The first clinical description of myocardial infarction (MI) was reported by Herrick in 1912.¹ He concluded from the clinical history that “while sudden death often does occur, yet at times it is postponed for several hours or even days, and in some instances, a complete, that is functionally complete, recovery ensues.” In the current era, a complete recovery after an acute MI has become the norm rather than the exception. Unfortunately however, the mortality for some patients remains devastatingly high. In particular, patients with cardiogenic shock after an acute MI have less than a 50 percent chance of surviving their hospital stay.^2,3

Cardiogenic shock in acute MI may result from a variety of mechanical complications. Most commonly it results from ventricular infarction and dysfunction alone, but other mechanical processes may contribute to the syndrome: ventricular septal rupture (VSR), ventricular free wall rupture, and ischemic mitral regurgitation (IMR).⁴ Although surgical therapies for these three conditions have long been recognized, the importance of timely revascularization in patients with cardiogenic shock in the absence of ventricular rupture or mitral regurgitation (MR) has received increased attention recently (see the decision-making flowchart; Fig. 31-1).

The topics covered in this chapter include (1) post-MI cardiogenic shock and ventricular dysfunction, (2) ischemic mitral valve (MV) disease, (3) postinfarction VSR, (4) postinfarction ventricular free wall rupture, and (5) ventricular aneurysms.

Introduction

Cardiogenic shock is a clinical syndrome that is characterized by hypotension and systemic hypoperfusion in the setting of ineffective cardiac function. Although the first report of circulatory collapse secondary to MI may have occurred as early as 1794 with Sir Everald Home’s description of the life of the British surgeon Sir John Hunter, Herrick first recognized the clinical signs of cardiogenic shock: cold clammy extremities, oliguria, and an altered mental status.^5,6 These clinical signs are accompanied by alterations in hemodynamic parameters: systolic blood pressure (SBP) less than 90 mm Hg, cardiac index (CI) less than 2.2 L/min/m², and pulmonary capillary wedge pressure greater than 15 mm Hg, indicating inadequate cardiac function despite adequate preload.

Pathophysiology

Myocardial Ischemia and Infarction

With progressive atherosclerosis of the coronary arteries, normal intraluminal diameter is preserved initially through compensatory outward remodeling; however, eventually these stenoses become functionally important and coronary artery disease becomes symptomatic.⁷ Plaque rupture may occur at any time, leading to intraluminal thrombosis.⁸ Usually this occurs in angiographically insignificant arteries, but it may cause total occlusion of epicardial arteries, resulting in acute myocardial hypoperfusion and ischemia. Occlusion of coronary arteries for less than 15 min results in reversible myocardial injury; longer periods result in irreversible damage.^9,10 Brief periods of ischemia correspond clinically to periods of angina (stable or unstable) and may occur on a daily basis¹¹; longer periods result in MI.

Stunned Myocardium

Within the first few minutes of ischemia, hypoxic myocytes stop contracting, resulting in regions of akinesia and dyskinesia.¹¹ After reperfusion (whether by relaxation of coronary artery spasm, cessation of exercise in stable angina, or pharmacologic or mechanical reperfusion), regions of viable post-ischemic myocardium may take hours to days to return to normal function; this delay has been termed myocardial stunning.^12–14 It originally was described in canine models of coronary occlusion and reperfusion and represents contractile dysfunction after acute ischemic injury. It includes left ventricular (LV) dysfunction after thrombolysis or angioplasty and may be involved in unusual cases of coronary spasm and severe exercise-induced ischemia. The pathogenesis of myocardial stunning is not completely understood. The primary mechanism is thought to be liberation of oxygen free radicals and myocyte adenosine triphosphate (ATP) depletion during reperfusion, but alterations in calcium homeostasis (including excitation-contraction decoupling resulting from sarcoplasmic reticulum dysfunction, calcium overload, and decreased responsiveness of myofilaments to calcium) may play a significant role.^11,15 Although investigators have suggested that calcium channel blockers or free radical scavengers may be useful in the treatment of myocardial stunning, inotropic support of the stunned myocardium until spontaneous recovery occurs remains the mainstay of treatment. Whatever the cause, stunned myocardium results in regions of reperfused, viable, but temporarily dysfunctional myocardium after an acute ischemic event. With sustained reperfusion, there is the potential for recovery of function.

Hibernating Myocardium

Historically, it was thought that ventricular wall dysfunction in patients with coronary artery disease results from regions of infarcted myocardium. However, with the advent of reperfusion therapies, it came to be recognized that some dysfunctional myocardium can recover after the return of blood flow to ischemic regions.^16,17 It is believed that these regions of chronically ischemic myocardium go into a state of “hibernation” in which metabolic activity is downregulated. This represents an adaptive process that reduces oxygen consumption and prevents irreversible ischemic damage.^16–18 Identification of patients with hibernating myocardium is important, because regions of hibernating myocardium consist of viable cells and revascularization may reverse the dysfunction and ameliorate LV failure.

Cardiogenic Shock

Acute MI leads to cardiogenic shock through ischemic dysfunction of myocytes and loss of effective contractility. The poor outcomes associated with this syndrome are due, at least in part, to the progressive nature of the dysfunction, in which worsening hypoperfusion leads to increasing ischemic and infarcted regions of myocardium. Cessation of this “vicious cycle” must occur early to increase survival rates in patients who present in cardiogenic shock after MI (Fig. 31-2).

Cardiac function depends on a complex interplay of a variety of factors: myocyte contractility, preload, afterload, and electrical coordination. After myocardial damage, ischemic myocytes lose contractile function. This results in a decrease in stroke volume and cardiac output. To compensate for this loss, sympathetic tone is increased, and this results in tachycardia, systemic vasoconstriction, and increased contractile function in the remaining, nonischemic myocardium. Although these mechanisms help maintain both systemic and coronary perfusion, they also lead to increasing cardiac workload and oxygen consumption in the remaining myocytes.

