeding or surgery in the previous 10 days are contraindications to
thrombolytic therapy. During therapy, warfarin and antiplatelet agents are
withheld and IM injections are avoided.
Complications
In case of severe bleeding, the tPA and heparin are stopped and the effects
of heparin may be reversed with protamine. Packed cells, FFP, and cryopre-
cipitate (1U/510 kg) are administered and may be repeated as required.
Recombinant factor VII is considered for persistent bleeding in spite of
above therapy.
Bibliography
1. Buck ML. Clopidogrel for platelet inhibition in pediatric patients: pediatric clinical trials.
Pediatr Pharm 2010;16(5). [Updated: 2010 June 22; accessed: 2012 Jan 31]. Available at: http://
www.medscape.com/viewarticle/723239.
2. Buck ML. Use of aminocaproic acid in children undergoing cardiac surgery or ECMO. Pediatr
Pharm 2006:12. [Updated: 2007 May 01; accessed: 2012 Jan 31]. Available at: http://www.
medscape.com/viewarticle/549277.
3. Chen CC, You JY, Ho CH. The aPTT assay as a monitor of heparin anticoagulation efficacy in
clinical settings. Adv Ther 2003;20:2316.
4. Clopidogrel. Drugs update. [Updated: 2011; accessed: 2012 Jan 31]. Available at: http://www.
drugsupdate.com/generic/view/594.
5. Eaton MP. Antifibrinolytic therapy in surgery for congenital heart disease. Anesth Analg
2008;106:1087100.
6. Harker LA, Kadatz RA. Mechanism of action of dipyridamole. Thromb Res Suppl 1983;4:3946.
7. Hirsh J, Warkentin TE, Shaughnessy SG, et al. Heparin and low-molecular-weight heparin:
mechanisms of action, pharmacokinetics, dosing, monitoring, efficacy, and safety. Chest
2001;119:64S94S.
8. Jennifer S, Yow E, Berezny KY, et al. Dosing of clopidogrel for platelet inhibition in infants and
young children. Circulation 2008;117:5539.
9. Massicot P, David M, Chan A. Thrombolytic therapy in children. Thrombosis interest group
of Canada. [Cited: July 2012] Available at: http://www.tigc.org/clinical-guides/Thrombolytic-
Therapy-in-Children.aspx.
10. Monagle P, Chan A, Massicotte P, Chalmers E, Michelson AD. Antithrombotic therapy in chil-
dren: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest
2004;126:645S87S.
11. Veldman A, Nold MF, Michel-Behnke I. Thrombosis in the critically ill neonate: incidence,
diagnosis, and management. Vasc Health Risk Manag 2008;4:133748.
ERRNVPHGLFRVRUJ
Management
of Anaphylaxis
Medicine sometimes snatches away health, sometimes gives it
Ovid (43 BCAD 17/18)*
Dose guide
<6 mo 6 mo6 yr 612 yr >12 yr
Adrenaline IM (1:1000) 150 mcg 150 mcg 300 mcg 500 mcg (0.5 mL);
(0.15 mL) (0.15 mL) (0.3 mL) 300 mcg (0.3 mL)
if child is small or
prepubertal.
Hydrocortisone IM/slow IV 25 mg 50 mg 100 mg 200 mg
Chlorpheniramine IM/slow IV 250 mcg/kg 2.5 mg 5 mg 10 mg
Crystalloid bolus 200 mL 400 mL 500 mL 500 mL
20 mL/kg IV
Presentation
The characteristic presentation of anaphylactic reaction involves two or

more systems, though it may also present with symptoms attributable only
to respiratory or circulatory systems, or the skin.
Sudden onset and rapid progression of symptoms following exposure to
an allergen.
Signs of airway obstruction (stridor, hoarseness, laryngeal or pharyngeal
edema) or breathing difculty (wheeze).
Signs of circulatory collapse (tachycardia, hypotension, cardiac arrest).
Skin and/or mucosal changes (ushing, urticaria, angioedema).
May have associated GIT symptoms (e.g., vomiting, abdominal pain,
incontinence).
*Excerpt from Tristia. Tristia (Sorrows or Lamentations) is a collection of letters written by

the Augustan poet Ovid during his exile from Rome.
ERRNVPHGLFRVRUJ
Laboratory Diagnosis
Serum Tryptase
Measurement of serum tryptase is a specic test to help conrm the diag-
nosis of anaphylactic reaction. Levels of serum tryptase peak 6090 min-
utes after the onset of anaphylaxis and last about 68 hour. Ideally, the
measurement should be obtained between 1 and 2 hour after start of
symptoms.
Emergency Management of Anaphylaxis
Adrenaline
Adrenaline reverses peripheral vasodilation (1 action) and increases the
force of myocardial contraction and cardiac output (1 action). It dilates
the bronchial airways, suppresses histamine and leukotriene release, and
attenuates the severity of IgE-mediated allergic reactions (2 actions).
In the rst instance, adrenaline is given IM because of ease of
administration and high incidence of arrhythmias associated with an
inappropriate IV dose. Intravenous administration is indicated with ECG
and arterial pressure monitoring in patients who respond poorly to IM
adrenaline.
IM dose (Adrenaline 1:1000 contains 1000 mcg/mL; and 1:10,000
contains 100 mcg/mL)
Children: 10 mcg/kg (0.01 mL of 1:1000/kg).
Adults: 300500 mcg (0.30.5 mL of 1:1000).
It is preferably administered on the lateral aspect of the thigh and may
be repeated every 510 min.
IV dose
Children: 1 mcg/kg (0.01 mL of 1:10.000/kg).
Adults: 50 mcg (0.5 mL of 1:10,000).
Dose is repeated according to response. IV adrenaline infusion in the
standard concentration (0.5 mg in 50 mL) may be started at a rate
titrated to response.
Positioning of Patient
The patient is placed in a supine position with elevation of the lower limbs,
particularly when there is hemodynamic compromise. It may be preferable
ERRNVPHGLFRVRUJ
Management of Anaphylaxis 275
Stop allergen
High flow oxygen
Adrenaline
10 mcg/kg IM or 1 mcg/kg IV
Hydrocortisone
4 mg/kg IM/IV
Chlorpheniramine
0.2 mg/kg IM/IV
Adrenaline
10 mcg/kg IM or 1 mcg/kg IV 510 minutes
Crystalloid 20 mL/kg
Fig. 1: Flow diagram for treatment of anaphylaxis in children.
to allow patients with airway and breathing problems to sit up, provided
there is no hemodynamic instability, as this will make breathing easier.
Oxygen
High ow oxygen (>10 L/min) is administered by face mask and reservoir.
Fluids
Hypotension because of vasodilatation and capillary leak may often
require large volumes of uid infusion. Saline is generally preferred to dex-
trose, because it stays in the intravascular compartment longer and does
not contain lactate, which may increase metabolic acidosis.
Saline bolus of 20 mL/kg in a child or 5001000 mL in an adult is given
initially and repeated depending on the response. If intravenous access is
delayed, the intra-osseous route can be used for uids or drugs.
Antihistaminics
Antihistamines (H1) help counter histamine-mediated vasodilatation and
bronchoconstriction. Inj. chlorpheniramine is administered slow IV/IM
(Dose: 1 mo1 yr, 0.25 mg/kg; >1 yr to adults, 0.20 mg/kg).
ERRNVPHGLFRVRUJ
Steroids
Inj. hydrocortisone 4 mg/kg IM/slow IV.
Other Drugs
IV glucagon is indicated in patients on -blockers who are unresponsive
to adrenaline and uids. Glucagon increases heart rate and myocardial
contractility, and improves atrioventricular conduction via non-adrenergic
pathways. The dose of glucagon required to reverse severe beta-blockade is
50150 mcg/kg IV (adults: 310 mg) followed by a continuous infusion of
50150 mcg/kg/h (adults: 310 mg/h), titrated to maintain the reversal.
Glucagon-treated patients should be monitored for side effects (nausea,
vomiting, hypokalemia, and hyperglycemia).
IV atropine may be required in patients who develop severe bradycardia
after an anaphylactic reaction. 0.02 mg/kg IV/IO (minimum 0.1 mg, maxi-
mum single dose in a child 0.5 mg, adult 1 mg). The dose may be repeated
once if needed.
Vasopressors such as dopamine, vasopressin, noradrenaline are indicated
if the hypotension is unresponsive to epinephrine and volume expansion.
Bronchodilators (salbutamol, ipratropium) may benet patients who
develop bronchospasm that is not relieved by adrenaline.
Bibliography
1. Emergency treatment for anaphylactic reactions. Guidelines for healthcare providers.
London: Resuscitation Council (UK). [Updated: 2008 Oct; cited: 2012 May 31]. Available at:
http://www.resus.org.uk/pages/reaction.pdf.
2. Kerns W. Management of beta-adrenergic blocker and calcium channel antagonist toxicity.
Emerg Med Clin N Am 2007;25:30931.
3. Lieberman P, Nicklas RA, Oppenheimer J. The diagnosis and management of anaphylaxis
practice parameter: 2010 Update. J Allergy Clin Immunol 2010;126:47780.
ERRNVPHGLFRVRUJ
Appendix A
International System
of Units (SI Units)
and Conversion Factors
SI Units of Measure
Prefix Symbol Factor Name

