Hemodynamic Case Studies

Edward G. Hamaty Jr., D.O. FACCP, FACOI

Pattern Recognition

Fluid Replacement Therapy-Goals

Fluid Therapy Protocol

Fluid Challenge Guideline Chart

Depressed Myocardium and Wedge

Pressure-Volume Compliance Relationship

PCWP and SV
Changes in preload are important primarily if they
affect stroke volume.
The next graphic illustrates the importance of
noting the PCWP in conjunction with the SV.
Notice that on the right side of the table no
optimal PCWP appears to exist.
The lack of determining an optimal wedge
pressure is more the rule than the exception.
Be very cautious in using the PCWP as the
primary guide to treating hemodynamics.
PCWP values are only useful when used in
conjunction with other hemodynamic information.
To use the PCWP as the primary indicator for
therapies runs the risk of employing unnecessary
or inappropriate therapies.

PCWP and SV

PCWP on EVLW

PCWP on EVLW

Practice Clinical Senarios

Simple and typical clinical senarios
for pattern analysis.

Practice Exercise 1

Practice Exercise 1 Answer

Practice Exercise 2

Practice Exercise 2 Answer

Practice Exercise 3

Practice Exercise 3 Answer

Practice Exercise 4

Practice Exercise 4 Answer

Practice Exercise 5

Practice Exercise 5 Answer

Practice Exercise 6

Practice Exercise 6 Answer

Practice Exercise 7

Practice Exercise 7 Answer

Practice Exercise 8

Practice Exercise 8 Answer

Practice Exercise 9

Practice Exercise 9 Answer

Practice Exercise 10

Practice Exercise 10 Answer

Practice Exercise 11

Practice Exercise 11 Answer

Total Peripheral Resistance

Current Treatment of Shock - General

The main determinants of tissue perfusion
are cardiac output and mean arterial
pressure. Although it has its limitations,
especially in certain distributive types of
shock, the MAP is a simple measure to
roughly determine the adequacy of tissue
perfusion.
MAP CVP is dependent on CO and SVR:
MAP-CVP = CO x SVR
MAP = (CO x SVR) + CVP [CO = SV x HR]
MAP = SV x HR x SVR + CVP [SV = EDV-ESV]

This brings us back to one of our initial

diagrams:

Determinants of Cardiac Output

[MAP = CO x SVR + CVP]

RVEDV
RAP, CVP

Complianc
PAD, PAWP e

SVR (LV)
PVR (RV)

SVI,
LVSWI,
RVSWI

Case 1 Pneumonia vs CHF

PATIENT 1: PNEUMONIA VERSUS

CONGESTIVE HEART FAILURE./Chaim Putterman, Charles L.
Sprung
A 22 year old woman with systemic lupus erythematosus (SLE) was
hospitalized in her 21st week of pregnancy for evaluation of anemia,
proteinuria and peripheral edema. She was diagnosed as suffering from
SLE two years previously based upon fever, lymphadenopathy,
arthalgia, pancytopenia, and a characteristic malar rash, accompanied
by a positive anti-nuclear factor and high levels of anti-DNA antibody.
An exacerbation of her disease one year previously responded to a
course of intravenous hydrocortisone, and she was recently reasonably
well controlled with a daily dose of 15 mg of prednisone.
During the first trimester of her pregnancy, she developed fever and
decreasing hemoglobin from 11 to 9 gr/dl. She was hospitalized in the
high risk obstetric ward for in-hospital evaluation. Despite an increase in
the daily dose of prednisone to 20 mg and subsequently to 60 mg. the
hemoglobin decreased to 6.9 gr/dl, the direct Coombs test was positive
and the lactic dehydrogenase increased. In addition, hyperkalemla.
hypoalbuminemia, severe proteinuria and a de-crease in creatinine
clearance developed, and she was transferred to the Internal Medicine
ward.

Case 1 Pneumonia vs CHF

On examination, the blood pressure was 105/70 mmHg, pulse

76 beats/min, respirations 20 breaths/min with slight dyspnea,
and normal temperature. The only notable physical findings
were slight pallor of the skin and conjuctivae, mild peripheral
edema, and a II/VI systolic non-radiating flow murmur heard at
the left sternal border.
Laboratory examinations: white blood count 3,200/cu mm with
66% neutrophils, hematocrit 21%, and platelets 115,000/cu mm.
Coagulation studies were normal. Abnormalities in the
biochemical profile included 'total protein 5.0 gr/dl. albumin 2.7
gr/dl, urea 34 mg/dl and creatinine 1.3 mg/dl. C4 was 14 mg%
(normal 20-50). C3 16 mg% (normal 50-120). anti-cardiolipin
was negative, anti-SS-A negative, anti-nuclear factor positive
+4/+4, anti-DNA 15.2 microgr/ml (normal 0-1.5), and anti-Sm
positive. Urinary albumin was 2.0 gr/dl, with a daily urinary
output of 800 to 1000 cc, and a creatinine clearance of 88
cc/min. The chest X-ray was normal and the electrocardiogram
showed sinus tachycardia. Obstetrical ultrasound showed a
viable infant appropriate for gestational age. with no obvious
anatomical abnormalities.

Case 1 Pneumonia vs CHF

A diagnosis of pregnancy-induced exacerbation of SLE was

made, based upon the hemolytic anemia, leukopenia,
thrombocytopenia and nephrotic syndrome, accompanied by
impressive laboratory evidence of disease activity. Intravenous
high dose hydrocortisone was begun, together with
azathioprine. Fluid therapy included diuretics and intravenous
albumin. Over the next month, the patient's nephrologic status
gradually stabilized with a decrease in urinary albumin
excretion, and serum urea and creatinine. After two months of
hospitalization, the patient began to complain of dyspnea, and
the temperature rose to 40.5C.

On examination, the patient was in moderate to severe

respiratory distress. Blood pressure was 160/90 mmHg, pulse
regular at 140 beats/min and respirations 50 breaths/min. The
jugular veins were not distended and anasarca was present. On
auscultation of the lungs, diffuse coarse crepitations were heard
throughout inspiration and expiration. A summation gallop was
heard on auscultation of the heart. The abdomen was soft, and
the uterine fundus was palpated at the level of the umbilicus.
Peripheral pulses were normal and Homan's sign was negative.

Case 1 Pneumonia vs CHF

The chest X-ray revealed borderline cardiomegaly, with signs of

diffuse bilateral infiltrates (Figure 12.1).
On room air, an arterial blood gas analysis showed pH 7.46, pO2 59 mmHg with
a saturation of 92%. and pCO2 28 mmHg. The patient was transferred to the
ICU.
Despite high concentrations of oxygen by mask and nasal
prongs, arterial blood gases improved only slightly. Due to the hypox
emia, tachypnea, and need for diagnostic bronchoscopy, the patient
was incubated and mechanical ventilation was instituted.
Because of the inability to determine by clinical means whether the diffuse
bilateral pulmonary infiltrates were secondary to congestive heartfailure (from
lupus myocarditis, toxemia of pregnancy, peripartum cardiomyopathy), volume
overload (due to glucocorticoid therapy or low serum protein and colloid osmotic
pressure), or progressive pneumonia in an immunocompromised host, a
pulmonary artery catheter (PAC) was inserted.
The central venous pressure (CVP) was 6 mmHg. pulmonary artery
pressure 20/12 mmHg. pulmonary artery occlusion pressure (PAOP) 8
mmHg, cardiac output 12.5 liter/ min, and cardiac index 7.2 liter/min/m2.
Bronchoscopy was performed at the bedside, but was negative for bacterial,
viral, fungal or parasitic organisms. A precise microbiological diagnosis was
deemed essential in this immunocompromised host, and an open lung biopsy
was performed.

Case 1 Pneumonia vs CHF

Figure 12.1. Chest roentgenogram demonstrating borderline cardiomegaly

and diffuse bilateral infiltrates. Pulmonary artery catheterization was
performed to differentiate between pneumonia and congestive heart
failure as an etiology.