If the remaining portions of the heart are able to maintain cardiac output and blood pressure, a compensated state may develop that allows for systemic and coronary perfusion without extension of the infarct. However, if the compensatory mechanisms cannot meet the increased demand, the area of ischemic and infarcted myocardium increases, leading to a downward spiral in cardiac function and ultimately to shock. Once mean arterial blood pressure falls below 70 mm Hg, coronary blood flow becomes severely restricted.¹⁹ This spiral toward shock and ultimately death is supported by autopsy studies that have shown that infarcted regions of myocardium contain varying degrees of progression, suggesting an initial insult followed by multiple subsequent infarction events.²⁰ Traditionally, cardiogenic shock was thought to occur after the loss of approximately 40 percent of LV muscle mass.²¹ Although studies have varied in the precise definition of hemodynamic variables, most would include SBP less than 90 mm Hg, cardiac index less than 2.2 L/min/m², and pulmonary capillary wedge pressure (PCWP) less than 15 mm Hg.^22,23

Right Ventricular Dysfunction

Most patients with cardiogenic shock related to ventricular dysfunction have primarily LV failure; in the SHOCK (SHould we emergently revascularize Occluded Coronaries in cardiogenic shoCK) trial, nearly 80 percent of patients presented with shock resulting from predominant LV failure.²⁴ In contrast, less than 3 percent of patients presented with isolated right ventricular (RV) failure. However, despite younger age and a lower incidence of multivessel disease, a similar mortality rate was observed in the group with RV infarcts.⁴ A variety of factors may contribute to this phenomenon, including RV dependence on atrial filling that may be compromised by atrioventricular (AV) dissynchrony, poor RV compensation for ischemia secondary to the large surface area and thin free wall, and concomitant LV dysfunction with loss of septal assistance to RV systole.

Peripheral Effects

Traditionally, the vicious cycle of ventricular dysfunction was thought to be the primary pathophysiologic process involved in the development of ventricular dysfunction and cardiogenic shock. More recently, data have begun to suggest that the pathophysiology of cardiogenic shock may be more complicated.²⁵ Patients in the SHOCK trial and registry have been found to have a wide range of ejection fractions with a mean of approximately 30 percent, and systemic vascular resistance (SVR) was not universally elevated despite the use of vasopressors.^23,25–27 Based on studies of nitric oxide species, Hochman²⁵ concluded that some patients may have a significant component of systemic hypoperfusion related to a systemic inflammatory response caused by the release of inflammatory cytokines, and the SHOCK-2 (Should we inhibit nitric Oxide synthase in patients with Cardiogenic Shock) trial was designed to evaluate additional medical therapies directed toward the inhibition of inflammatory and vasodilatory mediators of shock.²⁵

Clinical Features

Precise estimates of the incidence of cardiogenic shock after acute MI are difficult to obtain because many patients die before reaching medical care. Furthermore, varying definitions of cardiogenic shock may contribute to variation among studies. The early report by Griffith and associates²⁸ had an incidence of nearly 20 percent; however, more recent studies have shown a consistent incidence of 6 to 10 percent.^2,29–31 The high incidence reported by Griffith may have been due in part to the inclusion of patients with underresuscitated hypovolemic shock in an era before invasive hemodynamic monitoring.⁵ Despite advances in the diagnosis and treatment of patients with MI, the incidence of cardiogenic shock in this population over the past three decades has remained relatively constant.² Although mortality rates have improved (Fig. 31-2), patients diagnosed with cardiogenic shock during an admission for MI still have a substantially higher in-hospital mortality rate than do those without shock (59 vs 8 percent).^2,23 Overall cardiogenic shock accounts for more than 55 percent of the in-hospital mortality of MI.³⁰ In addition, long-term survival of patients with cardiogenic shock remains significantly lower than that in patients without it even after hospital discharge.³²

Interestingly, although patients may present to the hospital in cardiogenic shock, a significant proportion (anywhere from 44–90 percent) develop shock after admission.^30,33 In-hospital mortality is similar in both groups, although there may be a long-term survival advantage among patients who develop shock after hospital admission.^30,34,35 Median time to the development of shock has varied in reported series from 5 h to nearly 24 h.^24,30,33 This raises the question of whether initial therapies may contribute to the development of cardiogenic shock in some patients and, in light of the high mortality associated with the development of shock (independent of time to onset), suggests the importance of initiating early preventive measures.

The clinical presentation begins with the classic symptoms of MI. With the onset of cardiogenic shock, physical signs of hypoperfusion begin to predominate as oxygen delivery to vital organs becomes impaired: cold and clammy extremities, ashen or cyanotic skin, oliguria, and an altered sensorium.¹ Risk factors for the development of cardiogenic shock include age, diabetes, and a previous MI.^30,36 In addition, studies have demonstrated a correlation between large infarct size (as measured by peak cardiac enzyme levels), anterior MI, a depressed left ventricular ejection fraction (LVEF), and the development of shock.^36,37 Those who had undergone coronary artery bypass grafting (CABG) in the past, however, were less likely to develop shock during their admission.³⁰

Diagnostic Modalities

Assessment of a patient with systemic hypoperfusion should begin with the exclusion of noncardiac causes. Other causes of shock include hypovolemia, sepsis, pericardial tamponade, aortic rupture, tension pneumothorax, and anaphylaxis (Table 31-1). In light of the poor outcomes associated with the onset of cardiogenic shock after MI, initiation of therapies to improve systemic perfusion should not be delayed.

An electrocardiogram (ECG) should be performed immediately. Absence of electrocardiographic changes associated with ischemia essentially excludes the diagnosis of post-MI cardiogenic shock. A chest x-ray will rule out pneumothorax as a cause of circulatory collapse. History and physical examination also should assist in differentiating cardiogenic shock from other causes, such as sepsis, anaphylaxis, and neurogenic. In fact, despite the vast armamentarium of advanced diagnostic tests, physical findings remain significant predictors of in-hospital mortality. In the global utilization of streptokinase and tissue plasminogen activator (tPA) for occluded arteries (GUSTO trials), subjective signs of hypoperfusion were among the most significant predictors of 30-day mortality: altered sensorium [odds ratio 1.68, 95 percent confidence interval (CI) 1.19–2.39], cold clammy skin (1.68, 95 percent CI 1.15–2.46), and decreased urine output (2.25, 95 percent CI 1.61–3.15).³⁵

Initial laboratory investigations should focus on evaluating perfusion and oxygenation by measuring arterial blood gas as well as assessing levels of cardiac enzymes and electrolytes and measuring a hematocrit. Levels of cardiac enzymes and hematocrit in particular have prognostic significance in patients with acute MI.^38–42 Invasive monitoring of blood pressure should be initiated rapidly, as noninvasive cuff pressures may underestimate actual pressure significantly in the setting of peripheral vasoconstriction. In the absence of evidence of pulmonary edema (on physical examination or chest x-ray), volume status may be assessed by the patient’s response to intravenous (IV) fluid resuscitation. Perhaps most important in the final determination of cardiac function and etiology are pulmonary artery catheterization and echocardiography.