Peta P 1015
Tera T 1012
Giga G 109 Billion
6
Mega M 10 Million
Kilo k 103 Thousand
2
Hecto H 10 Hundred
Deka D 101 Ten
Liter: L
Base unit Meter: m
Gram: g
Deci d 101 One tenth
2
Centi c 10 One hundredth
Milli m 103 One thousandth
Micro * 10 6
One millionth
Nano n 109 One billionth
12
Pico p 10
Femto f 1015
*In drug prescriptions, to avoid confusing (micro) with m (milli), it is recommended that g should be written
as mcg.
The basic metric units are meters (for length), grams (for mass), and liters
(for volume). Higher and lower sized values are all multiples of ten of each
other and are indicated by the prexes kilo-, hecto-, deka-, deci-, centi-,
milli- and so on. Therefore, 1 kg = 1000 g; 1 g = 1000 mg; 1 mg = 1000 mcg;
1 mcg = 1000 ng (106 g). Similarly, 1 L = 10 dL; 1 dL = 10 cL; 1 cL = 10 mL
(i.e., 1 L = 1000 mL).
ERRNVPHGLFRVRUJ
Relationship among Units

1 L = 1 dm3, i.e., one liter has a volume equal to one cubic decimeter.
1 mL = 1 cm3, i.e., the milliliter is the same as a cubic centimeter.
1 L = 1 mm3 (= 0.001 mL = 0.001 cm3), i.e., a microliter has a volume of
one cubic millimeter.
1 L of water has a mass of approximately 1 kg.
1 mL of water has a mass of approximately 1 g.
1 L of water has a mass of 1 mg.
Thus, the range of normal platelet count may be written as:

150,000450,000/L (microliter) or 150,000450,000 106/L or
150,000450,000/mm3 or 150450 109/L
150450 103/mm3 or
Pressure Scales
cm H2O 12 3 4 56 7 8 910 11 12 1314 15 16 1718 19 2021 22

mmHg* 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
*Pressures in mmHg are the nearest whole numbers.
For converting values in centimeters of water to millimeters of mer-

cury, the value given in centimeters of water is divided by the factor 1.36
(1 mmHg = 1.36 cm H2O).
1 kilopascal (kPa) = 7.5 mmHg (10.2 cm H2O).
Temperature Scales
Celsius 33 34 35 36 37 38 39 40 41 42
Fahrenheit 91.4 93.2 95 96.8 98.6 100.4 102.2 104 105.8 107.6
Conversion of Fahrenheit to Celsius: C = (F 32) (5/9)

e.g., to convert 98.6F to C: (98.6 32) 5/9 = 37C
Conversion of Celsius to Fahrenheit: F = (C 9/5) + 32

e.g., to convert 100C to F: (100 9/5) + 32 = 212F
ERRNVPHGLFRVRUJ
SI Units and Conversion Factors 279
French Gauge Catheter Scale
French 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
mm 2 2.3 2.7 3 3.3 3.7 4 4.3 4.7 5 5.3 5.7 6 6.3 6.7
The French gauge (Fr) system is used as a measure of the sizes of the external
diameter of catheters. 1 Fr = 0.33 mm, and therefore the diameter in mm is
equal to Fr divided by 3, e.g., if the Fr size is 12, the diameter is 4 mm. An
increasing Fr gauge corresponds to a larger diameter catheter.
IV Cannula and Needle Gauge
Gauge 8 10 12 14 16 18 20 22 24
Outer diameter (mm) 4.19 3.40 2.77 2.11 1.65 1.27 0.91 0.72 0.57
The outer diameter of IV cannula and needles is commonly indicated

in gauge (Birmingham wire gauge, also referred to as the Stubs needle
gauge). There is an inverse relationship between size and gauge, and an
increasing gauge corresponds to a smaller outer diameter (gauge 14 has
a larger diameter than gauge 20). Inner diameter depends on both gauge
and wall thickness.
1214 gauge are large cannulae, which may be used for rapid infusions
during resuscitation.
16 gauge is midsize and can be used for blood transfusion.
1820 gauge are used for IV infusions and taking blood samples.
22 gauge lines are used in pediatric patients.
ERRNVPHGLFRVRUJ
Appendix B
Vital Signs
Vital Signs at Various Ages (at Rest)
Age Heart rate Respiratory rate Blood pressure

(beats/min) (breaths/min) (mmHg)
Premature 120170* 4070 5575/3545
03 mo 100150* 3555 6585/4555
36 mo 90120 3045 7090/5065
612 mo 80120 2540 80100/5565
13 yr 70110 2030 90105/5570
36 yr 65110 2025 95110/6075
612 yr 6095 1422 100120/6075
>12 yr* 5585 1218 110135/6585
th
Source: Kliegman RM, et al., eds. Nelsons Textbook of Pediatrics 19 ed. Philadelphia: Saunders Elsevier; 2011:27980.
*From Dieckmann R, Brownstein D, Gausche-Hill M, eds. Pediatric Education for Prehospital Professionals. Sudbury,
Mass, Jones & Bartlett, American Academy of Pediatrics; 2000:4345.

From American Heart Association ECC Guidelines, 2000.
Hypotension*
For purposes of resuscitation, hypotension has been dened as:

Age <1 mo: Systolic blood pressure <60 mmHg
1 mo1 yr: <70 mmHg
110 yr: <(2 age in yr) + 70 in mmHg
>10 yr: <90 mmHg
*Sources: Kleinman ME, Chameides L. et al. Pediatric Advanced Life Support 2010. American
Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular
Care. Circulation 2010;122:S876S908.
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Appendix C
Anthropometric
Measurements and
Major Motor Milestones
Age Groups in Children
Neonate Birth to 4 weeks

Infant 1 month to 1 year
Toddler 13 years
Pre-school 36 years
School 612 years
Age Weight Height/Length Surface Area
Age (years) Weight Weight Height/length Height/length BSA

boys (kg) girls (kg) boys (cm) girls (cm) boys m2
At birth 3.3 3.2 49.9 49.1 0.21
1 9.6 8.9 75.7 74.0 0.45
2 12.2 11.5 87.1 85.7 0.54
3 14.3 13.9 96.6 95.1 0.62
4 16.3 16.1 103.3 102.7 0.68
5 18.3 18.2 110.0 109.4 0.75
Adult 68 56 173 163 1.80
WHO growth standards, 50th percentile values for weight and height/length are shown in this table.
BSA calculated by Mostellars formula.
Calculation of Predicted Weight from Age
The following formulas can be used to provide an approximation of

median weight from age.
110 yr: Wt (kg) = (Age in yr + 4) 2
712 yr: Wt (kg) = (Age in yr 3) + 7
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In the rst few days after birth, children lose 10% of their birth weight,
and regain this weight by the 710th day. In the rst 3 months of age, the
rate of weight gain is 2530 g/day. Children double their birth weight by
5 months age, triple the birth weight by 1 year, and become 4 times their
birth weight by 2 years age.
Calculation of Body Surface Area from Weight and

Height/Length
Mostellars formula:
Ht (cm) Wt (kg)
BSA (m 2 ) =
60
Pediatric prescriptions based on body surface area: Percentage of the adult
dose based on body surface area may be used for calculation of pediatric doses
for drugs having a wide margin between the therapeutic and toxic doses.
Surface area of patient (m2 ) Adult dose

Approximate pediatric dose =
1.8
Major Motor Development Milestones
Milestone 1st percentile 99th percentile

(in months) (in months)
Sitting without support 3.8 9.2
Standing with assistance 4.8 11.4
Hands and knees crawling 5.2 13.5
Walking with assistance 5.9 13.7
Standing alone 6.9 16.9
Walking alone 8.2 17.6
The 1st to 99th percentiles reflect normal variation in age of milestone achievement in healthy children.
Sources
1. WHO child growth standards. [Updated: 2012; accessed: 2012 Mar 21). Available at: www.
who.int/childgrowth/standards/en/
2. Luscombe MD, Owens BD, Burke D. Weight estimation in paediatrics: a comparison of the
APLS formula and the formula Weight = 3 (age) + 7. Emerg Med J 2011;28:5903.
3. Mosteller RD. Simplified calculation of body-surface area. N Engl J Med 1987;317:1098.
4. WHO Multicentre Growth Reference Study Group. WHO Motor Development Study: win-
dows of achievement for six gross motor development milestones. Acta Paediatr Suppl
2006;450:8695.
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Appendix D
Hematological Parameters
Normal Hematology Values
Age Hb PCV RBC MCV MCH MCHC PLTS WBC Lymphs

