Definition

Circulatory shock is characterized by the inability of tissue blood flow and oxygen delivery to meet metabolic demands. Cardiogenic shock is a type of circulatory shock resulting from severe impairment of ventricular pump function rather than from abnormalities of the vascular system or blood volume. It is important to separate the shock state, in which tissue perfusion is inadequate, from hypotension, in which tissue metabolic demands may be met by increasing cardiac output or decreasing systemic resistance.

The diagnosis of cardiogenic shock should include the following:

The failure to define cardiogenic shock consistently or to confirm hemodynamically the presence of an elevated pulmonary capillary wedge pressure and low cardiac index have previously confused the clinician and confounded the literature.

Etiology

The most common cause of cardiogenic shock is acute MI.²⁰ Often, anterior MI from acute thrombotic occlusion of the left anterior descending artery results in extensive infarction. Alternatively, a smaller MI in a patient with borderline left ventricular function may be responsible for insufficient cardiac output. Large areas of ischemic nonfunctioning but viable myocardium occasionally lead to shock in patients with MI. The delayed onset of shock may result from reocclusion of a patent infarct artery, infarct extension, or metabolic decompensation of non–infarct zone regional wall motion. Occasionally, right ventricular MI from occlusion of a proximal large right coronary artery in a patient with inferior MI is the cause.²¹

Mechanical complications unrelated to infarct size account for approximately 12% of cases. The papillary muscle of the mitral valve may infarct or rupture, causing acute, severe mitral regurgitation.²² Rupture of the interventricular septum causing ventricular septal defect²³ or rupture of the left ventricular free wall producing pericardial tamponade²⁴ also needs to be considered. Other causes of cardiogenic shock that are not emphasized in this chapter include end-stage cardiomyopathy, myocardial contusion, myocarditis, hypertrophic cardiomyopathy, valvular heart disease, pericardial disease, and post–cardiopulmonary bypass.

Incidence

Before the emphasis on time-to-treatment and primary PCI, the incidence of cardiogenic shock had remained unchanged for more than 25 years with approximately 8% of patients with ST segment elevation myocardial infarction (STEMI)^25,26 and 2.5% of patients with non–ST segment elevation MI^27,28 developing cardiogenic shock. The latter group is more likely to have circumflex artery occlusion, comorbid disease, and severe three-vessel disease or left main disease.²⁸ Cardiogenic shock usually develops early after onset of symptoms, with approximately half of patients developing shock within 6 hours and 72% developing shock within 24 hours.²⁹ Others first develop a preshock state manifested by systemic hypoperfusion without hypotension.³⁰ These patients benefit from aggressive supportive therapy, and revascularization; early intervention may abort the onset of cardiogenic shock.

Pathology

The early development of cardiogenic shock is usually caused by acute thrombosis of a coronary artery supplying a large myocardial distribution, with no collateral flow recruitment.³¹ Frequently, this is the left anterior descending artery, although shock may result from coronary thrombosis in other sites if previous MI has occurred. Multivessel disease is present in two thirds of patients.³²

Autopsy studies have consistently shown that at least 40% of the myocardium is infarcted in patients who die of cardiogenic shock.³³ Various ages of infarction reflect previous infarction, reinfarction, or infarct extension.

The infarct border zone in patients without hypotension is clearly demarcated. In patients dying of shock, it is irregular, with marginal extension. Focal areas of necrosis remote from the infarct zone are also present. These findings result from progressive cell death owing to poor coronary perfusion, are reflected by prolonged release of cardiac enzymes, and contribute to hemodynamic deterioration.³⁴

Pathophysiology

Progressive hemodynamic deterioration leading to cardiogenic shock results from a sequence of events (Fig. 17-1). A critical amount of ischemic or necrotic myocardium decreases contractile mass and cardiac output. When cardiac output is low enough that arterial blood pressure declines, coronary perfusion pressure decreases in the setting of an elevated left ventricular end-diastolic pressure. The resulting reduction in coronary perfusion pressure gradient from epicardium to endocardium exacerbates myocardial ischemia, further decreasing left ventricular function and cardiac output, perpetuating a vicious cycle. The speed with which this process develops is modified by the infarct zone, remote myocardial function, neurohumoral responses, and metabolic abnormalities.