Echocardiography

Rapid echocardiography (ECHO) is an important tool in the diagnosis and management of patients with cardiogenic shock. It allows for an expedited and accurate assessment of overall cardiac function. Multiple studies have shown that the ejection fraction is an important predictor of outcome even when it is measured within 24 h of presentation.^26,43 In addition, it can exclude other causes of circulatory collapse unrelated to ventricular dysfunction such as pericardial tamponade, IMR, and ventricular free wall or septal rupture, which may require different therapies.

Pulmonary Artery Catheterization

Placement of a pulmonary artery catheter allows direct measurement of right-sided cardiac pressures and extrapolation to left-sided filling pressures. Patients in cardiogenic shock are expected to have poor cardiac function, with adequate ventricular preload leading to depressed cardiac output and hypotension (Table 31-2). In the setting of ventricular infarction, diastolic dysfunction may contribute to impaired ventricular filling, requiring an even higher PCWP to maintain cardiac output. Even in the absence of hypotension, some patients may have evidence of systemic hypoperfusion (and its accompanying clinical signs); their in-hospital mortality, although lower than that of patients with hypotension (43 vs 66 percent), is high. Although clinical characteristics are important, hemodynamic monitoring should be initiated rapidly to obtain measurements of ventricular preload and cardiac output.

Recently continuous, arterial pressure-based cardiac output measurement devices have been introduced. These devices provide real-time continuous hemodynamic monitoring using an arterial catheter. They can provide data to diagnose and guide treatment while avoiding the cost and complications of pulmonary artery catheters.⁴⁴

Medical Therapies

As was noted above, therapies should not be delayed while one awaits diagnostic test results. Initial management should be directed immediately toward improving systemic and coronary perfusion and oxygenation. Supplemental oxygen should be delivered, and mechanical ventilation should be initiated when appropriate. Electrical complications of acute MI are common and before the development of coronary care units, they constituted the most common cause of death.⁴⁵ Depending on the location of the infarct, a variety of rhythm disturbances may occur, including tachy- and bradyarrythmias in both the atria and the ventricles. Therefore, telemetry monitoring should be initiated to screen for electrical dysfunction and allow for early treatment. Rapid correction of rhythm disturbances with antiarrythmic agents or cardioversion may be required, as AV dissynchrony may contribute to poor cardiac function. The use of analgesics (morphine sulfate or fentanyl) to control pain is also an important tool in reducing sympathetic tone and thus decreasing preload, afterload, and myocardial work.

Volume Resuscitation and Electrolyte Replacement

Although cardiac dysfunction accounts for most of the decreased cardiac output and systemic hypoperfusion, relative hypovolemia may coexist in as many as 20 percent of patients with cardiogenic shock.⁴⁶ Hemodynamic parameters measured with a pulmonary artery catheter should guide resuscitation efforts. Optimal ventricular filling pressures may vary among patients. Initial infusion with either normal saline or Ringer’s lactate is appropriate, although blood products should be used early. In patients over 65 years of age with a hematocrit below 33 percent, blood transfusion during admission with MI is associated with a decrease in 30-day mortality (conversely, patients with an admission hematocrit above 36 percent who received a transfusion had a higher mortality rate).⁴² Among patients with a hematocrit below 27 percent who do not receive a transfusion, the mortality rate has been shown to be approximately 50 percent, three times higher than that of patients with a normal hematocrit (above 37 percent).⁴² Recently it has been suggested that patients requiring transfusions were more ill at baseline and at increased risk of death.⁴⁷ Cardiac myocyte dysfunction is worsened by alterations in the electrolyte and acid–base environment. Maintenance of appropriate electrolyte levels is therefore essential, as is optimizing the patient’s acid-base status.

Vasodilators

Pharmacologic therapies such as nitrates, angiotensin-converting enzyme (ACE) inhibitors, and β-blockers have proven effectiveness in reducing mortality in patients with MI. However, all these agents have the potential to cause systemic hypotension; their use should be limited in patients in cardiogenic shock. Nitroglycerin has been shown to improve myocardial oxygen delivery and reduce oxygen demand as well as augment the antiaggregatory effects of aspirin on platelets.^48–50 Nitroglycerin also has been shown to reduce ischemia and infarct size. Although it has been difficult to demonstrate a survival benefit among patients treated with nitrates in large trials such as the Grupo Italiano per lo Studio della Sopravivenza nell’infarto Miocardico (GISSI) 3 study,⁵¹ as many as half the patients in the placebo group received off-label nitrates, probably diluting the detection of a real benefit. Also, seven smaller studies demonstrated an impressive reduction (41 percent) in post-MI mortality with the use of nitroglycerin.⁵²

Although IV nitroprusside has many of the same pharmacologic effects as nitroglycerin, some differences make it less useful in patients with acute MI; most importantly, it may exacerbate coronary steal by failing to promote collateral blood flow to ischemic myocardium.⁵³ In light of the salutary effects of nitrates on cardiac work and the potential decrease in mortality, IV nitrate therapy (preferably with nitroglycerin) should be started when systemic arterial blood pressure allows. The initial doses should be low (5–10 mg/min) with rapid titration upward to optimize arterial blood pressure and LV filling pressures (PCWP between 15 and 22 for patients in severe cardiac failure).

Inotropic Support

If optimization of ventricular filling pressures fails to ameliorate systemic hypoperfusion and hypotension, the use of inotropic support and intra-aortic balloon counter-pulsation (IABP) should be considered. A variety of inotropic agents are available, and the choice of a specific drug should be tailored to the specific clinical and hemodynamic status of the patient, particularly the degree of systemic hypotension.

Dopamine.

In patients with an SBP below 80, dopamine is one of the first-line cathecholamines because it has both inotropic and vasoconstrictive effects. Dopamine interacts with a variety of receptors in a dose-dependent manner. These receptors include the dopamine (DA)-1 receptors in the renal vasculature that mediate renal vasodilatation,⁵⁴ β₁-adrenergic receptors in the heart leading to increased inotropy and chronotropy, and α-adrenergic receptors in the peripheral vasculature leading to increased vascular resistance. As the dose increases, the predominant effect changes; however, there are no precise cutoffs, and the response to dopamine may vary between patients.⁵⁴

At low doses (0.5–3.0 μg/kg/min) it acts primarily as a dopaminergic agonist, increasing renal blood flow. At higher doses (3–5 μg/kg/min) β-adrenergic effects become noticeable, although dopaminergic effects still dominate. At these doses, improvement in renal perfusion depends primarily on the increase in cardiac output rather than on dilatation of the renal arterial bed.^55,56 Between 5 and 10 μg/kg/min, β-adrenergic effects become dominant and α-adrenergic effects become noticeable. Finally, in the range of 10 to 20 μg/kg/min, dopamine functions primarily as an α-adrenergic agent, leading to significant peripheral vasoconstriction. At doses above 20 μg/kg/min, coronary vasoconstriction may predominate.⁵²

