Download Cardiogenic Shock

Cardiogenic Shock
Essentials of Diagnosis
►Tissue hypoperfusion: Depressed mental status, cool extremities, decreased urinary output.
►Hypotension: Systolic blood pressure < 90 mm Hg.
►Reduced cardiac output: Cardiac index < 2.2 L/min/m2.
►Adequate intravascular volume: Pulmonary artery wedge pressure > 15 mm Hg.
►General Considerations
A diagnosis of cardiogenic shock has historically conferred a very high mortality. Despite recent
advances in treating this condition, nearly 50% of patients with cardiogenic shock still do not
survive to hospital discharge. In a strict sense, cardiogenic shock develops as a result of the
failure of the heart in its function as a pump, resulting in inadequate cardiac output. This failure
is most commonly caused by extensive myocardial damage from an acute myocardial infarction
(MI), but other mechanical complications of an acute MI, valve lesions, arrhythmias, and endstage cardiomyopathies can also lead to cardiogenic shock.
►Definition
A number of definitions for cardiogenic shock have been proposed. Although these definitions
differ in some ways, there is general agreement that both hemodynamic and clinical
parameters should be included. There should be evidence of a reduced cardiac output without
hypovolemia. Clinical signs of decreased peripheral perfusion should be present and include
cool and clammy skin, weak distal pulses, altered mental status, and diminished urinary output
(less than 30 mL/h). A commonly used set of hemodynamic criteria for cardiogenic shock are (1)
a systolic blood pressure of less than 90 mm Hg for at least 30 minutes (or the need for
vasopressor or intra-aortic balloon pump support in order to maintain a systolic blood pressure
90 mm Hg), (2) a pulmonary capillary wedge pressure (PCWP) of greater than 15 mm Hg, and
(3) a cardiac index less than 2.2 L/min/m2. Using a combination of clinical and hemodynamic
criteria means that fewer patients are given an inappropriate diagnosis of shock.
►Etiology
Acute MI accounts for most cases of cardiogenic shock. Acute MI results in cardiogenic shock in
5–10% of patients; however, it is likely that cardiogenic shock develops in many more patients
following an acute MI, but they do not survive to receive medical attention. Cardiogenic shock
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may occur in a patient with a massive first infarction, or it may occur with a smaller infarction in
a patient with an already substantially infarcted myocardium. “Mechanical” complications of
acute MI can also cause shock, and these include ventricular septal rupture, acute mitral
regurgitation as a result of papillary muscle rupture, and myocardial free wall rupture with
tamponade. Right ventricular infarction in the absence of significant left ventricular infarction
or dysfunction can lead to shock. Refractory tachyarrhythmias or bradyarrhythmias, usually in
the setting of preexisting left ventricular dysfunction, are occasionally a cause of shock and can
occur with either ventricular or supraventricular arrhythmias. Cardiogenic shock may occur in
patients with end-stage cardiomyopathies (ischemic, valvular, hypertrophic, restrictive, or
idiopathic in origin). Cardiogenic shock may also be the presenting manifestation of acute
myocarditis (infectious, toxic, rheumatologic or idiopathic). A more recently recognized entity is
stress cardiomyopathy (also known as apical ballooning syndrome or tako-tsubo
cardiomyopathy) in which severe heart failure and sometimes cardiogenic shock result from
extreme emotional distress. Finally, certain endocrine abnormalities may cause severe cardiac
dysfunction and cardiogenic shock (Table 6–1).
Table 6–1. Causes of Cardiogenic Shock.
I. Acute myocardial infarction (MI)
A. Pump failure
B. Mechanical complications of acute MI
1. Acute mitral regurgitation
2. Ventricular septal defect
3. Free wall rupture/tamponade
C. Right ventricular MI
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II. End-stage, severe cardiomyopathies secondary to
A. Valvular disease
B. Chronic ischemic disease
C. Restrictive/infiltrative
D. Idiopathic
III. Acute myocarditis: viral/infectious, toxic
IV. Stress cardiomyopathy
V. Endocrine disease (eg, hypothyroidism, pheochromocytoma)
A. Bradyarrhythmias
B. Tachyarrhythmias
VII. Secondary to medications
VIII. Post-traumatic
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►Pathogenesis
The principle feature of shock is hypotension with evidence of end-organ hypoperfusion. In
cardiogenic shock, this occurs as a consequence of inadequate cardiac function. The usual
response to low cardiac output is sympathetic stimulation to increase cardiac performance and
maintain vascular tone. This results in tachycardia and increased myocardial contractility (βadrenergic mediated effects) and peripheral vasoconstriction (an α-Adrenergicmediated effect).