Case 1 Pneumonia vs CHF

Discussion
Catheterization of the pulmonary artery at the bedside with the
balloon-tipped PAC is frequently indispensable for an accurate
differentiation between cardiac and pulmonary etiologies of
respiratory distress and diffuse bilateral pulmonary infiltrates.
Heart failure and pulmonary edema are common situations in
every-day practice. Most clinicians are confident in their
diagnostic ability to accurately identify and reasonably quantify
the presence of heart failure. Suprisingly, it has been
demonstrated that non-invasive techniques are clearly
inadequate for predicting cardiovascular function in the critically
ill, and for correctly differentiating between cardiac and noncardiac pulmonary edema.
Bayliss et al (1) prospectively studied 55 patients in a cardiac
care unit to determine the accuracy of clinical evaluation,
relative to "hard" data obtained from invasive hemodynamic
monitoring. Physicians correctly predicted cardiac output in
71%, the PAOP in 62%, and the overall hemodynamic status
only in 55%. Fein et al (2) examined the ability of physicians to
differentiate cardiac from non-cardiac (permeability) edema on
the basis of clinical and radiographic criteria in 70 patients
admitted to the ICU with pulmonary edema.

Case 1 Pneumonia vs CHF

Clinical assessment of permeability pulmonary edema was correct in 17

of 20 patients (85%). However, of the 50 patients initially suspected of
having a cardiogenic cause for the edema, only 31 patients were
correctly classified (62%). Even in patients with known chronic heart
failure, Stevenson and Perloff)recently documented limited reliability of
physical signs for estimating hemodynarnics. Rales, edema and
elevated mean jugular venous pressure were absent in 18 of 43
patients with PAOP pressures equal or greater than 22 mmHg.
Stevenson and Perloff (3) concluded that reliance on physical signs
alone for the diagnosis of elevated ventricular filling pressure may result
in inadequate therapy.
The occurrence of pulmonary disease with diffuse bilateral in-filtrates is
a recognized and ominous manifestation of SLE. The differential
diagnosis is wide, and includes pulmonary hemorrhage, lupus
pneumonitis, uremia, drug reactions and congestive heart failure (4).
Heart failure in patients with SLE can also be multifactorial. Many
different mechanisms of heart involvement in SLE have been
recognized and have recently been summarized by Doherty and Siegel
(5). Lupus cardiomyopathy (6), valvular heart disease (7), premature
coronary artery disase (8) and myocarditis (9) can all lead to a
decrease in myocardial function and produce the clinical syndrome of
congestive heart failure.

Case 1 Pneumonia vs CHF

Recently, yet another cause of respiratory failure has been identified in

patients with severe SLE, particularly those treated with high doses of
corticosteroids. Andonopolous (10) found that 7 of 46 patients with SLE,
all female, died with a clinical, radiological, physiological and
pathological picture compatible with ARDS. In fact, the entire mortality
of the patient population was represented by the prevalence of ARDS.
In most patients with SLE and ARDS, infection was documented as the
probable link between these syndromes. However, ARDS also
appeared primarily in patients with SLE in whom no infectious process
could be identified (10-12).
What parameters derived from the PAC can assist in the differentiation
between a cardiac and pulmonary etiology of lung in-filtrates? The
patient with congestive heart failure typically has a decreased cardiac
output and an increased CVP and PAOP, whereas the patient with a
pulmonary disorder has a normal or increased cardiac output, normal or
low PAOP, and a CVP that may be elevated.
Another helpful parameter derived from the PAC is the gradient
between the pulmonary artery diastolic pressure and the PAOP. This
gradient is usually normal in patients with cardiac disorders, but may
increase in primary pulmonary disorders. Rahimtoola et al (13)
examined the relationship of the pulmonary artery diastolic pressure
(PADP) to left ventricular diastolic pressures in patients with acute
myocardial infarction.

Case 1 Pneumonia vs CHF

In patients without significantly increased pulmonary vascular resistance (PVR),

there were no significant differences between the PADP and mean PAOP. All
patients but one with a PADP > 15 mmHg had a PAOP > 12 mmHg and all but
one patient with a mean PAOP > 12 mmHg had a PADP > 15 mmHg.
However, with increased PVR, an average gradient of 6.7 mmHg existed
between the PADP and PAOP. Lappas et al (14) found good correlation between
left atrial pressure (LAP) and PAOP, and between LAP and PADP, in 161 paired
measurements in cardiac-surgical patients. Gabriel et al (15) investigated the
difference between PADP and the mean PAOP and its relationship to PVR in 24
patients with chronic lung disease. In patients with normal PVR, there was no
significant pressure difference either at rest or during exercise over a wide range
of PAOP values (6-27 mmHg), while in patients with increased PVR a significant
pressure difference was present.
A gradient of 4-5 mmHg allowed for differentiation between normal and
increased PVR. Several studies have shown that an in-creased gradient also
correlated with the presence of pulmonary hypertension, and may be predictive
of a higher mortality (16,17).
Sibbald et al (18) have summarized a practical approach to differentiate cardiac
from non-cardiac pulmonary edema in the critically ill. Definitive separation
between these two major types of edema necessitates demonstration of
increased microvascular permeability, which is characteristic of non-cardiogenic
pulmonary edema. However, this can be shown only by cumbersome radiotracer
techniques not generally available outside the research setting.
In most clinical situations, documentation of persistently increased extravascular
lung water [by direct measurement (or indirectly from the chest X-ray) and the
measurement of microvascular hydrostatic pressures with the PAC will allow
accurate diagnosis of the cause of the pulmonary edema.

Case 1 Pneumonia vs CHF

Traditionally, use of invasive hemodynamic monitoring has usually been

in the complicated, medical or surgical patient with multiorgan
dysfunction, either due to the current disease process or because of the
patient's premorbid health status. However, experience in recent years
supports an important role for the PAC for certain indications in
obstetrics and gynecology, particularly during complicated pregnancy.
Major hemodynamics adjustments occur in the pregnant woman, even
without cardiovascular disease. Important factors are increased uterine
blood flow, the placental circulation, and inferior vena cava obstruction.
Cardiac output increases by al-most 40% by the 28 to 32 week of
pregnancy, while vascular resistance tends to decrease. Further
changes in hemodynamic parameters during labor and delivery
increase the need for careful observation in the complicated obstetric
patient (19).
Several specific applications of the PAC in the critically ill obstetric
patient have been discussed in recent years (20-23). Pre-eclampsia
(toxemia) can be accompanied by significant hemodynamic changes
that can predispose to pulmonary edema. However, defining the exact
mechanism of the edema is essential for pro-per treatment.
Cardiogenic pulmonary edema may occur in this setting because of the
markedly increased systemic vascular resistance, leading to depressed
left ventricular function and congestive heart failure. The primary
therapy in this case would be aggressive afterload reduction and rigid
control of hypertension.

Case 1 Pneumonia vs CHF

On the other hand, pulmonary edema may also be caused by the decrease in
colloid osmotic pressure present in patients with severe eclampsia, or by an
increase in pulmonary capillary permeability.
Management in non-cardiogenic pulmonary edema consists of lowering the
PAOP (with fluid restriction and diuretics) to the lowest level compatible with
peripheral perfusion, while treating the responsible insult. The only reliable way
to distinguish between the cardiogenic and non-cardiogenic mechanisms of
edema in women with pre-eclampsia is by using the PAC.
Indeed, both aforementioned mechanisms may be operative, and defining their
relative contribution to the clinical situation is possible only by invasive
monitoring. Clark and Cotton (21) suggest that monitoring with the PAC in preeclamptic patients is also indicated in severe, unresponsive hypertension,
persistent oliguria unresponsive to fluid challenge, and for safe induction of
anesthesia in certain parturients.
Many indications for catheterization encountered in obstetric and gynecologic
patients are common to other areas of medicine, such as radical surgery, septic
shock, and acute myocardial infarction (22).
Unique indications include pre-eclampsia and rheumatic heart disease in
pregnancy. Although based on a retrospective summary, Clark et al (22)
advocate an important role for the PAC in the critically ill obstetric or
gynecological patient to ensure an optimal outcome-both for the mother and
fetus.