Many of the presumed renal protective effects of low-dose dopamine have come under attack recently.^54,57 The renal vasodilatation thought to be related to dopaminergic stimulation actually may be due to augmentation of cardiac output through both increased stroke volume and increased heart rate.⁵⁸ Thus, dopamine should be used with care in patients in cardiogenic shock, in whom the increased inotropy may increase myocardial oxygen demand beyond the increase in oxygen delivery, leading to further ischemia; this is particularly of concern at high doses, in which case coronary vasoconstriction may lead to infarction of at-risk myocardium. In fact, the recently published SOAP II study demonstrated that patients in shock treated with dobutamine were at increased risk of developing arrhythmias, and patients in cardiogenic shock treated with dobutamine had a significantly increased mortality at 28 days when compared with patients given norepinephrine.⁵⁹ However, dopamine remains an important agent in the initial management of hypotension unresponsive to fluid resuscitation, and the necessity for high-dose dopamine should lead to the insertion of an IABP to protect myocardium at risk for further ischemia and infarction.

Dobutamine.

In contrast to dopamine, dobutamine causes peripheral vasodilatation in association with its inotropic effects. Therefore, it is best used in patients with SBP greater than 80. Dobutamine originally was thought to be a selective β₁-adrenergic agonist, but it now is recognized that it also has α- and β₂-adrenergic effects. As with dopamine, the relative importance of these effects changes with the dose.⁵ At rates between 2.5 and 15 mg/kg/min, dobutamine increases cardiac output without significantly affecting peripheral vascular resistance (probably as a result of stimulation of both α₁-mediated vasoconstriction and β₂-mediated vasodilatation).⁶⁰ At higher doses, α₁-adrenergic effects may begin to predominate with an increase in heart rate, LV afterload, and myocardial oxygen demand. In contrast, at lower doses, myocardial oxygen demand may remain constant despite increased contractility because of the reduction in peripheral vascular resistance, ventricular volumes, and wall stress.⁶¹

Isoproterenol.

Isoproterenol is a β-adrenergic agonist used primarily in the treatment of postcardiotomy cardiogenic shock. It has both an inotropic and a chronotropic effect on the heart and results in systemic vasodilatation. The increase in cardiac output seen with isoproterenol infusion is due largely to a resultant increase in heart rate.⁶² Because heart rate is a major determinant of myocardial oxygen demand, isoproterenol infusion may increase myocardial oxygen consumption.⁶³ In addition, it has been shown to shunt blood from ischemic myocardium to nonischemic areas.⁶⁴ This also results in an increase in ventricular instability that may result in ventricular arrhythmias even at relatively low doses.⁶³ In light of these problems, the use of isoproterenol in the setting of post-MI cardiogenic shock largely has been abandoned. It may have some application in a hypotensive patient with bradycardia, but transvenous pacing is preferred.

Phosphodiesterase Inhibitors.

Milrinone and amrinone are nonadrenergic inotropic agents. In addition, they have peripheral and pulmonary vasodilatory effects. Although they have minimal chronotropic and arrhythmogenic actions compared with the cathecholamines,⁶⁴ they also have long half-lives. This mitigates their usefulness in the acute post-MI setting. Therefore, they are used only when other agents have proved ineffective.^65,66 Most commonly, this occurs in the setting of right-sided heart failure, in which the increased pulmonary vasodilation of these agents has added benefit.

Vasopressors

In patients without adequate arterial blood pressure, vasopressor agents may be required to maintain systemic perfusion.

Norepinephrine.

Norepinephrine is a combined α- and β-adrenergic agonist. At low doses, its effects include primarily increased cardiac output and arterial blood pressure (mainly β-adrenergic-mediated).⁶⁷ At higher doses, vascular resistance is markedly increased and cardiac output actually may fall. Treatment with norepinephrine in patients with cardiogenic shock results in rapid increases in blood pressure, vascular resistance, and the LV stroke work index.⁶³ The last effect presents the main downside to norepinephrine in the setting of post-MI shock. Although the increased blood pressure improves myocardial oxygen supply through increased coronary blood flow,⁶⁸ the increase in the stroke work index increases oxygen demand in a potentially ischemic heart. While a shift from anaerobic to aerobic metabolism was observed with norepinephrine infusion in patients with cardiogenic shock, myocardial oxygen extraction remained abnormally high.⁶⁸ Other side effects of norepinephrine infusion include aggravation of oliguria through constriction of the renal arterial supply, increased risk of ventricular arrhythmias, and peripheral ischemia and limb loss. Despite these drawbacks, norepinephrine is a potent vasopressor with a rapid onset; its use is appropriate in severely hypotensive patients to maintain mean arterial pressure in the range of 70 to 80 mm Hg while other therapies are instituted.

Vasopressin.

Arginine vasopressin has been used frequently in patients with vasodilatory shock. In a variety of circumstances that include septic shock and postcardiotomy vasodilatory shock, an endogenous vasopressin deficiency exists.^69,70 Although that deficiency has not been seen in small series of patients in cardiogenic shock,⁶⁹ the recent recognition of a possible vasodilatory component in some patients in the SHOCK trial²⁵ may indicate a role for vasopressin in this setting. Traditionally, vasopressin was thought to have a negative impact on coronary perfusion; however, this was based on experimental data in normotensive dogs. Data in hypotensive models suggest that vasopressin increases coronary perfusion.^71,72 In addition, clinical trials in critically ill patients with vasodilatory shock suggest that the use of a vasopressin infusion results in decreased norepinephrine requirements, an improved cardiac index, a decreased stroke work index, and better preservation of gastric perfusion.⁷³ Although further study is necessary, vasopressin may provide a useful adjunct to norephinephrine in the maintenance of systemic blood pressure during the initial phase of cardiogenic shock before the institution of more definitive therapies.

None of the pharmacologic agents listed above has been shown to have a survival benefit in the treatment of cardiogenic shock. They all have significant side effects, and any attempt to increase cardiac output or systemic blood pressure in an attempt to increase coronary perfusion carries a risk of increasing myocardial ischemia. The use of vasopressors should be limited to keep mean arterial pressure at 70 to 80 mm Hg, not to return patients to a normotensive state, and inotropes should be used sparingly and under careful monitoring of hemodynamic parameters. In all cases, the most appropriate uses of these agents are as temporizing measures until the initiation of IABP placement, mechanical circulatory support, and revascularization.