Figure 17-1 The vicious circle of mechanical and neurohormonal events that lead to progressive cardiogenic shock and death in acute myocardial infarction. ANP, atrial natriuretic peptide.

(Adapted from Califf RM, Bengston JR: Cardiogenic shock. N Engl J Med 1994;330:1724.)

The infarct zone can be enlarged by reocclusion of a patent infarct artery. Alternatively, infarct extension can result from side branch occlusion from coronary thrombus propagation or from thrombosis of a second stenosis stimulated by low coronary blood flow and hypercoagulability. Infarct expansion or aneurysm formation promotes left ventricular dilation, which increases wall stress and oxygen demand in the setting of decreased oxygen supply owing to low cardiac output.

Preclinical and clinical studies³⁵ have shown the importance of hypercontractility of remote myocardial segments in maintaining cardiac output in the setting of a large MI. This compensatory mechanism is lost when multivessel disease is present and produces ischemia in noninfarct segments.

A series of neurohumoral responses is activated in an attempt to restore cardiac output and vital organ perfusion. Decreased baroreceptor activity secondary to hypotension increases sympathetic outflow and reduces vagal tone; this increases heart rate, myocardial contractility, venous tone, and arterial vasoconstriction. Vasoconstriction is most pronounced in the skeletal, splanchnic, and cutaneous vascular beds to redistribute cardiac output to the coronary, renal, and cerebral circulations. An increase in the ratio of precapillary to postcapillary resistance decreases capillary hydrostatic pressure, facilitating movement of interstitial fluid into the vascular compartment. Increased catecholamine levels and decreased renal perfusion lead to renin release and angiotensin production. Elevated angiotensin levels stimulate peripheral vasoconstriction and aldosterone synthesis. Aldosterone increases sodium and water retention by the kidney, increasing blood volume. Release of antidiuretic hormone from the posterior pituitary by baroreceptor stimulation also increases water retention. Local autoregulatory mechanisms that decrease arteriolar resistance and increase regional blood flow are stimulated by hypoxia, acidosis, and accumulation of vasoactive metabolites (e.g., adenosine).

Enhanced anaerobic metabolism, lactic acidosis, and depleted adenosine triphosphate stores result when compensatory neurohumoral responses are overwhelmed, depressing ventricular function further. Arrhythmias may additionally reduce cardiac output and increase myocardial ischemia. Loss of vascular endothelial integrity because of ischemia culminates in multiorgan failure. Pulmonary edema impairs gas exchange. Renal and hepatic dysfunction can cause fluid, electrolyte, and metabolic disturbances. Gastrointestinal ischemia can lead to hemorrhage or entry of bacteria into the bloodstream, causing sepsis. Microvascular thrombosis owing to capillary endothelial damage with fibrin deposition and catecholamine-induced platelet aggregation impairs organ function further.

A systemic inflammatory state with high plasma levels of cytokines (e.g., tumor necrosis factor-α, interleukin-6) and inappropriate nitric oxide production additionally may depress myocardial function or impair catecholamine-induced vasoconstriction. All of these factors lead to diminished coronary artery perfusion and trigger a vicious cycle of further myocardial ischemia and necrosis resulting in even lower blood pressure, lactic acidosis, multiple organ failure, and ultimately death.³⁶

History and Physical Examination

The diagnosis of acute MI must be confirmed. Noncardiac causes of shock need to be ruled out, including aortic dissection, tension pneumothorax, massive pulmonary embolism, ruptured viscus, bleeding, and sepsis. Risk factors for developing cardiogenic shock include older age, anterior MI location, hypertension, diabetes mellitus, multivessel coronary artery disease, prior MI, prior congestive heart failure, STEMI, or left bundle branch block.^37,38

Patients usually appear ashen or cyanotic, with cold and clammy skin. They may be agitated, disoriented, or lethargic from cerebral hypoperfusion. The pulses are rapid and faint, the pulse pressure is narrow, and arrhythmias are common. Jugular venous distention and pulmonary rales are usually present in left ventricular shock, but they may be absent. Jugular venous distention, Kussmaul sign (a paradoxical increase in jugular venous pressure during inspiration), and absent rales are found in right ventricular shock. Left ventricular dyskinesis may produce a precordial heave. A systolic thrill along the left sternal border is consistent with mitral regurgitation or ventricular septal defect. The heart sounds are distant. Third and fourth heart sounds or a summation gallop can be auscultated. The systolic murmur of mitral regurgitation is often present; ventricular septal defect also produces a systolic murmur. The absence of a murmur does not exclude these complications, however. The extremities are usually vasoconstricted.

