Anasthesia Handout - Final-9awa3i8 PDF

Anesthesia handout
Academic secretary 9awa3i8 2014/15

^^ REMEMBER: If there is a WILL there is a WAY
1/1/2015
Prepared by: Tayba M. Ahmed & Esra Abdallah

:

^^"
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Table of content
topic
Page No.
1-Introduction to anaesthesia & intensive care
2-Body fluids & electrolytes
3-Basic life support
18
4-preanasthetic medications
23
5-preanasthetic assessment
26
6-Conduct of general anaesthesia
32
7-Intraoperative complication of GA
34
8-Intravenous anaesthetics
41
9-Inhalational anaesthetics
51
10-Management of critically ill patient
56
11-Muscle relaxants
74
12-Blood transfusion
78
13-Analgesics
87
14-Local analgesia
93
15-Neuraxial anaesthesia (spinal anaesthesia)
95
16-Oxygen therapy
101
17-shock
114
18-drugs that affects autonomic nervous system
129
19-Advanced life support
139
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Introduction to anaesthia and intensive care

Types:
1.
2.
3.
General Anesthesia
Local Analgesia
Regional Analgesia
1. General anesthesia:
Patient is unconscious (sleeping)
Not feeling pain (i.e. Analgesia)
Relaxed and quite :
Muscle relaxants.
Anesthetic Drugs (IV, Inh).

2. Local anesthesia:
Awake patient.
No pain (enough analgesia + Sedation).
+ sedation.
3. Regional anesthesia:
Spinal Anesthesia.
Epidural Analgesia.
Groups of nerves (e.g. Brachial P.B.)
Single nerve block (e.g. Radial ,etc)
Mucosal block (e.g. Oral cavity spray or gel )
Ssurface or topical infiltration
IV analgesia
Intensive care
An area where intensive and meticulous care are being provided to the
patient.
Monitoring :
Invasive .
Non invasive: Pulse , RR, PO2 % ,urine output, fluid
balance ,BP , etc
Types of patients presents:

1.
2.
3.
4.
Critically ill patients (e.g. Cardiac , respiratory , sever vital

organ affection e.g. Liver, brain , kidneys ,etc..).
Severe infection (e.g. sepsis,).
Shock .
Critical surgery . 5.Neonatal surgery
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Body Fluids
A proper management of patients with water and electrolyte disorders requires an
understanding of water and electrolytes physiology.
Distribution of Body Fluids:
Intracellular fluid (ICF)-Inside cells
Extracellular (ECF)-Outside cells
ICF and ECF are separated by the cell membrane.

ECF volume is subdivided into the interstitial and intravascular ( plasma)
volumes; separated by the vessel wall.
Body Fluid Volumes (The 60: 40: 20 Rule):
Total Body Water (TBW)= 60% Body weight (Kg)
ICF= 40% Body weight
ECF= 20% Body weight
Plasma Volume= 5% Body weight
Composition of Body Fluids

Intracellular Fluid
Two times the volume of extra cellular fluid
Potassium (K+) is the major cation
Immobile proteins and phosphates are the major anions

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Composition differs slightly in different tissues to enhance function
pH is close to 7.0.
The cell membrane is selectively permeable to ions but freely

permeable to water which moves to equilibrate intra and
extracellular osmolalities.
Extracellular Fluid
One-half the size of Intracellular Fluid
Sodium (Na+) is the major cation
Chloride (Cl-) is the major anion
pH is 7.45.
The capillary endothelium is freely permeable to water, ions and

many substances such as glucose (but not proteins); therefore, the
composition of interstitial fluid and plasma are similar.
Extracellular fluid is subdivided into three compartments:
Interstitial fluid:- between cells (largest)
Plasma fluid:- in the vascular space
Transcellular fluid:-highly specialized
Interstitial versus Plasma Fluid:

Virtually identical except:
Plasma contains about 5% protein
Albumen is the most abundant protein
Made in the liver to hold fluid in the vascular space against the
hydrostatic pressure created by the heart
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Transcellular Fluids
Cerebrospinal-Ventricles, spinal canal-outside the brain and spinal

cord
Intraocular-inside chambers of the eye
Pleural-between the lung and chest wall
Synovial-in the joints
Peritoneal-between the abdominal wall and the abdominal organs
Digestive secretions-inside GI tract
Pathophysiology of Transcellular Fluid:

Abnormal collection of transcellular fluid can lead to:
Cerebrospinal-hydrocephalus
Intraocular-glaucoma
Pleural-effusion
Peritoneal-ascities
Synovial-pain and restricted movement
GI secretions-ECF volume depletion, abnormal pH (acid-base

disturbances), abnormal ECF [K]
GI secretions volume (ml) per day:
Saliva
1500
Gastric
2500
Bile
500
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Pancreatic
700
3000
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to see in z world
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TOTAL
8000
Fluid Movement
1- Capillary Beds
Capillaries allow free movement of ECF fluid (ions and water).
Hydrostatic pressure (Hp) tries to push fluid out of the capillary

while colloid Osmotic Pressure (COP) of plasma proteins pulls fluid
into the capillary.
The net fluid movement is determined by the balance of Hp and COP
Normally no net fluid movement (exceptions are GI and renal

capillaries)
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2- Cell Membranes:
Osmotic Equilibrium between Body Fluid Compartments:
Body fluid compartments are in osmotic equilibrium
Water moves freely- driven by the osmotic gradient
Ratio of solute/volume = Osmolality
Normal value = 290 +/- 10 mOsm/liter
Osm of ICF = ECF = Plasma
Plasma Osm is 1 mOsm/l > interstitial fluid volume due to COP
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Water moves freely- driven by osmotic gradient
Energy is needed to move Ions /molecules against electrical

and concentration gradients (Active Transport) into and out of
the cells (exceptions e.g., urea, alcohols)
Hp and COP in capillaries do not affect the movement of water

and molecules between ICF and Interstitial fluid
Water homeostasis:
In an adult, the mean uptake and elimination of water per 24
hours, at conditions of rest, is as follows:
Source
Uptake (ml)
Elimination
Output (ml)
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Oral fluids
1300
kidneys
1500
Solid foods
800
skin
500
Oxidation
(metabolic
water)
400
Lungs
400
Intestine
100
Total
2500
2500
The daily fluid requirements:

Calculating the estimated fluid requirement of an adult per day
under conditions of rest can be achieved using:
1. Certain formulas.
2. Certain regimes.
3. Certain rules.
1. Formulas:
*Fluid requirement = 20 40 ml/kg/day
*4-2-1 formula:
This is the best assessment for almost all age groups except newborn
infants.
4 ml/kg/h (for each of the first 10 kg of BW)

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PLUS
2 ml/kg/h (for each of the second 10 kg of BW).

PLUS
1 ml/kg/h (for each subsequent kg of BW).
Example of 4/2/1 formula:

A 5 kg infant needs??
4 x 5 = 20 ml/h or 500 ml/day.
A 25 kg child needs??
4 x 10 = 40 ml/h +
2 x 10 = 20 ml/h +
1 x 5 = 05 ml/h.
i.e.
65ml/h.
OR 1550 ml/day
2. Regimes :
70 kg patient requires daily provision of 2000 2500 ml of water
and approximately 70 mmol each of Na+ & K+.
This could be administered as one of the following:
a) 2000 ml of glucose 5% + 500 ml of saline 0.9%
b) 2500 ml of glucose 4%/saline 0.18%; plus potassium as KC1, 1 g
(13 mmol) added to each 500 ml of fluid.
3. RULES (Practical fluid balance):

RULE (1) :
All infused Na+ remains in the ECF. Na+ cannot gain access to
the ICF because of the Na-K pump.
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If saline 0.9% is infused, all Na+ remains in the ECF. As this is

isotonic solution, there is no change in the ECF osmolality and
therefore no water exchange occurs across the cell membrane.
Thus saline 0.9% expands ECFV only and is the resuscitation

fluid of choice.
However, if saline o.45% (hypotonic) is given, ECF osmolality

decreases, this causes a shift of water from ECF to ICF (leading
to cellular swelling).
If saline 1.8% (hypertonic) is administered, all Na+ remains in

the ECF, its osmolality increases and water moves from ICF to
ECF to maintain osmotic equality (leading to cellular shrinkage
and intracellular dehydration).
RULE (2) :
IV of 1000 ml
Saline
Water without Na+ expands the TBW.
After infusion of a solution of glucose 5%, the glucose enters

cells and is metabolized.
The infused water enters both ICF and ECF in proportion to

their initial volumes
Change in Volume
)mL)
ECF
ICF
+ 1000
Remarks
Na+ remains in ECF
0.9 %
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Glucose
+ 333
+ 666
5%
66% of TBW is
ICF
Saline 0.45 %
+ 666
+ 333
33% of TBW is
ICF
RULE (3) :
The daily fluid requirements for surgical patients may be allocated
usefully into three processes:
Normal maintenance needs.
Abnormal losses resulting from underlying pathology.
Correction of pre-existing deficit
1- NORMAL MAINTENANCE NEEDS:

A. WATER:
Regardless of the disease process, water & electrolyte losses

occur in urine and as evaporative losses from skin and lungs.
A normothermic 70 kg patient with a normal metabolic rate

may loss 2500 ml of water per day.
Allowing for a gain of 400 ml from water of metabolism, this

hypothetical patient needs 2000 ml
As a rule of thumb:
a volume of 30 35 ml/kg/day of water is a useful estimate for
daily maintenance needs.
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B. SODIUM:
The normal requirement is:
1 mmol / kg / day, 50 80 mmol / day OR 2 3 mmol / hour.
C. POTASSIUM:
The normal requirement is:
1 mmol / kg / day, 50 80 mmol / day OR 2 3 mmol / hour.
2-ABNORMAL LOSSES:
These may be sensible or insensible.
May result from:
1. Prolonged lack of oral intake.
2. Diarrhea and vomiting.
3. Haemorrhage.
4. Diuretic use.
5. Sever inflammatory illness.
6. Surgery and trauma (Third space losses).
7. Fever/hyperventilation (increased insensible losses).
Fluids are needed to replace intraoperative blood losses, losses in the
third space, from the skin, gut and lungs.
Losses from the gut:

Nasogastric suction, diarrhea and vomiting or sequestration of fluid
within the gut lumen):
These should be replaced with saline 0.9% with 13-26 mmol/ L
Increased insensible losses: (fever or hyperventilation):

The usual insensible loss of 0.5 ml/ kg/hr increases by 12% for each 1
0
C rise in body temperature.
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Third space losses:

Sequestration of plasma-like fluid in any area of tissue injury or
surgical site:
Volume lost is proportional to the extent of trauma and contained
fluids are reabsorbed after 2-3 days. These losses are uneasy to
measure and requirements can be guided by measurement of CVP.
3-EXISTING DEFICITS:
These occur pre-operatively and arise primarily from the gut.
The difficulty in correcting these deficits relates to an inability to

quantify their magnitude accurately.
Fluids and electrolytes deficits occur directly from the ECF.
If the fluid lost is isotonic, only ECFV is reduced, however if water

alone or hypotonic fluid is lost, redistribution of the remaining TBW
occurs from ICF to ECF to equalize osmotic forces.
Dehydration with accompanying salt loss is a common disorder in

the acute surgical patient.
ASSESSMENT OF DEHYDRATION:
1-History:
How long has the patient had abnormal loss of fluid?
How much has occurred (e.g. frequency of vomiting)?
2-Examination:
Specific features are:
Thirst.
Dryness of mucous membrane.
Loss of skin turgor.
Orthostatic hypotension.
Tachycardia.
Reduced JVP.
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Decreased urine output:

In the presence of normal renal function, dehydration is associated
usually with a urine output of less than 0.5 ml/kg/h.
The severity of dehydration may be described clinically as mild,

moderate or severe and each category is associated with certain water
loss relative to body weight.
Fluid Replacement :
The postoperative stress response modifies homeostatic
mechanisms, causing retention of Na+ and water and increased renal
excretion of K+. However, fluid and sodium restriction in the
postoperative period is not recommended because of increased
losses by evaporation and into the 'third space'. Postoperative fluid
and electrolyte requirements should ideally be assessed by
measurement of CVP and serum electrolyte concentrations.
Normally, potassium is not administered in the first 24 h after
surgery as endogenous release of potassium from tissue trauma and
catabolism warrants restriction.
Patients with renal failure require fluid replacement determined by
the urine output plus insensible losses and any abnormal losses.
Fluid replacement can be undertaken with crystalloid, colloid or
blood products.
1. CRYSTALLOID:
Initially fluid should be replaced through the administration of an

isotonic salt solution.
There is no formula for calculating the amount of saline required
to correct extracellular fluid depletion.
The adequacy of repletion must be assessed clinically by heart
rate, blood pressure, urine output and haematocrit.
Further management of electrolyte and acid base abnormalities
should be based on laboratory studies.
When crystalloid solution containing a concentration of Na +
isotonic with plasma is used to replace blood, about of the
solution will pass into the interstitial space and will remain in
the intravascular space.
2. COLLOID:
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Are fluids containing particles that are large enough to exert an

oncotic pressure compared with crystalloid, they remain within
intravascular space longer.
3. BLOOD PRODUCTS:
Their use should be guided by laboratory measurement of:
a) Haematocrit.
b) Platelet count.
c) Coagulation parameters.
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BASIC LIFE SUPPORT

OBJECTIVES
How to assess the collapsed victim.
How to perform chest compression and rescue breathing.
How to place an unconscious breathing victim in the recovery position.
BACKGROUND
Survival to hospital discharge presently approximately 5-10%
Bystander CPR vital intervention before arrival of emergency services
Early resuscitation and prompt defibrillation (within 1-2 minutes) can

result in >60% survival
CHAIN OF SURVIVAL
APPROACH SAFELY!
CHECK RESPONSE
SHOUT FOR HELP
OPEN AIRWAY
CHECK BREATHING
Call for definitive help
30 chest compression
2 rescue breath
Approach safely:
Scene
Rescuer
Victim
Bystanders
NB.only isolated reports of infections such as tuberculosis (TB) and
severe acute respiratory distress syndrome (SARS). Transmission of HIV
during CPR has never been reported. barrier devices specially at times of
outbreaks
Other appropriate safety precautions
Check response:
Shake shoulders gently
Ask Are you all right?
If he responds
Leave as you find him.
Find out what is wrong.
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Reassess regularly.
If not.. SHOUT FOR HELP
Open airway
Turn the victim onto his back and then open the airway
using head tilt and chin lift.
Place your hand on his forehead and gently tilt his head
back.
With your fingertips under the point of the victim's chin, lift
the chin to open the airway.
NB. The jaw thrust technique is not recommended for lay
rescuers because it is difficult to learn and perform. Therefore,
the lay rescuer should open the airway using a head-tilt chin-lift
manoeuvre for both injured and non-injured victims.
Check breathing:
Look, listen and feel for NORMAL breathing

Do not confuse agonal breathing with NORMAL breathing
Look for chest movement.
Listen at the victim's mouth for breath sounds.
Feel for air on your cheek.
Check for no more than 10 s to determine if the victim is
breathing normally.
If you have any doubt whether breathing is normal, act as if it
is not normal.
o AGONAL BREATHING
Occurs shortly after the heart stops in up to 40% of cardiac
arrests
Described as heavy, laboured, noisy or gasping breathing
Open mouth
Loud
The patient may be barely breathing.
Recognise as a sign of cardiac arrest
Ask someone to:

Call for an ambulance.
Bring an AED (automated external defibrillator)
If you are on your own, use your mobile phone to call for an
ambulance.
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If in a hospital, call for Cardiac Arrest Team.

Or ask your colleagues to start Advanced Life Support.
Leave the victim only when no other option exists for getting
help.
NB.During the first few minutes after non-asphyxial cardiac
arrest the blood oxygen content remains high. Therefore,
ventilation is less important than chest compression at this
time.
CHEST COMPRESSIONS
Kneel by the side of the victim if on the ground.
Or bring the patients bed down to a convenient level.
Or kneel on top of the patients bed.
If the bed is not hard enough bring the patient down on the
ground.
Place the heel of one hand on the centre of the victims chest
This is the lower half of the victims sternum.
Place other hand on top
Interlock fingers
Position yourself vertically above the victim's chest.
With your arms straight at the elbow.
Ensure that pressure is not applied over the victim's ribs.
Do not apply any pressure over the upper abdomen or the
bottom end of the sternum.
Compress the chest:
Rate 100/min
Depth 4-5 cm
Equal compression : relaxation
Do not lose contact between your hands and the sternum.
When possible change CPR operator every 2 min
Ensure the minimum of delay during the changeover of rescuers,
and do not interrupt chest compressions.
Rescue breath:
Re-open the airway
Head tilt & chin lift
Pinch the nose closed
Take a normal breath
Place lips over mouth
Obtain a good seal
Take a normal breath
Blow until the chest rises
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Take about 1 second

Allow chest to fall
Repeat
This is an effective rescue breath.

The two breaths should not take more than 5 s.
NB.Mouth-to-nose ventilation is an effective alternative to mouth-to-mouth
ventilation. It may be considered if the victims mouth is seriously injured or
cannot be opened, if the rescuer is assisting a victim in the water, or if a
mouth-to-mouth seal is difficult to achieve.
Stop to recheck the victim only if he shows signs of regaining
consciousness, such as:
Coughing
Opening his eyes
Speaking
Moving purposefully
AND starts to breathe normally
Otherwise do not interrupt resuscitation until qualified help arrives and

takes over.
OR you become exhausted.
IF VICTIM STARTS TO BREATHE NORMALLY PLACE IN RECOVERY

POSITION
Recovery position
The position is:
Near a true lateral position
Stable.
With the head and mouth dependent
With no pressure on the chest to impair breathing.
Kneel beside the victim and make sure that both his legs are
straight.
Place the arm nearest to you out at right angles to his body,
elbow bent with the hand palm-up.
Bring the far arm across the chest, and hold the back of the
hand against the victims cheek nearest to you.
With your other hand, grasp the far leg just above the knee
and pull it up, keeping the foot on the ground.
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Keeping his hand pressed against his cheek, pull on the far
leg to roll the victim towards you on to his side.
Adjust the upper leg so that both the hip and knee are bent
at right angles.
Tilt the head back to make sure that the airway remains
open.
If necessary, adjust the hand under the cheek to keep the

head tilted and facing downwards to allow liquid material to
drain from the mouth.
Check breathing regularly.
Paediatric cpr
Give 5 initial rescue breaths before starting chest compressions
Compress the chest by one third of its depth.
Use two fingers for an infant under 1 year
Use one or two hands for a child over 1 year as needed to
achieve an adequate depth of compression.
Rate 100-120/min
C:V ratio of 15:2
C:V ratio at birth is 3:1
If you are on your own, perform CPR for 1 min before going
for help.
Drowning cpr
The same modifications of five initial breaths, and 1 min of
CPR by the lone rescuer before getting help, may improve
outcome for victims of drowning.
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Preanaesthetic assessment
Preanaesthetic assessment is made to assess the patient fitness to

anaesthesia and surgery, and to discuss different types of anaesthesia
that can be given and the complications which may arise from both
anaesthesia and the surgery.
When to do the assessment .
1. for elective surgery
In the referred clinic where the surgical diagnosis is
made (Combined discussion between the patient,
surgeon and anesthetist "which is best")
In the surgical word, if the patient is hospitalized
2. for emergency
In the surgical word
In the theatre reception "top emergency"
Types of patients for assessment

o
o
o
o
fit adult
Children and neonates for elective or emergencies.
old and elderly
Ill or sick patient
for emergencies.
Systems to be assessed
Routine history taking. (Name, sex, age ...etc)

General condition of patient (does the patient look ill, febrile,
etc..)
Assessment of systems :
CVS: pulse, cardiac examination, BP, signs of heart failure
murmurs, valvular lesions, cardiomyopathy.etc...
Respiratory system examination
Liver, renal and CNS systems to be examined as well.
Problems anticipated in adults:

Fit adult without systemic diseases
adult + systemic disease
High BP medication or no medication
- Effect of high BP on heart and kidneys.
Diabetes medication or no medication
- Effect of diabetes on heart, kidneys.. etc..
Jaundice - Effects on liver & kidneys
effects of drugs taken by the patient

Systems affected and anesthetic drugs given
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Children and neonates

o problems anticipated :
Congenital diseases and abnormalities affecting the
anesthetic management. eg. Con. Heart disease with
hernia
child cooperation
venous canulation
temperature regulation
blood volume and blood loss assessment
Investigations required
In a fit patient "no systemic disease"
Urine examination, CBC , ECG , chest x-ray ( for patient above
40 )
+ blood grouping, cross matching , preparation.
Specific investigations :
Investigations considering the affected systems:
Cardiac patient : chest x-ray ECG ,eco, referral to
cardiologist
Respiratory problems: lung functions, referral
to chest physician
Diabetes : blood sugar, urine for sugar and

acetone.
Chest x-ray and ECG, renal and liver function.
Liver problems : LFT, coagulation profile
Premedication:
Drugs given:
before anaesthesia and surgery

day or more before surgery
Immediately before induction.
Indication for premedication:

Optimal control of a preexisting disease e.g diabetes,
hypertension, etc...
continue same medication increase or decrease", or
change medication.
Assess in induction( to decrease induction agent)
Eg. Sedatives and tranqulizers
Decrease side effects of anaesthetic drugs. (anticholinergic

eg. Atropine )
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Analgesia : for a patient with pain

For specific patients: anti acids, H2 blocker, and drugs
increase gastric motility.
NB
The patient should be fasting before the surgery for at least 4 to 6

hours, even when local anaesthesia is being used .
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Premedication
Definition:
Premedication refers to the administration of drugs in the period 1-2 h before
induction of anaesthesia.
Objectives are:
Allay anxiety and fear.