Case 1 Pneumonia vs CHF

Microvascular disorders involving the pulmonary arterial tree such as

amniotic fluid embolism, fat embolism and lymphangitic carcinomatosis are
often a diagnostic challenge to the clinician. The differential diagnosis of
respiratory failure and pulmonary infiltrates can be extensive, as it was in our
patient, and may necessitate invasive investigation. In some cases, however,
a diagnosis cannot be made until autopsy.
Masson and Ruggieri in 1985 (24) hypothesized that fetal squamous cells,
fat globules, and malignant cells would be recognizable in microvascular
blood obtained from the pulmonary circulation via the lumen of a PAC in the
wedged position. Wedged pulmonary blood was found to almost invariably
contain megakaryocytes and megakaryocytic nuclei, which are particulary
abundant in the pulmonary capillary bed, indicating the microvascular source
of the blood obtained. In preliminary studies (24,25), fetal squamous cells in
amniotic fluid embolism and fat globules in fat embolism were easily
identified by cytologic study, and provided important confirmatory di-agnostic
information.
This information is available without risk in those patients in whom a PAC is
already present for hemodynamic monitoring. Masson et al (26) recently
evaluated this technique of cytologic analysis of blood from wedged PAC in 8
patients in whom lymphangitic carcinomatosis was subsequently confirmed
by other means. Malignant cells were found in 7 of the 8 patients. Cytologic
findings were normal in 16/17 patients with cancer but without pulmonary
metastases, and in 22/23 patients with non-malignant pulmonary disorders.

Case 1 Pneumonia vs CHF

Masson et al concluded that pulmonary microvascular cytology may be

especially valuable for the diagnosis of some patients with obscure
respiratory failure, when lung biopsy is refused or too dangerous, or
when a PAC is otherwise present for other purposes.
Although prognosis of cancer patients with such extensive spread is
generally dismal, a positive pulmonary microvascular cytology result
may allow for better planning of the subsequent management.
The present patient, based upon the above discussion, had several
indications for the insertion of the PAC upon the precipitous
deterioration in her respiratory status. The etiology of the diffuse
pulmonary infiltrates was unclear, and it was thought that further
diagnostic delay would only be to the patient's detriment.
The various-contributions of pregnancy, SLE, or complications of
therapy could not be determined, and the primary question of whether
the infiltrates resulted from a "cardiac" or "pulmonary" etiology could not
be resolved.
As can be seen from the initial hemodynamic data of a low PAOP, high
cardiac index, and low SVR, no cardiac dysfunction was presentwhether due to pregnancy or systemic vasculitis. The cardiac output
was appropriate for the metabolic demands of the mother and fetus.
The main diagnostic considerations at this stage became lupus
pneumonitis, an infectious pneumonia due to the immunosuppression,
or ARDS.

Case 1 Pneumonia vs CHF

Routine microbiology and bronchoalveolar lavage
failed to provide a definite pathogen and a diagnostic
open lung biopsy was performed. On histological
examination, severe interstitial inflammation was
present. In the alveolar spaces, an amorphic, necrotic
infiltrate was the dominant finding, in which small
corpuscles could be seen.
On silver staining, the diagnosis of Pneumocystis
carinii pneumonia was confirmed. High dose
cotrimoxazole therapy was initiated.
Two weeks later, there was spontaneous rupture of the
amniotic membranes, and the patient gave birth to a
900 gram, healthy female infant. After a pro-longed and
stormy hospital course, the patient slowly improved,
was weaned from mechanical ventilation, was
discharged from the ICU and finally sent home.

Pulmonary Disease-Acute Respiratory Distress

Case 2 Complicated MI

ATIENT 2: COMPLICATED MYOCARDIAL INFARCTION/John M.

Phelan, Joseph E. Parrillo

A 54 year old man with a history of non-insulin dependent diabetes and

hypercholesterolemia presented to the emergency room with 1 hour of
left arm discomfort with associated dyspnea, nausea and diaphoresis.
He also noted palpitations and lightheadedness. On arrival to the ER he
was given oxygen by nasal cannula and attached to a cardiac monitor.
His medications included micronase and mevacor.

Physical examination was remarkable for: marked diaphoresis with a

blood pressure of 105/60 mmHg, an irregular pulse of 115 beats/min,
and a respiratory rate of 22 breaths/min. Lung exam revealed few
bibasilar rales. Examination of the heart showed a focal non-displaced
PMI with normal S, and S2 and an S4 gallop. The abdomen was benign
and extremity exam unremarkable.

Laboratory analysis revealed: hemoglobin 13 gm/dl, white blood count

10,000 /cu mm, hematocrit 39%, ABG (on 2L 02) pH 7.46, P02 86
mmHg, PCO2 34 mmHg, BUN 17 mg/dl, creatinine 0.9 mg/dl, and CPK
200. The chest x-ray showed no evidence of congestive heart failure or
cardiomegaly. The electrocardiogram revealed 8 mm of ST elevation in
leads V2 thru V6 and in AVL and I. (see EKG, Figure 12.2).

Case 2 Complicated MI

Case 2 Complicated MI

Hospital Course
Sublingual nitroglycerin was administered without relief, and eventually
morphine sulfate was given to relieve his symptoms. Thrombolytic therapy was
initiated with intravenous t-PA and heparin was begun with a 5000 unit bolus and
1000 u/hr continuous drip. Aspirin 160 mg P.O. was given. Because of frequent
episodes of non-sustained ventricular tachycardia. lidocaine therapy was
initiated. He had a persistent tachycardia to 115-120 beats/min, and metoprolol 5
mg IV was administered three times.

Over the next three hours his symptoms were not ameliorated. In addition his
blood pressure fell to 75/40 mmHg with a pulse of 100 beats/min. Dopamine
therapy was initiated and the patient was transferred to the cardiac
catheterization laboratory where a pulmonary artery catheter was inserted and
showed the hemodynamic Pro-file 12.1, #1.

With these results an intraaortic balloon pump was inserted and a dobutamine
drip was started (see 12.1, #2). Coronary angiography was quickly performed
and revealed a 100% occlusion of the proximal left anterior descending artery.

On the basis of this man's hemodynamic profile and coronary anatomy the
decision was made to proceed with salvage angioplasty. This was successfully
performed and the patient was returned to the CCU where follow-up
hemodynamic monitoring was employed so that the PAOP and cardiac output
were optimized until inotropic support could be weaned after 2 days (Profile
12.1, #3).

Case 2 Complicated MI

Case 2 Complicated MI

Discussion
This patient's clinical course demonstrates the reduced mortality (27) associated
with cardiogenic shock and reflects our belief that incipient cardiogenic shock
following acute myocardial infarction (AMI) should be approached with
aggressive early efforts at revascularization. Prior efforts (28) to classify patient
outcomes based on bedside clinical examination demonstrated a high clinical
mortality as shown in the Killip classification (Table 12.1).

Of note, the incidence of cardiogenic shock in the 1970's was 10% to 20% and
the mortality remained high probably because pharmacotherapy alone was only
supportive.
As noted in Table 12.2, Forrester, et al (29) have correlated the clinical findings
with hemodynamic data from pulmonary artery catheterization. While these
hemodynamic subsets closely follow physical exam, there is enough disparity in
about 20-30% of patients to mandate the use of a pulmonary artery catheter
(PAC). In fact pulmonary catheterization is needed to optimize fluid and
pharmacologic therapy.

Crexell et al (30) have shown that when a PAOP is less than 14 in the face of LV
systolic impairment, patients derive great benefit from volume loading. In this
study optimal filling pressures of 14 to 18 mmHg resulted in significant
improvements in cardiac out-put and mean arterial pressure. This occurs as the
result of reduced left ventricular compliance produced by ischemia. Even higher
pressures may be tolerated so long as respiratory compromise is avoided.
Usually, filling pressures beyond this level result in further deterioration of
cardiac performance.

Case 2 Complicated MI

Case 2 Complicated MI

An intelligent use of the PAC in cardiogenic shock requires a

solid understanding of the underlying pathogenesis of this form
of shock (Figure 12.3).
When total myocardial necrosis exceeds 40% of left ventricular
myocardial mass, cardiogenic shock ensues. This may occur as
the result of one large infarction, infarct extension or a small
infarct in the setting of prior damage. Right ventricular infarction
may also be associated with cardiogenic shock, and mechanical
complications of MI should be excluded in every patient who
develops cardiogenic shock. Thus, the physician should always
look for the presence of an acute ventricular septal defect,
ruptured (or dysfunctional) papillary muscle, or free wall rupture.
When inserting a PAC in the setting of cardiogenic shock, blood
should be sampled for percent saturation in the right atrium,
right ventricle and pulmonary artery.
Generally an oxygen saturation step-up of 5% or greater
suggests left to right shunting characteristic of a VSD. A large v
wave (10 mmHg or greater above the PAOP) suggests mitral
regurgitation. Since other entities may yield similar findings, the
presence of mitral regurgitation should be confirmed with
echocardiography or left ventriculography.