(g/dL) (%) (mill/ (fL) (pg) (%) (103/ (103/ (%)
mm3) mm3) mm3)
03 day 15.020.0 4561 4.05.9 95115 3137 2937 250450 9.035.0 1929
12 wk 12.518.5 3957 3.65.5 86110 2836 2838 250450 5.020.0 3645
16 mo 10.013.0 2942 3.14.3 7496 2535 3036 300700 6.017.5 4171
7 mo to 2 yr 10.513.0 3338 3.74.9 7084 2330 3137 250600 6.017.0 4576
25 yr 11.513.0 3439 3.95.0 7587 2430 3137 250550 5.515.5 3565
58 yr 11.514.5 3542 4.04.9 7795 2533 3137 250550 5.014.5 2848
1318 yr 12.015.2 3647 4.55.1 7896 2535 3137 150450 4.513.0 2545
Adult male 13.516.5 4150 4.55.5 80100 2634 3137 150450 4.511.0 2444
Adult 12.015.0 3644 4.04.9 80100 2634 3137 150450 4.511.0 2444
female
Mean corpuscular volume (MCV) is expressed in femtoliters (fL, or 1015 L), the following formula is used:
MCV = 10 hematocrit (%)

RBC count (millions/mm3 )
Mean corpuscular hemoglobin (MCH) is the average mass of hemoglobin per red blood cell in a sample of blood.
10 Hb (g%)
MCH =
RBC count (millions/mm3 )
Mean corpuscular hemoglobin concentration (MCHC) is a measure of the concentration of hemoglobin in a
given volume of packed red blood cells. It is calculated by dividing the hemoglobin by the hematocrit.
Erythrocyte sedimentation rate (ESR) is <20 mm/h by Westergrens method

(<13 by Wintrobes method) provided the PCV is >35%.
Reticulocyte count: Newborns: 26%; 16 months: 02.8%; Adults:
0.51.55.
Differential counts:
In general, in age <7 days: Neutrophils > lymphocytes;
7 days 4 yr: Lymphocytes > neutrophils;
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47 yr: Neutrophils = lymphocytes;

7 yr: Neutrophils > lymphocytes;
Eosinophils: 23%;
Monocytes: 69%.
Source
Paediatric care online; American Academy Of Pediatrics (2012). Available at: www.pediatric-
careonline.org
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Appendix E
Normal Laboratory
Values for Children
Biochemistry
Albumin 01 yr 2.04.0 g/dL

1 yr to adult 3.55.5 g/dL
Ammonia Newborns 90150 mcg/dL
Children 40120 mcg/dL
Adults 1854 mcg/dL
Amylase Newborns 060 units/L
Adults 30110 units/L
Bilirubin, conjugated, direct Newborns <1.5 mg/dL
1 mo to adult 00.5 mg/dL
Bilirubin, total 03 day 2.010.0 mg/dL
1 mo to adult 01.5 mg/dL
Bilirubin, unconjugated, indirect 0.610.5 mg/dL
Calcium Newborns 7.012.0 mg/dL
02 yr 8.811.2 mg/dL
2 yr to adult 9.011.0 mg/dL
Calcium, ionized, whole blood 4.45.4 mg/dL
Chloride 95105 mmol/L
Cholesterol Newborns 45170 mg/dL
01 yr 65175 mg/dL
120 yr 120230 mg/dL
Creatinine 01 yr 0.6 mg/dL
1 yr to adult 0.51.5 mg/dL
Glucose Newborns 3090 mg/dL
02 yr 60105 mg/dL
Children to adults 70110 mg/dL
Lactic acid, lactate 220 mg/dL
Lipase Children 20140 units/L
Adults 0190 units/L
Magnesium 0.51.0 mmol/L
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Osmolality, serum 275296 mOsm/kg

Osmolality, urine 501400 mOsm/kg
Phosphorus Newborns 4.29.0 mg/dL
6 wk to 19 mo 3.86.7 mg/dL
19 mo to 3 yr 2.95.9 mg/dL
315 yr 3.65.6 mg/dL
>15 yr 2.55.0 mg/dL
Potassium, plasma Newborns 4.57.2 mmol/L
2 day to 3 mo 4.06.2 mmol/L
3 mo to 1 yr 3.75.6 mmol/L
116 yr 3.55.0 mmol/L
Protein, total 02 yr 4.27.4 g/dL
>2 yr 6.08.0 g/dL
Sodium 136145 mmol/L
Triglycerides Infants 0171 mg/dL
Children 20130 mg/dL
Adults 30200 mg/dL
Urea nitrogen, blood 02 yr 415 mg/dL
2 yr to adult 520 mg/dL
Uric acid Adult 3.07.0 mg/dL (M),
2.06.0 mg/dL (F)
Enzymes
Alanine aminotransferase 02 mo 878 units/L
(ALT) (SGPT) >2 mo 836 units/L
Alkaline phosphatase (ALKP) Newborns 60130 units/L
016 yr 85400 units/L
>16 yr 30115 units/L
Aspartate aminotransferase Infants 1874 units/L
(AST)(SGOT) Children 1546 units/L
Adults 535 units/L
Creatine kinase (CK) Infants 20200 units/L
Children 1090 units/L
Adults 0206 units/L (M),
0175 units/L (F)
Lactate dehydrogenase (LDH) Newborns 290501 units/L
1 mo to 2 yr 110144 units/L
>16 yr 60170 units/L
Source: Pediatric Care Online; the American Academy of Pediatrics. Available at:
www.pediatriccareonline.org.
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Appendix F
Composition of
Frequently Used
Parenteral Fluids
Crystalloids
Fluid Na K Ca Cl HCO3 Comments
(mmol/L) (mmol/L) (mmol/L) (mmol/L) (mmol/L) (pH/tonicity
[mOsm/L])
Plasma 140 4.5 2.3 100 26 pH 7.4, Osm 290
5% Dextrose Dextrose 50 g/L
Osm 277
10% Dextrose Dextrose 100 g/L
Osm 556
Normal saline 154 154 pH 5,
(0.9% NaCl) Osm 308
Normal 77 77 pH 5,
saline (0.45 NaCl) Osm 154
Glucose 5% + 77 77 Glucose 50 g/L
saline 0.45% Osm 431
Ringer lactate 130 4 1.5 109 28 Contains lactate
28 mmol/L; pH 6.5,
Osm 273
Plasmalyte 148 140 5 98 29 Contains acetate
27 mmol/L,
gluconate 23 mmol/L;
pH 5, Osm 294
Colloids
Fluid Na K Ca Cl Other (g/L) Comments
(mmol/L) (mmol/L) (mmol/L) (mmol/L) (pH/tonicity)
Haemaccel 145 5 6.25 145 Gelatin 35 g 7.4
Gelofusine 154 <0.4 <0.4 125 Gelatin 40 g 7.4
Hetastarch 154 154 Starch 60 g 5.5
Pentastarch 154 154 Starch 100 g 5.0
Albumin 5% <160 <2 136 Albumin 50 g 7.4
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Fluid Na K Ca Cl Other (g/L) Comments

(mmol/L) (mmol/L) (mmol/L) (mmol/L) (pH/tonicity)
Dextran 70 Dextran (long-
(and 40) 6% chain glucose
polysaccharides)
60 g + dextrose
50 g in water.
Intravenous uids are of two types:

Crystalloids are volume expanders of the intra- and extravascular
compartment and are further classied as Isotonic (D5W, 0.9% NaCl,

or Lactated Ringers), Hypotonic (0.45% NaCl), or Hypertonic (D5/0.9%
NaCl, D5/0.45% NaCl).
Colloids are a suspension of large molecules, usually in water or
saline, with a tonicity of 270300 mOsm/L, and tend to remain in the
intravascular compartment after infusion thus expanding the circulating
blood volume. These may be physiological (5% albumin, dextran
40/70), semi-synthetic (succinylated gelatin) or synthetic (hydroxyethyl
starch). Dextran 70, when given in large amounts, also prevents platelet
aggregation and facilitates brinolysis.
Sources
1. Intravenous fluids. Ganfyd. [Updated: 2011 Mar 11; accessed: 2012 Mar 21]. Available at:
www.ganfyd.org/index.php?title=Intravenous_fluids.
2. Anaesthesia UK. Summary of IV fluids composition. [Updated: 2004 Oct 26; accessed: 2012
Mar 21]. Available at: www.frca.co.uk/article.aspx?articleid=295.
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Appendix G
Size and Length of
Pediatric Endotracheal
Tubes and Suction Catheters
Age Weight (kg) Internal Length (cm) Suction

