Cardiogenic Shock

Circulatory shock is characterized by the inability of blood flow and oxygen delivery to meet metabolic demands.

Cardiogenic shock is a type of circulatory shock resulting from severe impairment of ventricular function, the diagnosis of which should include:

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  Systolic blood pressure (BP) less than 80 mm Hg without inotropic or vasopressor support, or less than 90 mm Hg with inotropic or vasopressor support, for at least 30 minutes

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  Low cardiac output (< 2.0 L/min/m ² ) not related to hypovolemia (pulmonary artery capillary wedge pressure < 12 mm Hg), arrhythmia, hypoxemia, acidosis, or atrioventricular block

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  Tissue hypoperfusion manifested by oliguria (< 30 mL/h), peripheral vasoconstriction, or altered mental status

The most common cause of cardiogenic shock is acute myocardial infarction (MI).

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  Often, anterior MI due to acute thrombotic occlusion of the left anterior descending artery results in extensive infarction.

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  Alternatively, a smaller MI in a patient with borderline left ventricle (LV) function may be responsible for insufficient cardiac output (CO).

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  Large areas of ischemic, nonfunctioning but viable myocardium or right ventricular (RV) MI from occlusion of a proximal large right coronary artery (CAD) can occasionally lead to shock (see Chapter 4 ).

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  Mechanical complications account for approximately 12% of cases (see Chapter 5 ), which include:

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    Infarction or rupture of the mitral valve papillary muscle causing acute, severe mitral regurgitation (see Chapter 14 )

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    Rupture of the interventricular septum causing ventricular septal defect (VSD)

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    Rupture of the LV free wall producing pericardial tamponade

Other cardiac causes include end-stage cardiomyopathy, myocardial contusion, myocar­ditis, hypertrophic cardiomyopathy, valvular heart disease, pericardial disease, RV myocardial infarction, and post-cardiopulmonary bypass.

LV dysfunction is not a requirement for cardiogenic shock as evidenced in RV MI, cardiac tamponade, massive pulmonary embolism, acute mitral regurgitation, and acute aortic regurgitation.

Noncardiac causes include aortic dissection, tension pneumothorax, massive pulmonary embolism, ruptured viscus, hemorrhage, and sepsis.

Approximately 50% of patients with acute MI develop cardiogenic shock within 6 hours and 72% within 24 hours of symptoms.

Others first develop a preshock state manifested by systemic hypoperfusion without hypotension and may benefit from aggressive supportive therapy aborting the onset of cardiogenic shock.

Risk factors for cardiogenic shock complicating acute MI, include older age, anterior MI, hypertension, diabetes mellitus, multivessel CAD, prior MI, prior LV failure, ST segment elevation myocardial infarction, or left bundle branch block.

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 narrow, and arrhythmias are common.

Jugular venous distention and pulmonary rales are usually present in LV shock.

Jugular venous distention, Kussmaul sign (a paradoxic increase in jugular venous pressure during inspiration), and absent rales are found in RV shock.

A systolic thrill along the left sternal border is consistent with mitral regurgitation (MR) or VSD.

The heart sounds are distant.

Third and fourth heart sounds or a summation gallop may be present.

The systolic murmur of MR is often present; VSD also produces a systolic murmur.

The Society for Cardiovascular Angiography and Interventions (SCAI) shock stages, akin to the AHA/ACC stages A-D of heart failure, help visualise the progression and improvement of patients from those patients merely at risk (A) of cardiogenic shock to those in extremis (E), see Figs. 6.1 and 6.2 .

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; frequently, this is the left anterior descending artery, but multivessel disease is present in two thirds of patients.

Autopsy studies have consistently shown that at least 40% of the myocardium is infarcted in patients who die of cardiogenic shock.

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  The infarct border zone in patients without hypotension is clearly demarcated. In patients succumbing to shock, however, it is irregular, with marginal extension.

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  Focal areas of necrosis remote from the infarct zone are also present.

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  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.

Progressive hemodynamic deterioration resulting in cardiogenic shock results from a sequence of events ( Fig. 6.3 ).

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  A critical amount of diseased myocardium decreases contractile mass and CO.

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  When CO is low enough that arterial BP falls, coronary perfusion pressure decreases in the setting of an elevated LV end-diastolic pressure.

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  The resulting reduction in coronary perfusion pressure gradient from epicardium to endocardium exacerbates myocardial ischemia, further decreasing LV function and CO, perpetuating a vicious cycle.

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  The speed with which this process develops is modified by the infarct zone, remaining myocardial function, neurohumoral responses, and metabolic abnormalities.

The infarct zone can be enlarged by reocclusion of a previously patent infarct artery, side branch occlusion from coronary thrombus propagation or embolization, or by thrombosis of a second stenosis stimulated by low coronary blood flow and hypercoagulability.

This promotes LV dilation, increasing wall stress and oxygen demand in the setting of low CO.

Preclinical and clinical studies have demonstrated the importance of hypercontractility of remaining myocardial segments in maintaining CO in the setting of a large MI.

This compensatory mechanism is lost when multivessel disease is present and severe enough to produce demand ischemia in noninfarcted segments.

A series of neurohumoral responses is activated in an attempt to restore CO and vital organ perfusion (see Chapter 7 ).

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  Decreased baroreceptor activity owing to hypotension increases sympathetic outflow and reduces vagal tone.

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  This increases heart rate, myocardial contractility, venous tone, and arterial vasoconstriction.

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  Vasoconstriction is most pronounced in the skeletal, splanchnic, and cutaneous vascular beds to redistribute CO to the coronary, renal, and cerebral circulations.

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  An increase in the ratio of precapillary to postcapillary resistance decreases capillary hydrostatic pressure, facilitating movement of interstitial fluid into the vascular compartment.

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  Increased catecholamine levels and decreased renal perfusion lead to renin release and angiotensin production.

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  Elevated angiotensin levels stimulate peripheral vasoconstriction and aldosterone synthesis.

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  Aldosterone increases sodium and water retention by the kidney, raising blood volume.

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  Release of antidiuretic hormone from the posterior pituitary by baroreceptor stimulation also increases water retention.

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  Enhanced anaerobic metabolism, lactic acidosis, and depleted adenosine triphosphate stores result when compensatory neurohumoral responses are overwhelmed, further depressing ventricular function.

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  Loss of vascular endothelial integrity because of ischemia culminates in multiorgan failure.

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  Pulmonary edema impairs gas exchange.

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  Renal and hepatic dysfunction results in fluid, electrolyte, and metabolic disturbances.

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  Gastrointestinal ischemia can lead to hemorrhage or entry of bacteria into the bloodstream, causing sepsis.

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  Microvascular thrombosis owing to capillary endothelial damage with fibrin deposition and catecholamine-induced platelet aggregation further impairs organ function.

A systemic inflammatory state with high plasma levels of cytokines and inappropriate nitric oxide production may also depress myocardial function or impair catecholamine-induced vasoconstriction, respectively.

All of these factors, in turn, lead to diminished coronary artery perfusion and thus trigger a vicious cycle of myocardial ischemia and necrosis resulting in even lower BP, lactic acidosis, multiorgan failure, and ultimately death.

The SCAI SHOCK stage is an indication of cardiogenic shock severity and

comprises one component of mortality risk prediction in such patients (see Table 6.1 ). A helpful SCAI 3-axis model of risk stratification in cardiogenic shock helps one to ­consider the risk factors, etiology and phenotype and severity of shock (see Fig. 6.4 ).