Case 2 Complicated MI

Case 2 Complicated MI

In the era of thrombolytic therapy, the incidence of cardiogenic shock has

fallen dramatically to about 5%. This reduction has probably resulted from
emphasis on the urgent need to re-establish myocardial blood flow to
salvage myocardium and pre-vent further pump failure. This must be
accomplished early, prior to the development of end organ manifestations
of pump failure (i.e. acute renal failure, shock liver).
As noted above, supportive therapy alone (i.e. inotropic, vasopressors,
vasodilators, diuretics) has little impact on survival in cardiogenic shock.
Use of the intraaortic balloon has improved mortality in patients with
cardiogenic shock insofar as it enables stabilization of the patient prior to
more invasive therapeutic modalities aimed at restoration of coronary
blood flow. However, if the balloon pump is utilized for support without
revascularization, prognosis remains poor (31).
As DeWood et al (32) demonstrated, patients with cardiogenic shock after
myocardial infarction have improved survival with surgical
revascularization. In the study, two groups of post MI patients with
cardiogenic shock were stratified. Those who received intraaortic balloon
pumping with pharmacologic therapy had a long-term mortality of 71%.
By contrast, those who received early surgical revascularization in
combination with an intraaortic balloon pump had a much lower mortality.
While these data show a significant survival advantage with this approach
to cardiogenic shock, not all hospitals are able to provide surgical
resources in such a timely fashion.

Case 2 Complicated MI
While thrombolytic therapy may have reduced the incidence of
cardiogenic shock, large clinical trials such as the GISSI (33)
trial have not demonstrated a reduction in mortality when
thrombolytic therapy is given to patients in cardiogenic shock
with an AMI.
Percutaneous transluminal coronary angioplasty has been
reported to improve survival in AMI complicated by cardiogenic
shock. This approach has the advantage that it is faster and less
invasive than surgery. In addition the rate of reperfusion is
greater with direct PTCA compared to thrombolytic therapy and
there is a lower rate of residual stenosis.
In a retrospective trial, Lee et al (34) showed an impressive
survivor benefit (50% vs 17%) in those patients undergoing
emergent PTCA for cardiogenic shock compared with those who
were managed with conventional therapy. This trial was
performed retrospectively and the controls were not completely
comparable to the angioplasty group; however, it represents the
best data presently available.
Therefore, our approach is to stabilize patients with cardiogenic
shock with pharmacological support and the intraaortic balloon
pump and then proceed directly to the catheterization laboratory.

Case 2 Complicated MI

Pharmacotherapy in cardiogenic shock is important in order to stabilize patients prior to

definitive coronary flow restoration. Clearly, in this clinical situation the goal is to optimize
myocardial oxygen supply and minimize oxygen consumption. In patients who have isolated
pulmonary congestion, therapy consists mainly of diuretics and anti-ischemic agents. This
group of patients does not require emergent intervention except when post infarction angina
occurs. Recent data prove the mortality benefit of ACE inhibitors in patients with chronic
heart failure (35), and other information (36) suggests that treatment with captopril following
myocardial infarction leads to lower left ventricular filling pressure and a smaller enddiastolic volume at one-year follow-up. In addition, exercise capacity appears to be
improved. Whether these latter two effects will translate into improved longevity re-mains to
be seen.
In patients who have peripheral hypoperfusion without pulmonary congestion (Forrester
Class III) an effort is made to find the optimal combination of PAOP and cardiac output (i.e.
a clinical application of Starling's law). As previously noted this usually occurs at a PAOP
between 14-18 mmHg. Beyond this range, further volume loading, usually precipitates
hemodynamic and respiratory decompensation. If the patient remains hypotensive in spite
of volume loading, inotropic therapy with agents such as dobutamine and dopamine are
indicated. Pressor and inotropic support have multiple effects on myocardial oxygen supply
and demand. Oxygen demand is increased by virtue of enhanced con-tractility and heart
rate, whereas the increase in aortic diastolic pressure leads to improved oxygen supply.
The net effect is to cause increase oxygen demand and this may precipitate further
episodes of ischemia.
In some circumstances, patients will respond nicely to inotropic support with dobutamine
and with reasonable systolic blood pressure (> 100 mmHg) afterload reduction with sodium
nitroprusside may be initiated thereby enhancing peripheral perfusion. For most Class III
patients who require pressor support, the prognosis remains poor and the clinical strategy
should revolve around early definitive revascularization of jeopardized but viable
myocardium. This point is particularly obvious when one remembers the survival benefit
from pharmacotherapy alone remains negligible.

Case 2 Complicated MI

In the patient example above incipient cardiogenic shock was

identified when insertion of the PAC revealed a cardiac index of
1.8 L/min/m2 with a PAOP of 18 mmHg, a mean artertial
pressure of 65 mmHg and a low mixed venous saturation of
0.51.
Dobutamine therapy was selected for this patient because of its
selective, almost purely inotropic properties. By contrast
dopamine, which also may be used, usually produces a
significant chronotropic effect which may be deleterious to the
balance between myocardial oxygen demand and supply. As
shown in this case example our patient responded well to
dobutamine and insertion of the intra-aortic balloon pump. This
was manifested by the increase in cardiac index to 2.4
L/min/m2, the fall in PAOP to 14 mmHg, the improvement of
mean arterial pressure to 75 mmHg and the increase in mixed
venous saturation to 0.66.
During his hospital course his CPK/MB peaked at 4800 IU with
20% MB. While there is no perfect correlation, CPK elevations
of this magnitude usually signify extensive myocardial necrosis
and a potentially fatal outcome from pump failure.

Cardiac Disease Acute MI

Cardiac Disease Acute MI

Cardiac Disease Acute MI

Case 3 Ruptured Ventricular Septum

PATIENT 3: RUPTURED VENTRICULAR SEPTUM / John M. Phelan, Joseph

E. Parrillo

A 54 year old woman with hypertension and non-insulin dependent diabetes

presented to the emergency room with chest pain. She de-scribed substernal
heaviness radiating to her back and left shoulder beginning four hours earlier
with associated nausea and diaphoresis. The ECG revealed 3 mm ST segment
elevation in V2 through V4 with ST depression in leads II, III, and AVE
Examination revealed a pulse of 110 beats/min with a BP of 150/90 mmHg.
There were no bruits and the neck veins were not distended. The lungs were
clear. Cardiac exam revealed normal S, and S2 with a prominent S4. No
murmurs were heard. The distal pulses were intact and the remain-der of the
exam was normal. The chest x-ray was normal. Therapy was initiated with
chewable aspirin, intravenous metoprolol, nitro-glycerin, heparin and t-PA. The
CPK peaked at 3564 with 14% MB.
During the first 5 days the patient did remarkably well without evidence of heart
failure, hypotension, ventricular arrhythmia or further chest pain. On day 6 she
complained of dyspnea and weakness. Examination revealed a BP of 90/60
mmHg with a pulse of 95 beats/min. Rales were heard in the lower half of her
lung fields. Cardiac examination revealed a new third heart sound with a grade
IV murmur heard best along the lower left parasternal border. The chest x-ray
showed pulmonary vascular redistribution and the patient was transferred back
to the CCU.
A pulmonary artery catheter was inserted using the right internal jugular vein and
the following hemodynamic data were demonstrated:

Case 3 Ruptured Ventricular Septum

These data demonstrated the presence of a step-up in oxygen saturation

between the right atrium (60%) and right ventricle (82%) signifying a left to
right shunt from an acute rupture of the inter-ventricular septum.

Case 3 Ruptured Ventricular Septum

This calculation shows that pulmonary flow is 2.5 times
systemic flow. In this patient, the thermodilution cardiac
output yielded a CO of 5.5 L/min. Thus, the systemic
output is 2.2 L/min (5.5/2.5).
With these hemodynamic data, the patient was
managed with sodium nitroprusside and dobutamine.
Repeat hemodynamic and oximetry data several hours
after initiation of therapy were:

Case 3 Ruptured Ventricular Septum

These hemodynamic data reveal that following therapy with dobutamine

and sodium nitroprusside the new step-up from the right atrium (66%)
to right ventricle (74%) was smaller signifying diminution of the left to
right shunt.

This was confirmed by the shunt calculation (Qp/Qs) which shows the
Qp/Qs, 1.3:1.0 following therapy compared with the Qp /Qs of 2.5:1.0
prior to the initiation of therapy. Of note, the total cardiac output
increased from 5.5 L/min to 6.2 L/min with the effective systemic output
rising from 2.2 L/min to 4.1 L/min following therapy.