diameter (mm) Oral Nasal catheter (Fr)
Premature 1.5 2.53.0 10.5 9.013.0 6

Newborn 3.0 3.0 10.5 13.0 68
23 mo 5.05.5 3.5 11.0 14.0 8
36 mo 6.0 4.0 12.0 14.5 8
1 yr 10.0 4.0 13.5 15.0 8
2 yr 14.0 4.5 14.0 16.0 8
24 yr 14.017.0 5.0 15.0 17.0 10
45 yr 17.020.0 5.5 16.0 18.0 10
57 yr 20.023.0 6.0 17.0 19.0 10
78 yr 23.030.0 6.5 19.0 21.0 10
812 yr 30.045.0 7.0 21.0 22.0 10
1214 yr 45.070.0 7.07.5 22.0 23.0 1214
The following formula may be used for assessment of size of required ET tube
and suction catheter. ET tubes are measured in sizes by internal diameter in mm.
Internal diameter (mm) of ET tube = (age/4) + 4
Length (cm) of oral ET tube = (age/2) + 12
Length (cm) of nasal ET tube = (age/2) + 15
The above calculation is applicable after 1 year of age. Neonates generally
require a tube of internal diameter 33.5 mm.
For tracheal suction catheters, in general, the suitable size in French
gauge is twice the internal diameter of the ET tube, e.g., for an ET tube of
4 mm diameter the suction catheter should be 8 F size. Same size of suc-
tion catheter can be used as a feeding tube.
Source
Mackway-Jones K, et al. Advanced Paediatric Life Support: The Practical Approach 3rd ed.
London: BMJ books; 2001:378.
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Appendix H
Postoperative
Checklist
on Arrival in ICU
Ventilation
Select initial ventilator settings.
Transfer patient to ventilator and check bilateral breath sounds.
Fix endotracheal tube in position. Mark the position.
ICU monitor
Transfer ECG, pressure lines (LA/RA/PA), pulse oximeter, end-tidal
CO2, rectal/skin temperature to ICU monitor.
Zero transducers and secure the lines.
Intracardiac and IV lines
Transfer all infusion pumps to bedside.
Check all IV lines for patency and secure.
Review, recalculate, and note all infusion doses.
Other lines and tubes
Connect thoracic drains to appropriate suction.
Aspirate nasogastric tube and place on gravity drainage.
Secure the urinary catheter and record the initial urinary output.
Pacemaker
Check pacing wires/pacemaker leads.
Note pacemaker settings.
Physical examination
Check all vital signs, and perform a physical examination.
Record level of consciousness, liver size, and fontanelles (in infants).
Arterial blood gases and lab samples
Portable chest X-ray
Note the position of the endotracheal tube, bilateral lung elds
(pneumothorax, opacities, etc.), location of intracardiac lines,
position of nasogastric tube, and conguration of cardiac
silhouette.
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Appendix I
Postoperative Instructions
Date of surgery:
Procedure done:
Preoperative weight:
Preoperative medications:
Allergies:
1. Vital signs q30min

2. Elevate head of bed 30
3. NPO
4. N/G tube open to gravity drainage
5. Chest drain negative suction: 10 to 20 cm H2O
6. Hourly intake-output
7. Milk chest drains q15min 2 h, then q1h and PRN
8. Weight q AM if hemodynamically stable
9. Portable X-ray chest stat and in the morning
10. ECG stat and in the morning
11. Serum electrolytes, acid/base, and blood gases q4h (or PRN)
12 hours, then q6h 12 hours
12. Blood glucose q4h (or q1h if required)
13. Laboratory studies
Total blood count, PT, PTT, platelet count, BUN, Se creatinine, stat and
in the morning.
14. Respiratory care
Turn side to side and chest physiotherapy after 4 hours and
thereafter every 2 hours if hemodynamically stable.
Endotracheal suction gently and irrigation with 1 mL normal
saline q1-3h and PRN.
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15. IV uids
normal saline in 5% dextrose ( saline in 10% dextrose, in
neonates) mL/h.
Calculated as maintenance (including all drips) on the day of surgery;
increased by 25% every subsequent day till full maintenance. Alternatively,
plain 5 or 10% dextrose is administered for the rst 48 hours and dextrose
saline instituted only if the plasma sodium is low.
Potassium chloride mmol in 50 mL of maintenance uid.
The concentration of potassium is calculated for 50 mL of maintenance
uid based on the daily requirement (2 mmol/kg/day). The amount added
is altered depending upon the serum potassium level and urinary output.
If serum K+ falls to <3.4 mmol/L, potassium chloride 0.51 mmol/kg
is administered in a saline or dextrose infusion at a rate of 0.5 mmol/h
via infusion pump. Higher rates up to 2 mmol/kg/h IV may be given in
arrhythmias. Maximum recommended concentration for a central line is
20 mmol/100 mL and peripheral line 4 mmol/100 mL. K+ levels are checked
after the infusion, and the dose is repeated if required.
Inj. calcium gluconate 10% mL in 50 mL of maintenance uid.
Daily requirement of calcium is 0.20.4 mmol/kg (100200 mg/kg) of
calcium gluconate, which may be added to the maintenance uid or
administered intermittently.
(1 mL/100 mg of 10% calcium gluconate provides 0.23 mmol of Ca++)
Arterial ushing uid: Normal saline with heparin 1 unit/mL,
at 1 mL/h.
16. Antibiotics
Inj. teicoplanin 10 mg/kg q12h for 3 doses, then 610 mg/kg q24h.
Administer IV bolus over 35 minutes.
Inj. amikacin 57.5 mg/kg q12h IV.
17. Analgesics and sedatives
Inj. dexmedetomidine 100 mcg in 50 mL 5% dextrose;
IV infusion at mL/h.
With this concentration 0.25 body wt (in mL/h) = 0.5 mcg/kg/h;
Dose: 0.250.5 mcg/kg/h, titrated to response.
Inj. fentanyl (250 mcg/kg) mcg in 50 mL 5% dextrose.
With this concentration 1 mL/h = 5 mcg/kg/h;
Dose: 25 mcg/kg/h IV infusion.
Inj. midazolam (2.5 mg/kg) mg in 50 mL 5% dextrose.
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Postoperative Instructions 293
With this concentration 1 mL/h = 50 mcg/kg/h.

Dose: 60120 mcg/kg/h.
18. Gut prophylaxis
Sucralfate suspension (1 g in 5 mL) mL q4h PO.
Dose:
01 yr: 6 mL/day in divided doses q4h PO.
>12 yr: 30 mL/day in divided doses q4h PO.
19. Inotropes and vasodilators
Dopamine/dobutamine 100 mg in 50 mL 5% dextrose;
Sodium nitroprusside/NTG/milrinone 10 mg in 50 mL
5% dextrose;
Adrenaline/isoprenaline/noradrenaline 1 mg in 50 mL
5% dextrose;
Vasopressin 10 units in 50 mL 5% dextrose;
IV infusion at units/h.
20. Other medication as indicated
IV furosemide 100 mg in 50 mL 0.9% saline (not 5% dextrose)
Dose: 0.052.0 mg/kg/h IV infusion.
Inj. magnesium sulfate 50% mL in mL of 0.9% isotonic
saline or 5% dextrose (diluted 1 in 10) given at a rate of <1 mL/min
(max 2 g of magnesium sulfate).
Daily requirement of magnesium is 0.2 mmol/kg/day (50 mg/kg/day of
magnesium sulfate).
(1 mL/500 mg of 50% magnesium sulfate provides 2 mmol of Mg++)
Hypoglycemia (<70 mg%): dextrose 0.51 g/kg (dextrose 25%:
24 mL/kg) slow IV.
Hyperglycemia (>150 mg%): Inj. insulin 0.10.2 U/kg IV.
21. Blood products
Packed cell at mL/h to replace drainage and achieve desired
hematocrit (e.g., 4 mL/kg/h 3 hours).
Thereafter, FFP PRN to maintain LAP/CVP (e.g., 10 mL/kg over 2 hours).
22. Ventilator settings
FiO2 (initial setting 100%)
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Respiratory rate (1525/min)

Inspiratory time (0.51.0 sec)
Peak inspiratory pressure cm H2O (<25)
Tidal volume mL (1012 mL/kg)
PEEP cm H2O (35)
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Appendix J
Fluid Prescription
after Open Heart Surgery
Weight (kg) Op day 1st Post op day 2nd Post op day 3rd Post op day
mL/h mL/day mL/h mL/day mL/h mL/day mL/h mL/day
2 2.0 48 4.0 96.0 6.0 144.0 8.0 190.0
3 3.0 72 6.0 144 9.0 216 12.0 290
4 4.0 96 8.0 192 12.0 288 16.0 380
5 5.0 120 10.0 240 15.0 360 20.0 480
6 6.0 144 12.0 288 18.0 432 24.0 580

7 7.0 168 14.0 366 21.0 504 28.0 670
8 8.0 192 16.0 384 24.0 576 32.0 770
9 9.0 216 18.0 432 27.0 648 36.0 860
10 10.0 240 20.0 480 30.0 720 40.0 960
11 10.5 252 21.0 504 31.5 756 42.0 1010

12 11.0 264 22.0 528 32.0 792 44.0 1060
13 11.5 276 23.0 552 34.5 328 46.0 1100
14 12.0 288 24.0 576 36.0 864 48.0 1150
15 12.5 300 25.0 600 37.5 900 50.0 1200
16 13.0 312 26.0 624 39.0 936 52.0 1250

17 13.5 324 27.0 648 40.5 972 54.0 1300
18 14.0 336 28.0 672 42.0 1008 56.0 1340
19 14.5 348 29.0 696 43.5 1044 58.0 1390
20 15.0 360 30.0 720 45.0 1080 60.0 1440
21 15.3 367 30.3 727 45.7 1097 61.0 1460

22 15.6 374 30.6 734 46.4 1114 62.0 1510
23 15.9 381 30.9 742 47.0 1130 63.0 1560
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Weight (kg) Op day 1st Post op day 2nd Post op day 3rd Post op day
mL/h mL/day mL/h mL/day mL/h mL/day mL/h mL/day
24 16.2 388 31.2 749 47.8 1147 64.0 1540
25 16.5 396 31.5 756 48.8 1164 65.0 1560
26 16.8 408 31.7 763 49.2 1181 66.0 1580