The classic patient with cardiogenic shock has evidence of peripheral vasoconstriction (cool,
clammy skin) and tachycardia. Corresponding classic hemodynamics are a reduced cardiac
output and increased systemic vascular resistance (SVR), defined as:
(SVR) = (mean arterial pressure central venous pressure) x 80 (dynes x s x cm-5)
--------------------------------------------------------------cardiac output
Recent evidence suggests that many patients with cardiogenic shock do not have these classic
hemodynamics and instead have a lower SVR much like patients in septic shock. In fact, it has
been postulated that a systemic inflammatory response-like syndrome with a low SVR may be
encountered in up to 25% of patients in cardiogenic shock. Furthermore, patients with severe
septic shock often have depressed myocardial function, and patients with cardiogenic shock can
have a component of hypovolemia. Thus, there can be considerable overlap in
pathophysiologies.
A. Cardiogenic Shock after Acute MI
If at least 40% of the left ventricular myocardial muscle mass is lost, either acutely or as a result
of prior damage, cardiogenic shock can result from pump failure (ie, there is not sufficient left
ventricular muscle mass to maintain forward cardiac output). This usually occurs as a
consequence of an MI. The initial event in an acute MI is obstruction of a coronary artery,
commonly termed the “infarct-related artery.” The acute obstruction decreases oxygen supply
to a portion of the heart, resulting in myocardial ischemia and infarction, which in turn leads to
diminished myocardial contractility. The ensuing drop in cardiac output and blood pressure
leads to decreased perfusion pressures in other coronary beds. (Coronary perfusion becomes
compromised when the aortic diastolic pressure falls below 50–55 mm Hg.) This results in
further ischemia, especially if stenoses are present in these non–infarct-related vessels, and
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additional deterioration in left ventricular function occurs. Indeed, most patients with shock
after acute MI have extensive coronary disease, and mortality correlates with the extent of
coronary disease (Figure 6–1).
The process of ischemia and infarction leading to myocardial dysfunction leading to further
ischemia and so on has been appropriately termed “a vicious cycle.” Evidence for this vicious
cycle is found in autopsy studies that show infarct extension at the edges of an infarct in
addition to discrete, remote infarctions throughout the ventricle. This also explains the finding
that cardiogenic shock can occur immediately, provided sufficient myocardium is dysfunctional,
or occur hours after the initial infarct as a consequence of the vicious cycle. Tissue
hypoperfusion also leads to accumulation of lactic acid. Acidemia is detrimental to left
ventricular contractility, and this is another example of a vicious cycle contributing to the
pathophysiology of cardiogenic shock.
B. Mechanical Complications of Acute MI
The pathophysiology of cardiogenic shock due to mechanical complications of acute MI is
somewhat different. The three main mechanical problems are (1) acute mitral regurgitation as
a consequence of papillary muscle rupture, (2) ventricular septal defect (VSD), and (3)
myocardial free wall rupture leading to cardiac tamponade. These mechanical problems all
occur in a bimodal distribution, with some occurring earlier in the presentation and others
occurring later, and are a consequence of weakened, necrotic myocardium.
The papillary muscles anchor the the mitral valve apparatus to the left ventricle. Proper
papillary muscle function is vital in ensuring that the two mitral valve leaflets close completely
to prevent leakage or regurgitation of blood backwards into the left atrium. Papillary muscle
rupture is a term used somewhat erroneously; rupture and avulsion of the entire papillary
muscle usually results in such severe regurgitation that it is rapidly fatal. If only a portion of the
papillary muscle ruptures, then severe mitral regurgitation ensues, leading to pulmonary
edema and a reduced forward cardiac output. This accounts for up to 7% of patients with
cardiogenic shock after an acute MI. The sympathetic nervous system response to cardiac
failure results in increased SVR (afterload) and a further increase in the regurgitant fraction,
another example of a vicious cycle contributing to cardiogenic shock.
Rupture of the myocardial free wall results in bleeding into the relatively nondistendible
pericardial space and leads rapidly to pericardial tamponade and cardiovascular collapse. Often
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this is immediately fatal, but occasionally patients survive and cardiogenic shock develops. The
incidence of free wall rupture in patients with cardiogenic shock is as high as 3%.
Rupture of the intraventricular septum with the formation of a VSD has an incidence of
approximately 0.3% in patients with acute MI and accounts for up to 6% of patients with
cardiogenic shock after an acute MI. A large VSD causes significant shunting of blood from the
left ventricle to the right ventricle, and results in right ventricular volume and pressure overload
(Figure 6–2). Shock usually develops as a consequence of reduced forward cardiac output. As
with acute mitral regurgitation, the sympathetic nervous system response results in increased
afterload, thereby shunting an even larger fraction of the cardiac output across the
interventricular septum.