Thus the patient remained stable and was brought to the cardiac
catheterization lab the following morningwhere coronary angiography
revealed a 90% mid LAD obstruction, 70% proximal circumflex stenosis
and 60% stenosis of the distal right coronary artery. Left
ventriculography demonstrated severe anterolateral and apical
hypokinesis with an LVEF of 38%. The LAO projection of the
ventriculogram showed evidence of the interventricular septal defect.

The patient was taken to the operating room where the VSD was closed
with a dacron patch and 3 vessel coronary artery bypass was
performed. One year later she remains well, has returned to work as a
computer operator and is functionally class II (NYHA).

Case 3 Ruptured Ventricular Septum

Discussion
This case demonstrates many of the features found in the acute rupture of the
interventricular septum following myocardial infarction (37). This complication
occurs in approximately 2% of all patients with myocardial infarction and is more
common with anterior wall infarctions. When the VSD occurs in this setting, the
apical septum is more commonly involved. By contrast in the setting of an
inferior wall MI, rupture of the basal septum is more likely. Clinically one usually
finds a harsh holosystolic murmur along the lower left sternal border with an
associated thrill. The patient usually evolves biventricular failure over hours and
survival appears to be dependent in part on right ventricular performance. In
those patients who have sustained a right ventricular infarction (or have RV
failure) outcome is considerably reduced. Medical management clearly is
unacceptable because of a mortality that exceeds 90%. Prompt surgical
intervention reduces mortality to 50% and should not be delayed.
Analysis of the preceding case example demonstrates the valuable role of the
pulmonary artery catheter in yielding the correct diagnosis. The presence of a
significant step-up in oxygenation between the right atrium and right ventricle
established the diagnosis of VSD. The large "v" wave (23 mmHg above the
mean PAOP) also raised the possibility of acute mitral regurgitation. The
specificity and sensitivity of this finding have been shown to be suboptimal. One
report showed that large "v" waves were present in only 33% of patients with
mitral regurgitation (38). Conversely 18% of patients with large v waves do not
have mitral regurgitation. Other causes of prominent v waves are listed in Table
12.3. This patient's v wave clearly was not the result of mitral regurgitation as
only a trivial amount of regurgitant flow was seen on left ventriculography. The
likely explanation for the v wave in this example is the presence of an acute VSD
with a non-compliant left atrium.

Case 3 Ruptured Ventricular Septum

Table 12.3. Differential diagnosis of a large v
wave in the pulmonary artery occulsion
pressure tracing

.Mitral Regurgitation/Stenosis
Aortic Regurgitation
Aortic Stenosis
Multivalvular Disease
Cardiomyopathy (Dilated and Hypertrophic)
Ventricular Septa] Defect
Pulmonary Hypertension
Pericardial Constriction
ASD

Case 4 Cardiac Tamponade

PATIENT 4: CARDIAC TAMPONADE/John M. Phelan,

Joseph E. Parrillo
A 37 year old man had undergone coronary artery bypass
surgery 4 weeks earlier. He returned to see his physician with
complaints of lethargy and lightheadedness. His family had
noted that the patient was intermittently confused.

Physical examination revealed a BP of 85/55 mmHg with a

pulsus paradoxus of 20 mmHg. The pulse was 125 beats/min
and the temperature was 100.5F. There, was jugular venous
distension 8 cm above the clavicle at 45 degrees. The lungs
were clear except for diminished breath sounds at the left base
and cardiac examination revealed a normal S, and S2 without
murmurs. gallops or rubs. The remainder of the exam was
normal except for trace pretibial edema.

The ECG showed sinus tachycardia with non-specific T wave

abnormalities and the chest x-ray revealed marked
cardiomegaly with a small left pleural effusion.

Case 4 Cardiac Tamponade

The patient was admitted to the hospital through the emergency

room where efforts to raise his blood pressure with fluids were
unsuccessful; dopamine was begun. He developed tachypnea
and a room air arterial blood gas showed: pH 7.47, PO2 54
mmHg with a saturation of 87% and PC02 28 mmHg. Upon
transfer to the MICU, insertion of a pulmonary artery catheter
yielded the following information:
Site
Pressure
Right Atrium
22 (mean)
Right Ventricle
42/24
Pulmonary Artery
40/22
Pulmonary Artery
Occlusion Pressure 23 mmHg
Cl = 1.8 L/min/m2
Equalization of diastolic pressures was clearly demonstrated.
Therefore, an echocardiogram was obtained and revealed
evidence of a large pericardial effusion with diastolic collapse of
the right ventricle. The patient was immediately transferred to
the operating room where pericardial drainage was performed.
His blood pressure improved and pressor support was weaned.

Case 4 Cardiac Tamponade

Discussion
This case clearly points out the utility of pulmonary catheterization in arriving at the proper
diagnosis. On a clinical basis, the diagnosis of cardiac tamponade is difficult. The most
common physical finding is jugular venous distension. One may also observe tachypnea,
tachycardia and pulsus paradoxus in about 80% of patients.

Hemodynamic monitoring typically shows elevation and equalization of all diastolic

pressures. The right atrial pressure tracing demonstrates a characteristic prominent systolic
X descent with an absent Y descent. Right ventricular end diastolic pressure is elevated
and equal to the right atrial, pulmonary artery diastolic and mean wedge pressures. The dip
and plateau pattern characteristic of constrictive pericarditis is not seen. These findings are
explained by the fact that the intrapericardial pressure is elevated and equal to the diastolic
right atrial pressure so that the net transmural pressure is zero (Figure 12.4, panel A).

Thus, rapid diastolic emptying of the right atrium (corresponding to the Y descent) is
impeded. With compression of the cardiac cycle, the stroke volume falls prompting
increased adrenergic tone leading to tachycardia and increased ejection fraction to
maintain cardiac output. Systemic vascular resistance also in-creases in order to maintain
blood pressure. Initial treatment of cardiac tamponade includes volume expansion with
fluids and, if necessary, inotropic agents such as dobutamine. Rapid drainage should be
performed. With pericardiocentesis, right atrial and intrapericardial pressures begin to fall
(Figure 12.4, panel B) and when a sufficient amount is aspirated (panel C) all pressures return to normal with reappearance of the Y descent. In post-operative cardiac surgical
tamponade, pericardiocentesis should be employed only as a temporizing measure in order
to stabilize the patient prior to surgical intervention.

Pericardiocentesis may be used as definitive treatment in patients with a pericardial

effusion due to malignancy, collagen vascular disease, or an inflammatory pericarditis.

Restriction Summary Table

Constrictive
Pericarditis

Diastolic
Equilibration

Dip and
Plateau
Physiology

YES

YES

Restrictive
NO
Cardiomyopathy

YES

Cardiac
Tamponade

NO

YES

Case 4 Cardiac Tamponade

Finally, the diagnosis of pericardial tamponade is
frequently suggested by the echocardiogram.
By itself, this technique may provide compelling
evidence for emergency pericardial drainage in
hypotensive patients refractory to fluids or pressors.
However, we believe that in the majority of
circumstances the diagnosis of tamponade should be
established by a pulmonary artery catheter. These
critically ill patients frequently have co-existing
problems (e.g. LV dysfunction, sepsis) that may
obscure the response to pericardial drainage.
We believe that baseline hemodynamic variables
provide a crucial reference point for the management
of these patients in the critical care setting.

Case 5 Vasodilator Therapy

PATIENTS 5a AND 5b: VASODILATOR
THERAPY/ Charles M. Carpati, Mark E. Astiz,
Eric C. Rackow
Patient 5a:
A 71 year old man with a history of coronary artery
disease was admitted with an anterior wall
myocardial infarction. On exam ne was in moderate
distress, blood pressure 132/82 mmHg. pulse 116
beats/ min, and respirations 28 breaths/min.
Jugular venous distention was present at 45
degrees. Lung examination was remarkable for
rales to the apices. The PMI was in the 5th
intercostal space in the anterior axillary line. On
auscultation both an S3 and an S4 were present,
and a grade III/VI blowing holosystolic murmur
radiating to the axilla was heard. The liver span
was 13 cm, and there was +2 edema of the lower
extremities. On laboratory exam sodium was 132
meq/1, BUN was 31 mg/dl and creatinine was 1.0
mg/dl. The electrocardiogram revealed anterior
lead S-T elevations and the chest X-ray showed
cardiomegaly with pulmonary edema.
The patient was admitted to the coronary care unit
and a pulmonary artery catheter (PAC) was placed
for optimization of cardiac status. The initial
physiologic profile is seen in Profile 12.2. #1.
Profile 12.2, #2 shows a repeat hemodynamic
study taken after nitroprusside was titrated to
decrease the MAP approximately 10 mmHg.