Thrombolysis

The improvement in outcome with thrombolysis in patients with acute MI has been well established,^74–76 but in patients with cardiogenic shock, the benefits of this therapy are less clear. Many studies explicitly excluded patients with cardiogenic shock, and even more failed to describe the inclusion or exclusion of those patients.^74,77,78 Thrombolytics may decrease the incidence of the subsequent development of cardiogenic shock,^75,76,79 but no trial has demonstrated a convincing reduction in mortality in patients with already established cardiogenic shock.

Mathey and associates reported the survival of three patients with cardiogenic shock treated with streptokinase in 1980.^80,81 In a larger series of 44 patients, however, mortality remained at 66 percent.⁸² The GISSI-1 trial randomized a total of 280 patients with cardiogenic shock. Overall mortality in that group was 70 percent and did not differ between those treated with streptokinase (69.9 percent) and controls receiving placebo (70.1 percent).⁷⁵ Mortality rates were similar in trials comparing various thrombolytic regimens: The International Study Group reported mortality rates of 78.1 and 64.9 percent among 246 patients with cardiogenic shock treated with tPA or streptokinase⁸³; the GUSTO trial also had a high 30-day mortality among 2972 patients treated with streptokinase (51 percent) or tPA (57 percent).³⁰

Interestingly, among the 44 patients in the Society for Cardiac Angiography registry, arterial patency was achieved in only 19 patients (44 vs 71 percent in the registry as a whole), among whom mortality dropped to 42 percent (vs 84 percent in patients without reperfusion, p = 0.0005). In the GUSTO trial, lytic therapy was less likely to be successful in patients with cardiogenic shock [Thrombolysis in Myocardial Infarction (TIMI) 0 or 1 flow 42.9 vs 27.7 percent, p <0.001].³⁴ However, with successful reperfusion, mortality can be decreased significantly.^34,82,84 Thus, the poor performance of thrombolysis in the setting of cardiogenic shock may be secondary to an inability to achieve patency.

The decreased ability of thrombolysis to achieve successful reperfusion in the setting of cardiogenic shock is not completely understood and probably involves a combination of hemodynamic, metabolic, and mechanical factors.⁸⁵ Hypotension and coronary hypoperfusion probably play a significant role. In the setting of cardiogenic shock, research in canine models has suggested that the rate and degree of thrombolysis after intracoronary injection of tPA are depressed compared with those in normotensive controls,^86,87 and in clinical trials, hypotension was associated with lower TIMI flow grades after thrombolysis.⁸⁸ The augmentation of blood pressure through vasopressors or an IABP may improve the success rate of thrombolysis in patients with cardiogenic shock.^87,89,90

Despite these limitations, thrombolysis remains an important treatment for acute ST-elevation MI when percutaneous catheter-based interventions are not available. Indications and contraindications for thrombolytic therapy are well established (Table 31-3).⁹¹ However, recent data suggest that even when percutaneous catheter-based interventions are unavailable, transport to a facility with those services improves survival and decreases complications.⁹² Furthermore, the use of IABPs (see below) to stabilize patients for transport to a tertiary care facility has been shown to be a safe alternative to treatment with thrombolytics.⁶⁶ Although thrombolysis is an option in limited circumstances, mechanical revascularization delivers the best outcomes in acute MI patients.

Intra-Aortic Balloon Counterpulsation

In 1958, Harken described a mechanism for diastolic augmentation of blood flow.^93,94 However, initial attempts to use femoral–femoral bypass to augment diastolic flow met with technical difficulties, including the need for bilateral femoral arteriotomies and problems with the extracorporeal pump. Efforts at demonstrating increased cardiac perfusion failed. However, after work by Moulopoulos and associates^95,96 in 1968, Kantrowitz and coworkers described the first use of an IABP to provide diastolic flow augmentation in patients with cardiogenic shock.⁹⁷ Initial models required operative placement via a femoral arteriotomy, but in 1979 Bregman and Casarella introduced a percutaneously placed model inserted through a 12F sheath.⁹⁸ Further refinements have included a dual-lumen design, wire-guided placement, reduced sheath sizes (8F or 9F for 30–50-mL balloons), and the use of helium to inflate and deflate the balloon rapidly.^99,100

Most commonly, the IABP is inserted percutaneously into the femoral artery, using a modified Seldinger technique. After puncture of the artery, a J-wire is advanced into the aorta. The needle is removed, and the IABP catheter is inserted over the wire into the descending aorta. When properly placed, the balloon should lie immediately distal to the origin of the left subclavian artery (Fig. 31-3). In specialized cases such as pediatric patients and those with significant peripheral vascular disease that precludes the use of the femoral artery, other insertion sites may be used, including the ascending aorta, aortic arch, and subclavian, axillary, and iliac arteries.^101–107

After insertion, the balloon is connected to a pump console that controls its inflation and deflation. The timing of these events is synchronized to the patient’s cardiac cycle through the use of either electrocardiographic or aortic pressure-sensitive timing. The balloon inflates with the onset of diastole, displacing blood both proximally and distally and increasing intra-aortic pressure (diastolic augmentation). Immediately before systole, the balloon deflates, reducing obstruction to LV ejection (decreased afterload). With electrocardiographic timing, balloon inflation occurs (Fig. 31-4).

The decreased afterload results in a reduction in enddiastolic LV diameter and volume and a reduction in ventricular wall stress; a slight decrease in heart rate also is seen.¹⁰⁸ Multiple studies have shown that, as expected, the reductions in wall stress and heart rate, lead to a decrease in myocardial oxygen demand and consumption.¹⁰⁹ Through diastolic augmentation, the IABP increases coronary perfusion and myocardial oxygen delivery.¹¹⁰ This increase in coronary blood flow has been observed in both hypotensive animals and patients with cardiogenic shock (Fig. 31-4).^109,111 Overall, these effects lead to improved hemodynamics (increased cardiac output, decreased PCWP, improved arterial blood pressure, and improved urine output)^112–114 along with improvement in myocardial metabolism (as reflected in decreasing oxygen extraction and a shift toward aerobic metabolism).⁶⁸