Reduce salivary secretions.
Enhance the hypnotic effect of general anaesthetic agents.
Reduce postoperative nausea and vomiting.
Produce amnesia.
Reduce the volume and increase the ph of gastric contents.
Attenuate vagal reflexes.
Attenuate sympathoadrenal responses.
Drugs Used for Premedication:

SEDATIVES
1. Benzodiazepines
Effects:
Sedation
Anterograde amnesia
Anxiolysis
Potentiation of some IV induction agents e.g propofol &
thiopentone
Action
On GABA receptors
Examples
Temazepam 0.5mg/kg orally
Midazolam (Hypnovel) 70-100mcg/kg IM or IV
Lorazepam (Ativan) 30-50 mcg/kg oral - IM
Diazepam (Valium) 10-20mg oral - IV
Reversal:
Flumazenil (Anexate) 100-200 mcg IV up to 1mg
2. Phenothiazines:
Effects:
Central antiemetic action
Sedation
Anxiolysis
H2 receptor antagonism
adrenergic antagonism
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Adverse Effects:
Potentiation of opioid analgesia

Extrapyramidal side effects
Synergism with opioids which may delay postop recovery
Potentiation of the hypotensive effects of anaesthetic
agents
Especially in children; they may show signs that mimick
that of hypovolemia i.e pallor, tachycardia and
hypotension
Examples
a.Promethazine (Phenergan)
Dose 25-50 mg 1m
b. Trimeprazine tartrate (Vallergan)
Dose 2mg/kg 2hrs preop. Orally
Suitable premedicant for small children
3.Butyrophenones:
Effects
Neuroleptic effects (withdrawal & seclusion).
blocking actions.
Antiemetic effects.
Adverse Actions
Dose dependent dysphoric reactions.
Extrapyramidal side effects.
Delay recovery from GA.
Examples
a. Haloperidol
Not much used in anaesthesia
b. Droperidol
Very popular in anaesthesia as an antiemetic
Dose 1.25mg - IV
ANALGESICS:
1.Opioids:
Effects
Powerful analgesics
Sedation but not anxiolysis
Decease the concentration of volatile anaesthetics
used for maintenance of anaesthesia
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Adverse Actions
Depression of ventilation and delayed resumption of
spontaneous ventilation at the end of NO2 /Os
relaxant technique
Nausea and vomiting
Should be used in combination with an antiemetic e.g.
hyoscine, phenothiazine or a butyrophenone
Morphine cause spasm of the sphincter of Oddi rt upper
quadrant pain
It also causes histamine release & therefore contraindicated in
asthmatics
Examples:
Morphine - single bolus dose 10-15mg IV
or 2-5 mg IV at 20 min interval
Pethidine - 25-50 mg IV
or 100-150 mg IM
Fentanyl - 50-100mcg IV
Al Fentanil 500 mcg
Others
Antagonist:
Naloxone
Adult dose 200-400 mcg IV
NS A I Ds
Effects
Give useful background analgesia upon which intra &

postop. opiates develop an enhanced analgesic
effects.
Examples
Ketoprofen - dose 100-200 mg oral or rectal 30mg
Im/IV
Diclofenac - dose 50-100 mg oral or rectal or Im
Others
Anticholinergic Agents
Effects
Antisialagogue effects
Sedative and amnesic effects
Prevention of reflex bradycardia
Block ocuto cardic reflex in ophthalmic surgery
In association halothane anaesthesia
28 | P a g e

Adverse Effects
a. CNS toxicity manifested by the central
anticholinergic syndrome which include
restlessness, agitation & somnolence
convulsion + coma
M ad as a h at t e r
Hot as a hen
Blind as a bat
Red as a beetroot
Dry as a Bone
- commonly seen with atropine
- treated with physostigmine and
glycopyrronium
b. Reduction in LOS tone
c. Tachy cardia
- should be avoided in cardiac condition
d. Mydriasis and cycloplegia
e. Pyrexia
f. Excessive drying
g. Increased Physiological dead space by 20-25%
compensated for by in ventilation
Examples
Atropine tertiary amine

Dose 0.015 0.02 mg/kg Iv
Adult dose 0.6 mg IV
Adult 2 mg oral dose
Children 0.03 mg/kg oral
Hyoscine (Scopolamine) tertiary amine
Adult dose 0.3 0.6 mg Im
Glycopyrronium Bromide
- quaternary ammonium compound
Adult dose 0.2 0.4 mg IV
Children 4 mcg/kg
ANTIACIDS:
Effects
Raise the ph of gastric juice
Facilitate ulcer healing when given in high doses
Examples
Mg Al antiacids
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Non particulate antiacids, e.g Sodium Citrate

Dose 30 mls of 0.3 mol/L
1.H2 receptor blockers:

Effects
Reduce acid content
Reduce volume of gastric secretion
Examples
Raritidine dose 150 mg IV or Im 60-90 min preop.
Famotidine dose 40 mg
Nizatidine dose 150 mg
2.Proton-Pump Inhibitors
Effect
Reduction of acid secretion by inhibition of the
terminal stage of acid secretion (the proton pump)
Example: Omeprazole dose 20mg oral
3.Prokinetic Drugs
Effects
Increase the tone of LOS
Increase gastric and intestinal motility
Decrease stomach emptying time and reduce
incidence of regurgitation
Example: Metclopramide dose 10 mg Im or IV
Paediatric Premedication
Aims
1.
2.
3.
Reduce parental anxiety

Improve pt compliance
Decrease incidence of postop. Behavioural changes
Target Groups
Routine is unnecessary
Some children need it including the excessively upset,
those with previous unpleasant experience, pt with
developmental delay and the preschool age group
Suggested Premedicants are:

1.
2.
Midazolam 0.5 mg/kg orally 30 min preop

Trimeprazine 3mg/kg orally
30 | P a g e

3.
4.
Thiopentone 5 or 10 % solution administered rectally to induce basal

narcosis in children, dose 44 mg/kg
Ketamine
Some Suggested Combination Used for Premdication:
Papaveretum 20mg Im & Hyoscine 0.4 mg Im
Diazepam 10-15 mg oral or Lorazepam 2-3 mg oral
Atropine 0.6 mg Im & Promethazine 50 mg Im
For asthmatic patients:
Morphine 10 mg Im & Atropine 0.6 mg Im
Lastly:
Sedative Premedication Does Not Lessen the Need for Kind, Sympathetic care for
patients at a time of great stress
31 | P a g e
Conduct of general anaesthesia

Phases of anaesthesia;
Induction,,,,,,,maintenance,,,,,,,,recovery
Induction:
is of two types;
1. Intravenous e.g thiopentone,propofol,midazolam,ketamine
2. Inhalational e.g halothane,isoflourane,sevoflourane
Patient is checked in the preoperative visit by history ,
examination , investigations.
He is reassured, anaesthesia is explained and premedication given.
His airway is assessed.
Blood is prepared if needed for certain operations.
The patient is called to theatre.
History , examination and investigations revised. His blood is
checked for availability if relevant for the particular operation.
Check the anaesthetic machine for leaks, gases, alarms etc.
Prepare the emergency drugs
Prepare the anaesthetic drugs needed for the specific case
Prepare the laryngoscope , airway , mask and different sizes of
endotracheal tubes.
According to the type and length of operation the appropriate type
of anaesthesia is chosen.
For short procedures a purely inhalational technique with

spontaneous breathing is chosen either using a face mask or a
laryngeal mask airway.
For face , or ENT operations the airway should be secured by

endotracheal tube.
For long operations like abdominal operations, chest ,
cardiovascular and neurosurgical operations ETT is mandatory.
After the patient has slept , a muscle relaxant is given and the ETT
is introduced using a laryngoscope.
The ETT is checked by chest auscultation and capnograph and then
fixed with tape or adhesive plaster.
The patient is connected to the ventilator and artificial ventilation
is commenced after setting the ventilator.
Maintainance:
Anaesthesia is maintained by oxygen, nitrous oxide , halothane or
isoflourane plus opiod analgesic and or nonsteroidal
antiinflammatory drugs and or propofol infusion.
Top up doses of muscle relaxants can be given when needed.
32 | P a g e
Balanced anaesthesia is the recent type of anaesthesia where small

doses of a set of drugs are used to achieve all aspects of anaesthesia
with minimal side effects
Recovery;
When the operation is over , the patient is warmed up and given

100% oxygen.
All anaesthetics are stopped.
If only inhalational anaesthetics are given they will be excreted by

the lungs.
If muscle relaxants are given reversal drugs like neostigmine are

given to reverse paralysis.
When the patient is fully awake the ETT is removed .
The patient is transferred to the recovery room
He should be connected to the monitor to check the vital signs
The patient is then discharged to the ward or ICU according to the

patients condition.
33 | P a g e
Intraoperative complications of general anaesthesia

One per 9% of patients undergoing surgery
Risk factors :
a) Duration of surgery
b) Obesity
c) At extremes of age
d) Pts. undergoing obstetric& emergency anaesthesia.
Are they avoidable?
Most but not all.
*Assessment& preparation of pts.
*Assessment& preparation of anesthetic equipments.
CVS complications:
Arrhythmias
The most commonly reported CVS complications.

All types of arrhythmias can occur e.g. Tachycardias, bradycardias,
atrial arrhythmias, ventricular arrhythmias &cardiac arrest.
Most are caused by alteration in autonomic tone& hence
potentially avoidable.
Causes:
(Cardio-respiratory, metabolic, surgery& drugs)
1-Cardio-respiratory: Hypoxia, Hypo& hypercapnea, Hypotension.& MI.
2- Metabolic:
a) Catecholamines:
Exogenous e.g. Sympathomimetics.
Endogenous e.g. Light anaesthesia
* Light analgesia
*Airway manipulation
*Hyperthyroidism.
b) Hypo &hyperkalaemia.
3-Surgical:
*Vagal stimulation
*Direct cardiac stimulation (C.V.line ).
*Dental surgery.
4-Drugs:
*Vagolytics *Sympathomimetics
*Halothane *Digoxin.
34 | P a g e
Management:
o Correct the precipitating cause before giving anti-arrhythmic drugs.
Hypertension
Definition: Intraoperative hypertension is defined as systolic BP 25%
than the preoperative level.
Effects:
BP
afterload
myocardial work & ventricular wall tension
risk of ischaemia & infarction
risk of haemorrhage in other
organs( e.g. Brain ).
Etiology:
a). Preexisting :
Undiagnosed, poorly controlled, pregnancy induced.
b).Increased sympathatic tone:
*Hypoxia
*Hypercapnea
* Inadequate anaesthesia & analgesia.
*Airway manipulation (Endotracheal intubation ).
c). Drug overdose:
e.g. Ketamine, adrenaline, ephedrine, ergometrine.
d). Others:
Hypervolaemia, aortic cross-clamping, pheochromocytoma.
Management:
Preoperative control is essential. Surgery should be postponed to
achieve adequate control& to assess target organs function (e.g.
Brain, kidneys).
Premedication is indicated to reduce anxiety.
Anticipate the anaesthetic& surgical events that increases
sympathetic tone e.g. Laryngoscopy, extubation ,aortic crossclamping.
Avoid induction agents that increases BP
If hypertension occurs in other clinical situation, ensure adequate
oxygenation, anaesthesia& analgesia
The use of hypotensive agents, such as blockers, vasodilators, may
then be indicated for persistent hypertension.
Myocardial ischaemia (M.I.)

Aetiology: Occurs when myocardial O2 demand exceeds supply as in
hypotension, hypertension& tachycardia.
35 | P a g e
Clinical features:
o Pts. With coronary heart diseases are most at risk (suspicion should
be increased).
o Intraoperative M.I. manifests as arrhythmias, hypotension or
pulmonary oedema.
o Diagnosis is by S-T segment changes, so ECG monitoring is essential
in susceptible pts.
o Transoesophageal echo can detect abnormal myocardial wall
tension.
Management:
Aims of management are :
1-Prevension of ischaemia by appropriate anaesthetic technique.
2-Early detection in susceptible pts. by appropriate monitoring.
If M.I. is detected, insure adequate oxygenation, normocapnia,

analgesia& anaesthesia.
Significant hypertension, hypotension& tachycardia, can then be

controlled pharmacologically.
If signs persist, use coronary artery vasodilators eg.GTN.
Respiratory complications:
Hypoxaemea:
Refers to arterial haemogoblin desaturation or reduced arterial

oxygen tension.
In contrast hypoxia is O2 deficiency at tissue level.

Aetiology:
1- Hypoxic inspired gas mixture:Equipments :- Low O2 supply , flow meter & breathing system
malfunction.
2- Hypoventilation: Pt :- Respiratory depression in spontaneously
breathing pt. Respiratory obstruction
Equipment: - Ventilator failure , breathing system
&ETT obstruction.
3- V/Q mismatch: * Inadequate ventilation: (Secretions, bronchospasm , pulmonary
Oedema)
* Inadequate perfusion: (Embolus , low cardiac output)
4- Other:- Methaemoglobinaemia, malignant hyperthermia.
Clinical Features:
Cyanosis:- Unreliable
36 | P a g e

Tachycardia , hypertension , arrhythmias ,

sweating.
Tachypnoea in spontaneously breathing pt.
Later, hypotension , bradycardia & cardiac arrest.
Management:
Good monitoring(SpO2 , ECG)
If hypoxaemia is detected:o Check pulse & ECG; treat as cardiac arrest if there
is low cardiac output , V.T. or V.F
o Give 100% O2 & exclude delivery of hypoxic gas
mixture.
o Confirm the position &patency of E.T.T.
o Search for causes of V/Q mismatch.
o If diagnosis is difficult, measure arterial blood
gas, temp.& CXR.
2. Hypercapnoea:
Hypercapnoea is Co2 accumulation in blood

indicated by:Pa Co2 of
6 Kpa or EtCo2 > 6%.
Aetiology :
* Inadequate Co2 removal : -Hypoventilation
-Low fresh gas flow or exhausted soda lime
* Increased Co2 production:Fever, sepsis, hyperthyroidism, malignant hyperthermia, drug
reaction, use of Co2 in laparoscopy.
Clinical Features: Sympathetic stimulation:- HR, BP,
arrhythmias , sweating.
Tachypnoea in spontaneously breathing pt.
Acidosis
Hyperkalaemia
Management:
Treat the underlying cause
If signs of Co2 detected then control ventilation
3-Respiratory Obstruction:
It is a common & potentially hazardous anaesthetic complication.
Aetiology :1- Equipment :
Breathing system (kinking, valve malfunction)
37 | P a g e
ETT : External compression , internal occlusion.
2. Patient:*Oropharyx:(Oedema , tumor , secretion).

*Larynx: ( laryngospasm , recurrent laryngeal nerve palsy,
oedema, tumor.
*Trachea: (surgical manipulation, haematoma, tumeur
*Bronchi: ( secretion , tumor , bronchospasm , pneomothorax.
Clinical features:Spontaneously breathing :
Noisy breathing( strider) on partial obstruction.
Silent breathing if obstruction is complete.

Other signs include paradoxical chest & abdominal movements,
inadequate reservoir bag movement.
In some pts. negative intrathoracic pressure can precipitate
pulmonary oedema.
Artificially ventilated pts:
Increased inflation pressure, signs of hypoxia &hypercapnea.
Management:Early deletion & management of hypoxaemia is essential.
Spontaneously breathing pts:
* Respiratory obstruction by tongue or pharyngeal tissues may be
overcomed by jaw lift & the use of airways.
* Suction to remove oropharyngeal secretions.
* If persistent, ventilate manually 100% O2 & check breathing
system obstruction.
* Confirm the presence of bilateral chest movement (breath
sound) & exclude laryngospasm, bronchospasm
&pneumothorax.
If airway is difficult to maintain, intubate & ventilate.
Artificially ventilated pts:
* Systematically exclude causes of obstruction in breathing system
& pt.; complete obst. is usually due to equipment problem.
* Pass a suction catheter through the ETT to confirm patency.
* Surgical manipulations may distort or displace ETT.
* If persistent, ventilate with 100% O2 & replace the ETT.
* Treat specific causes e.g.. bronchospasm, penmothorax.
Intubation problems:
1- Endobroncheal Intubation: 38 | P a g e
This produces one lung ventilation leading to large

shunt
and consequently leading to hypoxaemia &
lung collapse.
Intubation of the Rt) main bronchus is more common.
Confirm the position of ETT by auscultation & draw ETT
out towards the trachea in case of endobroncheal
intubation.
2. Oesophageal Intubation: An important cause of anaesthetic mortality.