27 17.1 410 32.0 770 49.9 1198 67.0 1610
28 17.4 418 32.4 778 50.6 1214 68.0 1630
29 17.7 424 32.7 785 51.3 1231 69.0 1660
30 18.0 432 33.0 792 52.0 1248 70.0 1680
Day of surgery: 1/4th of the daily maintenance requirement: 1 mL/

kg/h (for 1st 10 kg) + 0.5 mL/kg/h (for weight >10 kg);
in infants, one may start with 2 mL/kg/h and increase
daily.
1st day: Half maintenance requirement: 2 mL/kg/h (for 1st
10 kg) + 1 mL/kg/h : (next 10 kg) + mL/kg/h (for
weight >20 kg).
2nd day: 3/4th maintenance requirement: 3 mL/kg/h (for 1st
10 kg) + 1.5 mL/kg/h : (next 10 kg) + 0.75 mL/kg/h
(for weight >20 kg).
3rd day: Full maintenance requirement: 4 mL/kg/h (for 1st
10 kg) + 2 mL/kg/h (next 10 kg) + 1 mL/kg/h (for
weight >20 kg).
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Appendix K
Calculations
of Drug Infusions
To Calculate the Dose for a Given Infusion Rate
1. Convert drug into required measurement if necessary (mg into mcg)

2. Calculate how much of the drug is in one mL (mcg/mL)
3. Divide by patients weight (mcg/kg/mL)
4. Multiply by the rate of the infusion to obtain dose (mcg/kg/h)
Dose (mcg/kg/h) = Concentration (mcg/mL) Weight (kg) Rate (mL/h).

Example: 12 kg ChildFentanyl made up as 1 mg in 50 mL 5% glucose. Infusion
running at 1.8 mL/h. Calculate the dose in mcg/kg/h.
1. Convert mg to mcg (1 1000 = 1000 mcg)

2. 1000 mcg in the 50 mL syringe (1000 50 = 20 mcg/mL)
3. Patient weight 12 kg (20 12 = 1.67 mcg/kg/mL)
4. Infusion rate 1.8 mL/h (1.67 1.8 = 3 mcg/kg/h)
1.8 mL/h gives 3 mcg/kg/h.
Dose (mg/kg/h) = Concentration (mg/mL) Weight (kg) Rate (mL/h)

Example: 14 kg ChildMidazolam syringe made up as 50 mg in 50 mL water for
injection. Infusion running at 3 mL/h. Calculate the dose in mg/kg/h.
1. Midazolam IV expressed as mg/kg/h. No need to convert mg to mcg

2. 50 mg in the 50 mL syringe (50 50 = 1 mg/mL)
3. Patient weight 14 kg (1 14 = 0.071 mg/kg/mL)
4. Infusion rate 3 mL/h (0.071 3 = 0.2 mg/kg/h)
3 mL/h gives 0.2 mg/kg/h.
Dose (mcg/kg/min) = Concentration (mcg/mL) Weight (kg)

Rate (mL/h) 60
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To Calculate the Infusion Rate for a Specific Dose
Dose (mcg/kg/h) Weight (kg)

Infusion rate (mL/h) =
Concentration (mcg/mL)
Dose (mg/kg/h) Weight (kg)
Concentration (mg/mL)
Dose (mcg/kg/min) Weight (kg)
Concentration (mcg/mL) 60
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Appendix L
Preparation of Various
Concentrations of Solutions
Dilution of Solutions
A concentrated solution must often be diluted before administration.

To determine the volume of water required to be added for dilution to
achieve the desired concentration can be calculated by the formula:
C1 V1 = C2 V2
where, C1, concentration of the primary solution; V1, volume of the
primary solution; C2, concentration of the nal solution; V2, volume of the
nal solution.
Example: How many mL of water must be added to 250 mL of a 3% sodium chlo-

ride to prepare a 0.9% w/v sodium chloride solution?
C1 V1 = C2 V2
C1 = 3% C2 = 0.9% w/v
V1 = 250 mL V2 = ?
3 250 = 0.9 V2
Therefore, V2 = (3 250) 0.9 = 833 mL.

However, to carry out the dilution (833 250) 583 mL must be added.
Mixing of Solution
When a particular concentration of a solution is required to be prepared

from available solutions, the quantities needed to be mixed are deter-
mined by the formula:
C1V1 + C2V2 = C3V3
where, C1, Concentration of 1st solution; V1, Volume of 1st solution; C2,
Concentration of 2nd solution; V2, Volume of 2nd solution; C3, Percentage of
solution to be prepared; V3, Volume of solution to be prepared.
ERRNVPHGLFRVRUJ
Example 1:
How many mL of 50% dextrose solution and how many mL of 5% dextrose solu-
tion are required to prepare 510 mL of a 10% dextrose solution? When two solu-
tions are combined to make a third one, the following formula is used:
C1V1 + C2V2 = C3V3
C1 = 5% C2 = 50% C3 = 10%
V1 = ? V2 = ? V3 = 510 mL
It is evident that V2 = V3 V1, then from the above formula, the following can be
derived:
(C2 C3) V3
V1 =
(C2 C1)
(50 10) 510
First V1 is calculated = 453 mL
(50 5)
V2 = V3 V1, i.e., (510 453) = 57 mL
453 mL of 5% dextrose and 57 mL of 50% dextrose are required to make 510 mL of
10% dextrose.
Example 2:
How many mL of 50% dextrose solution needs to be added to 1 L of dialysis uid
(1.7% dextrose) to make a 3% solution.
C1V1 + C2V2 = C3V3
C1 = 1.7% C2 = 50% C3 = 3%
V1 = 1000 mL V2 = ? V3 = ?
Knowing that V3 = (V1 + V2) mL

The following formula for V2 can be derived:
V1(C3 C1) 1000(3 1.7)
V2 = i.e., = 27.6 mL
(C2 C3) (50 3)
27.6 mL of 50% dextrose needs to be added to 1 L of 1.7% dialysis uid to make a

3% concentration.
ERRNVPHGLFRVRUJ
Appendix M
Cries Pain Scale
Crying Characteristic cry of pain is high pitched

0 - No cry or cry that is not high-pitched
1 - Cry high pitched but baby is easily consolable
2 - Cry high pitched and baby is inconsolable
Requires O2 for SaO2 Babies experiencing pain manifest decreasing oxygenation. Consider other
<95% causes of hypoxemia (e.g., oversedation, atelectasis, pneumothorax)
0 - No oxygen required
1 - <30% oxygen required
2 - >30% oxygen required
Increased vital signs Take BP last as this may awaken child making other assessments difficult
(BP and HR) 0 - Both HR and BP unchanged or less than baseline
1 - HR or BP increased but increase is <20% of baseline
2 - HR or BP is increased >20% over baseline
Expression The facial expression most often associated with pain is a grimace. A grimace
may be characterized by brow lowering, eyes squeezed shut, deepening
nasolabial furrow, or open lips and mouth
0 - No grimace present
1 - Grimace alone is present
2 - Grimace and non-cry vocalization grunt is present
Sleepless Scored based upon the infants state during the hour preceding this recorded
score
0 - Child has been continuously asleep
1 - Child has awakened at frequent intervals
2 - Child has been awake constantly
The CRIES Pain Scale is a pain assessment scale generally used for infants <6 months age. Each of the five (5)
categoriescrying oxygenation, vital signs, facial expression, and sleeplessnessin relation to pain is scored from
0 to 2, which results in a total score between 0 and 10.
For assessment of HR and BP multiply the baseline HR and mean BP by 0.2 then add to baseline HR/BP to
determine the HR/BP that is 20% over baseline.
Source
Krechel SW, Bildner J. CRIES: a new neonatal postoperative pain measurement scoreinitial
testing of validity and reliability. Paediatric Anaesthesia 1995;5:53.
ERRNVPHGLFRVRUJ
Appendix N
Drug Prescription in Renal Failure
Cardiac Drugs and Diuretics
Drug/dose in Change GFR Supplemental

children in dose >50 1050 <10 dose for dialysis
(I/D) (HD/PD/CRRT)
Acetazolamide I q6h q12h NR HD/PD/CRRT
510 mg/kg/day
PO/IV in divided
doses q612h
(max 750 mg/day)
Atenolol D, I 100% or 50% or 3050% HD+
11.2 mg/kg q24h q48h or q96h PD
q24h PO CRRT + (dose for
GFR 1050)
Captopril D, I 100% or 75% or 50% or HD + (2530% of
0.33.0 mg/kg/day in q812h q1218h q24h dose)
divided doses q8h PO. PD
(dose in CCF) CRRT + (dose for
GFR 1050)
Digoxin D, I 100% or 2575% 1025% HD
Neonate10 yr: q24h or q36h or q48h PD
5 mcg/kg q12h PO CRRT + (dose for
>10 yr: 2.5 mcg/kg GFR 1050)
q12h PO
Enalapril D 100% 75100% 50% HD + (2530%
0.10.5 mg/kg/day dose)
divided q12h24h PO PD
CRRT + (dose for
GFR 1050)
Hydrochlorothiazide D 100% 100% NR
24 mg/kg/day
divided q612h PO.
ERRNVPHGLFRVRUJ
Drug Prescription in Renal Failure 303