Electrocardiography and Laboratory Testing

A large anterior or anterolateral MI pattern is often present. Old anterior Q waves or new ST segment elevation in the right precordial leads consistent with right ventricular MI may be noted with acute inferior MI. Multiple lead ST segment depression without an injury current is another pattern that can occur with multivessel or left main disease. New left bundle branch block and third-degree atrioventricular conduction block are ominous findings. A relatively normal electrocardiogram (ECG) should alert one to other causes of shock.

Troponin and creatine kinase levels are elevated, may peak late because of prolonged washout or ongoing necrosis, and can increase secondarily with infarct extension. Lactic acidosis, hypoxemia, and mixed venous oxygen desaturation are usually present.

Echocardiography

Echocardiography can be performed rapidly and offers valuable information on the extent of left ventricular dysfunction. A dilated, hypokinetic left ventricle suggests left ventricular shock, whereas a dilated right ventricle suggests right ventricular involvement. Normal ventricular function, low cardiac output, and mitral regurgitation are consistent with acute severe mitral regurgitation. Pericardial tamponade from hemorrhagic effusion or free wall rupture can be detected quickly. The Doppler evaluation can easily confirm the presence of significant mitral regurgitation or ventricular septal rupture. Transesophageal echocardiography is helpful in patients in whom image quality is inadequate, or when a flail mitral leaflet is suspected but not seen on transthoracic echocardiography.

General Measures

Numerous supportive measures need to be instituted quickly (Fig. 17-2). If there is no clinical evidence for pulmonary edema, a fluid bolus should be given to exclude hypovolemia as a cause of hypotension. Patients with a history of inadequate fluid intake, diaphoresis, diarrhea, vomiting, or diuretic use may not have pump failure and improve dramatically with fluid administration. Because preload is critical in patients with right ventricular shock, fluid support and avoidance of nitrates and morphine are indicated (Table 17-2).

Figure 17-2 Emergency management of complicated ST segment elevation myocardial infarction. ACE, angiotensin-converting enzyme; BP, blood pressure; MI, myocardial infarction; SBP, systolic blood pressure; SL, sublingual.

(From Antman EM, Anbe DT, Armstrong PW, et al: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction]. Circulation 2004;110:e82.)

Table 17–2 Conventional Therapy for Cardiogenic Shock

Oxygenation and airway protection are crucial. Intubation and mechanical ventilation are usually required, followed by sedation, and often muscular paralysis. These interventions also improve the safety of electrical cardioversion or cardiac catheterization, if needed, and decrease oxygen demand. Positive end-expiratory pressure decreases preload and afterload.

Hypokalemia and hypomagnesemia predispose patients to ventricular arrhythmias and should be corrected. Because metabolic acidosis decreases contractile function, hyperventilation should be considered, but sodium bicarbonate should be avoided because of a short half-life and the large sodium load.

Arrhythmias and atrioventricular heart block have a major influence on cardiac output. Atrial and ventricular tachyarrhythmias should be electrically cardioverted promptly, rather than treated with pharmacologic agents. Severe bradycardia secondary to excess vagotonia can be corrected with atropine. Temporary pacing should be initiated for high-degree heart block, preferably with a dual-chamber system. This is especially important in patients with right ventricular infarction who depend on the right atrial contribution to preload.