An endotracheal tube passing into the larynx
confirms correct placement although it may be
displaced later.
If direct vision is not possible, proper placement
should be confirmed by: * Auscultation of breath sounds.
*Normal capnographic wave form.
*Self-inflating bulb.
*Fibro- optic laryngoscopy.
If there is doubt regarding the position of ETT or if
hypoxaemia develops , remove ETT& give 100% O2 .
3. Difficult Intubation
This is a significant cause of anaesthetic morbidity &
mortality (Dental & airway trauma, pulmonary aspiration &
hypoxaemia ) .
Aetiology :
1-Anesthetist:Inadequate assessment of patient, equipment &
inexperienced anesthetist.
2-Equipment: Malfunction, unavailability of equipments & untrained
assistant.
3-Patient:* Reduced jaw movement.
* Reduced neck movement.
*Airway abnormality.
*Obesity.
Management:
Preoperative assessment:
*Preoperative airway examination to detect those with a
potentially difficult airway for planning an appropriate
anesthetic technique.
*Check the presence of strider , hoarseness of voice & previous
anesthetic records.
39 | P a g e
*Clinical tests to predict difficulty. e.g.Mallampati test,

thyromental distance.
Preoperative Preparation:*Antisialagogue & anxiolytics.
*Trained assistant is essential.
*Availability of experienced anesthetist.
*Difficult Intubation trolley with range of equipments.
Anaesthesia:
a) Regional anaesthesia is preferable where possible, but
preparation for general anaesthesia & difficult airway should
be available.
b) General anaesthesia:
Use of spontaneous ventilation with mask or laryngeal
mask is a safe technique.
If intubations is essential the technique depends on
the:
* Anticipated degree of difficulty.
*Presence of airway obstruction
*Risk of regurgitation.
Awake intubation.
Other intraoperative complications of common occurrence are: Aspiration of gastric content.
Adverse drug reactions.
Hypothermia and hyperthermia.
Injuries ( neural , dental , ophthalmic ,
thermal,e.t.c.).
40 | P a g e
Intravenous anasthetics
History
Introduction of hollow needles, syringes and IV fluid therapy in the
late 19 century.
Induction of anaesthesia with inhalation of gases and vapors' ( nitrous
oxide, ether, and chloroform) preceded the intravenous induction.
In 1926 the concept of balanced anaesthesia was introduced.
Definition:
A drug or combination of drugs which will induce anaesthesia safely and
reversibly when injected in sufficient doses and which could also be used
intermittently or by infusion for maintenance of anaesthesia.
What are intravenous induction agents?
These are drugs that, when given intravenously in an appropriate dose,
cause a rapid loss of consciousness. This is often described as occurring
within one arm-brain circulation time that is simply the time taken
for the drug to travel from the site of injection (usually the arm) to the
brain, where they have their effect ( approximately 20 seconds)
THEY ARE USED TO:To induce anesthesia prior to other drugs being given to maintain
anesthesia.
As the sole drug for short procedures.
To maintain anaesthesia for longer procedures by intravenous
infusion.
.To provide sedation.
The commonest drugs currently in use can be classified according
to their chemical structure and include:
Barbiturates
Phenols
Imidazoles
Phencyclidines
Benzodiazepines
Classification:
Rapid acting: Barbiturates, imidazoles, phenols

Slower acting: Phencyclidines, benzodiazepines, opioids,
neurolept combinations
41 | P a g e

Mechanism of action:
The target of intravenous agents are ion-channel linked receptors
for the endogenous neurotransmitters glutamate and gamma
amino butyric acid (GABA.).
GABA receptors:
conduct chloride and bicarbonate anions to hyperpolarize the
membrane of mature neurons.
They are the primary target for the anesthetic effect.
NMDA receptors:
the ionotropic glutamate receptors
Classified into n methyl d aspartate or Non N methyl D aspartate types.
The NMDA receptors conduct sodium and calcium cations--- depolarize
the membrane---- activate multiple intracellular pathways involved in
learning and memory.
KETAMINE
Non competitive blockade of NMDA receptors
is the primary mechanism of the dissociative anaesthetic ketamine
Anaesthetic effect
1- sedation .
2- anxiolysis.
3- hypnosis.
4- amnesia.
From induction to wake up: what happens to a bolus of IV induction drug?

The drug then passes along a concentration gradient from the blood into
the brain.
the rate of transfer is dependent on : the arterial concentration of the unbound free drug .
the lipid solubility of the drug
the degree of ionization.
Unbound, lipid soluble, unionized molecules cross the blood brain barrier
the quickest.
Like most anaesthetic drugs, the exact mode of action of the intravenous
drugs is unknown. It is thought that each drug acts at a specific receptor
GABA-A, NMDA and acetylcholine receptors have all been studied as
potential sites of
42 | P a g e
action.
Redistribution of drug into other tissues that leads to the rapid wake up
seen after a single dose of an induction drug. Metabolism and plasma
clearance have a much less important role following a single bolus, but
are more important following infusions and repeat doses of drug
The properties of an ideal IV induction drug:

PHYSICAL PROPERTIES
Water soluble & stable in solution
Stable on exposure to light
Long shelf life
No pain on intravenous injection
Painful when injected into an artery
Non-irritant when injected subcutaneously
Low incidence of thrombophlebitis
Cheap
PHARMACOKINETIC PROPERTIES
Rapid onset in one arm-brain circulation time
Rapid redistribution to vessel rich tissue
43 | P a g e
Rapid clearance and metabolism

No active metabolites
PHARMACODYNAMIC PROPERTIES
High therapeutic ratio ( ratio of toxic dose : minimally effective
dose )
Minimal cardiovascular and respiratory effects( ETOMIDATE).
No histamine release/hypersensitivity reactions( PROPOFOL)
No emetic effects( PROPOFOL).
No involuntary movements( PROPOFOL AND ETOMIDATE HAVE).
No emergence nightmares ( KETAMINE).
No hang over effect
No adrenocortical suppression (ETOMIDATE HAS
ADRENOCORTICAL SUPPRESSION EFFECT)
Safe to use in porphyria (THIOPENTONE NOT SAFE).
Thiopentone and methohexitone are barbiturate induction agents used
intravenously. Their brief duration of action results from rapid
distribution from the vessel-rich group into skeletal muscle and then fat.
Methohexitone is slightly less dependent on redistribution for its
duration of action as its rate of hepatic metabolism and renal clearance is
significantly higher.
THIOPENTONE:
Pharmaceutics
Presented as the Na+ salt of the enol form 0.5 g in 20 ml ampoule
with N2, Na2CO3 30 mg to pH 11
Prepared with water or saline to 25 mg/ml solution
pH 11-12 precipitates in neutral or acid solution
Stable (<7% loss of potency) for 5 days at 25C or 45 days at 5C
Pharmacokinetics
Distribution
- pKa 7.6
- 85% protein bound
- Vdss 1-2 l/kg
Metabolism
- t1/2a fast 8 min, slow 60 min, t1/2 11 h
- Clearance 3 ml/min/kg
- Rapid redistribution from VRG into muscle (30 min peak) and fat
- Slow hepatic metabolism, easily saturated in infusion
- Pentobarbitone is one metabolite
44 | P a g e
Pharmacodynamics
CNS:
- Potentiates GABAA transmission, prolongs channel opening
- May depress excitatory transmission by inhibiting Ca2+ transport
- Acts at reticular formation, hypothalamus and limbus
- Brief stimulatory phase before sleep
- Anticonvulsant at hypnotic doses
- Decrease in CMRO2, CBF, vasoconstrictor (may cause inverse steal)
- Not analgesic
Respiratory
- Central depressant.
- Decreased rate, increased VT followed by apnoea.
- Decrease in CO2 sensitivity.
- Decrease in upper airway reflexes when deep
CVS
- Effects depend on dose and rate of administration and filling
- Venodilator: decrease in LVEDV
- Myocardial depressant at high doses: decrease in SV, CO, MAP
- But increase in myocardial O2 demand in anesthetic doses
- Not an arterial vasodilator: baroreceptor reflex increase in SVR
Renal & Hepatic:

- Minimal decrease in function.
Uterine:- Crosses placenta readily, no effect on tone
Local:
- Thrombophlebitis, pain, thrombosis.
- Intraarterial injection causes vasospasm due to endogenous
vasoconstrictor release.
- Treat with local anaesthetic, vasodilator, heparin, regional
Contraindicated
-No IV access, no airway support equipment.
- Respiratory obstruction (croup, epiglottitis)
- Allergy.
- Porphyria
45 | P a g e
Relative contraindications
- Cardiac disease
- Septicaemia, acidosis
- Adrenocortical insufficiency
PROPOFOL
Physicochemical properties: Very weak acid.
Non-ionized at physiologic PH.
Insoluble in water.
Formulated at 1% in an oil-water emulsion containing 10% soya
bean oil, 1.2% egg lecithin, and 2.25% glycerol with a PH range of 68.5.
The emulsion is an excellent medium for microbial growth.
KETAMINE
Ketamine has hypnotic, analgesic and local anaesthetic properties. Its
effects are mediated primarily by noncompetitive antagonism at the
N-methyl-D aspartate (NMDA) receptor in the brain and spinal cord.
Pharmacokinetics
-Vd 3 l/kg
-Hepatic metabolism hydroxylation or N-demethylation, conjugation.
-Norketamine has 20% potency.
-Clearance 18 ml/kg/min
-t1/2a 10 min, t1/2 3 h
Pharmacodynamics
NMDA antagonist
CNS
Dissociative anesthesia
-Inhibits thalamic transmission to cortex
-Increased CBF, ICP, IOP
-Hallucinations on emergence
CVS
-Increased sympathetic tone (central and decreased NA uptake)
-Increased HR, MAP, PVR
-Direct cardiac depressant
Respiratory
46 | P a g e
-Retention of airway reflexes in low dose

-Increased secretions, bronchodilation
Muscle: Increased tone, movements, inhibits PlChE
KETAMINE
It has got important role in induction of anaesthesia under specific conditions.(
due to its sympathomimetic activity.)
eg: Hypotension.
Hypovolemia.
Constrictive pericarditis.
Cardiac tamponade.
Another unique advantage of ketamine is the versatility of administration routes.
IM, IV oral, rectal.,epidural and intrathecal (preservative-free.)
BENZODAZEPINES:
Act by binding to a specific receptor site on GABA receptors, facilitating
GABAergic transmission.
In the CNS, it acts predominantly in the cortex
The concentration of GABA receptors being less in the more primitive parts
of the CNS.
There are GABA receptors on spinal motor interneurones, which may
account for the activity of diazepam in reducing muscle tone
Diazepam and midazolam are benzodiazepines which are active orally,
transmucosally, intravenously, and in the case of midazolam, epiduralY.
Midazolam is used as a sedative and co induction agent. They are both highly
lipid soluble and 9698% protein bound.
Diazepam:
-Diazepam is oxidized in the liver to desmethyldiazepam, oxazepam and
temazepam all of which are active.
-Desmethyldiazepam has an elimination half-time of 48-96 hours, greatly
prolonging the clinical effect of diazepam.
-The elimination half-time of diazepam increases with age and hepatic
impairment to over 100 h. in the elderly
Etomidate:
An imidazole containing compound which can be used as an induction
agent.
It is water-soluble at acidic pH and is used intravenously.
Its brief duration of action is a result of redistribution as with thiopentone.
It is moderately lipid-soluble at physiological pH.
It is 76% protein bound
47 | P a g e
Etomidate probably acts to increase GABA transmission.lowers the seizure

threshold and causes myoclonic movements.
Inhibit 11--hydroxylase in the adrenal, reducing synthesis of cortisol and
inhibiting the normal stress response.
Physical properties
thiopental
propofol
ketamine
etomidate
Water soluble
Stable in soln.
Long shelf life
Pain on IV injection
++
++
Non-irritant on
subcutaneous
injection
Painful on arterial
injection
Low incidence of
venous thrombosis
No sequel from intraarterial inj.
48 | P a g e
Effects on body
thiopentone
propofol
ketamine
etomidate
Rapid onset
Recovery due to
redistribution
cumulating
++
Induction excitatory
effect
+++
Respiratory
complication
Cardiac hypotension
++
analgesia
++
antianalgesic
Emergence delerium
++
Safe in porphyria
49 | P a g e
50 | P a g e
Inhalational Anaesthesia
Remmember!
General anaesthesia: loss of consciousness, analgesia, amnesia and muscle
relaxation.
History:
-Nitrous oxide, chloroform, ether were the first.
-Methoxyflourane, enflourane.
-Ethyl chloride, cyclopropane were abandoned toxicity and flammability.
Enflourane: seizures, arrhythmias, increase ICP.
Methoxyfluorane: free flouride-nephrotoxic
NOW: FIVE in use:
1-Nitrousoxide.
2-Halothane.
3-Isoflourane.
4-Sevoflourane.
5-Desflourane.
Induction, maintenance and emergence.
Pharmacokinetics: How a body affects a drug-dose, tissue concentration.
Pharmacodynamics: How a drug affects a body, drug action, toxic responses.
Mechanism unknown therapeutic level in brain.
Inspired gas concentration depends on:
1. Fresh gas flow rate.
2. Breathing circuit volume.
3. Circuit absorption.
Alveolar gas concentration depends on:
1. Uptake.
2. Ventilation.
3. Concentration effect and second gas effect.
Arterial gas concentration: Affected by ventilation perfusion mismatching.
Uptake: depends on solubility, more soluble-less concentration in alveoli, slow
induction and vice versa.
Uptake depends on:
1. solubility:
Nitrous oxide 0.47.
isoflourane 1.4.
halothane 2.4.
desflourane 0.42.
sevoflourane 0.65.
51 | P a g e
2. Alveolar blood flow-cardiac output:

3. Tissue uptake-difference between pp in alveoli and venous blood.
Elimination:
Mainly exhalation drops brain concentration.
Transcutaneous minimal.
Rebreathing: anaesthetic circuit volume, FGF rate, circuit absorption,
solubility, CBF, ventilation.
Elimination of N2O is so rapid it dilutes O2 an CO2 causing diffusion
hypoxia. Prevented by 100% O2 for 10 min.
Pharmacodynamics:
Theories: GA ,altered physiological state.
Many theories.
Many elements: some inert like xenon,
Inorganic N2O
Halogenated hydrocarbons (Halothane).
Complex organic barbiturates.
Inhibition of specific brain areas and excitatory spinal nerves.
The UNITARY HYPOTHESIS-all agents share same mechanism of action at
molecular level.
Action correlates with lipid solubility-MEYER OVERTON RULE.
MINIMUM ALVEOLAR CONCENTRATION

Is the alveolar concentration that prevents movement in 50% of patients in
response to surgical stimulus.
It mirrors brain partial pressure and allows comparison between agents.
6% drop in MAC per decade of age.
Clinical pharmacology
The Inhalational Agents
About Each: 5 points:
1-Characteristics.
2-Picture (the structure, bottle and the vaporizer)
3-Effect on the body systems.
4-Biotransformations.
5-Contraindications.
1-Nitrous Oxide:
Colorless, odorless, nonexplosive.
Laughing gas-the only inorganic gas in use.
Nonflammable, gas at room temperature
52 | P a g e
Effects on systems:
1-CVS: Stimulates sympathetic NS, myocardial depression. No change
in B.P. unless patient has CAD, or hypovolemic.
2-Respirotary: Increases RR and drops TV.
3-cerebral: increases CBV , increases ICP and O2 consumption.
4-Neuromuscular: no change , no trigger for malignant hyperthermia.
5- Renal: decreases RBF by increase in resistance. Decreases GFR and
urine output.
6- Hepatic: hepatic blood flow decreases to a lesser extent.
7- G.I.: Vomiting ?
Biotransformation and toxicity
Exhalation mostly, small amount by skin.
Irreversibly oxidizes cobalt atom in vitamin B12. So methionine synthetase
enzyme is inhibited and myelin formation. Also thymidylate synthetase for
DNA synthesis.
Prolonged use ,megaloblastic anemia, peripheral neuropathy and
pernicious anemia.
Also teratogenic.
Contraindications
Insoluble as compared to others.
35 times more soluble than nitrogen in blood, so occupies N2 spaces.
Contraindicated in pneumothorax,air embolism ,intracranial air, tympanic
membrane grafting. Even tracheal tube cuffs.
Decreases the MAC of other inhalational.
2-Halothane
Halogenated alkane.
Nonflammable nonexplosive bec. of C-F bond.
Thymol preservative and amber coloured bottles.
Least expensive.
Effects on Systems:
1-CVS: Dose dependent drop in B.P. Myocardial depressant. Sensitizes the
heart to catecholamines. Arrhythmias with doses of >1.5 mic/kg adr.
2- Respiratory: increases RR and drops TV. Bronchodilator, drops reflexes.
3-Cerebral: dilates vessels increases CBF.
4-Neuromuscular: relaxes skeletal muscles and potentiates NMBA.
5- Renal: increases RBF preop. Hydration.
6- Hepatic: drops blood flow.Increases transaminases.
Biotransformation:
Oxidized by cytochrome p-450 to trifluoroacetic acid.
53 | P a g e
Hepatic dysfunction, halothane hepatitis ,1 in 35,000. middle aged ladies,

familial, multiple exposures.
Contraindications:
Increases ICP,
Friable patients arrhythmias, catecholamines, pheochromocytoma.
Drug interactions, verapamil,and B.blockers, further depress myocardium.
3-Isoflurane
Nonflammable, with pungent odour.
Effects on Systems:
1-CVS:minimal changes, coronary steel syndrome.
2-Respirotary: less drop in T.V. and increase in RR.
Good bronchodilator.
3-Cerebral: increases CBF and ICP, less than halothane.
Drops cerebral metabolism and O2 requirements. Brain protection in 2 MAC.
4-Neuromuscular: relaxes skeletal muscles
5-Renal: increases RBF and GFR and urine output.
6-Hepatic: reduces blood flow.
Biotransformation:
Trifluroacetic acid, increases fluride, no much nephrotoxicity.
Contraindications:
None.
Interactions: adrenaline dose up to 4.5 mic/kg.
4-Sevoflurane:
Halogenated with F. like des.
Nonpungent,rapid induction and recovery.
Excellent for all ages.
Effects on Systems:
1-CVS: slight drop in B.P.
2-Respiratory: drops RR and reverses bronchospasm.
3-Cerebral: slight increase in CBF and ICP. Drops O2 req. no fits.
4-Neuromuscular: good muscle relax. For children intubation.
5-Renal: drops RBF.
6-Hepatic: no change.
Biotransformation:
Metabolized by p-450
No renal toxicity.
54 | P a g e
Contraindications:
Hypovolemia, suspect to malignant hyperthermia and high ICP.
Interactions: potentiates NMBA.
No sensitization to catecholamines.
5-Desflurane:
Similar to iso. F for CL.
Vapour pressure at 20 is 681mmhg.
At high altitudes it boils ,so special vaporizer.
Low solubility ,so rapid induction and recovery
Moderate potency.
Structure, Vaporizer and bottle:
Effects on Systems:
1-CVS: increases HR drops BP , myocardial depressant.
2-Respiratory: similar to iso. Drops TV and increases RR.
Pungent, not nice for inhalational induction.
3-Cerebral: increases CBF and ICP, reduces BMR and O2 consumption.
4-Neuromuscular: drops response to train of four and tetany.
5-Renal: no nephrotoxicity.
6-Hepatic: no injury.
Biotransformation:
Minimal metabolism.
Dissicated by soda lime-barium OH NAOH, KAOH. Calcium OH Better used.
Contraindication:
Severe hypovolemia, increased JCP.
Drug interactions: potentiates muscle relaxants. Adrenaline can be used up
to 4.5 mic/kg.
55 | P a g e
Management of the Critically Ill Patient

Definition: Critical illness is any disease process which causes physiological instability
leading to severe disability or death within minutes or hours.
An immediately life-threatening health problem.
Recognizing Critical Illness
56 | P a g e
57 | P a g e
Monitoring at least hourly
Medium
Urgent assessment by a clinician competent in

assessing acutely ill patients
Clinical care in an environment with monitoring
facilities
Continuous monitoring of vital signs
High
Emergency assessment by a clinical team with

critical care competencies, which also includes a
practitioner/s with advanced airway skills
Consider transfer of clinical care to a HDU or ICU
58 | P a g e
Ask: are you alright?