Case 5 Vasodilator Therapy

Patient 5b:
A 42 year old man with a history of essential hypertension
and medical noncompliance was admitted to the hospital with
progressive shortness of breath, associated with headache
and blurred vision. On physical exam he was in severe
respiratory distress, blood pressure 244/178 mmHg, pulse 104
beats/min, and respirations 36 breaths/min. Fundoscopic
examination revealed papilledema. Jugular venous distention
was present to the angle of the jaw at 90 degrees. Lung
examination revealed rales at the bases. The PMI was present
in the 6th intercostal space in the midclavicular line and there
was an S3 gallop. Abdominal exam was remarkable for
paradoxical inspiratory movements. Lower extremities had +2
pitting edema.
An electrocardiogram showed sinus tachycardia with left
ventricular hypertrophy. A chest X-ray revealed a markedly
enlarged cardiac silhouette and an alveolar pattern consistent
with pulmonary edema. The hematocrit was 30.4%.
Electrolytes were normal. The BUN was 52 mg/dl and
creatinine 4.8 mg/dl. Urinalysis was remarkable for
hemoglobin without red cells. Arterial blood gas on 100% FIO2
showed: pH 7.30, P02 57 mmHg and PCO2 51 mmHg.
The patient was intubated and admitted to the intensive care
unit where a PAC was placed. The initial hemodynamic profile
is shown in Profile 12.3, #1.
He was started on intravenous nitroprusside, but proved
extremely sensitive to this drug as shown in Profile 12.3. #2.
Profile 12.3, #3 shows the patient's profile after fluid
resuscitation.

Case 5 Vasodilator Therapy

Discussion
The treatment of acute and chronic congestive heart failure (CHF) has
continued to evolve over the past 10 years, coincident with further
insight into the physiologic contributions of the endocrine and nervous
systems to the syndrome. In addition to a better understanding of the
benefits of digitalis and diuretics, vasodilator therapy has moved to the
forefront of the treatment of this disease.
Clinically, syndromes of heart failure are manifested to varying degrees
by poor exercise tolerance, dyspnea and edema, as well as signs such
as rales, gallops and elevated venous pressures. The hemodynamic
hallmarks of congestive heart failure include a low cardiac output state
induced by the inability of the ventricle to mount an adequate stroke
volume. The decrease in effective circulating blood volume triggers a
sympathetic release of catecholamines and activation of the reninangiotensinaldosterone axis, as well as release of antidiuretic hormone.
The catecholamines and angiotensin II are potent vasoconstrictors.
Although adaptive for the maintenance of blood pressure, this effect
results in an increased cardiac afterload and may worsen perfusion of
vascular beds, contributing to organ dysfunction. Aldosterone and
antidiuretic hormone release result in renal salt and water retention, an
effect which may be exacerbated by renal vasoconstriction. These
"maladaptive" responses perpetuate a vicious circle. Current therapy
rests on manipulating contractility, preload and afterload.

Case 5 Vasodilator Therapy

Although potent intravenous inotropes exist to increase contractility

(dobutamine, amrinone, dopamine), their use is limited by a lack of oral
analogues. Of the oral inotropes, only digoxin has proven to be of long-term
benefit (39). It has been suggested that digoxin is less efficacious than
vasodilator therapy in improving exercise tolerance (40). Vasodilators can act
preferentially on the venous bed, the arterial bed or can be balanced in activity
(Table 12.4). Agents acting to increase the capacitance of the venous bed may
be effective in heart failure by decreasing preload and wall tension. Arterial
vasodilation decreases afterload, i.e. the impedance to left ventricular ejection,
thereby increasing cardiac output and stroke volume. Vasodilator therapy may
result in hypotension and tachycardia either through excessive reduction in
venous return or preload, or through excessive decrease in arterial resistance.
Table 12.4. Mechanisms of action of vasodilators
VENODILATION
Diuretics
Nitrates (Low Dose)
ARTERIAL DILATION
Hydralazine Diazoxide
Minoxidil
Nifedipine
MIXED VENOUS AND ARTERIAL
ACE Inhibitors Nitroprusside Nitrates (High Dose)
Prazosin
Trimethaphan Phentolamine

Case 5 Vasodilator Therapy

Patients in acute heart failure manifest low cardiac outputs, high filling (wedge)
pressures, and high systemic vascular resistances. In the acute setting a
parenteral vasodilator with a short half-life that is easily titratable should be
utilized. This therapy should only be used in an intensive care setting with
continuous blood pressure monitoring. Nitroprusside toxicity usually consists of
reflex tachycardia or the toxicity of its breakdown product, thiocyanate. In
congestive heart failure with systolic dysfunction, filling pressures will be high
and vasodilation will result in decreased afterload and decreased end-diastolic
volume as manifested by a decrease in wedge pressure. Goals of therapy
should be the reduction of filling pressures and an increase in cardiac index
without a deleterious fall in blood pressure. This is seen in Patient 5a, Profile
12.2.
Note that in accelerated or malignant hypertension, filling pressures may actually
be low. Vasodilation may then result in precipitous hypotension which should be
treated by lowering the dose of vasodilator; blood pressure lability in this setting
may re-quire the infusion of fluid. This is shown in Patient 5b, Profile 12.3.
Treatment with nitroprusside resulted in a decrease in the filling pressures, an
increase in cardiac output and decrease in systemic resistance but the decrease
in blood pressure and after-load was too great and caused severe tachycardia. A
decrease in nitroprusside together with fluid therapy led to a more gradual
decrease in blood pressure and resistance, a greater cardiac out-put, stroke
volume index, stroke work, mixed venous oxygen saturation and oxygen delivery
and a lower arteriovenous oxygen content difference and oxygen utilization ratio.
As noted, dose optimization in hypertension is achieved by measuring cardiac
out-put, stroke volume or stroke work at sequentially titrated blood pressures;
other indices of perfusion, such as mixed venous oxygen tension and arterial
lactates, may also be followed. Conversion to oral therapy can then accompany
tapering of intravenous therapy.

Case 5 Vasodilator Therapy

Other intravenous agents, such as hydralazine (direct arteriolar dilator),

diazoxide (direct arteriolar dilator), trimethaphan (ganglionic blocker), and
phentolamine (alpha-blocker) are less ideal than nitroprusside in the acute
setting because of longer half-life, lack of titratability or expense. Intravenous
nitroglycerin may accomplish similar goals as nitroprusside; however, this agent
causes more venodilation at low doses.
At present, angiotensin converting enzyme (ACE) inhibitors or the combination
of isosorbide dinitrate with hydralzine are themost commonly used oral therapy
for vasodilation. Studies have demonstrated long-term benefit of these agents in
improving survival in chronic CHF (41,42). Both ACE inhibitors and
hydralazine/isosorbide dinitrate maintain a long-term increase in cardiac ejection
fraction. Captopril has been associated with an increase in long-term exercise
tolerance in patients with congestive heart failure (43).
Hydralazine/isosorbide dinitrate is associated with lowered norepinephrine levels
when compared to captopril in chronic CHF (44). ACE inhibitors may affect
renal and hepatic function adversely, as well as lower white blood cell counts.
Hydralazine is associated with reflex tachycardia and a lupus-like syndrome.
Other oral vasodilators, such as nifedipine (calcium channel blocker), although
possibly useful in the acute setting, have not been shown to improve mortality.
Both nifedipine and minoxidil (direct arteriolar dilator) have been associated with
no-table renal salt and water retention.
Although the short-term effects of prazosin (alpha-1 blocker) are similar to those
of the other vasodilators, the development of tachyphylaxis, possibly as a result
of alpha-1 receptor downregulation, mitigates against its long-term benefit (45).