Aspirin and monitored unfractionated heparin should be administered to decrease the likelihood of reinfarction, ventricular mural thrombus formation, or deep venous thrombosis in the setting of low flow and hypercoagulability. Clopidogrel is best withheld until cardiac catheterization has determined the need for emergency surgery because of its prolonged action and increased risk for perioperative bleeding. Morphine sulfate decreases pain and anxiety, excessive sympathetic activity, preload, and afterload, but should be administered only in small increments. Diuretics decrease filling pressures and should be used to control volume. β blockers and calcium channel blockers should be avoided because they are negative inotropic agents. An insulin drip may be required to control hyperglycemia.

Hemodynamic Monitoring

Central hemodynamic monitoring is crucial for confirming the diagnosis and guiding pharmacologic therapy (Table 17-3). Urine output needs to be monitored hourly through catheter drainage. An arterial catheter allows constant monitoring of the blood pressure. A pulmonary artery catheter should be inserted as soon as feasible to measure intracardiac pressures, cardiac output, systemic resistance, and mixed venous oxygen saturation. Although use of the pulmonary artery catheter has not been associated with mortality benefit in patients without MI, it is very helpful in the titration of fluids and medications in patients with cardiogenic shock.

Table 17–3 Hemodynamic Profiles

The hemodynamic profile of left ventricular shock, as defined by Forrester and coworkers,¹² includes pulmonary artery wedge pressure greater than 18 mm Hg and a cardiac index less than 2.2 L/min/m². Others have used a pulmonary wedge pressure of 15 mm Hg or 12 mm Hg and a cardiac index of 2 L/min/m² or 1.8 L/min/m². The hemodynamic profile of right ventricular shock includes right atrial pressure of 85% or more of the pulmonary artery wedge pressure, steep y descent in the right atrial pressure tracing, and the dip and plateau (i.e., square root sign) in the right ventricular waveform. Large v waves in the pulmonary artery wedge tracing suggest the presence of severe mitral regurgitation. An oxygen saturation step-up (>5%) from the right atrium to the right ventricle confirms the diagnosis of ventricular septal rupture. Equalization of right atrial, right ventricular end-diastolic, pulmonary artery diastolic, and pulmonary capillary wedge pressures occurs with severe right ventricular infarction or pericardial tamponade owing to free wall rupture or hemorrhagic effusion. Cardiac power (mean arterial pressure × cardiac output/451) is the strongest hemodynamic predictor of hospital mortality.³⁹

Pharmacologic Support

Vasopressor and inotropic drug support are the major initial interventions for reversing hypotension and improving vital organ perfusion (Table 17-4). Failure to improve blood pressure with these agents is an ominous prognostic sign. Continued hypotension results in progressive myocardial ischemia and deterioration of ventricular function. Although many patients temporarily respond to therapy, hospital mortality rates remain unchanged without successful reperfusion therapy.

Table 17–4 Pharmacologic Treatment for Cardiogenic Shock

Dobutamine, a synthetic catecholamine with predominantly β₁-adrenergic effects, is the initial inotropic agent of choice for patients with systolic pressures greater than 70 mm Hg. It has some chronotropic effect, but it has no significant vasoconstrictor, arrhythmogenic, or renal effects. Cardiac output is increased, and filling pressures are decreased.

Dopamine, a natural catecholamine, is the initial vasopressor of choice when the systolic pressure is greater than 70 mm Hg. Low dose (2 to 5 μg/kg/min) increase stroke volume and renal perfusion by stimulating dopamine receptors. Intermediate doses have a dose-dependent β₁-adrenergic receptor effect, increasing inotropy and chronotropy. High doses (15 to 20 μg/kg/min) activate α-adrenergic receptors, increasing vascular resistance.

Norepinephrine is a natural catecholamine with predominately peripheral α-adrenergic effects. It is used when the systolic pressure is less than 70 mm Hg because it is a potent venous and arterial vasoconstrictor.

Catecholamine infusions should be carefully titrated. A delicate balance must be obtained between increasing coronary perfusion pressure and increasing oxygen demand, so that myocardial ischemia is not exacerbated. Excessive peripheral vasoconstriction decreases tissue perfusion, increased afterload increases filling pressures, and excessive tachycardia or arrhythmias can be stimulated. Extravasation of dopamine or norepinephrine can cause tissue necrosis.

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