(I/D) (HD/PD/CRRT)
Spironolactone I 612 1224 NR
1.53.5 mg/kg/day hours hours
divided q624h PO
Verapamil 100% 100% 5075% HD
36 mg/kg/day in PD
divided doses CRRT + (dose for
q8h PO GFR 1050)
NR: not recommended, +: additional dose is indicated, : additional dose is not indicated, PD: peritoneal dialysis,
HD: hemodialysis, CRRT: continuous renal replacement therapy. D: method of dose reduction by administration of a
percentage of the usual dose. I: method of dose reduction by increase in the dosing interval. D, I: Either the dose or
the interval can be changed.
Noncardiac Drugs

(I/D) (HD/PD/CRRT)
Aspirin I q4h q46h NR HD+
3060 mg/kg/day PD+
PO divided q46h CRRT + (dose for
(anti-inflammatory GFR 1050)
dose)
Cisapride D 100% 100% 50% HD/PD not known
0.20.3 mg/kg CRRT +
q68h PO (50100% dose)
Famotidine D, I 100% or 50% or 25% or HD
0.5 mg/kg/day q1224h q24h q3648h PD
in divided doses CRRT + (dose for
q1224h PO GFR 1050)
Fentanyl D 100% 75% 50% HD/PD/CRRT: not
12 mcg/kg IV known
bolus. May be
repeated every
30 minutes1 hour
Insulin D 100% 75% 50% HD
0.1 U/kg/h IV PD
infusion or 0.10.2 CRRT + (dose for
U/kg IV stat PRN GFR 1050)
ERRNVPHGLFRVRUJ

(I/D) (HD/PD/CRRT)
Metoclopramide D 100% 5075% 2550% HD
0.10.2 mg/kg/dose PD: not known
q68h PO/IM/IV CRRT + (dose for
(anti-emetic dose). GFR 1050)
Midazolam D 100% 100% 50% HD/PD/CRRT: not
0.050.1 mg/kg known
IV bolus
Morphine D 100% 75% 50% HD
16 mo: 0.2550 PD: not known
mg/kg may repeat CRRT + (dose for
up to q6h IV. GFR 1050)
6 mo1 yr: 0.10.2
mg/kg may repeat
up to q4h IV.
Paracetamol I q4h q46h NR HD
(Acetaminophen) PD
4060 mg/kg q46h CRRT + (dose for
PO or 5 mg/kg GFR 1050)
q46h IV
Phenobarbitone I q812h q812h q1216h HD+
1020 mg/kg PD + (50% of
slow IV. dose)
Maintenance CRRT + (dose for
510 mg/kg/day GFR 1050)
in divided doses
q812h PO/IV
Ranitidine D 100% 75% 50% HD
IV (<12 yr): 3 mg/ PD
kg/day in divided CRRT + (dose for
doses q8h GFR 1050)
PO: 24 mg/kg in
divided doses q12h
Thiopental sodium D 100% 100% 75% HD/PD/CRRT: not
26 mg/kg IV bolus known
Normal glomerular ltration rate is approximately 100 mL/min/1.73 m2.

For prescribing purposes, renal impairment is usually divided into three
categories: (i) Mild impairment: GFR 5020 mL/min (serum creatinine
approximately 25 mg/dL); (ii) Moderate: GFR 1020 mL/min (serum
creatinine approximately 510 mg/dL); and (iii) Severe: GFR <10 mL/min
(serum creatinine >10 mg/dL).
ERRNVPHGLFRVRUJ
Drug Prescription in Renal Failure 305
Patients with a GFR above 50 mL/min do not usually require any dosage
adjustment; however, nephrotoxic drugs (e.g., many antibiotics, NSAIDs)
are best avoided in patients with acute kidney injury. Drugs that are excreted
by the kidneys but are in themselves not nephrotoxic require dose reduc-
tion to prevent dose related side effects. The total daily maintenance
dose of a drug can be reduced either by reducing the individual dose or
by increasing the interval between doses. It is however important to give a
normal initial dose if an immediate effect is required.
No change in dose in renal dysfunction is required for the following
drugs:
Analgesics, sedatives, muscle relaxants: Diazepam, diclofenac, ibuprofen,
ketamine, lorazepam, propofol, or vecuronium.
Steroids and antihistaminics: Dexamethasone, hydrocortisone,
prednisolone, methyl prednisolone (additional dose required following
HD), and chlorpheniramine.
Anti-convulsants: Carbamazepine, phenytoin or sodium valproate,
however, drug levels need careful monitoring.
Drugs used in GI disorders: Omeprazole and ondansetron.
Anticoagulants: Heparin (dose of LMW heparin however requires
reduction to 50% with GFR <10, no change is required with a GFR >10)
and warfarin.
Cardiac drugs and diuretics: Adenosine, amiodarone, diltiazem,
labetalol, metoprolol, nifedipine, xylocard, and furosemide.
Sources
1. Arnoff GR, Brier ME. Prescribing drugs in renal disease. Brenner and Rectors The Kidney 7 ed.
Philadelphia: Saunders; 2004:284970.
2. Robertson J, Shilkofski N. Drugs in renal failure. The Harriet Lane Handbook 17 ed.
Philadelphia: Mosby; 2005:105368.
ERRNVPHGLFRVRUJ
Appendix O
Pediatric Blood Levels

of Commonly Used Drugs
Drug Optimal range Remarks

Amikacin Peak: 1525 mcg/mL Suggested sampling time at 3rd dose or
Trough: 25 mcg/mL later. Peak 30 min after end of infusion.
Trough levels are estimated before next
dose.
Amiodarone 0.52.5 mcg/mL Trough level after steady state has been
achieved.
Carbamazepine 612 mcg/mL Trough level after 12 weeks
Digoxin 0.81.2 ng/mL Oral trough level after 1 week
Gentamicin Peak: 510 mcg/mL Peak 60 minutes after IV or IM dose
Trough: <2 mcg/mL
Netilmicin Peak: 412 mcg/mL Peak 60 minutes after IV or IM dose
Trough: <2 mcg/mL
Lignocaine 1.55 mcg/mL Sample for drug level can be drawn at any
time during infusion
Phenobarbitone 1525 mcg/mL Trough level after 12 weeks of oral
therapy.
Phenytoin 1020 mcg/mL Trough level after 1 week of oral therapy.
IV 24 hours after loading dose
Salicylate 100300 mcg/mL Suggested sampling time at 5th dose. Peak
level 12 hours after dose.
Theophylline 1020 mcg/mL Peak level 12 hours after dose following
(for asthma) 12 days of oral drug therapy; IV, 30
minutes after completion of loading dose
and anytime during continuous infusion.
Valproic acid 50100 mcg/mL Trough level after 23 days of oral therapy.
Vancomycin Peak: 1826 mcg/mL Peak level at 4th dose, 2 hours after
Trough: 510 mcg/mL completion of infusion. (2 hours after start of
infusion level 2540 mcg/mL).
Sources: Rylance GW, Moreland TA. Review article: Drug level monitoring in paediatric practice. Archives of Disease
in Childhood 1980;55:8998. AND Therapeautic drug level monitoring. Alder Hey Book of Childrens Doses 6th ed.
Liverpool: Royal Liverpool Childrens Hospital; 1994:2523.
ERRNVPHGLFRVRUJ
Index
A Anaerobic pathogens 184