Despite these improvements in hemodynamic performance and myocardial metabolism, initial results with the IABP alone in the treatment of cardiogenic shock failed to demonstrate improvement in survival.^115,116,117 In a small randomized trial (30 patients) that compared optimal medical therapy for cardiogenic shock with IABP, in-hospital mortality was similar in both groups (50 percent with IABP vs 44 percent with medical management).¹¹⁵ However, when IABP is combined with revascularization (via thrombolysis, angioplasty, or surgery), it appears that IABP improves both short- and long-term survival, though patient selection remains a confounding factor in these trials. As was noted above, in the setting of cardiogenic shock or hypotension, the rate and degree of thrombolysis are depressed.⁸⁷ Additional work with canine models demonstrated improvement in the rate and degree of thrombolysis as well as the time to reperfusion when IABP was added to thrombolytic therapy.^89,90 Observational studies in humans confirmed an advantage for IABP when it was used with thrombolytics.^118,119

The GUSTO-1 trial was a large randomized trial that investigated the benefits of thrombolysis. In this trial, analysis of patients with cardiogenic shock who had an IABP placed on hospital day 0 or 1 showed a trend toward improved short-term survival (30-day mortality 48 vs 59 percent) when IABP was used and a significant reduction in 1-year mortality (57 vs 67 percent, p = 0.04).¹²⁰ The trend toward improved 30-day mortality with IABP remained when only patients undergoing revascularization were analyzed (47 vs 64 percent).¹²⁰ However, the 310 patients included were not randomized to IABP therapy, and the IABP group had significantly higher use of inotropes, pacemakers, pulmonary artery catheters, diagnostic angiography, and revascularization (both percutaneous and surgical). Most of the difference in survival occurred in the first days; this might have been due to earlier use of IABP but also might have resulted from selection of patients with a better prognosis for more aggressive interventions (including IABP and revascularization).

The larger SHOCK registry included nearly 900 patients who were collected prospectively but not randomized. Analysis of this group showed that patients with IABP use had lower in-hospital mortality than did those without it whether thrombolysis was used (47 vs 63 percent) or not (52 vs 77 percent).¹²¹ Unfortunately, these data also were subject to significant selection bias, and the groups that had the best outcomes included those individulas who underwent revascularization regardless of the adjunctive treatment (thrombolysis with or without IABP support) they received. These results were supported by an analysis of the 23,180 patients with cardiogenic shock enrolled in the National Registry of Myocardial Infarction-2. In this group, use of IABP improved 30-day survival in patients receiving thrombolytics (adjusted odds ratio 0.82; 95 percent CI 0.72–0.93), but a slight increase in mortality was noted in patients undergoing percutaneous coronary angioplasty (PTCA) who had placement of an IABP.

These data suggest that the improvement in thrombolysis noted in the canine models when IABP was used for patients in cardiogenic shock may result in a real improvement in outcomes in those patients.^89,90 For patients not receiving thrombolysis, significant patient selection bias exists in all these studies; however, it is clear that IABP alone does not improve survival over medical therapy. Its use, as with inotropic support, should be as an adjunct to maintain systemic and coronary perfusion and minimize infarct expansion before revascularization. Thus, in hospitals without cardiac catheterization capability, stabilization with IABP and transfer to a tertiary care facility may be the best option.⁶⁶ Although selection bias is again a confounding factor, retrospective analysis has suggested improvement in community hospital survival (93 vs 37 percent, p = 0.0002), transfer to a tertiary care center (85 vs 37 percent), and 1-year survival (67 vs 32 percent, p = 0.019) with the use of IABP in this setting.¹²² A recent retrospective study suggests that placement of an IABP prior to PCI results in decreased in-hospital mortality and incidence of major adverse cardiac events when compared to patients having IABP placed after PCI (19 vs 59 percent and 23 vs 77 percent, p = 0.007 and 0.0004, respectively).¹²³ After revascularization, prophylactic use of IABP for 48 h has been shown to maintain patency of revascularized arteries.¹²⁴ Weaning of the IABP should be performed before weaning from inotropic and pressor support except when limb ischemia intervenes.

Surgical Therapies

Multiple studies have shown that the patency of an infarct-related artery is an important predictor of LV function and mortality after acute MI.^125–131 In addition, most studies have demonstrated worse outcomes with increasing time between symptom onset and reperfusion.^{74,75,125,132} These findings were extrapolated to patients with cardiogenic shock, supporting an aggressive approach to early mechanical reperfusion for patients in shock after MI. Recently, prospective, randomized data in patients with post-MI cardiogenic shock have become available to define further the indications for and outcomes with emergent revascularization.

Angioplasty

The SHOCK trial enrolled 302 patients with post-MI cardiogenic shock resulting from LV dysfunction and randomized them to receive either optimal medical management (including IABP and thrombolysis) or emergent mechanical revascularization [either percutaneous coronary intervention (PCI)(PTCA with or without stenting) or coronary artery bypass surgery]. Revascularization in this group occurred on average within 1 h of randomization for patients undergoing PTCA and within 3 h for those undergoing CABG. There was a trend toward improved 30-day mortality in the revascularization group (46.7 vs 56.0 percent, p = 0.11) and a significant reduction in 6-month mortality (50.3 vs 63.1 percent, p = 0.027) and 1-year mortality (53 vs 66 percent, p = 0.025).^23,43,133 Patients who had successful angioplasty (TIMI grade 2 or 3¹³⁴) had very low mortality rates at 30 days (38 vs 79 percent, p = 0.003), and no patient who had a post-PCI occluded infarct artery survived (Fig. 31-5).^23,135 The only group that did not appear to benefit from a strategy of emergent revascularization were those over age 75 (30-day mortality 75.0 vs 53.1 percent, p = 0.01), although these results may have been affected by patient selection and a 25-percent revascularization rate before discharge among medically treated patients²³ and have been called into question by results from other studies.¹³⁶ The survival advantage seen in the early revascularization group remained at 3 and 6 years.¹³⁷ The importance of reducing time to reperfusion in patients with cardiogenic shock after MI has been reinforced by other nonrandomized studies.^138,139 In fact, the goal time period from presentation to the hospital to angioplasty balloon inflation (door-to-balloon time) is 90 min.¹⁴⁰ Significant predictors of poor outcomes in all patients include severity of MR,²⁶ initial TIMI flow, and culprit vessels other than the right coronary artery.⁴³

Stenting

Percutaneous coronary stenting has been shown to improve outcomes and reduce angiographic restenosis during elective PTCA.^141–144 Although there was initial reluctance to use stents in the setting of a potentially unstable coronary thrombus, randomized studies have demonstrated that stenting in the setting of acute MI can be performed safely.¹⁴⁵ Unfortunately, the largest studies have failed to demonstrate a survival benefit from the use of stenting in the setting of MI and instead have shown a trend toward increased mortality with the use of primary stenting (although some have shown reductions in combined endpoints such as recurrent ischemia, infarction, and angina).^144,146,147 However, none of these studies included patients with post-MI cardiogenic shock.