Shake gently and ask again: are you alright?
If the patient answers:
Patient is breathing (B)

Brain is perfused (C)
If the patient answers in short sentences:
Patent airway (A)
Problem in breathing
If no answer:
This is a critically ill patient

Go for the ABCDE approach
Call for help
59 | P a g e
How much time? Amount of time available for assessment is a key early
decision.This judgement is often based on the appearance of the patient as well
as vital signs
Initial Management
ABCDE approach: aiming to keep the patient alive.
Airway
Breathing
Circulation
Disability
Exposure
Assess, manage, monitor & reassess all of ABCDE
Airway:
Assess for:
Paradoxical (seesaw) respirations

Absence of breath sounds at the nose and mouth
Stridor
Choking sign
Diminshed air entry
Central cyanosis
Possible causes:
LOC
Foreign body
Blood
Vomitus
Solid object
Secretions
Blocked airway device
Airwaysswelling
Direct trauma
Laryngospasm
Bronchospasm
Manage:
Headtilt/chinlift
60 | P a g e

Jaw thrust
Finger sweep
Suction
Oropharyngeal/nasopharyngeal airway
Recovery position
Endotracheal intubation
Cricothyroidotomy
Call for help
Give oxygen
Monitor
Pulse oxymetry
Goal SpO2:
94-98%
88-92% in chronic CO2 retainers
ABG
PaO2 > 60 mmHg
Keep reassessing the patient
Breathing:
Assess:
RR: apnoea, <8 bpm, >25 bpm (decreased drive)

Depth: shallow breathing (decreased effort)
Respiratory distress:
Abdominal breathing
Use of accessory muscles
Pattern: gasping
Tracheal deviation
One side moves less
Surgical emphysema
61 | P a g e

Dullness
Hyperresonance
Stridor
Rattling of secretions
Decreaed breath sounds
Bronchial breathing
Crepitations
Wheeze
Check chest tubes
Check for abdominal distension
Possible causes:
Pneumothorax and tension pneumothorax
Massive hemothorax
Pulmonary oedema
PE
Acute severe asthma
Pneumonia
COPD
CNS depression
Exhaustion
Spinal cord injury
Deformity
Pain
Manage
Give Oxygen
Treat the life-threatening conditions
Support ventilation
BVM
NIV
Invasive MV
Treat the underlying cause
Monitor
62 | P a g e
Pulse oxymetry
SpO2 >94
ABG
PaO2 < 60 mmHg
PaCO2 <45 mmHg
Reassess
Circulation
Assess
Peripheries: cool, sweaty, pale, blue, mottled, delayed CR

Pulse: pulseless, weak, <50 bpm, >140 bpm, irregular, abnormal character
BP: SBP <90 mmHg
Raised JVP
Altered mental status
Auscultation: crepitations,
3 heart sound, murmurs
rd
Oliguria
Hemorrhage
Possible Causes:
Hypovolemia
Hemorrhage
Cardiogenic
MI
Arrhythmias
Obstructive
Distributive
Septic shock
Anaphylaxis
Manage:
Treat as hypovolemia until proven otherwise

Insert 2 wide-bore cannulae
Take blood samples:
Cross-matching
63 | P a g e

Hematology
Chemistry
Microbiology
Coagulation
Give 20 ml/kg crystalloids over 5-10 minutes

Give 250 ml if suspecting cardiogenic causes and listen to chest after each
bolus
Use inotropes/vasopressors
Treat the underlying causes
Monitor
Pulse oxymetry
Blood pressure every 5 minutes initially

*Reassess
Disability:
Assess
Level of consciousness( AVPU, GCS)

Pupils: ( size, shape, reactivity)
Blood glucose (bedside)
Possible causes:
Hypoxia
Hypercapnia
Hypoglycemia
Acidosis
Electrolyte disturbances
Hypothermia
Drugs: opiods, sedatives
Toxicity
Manage:
ABCs
64 | P a g e

Drug antidotes: naloxone, flumazenil, etc

Abort seizures
Give glucose 50 mls of D10% up to 250 and repeat meseaurement
Put in recovery position
Reassess
Exposure
Facilitates examination
Maintain the patients dignity
Minimize heat loss
Do NOT leave the patient until he/she is stable
Further management
Take full history

Review notes and charts
Review drugs
Perform head to toe examination
Investigate accordingly
Plan your management
Definitive diagnosis and treatment
Assess patients response to your management
Intensive Care Unit

The hospital facility within which the highest levels of continuous
patient care and treatment are provided.
More detailed observation and monitoring
Minimum nurse: patient ratio of 1:1
A nurse in charge at all times
24 h cover by resident medical staff
The facilities to support organ system failures.
Criteria of admission:
Reversible conditions
1.
2.
3.
Patients requiring, or likely to require, advanced respiratory support

alone.
Patients requiring support of two or more organ systems.
Patients with co-morbidity who require support for an acute
reversible failure of another organ system.
Advanced respiratory support

65 | P a g e
Mechanical ventilator support or non-invasive ventilation

The possibility of sudden deterioration in respiratory function
requiring immediate intubation and ventilation.
Basic respiratory monitoring and support:
The need for an inspired oxygen concentration of more than 40%.
The possibility of progressive deterioration to the point of needing

advanced respiratory support.
The need for physiotherapy to clear secretions at least 2-hourly.
Recent extubation
CPAP
Circulatory support
The need for vasoactive drugs.

Support for circulatory instability caused by hypovolaemia from any
cause unresponsive to modest volume replacement.
Patients resuscitated after cardiac arrest where ICU or HDU care is
considered clinically appropriate.
Neurological monitoring or support
Central nervous system depression sufficient to compromise the airway
and impair protective reflexes.
Invasive neurological monitoring.
Renal support:
The need for acute renal replacement therapy.
Core Values:
Advanced treatment
Organ system support
Relief suffering and distress
Compassion
Maintain patients dignity
Provide proper information
Specific Conditions:
Respiratory Failure:
Type I RF:
hypoxia (PaO2 < 60 mmHg, SpO2 >94) without hypercapnia, (PaCO2
(<45 mmHg)
Type II RF:
66 | P a g e
Hypoxia (PaO2 < 60 mmHg) with Hypercapnia (PaCO2 >45 mmHg)*

Management:
1-Supportive:
Hypoxemia:
o Escalated and titrated oxygen therapy
o CPAP
o Invasive mechanical ventilation
Hypercarbia
o Mechanical ventilation.
o BVM temporarily
2-Treat the underlying condition
Bronchodilators
Intravenous antibiotics
Diuretics for fluid overload
Ensuring optimal cardiac function
Aminophylline infusions can improve diaphragmatic function.
Pulmonary oedema:
Transudation of fluid, from pulmonary capillaries into interstitial

spaces and then into alveoli
Stage I: Only interstitial pulmonary edema is present. Patients often
become tachypneic as pulmonary compliance begins to decrease. The
chest radiograph reveals increased interstitial markings and
peribronchial cuffing.
Stage II: Fluid fills the interstitium and begins to fill the alveoli. Gas
exchange may remain relatively preserved.
Stage III: Alveolar flooding most prominent in dependent areas. Results
in a large increase in intrapulmonary shunting. Hypoxemia and
hypocapnia.
Stage IV: Fluid spills over into the airways as froth. Gas exchange is
severely compromised due to both shunting and airway obstruction.
Progressive hypercapnia and severe hypoxemia follow.
Classification:
Cardiogenic:
o Increase in the net hydrostatic pressure across the capillaries
o PAOP greater than 18 mm Hg
o Low protein content,
Noncardiogenic
o Increase in the permeability of the alveolarcapillary membrane
67 | P a g e
o PAOP less than 18 mm Hg

o High protein content.
Less common causes :
o Prolonged severe airway obstruction,
o Sudden reexpansion of a collapsed lung
o High altitude
o Pulmonary lymphatic obstruction, and
o Severe head injury
o The same mechanisms also account for these diagnoses.
Mangement
Cardiogenic:
o Supportive
o Correct fluid overload with diuretics.
o Decreasing the pressure in the pulmonary capillaries.
o Reduce pulmonary blood flow.
o Improve left ventricular function,
o Oxygen therapy
o CPAP
o Invasive MV
o Diuretics
o Vasodilators such as nitrates
o By reducing preload, pulmonary congestion is relieved.
o By reducing afterload, cardiac output may be improved.
o Inotropes such as dobutamine.
Noncardiogenic
Treat the underying cause:
o sepsis or hypotension.
o oxygen therapy.
o Milder cases may be treated with a CPAP
o most patients require intubation and at least some degree of
mechanical ventilatory support.
o Use protective lung strategy.
o If possible, the FIO2 should be maintained at 0.5, primarily by
increasing PEEP
o Inhaled nitric oxide
o Ventilation in the prone position.
Acute Myocardial Infarction:
MONA
Oxygen (46 L/min),
68 | P a g e

Aspirin (160325 mg),

Nitroglycerin (sublingual or spray)
Morphine (24 mg intravenously every 5 min) until the pain is
relieved.
Early reperfusion is the mainstay.
Prognosis following AMI is generally inversely proportionate to the
extent of necrosis.
PCI
Alternately, thrombolysis will improve survival.
The greatest benefit is if treatment is given within the first hour, but
benefit can be seen if treatment is given within 12 h of the AMI.
Patients with nonSTEMI benefit from antithrombin (heparin) and
antiplatelet (aspirin) therapy.
Intraaortic balloon counterpulsation is usually reserved for
hemodynamically compromised patients with refractory ischemia.
Temporary pacing for Mobitz type II and complete heart block.
Antiarrhythmic drugs for aeehythmias.
Renal Failure:
o Acute renal failure (ARF) is a rapid deterioration in renal function
that is not immediately reversible by altering extrarenal factors,
such as blood pressure, intravascular volume, cardiac output, or
urinary flow.
o The hallmark of renal failure is azotemia and frequently oliguria.
o Typically, ARF is diagnosed by documenting an increase in BUN
and plasma creatinine over 2472 h
Classification:
Management:
o
o
o
o
o
o
o
Pre-renal
Renal
Post-renal
Primarily supportive.
Diuretics may be used to maintain urinary output in nonoliguric
patients.
ARF due to glomerulonephritis or vasculitis may respond to
glucocorticoids.
Standard treatment for oliguric and anuric patients includes
restriction of fluid, sodium, potassium, and phosphorus.
Daily weight measurements help guide fluid therapy.
Fluid intake should generally equal 500 mL plus urinary output.
Sodium and potassium intake is limited to 1 mEq/kg/d,
69 | P a g e

o The dosages of renally excreted drugs should be adjusted to the

estimated glomerular filtration rate or measured creatinine
clearance to prevent accumulation.
o Dialysis may be employed to treat or prevent uremic
complications.
Sepsis & Septic Shock

Sepsis= SIRS + infection
SIRS:
High heart rate

High respiratory rate
Hypo or hyperthermia
High or low TWBC
o Severe sepsis exists when the response is associated with organ
dysfunction.
o MODS describes progressive dysfunction of two or more organs
that is associated with sepsis.
Septic shock:
o Acute circulatory failuresustained hypotension despite
adequate volume resuscitationin a patient with sepsis.
Mangement
1.
2.
3.
Treat the infection

Intravenous antibiotics within 1 hour (protocols, take culture
and start empirical)
Drainage of abscesses
Debridement of necrotic tissues
Removal of infected foreign bodies
Maintenance of adequate perfusion with intravenous fluids and
inotropic and vasopressor agents
Supportive treatment of complications such as ARDS, ARF, GI
bleeding, and DIC.
Gastrointestinal Hemorrhage
Hematemesis
70 | P a g e

Melena
Hematochezia
Management:
Consists of simultaneous and rapid evaluation and identification of the site
of bleeding and stabilization.
At least two large-bore (1416 gauge) intravenous cannulas should be
placed, and blood should be sent for laboratory analysis
The patient should also be typed and crossed for at least 46 units.
IVF
Intra-arterial blood pressure monitoring is very helpful.
Central venous cannulation is useful for both venous access and pressure
measurements.
Upper GI bleeding:
Peptic ulcer
Oesophageal varices
OGD
Nasogastric lavage
Arteriography
Injection sclereothreapy
Electrocoagulation
Embolization
Balloon tamponade
Surgery
PPI
Lower GI bleeding:
o Diverticulosis
o Angiodysplasia
o Neoplasms,
o Anorectal disease
-Rectal examination, anoscopy, and sigmoidoscopy can usually diagnose
very distal lesions.
-Colonoscopy usually allows definitive diagnosis and is often useful
therapeutically. -Cauterization
-Technetium-99labeled red blood scan.
-Selective arteriography can be used to identify the source, which is either
embolized or infused with vasopressin.
-Surgical treatment is reserved for severe or recurrent hemorrhage.
CNS disorders:
Raised ICP
Brain Oedema
71 | P a g e
Space occupying lesion

Traumatic
Intracranial hemorrhage
Hypertensive crisis
Stroke
Status epilepticus
Brain protective strategy

o Abolish fits immediately
o Avoid hypoxia (PaO2 >60 mmHg, SpO2 >94)
o PaCO2 between 25 and 35 mmHg
o Avoid fever
o Mild hypothermia 33-34o (avoid shivering)
o Maintain CPP between 70 and 80 mmHg
o Avoid hypotension and hypertension
o Maintain normoglycemia
o Avoid hypotonic IV fluids
o Abolish pain
o Avoid excessive stimulation (suctioning, cough, straining, etc)
o Adequate sedation
o
Head up at 30o
o Maintain cerebral venous drainage
o Osmodiuretics (mannitol and hypertonic saline) to buy time
when there is a servere increase in ICP and risk of coning
(awaiting ventriculostomy, decompressive surgery)
Specific components of care
Nutritional Support:
o Severe malnutrition causes widespread organ dysfunction and
increases morbidity and mortality.
o Nutritional repletion may improve wound healing, restore
immune competence, and reduce morbidity and mortality.
o Oral intake whenever possible
o NG feeding
o TPN
Sedation and delirium:
o The provision of adequate analgesia and anxiolysis and the
management of delirium are essential components of care in the
critically ill
o Delirium: an acutely fluctuating mental status, inattention,
disorganized thinking, and an altered level of consciousness.
o Can be hypoactive, hyperactive or mixed.
72 | P a g e
o Associated with increased length of ICU and hospital stays, time

on the ventilator, mortality, and long-term neuropsychological
deficits.
o Assess routinely for delirium
o Treat the underlying causes
o A number of opioids, benzodiazepines and anesthetic drugs can
be used.
o The drug should be titrated according to the patients response.
o Avoid oversedation
o Implement sedation vacations
Thromboembolism Prophylaxis
VTE (DVT and PE) has a higher prevalence among critically ill patients
It is an important cause of morbidity and mortality
Early mobilization
LMWH e.g. enoxapram 1 mg/Kg SC OD
HMWH 5000 units SC BD or TDS
Graded compression stocking
Intermittent pneumatic compression pumps
Stress Ulcer Prophylaxis
Stress related mucosal disease (SRMD) is erosion of the gastric mucosa that
occurs in critically ill patients and can cause significant blood loss
Routine prophylaxis for all patients
I.V. ranitidine 50 mg TDS
Enteral feeding has a protective effect
Blood Glucose Management
Stress hyperglycemia is associated with poor clinical outcomes in critically
ill patients.
Hypoglycemia can be rapidly fatal
Keep blood glucose between 110 and 180 mg/dL
Use the available protocols for insulin administration.
73 | P a g e
Muscle Relaxants
Introduction
Was first introduced in practice in 1942 by Griffith and Johnson in Montreal.
Acetylcholine (Ach) is the neurotransmitter at the NM junction .
Ach is released on passage of a nerve impulse down the axon
On arrival of an action potential storage vesicles are transferred to the

active zone fusion with the terminal wall occurs leading to release of Ach.
There are thousand active sites at each nerve ending and 1 action potential
leads to the release of 200-300 vesicles.
Spontaneous release of Ach at the NM junction produce MEPPs.
The junctional cleft, which is the gap between the nerve terminal and the
muscle membrane is 60 nm and contains acetylcholinesterase which is
responsible for the breakdown of Ach.
The postsynaptic membrane contains clusters of nicotinic Ach receptors on the
shoulders of the junctional folds.
Each receptor has 5 subunits and activation cause ion channel opening with
influx of Na, K, Ca and Mg with change in action potential from -90 to -50mv
resulting in muscle contraction
Neuromuscular blocking Agents:
Depolarizing (non-competitive)
Non-depolarizing (competitive)
Depolarizing muscle Relaxants

Suxamethonium chloride(Scoline):
Is a quaternary ammonium cmpd.
2 molecules of Ach linked together that bind to units of the Ach
receptors _ causes depolarization known as fasiculations repolarization
does not occur and the muscle is flaccid. This takes place in 1 min.
Dose: Intubating dose is 1- 1.5mg/ kg.
Is useful in emergency cases , full stomach , obestetric cases etc.
Metabolism: In the plasma by the plasmacholinesterase, an enzyme producded by the
liver. Recovery occurs in 3 min Complete reversal occurs in 12 15 min
Prolongation of suxa. Action(scoline apnoea) can be due to either:
1.
Inherited factors
2.
Acquired factors.
1. Inherited Factors
74 | P a g e
The structure of the enzyme is determined genetically by

autosomal genes
A normal individual E1u E1u
Atypical gene Ea1 exists in 4% of population.
A heterozygous E1u Ea1 has longer duration of action ie up to 30
min.
A homozygote Ea1 Ea1 has an effect over 2 hrs .
Other abnormal genes include the fluride and the silent ones.
Management: s by transfusion of FFP and artifically ventilating the lungs.

Take a blood sample to determine the genotype.
Give the pt a card or a bracelet determining the
genotype.
2. Acquired factors
Normal structure but reduced activity.
Causes include:1. Liver disease.
2. Carcinomatosis , starvation.
3. Pregnancy.
4. Anticholinesterases e.g neostigmine.
5. Other drugs which are metabolized by plasmacholinesterase e.g
ester L A , etomidate , methotrexate etc.
6. Hypothyriodism.
7. Cardiopul. Bypass
8. Renal disease. , plasmapheresis.
Side Effects :1. Muscle pain.
2. Increased intraocular pressure.
3. Hyperkalaemia is marked in renal failure pts, burned pts,
muscle and nerve disease etc.
4. CVS effects e. g bradycardia.
5. Anaphylaxis.
Non- depolarizing NM blocking agents:

Action: Competitive inhibition of the receptors_ small or no EPP no
muscle contraction.
Metabolism : No metabolism occurs in the NM junction and reversal is by
diffusion down its concn gradient into the plasma and the use
of an antagonist.
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Types of Non depolarizing NM blocking agents

1.
Benzylisoquinolinium cmpd.
2.
Aminosteroid cmpd.
1.Benzylisoquinolinium agents:e.g.Tubocurarine chloride
Naturally occuring used as an arrow poison by Indians.
Dose is 0.5 -0.6 mg /kg .
Side effects include histamine release, hypotension.