C. Right Ventricular Infarction
Right ventricular infarctions occur in approximately 40% of patients with inferior MIs. Right
ventricular infarctions may result in cardiogenic shock without significant left ventricular
dysfunction. Failure of the right ventricle leads to diminished right ventricular stroke volume,
which results in a decreased volume of blood returning to the left ventricle. This markedly
diminished left ventricular preload, even with normal left ventricular contractility, causes a
decreased systemic cardiac output. The right ventricle also becomes dilated, which results in
displacement of the intraventricular septum to the left. If severe, this can actually impair left
ventricular filling, with physiology similar to that seen in cardiac tamponade. Since left
ventricular filling pressures are not elevated in pure right ventricular failure, pulmonary
congestion will not be evident.
D. Arrhythmias
A variety of arrhythmias can contribute to the development of shock. A sustained arrhythmia,
that is, one that does not culminate in ventricular fibrillation and sudden death, is generally a
cause of shock only in the already compromised ventricle. Atrial and ventricular
tachyarrhythmias can result in diminished time for ventricular filling in diastole as well as the
loss of the atrial contribution to ventricular diastolic filling. This results in a diminished preload,
which in turn results in a decreased stroke volume. These factors may be enough to result in
cardiogenic shock in patients with already impaired left ventricular function or with conditions
such as severe aortic stenosis in which the left ventricle is especially sensitive to filling
pressures. Bradyarrhythmias reduce cardiac output as a consequence of the slow heart rate.
Because total cardiac output is a function of heart rate and stroke volume (cardiac output =
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stroke volume x heart rate), a markedly decreased heart rate, especially with concomitant left
ventricular dysfunction may, result in shock.
E. Other Causes of Cardiogenic Shock
Many forms of heart disease can result in an end-stage dilated cardiomyopathy. These patients
may be in such acutely decompensated states that they are in frank cardiogenic shock.
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Menon V et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial
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Slater J et al. Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a
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►Clinical Findings
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A. History
The symptoms that precede the development of cardiogenic shock depend on the cause.
Patients with acute MIs often have the typical history of acute onset of chest pain, possibly in
the setting of known coronary artery disease. Often, however, patients seek medical care days
later following unrecognized MIs once cardiogenic shock has developed. In such cases, there is
no history of antecedent chest pain, but instead the insidious onset of dyspnea and weakness
culminating in shock. Patients may be obtunded and lethargic as a result of decreased central
nervous system perfusion. Mechanical complications of acute MI tend to occur several days to
a week following the initial infarction but can occur earlier. They may be heralded by chest
pain, but they more commonly present abruptly as acute dyspnea. Patients with arrhythmias
may have a history of palpitations, presyncope, syncope, or a sensation of skipped beats.
Regardless of the cause, however, by the time shock develops, the patient may be unable to
give any useful history.
B. Physical Examination
The physical examination reveals signs consistent with hypoperfusion.
1. Vital Signs – Hypotension is present (systolic blood pressure < 90 mm Hg). The heart rate is
commonly elevated, and the respiratory rate is generally increased as a result of hypoxia from
pulmonary congestion.
2. Neurologic – Patients may be confused, lethargic, or obtunded as a consequence of cerebral
hypoperfusion.
3. Pulmonary – Patients may use accessory muscles of respiration and may have paradoxical
respirations. The chest examination in most cases shows diffuse rales, often to the apices.
Patients with isolated right ventricular infarction will not have pulmonary congestion.
4. Cardiovascular System – Jugular venous pulsations are commonly elevated. Peripheral pulses
will be weak. The apical impulse is displaced in patients with dilated cardiomyopathies, and the
intensity of heart sounds is diminished, especially in patients with pericardial effusions. A third
or fourth heart sound suggesting significant left ventricular dysfunction and/or elevated filling
pressures may be present. A mitral regurgitation murmur (holosystolic, usually at the apex) or a
VSD murmur (harsh, holosystolic at the sternal border) can help in diagnosing these causes.
Patients with a free wall rupture that is partially contained may have a pericardial friction rub.
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Patients with significant right heart failure may have signs on abdominal examination of liver
enlargement with a pulsatile liver in the presence of significant tricuspid regurgitation.
5. Extremities – Peripheral edema may be present. Cyanosis and cool, clammy extremities are
indicative of diminished tissue perfusion. Profound peripheral vasoconstriction can result in
mottling of the skin (livedo reticularis).
C. Laboratory Findings
Patients with recent or acute MIs will have elevations in cardiac-specific enzymes (CPK-MB,
troponin). Renal and hepatic hypoperfusion may result in elevations in serum creatinine and in
transaminases (alanine transaminase [ALT] and aspartate transaminase [AST]). Coagulation
abnormalities may be present in patients with hepatic congestion or hepatic hypoperfusion. An
anion gap acidosis may be present and the serum lactate level may be elevated.
