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Pattern Recognition
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 Exercise 1
Practice Exercise 2
Practice Exercise 3
Practice Exercise 4
Practice Exercise 5
Practice Exercise 6
Practice Exercise 7
Practice Exercise 8
Practice Exercise 9
Practice Exercise 10
Practice Exercise 11
RVEDV
RAP, CVP
Complianc
PAD, PAWP e
SVR (LV)
PVR (RV)
SVI,
LVSWI,
RVSWI
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.
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 2 Complicated MI
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
Case 2 Complicated MI
Case 2 Complicated MI
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
Case 2 Complicated MI
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).
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.
.Mitral Regurgitation/Stenosis
Aortic Regurgitation
Aortic Stenosis
Multivalvular Disease
Cardiomyopathy (Dilated and Hypertrophic)
Ventricular Septa] Defect
Pulmonary Hypertension
Pericardial Constriction
ASD
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.
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.
Constrictive
Pericarditis
Diastolic
Equilibration
Dip and
Plateau
Physiology
YES
YES
Restrictive
NO
Cardiomyopathy
YES
Cardiac
Tamponade
NO
YES
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.
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.
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).
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.
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).
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.
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.
Discussion
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.