Metabolism:unchanged by the kidney.
Atracurium besylate
Introduced in 1982 .
Dose is 0.5 mg/kg can be reversed in 20 25 min.
Metabolized mainly by Hofmann degradation, ester hydrolysis & a small
amount via kidney.
Suitably used in hepatic & renal fn.
2.Aminosteroids Agents
One ammonium group plus a steroid nucleus
Fewer S/E .
No histamine release.
Excreted unchanged via the kidney ,some in the bile & liver.
Examples:Pancronium bromide: Is a bisquaternary amine used in 1964.
Dose is 0.1 mg/kg and maximum effect takes 3---4 min.
Duration of action is long and potentiated by inhalational agents & opoids.
It causes tachycardia and hypertension.
General factors that affect the duration of action of non

depolarizing blockers:
1.
2.
3.
4.
5.
6.
Prior administration of suxa

pH changes e.g metabolic acidosis prolongs the duration of block.
Use of inhalational agents.
Body temperature ,hypothermia potentiates the block
Electrolyte changes e.g.low K , Ca , potentiates the block.
Myasthenia gravis due to reduction in receptors number.
76 | P a g e
Anticholinesterases
Commonest use for reversal of residual amounts of non depolarizing agents
at the end of surgery.
Action: Inhibition of the action of acetylcholinesterase at NM junction.
Examples: Neostigmine ( used in anaesthesia) ,
edrophonium,pyridostigmine , & physostigmine (orally used)
Neostigmine
Forms a reversible ester link with the cholinesterase that lasts
for 30 min .
Excretion is via kidney & half life is 45 min
S/E includes bradycardia , salivation , sweating, bronchospasm
, increased GIT motility.These are counteracted by the use of
an anticholinergic agents e. g atropine
Dose is 0.035---0.05mg/kg.
Pyridostigmine
Used as oral therapy for treatment of myasthenia gravis.
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BLOOD TRANSFUSION
Introduction: Blood used correctly can be life saving, used inappropriately it can
endanger life.
It is important to remember that blood transfusion is only one part of
the patients management.
Indications of blood transfusion
1. Acute massive blood loss;
2. Anemia and hypoalbuminemia;
3. Overwhelming Infection;
4. Dysfunction of Coagulation
We compensate for:
1- Components: R.B.Cs, platelets, Coagulation factors & plasma
proteins.
2- Volume
Old concept: Hb.<10 gm & Hct.< 30%?
New concepts: Clinical assessment:
*C.V.S. function. * Age.
*Anticipated loss. *Cardiac output & blood volume.
Oxygen delivery is adequate in most individual at Hb as low as 7g/dl.

In acute anemia, oxygen content is usually maintained by compensatory
increased in cardiac output.
In chronic anemia, oxygen delivery is facilitated through increases in 2,3-DPG
level in RBCs.
In healthy, normovolaemic individuals, tissue oxygenation is maintained and
anemia tolerated at Hct as low as 25%
Hct 20% the heart begins producing lactic acid
Hct 10% heart failure occurs
Human may tolerate lower Hb and O2 to tissues during general anaesthesia
than awake due to an anaesthetic and neuromuscular blockade induced
reduction of oxygen consumption
The impact of regional anaesthesia on O2 transport is unclear
Preparations before transfusion

1- Selection of donors
2- Compatibility testing
3- Screening for infection
4- Processing before transfusion
78 | P a g e
1-Blood donation
Blood is donated as whole blood by inserting a catheter into a vein

and collecting it in a plastic bag (containing anticoagulant) via
gravity.
Collected blood is then separated into components to make the best
use of it.
1. Ineligible donor:
Current disease or at high risk for a disease that can be
transmitted by transfusion(malaria, hepatitis, HIV)
Donors who are not healthy enough to tolerate the process e.g.
CVS diseases, pregnancy, high blood pressure, tuberculosis,
seizures
Younger donors are excluded from donating blood because
they cannot give legal consent for the process.
2-Compatibility testing:
These tests are done in vitro, so that antigen-antibody

reactions can be prevented.
These are : 1- Blood grouping.
2- Cross matching.
3- Antibody screening.
1. ABO-Rh Typing
Phenotype
A
B
AB
O
A blood type (also called a blood group) is a classification of

blood based on the presence or absence of inherited
antigenic substances on the surface of red blood cells.
Genotype
AA or AO
BB or BO
AB
OO
The associated anti-A and anti-B antibodies, in the plasma, are

usually IgM antibodies.
ABO IgM antibodies are said to be naturally occurring
antibodies, although produced in the first years of life by
sensitization to environmental substances such as food,
bacteria and viruses.
Antibodies in the plasma are directed against antigens that are
lacking in the individual's own cells.
79 | P a g e

Blood grouping is done by testing RBCs for A&B antigens&

serum for A&B antibodies before transfusion.
An additional test is done for Rh(D) antigen.
About 85% of individual posses the D antigen & are termed
Rh+ve (Rh antibodies(IgG) are immune type).
2. Cross-matching
This test is done to detect the potential for transfusion

reaction by mixing the doner RBSs with the recipient serum in
a test tube.
Cross matching is completed in about 45 -60 min & is carried
out in three phases :
a) Immediate phase:
Is a check against errors in ABO typing ,takes about 1-5 min
& is able to detect incomplete antibodies.
b) Incubation phase :
(30-45 min in albumin )
The incubation allows a sufficient duration for antibody
uptake by cells.
c) Antiglobulin phase :
It is done by adding antiglobulin to the incubated test tube.
Antiglobulin becomes attached to globulin antibodies on
RBCs causing agglutination. This will detects most
incomplete antibodies in the blood.
The most serious antibodies are those appearing in the
immediate phase ; others are less sever clinically.
3. Antibody screening
This is a trial transfusion between the recipient serum & a

commercially supplied RBCs containing optimal number of
RBCs antigen.
The same test is done for donner serum , shortly after blood
withdrawal.
3-Screening for infection

All donors &donated blood should be screened for the following infectious
agents:
HIV
Hepatitis B & C viruses
Malaria
Treponema pallidum
80 | P a g e
4-Processing
Component seperation
Leukoreduction
Irradiation
CMV screening
Red cells, plasma and platelets are separated into different containers and
stored in appropriate conditions so that their use can be adapted to the
patient's specific needs. Temperature also plays a capital role into
component storage: plasma must be frozen as soon as possible 18 C or
colder, red cells must be refrigerated (1-6C) and platelets are kept in
continuous shaking platforms at room temperature (20-24C).
Leukoreduction greatly reduces the chance of cytomegalovirus (CMV)
transmission. Leukoreduced blood is appropriate for:
Chronically transfused patients
Potential transplant recipients
Patients with previous febrile nonhemolytic transfusion
reactions
CMV seronegative at-risk patients for whom seronegative
components are not available
In patients who are severely immunosuppressed and at risk for transfusionassociated graft-versus-host disease, to prevent the donor T lymphocytes
from dividing in the recipient.
CMV, is a virus which infects white blood cells. In patients with significant
immune suppression (e.g. recipients of stem cell transplants) who have not
previously been exposed to CMV, blood products that are CMV-negative are
preferred.
Technique of Transfusion:
o
o
o
o
o
o
o
Approach Route: Peripheral vein, central vein

Double Check: Name, type and cross match to minimize risk of
clerical error.
Check storage time
Pre-heat
Filtration before transfusion
A unit (up to 500 ml) should be administered slowly (up to 4
hours).
Observation during / after transfusion
In patients at risk of congestive heart failure, packed RBCs are
advisable, or furosemide (with whole blood) to prevent fluid
overload.
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Storage of blood:
Blood is stored in special refrigerators at 1-6 C.
Different solutions are added in the blood collecting bag to act as
preservatives & anticoagulants.
Preservatives:
a) C.P.D. :
Citrate is an anticoagulant which prevents clotting by binding
calcium, phosphate acts as a buffer & dextrose allows RBCs to
continue glycolysis to provide ATP for metabolism & hence
survival.
Storage at 1-6 C slows the rate of metabolism .
C.P.D. maintain 70% RBCs survival for 28 days.
b) CPD-A:
Addition of adenine to CPD has increased the RBCs storage time to 35
days. Adenine allows the RBCs to resynthesise ATP .
c) Adsol (SAGM):
The half life of RBCs can be increased to 42 days when Adsol is added.
Adsol contains sodium chloride , adenine , glucose & mannitol.
d) Frozen storage:
Blood mixed with glycerol & stored at -79 C has a shelf life of almost
10 years. It must be free of glycerol before transfusion.
Effects of storage
*Stored blood is an unphysiological solution???
*Progressive decrease in the content of ATP & 2,3-DPG & decreased
activity of Na-K pump.
*Reduced plasma pH.
*Other constituents can not withstand storage , e.g.. : platelets,
granulocytes& coagulation factors.
Complications of blood transfusion
Most of the complications are the result of massive blood transfusion.

Massive blood transfusion is the replacement of blood loss equivalent to
or greater than the patients total blood volume in less than 24 hrs.
These are:
1- Change in O2 transport :
This is because of left ward shift in oxyhaemoglobin dissociation
curve (from low pH), leading to tissue hypoxia.
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2- Changes in coagulation :
In massively transfused pt. and is due to:
*Delusional thrombocytopenia: At 4C platelets are sufficiently
damaged& those infused have a reduced survival time. Platelets
activity is also reduced, being 50% after 6 hrs.,10% after 24 hrs.&
5% after 48 hrs. of storage.
*Low levels of coagulation factors: Most factors are stable at 4C
with exception of factor V & VIII which decreases to 15 & 50% of
normal, respectively, after 21 days of storage.
*D.I.C. : This is induced by massive transfusion.
3-Citrate intoxication:
Citrate binds calcium & thus signs are those of

hypocalcaemia.
Serum Ca. returns normal after transfusion because citrate
is rapidly metabolized by the liver.
Very high rates of infusion are required to produce
hypocalcaemia (1 unit of blood per 5 min.)
Hypothermia, liver impairment and hyperventilation
increase the possibility of citrate intoxication.
4-Hyperkalaemia:
o Serum potassium may be as high as 30mmol/L in stored
blood after 21 days of storage.
o Insignificant with small volumes as a result of
redistribution.
o A bank blood should be given at a rate of 120 ml/min to
produce significant hyperkalemia.
5-Hypothermia:
If core temperature declines to 30C, ventricular
arrhythmias& cardiac arrest may occur.
6-Infusion of microagrigates:
Amount of clots& debris in stored blood increase with duration
of storage. For this reason, stored blood is infused through a
giving set with standard filter (170 micrometer).
Some particulates are not filtered& enter the blood
stream. ARDS after massive transfusion may be the
result of accumulation of these particulate materials
in the lungs, resulting in vascular obstruction.
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7-Transfusion reactions:
a).Hemolytic reactions:
It is the most serious reaction which arise from intravascular
haemolysis caused by incompatible transfusion. It can occur
after transfusion of as little as 10 ml of blood. Mortality is 2060%.
Acute transfusion reactions occur during or shortly after
(within 24 hrs) the transfusion.
Classic symptoms& signs are: (Fever, Rigors, Chest pain,
Nausea, Flushing, Hypotension, Haemoglobinurea).
These symptoms& signs are masked by general anesthesia. The
only signs may be haemoglobinurea, bleeding diathesis or
hypotension.
Mainly renal& coagulation systems are affected.
Hemoglobin, as acid haematin, precipitates in the distal
tubules, causing mechanical obstruction.
Management is directed towards stopping infusion,
maintaining good urinary out put through I.V. fluid
administration with diuretics, alkalinizing urine& retaining
blood for recrossmatching.
Haemoglobinurea occurs when the plasma level of free
hemoglobin reaches150mg/100ml plasma (i.e. Beyond the
capacity of haptoglobulin).
Management:
1. Stop transfusion and treat as anaphylaxis
2. Replace infusion set with normal saline.
3. Maintain airway, give high flow oxygen.
4. If there is severe hypotension or bronchospasm give
adrenaline, corticosteroids and bronchodilators.
b).Non hemolytic reactions:

(These are usually less serious)
*Febrile reactions: They are due to WBCs& have the same
symptoms( but less sever) of hemolytic reactions.
*Allergic reactions: They are caused by donner plasma protein
in the transfused blood.
Common symptoms are urticarea, itching& facial flushing.
Antihistamines are used to treat these symptoms.
8- Infectivity of blood:
Many diseases can be transmitted by blood transfusion:
*Viral: Hepatitis, HIV, cytomegalovirus
*Bacterial: Salmonella, brucella
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*Spirochetal: Syphilis
*Parasitic: Malaria, filariasis.
9-Immunodepression:
The cause is unknown, but present data indicate that blood
transfusion increases the susceptibility to infection& enhances
progression of malignant tumors.
How to minimize preoperative blood transfusion?

o Preoperative screening and treatment of anaemia for elective
surgical patients.
o Intraoperative surgical& anaesthetic precautions to minimize
bleeding.
o Autologous transfusion.
o Blood substitutes.
Anesthetic techniques:
Avoid hypertension and tachycardia due to sympathetic

overactivity by ensuring adequate levels of anesthesia and
analgesia.
Avoid coughing, straining and patient maneuvers, which increase
venous blood pressure.
Avoid hypercarbia causing vasodilatation which will increase
operative blood loss.
Use regional anaesthesia, such as epidural and spinal, where
appropriate
Avoid hypothermia in the perioperative period.
Controlled hypotension in experienced hands.
Surgical techniques:
Meticulous attention to bleeding points - use of diathermy.

Posture - the level of the operative site should be a little above
the level of the heart.
Tourniquets.
Use of vasoconstrictors.
Blood substitute:
Often called artificial blood, are used to expand the plasma volume
and/or carry blood gases in the circulation.
Although commonly used, the term is not accurate since human

blood performs many important functions.
85 | P a g e

The more accurate terms are volume expanders for inert products,
and oxygen therapeutics for oxygen-carrying products.
Volume expanders:
Inert and merely increase blood volume. These may be crystalloidbased (Ringer's lactate, normal saline, D5W) or colloid-based
(Gelatins, dextrans, albumins& HES).
Oxygen therapeutics: mimic human blood's oxygen transport ability.
Examples: Hemopure, Oxygent, PolyHeme.
There are two basic approaches to constructing an oxygen therapeutic:
Perfluorocarbons (PFCs): Chemical compounds which can carry

and release oxygen. The specific PFC usually used is
perfluorocarbon.
Hemoglobin: Derived from humans, animals, or artificially via

recombinant technology.
86 | P a g e
Analgesic Drugs
The ascending pain pathway
The descending pathway
A descending inhibitory pathways from the brain to the spinal cord

arise from discrete centres in the mid-brain and medulla.
These centres contain high concentrations of endogenous opioids and
opioid receptors.
Activation of these receptors increases activity in descending pathway
that project to the dorsal horn.
Pain can be interrupted at any stage of this pathway by variety of
drugs and procedures.
Specific drugs (analgesics) designed for such specific purpose are the
opioids and the non-steroidal anti inflammatory drugs.
Opioids
Opioids produce analgesia through their action on naturally

occurring opioid receptors { (mu), (kappa) and (delta)}.
These receptors are found mainly in the CNS, but also in other
tissues, and are the site of action of the naturally occurring opioids,
the encephalins and endorphins, that modify pain perception.
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Classification
Naturally occurring alkaloids: alkaloids derived from opium poppy,

primarily morphine, codeine.
Semi-synthetic opioids: created from the natural opiates, such as
diamorphine, dihydrocodiene.
Synthetic opioids e.g. pethidine, fentanyl, alfentanil, e.t.c.
Mechanism of action
Opioids exert their action through binding to opioid receptors in these
sites:
*presynaptic nerve terminal: prevents excitatory neurotransmitter release.
*Post synaptic terminal: causes hyperpolarization and making the cell less
excitable.
*Activation of the descending inhibitory pathways in the central nervous
system.
Indications
1- Moderate to severe pain.
2- Cough e.g. codeine.
3- Diarrhea e.g. loperamide.
4- Anxiety.
Systemic actions
CNS
Analgesia:
Effective in most kinds of pain.
Less effective in neuropathic pain & sharp pain of movement e.g. un

supported fracture.
Hallucination.
Respiratory system
Respiratory depression:
Due to reduced sensitivity of the respiratory centre to hypoxia and
hypercapnea.
Cough suppression:
Especially with codeine.
GIT
o Constipation: They increase sphincter tone and decrease gut motility.
o Nausea and vomiting are the result of chemoreceptor trigger zone
stimulation.
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CVS
No direct effects on the force of myocardial contraction.

They cause bradycardia through vagal stimulation.
Histamine release and urticaria

They release histamine from the mast cells leading to urticaria ,
itching, bronchoconstriction and hypotension.
This is more pronounced with morphine and less with others.
Immunity
Immunity is depressed with chronic use.
Dependence and tolerance
They occur together.
Physical dependence is the increasing effect of drug withdrawal.
Tolerance is the process whereby neuroadaptation occurs (through
receptor desensitization due to fixed concentration of the drug)
resulting in reduced drug effects.
Pharmacokinetics
All routes of administration can be used.
Opioids are mainly metabolized by the liver e.g. morphine is
converted to morphine -6-glucuronide.
Morphine and other opioids are excreted through the kidney and
bile.
Adverse effects
Common adverse reactions include:
1- Nausea and vomiting.
2- Constipation.
3- Itching.
4- Dry mouth.
5- Miosis.
6-Drowsiness.
Adverse effects
Infrequent adverse reactions include:
1- Respiratory depression.
2- Bradycardia.
3- Hypothermia.
4- Confusion, hallucinations and delirium.
5- Urinary retention.
6- Ureteric or biliary spasm.
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N.S.A.I.Ds.
These are drugs with analgesic, antipyretic & anti-inflammatory

effects.
The inflammatory process:
tissue becomes red, swollen& tender.

The capillaries become more permeable, leaking fluids&
other elements into tissue spaces.
Leucocytes migrate into the area& rupture the cell
lysosomes releasing lytic enzymes into the tissues.
Local liberation of chemical mediators (Histamine, 5H.T,
bradykinin &eicosanoids).
Every mediator has a special importance for a specific
type of inflammation
e.g. histamine in urticareal reactions (so antihistamines
are only effective in treatment).
Eicosanoids however , are involved in most types of
inflammation.
Eicosanoids are a group of unsaturated fatty acids formed
in almost every tissue in the body &their biosynthesis is
the base for current
anti inflammatory therapy.
Action of N.S.A.Ds.
Reduce nociception related to inflammation& modify the inflammatory

reaction& lower temperature.
All N.S.A.I.Ds. Inhibit prostaglandin synthesis by inhibiting the enzyme
cyclo-oxygenase.
Indications:
General indications:
These drugs are usually indicated for the treatment of acute or chronic
conditions where pain & inflammation are present.
Specific indications:
Symptomatic relief of the following conditions:
1) Rheumatoid arthritis.
2) Osteoartheritis.
3) Acute gout.
4) Dysmenorrhoea.
5) Metastatic bone pain.
6) Headache& migraine.
7) Postoperative pain.
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8) Pain due to inflammation& tissue injury.

