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CURRENT Diagnosis & Treatment in Cardiology > Chapter 6. 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 end-stage cardiomyopathies can also lead to cardiogenic shock.


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.


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 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
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
Babaev A et al. Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. JAMA. 2005 Jul 27;294(4):448–54. [PMID: 16046651]

Hochman JS et al. Cardiogenic shock complicating acute myocardial infarction–etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol. 2000 Sep;36(3 Suppl A):1063–70. [PMID: 10985706]

Sharkey SW et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation. 2005 Feb 1;111(4):472–9. [PMID: 15687136]


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 (β-adrenergic mediated effects) and peripheral vasoconstriction (an -adrenergic mediated 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:

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.

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 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).

Figure 6–1.

Coronary angiogram of patient with an acute myocardial infarction and cardiogenic shock. Severe disease in left coronary system (A) and acute occlusion with thrombus in the right coronary artery (B).

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.

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 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.

Figure 6–2.

Left ventriculogram of patient with ventricular septal defect. Note that contrast injected into the left ventricle (LV) opacifies both the aorta (AO) and the pulmonary artery (PA). (The right ventricle is superimposed upon the left in this projection and therefore is not visualized.)

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.


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 = stroke volume x heart rate), a markedly decreased heart rate, especially with concomitant left ventricular dysfunction may, result in shock.

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.

Birnbaum Y. Ventricular septal rupture after acute myocardial infarction. N Engl J Med. 2002 Oct 31;347(18):1426–32. [PMID: 12409546]

Bowers TR et al. Patterns of coronary compromise resulting in acute right ventricular ischemic dysfunction. Circulation. 2002 Aug 27;106(9):1104–9. [PMID: 12196336]

Crenshaw BS. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Arteries) Trial Investigators. Circulation. 2000 Jan 4–11;101(1):27–32. [PMID: 10618300]

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]

Kohsaka S et al. Systemic inflammatory response syndrome after acute myocardial infarction complicated by cardiogenic shock. Arch Intern Med. 2005 Jul 25;165(14):1643–50. [PMID: 16043684]

Menon V et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK trial registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol. 2000 Sep;36(3 Suppl A):1110–6. [PMID: 10985713]

Slater J et al. Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a report from the SHOCK trial registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol. 2000 Sep;36(3 Suppl A):1117–22. [PMID: 10985714]

Webb JG et al. Implications of the timing of onset of cardiogenic shock after acute myocardial infarction: a report from the SHOCK trial registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol. 2000 Sep;36(3 Suppl A):1084–90. [PMID: 10985709]

Wong SC et al. Angiographic findings and clinical correlates in patients with cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK trial registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol. 2000 Sep;36(3 Suppl A):1077–83. [PMID: 10985708]

Clinical Findings


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.

Physical Examination

The physical examination reveals signs consistent with hypoperfusion.

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.


Patients may be confused, lethargic, or obtunded as a consequence of cerebral hypoperfusion.


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.

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. 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.


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).

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.

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.


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.

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.


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.

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.

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.

Left Heart (Cardiac) Catheterization

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.


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
  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

1Patients 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.

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.


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.

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.

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.


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).

-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.


Vasodilation (especially of the arterioles to reduce SVR) can be effective in increasing cardiac output in patients with heart failure by countering the peripheral 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.

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.


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 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.

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.

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.

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 therapy for patients with an acute MI complicated by cardiogenic shock who cannot proceed directly to cardiac catheterization and PCI.

Other Medical Therapies

Aspirin and heparin are indicated in patients with MIs and cardiogenic shock, provided mechanical complications requiring surgery are not present. -Blockers 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.

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.

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 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.


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.

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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]

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 emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol. 2000 Sep;36(3 Suppl A):1123–9. [PMID: 10985715]

White HD et al. Comparison of percutaneous coronary intervention and coronary artery bypass grafting after acute myocardial infarction complicated by cardiogenic shock: results from the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK (SHOCK) trial. Circulation. 2005 Sep 27;112(13):1992–2001. [PMID: 16186436]


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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