D. Diagnostic Studies
While further diagnostic studies are important in clarifying the diagnosis, it must be emphasized
that rapid, definitive therapy should not be delayed once the diagnosis is apparent. In general,
patients with cardiogenic shock and suspected acute MI should proceed to cardiac
catheterization as quickly as possible.
1. Electrocardiography – The electrocardiogram (ECG) may be helpful in distinguishing between
causes of cardiogenic shock. Patients with coronary disease and acute MI may show evidence of
both old (Q waves) and new infarctions (ST segment elevation). Right-sided chest leads in
patients with inferior MIs can detect the presence of a right ventricular infarction (ST elevation
in V4R). While ST elevations are often present on the ECGs of patients with cardiogenic shock,
patients with non–ST-segment elevation MIs represent up to 50% of patients with cardiogenic
shock. The ECG also readily aids in the diagnosis of arrhythmias contributing to cardiogenic
shock.
2. Chest Radiography – The chest radiograph may show an enlarged cardiac silhouette
(cardiomegaly) and evidence of pulmonary congestion in patients with severe left ventricular
failure. A VSD or severe mitral regurgitation associated with an acute infarction will lead to
pulmonary congestion but not necessarily cardiomegaly. Findings of pulmonary congestion may
be less prominent—or absent—in the case of predominantly right ventricular failure or in
patients with superimposed hypovolemia.
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3. Echocardiography – Given that it is noninvasive and able to be performed rapidly at the
bedside, echocardiography is extremely useful in the diagnosis of cardiogenic shock.
Furthermore, mechanical complications of an acute infarction can be readily diagnosed via
echocardiography. Information obtained by echocardiography includes assessment of right and
left ventricular size and function, valvular function (stenosis or regurgitation), right and left
ventricular filling pressures, and the presence of pericardial fluid with tamponade.
4. Hemodynamic Monitoring – Routine use of invasive pulmonary artery catheters in critically
ill patients is controversial. However, this procedure is recommended in certain situations and
can help in establishing the diagnosis and cause of cardiogenic shock. Catheters are usually
placed from a central vein into the right heart and advanced into a pulmonary artery. By
occluding flow temporarily in a branch of the pulmonary artery (“wedging” the catheter), an
estimate of left atrial pressure can be obtained (the PCWP). The presence of a wedge pressure
higher than 15 mm Hg in a patient with acute MI generally, but not always, indicates adequate
intravascular volume. Patients with primarily right ventricular failure or significant
superimposed hypovolemia may have cardiogenic shock with a normal or reduced PCWP. The
presence of a large “v wave” on the PCWP tracing is consistent with significant mitral
regurgitation, but may also be seen with a VSD or a very stiff left ventricle. A pulmonary artery
catheter also allows calculation of the SVR. Hemodynamic criteria for cardiogenic shock vary
and include a cardiac index of less than 2.2 L/min/m2. (Cardiac index is preferred to cardiac
output as a measure because it normalizes the cardiac output for body size.) It is important to
note that some patients with chronic heart failure but not in cardiogenic shock have cardiac
outputs in this range and are in fact ambulatory in a “compensated” state. Patients in
cardiogenic shock usually have suffered an acute insult and cannot compensate.
5. Oxygen Saturation – Invasive measurement of the mixed venous oxygen saturation can be
obtained from pulmonary artery catheters and may be helpful in two ways. First, knowing the
mixed venous oxygen saturation allows the arteriovenous difference in oxygen content to be
calculated. The arteriovenous difference in oxygen content is inversely proportional to the
cardiac output; it increases as more oxygen is extracted from the blood in the setting of low
cardiac output. Serial determinations can be useful in monitoring a patient’s course and
response to therapy. Secondly, oxygen saturations obtained invasively with a pulmonary artery
catheter may also be helpful in diagnosing a VSD. The shunting of oxygenated blood from the
left ventricle to the right ventricle across the septal defect results in an abnormal “oxygen
saturation step-up” when comparing oxygen saturations from the right atrium with those
obtained from the right ventricle.
E. Left Heart (Cardiac) Catheterization
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Left heart catheterization and invasive coronary angiography should be performed without
delay in patients with ST-segment elevation MI, since survival and myocardial salvage depend
on the time to reperfusion. This also applies to patients in cardiogenic shock with ST-segment
elevation. In patients with cardiogenic shock without ST-segment elevation but with evidence
of MI, cardiac catheterization should be expedited as well. In the cardiac catheterization
laboratory, obstructions in coronary arteries or bypass grafts can be detected, appropriate
treatments planned (either bypass surgery or percutaneous coronary intervention [PCI]) and an
intra-aortic balloon pump (IABP) placed if necessary.