9) Renal colic.
10) Pyrexia.
11) Within 24 hours of birth to close a patent ductus arteriosus.
Pharmacokinetics:
(a).Absorption:
Absorption of all N.S.A.I.Ds is facilitated in the stomach as they are

weak acids & mainly un-ionized in the acid media of the stomach.
Most absorption occurs in the small intestine because the un-ionized

form may be insoluble & the absorptive area of microvilli is much more
extensive.
(b). Protein binding:
Most N.S.A.I.Ds. Are extensively protein- bound (90-99%).
Aspirin is bound to the same site on albumin as warfarin , potentiating

its effect.
(c).Metabolism &excretion:
They are oxidized or hydroxylated &then conjugated in the liver& excreted
in the urine. Some have active metabolites.
Adverse effects of N.S.A.I.Ds.:

Most side effects are due to inhibition of prostaglandin
1.G.I.T.:
These are the commoner side effects. They include dyspepsia, gastric
erosion , nausea vomiting ,diarrhea & constipation.
Gastric erosion is caused by uninhibited acid secretion, reduced mucous &
bicarbonate secretion& reduced mucosal blood flow.
Prostaglandin is mandatory for all these functions & its inhibition by

N.S.AI.Ds. produces these side effects.
These effects may be reduced by administration of prostaglandin

analogue e.g. misoprostol or H2-receptor antagonist.
2. Renal:
When renal blood flow is normal or high, little prostaglandin is

released by the kidney.
When renal blood flow is reduced, prostaglandins are released causing

compensatory vasodilatation.
N.S.A.I.Ds. May cause acute renal failure when given during acute blood
loss, hypotension , cardiac failure, liver cirrhosis, glomerulonephritis &
nephrotic syndrome.
N.S.A.I.Ds. may cause salt& water retention&
may exacerbate heart failure.
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chronic N.S.A.Ds. administration may cause analgesic nephropathy&

renal papillary necrosis.
N.S.A.I.Ds.
3.Clotting:
Vascular damage causes platelets to aggregate & release thromboxane

which causes further aggregation. Platelets aggregation is inhibited by
prostacyclin.
Aspirin inhibits cyclo-oxygenase & therefore diminishes both
prostacyclin in the endothelial cell &thromboxane in platelets.
Low dose aspirin alter the balance towards prostacyclin, where as high
dose reduces both prostacyclin& thromboxane.
4.Asthma & bronchospasm:
Bronchospasm may occur as a part of anaphylactic reaction or may be

due to inhibition of bronchodilator prostaglandin.
5. Skin reactions:
This include mild rash, urticaria, photosensitivity.

They are common with mefenamic acid.
6.C.N.S.:
Regular high doses of aspirin may cause 8th nerve damage( tinnitus,
reduced hearing &vertigo ).
Overdose may cause medullary stimulation & hyperventilation.
7.Reproductive system:
Prostaglandin synthesis by the uterus increases substantially in the

hours before delivery.
N.S.A.I.Ds. Inhibit uterine contractions & prolong labour.
8 Ductus arteriosus:
Prostaglandin is a potent dilator of ductus arteriosus & it is important

for its patency in utero.
N.S.A.I.Ds. , especially indomethacin may cause closure (even
prematurely) of ductus arteriosus & may be used in the newborn for this
purpose to escape the alternative of surgical ligation.
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LOCAL ANALGESICS
Techniques of Local Analgesia
There are either peripheral or central:-
A-Peripheral:
1. Local infiltration around where surgical incision is intended. (Lipoma,
sebacious cyst, cut wounds etc.)
2. Individual nerve blocks, e.g ulnar, radial, sciatic nerves
3. Regional block, where more than one nerve supplying a region of the body
e.g Brachial plexus, Lumbar plexus and Three in one block of the lower
limb(includes sciatic, femoral and obturator nerves)
4. Intravenous(Beirs) block for upper and lower limbs.
B-Central or spinal:
As it is performed by depositing the agent inside the spinal canal, either
outside the covering meninges of the spinal cord or inside the meninges in
the subarachnoid space between the arachnoid and the pia matter also
called thecal space.
CENTRAL BLOCKS
A- INTRATHECAL,(SUBARACHNOID), (SPINAL) BLOCK:
It is attained by deposition of the local agent inside the subarachnoid space
of the spinal cord.
Indications:
Suitable for surgical procedures of the lower abdomen and lower
extremities; as it provides analgesia at level determined by the level of
block. e.g. groin hernia, vesical lithotomy, prostatectomy, caeserian
section, varicose veins and amputations of the lower limbs
It is performed under complete aseptic conditions. The lumbar puncture is
usually performed at a spinal level avoiding direct injury to the spinal cord.
This is done by choosing a level below the lower end of the spinal cord at
the level of the lower end of the first lumbar vertebra i.e. Anywhere below
lumbar vertebra number two. The spinal needle penetrates the back of the
patient passing through the skin first, then the subcutaneous tissues, the
supra spinous ligament, the inter spinous,the ligamentum flavum, the
extradural space, the duramatter and the arachnoid into the subarachnoid
space.
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The indicator that the needle is in the correct site is the flow of the
cerebrospinal fluid
Through the needle to the outside. Then the local agent will be injected.
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Neuraxial Anesthesia
A. General Information
B. Spinal Anesthesia
C. Epidural and Caudal Anesthesia
D. Assessing level of blockade
E. Complications
Neuraxial anesthesia is the name used for spinal, epidural and caudal blocks.
Each of these different blocks can be achieved either with a single injection or
through intermittent boluses or constant infusions delivered through a catheter.
Indications for Neuraxial blockade include:

1. Surgery of lower abdominal, inguinal, urogenital, gynecologic and rectal
regions and the lower extremity including orthopedic and vascular
procedures
2. Obstetrics
Labor analgesia
Surgical anesthesia for c-sections
3. Post-operative pain control
Thoracic surgery
Major abdominal surgery
Orthopedic surgery (hip, knee)
4. Pain Control
Rib fractures
Contraindications:
Absolute:
-patient refusal
-bleeding diathesis
-infection at the proposed site of injection
-severe hypovolemia
-elevated intracranial pressure
Relative:
-sepsis
-uncooperative patient
-severe spinal deformity
-demyelinating lesion
-severe stenotic heart valvular disease or ventricular outflow
obstruction
Controversial:
-prior back surgery at injection site
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-prolonged and complicated operation with severe blood loss
Sites of Action:
The main site of action for neuraxial blockade is the nerve root.
In spinal blocks, LA is injected around the nerve root in the
subarachnoid space. Direct injection into the CSF allows a relatively
small dose and volume to achieve a dense sensory and motor
blockade.
In epidural and caudal blocks, LA is injected into the epidural space
to bathe the nerve root. In contrast to spinal blocks, a higher volume
and dose of LA is needed to achieve the same concentration of LA.
Mechanism of Action:
Conduction blockade of posterior nerve roots interrupts somatic and
visceral sensation whereas blockade of anterior nerve root fibers
prevents efferent motor and autonomic transmission.
Somatic and Motor Blockade:

Blocking painful stimuli and abolishing skeletal muscle tone is ideal
for surgical procedures, providing analgesia and muscle relaxation.
The mechanism of action of LAs and differences in nerve fiber type
has been discussed in previous sections. Briefly, smaller and
myelinated fibers are blocked before larger, unmyelinated fibers.
This and the fact that the concentration of LA decreases with
increasing distance from the site of injection leads to the
phenomenon of differential blockade:
-sympathetic blockade (tested by temperature) occurs two levels
above . . .
-sensory blockade (tested by pin prick or light touch) occurring two
levels above . . .
-motor blockade
Autonomic Blockade
Interruption of efferent autonomic transmission at spinal nerve roots
produces sympathetic and some parasympathetic blockade.
Sympathetic nerve fibers exit from T1-L2 (thoracolumbar) while
parasympathetics exit with cranial and sacral nerves (craniosacral).
Neuraxial anesthesia does not block the Vagus nerve.
What results from blockade is either decreased sympathetic tone or unopposed
parasympathetic tone.
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Organ System Effects:

Cardiovascular:
Due to sympathetic blockade, neuraxialblocks produce varying
degrees of decreased blood pressure, heart rate and cardiac
contractility depending on the level of sympathectomy.
Vascular toneis determined mainly by sympathetic fibers arising
from levels T5-L1 which innervate vascular smooth muscle. Blockade
of these fibers results in venous vasodilation, pooling of blood, and
decreased venous return to the heart. Compensatory
vasoconstriction at levels above the block may compensate for this
vasodilation.
Blockade of higher levels (T1-T4) prevents compensatory
vasoconstriction and interrupts sympathetic fibers leading to
compensatory tachycardia. The resulting hypotension and
bradycardia(unopposed vagalor parasympathetic tone) can result in
the sudden cardiac arrest sometimes seen with spinal anesthesia.
Clinical Pearl: To avoid hypotension and bradycardia, volume load, place patient in
supine position, and if a gravid uterus is present place patient in lateral decubitus
to avoid obstruction of venous return.
NOTE: ALWAYS HYPOTENSION COMES WITH TACHYCARDIA, SPINAL
ANASTHESIA IS ONLY PLACE THAT YOU FIND HYPOTENSION+BRADYCARDIA
Pulmonary:
Pulmonary manifestations are generally minimal in healthy patients
as the diaphragm is innervated by C3-C5. In patients with little
pulmonary reserve, however, who depend on accessory muscles for
respiration, higher blockade will impair these muscles. Coughing and
clearing secretions also depends on these muscles for expiration.
Gastrointestinal
Unopposed vagal tone via sympathetic blockade from T5-L1 results in
a contracted gut with active peristalsis. This is a helpful adjunct to
general anesthesia in laparoscopic surgery.
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Urinary Tract
Neuraxial anesthesia at the lumbar and sacral levels blocks both
sympathetic and parasympathetic outflow to the bladder. This results
in urinaryretention until the block wears off.
Metabolic and Neuroendocrine
Surgical manipulation evokes the stress response leading to an
increase in ACTH, cortisol, epinephrine, norepinephrine, and ADH
levels as well as the activation of the renin-angiotensinaldosteronesystem. This leads to intra-and post-operative
hypertension, tachycardia, hyperglycemia, protein catabolism,
suppressed immune responses and altered renal function. Neuraxial
anesthetic techniques can wholly or partially block this response if
initiated before and continued after surgery.
Spinal Anesthesia -Factors affecting level of the block

Baricity
Baricity of a LA solution is its specific gravity relative to that of CSF. A
hyperbaric solution is more dense than CSF while a hypobaric
solution is less dense.
In general, the higher the level of injection, the higher the level of
the block. However, when a hyperbaric solution is injected into a
patient in the head down position, it will migrate cephalad, and vice
versa. Likewise, a hypobaric solution will move caudad.
The same holds true when a patient is in the lateral decubitus
position -a hyperbaric solution will move towards the dependent side
while the hypobaric solution to the non-dependent.
With normal spinal anatomy, the apex of the thoracolumbar
curvature is T4. When the patient is in the supine position, this
should limit a hyperbaric solution spread and level of block to T4 or
below.
Positioning
As described above level of anesthesia is dependent on patient
positioning. If the patient is seated for 3-5 minutes after injection of a
hyperbaric solution into the lumbar region, only the lumbar and
sacral nerves are blocked.
Moving the patient from seated to supine immediately following
injection moves the solution more cephalad.
A patient can also be placed in the lateral decubitus position if
unilateral block is desired (the hyperbaric solution will move to the
operative side if the patient is appropriately positioned.)
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Local Anesthetic and dosage

In general, the higher the dosage, the higher the level of the block.
Hyperbaric bupivacaine and tetracaineare two of the most commonly
used agents.
Both are relatively slow in onset (510 min) and have a prolonged
duration (90120 min).
Tetracaine generally produces more motor blockade than the
equivalent dose of bupivacaine.
Addition of epinephrine to spinal bupivacaine prolongs its duration
only modestly.
In contrast, epinephrine can prolong the duration of tetracaine
anesthesia by more than 50%.
Other factors potentially affecting level of block

1.
2.
3.
4.
5.
6.
7.
8.
Age
CSF volume
Curvature of spine
Drug volume
Intraabdominal pressure
Needle direction
Patient height
Pregnancy
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Oxygen therapy
Why is oxygen required for survival ?
Oxygen is required for aerobic metabolism.

Oxidative phosphorylation in mitochondria -
6o2+ glucose___ 6H2o +6co2+36ATP.-
Anaerobic metabolism in cytoplasm-
Glucose___ lactic acid+2ATP-
What is Pasteur Point ?

The critical level of Po2 below which aerobic metabolism fails (1-2 mmhg in
mitochondria).
Oxygen therapy:
Oxygen therapy is the administration of oxygen as a medical
intervention, which can be for a variety of purposes in both chronic
and acute patient care.
Oxygen is essential for cell metabolism, and in turn, tissue
oxygenation is essential for all normal physiological functions.
Room air only contains 21% oxygen, and increasing the fraction of
oxygen in the breathing gas increases the amount of oxygen in the
blood.
The fraction of inspired oxygen, Fio2.
Recommendations for instituiting oxygen therapy:1-cardiac and respiratory arrest.

2-hypox.aemia(pao2<59mmhg,sao2<90.)
3-systemic hypotension( systolic BP<100.)
4- low cardiac output and metabolic acidosis.( Hco3<18mmol/l).
5-in anaesthesia added oxygen should be used pre, during and after
anaesthesia.
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Oxyhemoglobin dissociation curve:
MEDICAL GAS THERAPY

AVAILABLILITY:1- High pressure cylinders.
2- Pipeline systems.
3- Oxygen concentrators.
4- Liquid oxygen.
Oxygen cascade
Oxygen moves down the pressure or concentration gradient from
high level in air to the levels respiratory tract and then alveolar gas,
the arterial blood, capillaries and finally the cells.
Oxygen carriage in the blood

Oxygen is carried in the blood in two forms:
Bound to hemoglobin.
A very small amount is dissolved in plasma
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Oxygen stores
The store of oxygen in the body is small and would be unable to
sustain life for more than a few minutes.
Oxygen stores are limited to the oxygen in the lung and in the blood.
Breathing 100% oxygen:

Breathing 100% oxygen causes a large increase in the total stores as
the FRC fills with oxygen.
The major component of the store is now in the lung
80% of this store is now can be used without .any reduction in Hb
saturation
Breathing air
Breathing 100%
oxygen
In the lung
450 ml
3000 ml
In the blood
850 ml
950 ml
Dissolved or bound in
tissues (FRC)
250 ml
300ml
total
1550 ml
4250 ml
Oxygen content of blood:

The volume of oxygen carried in each 100 ml of blood
O2 carried by Hb) + (o2 in solution) = 1.34x Hb x Spo2 x 0.01) +0.023x
PaO2)
Oxygen content of arterial blood ( CaO2) is 20.4ml/100 ml.
Oxygen Delivery
Tissue oxygenation is primarily dependent on mill. Of o2 delivered to
the tissues.
Oxygen delivery is the amount of oxygen made available to the body
in one minute.
Do2 (ml/min)=
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Oxygen content(ml/dl)x cardiac output

Oxygen Content Cao2=(Hb)(percent saturation)(1.34)+(Pao2)(0.003)
5000X200ml/1000ml of blood = 1000ml of oxygen /min.
Oxygen returned=mixed venous oxygen content x cardiac output=
15.2X5=760
Oxygen consumption:
Approximately 250 ml of oxygen are used every minute by a conscious
resting person, therefore about 25% of the arterial oxygen is used
every min.( the Hb in mixed venous blood is 70% saturated.
Hypoxemia :
Clinically defined as a relative deficiency of oxygen in the arterial
blood.
Assuming normal Hb content, an arterial po2 (Pao2) measurement of
less than 80mmhg signifies hypoxemia
Hypoxia:
defined as inadequate oxygen tension at the cellular level.
Recognition of hypoxia
Signs and symptoms:1-Altered mental status.
2-Dyspnoea.
3-Arrhythmias.
4-Nausea , vomiting and other GIT signs.
5-Cyanosia.
6-Systemic hypotension or hypertension.
Cyanosis
Bluness of the tissues.(due to excessive amount of deoxygenated
haemoglobin in the peripheral blood vessels).
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Classification of hypoxia
Histotoxic hypoxia
Inability of cells to
utilize o2
Cyanide toxicity
Hypoxic hypoxia
Reduced fio2 alveolar

hypoven. R-L shunt
Circulatory hypoxia
Reduced Cardiac
output.
Emphysema. pul.
Fibrosis. asthma
atelectasis. cynotic C H D.
drug overdose. o2
equipment error.
Congestive heart failure.
MI. dehydration.
Haemorhage.
Hemic hypoxia
Reduced HB content.
Reduced HB function.
Anemias.
Carboxyhemoglobinemia.
methemoglobinemia
Demand hypoxia
Increased o2
consumption
Fever. seizures
INDICATIONS FOR OXYGEN SUPPLEMENTATION

Po2< 60mmhg or Spo2< 90%.
It is also indicated for the following
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ARDS.
-Pulmonary fibrosis.
-Myocardial infarction.
Cardiogenic pulmonary
edema.-Cyanide poisoning.
-CO inhalation.
Supplemental oxygen during the perioperative period:

Supplemental o2 is given during the per operative period
because general anaesthesia commonly causes a decrease in
po2 secondary to increased pul. Ventilation perfusion
mismatching and decreased FRC.
Postoperative prolonged oxygen supplementation is needed

in the following:
Ischemic heart
disease.
Reduced cardiac
output.
Anaemia.
Obesity.
Shivering.
Hypothermia &
Hyperthermia.
Pulmonary oedema.
Airway obstruction.
Major surgery.
Hypotension .
What might be done to improve oxygenation

Increase Fio2.
Increase minute ventilation.
Increase cardiac output.
Increase oxygen carrying capacity (Hb)
Decrease oxygen consumption from pain, shivering or fever.
Cardiopulmonary Bypass.
Hypoventilation
Oxygen therapy is particularly beneficial in treating
hypoxemia caused by hypoventilation.
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Causes of hypoventilation in the immediate postoperative

period:Factors affecting the airway.
Factors affecting the ventilatory drive.
Peripheral factors.
Oxygen delivery devices

1-Fixed-Performance devices.
2-Variable-Performance devices.
1. Fixed-Performance devices:
They are also called high air flow oxygen enriched
devices(HAFOE).
They provide a constant & predictable inspired oxygen
concentration irrespective of the pt. ventilatory pattern.
AIR - ENTRAINMENT VENTURI MASKS:

Venturi masks provide fixed Fio2 through an open system
with high flow about the nose and mouth.
Oxygen is directed by a small- bore tubing to a mixing-jet.
The mask can either provide a fixed Fio2 or can be adjusted
to different Fio2 selections.
FIXED PERFORMANCE OR HIGH-FLOW SYSTEM:

1- anaesthesia bag.
2- bag-mask-valve system.
3- air-entrainment venturi mask.
4-air-entrainment nebulizers.
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PROBLEMS WITH HAFOE SYSTEM:

Fio2 can increase if the entrainment ports are obstructed by
the patient's hands, bed sheets, water condensate.
2.Variable-Performance devices:
These devices are popular because of their simplicity,pt. comfort&
economics.
Fio2 in these devices is determined by:1-The size of the oxygen reservoir.
2-The oxygen flow rate.
3-The breathing pattern of the patient.
Guidelines for estimating Fio2 with variable-performance

devices:
O2 flow rate(L)
1-Nasal cannula 1
2
3
4
5
6
2-Oxygen mask 5-6
6-7
7-8
3-Mask with reservoir
bag
6
7
8
9-10
Fio2
0.24
0.28
0.32
0.36
0.40
0.44
0.40
0.50
0.60
0.60
0.70
0.80
> 0.80
Hyperbaric oxygen therapy

Breathing pure oxygen in a pressurized room.
The air pressure is raised up to 3 times higher than normal
air pressure .
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HYPERBARIC OXYGEN:
Oxygen therapy at greater than atmospheric pressure ,
usually 2-3 atmosphere by using a pressurized or hyperbaric
chamber.
Indications:
Air or gas embolism.