AAI mode 66 Analgesics 223
Accelerated idioventricular rhythm 50 Anidulafungin 212, 215
Acidbase disorder 115 Anion gap acidosis 119
Acinetobacters 184 Anthropometric measurements 281
Activated clotting time 260 Anti-emetics 136
Activated partial thromboplastin Antidromic AVRT 45
time 257 Antibrinolytic agents 264
Acute kidney injury 241 Antithrombin III 261, 262
Acute lung injury 146 AOO mode 66
Acute renal failure 241 Approximate pediatric dose 282
Acute respiratory distress syndrome Aspergillosis 211
146 Aspiration pneumonia 147
Adenosine 52, 57, 61, 89 Aspiration pneumonitis 144
Adrenaline 25, 26, 89, 93, 273, 274 Aspirin 222, 267
Adrenergic receptors 24 Assist control 161
Afterload 20 Asynchrony 173
Age groups in children 281 Asystole 96
Alpha-2-antiplasmin 262 Atelectasis 143
Alpha-2-plasmin inhibitor 261 Atenolol 79
Alprostadil 26, 28 Atrial demand pacing 71
Alveolararterial oxygen gradient 114 Atrial ectopics 42
Amikacin 187, 190 Atrial ectopic tachycardia 43
Amino acids 125 Atrial electrocardiograms 38
Aminopenicillins 185 Atrial brillation 44, 59
Amiodarone 53, 58, 89, 93 Atrial utter 44
Amlodipine 79 Atrioventricular interval 69
Amoxicillin 190 Atrioventricular reentrant
Amoxicillinclavulanate 185, 190 (or reciprocating) tachycardia 45
Amphotericin B 214 Atropine 89, 93, 276
Amphotericin B deoxycholate 211 AV nodal reentrant tachycardia 46
Amphotericin B lipid complex 212 AV sequential pacing 70
Amphotericin B liposomal 212 AVPU scale 234
Ampicillin 191 Azithromycin 189
Ampicillinsulbactam 185, 191 Aztreonam 188, 192
ERRNVPHGLFRVRUJ
308 Index
B CAVH 250
Cefaclor 186, 192
Bacteroides fragilis 184
Cefazolin 186, 192
Base excess 115
Cefepime 187, 193
Benzathine penicillin 184
Cefoperazone 186, 193
Beta-blockers 58
Cefotaxime 186, 193
Beta-lactamase 182
Cefoxitin 186
Beta-lactamase inhibitors 182
Cefpirome 187
Bicarbonate (HCO3) level 114
Ceftazidime 186, 193
BIPAP 165
Ceftriaxone 186, 194
Bisferiens pulse 4
Cefuroxime 186, 194
Bleeding time 259
Central venous pressure 6
Blood components 265
Cephalexin 186, 194
Blood gas analysis 116
Cephalosporins 186
Blood glucose control 103
Cerebral perfusion pressure 237
Blood sugar 110
Cheynestokes respiration 235
Bolus feedings 131
Chloral hydrate 217
Bradycardia 98
Chloride-resistant metabolic
Brain death 234
alkalosis 120
Broad QRS complex tachycardia
Chloride-responsive metabolic
60, 61
alkalosis 120
Bronchial asthma 150
Chlorpheniramine 273, 275
Bronchospasm 150
Chylothorax 141
Budesonide 152
Ciprooxacin 187, 195
Cisapride 136
C Clarithromycin 189, 195
Calcium 94 Clindamycin 188, 195
Calcium channel blockers 58 Clinical criteria for VAP 177
Calcium gluconate 89 Clopidogrel 267
Calculation of body surface area from Clotrimazole 215
weight and height/length 282 Cloxacillin 185
Calculation of predicted weight from CockcroftGault equation 243
age 281 Collapsing pulse 4
Calculations of drug infusions 297 Colloids 287
Caloric requirements 125 Colorimetry 93
Candidiasis 211 Coma 234
Capnography 93 Combination or dual modes 157
Captopril 35, 80 Common pathway 257
Carbamazepine 229 Compensation 117
Carboxypenicillin 186 Compensatory pause 42, 46, 48
Cardiac index 10 Competition 72, 74
Cardiac output 10 Complete heart block 64
Cardiopulmonary resuscitation 90 Complications of tube feeding
Cardioversion 61 133
Care of the ventilated patient 178 Composition of frequently used
Carvedilol 36 parenteral uids 287
Caspofungin 213, 215 Congestive heart failure 32
ERRNVPHGLFRVRUJ
Index 309
Continuous feedings 131 Dolls eyes movement 236

Controlled mechanical ventilation 158 Domperidone 136
Control of seizures 227 Dopamine 25, 26
Conversion of Celsius to Fahrenheit Drug prescription in renal failure 302
278 Dual/combination modes 166
Conversion of Fahrenheit to Celsius DVI pacing 66
278
CounahanBarratt equation 243 E
CPAP 164 E. coli 183
Creatinine clearance 242 Ejection fraction 11
Cries pain scale 301 Electrolyte requirements 100
Cryoprecipitate 264, 266 Electrolytes 126
Cryptococcosis 211 Elemental formulas (monomeric
Crystalloids 287 formulas) 132
CT scan 237 Enalapril 35, 78, 80
Cushings triad 235 End tidal carbon dioxide monitoring
CVVH 251 93
CVVHD 251 Enteral tube feeding 130
CVVHDF 252 Enterobacter 183
Cyanide toxicity 2731 Enterobacteriaceae 183
Cyanotic spells 88 Enterococci 183
Epicardial pacing 67
D Epoprostenol 26, 28
D-dimer 259 Ertapenem 187
Damping 3 Erythrocyte sedimentation rate 283
DC cardioversion 57 Erythromycin 189, 196
DDD device 66 Esmolol 54, 78, 87
Decerebrate rigidity 236 Established ARF 241
Decorticate posture 236 Etomidate 220
Debrillation 92 Expressed breast milk 131
Decit therapy 100, 102 External chest compressions 90
Dehydration 102 Extrinsic coagulation pathway 257
Delirium 234
Dexamethasone 240 F
Dexmedetomidine 217, 225 Failure to capture 71, 72
Dextrose 89, 126 Failure to pace 71, 74
Diaphragmatic paralysis 142 Failure to sense 71, 73
Diazepam 217, 227, 230 Fat 125
Diazoxide 78 Febrile seizures 232
Differential counts 283 Fentanyl 87, 219, 225
Digoxin 33, 58 Fibrinogen 259, 261, 262
Diltiazem 54, 80 Fibrinogen degradation products 259
Dilution of solutions 299 Fibrinolysis 257
Dipyridamole 267 FiO2 169
Disseminated intravascular First-degree AV block 64
coagulation 260 First-degree heart block 63
Dobutamine 25, 26 Flow rate 168
ERRNVPHGLFRVRUJ
310 Index
Flow waveforms 170 Hyponatremia 108

Fluconazole 213, 215 Hypothermia 99
Fluid prescription after open heart
surgery 295 I
Fluid therapy 102 I:E ratio 168
Fluoroquinolones 187 Ibuprofen 222
Fosphenytoin 228 Idioventricular rhythm 50
FrankStarling law 18 ImipenemCilastatin 187, 196
French gauge catheter scale 279 Infection 202
Fresh frozen plasma 263, 265 Inj. ranitidine 137
Furosemide 34 Inspiratory pause 170
Fusobacterium 184 Intermittent mandatory ventilation
159
G International normalized ratio 258
Gastric residue 134 Intracranial pressure 237
Generic code for pacemakers 65 Intrinsic coagulation pathway 257
Gentamicin/tobramycin 196 Ipratropium 152
Gentamicin 187 Isoproterenol 25, 26
Glasgow coma scale 233 Itraconazole 215
Glomerular ltration rate 242 IV cannula and needle gauge 279
Glucagon 276
Glucose homeostasis 110 J
Glycopeptides 188 JET 59
Gram-negative bacilli 183 Junctional ectopics 46
Gram-positive cocci 182 Junctional ectopic tachycardia 46
Griseofulvin 215 Junctional rhythm 46
H K
H. inuenzae 183 Ketamine 87, 220
Heart blocks 63 Ketoconazole 215
Hematological parameters 283 Kitchen based feeds 132
Heparin 127 Klebsiella 183
Histoplasmosis 211
Human milk fortier 132 L
Hydralazine 78, 80 L-adrenaline 152
Hydrochlorothiazide 34 Labetalol 79, 80
Hydrocortisone 152, 273, 276 Laryngeal mask airway 92
Hydrogen ion 112 Left atrial pressure 8
Hypercarbia 172 Left heart failure 147
Hyperkalemia 104 Left ventricular end diastolic
Hypernatremia 109 pressure 8
Hypertensive crisis 81, 84 Levetiracetam 229
Hypertensive emergency 81 Levooxacin 187, 197
Hypertensive urgency 81 Lignocaine 54, 89, 94
Hypertonic saline 239 Lincosamides 188
Hypocalcemia 105 Linezolid 188, 197
Hypokalemia 103 Lorazepam 217, 227
Hypomagnesemia 107 Losartan 35
ERRNVPHGLFRVRUJ
Index 311
Low cardiac output 15 N

Lumbar puncture 237
Naloxone 90
M Narrow QRS complex arrhythmias 52
Narrow QRS complex tachycardias 57
Macrolides 189
Natural penicillins 184
Magnesium 90, 94
Netilmicin 187
Magnesium sulfate 54, 90
Nicardipine 79
Maintenance uid requirement 101
Nifedipine 80
Maintenance therapy 100
Nimesulide 222
Management of sepsis 206
Nitroglycerin 25
Mannitol 239
Non-anion gap acidosis 119
Mean arterial pressure 1
Nonsustained VT 50
Mean corpuscular hemoglobin 283
Noradrenaline 25, 27
Mean corpuscular hemoglobin
Normal breathing 156
concentration 283
Normal ECG 37
Mean corpuscular volume 283
Normal hemostasis 256
Meropenem 187, 197
Normal laboratory values for
Metabolic acidosis 119
children 285
Metabolic alkalosis 120
Normal sinus rhythm 39
Methicillin-resistant Staph. aureus
NTG 27
183
Nutritional requirements 124
Methicillin 185
Nystatin 215
Methylprednisolone 152
Metoclopramide 136
O
Metolazone 34
Metoprolol 35, 55, 80, 87 Oculocepahalic reex (Dolls eyes
Metronidazole 198 movement) 236
Micafungin 213, 215 Oculovestibular reex 236
Midazolam 87, 218, 225, 227, 230 Ooxacin 187
Milrinone 26, 27 Omeprazole 137
Mixing of solution 299 Ondansetron hydrochloride 136
Mobitz type 1 second-degree heart Organ dysfunction criteria 203
block 63 Orthodromic AVRT 45
Mobitz type 2 second-degree heart Osmotic diuresis 239
block 63 Overdrive pacing 59
Modied Ramsay sedation scale 223 Oxazolidinones 188
Modular formulas 132 Oxygen 98
Monobactams 188 Oxygenation 172
Monomorphic VT 49, 61 Oxygen content 113
Morphine 87, 219, 225
Mostellars formula 282 P
Motor milestones 281 Pacemaker mediated tachycardia
MRI 237 72, 75
MRI in patients with pacing Pacemaker output 67
wires 76 Pacemaker parameters 67
Multifocal atrial tachycardia 43 Pacemaker settings 69
Muscle relaxants 222 Pacing modes 65
Myoclonus 236 Pacing rate 68
ERRNVPHGLFRVRUJ
312 Index
Packed RBCs 263 Prerenal failure 246