► Treatment
Although some general therapeutic considerations are applicable to all patients in cardiogenic
shock, treatment is most effective when the cause is identified. In many situations, this
identification allows rapid correction of the underlying problem. In fact, survival in most forms
of shock requires a quick, accurate diagnosis. The patient is so critically ill that only prompt,
directed therapy can reverse the process. The already high mortality rates in cardiogenic shock
are even higher in patients for whom treatment is delayed. Therefore, although measures
aimed at temporarily stabilizing the patient may provide enough time to start definitive
therapy, potentially lifesaving treatment can be carried out only when the cause is known
(Table 6–2).
Table 6–2. Management of Cardiogenic Shock.
I. Diagnosis1
A. Electrocardiogram
B. Chest radiography
C. Laboratory tests (complete blood count, coagulation
profile, CK-MB, cardiac troponin, electrolytes + blood urea
nitrogen/creatinine, arterial blood gases)
D. Echocardiography
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E. Pulmonary artery catheterization (if diagnosis is in
question, patient receiving inotropes/vasopressors, or patient
is not responding to treatment)
F. Cardiac catheterization
II. Treatment
A. Oxygen supplementation; intubation, ventilation
B. Vasopressors/inotropes; consider careful intravenous
fluids, arterial line and pulmonary artery catheter insertion to
guide management; correct underlying causes of acidemia
C. Intra-aortic balloon pump, if needed
D. For suspected acute MI: aspirin, heparin, urgent cardiac
catheterization, revascularization (PCI, CABG); fibrinolysis if a
delay in PCI is anticipated
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Patients with suspected acute MI should proceed directly to cardiac catheterization; this should generally not be
delayed to facilitate additional diagnostic tests.
CABG, coronary artery bypass grafting; MI, myocardial infarction; PCI, percutaneous coronary intervention.
A. Acute MI
In patients with cardiogenic shock caused by a large amount of infarcted or ischemic
myocardium, the most effective treatment for decreasing mortality is prompt revascularization,
with either PCI or coronary artery bypass grafting (CABG) surgery. A number of pharmacologic
and nonpharmacologic measures may be helpful in stabilizing the patient prior to
revascularization.
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1. Ventilation-Oxygenation – Because respiratory failure usually accompanies cardiogenic
shock, every effort should be made to ensure adequate ventilation and oxygenation. Adequate
oxygenation is essential to avoid hypoxia and further deterioration of oxygen delivery to
tissues. Patients with cardiogenic shock should receive supplemental oxygen and many require
mechanical ventilation. Hypoventilation can lead to respiratory acidosis, which could
exacerbate the metabolic acidosis already caused by tissue hypoperfusion. Acidosis worsens
cardiac function and makes the heart less responsive to inotropic agents. A substantial
proportion of the cardiac output in patients with cardiogenic shock is devoted to the “work of
breathing,” so mechanical ventilation is also advantageous in this regard.
2. Fluid Resuscitation – Although hypovolemia is not the primary defect in cardiogenic shock, a
number of patients may be relatively hypovolemic when shock develops following MI. The
causes of decreased intravascular volume include increased hydrostatic pressure and increased
permeability of blood vessels as well as patients simply being volume depleted for many hours.
The physical examination may not always be helpful in determining the adequacy of the left
ventricular filling pressure. In select patients, invasive monitoring with a pulmonary artery
catheter can be helpful in determining the optimal volume status. Some patients with
cardiogenic shock will actually have improved hemodynamics with slightly higher than normal
filling pressures. Ventricular compliance is reduced in acute ischemia; the pressure–volume
relationship changes such that cardiac output may be optimized at slightly higher filling
pressures. In general, a PCWP of 18–22 mm Hg is considered adequate; further increases will
lead to pulmonary congestion without a concomitant gain in cardiac output. Fluid
administration, when indicated by low or normal PCWP, should be undertaken in 200–300 mL
boluses of saline, followed by careful reassessment of hemodynamic parameters, especially
cardiac output and PCWP, and generally should not be undertaken in patients with marginal
oxygenation or in those not already mechanically ventilated.
3. Inotropic/Vasopressor Agents – A variety of drugs are available for intravenous
administration to increase the contractility of the heart, the heart rate, and peripheral vascular
tone. It is important to note that these agents also increase myocardial oxygen demand;
improvements in hemodynamics and blood pressure therefore come at a cost, which can be
deleterious in patients with ongoing ischemia. Furthermore, -agonists can precipitate
tachyarrhythmias and -agonists can lead to dangerous vasoconstriction and ischemia in vital
organ beds. When using these agents, attention should be given to the patient as a whole
rather than focusing solely on a desired arterial pressure.
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A. DIGOXIN – Although digoxin benefits patients with chronic congestive heart failure, it is of
less benefit in cardiogenic shock because of its delayed onset of action and relatively mild
potency (compared with other available agents).