Carbon monoxide poisoning.
Intestinal obstruction
Indications for hyperbaric oxygen

1- intracranial abscess.
2-thermal burns.
3- skin graft and flaps.
4- osteomyelitis.( refractory).
5- decompression sickness.
6-Air or gas embolism.
7-Carbon monoxide poisoning.
8-Severe anaemia.
9-Arterial insufficiences (central retinal artery occlusion).
Adverse Effects of Oxygen

The clinically effective range of Fio2 for prolonged oxygen
therapy is from 0.2- 0.5.
Prolonged administration of 1.0 Fio2 to patients with
diseased lungs often has detrimental physiologic&
cytotoxic effects .
Factors leading to oxygen toxicity:1- patient susceptibility.

2- Fi o2.
3- duration of therapy.
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Oxygen toxicity
O2 toxicity is caused by free radicals. These affect the
nervous system resulting in anxiety, nausea and seizures
when the partial pressure exceeds 200kPa. The alveolar
capillary membrane undergoes lipid peroxidation and
regions of lung may collapse
SYMPTOMS OF OXYGEN TOXICITY:
Substernal distress.
Paroxysmal coughing.
Pain.
Dyspnoea.
THE MODE OF ACTION OF TOXICITY:

O2- derived free radicals inactivates enzymes; neutrophil
recruitment and release of mediators of inflammation occur next
and greatly accelerate the extent of endothelial and epithelial
damage and impairment of thesurfactant system.
Adverse Effects
1.
2.
3.
4.
Absorption Atelectasis.
CO2 narcosis.
Pulmonary oxygen toxicity.
Central nervous system
toxicity.
5. Depressed hemopoisis.
6. Retrolental fibroplasia
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PULMONARY OXYGEN TOXICITY:

Oxygen toxicity is thought to be a result of intracellular
generation of free radicals .
A high conc. Of oxygen increases the likelihood of generating toxic
species.
PULMONARY TOXICITY:
Oxygen - mediated injury of the alveolar - capillary membrane
results in a clinically & pathologically ARDS similar picture.
Pulmonary capillary permeability increases & the membrane
thickens (type 1 alveolar cells decreases & type 11) cells proliferate.
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113 | P a g e
Shock
Definition
Acute circulatory failure. -Acute, significant systemic hypo-perfusion.
-Acute condition in which the circulatory system fails to
provide the body with adequate perfusion to meet the
cellular metabolic needs.
-Medical emergency.
Can lead to multi-organ failure and death. -Hypotension is the major (though late) sign.
Hemodynamics:
F=blood flow,
P= pressure gradient,
R=resistence to flow,
PA=arterial pressure,
PV=venous pressure
L = length of the vessel

= viscosity of the blood
r4 =radius to the fourth power
114 | P a g e
CVS Components:
1- the blood(fluid) , 2- the heart (pump) , 3- the vesseles(tubes)
Myocardial
Contractility
Stroke Volume
Afterload
Cardiac Output
Blood
Pressure
Preload
Heart Rate
Systemic Vascular
Resistance
Preload:
The degree of stretch of the cardiac myocytes at end
diastole.
The ventricular end-diastolic volume.
The ventricular end-diastolic pressure.
Afterload:
The load against which the heart must contract to eject
blood.
Is the stress developed in the wall of the ventricle during
ejection.
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Systemic Vascular Resistance:

Vasoconstriction increases SVR, while Vasodilation
decreases SVR.
Etiological Classification of Shock
1. Hypovolemic: fluid loss reduced preload
2. Obstuctive: obstruction to blood flow increased afterload or
reduced preload reduced stroke volume
3. Cardiogenic: decreased contractility or heart rate decreased
cardiac output
4. Distributive: generalized vasodilation decreased SVR &
decreased preload
**The patient can have various combinations of the
different types of shock.
Pathophysiology of Shock
Role of the circulatory system:
1. Deliver Oxygen and nutrients
2. Remove toxic and waste products
Thus shock leads to 1-Tissue hypoxia
2-Accumulation of toxic waste products
-Lack of O2 becomes lethal when arterial oxygen partial pressure falls
to 35 mmHg or below.
-Lack of substrates makes the cell use its own phospholipids as fuel
Anaerobic Metabolism
-Glycolysis only; No citric acid cycle, no oxidative
phosphorylation
-Almost 20 times less efficient than aerobic
116 | P a g e
-Low ATP failure of Na+/K+ pump K+ efflux + Na+ (and

water) influx cell swelling cell burst and death
-Low ATP Ca2+ influx;
-Ca2+ influx activation of proteases and phospholipases
membrane disruption
-Ca2+ influx accumulation in the mitochondria
irreversible structural damage
-Hypoxia and lack of ATP lysosomal membrane
disruption cell auto-digestion.
-Hydrogen will be shifted to pyruvate converting it to lactic
acid (to free more NAD+)
-Increased lactic acid production lactic acidosis;
-Acidosis vasodilation low effective circulating volume
-Acidosis impaired enzymatic function
-Acidosis myocardial depression
-Acidosis DIC
Stages of Shock
1-Compensated:
-The body senses and responds to the circulatory inadequacy
-Modifications at the components that control blood pressure
(see Hemodynamics)
Defending Blood Pressure:
Detection:
-Baroreceptors: Carotid sinus and Aortic Arch
-Volume receptors: Right Atrium and Pulmonary
vasculature
-Chemoreceptors: Aortic and carotid bodies and Medullary
>>Response: neural and humoral.
The Neural:
Stimulate sympathetic:
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-Tachycardia
-Increased contractility
-Vasoconstriction
Inhibit parasympathetic
The Humoral:
Adrenal medulla :Catecholamines
Hypothalamopituitary response : Adrenocorticotropic
hormone, Vasopressin
Renin-angiotensin-aldosterone system
>>Fluid Shift response:

-Blood is diverted through vasoconstriction from the
kidneys, GIT, skin, etc. to the vital organs (brain, heart,
and lungs)
-Blood pressure is normal. Vital organ function is maintained
2-Uncompensated:
-Positive feedback progression
-If the initial causative agent is not corrected the compensatory
mechanisms will soon be overwhelmed.
Inadequate perfusion of vital organs.
SVR and HR LV afterload, LV work, and cardiac
oxygen consumption
3-Irreversible:
-Irreparable damage in the vital organs.
-Death cannot be prevented.
-Even the restoration of O2 will not be able to correct the
situation.
>>Death;
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Brain and Lungs : Die within 4 to 6 minutes without oxygen

Organs : Die within 45 to 90 minutes without oxygen
Skin and muscle :Die within 4 to 6 hours without oxygen
Hypovolemic Shock
intravascular volume preload CO BP
Causes:
1-Hemorrhage (internal or external) haemorrhagic shock
(Normal blood volume is about 5 L)
2-Vomiting
5-Burns
3-Diarrhea
6-Adrenal crisis
4-Third-space loss
(peritonitis,
pancreatitis, etc)
7-Diabetes insipidus
Clinical picture:
>Manifestations s of system organ hypoperfusion:
-CNS: Altered mental state : restlessness, agitation
lethargy, coma
-Pulse: rapid, weak pulse
-Skin: pale, cold, clammy (moist), delayed capillary refill
-Lungs: deep rapid breathing
-Kidney: oliguria
-Thirst and dry mouth
-Hypotension is a late sign (initially orthostatic)
-Bradycardia is a late sign
Hypotension:
systolic BP 90 mm Hg
mean arterial pressure 60 mm Hg
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Systolic BP > 30 mmHg below the patients baseline

pressure
Investigations: High serum lactate
Classes of hemorrhagic Shock:
Class
IClassI
Class II
3 Class III
33C
<750
750-1500
1500-2000
Class IV Cl
Class IV
ass IV
>2000
% blood
vol.
Pulse
Blood
pressure
Pulse
pressure
Resp. rate
UOP ml/hr
Mental
status
Fluids
<15
15-30
30-40
>40
<100
normal
>100
normal
>120
decreased
>140
decreased
normal
decreased
decreased
decreased
14-20
>30 ml/hr
Sli. anxious
20-30
20-30
anxious
30-40
5-15
confused
>40
negligible
lethargic
crystalloids
crystalloids
blood
blood
Management:
-ABC
-Call for help
Airway, Breathing and oxygen
Circulation;
Trendelenberg position
I.V. Fluids
Treatment of initial causes
+/- Drugs
*Fluids:
Rapid restoration of intravascular volume:
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1-Peripheral Intravenous- Insertion of two wide-bore

cannulae
-If unstable you have 60-90 seconds
2-intraosseous access; 2nd line for both paediatric and
adults.
3- Central venous access
-Use isotonic fluids (to remain inside ECF)
-1 L crystalloid 250 ml colloid
-Give 20 to 50 ml/kg bolus of crystalloids rapidly if
cardiac function is normal
-Use whole blood to replace blood loss, or if still
unstable after 60 cc/kg of crystalloids.
-anemia is poorly tolerated in the stressed, hypoxic,
hemodynamically unstable patient.
Crystalloids:
1-Normal Saline
2-Ringer Lactate
-Salt solutions that freely cross capillary walls.
-Stay in the intravascular space for a shorter time than
colloids, T1/2 = 20 to 30 minutes
-3 times the volume lost has to be given.
-Only one-third of the fluid administered will stay in the
intravascular space, with two-thirds passing directly into
the interstitial compartment
Colloids:
1-Gelatins.
5-Dextran.
2-Hetastarch.
6-Blood
3-Albumin.
7-Fresh Frozen
Plasma
4-Plasma protein
fraction.
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-Theoretically better than crystalloids at expanding the circulatory

volume, because their larger molecules are retained more easily in
the intravascular space.
-Some can cause anaphylactic reactions
Cardiogenic Shock
-Caused by a primary failure of the ventricles to generate
adequate CO
-Sustained hypotension despite adequate preload
-Associated with systemic hypoperfusion and high lactate.
Causes may include:
1-Myocardial infarction
2-Arrhythmia ( brady or
tachy)
3-Cardiomyopathy
5-Valvular lesions
6-Myocarditis
7-Myocardial contusion
4-Late septic shock
8-Infiltrative diseases
Clinical picture:
1-Manifestations of system organ hypoperfusion:
Altered mental status
Hypotension
Rapid weak pulse
Tachypnoea
Cold clammy skin
Oliguria
Slow capillary refill
High serum lactate
2-Pulmonary Edema (S & S); SOB and Bibasal creps

3-Jugular and neck venous distention
Diagnosis: ECG and echocardiography aid in diagnosis
Management:
- ABC
-Call for help
-Cautious fluid (challenge): 250-500 ml
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-Cautious pharmacological support (inotropes and

vasopressors)
-Other treatments according to the cause:
-Antiarrthytmic measures
- PCI
-Balancing fluid therapy and inotropic support can be very

difficult.
-If inotropes and vasopressors fail, intra-aortic balloon pump
*Pressors & inotropes:
-Vasopressors increase SVR and BP
-Inotropes augment contractility (after preload has been

established) thus improving cardiac output.
-Risk of tachycardia and increased myocardial oxygen

consumption if used too soon.
Ensure adequate fluid volume

Administer via a Central Venous Catheter
Pressors & inotropes
*Vasoactive/Cardiotonic Agents :
Norepinephrine
0.05-0.2mcg/kg/min: only alpha and beta-1
Dopamine
Low: 1-5 mcg/kg/min: dopaminergic (renal a. dilation)
Moderate: 5-10 mcg/kg/min: more beta-1 (+inotropic)
High: 10-20 mcg/kg/min: more alpha-1 (vasoconstriction)
Dobutamine
2.5-15 mcg/kg/min: mostly beta-1, some beta-2
potent inotrope, variable chronotrope
may be useful in cardiogenic shock
123 | P a g e

Epinephrine
0.05-0.1 mcg/kg/min: mostly beta-1, some beta-2
> 0.1 to 0.2 mcg/kg/min: alpha-1
potent inotrope and chronotrope
Obstructive Shock
Causes:
-Tension Pneumothorax
-Massive Pulmonary Embolism
-Cardiac Tamponade
-Constrictive pericarditis
-Severe pulmonary hypertension
Presentation:
-Similar to hypovolemic and cardiogenic shock
-S & S of the cause
-Jugular and neck venous distention
Treatment of the cause

Distributive Shock
-Caused by excess vasodilatation leading to low SVR
Types:
1-Septic
2-Anaphylactic
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3-Neurogenic
4-Vasodilator Drugs
5-Addisonian crisis
Septic Shock
-Results from sepsis (systemic inflammatory response
syndrome SIRS due to infection)
Mechanism:
-release of inflammatory mediators leading to:
1. Disruption of the microvascular endothelium
extravasation actual hypovolemia
2. Vasodilation and sequestration of blood in
cutaneous venules and small veins relative
hypovolemia
SIRS:
-High heart rate
-High respiratory rate
-Hypo or hyperthermia
-High or low TWBC
Clinical picture:
-Hypotension not responding to adequate fluid
resuscitation
-Manifestations of hypoperfusion except:
Warm flushed and sweaty skin due to vasodilation
Early: bounding pulse (collapsing)
Altered mental status -Rapid pulse

-Hypotension
-Tachypnoea
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-Oliguria
-High serum lactate
-Gram negative or other overwhelming infection.
Treatment:
-Intravenous fluids- fill the tank
-Vasopressors
-Early antibiotic administration
-Inotropes as sepsis depresses the myocardium
Neurogenic Shock
Mechanism: Loss of autonomic innervation of the
cardiovascular system (arterioles, venules, and the heart)
Causes:
1-Spinal cord injury
2-Regional anesthesia
-Presentation as above
-Bradycardia in high spinal injury (T1-T4)
Treatment:
-IVF
-Vasopressors
Anaphylactic shock
-Severe generalized life-threatening type I
hypersensitivity allergic reaction.
-Systemic release of histamine and other
inflammatory mediators from mast cells and
basophils.
-Triggered by antigen binding to cell-bound IgE
antibodies.
-Non-IgE-mediated reactions also occur:
anaphylactoid reactions
126 | P a g e
-Likely triggers: drugs (e.g. muscle relaxants,

antibiotics), foods (e.g. nuts), venoms (e.g. bee stings)
Criteria:
-Sudden onset and rapid progression
-Life-threatening Airway, Breathing, or Circulation
problems
-Skin or mucosal changes: flushing, urticaria,
angioedema. (can be absent in about 20% of the cases)
**Angioedema :Can cause airway obstruction.
Airway:
Airway swelling and airway obstruction (tongue,
pharyngeal and laryngeal swelling) may lead to
stridor.
Chest:
bronchoconstriction dyspnoea, cough and wheeze.
Can lead to confusion and cyanosis
Vasculature:
generalized vasodilation distributive shock
Treatment:
-ABCs approach
-Remove the causative agent
-100% oxygen
-Epinephrine 0.5 mg I.M. (anterolateral aspect of the
middle third of the thigh):*
-Alpha receptors: reverses the peripheral vasodilation.
-Beta receptors: bronchodilation, increases myocardial

contraction, suppresses histamine release.
-Further doses can be given at about 5 min intervals

according to patient response.
*IV epinephrine is only used by experienced individuals

(e.g. anaesthetists)
127 | P a g e
Intravenous fluids:
--Rapid IV fluid challenge (500-1000 ml in adults)
--Use crystalloids
--Give further doses according to the response
Antihistamines:
-Adjuvant treatment
-Not life-saving if used alone
-May help counter histamine mediated vasodilation
and bronchoconstriction
--Chlorphenamine 10 mg I.V. or I.M.
Hydrocortisone:
--May help prevent or shorten protracted reactions.
--200 mg I.M or I.V slowly
Summary
>Prompt recognition of systemic hypoperfusion.
>Call for help.
>Check: lungs, neck veins, hands, history
>ABC
> treat according to type.
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Autonomic Nervous System pharmacology and

anesthesia
Receptors
Definition: a receptor is a component of a cell that interacts selectively with
an extra-celluar compound to initiate a biochemical change.
Advances in molecular biology are promising in the future to discover new
receptors that will revoultionalize pharmacology and therapeutics .
Adrenergic Receptors
Adrenergic receptors are the sites where adrenergic drugs bind and produce
their effects.
Adrenergic receptors are divided into alpha-adrenergic and beta-adrenergic
receptors depending on whether they respond to norepinephrine or
epinephrine.
Both alpha- and beta-adrenergic receptors have subtypes designated 1 and
2.
Alpha Receptors
Alpha1-adrenergic receptors are located on the postsynaptic effector cells.
Generally excitatory: except in the GIT where they cause relaxation.
Alpha2-adrenergic receptors are located on the presynaptic nerve terminals
and smooth muscles. pre-junctional activation inhibit NT release
.activation of receptors in the vasomotor center in the medulla reduces
sympathetic tone.
Beta Receptors
Both beta-adrenergic receptors are located on the postsynaptic effector
cells.
Beta1-adrenergic receptors are primarily located in the heart.
Beta2-adrenergic receptors are primarily located in the smooth muscle of
bronchioles, arterioles, and visceral organs.
Dopaminergic Receptors
Dopaminergic receptors are only stimulated by dopamine which causes the
vessels of renal, mesenteric, coronary, and cerebral arteries to dilate and
the flow of blood to increase.
129 | P a g e
Adrenergic Receptor agonists

Adrenergic antagonists
Alpha-blockers and beta-blockers bind to the receptor sites for

norepinephrine and epinephrine blocking the stimulation of the SNS.
Cholinergics
Drugs that stimulate the parasympathetic nervous system are called
cholinergics.
Sometimes called cholinergic agonists or parasympathomimetics, these
drugs mimic the effect of acetylcholine, which is the neurotransmitter
responsible for the transmission of nerve impulses to effector cells in the
PSNS.
Cholinergic Receptors
The receptors that bind the acetylcholine and mediate its actions are called
cholinergic receptors.
These receptors consist of nicotinic receptors and muscarinic receptors.
Nicotinic receptors are located in the ganglia of the PSNS and SNS and are
stimulated by nicotine.
Muscarinic Receptors
Muscarinic receptors are located postsynaptically in the smooth muscle,
cardiac muscle, and salivary glands.
These receptors are stimulated by muscarine (found in mushrooms).
Cholinergic Drugs
Cholinergic drugs can be direct-acting (bind to and activate cholinergic
receptors) or indirect-acting (inhibit cholinesterase which is the enzyme
responsible for breaking down acetylcholine).
Cholinergic Blockers
Cholinergic blockers are competitive antagonists that compete with
acetylcholine for binding at the muscarinic receptors of the PSNS,
inhibiting nerve transmission.
This effect occurs at the neuroeffector junctions of smooth muscle, cardiac
muscle, and exocrine glands.
Drugs Affecting the Sympathetic System:

Adrenergic Agonists
Adrenergic Antagonists
130 | P a g e
Adrenergic agonists:
Classified into two groups - catecholamines and noncatecholamines.