Among patients with cardiogenic shock, Antoniucci and associates described a short- and long-term survival advantage to stent placement over angioplasty alone; however, again, selection bias may have played a role in those patients.¹⁴⁸ Similar results to those for MI alone have been obtained in other nonrandomized trials.¹⁴⁹ The Global Registry of Acute Coronary events has provided observational data that suggest an improvement in outcomes (PCI with stenting predicted hospital survival: odds ratio 3.99, 95 percent CI 2.41–6.62).¹⁵⁰ Thus, some evidence exists to support the use of stents in patients with cardiogenic shock; even without strong prospective evidence, it has become common practice (as many as 85 percent of the patients enrolled in the SHOCK trial between 1997 and 1998¹³⁵). A prospective observational study utilizing the National Registry of Myocardial Infarction examined almost 300,000 patients presenting with ST elevation MI and cardiogenic shock. It was seen that patients undergoing primary PCI had decreased odds of death during the index hospitalization (odds ratio, 0.46; 95 percent CI, 0.40–0.53).¹⁵¹ Further prospective, randomized investigations are needed to define the indications for stent placement in patients with MI and cardiogenic shock.

Antiplatelet Agents.

Among patients who have stents placed after MI, antiplatelet agents have become standard practice, as they appear to reduce short-term restenosis and the need for repeat revascularization.^152–155 In nonrandomized trials, combination treatment with abciximab (a glycoprotein IIb/IIIa inhibitor) decreased 1-month overall mortality (18 vs 42 percent, p = 0.020) and improved TIMI flow in the infarcted artery compared with stenting alone.^156,157 However, these mortality rates are low, suggesting that the population studied may have been selected for more aggressive treatment. Additional large randomized trials are needed to assess the impact of adding antiplatelet agents to percutaneous stenting of stenosed arteries in patients with acute MI with cardiogenic shock. Currently all patients receiving drug eluting stents (DES) are placed on antiplatelet therapy for at least 1 year, as they are at increased risk for late in-stent thrombosis, a catastrophic complication.^158–161

Coronary Artery Bypass

Early outcomes with CABG in the setting of acute MI were poor,^162,163 but surgical revascularization within 6 h has shown to improve survival compared with medically treated patients.^164–169 These reports, however, were published as medical management was changing: Randomized trials were evaluating the efficacy of thrombolysis and PCIs in post-MI patients.^75,76,170 Unfortunately, CABG was not included in these studies. Furthermore, subsequent improvements in both interventional and surgical techniques may make comparisons to contemporary populations and treatments meaningless. Thus, the appropriate use of CABG in the setting of MI in general and cardiogenic shock in particular remains a matter of debate.

The results of the SHOCK trial demonstrated that early revascularization improved survival, and despite more severe disease, mortality in the group receiving CABG (guidelines for the use of emergent CABG included left main stenosis equal to or greater than 50 percent, stenoses greater than 90 percent in two nonculprit major vessels, and patients in whom PCI was unsuccessful or who had disease unsuitable for PCI) was similar to that in patients undergoing percutaneous interventions.²³ Large observational studies support the selective use of CABG in patients with cardiogenic shock; although patients in Killip class IV have seven times the CABG-associated mortality of those in Killip class I, mortality in this group is 27 percent, substantially lower than that in patients who do not receive revascularization and comparable to survival in patients undergoing PCI.¹⁷¹ Although surgery within 3 days of transmural and 6 h of nontransmural MI has been associated with a higher mortality rate (Table 31-4),^172,173 Lee and associates documented decreased early mortality rates when operation occurs before 18 h in patients with cardiogenic shock (7 vs 31 percent).¹⁷⁴ Thus, in patients with ongoing ischemia or cardiogenic shock that is not amenable to medical stabilization, early revacularization with CABG is indicated; however, when possible, surgery should be delayed, especially in patients with transmural infarction.

Unfortunately, randomized data are not available, and the optimal indications for CABG in the setting of MI and cardiogenic shock remain ill-defined. In light of the excellent results obtained with thrombolysis and percutaneous revascularization, CABG probably will not become a primary therapy after MI whether or not cardiogenic shock intervenes; instead, it is best reserved for specific indications for which percutaneous revascularization is unsuccessful or inappropriate. One such indication for CABG surgery may be cardiogenic shock in the setting of left main coronary artery infarction. A recent study demonstrated that patients undergoing CABG in this situation had better survival at 30 days than those having PCI, 40 percent in the surgical group (n = 6) and 16 percent in the PCI group (n = 15; p = 0.03).¹⁷⁵ In addition, current American College of Cardiology/American Heart Association Guidelines Committee recommendations for initial reperfusion therapy in patients with three-vessel coronary disease in cardiogenic shock from AMI is CABG.¹⁷⁶

Perioperative Considerations.

When emergent revascularization by CABG is indicated, timing is important and rapid transport to the operating room is critical; however, some techniques are available to assist in maintaining coronary and systemic perfusion during transport. As was noted above, the use of IABP is preferable to the use of inotropes and vasopressors because of the improvement in myocardial oxygenation and workload. In patients with circulatory collapse, percutaneous cardiopulmonary bypass (CPB) may be initiated via the femoral artery and vein. Flow rates of 3.5 to 5.0 L have been obtained with this method.¹⁷⁷

Once the patient is in the operating room, anesthetic induction may lead to catastrophic hypotensive circulatory collapse. It is important that both surgery and perfusion teams be prepared for decompensation before the onset of anesthesia. Although the specific type of anesthetic agent used does not appear to alter myocardial oxygen utilization efficiency significantly,¹⁷⁸ a rapid narcotics-based regimen has been recommended.¹⁷⁹ Rapid institution of CPB to provide perfusion to threatened myocardium is essential.

Patients undergoing emergent CABG have high mortality rates; bleeding may contribute to that rate by decreasing myocardial oxygen delivery. In addition, release of cytokines in response to large-volume transfusions as well as thromboxane A₂ release during CPB may worsen coagulopathy, pulmonary hypertension, and myocardial microvascular contraction responses worsening ventricular ischemia.¹⁸³

The choice of a conduit should not be altered from that for elective cases. Although most surgeons use saphenous vein grafts (SVGs) to minimize bypass time, internal mammary artery (IMA) grafting has not been associated with increased complications compared with saphenous vein grafting even in the setting of cardiogenic shock, and late results with IMA grafts are significantly better than those with SVG.^184–186 To reduce MI, harvesting of the IMA can be performed after the initiation of CPB, cross-clamping, and cardioplegia.