Packed red cells 265 Pressure assist control 163
PALS protocols 94 Pressure controlled ventilation 162
Pancuronium 221 Pressure control ventilation 171
PAP complexes 262 Pressure limit 170
Paracetamol 222 Pressure preset modes 162
Partial pressure of carbon dioxide 113 Pressure preset SIMV 163
Partial pressure of oxygen 113 Pressure preset ventilation 157
Peak airway pressure 173 Pressure regulated volume control
Pediatric advanced life support 91 167
Pediatric basic life support 90 Pressure scales 278
Pediatric blood levels of commonly Pressure support ventilation 163
used drugs 306 Pressure support weaning 174
PEEP 169 Prevotella 184
Penicillinase-resistant penicillins 185 Primary brinolysis 261
Penicillin G 184 PR interval 37
Peritoneal dialysis 246 Procainamide 55
pH 112 Procaine penicillin 184
Phenobarbitone 228 Prochlorperazine 136
Phenylephrine 25, 27, 88 Propofol 220, 230
Phenytoin 228 Propranolol 81, 87
Phenytoin sodium equivalent units Prostacyclin 28
228 Proteus 183
PIP 170 Prothrombin time 258
Piperacillin 198 Pseudomonas 183
Piperacillintazobactam 185, 198 Pulmonary arterial hypertension 83
Plasmin-antiplasmin complex 261 Pulmonary artery (PA) pressure 83
Plateau pressure 170 Pulmonary artery pressure 8
Platelet count 259 Pulmonary blood ow 85
Platelet transfusion 263 Pulmonary capillary wedge pressure 8
Pleural effusion 140 Pulmonary dysfunction 140
Pneumonia 176 Pulmonary hypertensive crisis 84
Pneumothorax 142 Pulmonary vascular resistance 10, 83
Polymorphic VT 49 Pulmonary vasoconstrictors 83
Posaconazole 213, 215 Pulmonary vasodilators 83
Positive end-expiratory pressure 164 Pulseless electrical activity 51, 96
Post CPB bleeding 260 Pulseless ventricular tachycardia 95
Postoperative bleeding 262 Pulseless VT 50
Postoperative checklist on arrival in Pulse pressure 2
ICU 290 Pulsus alternans 4
Postoperative instructions 291 Pulsus paradoxus 5
Postoperative seizures 231 Pulsus tardus et parvus 4
Post ventricular atrial refractory P wave 37
period 69
Preload 19 Q
Preparation of various concentrations QRS complex 38
of solutions 299 QT interval 38
Prerenal azotemia 241 Quinupristindalfopristin 199
ERRNVPHGLFRVRUJ
Index 313
R Size and length of pediatric

endotracheal tubes and suction
Random donor platelets 265
catheters 289
Ranitidine 137
Sodium bicarbonate 87, 90, 94
Rapid sequence intubation 224
Sodium nitroprusside 25, 27, 79
Re-exploration 263
Sodium valproate 229
Recombinant factor VII 264
Sources of sepsis 204
Refractory seizures 230
Spironolactone 35
Relationship among units 278
Standard bicarbonate 115
Removal of pacing wires 76
Standard infant formula 131
Renal replacement therapy 246
Staphylococci 182
Respiratory acidosis 118
Streptococci 183
Respiratory alkalosis 118
Stress ulceration 137
Respiratory rate 168
Stroke volume 11, 18
Reticulocyte count 283
Stupor 234
Rifampin 199
Succinylcholine 221
RIFLE criteria 243
Sucralfate suspension 137
Right ventricular end diastolic
Supraventricular tachycardia 51, 60
pressure 8
Sustained VT 50
Rocuronium 221
Synchronized intermittent mandatory
ventilation 159
S Synchronized ventricular pacing 70
Salbutamol 151 Systemic arterial oxygen saturation
Same direction rule 115 8, 113
Schwartz equation 243 Systemic inammatory response
SCUF 251 syndrome 202
Second-degree AV block 64 Systemic vascular resistance 10
Sedation for short procedures 224 Systemic venous oxygen saturation 10
Sedatives 217, 223 Systolic overshoot 3
Sensing threshold 68
Sensitivity 169 T
Sepsis 202, 203 TAT complexes 261, 262
Septic shock 17, 202, 203 Teicoplanin 188, 200
Serratia 183 Temperature scales 278
Serum tryptase 274 Terbinane 215
Severe sepsis 202, 203 Terbutaline 153
Sigh 169 Theophylline 152
SIMV 167 Therapeutic overdrive pacing 75
SIMV + PS 166 Thiocyanate toxicity 2731
SIMV weaning 174 Thiopental sodium 220, 230
Single donor platelet 265 Third-degree AV block 64
Sinus arrest 41 Thrombin time 258
Sinus arrhythmia 41 Thrombin-antithrombin
Sinus bradycardia 40 complex 261, 262
Sinus tachycardia 40 Ticarcillin 199
SIRS 200, 202 Ticarcillinclavulanate 186, 200
SI units and conversion factors Tidal volume 167
277 Tobramycin 187
ERRNVPHGLFRVRUJ

Manual of Pediatric Cardiac Intensive Care

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Graham Nunn FRACS

2 Low Cardiac Output 15

3 Inotropes and Other Vasoactive Drugs 24

4 Congestive Heart Failure 32

6 Bradyarrhythmias and Pacemakers 63

11 Fluid and Electrolytes 100

12 Arterial Blood Gas Analysis 112

13 Parenteral Nutrition 124

14 Enteral Feeding 130

15 Gastrointestinal Drugs 136

16 Postoperative Respiratory Complications 140

17 Acute Respiratory Distress Syndrome 146

18 Postoperative Bronchospasm 150

20 Ventilator Associated Pneumonia 176

22 Sepsis and Multiorgan Dysfunction 202

23 Systemic Antifungal Agents 211

24 Sedatives, Analgesics, and Muscle Relaxants 217

26 Management of the Comatose Child 233

27 Acute Kidney Injury 241

28 Coagulation Disorders in the Postoperative Period 256

29 Antithrombotic Agents 267

30 Management of Anaphylaxis 273

100 valve closes

Fig. 1: Cardiac cycle.

Mean Arterial Pressure

The mean arterial pressure (MAP) determines the volume of blood ow to

MAP = (CO SVR) + CVP

MAP = DBP + 1 3 (SBP DBP)

(SBP: systolic blood pressure, DBP: diastolic blood pressure)

Fig. 2: Normal arterial pressure waveform.

Analysis of the Arterial Pressure Waveform

The arterial pressure waveform consists of an upstroke to the level of the

Site of recording: The arterial pressure waveform also changes as it

Pulses tardus et parvus

Pulsus paradoxus is an exaggeration of the inspiratory fall in systolic

Blood pressure variation during positive pressure ventilation: A phe-

Analysis of the Central Venous Pressure

x descent: The x descent is caused by the downward movement of the

Abnormal CVP Waveforms

Canon a waves are produced in AV dissociation because of contraction of

Normal Pressures and Saturations in Pediatric Heart

Chamber Pressure (mmHg) O2 saturation (%)

Chamber Pressure (mmHg) O2 saturation (%)

Left ventricular end diastolic pressure (LVEDP) is a reection of LV function,

Right ventricle Pulmonary artery

Systemic Arterial Oxygen Saturations

In normal individuals, systemic arterial oxygen saturation (SpO2) is

Systemic Venous Oxygen Saturation

Systemic venous oxygen saturation (SvO2, normal range: 6080%) can be

Calculation Child normal Adult normal

Arterial O2 content Venous O2 content is also known as the arterio-venous

Systemic Vascular Resistance

peripheral vasodilation (e.g., in septic shock or as a result of administra-

Pulmonary Vascular Resistance

The ratio of pulmonary to systemic blood ow (Qp/Qs) is used to

more accurately by obtaining systemic and pulmonary blood ows by the

Clinical Evaluation of Low Cardiac Output

Parameter Normal perfusion Low cardiac output

Skin, Temperature, and Peripheral Pulses

Mixed Venous Saturation

The clinical manifestations are different in patients with vasodilatory

Factors Controlling Cardiac Output