Also classified according to their action - direct-acting, indirect-acting, and
dual-acting.
Therapeutic uses depend on which receptors they stimulate and to what

degree - alpha-adrenergic, beta-adrenergic, and dopamine receptors.
Most adrenergic drugs stimulate alpha and beta receptors mimicking the
action of norepinephrine and epinephrine.
Caticholamines and noncaticholamines:

caticholamines have got 3,4-hydroxyl substitution on the benzene ring
combined with the ethanolamine side chain.
Catecholamines
Stimulate the nervous system, constrict peripheral blood vessels, increase
heart rate, and dilate the bronchi.
Can be natural or synthetic and include: dobutamine, dopamine,
epinephrine, norepinephrine, and isoproterenol.
Pharmacokinetics:
Not administered orally; when administered sublingually are absorbed
rapidly through the mucous membranes; when administered SC absorption
is slowed due to vasoconstriction around the injection site; when
administered IM absorption is more rapid.
Widely distributed throughout the body; predominantly metabolized by the
liver; excreted primarily in the urine.
Pharmacodynamics:
Are primarily direct-acting.
Positive inotropic effects - heart contracts more forcefully.
Positive chronotropic effects - heart beats faster.
Positive dromotropic effects - increased conduction through the AV node.
Pharmacotherapeutics:
Use depends on the particular receptor site that is activated.
Norepinephrine - alpha activity.
Dobutamine and isoproterenol > B1. at high doses they become mild B2
agonists.
Epi= upon .nephros=kidney.
Epinephrine - alpha and beta activity.
Dopamine dopaminergic, beta, and alpha activity.
131 | P a g e
Catecholamines that stimulate alpha receptors are used to treat

hypotension caused by a loss of vasomotor tone or hemorrhage.
Catecholamines that stimulate beta1-receptors are used to treat
bradycardia, heart block, low cardiac output, paroxysmal atrial or
junctional tachycardia, ventricular fibrillation, asystole, and cardiac arrest.
Catecholamines that stimulate beta2-receptors are used to treat acute and
chronic bronchial asthma, emphysema, bronchitis, and acute
hypersensitivity reactions to drugs.
Dopamine that stimulates dopaminergic receptors is used to improve blood
flow to kidneys.
Non-catecholamines
Examples:
Ephidrene .
Amphytamine.
Methamphitamine.
Phenylephrine.
Non-catecholamines
Uses include:
For hypotension. however treatment depends on the cause .
nasal and eye decongestion and dilation of bronchioles - albuterol
(Proventil/Ventolin).
smooth muscle relaxation terbutaline sulfate (Brethine, Bricanyl).
Pharmacokinetics:
Since the drugs have different routes of administration, absorption and
distribution vary; can be administered orally; metabolized primarily by the
Pharmacodynamics:
Direct-acting noncatecholamines that stimulate alpha activity include
phenylephrine (Neo-Synephrine).
Direct-acting noncatecholamines that stimulate beta2 activity include
albuterol (Proventil/Ventolin) and terbutaline (Brethine).
Indirect-acting - phenylpropanolamine (Acutrim).
Dual-acting - ephedrine.
Metraminol direct and indirect.
Ephedrine:
an indirectly acting sympathomimetic. It is taken up into presynaptic nerve
terminals, thereby displacing noradrenaline resulting in alpha mediated
vasoconstriction. Ephedrine also has a direct beta agonist effect increasing
132 | P a g e
heart rate and cardiac output, the overall effect increasing blood pressure.
These actions last for 10-15 minutes and repeated doses have a gradually
decreasing effect (tachyphylaxis). Commonly used to treat nasal congestion
,bronchospasm and the hypotension associated with neuro-axial blocks.
Stimulate the sympathetic nervous system and produce a variety of effects
in the body.
Example - ritodrine (Yutopar) - used to stop pre-term labor.
Drug interactions/adverse reactions:
Taken with monoamine oxidase inhibitors can cause severe hypertension
and death
Adrenergic antagonists
Called sympatholytic drugs.
Used to disrupt SNS function by blocking impulse transmission at
adrenergic receptor sites.
Classified according to their site of action: alpha-adrenergic blockers and
beta-adrenergic blockers.
Alpha1 Antagonism:
Inhibits peripheral vasoconstriction
Used for hypertension
prazosin (Minipress)
doxazosin (Cardura)
phentolamine (Regitine)
Alpha-Adrenergic antagonists:
Work by interrupting the actions of the catecholamines norepinephrine
and epinephrine at the alpha receptors resulting in: relaxation of the
smooth muscle in the blood vessels; increased dilation of blood vessels; and
decreased blood pressure.
Prototype drug -prazocin (Minipress)
Pharmacokinetics:
The metabolic fate of alpha blockers in the body is poorly
understood.
Pharmacodynamics:
Block the synthesis, storage, release, and uptake of norepinephrine by
neurons.
Antagonize epinephrine and norepinephrine at alpha receptor sites.
133 | P a g e
Occupy alpha receptor sites on the smooth muscle of blood vessels

resulting in vasodilation, decreased peripheral vascular resistance, and
decreased blood pressure.
Used to treat: hypertension; peripheral vascular disorders, and
pheochromocytoma (a catecholamine-secreting tumor causing severe
hypertension).
Beta Antagonists ( Blockers)
Frequently used
Lower Blood Pressure
Negative chronotropes & inotropes
Prevent stimulation of the sympathetic nervous system by inhibiting the
action of catecholamines at the beta-adrenergic receptors (beta-blockers).
Are selective or nonselective.
Beta1 Selective Blockade:
atenolol (Tenormin)
esmolol (Brevibloc)
metoprolol (Lopressor)
Nonselective beta-blockers: affect beta1 receptor sites located mainly in the

heart and beta2 receptor sites located in the bronchi, blood vessels, and
uterus.e.g:
propranolol (Inderal)
labetalol (Normodyne, Trandate)
sotalol (Betapace)
Pharmacokinetics:
Absorbed rapidly and are protein-bound; the onset of action is primarily
dose and drug-dependent; distributed widely with the highest
concentrations in the heart, lungs, and liver; metabolized primarily in the
Pharmacodynamics:
Effect adrenergic nerve endings as well as the adrenal medulla.
Effects on the CVS include: decreased peripheral vascular resistance;
decreased blood pressure; decreased force of heart contractions; decreased
oxygen consumption; slowed impulse conduction; and decreased cardiac
output.
Selective beta1-blockers (also called cardioselective beta-adrenergic
blockers).
134 | P a g e
Nonselective beta1 and beta2-blockers not only reduce stimulation of the

heart but can also cause the bronchioles of the lungs to constrict.
Clinical usefulness is based largely upon how they affect the heart.
Used to treat heart attacks, angina, hypertension, hypertrophic
cardiomyopathy, and supraventricular arrhythmias.
Also used to treat anxiety, cardiovascular symptoms associated with
thyrotoxicosis, essential tremor, migraine headaches, open-angle
glaucoma, and pheochromocytoma.
Adrenergic drugs and anaesthesia:
Pre-operative withdrawal of B receptor antagonists? NO need to stop them.
Many sympathomemtic drugs e.g aminophyline can interact with volatile
anaesthetics specially with halothane to cause ARRYTHMIAS
Ophthalmic drugs e.g phynliphrene eye-drops can cause severe
hypertension ,arrythmias and myocardial ischemia .
The major peri-operative use of drugs active in the SNS is to treat or prevent
tachycardia ,arrythmia ,hypotension or hypertension .
One ounce of Prevetion is worth a pound of cure. Treatment of the cause.
Titration of drugs is the secret of safety .
Interaction of MAO with indirectly acting sympathommeticamines can

precipitate HYPETENSIVE CRISIS.
Clonidine (A2 blocker) : can reduce the MAC of halothane .
Drugs Affecting the Parasympathetic System
Cholinergics
Anticholinergics
Ganglionic Blocking Agents( not used now) may be trimetaphan.
Cholinergic Drugs
Two major classes of cholinergic drugs: cholinergic agonists and
anticholinesterase drugs.
Cholinergic agonists:
Cholinergic agonists mimic the action of the neurotransmitter
acetylcholine.
Anticholinesterase drugs inhibit the destruction of acetylcholine at the
cholinergic receptor sites.
Include the drugs acetylcholine (rarely used), bethanechol (Urocholine),
carbachol (Miostat), and pilocarpine.
135 | P a g e
Pharmacokinetics:
Administered topically (eye), orally, and subcutaneously; metabolized by
cholinesterases; excreted by the kidneys.
Pharmacodynamics:
Mimic the action of acetylcholine on the neurons of target organs
producing: salivation, bradycardia, vasodilation, constriction of
bronchioles, increased GI activity, increased tone and contraction of the
bladder muscles, and constriction of pupils.
Used to treat: atonic bladder conditions and post-operative and postpartum
urinary retention; GI disorders such as post-operative abdominal distention
and GI atony; reduce eye pressure in glaucoma patients and during eye
surgery; and salivary hypofunction.
Cholinergic Agonists causes SLUDGE:
Salivation
Lacrimation
Urination
Defecation
Gastric motility
Emesis
Anticholinesterase Drugs
Block the action of the enzyme acetylcholinesterase, which breaks down
acetylcholine, at the cholinergic receptor sites.
Divided into two categories - reversible and irreversible.
Reversible have a short duration and include: donepezil (Aricept) and
edrophonium (Tensilon).
neostigmine (Prostigmine)
Myasthenia Gravis at nicotinicM receptors
Used to reverse nondepolarizing neuromuscular blockade
physostigmine (Antilirium)
Shorter onset of action
Used for iatrogenic atropine overdoses at muscarinic receptors
Irreversible anticholinesterase drugs:
have long-lasting effects.
Used primarily as toxic insecticides and pesticides or as a nerve gas in
chemical warfare.
Very common in insecticides & chemical weapons
VX and Sarin gas
Cause SLUDGE paralysis
136 | P a g e
Tx: atropine and pralidoxime (2-PAM)

Anticholinergics
Pharmacokinetics:
Most are readily absorbed from the GI tract, SC, and mucous membranes;
distribution varies among drugs; metabolized by enzymes in the plasma;
excreted in the urine.
Therapeutic uses include: reduce eye pressure; increase bladder tone;
improve GI tone and peristalsis; promote muscular contraction; diagnose
myasthenia gravis; an antidote to cholinergic blocking drugs.
Echothiophate : long acting Anticholinestrease ,is used in gulcoma to cause
meiosis. Enough can be absorbed from the eye to potentiate cholinergic
drugs and suxamethonium .
Interrupt parasympathetic nerve impulses in the central and autonomic
nervous systems.
Also referred to as anticholinergic drugs because they prevent acetylcholine
from stimulating the muscarinic cholinergic receptors.
Drugs include the belladonna alkaloids- the prototype is atropine.
Pharmacokinetics:
Absorbed from the eyes, GI tract, mucous membranes, and skin; when given
IV atropine works immediately; distributed widely; cross the BBB;
moderate protein-binding; metabolized in part by the liver; and in part
excreted un changed by the kidneys.
Often used to treat GI disorders and complications.
Atropine is administered pre-operative to reduce GI and respiratory
secretions and prevent bradycardia caused by vagal nerve stimulation
during anesthesia.
Other uses include bradycardia, pupil dilation, and organophosphate

pesticide poisoning.
Dry mouth, reduced bronchial secretions, increased heart rate, and
decreased sweating can occur.
Muscarinic antagonists
Atropine
Ganglionic antagonists
block nicotinicN receptors
Turns off the ANS.
trimethaphan (Arfonad)
137 | P a g e
Atropine Overdose
Dry mouth, blurred vision, anhidrosis
Hot as Hell
Blind as a Bat
Dry as a Bone
Red as a Beet
Mad as a Hatter
Anticholinergics and anaesthesia:

There are drugs similar to atropine e.g 1.hyocine (scopolamine): has
sedative effect, the old are often confused by hyocine and so it is avoided in
their anaesthetics pre-medications.
2.Glycopyrrolate: produces less tachycardia, pyrexia and blurred vision than
atropine.
Stress response and anaesthia:
Anaesthia may be considered as a tress pass over physiology and it causes
stress response that has been well documented by the measurement of
many markers of stress
E.g caticholamines, cortisol, growth hormones, prostaglandins.
Causes of elaboration of this substances include e.g endtracheal intubation,
pain, anxiety hypotension hypothermia anaemia.
Can be blunted by increasing the depth of anaesthesia, but one can wonder
whether the stress response is one of the defencer mechanisms in the body
specially in children ???
138 | P a g e
ADVANCED LIFE SUPPORT

The ALS Algorithm For
The Management Of
Cardiac Arrest In Adults
CARDIAC ARREST
BLS Algorithm
If appropriate
Give Oxygen
If available
Attach Defibrillator / Monitor
Assess Rhythm
+/- Check Pulse
shockable
VF / VT
non shockable
Non VF / VT
Defibrillate as necessary
as necessary
CPR (1 min.)
5 Cycles CPR
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During CPR:
If not already:
Check electrode / paddle positions & contact

Attempt / verify: ETT; IV access
Give adrenaline every 3 min
Correct reversible causes
Consider : buffers, antiarrhythmics, atropine / pacing
Potentially Reversible Causes

Hypoxia
Hypovolaemia
Hyper/hypokalaemia& metabolic disorders
Hypoglycemia
Hydrogen Ion (acidosis)
Hypothermia
Tension Pneumothorax
Tamponade
Toxic/therapeutic disturbances
Thromboembolic/mechanical obstruction
Trauma
VF / Pulseless Ventricular Tachycardia
DC shock 360J/200J (1)
Give 5 Cycles of CPR
Check Rhythm
DC shock 360J/200J
(2)
Give 5 Cycles of CPR

Check Rhythm
DC shock 360J/200J
(3)
140 | P a g e
If not already:
intubate & IV access
Adrenaline 1mg or vasopressin

40u IV or 2-3mg ET
5 CPR sequences of 30:2
Check Rhythm
NOTE:
Interval between shocks should not be more than 2min.

Adrenaline given during the loop approximately every 2-3 minutes
Continue CPR for as long as defibrillation is indicated
Consider antiarrhythmic drugs during CPR
alkalizing agent: NaHCO3 50ml IV every 10min
antiarrhythmic agent e.g.
Amidarone 5mg/kg (300mg)
Lignocaine 1mg/kg IV every 5min or
Magnesium Sulphate 8 mmole/kg (1-2gm)
Asystole/PEA
CPR 5 cycles
Give Adrenaline 1mg
or
Vasopressin 40u
Consider Atropine 1mg up to 3 doses
CPR for 5 Cycles
141 | P a g e
If not already:
intubate & IV access
Check Rhythm
Shockable or not
Electrical Activity Evident?

yes
Shockable or not
no
Push Hard and Fast (100/min)

Ensure Full Chest Recoil
1 cycle of CPR 30:2
After ETT placement, RR = 10breath/min
Rotate Compressors Every 2mins
with Rhythm Checks
Think of & if indicated,
give specific treatment for :
Hypovolaemia
Tension Pneumothorax
Cardiac Tamponade
Pulmonary Embolism
Drug Overdose/Intoxication
Hypothermia
Electrolyte Imbalance
142 | P a g e
Paediatric advanced life support
BLS Algorithm
Oxygenate
Ventilate
Attach Defibrillator/Monitor
Assess Rhythm
+/- Check Pulse
VF/VT
Non VF/VT
Asystole,Pulseless Electrical Activity
Defibrillate
As necessary
Adrenaline
CPR
CPR
1 min
1 min
143 | P a g e

During CPR
Attempt/verify : tracheal intubation & vascular access
Check: electrode/paddle position & contact
Give: adrenaline every 3 min.
Correct acidosis: consider NaHCO3
Correct reversible causes:
hypoxia , hypovolaemia, hypothermia, hypo/hyperkalaemia,tension

pneumothorax, tamponade, toxic/therapeutic disturbances,
thromboemboli.
Management of life-threatening arrhythmias in infants and

children:
Unconscious, apnoeic,
VF / VT
pulseless Basic life support
intubate, ventilate with 100% O2
display ECG
get access to circulation:IV, IO, ETT
Asystole / severe HR
EMD
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Doses of Drugs Used in CPR in Neonates
Adrenaline 1:10,000
Atropine
Bicarbonate 8.4%
Calcium chloride
Lignocaine
Initial DC defibrillation
0.1ml/kg
0.02mg/kg
1ml/kg
0.2 mmol/kg
1mg/kg
2J/kg up to 4J/kg
POST CARDIAC ARREST CARE

Patients need a high dependency unit : ICU or CCU
147 | P a g e
Cause of Death:
Mainly shock with low cardiac output, tachycardia & intense
vasoconstriction leading to poor tissue perfusionThe use of
inotropes may be beneficial.
Monitoring of:
Fluids by urinary catheterization
Electrolyte balance: especially serum potassium level since high levels
increase myocardial irritability and precipitate arrhythmias
Measures to be considered:
Cerebral Hypoxia;
Respiratory arrhythmias like Chyene Stokes breathing imply brain
stem damagesuch cases need artificial ventilation for 2 days
Psychological dreams
like dreams of violent death may follow
Post cardiac arrest care remains an area of active research to improve

patient recovery
Controlled hypothermia has been proposed to improve neurological

outcome..No adverse haemodynamic effects were reported
Quick restoration of an efficient cardiac function has been postulated to

improve outcome
Treatment of an existing underlying coronary disease that limits cardiac

function is also useful
148 | P a g e

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Anesthesia handout

Academic secretary 9awa3i8 2014/15

Prepared by: Tayba M. Ahmed & Esra Abdallah

1-Introduction to anaesthesia & intensive care

2-Body fluids & electrolytes

3-Basic life support

6-Conduct of general anaesthesia

10-Management of critically ill patient

15-Neuraxial anaesthesia (spinal anaesthesia)

18-drugs that affects autonomic nervous system

19-Advanced life support

Introduction to anaesthia and intensive care

Anesthetic Drugs (IV, Inh).

Types of patients presents:

Critically ill patients (e.g. Cardiac , respiratory , sever vital

Academic secretary 9awa3i8 2014/15

Intracellular fluid (ICF)-Inside cells

Extracellular (ECF)-Outside cells

ICF and ECF are separated by the cell membrane.

Body Fluid Volumes (The 60: 40: 20 Rule):

Total Body Water (TBW)= 60% Body weight (Kg)

ICF= 40% Body weight

ECF= 20% Body weight

Plasma Volume= 5% Body weight

Composition of Body Fluids

Two times the volume of extra cellular fluid

Potassium (K+) is the major cation

Immobile proteins and phosphates are the major anions

Academic secretary 9awa3i8 2014/15

Composition differs slightly in different tissues to enhance function

The cell membrane is selectively permeable to ions but freely

One-half the size of Intracellular Fluid

Sodium (Na+) is the major cation

Chloride (Cl-) is the major anion

The capillary endothelium is freely permeable to water, ions and

Interstitial fluid:- between cells (largest)

Plasma fluid:- in the vascular space

Transcellular fluid:-highly specialized

Interstitial versus Plasma Fluid:

Plasma contains about 5% protein

Albumen is the most abundant protein

Cerebrospinal-Ventricles, spinal canal-outside the brain and spinal

Intraocular-inside chambers of the eye

Pleural-between the lung and chest wall

Synovial-in the joints

Peritoneal-between the abdominal wall and the abdominal organs

Digestive secretions-inside GI tract

Pathophysiology of Transcellular Fluid:

Synovial-pain and restricted movement

GI secretions-ECF volume depletion, abnormal pH (acid-base

Capillaries allow free movement of ECF fluid (ions and water).

Hydrostatic pressure (Hp) tries to push fluid out of the capillary

The net fluid movement is determined by the balance of Hp and COP

Normally no net fluid movement (exceptions are GI and renal

Body fluid compartments are in osmotic equilibrium

Water moves freely- driven by the osmotic gradient

Ratio of solute/volume = Osmolality

Normal value = 290 +/- 10 mOsm/liter

Osm of ICF = ECF = Plasma

Plasma Osm is 1 mOsm/l > interstitial fluid volume due to COP

Water moves freely- driven by osmotic gradient

Energy is needed to move Ions /molecules against electrical