B. β-ADRENERGIC AGONISTS – Dopamine is an endogenous catecholamine with qualitatively
different effects at varying doses. At low doses (< 3 mcg/kg/min), it predominantly stimulates
dopaminergic receptors that dilate various arterial beds, the most important being the renal
vasculature. Although used frequently in low doses to improve renal perfusion, there is scant
evidence to support the clinical usefulness of this strategy. Intermediate doses of 3–6
mcg/kg/min cause 1-receptor stimulation and enhanced myocardial contractility. Further
increases in dosage lead to predominant -receptor stimulation (peripheral vasoconstriction) in
addition to continued 1 stimulation and tachycardia. Dopamine increases cardiac output, and
its combination of cardiac stimulation and peripheral vasoconstriction may be beneficial as
initial treatment of hypotensive patients in cardiogenic shock.
Dobutamine is a synthetic sympathomimetic agent that differs from dopamine in two
important ways: It does not cause renal vasodilatation, and it has a much stronger 2 (arteriolar
vasodilatory) effect. The vasodilatory effect may be deleterious in hypotensive patients because
a further drop in blood pressure may occur. On the other hand, many patients with cardiogenic
shock experience excessive vasoconstriction with a resultant elevation in afterload (SVR) as a
result of either the natural sympathetic discharge or the treatment with inotropic agents, such
as dopamine, that also have prominent vasoconstrictor effects. In such patients, the
combination of cardiac stimulation and decreased afterload with dobutamine may improve
cardiac output without a loss of arterial pressure.
Other agents that are occasionally used include isoproterenol and norepinephrine.
Isoproterenol is also a synthetic sympathomimetic agent. It has very strong chronotropic and
inotropic effects, resulting in a disproportionate increase in oxygen consumption and ischemia.
It is therefore not generally recommended for cardiogenic shock except occasionally for
patients with bradyarrhythmias. Norepinephrine has even stronger and 1 effects than
dopamine and may be beneficial when a patient continues to be hypotensive despite large
doses of dopamine (more than 20 mcg/kg/min). Because of the intense peripheral
vasoconstriction that occurs, perfusion of other vascular beds such as the kidney, extremities,
and mesentery may be compromised. Therefore, norepinephrine should not be used for any
extended time unless plans are made for definitive treatment.
4. Vasodilators – Vasodilation (especially of the arterioles to reduce SVR) can be effective in
increasing cardiac output in patients with heart failure by countering the peripheral
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vasoconstriction caused by endogenous catecholamines. Although these agents have a role in
treating acute, decompensated heart failure, they are rarely used in patients with cardiogenic
shock given the risk of worsening hypotension. The IABP (see below) is generally more effective
for reducing SVR without the risk of untoward hypotension.
5. Circulatory Support Devices – Among the mechanical devices developed to assist the left
ventricle until more definitive therapy can be undertaken, the intra-aortic balloon pump (IABP)
has been in use the longest and is the most well studied. The IABP is placed in the descending
aorta, usually via the femoral artery. Its inflation and deflation are timed to the cardiac cycle
(generally synchronized with the ECG). The balloon inflates in diastole immediately following
aortic valve closure. The augmentation of diastolic pressure that occurs when the balloon
inflates increases coronary perfusion as well as that of other organs. The balloon deflates at the
end of diastole, immediately before left ventricular contraction, abruptly decreasing afterload
and thereby enhancing left ventricular ejection. Unlike -agonists, these benefits come without
increases in myocardial demand.
Indications for use of the IABP include cardiogenic shock, especially when caused by ventricular
septal rupture and acute mitral regurgitation. In both ventricular septal rupture and mitral
regurgitation, the principle benefit is the decrease in afterload that occurs as the balloon
deflates; this results in a larger fraction of the left ventricular volume being ejected forward
into the aorta rather than into the left atrium (mitral regurgitation) or the right ventricle
(ventricular septal rupture). An IABP should be placed as soon as possible in an effort to
support these patients until emergency surgery can be performed. The most common side
effects of the IABP are local vascular complications, but these have diminished substantially
with the smaller caliber devices used currently. Nonrandomized data have shown that patients
in cardiogenic shock treated with an IABP fare better than those not treated with an IABP.
A number of other circulatory support devices have been developed in recent years with the
ability to provide even more circulatory support than the IABP. Devices can be implanted
surgically (such as the left ventricular assist device or LVAD) or percutaneously, and are capable
of creating flow rates of 3–5 L/min (close to a normal cardiac output). These devices can be
used until cardiac transplantation can be facilitated, or occasionally to support patients who
ultimately recover.
6. Revascularization – Revascularization, either by PCI or CABG surgery, decreases mortality in
patients in whom cardiogenic shock develops following MI. The multicenter, randomized
SHOCK trial (SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK)
showed a trend toward improved survival at 30 days in patients randomized to early
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revascularization (either PCI or CABG within 6 hours of enrollment). The survival benefit for
early revascularization became significant at 6 months, a benefit that persisted to 6 years.