Case 9 Septic Shock

PATIENT 9: SEPTIC SHOCK/Debora G. Geber, Charles L. Sprung

A 52 year old woman presented with chills, fever, disorientation, re-current
vomiting and oliguria, three days after an uneventful elective extracorporeal
shock wave lithotripsy. She had a previous history of nephrolithiasis, non-insulin
dependent diabetes mellitus and recurrent urinary tract infections.
The physical examination revealed a prostrated patient with blood pressure
100/45 mmHg, pulse 120 beats/min, respirations 40 breaths/min and
temperature 39C. The laboratory data showed hemoglobin 8 gm/dl, white blood
cell count 13,100/cu mm, platelets133,000/cu mm, sodium 138 meq/1,
potassium 5.1 meq/1, BUN 44 mg/dl, glucose 180 mg/dl, and creatinine 2.5
mg/dl. Chest x-ray was normal and EKG showed sinus tachycardia. Cultures
were obtained and the patient was started on mezlocillin and gentamicin.
The day after admission the patient's systolic blood pressure dropped to 70
mmHg and the arterial blood gases on FI02 0.6 were: pH 7.38, PaO2 42 mmHg,
PaCO2 49 mmHg, and 02 saturation 75%. Another chest x-ray showed diffuse
bilateral infiltrates. The patient was transferred to the intensive care unit, volume
resuscitated, intubated and started on intravenous inotropes and vasopressors.
A pulmonary artery catheter was inserted and the initial hemodynamic profile
can be seen in Profile 12.7, #1. Blood cultures taken on admission grew E. coll.
The patient also received monoclonal anti-bodies against endotoxin (HA-1A) as
part of a clinical research study. The patient remained oliguric, uremic and
therefore hemodialysis was started. Mechanical ventilation was maintained with
high FI02 and high PEEP values.

Case 9 Septic Shock

Case 9 Septic Shock

The next day's hemodynamic profile measured when the patient

was under treatment with dopamine 12 mcg/ kg/min,
dobutamine 10 mcg/kg/min and norepinephrine 3 mcg/min is
shown in Profile 12.7, #2.
Four days after admission to the ICU and aggressive treatment
with fluids, dopamine, dobutamine, norepinephrine, antibiotics,
TPN, blood components and hemodialysis, her hemodynamic
parameters became more stable. The dopamine dose was
reduced to 3 mcg/kg/min, the dobutamine dose to 5 mcg/
kg/min, and the norepinephrine was discontinued (Profile 12.7,
#3).
Two days later the patient was successfully weaned from the
ventilator. She had no fever and good urinary output, therefore
no further hemodialysis was needed. Nine days after admission
the patient was discharged from the intensive care unit and
subsequently to her home.

Case 9 Septic Shock

Discussion
Septic shock is a severe medical problem that has been increasing in incidence
over the past few years (61). It is now the most common cause of death in
intensive care units (61). The high incidence of sepsis today is paradoxically
linked to advances in modern medical technology including an increase in
patient age, greater number of immunocompromised patients as a consequence
of the use of cytotoxic drugs and radiotherapy, the wider use of invasive
techniques and devices such as catheters, and the emergence of antibiotic
resistant microorganisms (61,62). De-spite all of the medical progress, septic
shock still carries an unacceptably high mortality. Therefore it is imperative to
elucidate the pathophysiology of sepsis and septic shock in order to provide our
patients with better treatment and an improved outcome.
The most common pathogens that cause sepsis are the gram-negative bacilli
but sepsis may also follow gram-positive infections (62). It is believed that many
of the profound hemodynamic changes that occur in septic shock are due to
endotoxin released by microorganisms, which activate other mediators such as
cytokines, tumor necrosis factor, interleukins, myocardial depressant substance
and others. The latter appears to exert direct myocardial effects responsible in
part for the abnormal myocardial function seen in septic shock (63).
The action of endotoxins in septic patients results in an impairment of vasomotor
control (64). The loss of vasomotor tone decreases systemic vascular resistance
(SVR) resulting in hypotension and shock. A baroreceptor reflex increases
cardiac output and a hyperdynamic cardiovascular state ensues with an
elevated cardiac index (64,65). Ventricular function is abnormal with a
decreased right and left ventricular ejection fraction. (61-64,66).

Case 9 Septic Shock

As a consequence, end-systolic and diastolic volumes will increase and

ventricular dilation occurs (63). The cardiac output remains elevated despite the
decreased ejection fraction because of the increased heart rate. Failure to
achieve an appropriately augmented cardiac output results in hypotension which
together with the decreased SVR further aggravates shock. In septic shock
there, is an increase in microvasculac permeability which leads to extravasation
of albumin and fluid. from the intravascular compartment causing generalized
tissue edema. This edema further impairs the micro-circulation aggravating the
maldistribution of blood flow (64).

Patients suffering from septic shock fail to extract oxygen normally and are
highly dependent on oxygen supply (DO2) to maintain oxygen consumption
(VO2) and aerobic metabolism (67,68). The maldistribution of blood flow,
peripheral arteriovenous shunting, cellular damage and tissue edema have all
been implicated as causative factors of the ineffective oxygen utilization (66).
The impaired capacity of oxygen metabolism results in a high mixed venous
blood oxygen saturation and narrow arteriovenous oxygen difference (avDO2)
(66,67). On the other hand, because of the hyperdynamic state, patients have
high oxygen requirements. When oxygen delivery, even though augmented, is
not sufficient to maintain aerobic metabolism, oxygen extraction by peripheral
tissues will be deficient and blood lactate concentrations will in-crease (68). If
the relationship between oxygen supply and demand is not restored quickly and
the shock state is inadequately treated, irreversible tissue damage occurs in
multiple sites. Multiple organ failure is most common in septic patients and
worsens the clinical picture and prognosis.

Case 9 Septic Shock

In addition to lactic acidosis other metabolic derangements occur in sepsis

including hypoxemia, hyperglycemia, hyperuricemia, hypocalcemia,
hypertriglyceridemia, and respiratory alkalosis (62,66).
Successful management of septic shock requires an organized strategy and
aggressive therapy from the onset. The corner-stone of management is the use
of broad spectrum antibiotic agents, until the pathogen it definitely isolated and
the sensitivity to antibiotics veriiicd, a.id removal of any possible source of
infection such as pus, catheters or prostheses. Correction of hypotension must
be made with adequate fluid resuscitation. The use of the pulmonary artery
catheter (PAC) may help to ensure an adequate left ventricular preload while
avoiding pulmonary edema (68,69). Despite adequate volume infusion,
hypotension frequently persists. It is then necessary to add inotropic and vasopressor agents such as dopamine, dobutamine, norepinephrine and/or
epinephrine (61,62,69,70). Maximizing DO2 is also an important part of
hemodynamic resuscitation and prevention of multiple organ failure (68,71). To
achieve this goal, one can in-crease cardiac output by the use of volume and/or
inotropes. In addition, the arterial oxygen saturation should be maintained above
90% by the use of increasing FIO2. mechanical ventilation. PEEP, respiratory
physiotherapy and/or pulmonary toilet. When anemia is present, transfusion of
packed red blood cells should be considered (71).
The use of high dose corticosteroids is no longer controversial. In addition to the
possibility of superinfection, hyperglycemia and gastrointestinal bleeding in
corticosteroid-treated patients, large trials have shown some evidence of
increased mortality and no beneficial effect of corticosteroids in preventing or
reversing shock in septic patients (72-74).

Case 9 Septic Shock

Recently, trials employing human monoclonal antibodies against endotoxin have

shown improved survival in patients with gram-negative bacteremia (75). The
use of continuous arteriovenous hemofiltration associated with plasmapheresis
and dialysis may also be of use in patients suffering from sepsis and multiple
organ failure (76). The search for new methods to treat patients with sepsis and
septic shock continues. Trials are currently under way to assess monoclonal
antibodies to tumor necrosis factor and to interleukin-1 receptor antagonists.

The present patient developed septic shock four days after an extracorporeal
shock wave lithotripsy. When analyzing the initial hemodynamic profile (Profile
12.7, #1), one can see that the patient had a rapid heart rate which maintained
the high cardiac output despite the low stroke index. The high cardiac output,
low systemic vascular resistance and narrow arterio-venous oxygen difference
are typical of the hyperdynamic picture found in patients with septic shock.

Arterial hypoxemia was also present, despite mechanical ventilation with high
FIO2 and PEEP, secondary to an increased pulmonary shunt fraction related to
the adult respiratory distress syndrome (ARDS), frequently accompanying septic
shock. This hypoxemia associated with the low hemoglobin contributed to the
relatively low oxygen delivery. In clinical circumstances, oxygen delivery is in
excess of what is needed and oxygen consumption is supply independent. As
stated before, beyond a critical level, tissues fail to extract oxygen adequately
and are unable to sustain aerobic metabolism, switching then to anaerobic
metabolism and increasing the lactate production (77).