Although the mortality of patients treated with a strategy of early revascularization was still
high, the absolute reduction in mortality was substantial (13% at 1 year); stated alternatively,
the “number needed to treat” with revascularization was approximately nine to prevent one
death at 1 year, which is low and provides strong support for revascularization in these
circumstances. Of note, patients 75 years of age and older did not benefit from
revascularization at 1 year in the randomized trial but did benefit in the nonrandomized but
much larger SHOCK registry. Many experts believe that the SHOCK trial was underpowered to
show a mortality difference at 30 days and, based on the 6-month and now 6-year data,
ACC/AHA guidelines recommend emergency revascularization for patients (especially those
under the age of 75) with cardiogenic shock complicating acute MI.
A. PERCUTANEOUS CORONARY INTERVENTION – Patients undergoing PCI in the SHOCK trial had
a similar benefit to those having bypass surgery. Mortality from cardiogenic shock has
decreased over the past decade in parallel with increasing use of PCI for these patients.
Although retrospective, other studies from large populations have shown that PCI use is
associated with lower mortality in patients with cardiogenic shock.
B. CABG SURGERY – Despite the marked absolute reduction in mortality observed among
patients treated with bypass surgery in the SHOCK trial, only a small proportion of patients with
cardiogenic shock undergo urgent bypass surgery (approximately 3% in the National Registry of
Myocardial Infarction 2004 database). Nevertheless, patients with multivessel disease in
cardiogenic shock should be evaluated for bypass surgery, and for patients with mechanical
complications of MI, surgery offers the best hope for survival at present.
7. Fibrinolytic Therapy – Fibrinolytic therapy refers to treating patients with acute ST-segment
elevation MIs with drugs that have fibrinolytic properties (that dissolve occlusive thrombus
within coronary arteries or grafts). While PCI is superior therapy to fibrinolysis for ST-segment
elevation MI, fibrinolysis is the recommended therapy if there will be a considerable delay in
facilitating PCI. Most trials of fibrinolytic therapy excluded patients with cardiogenic shock. In
earlier trials that included patients with cardiogenic shock, there was no benefit to fibrinolytic
therapy over placebo. It has been suggested that the low flow state present in shock may
contribute to the limited efficacy of fibrinolytic therapy. In contrast to these older studies, in
the SHOCK trial and registry, patients treated medically with fibrinolytic therapy fared better
than those medically treated without fibrinolytic therapy. Additional evidence comes from
meta-analyses of more recent fibrinolytic trials that revealed improved survival among
hypotensive patients treated with fibrinolytics. Current guidelines recommend fibrinolytic
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therapy for patients with an acute MI complicated by cardiogenic shock who cannot proceed
directly to cardiac catheterization and PCI.
8. Other Medical Therapies – Aspirin and heparin are indicated in patients with MIs and
cardiogenic shock, provided mechanical complications requiring surgery are not present. βBlockers are contraindicated in patients in cardiogenic shock. Platelet IIb/IIIa inhibitors block
the final pathway of platelet activation and aggregation and are beneficial in patients with
acute coronary syndromes. Several clinical trials of IIb/IIIa inhibitors included patients with
cardiogenic shock. Patients in cardiogenic shock treated with the IIb/IIIa inhibitor eptifibatide
had improved survival in the PURSUIT trial, and patients in cardiogenic shock at presentation
who undergo PCI and are treated with the IIb/IIIa inhibitor abciximab have improved survival.
For patients who eventually stabilize and in whom hypotension is no longer a concern, most
clinicians would recommend other medical therapies benefiting patients with heart failure
including ACE inhibitors.
B. Mechanical Complications
Acute mitral regurgitation secondary to papillary muscle dysfunction, myocardial free wall
rupture, and VSD are true emergencies. The definitive therapy for these catastrophes is surgical
repair, although there are reports of using percutaneously placed devices to successfully repair
VSDs. If the patient is to survive, all efforts must be made to get the patient to the operating
room as soon as possible after the diagnosis is made. Pharmacologic agents and the IABP (see
section on Circulatory Support Devices) are useful as temporizing measures.
C. Right Ventricular Infarction
Cardiogenic shock may occur with right ventricular MI and no or only minimal left ventricular
dysfunction. Recent data have questioned the long-accepted notion that patients with shock
from an islolated right ventricular MI have a better prognosis than those with primarily left
ventricular dysfunction. In the SHOCK registry, patients with a right ventricular MI and shock
fared similarly to those with primarily left ventricular dysfunction. Hemodynamic data
suggesting right ventricular dysfunction out of proportion to left ventricular dysfunction and ST
elevation in lead RV4 on a right-sided ECG are helpful in establishing the diagnosis, and
assessment of right ventricular function on echocardiography can confirm the diagnosis. In
cases of shock from right ventricular failure, initial treatment is aggressive fluid resuscitation to
increase right ventricular preload and output. Significant amounts of fluid (1–2 L or more) may
be required to develop an adequate preload for the failing right ventricle. Inotropic agents are
usually necessary when the right ventricular failure is so profound that shock continues despite
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adequate volume administration, and the IABP may be helpful in this situation. Heart block is
common in patients with right ventricular MIs. Patients with right ventricular infarction are
relatively dependent on right atrial contraction. As a result, single-chamber right ventricular
pacing may be inadequate in patients who require pacing, and atrioventricular sequential
pacing may be required to improve cardiac output.