Case 9 Septic Shock

At this stage oxygen consumption is decreased and so one can say it becomes
supply dependent. In normal individuals this critical level is about 300
ml/min/m2. In septic shock patients it is necessary to have a higher delivery as
the critical level is about 600 ml/min/m2 which corresponds to an oxygen
consumption of 170 mUmin/m2 (78,79). In Profile #1, it can be seen that oxygen
de-livery is far below the amount needed and so is oxygen consumption. The
decreased oxygen consumption and low extraction ratios lead to normal or even
high mixed venous saturation in septic patients. The low V02 and high venous
oxygen saturation associated with the arteriovenous peripheral shunt are
responsible for the narrow a-v oxygen difference found.
A repeated hemodynamic study (Profile 12.7, #2) was taken after the patient
was better ventilated and oxygenated with a high FI02 and PEEP and received
blood components. She was also receiving inotropic and vasopressors agents. It
demonstrated improvement of arterial oxygen saturation and an increase in
oxygen delivery and consumption and consequently a better oxygen extraction
ratio. The avDO2 was wider, however there was still a hyperdynamic state with
high CO and heart rate and low systemic and pulmonary resistances. The next
hemodynamic profile (Profile 12.7, #3) shows an increase in systemic vascular
resistance and arterial blood pressure and lower heart rate. All of this was
probably related to the resolution of the septic shock state, resulting in a
decrease in cardiac output. The pulmonary shunt fraction was much lower and
the arterio-venous 02 difference wider. The patient had almost normal
parameters and was successfully recovering from the severe illness which made
it possible to wean the dopamine, dobutamine and norepinephrine. Cardiac
index was restored to almost normal values. Two days later the patient had good
urinary output and tachypnea disappeared. She was transferred from the
intensive care unit four days after this last profile was taken.

Case 9 Septic Shock

Case 10 Post Traumatic Shock and ARDS

PATIENT 10: POST TRAUMATIC SHOCK AND THE ADULT

RESPIRATORY DISTRESS SYNDROME (ARDS)/Loren D. Nelson
A 17 year old woman was ejected from a high speed motor vehicle
crash. She sustained severe multiple trauma and was brought to the
Trauma Center with a known closed head injury, multiple facial
lacerations, bilateral femur fractures, bilateral pneumothoraces, and
multiple rib fractures bilaterally, bilateral pulmonary contusions, and
significant hypotension with a distended abdomen. She was taken
immediately to the operating room where an exploratory laparotomy
was performed.
She was found to have a grade IV liver laceration and a splenic
avulsion at the hilum. A splenectomy was rapidly performed and
attention was turned to the liver laceration. Marked bleeding from deep
in the parenchyma of the liver could not be controlled by the usual
surgical methods. The patient, at this time, had lost more than 15 units
of blood and was becoming hypothermic with a core temperature of
33C. Because of her falling temperature and continued bleeding, the
liver injury was packed with laparotomy sponges and the abdomen was
closed.
The patient was taken to the Surgical Intensive Care Unit for
hemodynamic monitoring and ventilatory support. A chest x-ray
demonstrated diffuse bilateral pulmonary infiltrates consistent with
ARDS.

Case 10 Post Traumatic Shock and ARDS

On arrival in the SICU, the patient was on 100% oxygen, 5 cm H2O of PEEP,
and an IMV rate of 14. Initial arterial blood gases showed: pH 7.3, PO2 40
mmHg with a saturation of 75%, PCO2 30 mmHg, and Sv02 of .45, and a
cardiopulmonary profile demonstrated in Profile 12.8, # I. The initial CI was low
but yet the oxygen utilization coefficient or oxygen extraction ratio (OUC) was
greatly elevated implying that oxygen delivery (D02) was inappropriately low for
the current (normal or slightly elevated) oxygen consumption (V02). However, Cl
was being maintained by a very high heart rate, indicating a low stroke index.
The low stroke index with tachycardia and high OUC in the presence of a low
PAOP suggested intravascular volume depletion.
Because of the profound acute respiratory failure (99/9-0.57), the patient was
treated with increasing levels of positive end-expiratory pressure in order to
improve the functional residual capacity and peripheral oxygen delivery. Using
the pulse oximeter and continuous mixed venous oximeter, the end-expiratory
pressure was titrated up and the FIO2 was reduced in an attempt to lower the
toxic inspired oxygen concentration and improve intrapulmonary shunting.
Because the patient had initially low filling pressures (CVP = 10 mmHg, PAOP =
12 mmHg), she received additional intravenous fluid boluses to augment
ventricular preload to improve stroke volume and cardiac output. This is
especially important in patients on PEEP since some of the increases in airway
pressure (de-pending upon the relationship between lung and chest wall
compliances) will be transmitted to the pulmonary vasculature and
perimyocardial space. The effect of increases in transmitted pressure will be to
increase right ventricular afterload and decrease left atrial transmural pressure.
Both of these effects may lower left ventricular preload and may account for a
reduction of cardiac index sometimes seen during high levels of PEEP.

Case 10 Post Traumatic Shock and ARDS

Fifteen minutes after admission, the patient was on 18 cm H2O

of PEEP and the FIO2 was reduced to 0.6. This produced a
90% arterial saturation and a 62% venous saturation with an
estimated oxygen utilization coefficient of 0.31 and
intrapulmonary shunt of 0.39.
The PEEP was further increased and the second arterial blood
gas was obtained. At this point, the FI02 was 0.5 and the shunt
was reduced to 0.32. Fifteen minutes later following an IMV
change andan increase in the PEEP to 22, the FI02 was
reduced to 0.4 and the arterial oxygen tension had increased to
80 with a saturation of 96%.
The mixed venous oxygen saturation, however, had fallen to
0.60 and the OUC had increased to 0.38. The shunt fraction had
decreased to 0.17 but because the patient was showing signs of
impaired oxygen transport with a worsening of her metabolic
acidosis, a fluid bolus was administered and 15 minutes later,
another blood gas was obtained.
At this time, the intrapulmonary shunt fraction was 0.19, the
oxygen utilization coefficient was 0.28, and the PaO2 was now
85 on 22 of PEEP, and IMV of 4, and 40% oxygen.

Case 10 Post Traumatic Shock and ARDS

Discussion

This patient demonstrated the utility of arterial and venous

continuous saturation measurements in the titration of high
levels of positive end-expiratory pressure (PEEP). The rapid
titration ofincreasing levels of PEEP and decreasing FI02 was
accomplished over a period of 15 minutes without additional
blood gases. Several other alterations in ventilatory support
were achieved. Blood gases were obtained for the evaluation of
pH and PCO2 following IMV changes.

A total of 14 ventilator changes were made in a period of less

than 60 minutes. The patient's oxygenation support with increased levels of PEEP allowed normalization of the
intrapulmonary shunt to 0.19 and an improvement in the
Pa02/FI02 ratio from 40 to 213 mmHg. It is generally true that
diverging values of SaO2 and SvO2 indicate greater peripheral
utilization of oxygen or lower central shunting. Converging
values, on the other hand, generally indicate lesser peripheral
oxygen utilization or greater venous admixture (right-to-left
shunting).

Case 10 Post Traumatic Shock and ARDS

If SaO2 decreases, the oxygen utilization coefficient will increase implying a greater consumption of delivered oxygen.
OUC = V02/D02 but if the small amount of oxygen dissolved in
the plasma is ignored OUC = (SaO2 - SvO2)/SaO2. The
diverging SaO2 and SvO2 indicate greater utilization of oxygen.
If SvO2 is stable and SaO2 decreases, it is most likely that rightto-left intrapulmonary shunting has increased. Normally the
magnitude of shunting is estimated by calculating the
physiologic shunt fraction (venous admixture):
Qs/Qt = (Cc'02 - CaO2)/ (Cc'02 - Cv02)
If the small volumes of oxygen dissolved in the plasma are
ignored, an estimate of venous admixture can be calculated as:
1 - SaO2/ 1 - SvO2
Thus converging values of SaO2 and SvO2 (when SvO2 is
stable) imply worsening venous admixture. Obviously, these
hold true only when hemoglobin concentration and FI02 are
constant. The combined use of arterial and venous oximetry in
this critically ill patient shortened the time to the therapeutic endpoint and al-lowed more frequent measurements with fewer
expenditures of resources.

SvO2 Decision Tree