D. Arrhythmias
Arrhythmias contributing to cardiogenic shock are readily recognized with ECG monitoring and
should be promptly treated. Tachyarrhythmias (ventricular tachycardia and supraventricular
tachycardia) should be treated with electrical cardioversion in patients with hemodynamic
compromise. Bradyarrhythmias may respond to pharmacologic agents (atropine, isoproterenol)
in some circumstances, but external or transvenous pacing may be required.
Antoniucci D et al. Abciximab therapy improves survival in patients with acute myocardial infarction complicated
by early cardiogenic shock undergoing coronary artery stent implantation. Am J Cardiol. 2002 Aug 15;90(4):353–7.
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Barron HV et al. The use of intra-aortic balloon counterpulsation in patients with cardiogenic shock complicating
acute myocardial infarction: data from the National Registry of Myocardial Infarction 2. Am Heart J. 2001
Jun;141(6):933–9. [PMID: 11376306]
Brodie BR et al. Comparison of late survival in patients with cardiogenic shock due to right ventricular infarction
versus left ventricular pump failure following primary percutaneous coronary intervention for ST-elevation acute
myocardial infarction. Am J Cardiol. 2007 Feb 15;99(4):431–5. [PMID: 17293178]
Dzavik V et al; SHOCK Investigators. Early revascularization is associated with improved survival in elderly patients
with acute myocardial infarction complicated by cardiogenic shock: a report from the SHOCK trial registry. Eur
Heart J. 2003 May;24(9):828–37. [PMID: 12727150]
Fang J et al. Trends in acute myocardial infarction complicated by cardiogenic shock, 1979–2003, United States. Am
Heart J. 2006 Dec;152(6):1035–41. [PMID: 17161048]
Hasdai D et al. Platelet glycoprotein IIb/IIIa blockade and outcome of cardiogenic shock complicating acute
coronary syndromes without persistent ST-segment elevation. J Am Coll Cardiol. 2000 Sep;36(3):685–92. [PMID:
10987585]
Hochman JS et al. Early revascularization and long-term survival in cardiogenic shock complicating acute
myocardial infarction. JAMA. 2006 Jun 7;295(21):2511–5. [PMID: 16757723]
Hochman JS et al. One year survival following early revascularization for cardiogenic shock. JAMA. 2001 Jan
10;285(2):190–2. [PMID: 11176812]
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Jacobs AK et al. Cardiogenic shock caused by right ventricular infarction: a report from the SHOCK registry. J Am
Coll Cardiol. 2003 Apr 16;41(8):1273–9. [PMID: 12706920]
Martinez MW et al. Transcatheter closure of ischemic and post-traumatic ventricular septal ruptures. Catheter
Cardiovasc Interv. 2007 Feb 15;69(3):403–7. [PMID: 17195200]
Sanborn TA et al. Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in
cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK trial registry. SHould we
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►Prognosis
Over the past 25 years, the prognosis of patients with cardiogenic shock has improved from
over 80% in hospital mortality in the late 1970s to under 50% mortality in recent years.
Revascularization (primarily PCI) appears to be the major contribution to improved outcomes.
Demographic features associated with a better prognosis include younger age and male gender.
Delayed time to revascularization predicts a worse outcome. Other clinical predictors of poorer
outcome include a lower ejection fraction, extensive coronary disease, a left main or vein graft
acute occlusion, higher heart rate, lower systolic blood pressure, and severe mitral
regurgitation. Cardiac power (mean arterial pressure x cardiac output) was the strongest
hemodynamic predictor of outcome in the SHOCK registry.
Fang J et al. Trends in acute myocardial infarction complicated by cardiogenic shock, 1979–
2003, United States. Am Heart J. 2006;152(6):1035–41. [PMID: 17161048]
Fincke R et al. Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic
shock: a report from the SHOCK trial registry. J Am Coll Cardiol. 2004 Jul 21;44(2):340–8. [PMID:
15261929]
Klein LW et al. Mortality after emergent percutaneous coronary intervention in cardiogenic
shock secondary to acute myocardial infarction and usefulness of a mortality prediction model.
Am J Cardiol. 2005 Jul 1;96(1):35–41. [PMID: 15979429]
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