In all cases, both antegrade and retrograde cardioplegia should be used for myocardial protection to ensure the delivery of cardioplegia to ischemic areas. Both antegrade and retrograde catheters can be placed before placement of the aortic cross-clamp to ensure rapid delivery of cardioplegia to the entire myocardium. The placement of a “bail-out” catheter across stenotic regions during PCI may assist in the delivery of cardioplegia to ischemic regions.¹⁷⁷ Various authors have advocated a variety of techniques for myocardial protection, including hypothermic fibrillatory arrest,^187,188 oxygenated crystalloid cardioplegia,^187,189 blood cardioplegia,^190,191 and substrate-enriched blood cardioplegia.^187,190 However, in a series of experimental studies, Buckberg and coauthors developed specific modifications of the reperfusion process that reduce myocardial oxygen demand and reperfusion injury in ischemic myocardium. These experimental studies subsequently were validated clinically.¹⁹¹ Conditions favoring recovery of ischemic myocardium include the following: Decompression of the heart, which reduces myocardial oxygen demand by approximately 50 percent¹⁹²; cardioplegic arrest reduces oxygen demand by approximately 90 percent compared with a beating heart¹⁹³; myocardial metabolism is enhanced by warm blood cardioplegia that maintains normal energy production while decreasing energy demands¹⁹⁴; low perfusion pressure reduces postischemic edema¹⁹⁵; and prolonged reperfusion with cardioplegic arrest permits resuscitation of energy-depleted myocardium.¹⁹⁶ Therefore, the standard Buckberg protocol should be used to maximize myocardial protection in patients undergoing CABG who are in cardiogenic shock. This includes induction of cardioplegia with substrate-enriched warm blood cardioplegia for 3 to 5 min, followed by cold blood cardioplegia for 2 to 3 min and then by periodic small-volume infusions. In addition, an infusion of warm blood cardioplegia before removal of the cross-clamp (“hot shot”) may improve myocardial recovery.¹⁹⁷

The occluded artery supplying the largest region of ischemic but viable myocardium should be reperfused first. When vein grafts are used, after completion of the distal anastomosis, regional blood cardioplegia can be delivered to the ischemic area through a side branch of the graft while the proximal anastomosis is completed.

Ventricular Assist Devices and Heart Transplantation

In patients with cardiogenic shock refractory to maximal medical management and unimproved by percutaneous intervention or an IABP, implantation of a ventricular assist device (VAD) is a potentially lifesaving maneuver. Two classes of patients may benefit from the use of a VAD: (1) patients with stunned myocardium as a bridge to recovery and (2) patients with extensive infarction requiring a bridge to heart transplantation. Outside clinical trials, VADs are approved for use in patients pending transplantation; therefore, all patients should fulfill the general criteria for transplant recipient selection (Table 31-5).¹⁹⁸ Although complete evaluation is usually impossible in the acute setting, patients with obvious contraindications to transplantation (irreversible neurologic defects, coexisting active neoplasm, etc.) should not be considered for VAD implantation.

When used as a bridge to recovery for myocardial stunning, VAD implantation should be accompanied or preceded by mechanical revascularization, whether percutaneous or surgical. In this setting, the use of short-term VAD is appropriate. VADs suitable for short-term implantation include the Bio-medicus centrifugal pump and the Abiomed and Thoratec pumps. Although the centrifugal pump is easy to insert, it has a significant incidence of thromboembolic complications despite systemic heparinization, and its use largely has been supplanted by use of the pump devices.¹⁹⁹ The Abiomed VAD (AB5000) is a system recently approved by the Food and Drug Administration that consists of a fully automatic, vacuum-assisted console and a paracorporeal, pneumatically driven blood pump. The VAD is designed for short or intermediate termuse. The Thoratec pneumatically driven extracorporeal pump is also suitable for left, right, or biventricular short-term support and has the advantage of allowing significant patient mobility. Both devices require systemic anticoagulation. Percutaneous devices, such as the Abiomed Impella and the Cardiac Assist TandemHeart Pump, are being placed as a bridge to long-term VAD placement and bridge to recovery.^200,201

In patients with large infarcts without the potential for myocardial recovery, the insertion of a longer-term VAD is required as a bridge to transplantation. Historically, the two most commonly used pulsatile devices were the Heartmate XVE and Novacor pumps. Both are wearable, pulsatile intracorporeal VADs with only a driveline traversing the skin. The Heartmate has the advantage of requiring only aspirin for antiplatelet activity, not systemic anticoagulation; this is achieved through the use of textured blood contact surface that forms a stable biological lining that is resistant to thrombus formation.²⁰² The Novacor device was discontinued by its manufacturer, World Heart in 2008. It was the first mechanical circulatory support device to support a single patient for more than 6 years.

Other devices with different pump mechanisms have been developed (Table 31-6). The Heartmate II, a continuous-flow VAD, was approved for bridge to transplantation use in 2007. Direct comparison of the Heartmate XVE and II demonstrated increased survival without disabling stroke or need for device related reoperation [62 of 134 (46 percent) vs 7 of 66 (11 percent), p <0.001], and improved survival rates at 2 years (58 vs 24 percent, p = 0.008).²⁰³ After clinical stabilization of the patient, a complete evaluation for heart transplantation can proceed. In light of the potential for discovery of contraindications to transplantation after emergent placement of a VAD, consideration—including discussions with patients and families—must be given to the potential need to withdraw support in patients who are found to be unsuitable recipients for heart transplantation.

Outcomes and Prognosis

Survival after CABG for patients in cardiogenic shock or those receiving cardiopulmonary resuscitation (CPR) remains poor; 1- and 10-year survival rates are 59.4 and 47.5 percent.²⁰⁴ However, these rates compare favorably to medical therapy alone, in which mortality rates in excess of 65 percent at 1 year have been reported.¹³³ Predictors of poor outcomes after CABG in this population include extent of coronary disease, presence of drug-treated diabetes, and lower arterial pH at entry into the operating room.²⁰⁴

Summary

Cardiogenic shock after MI continues to occur in approximately 10 percent of patients who reach the hospital. Though improving slightly, mortality rates remain approximately 60 percent. Patients with hypoperfusion after acute MI should be evaluated rapidly with electrocardiography (ECG), chest x-ray, and echocardiography to determine the cause of shock. In those with cardiogenic shock, therapies should be directed toward stabilization of patients with IV fluid resuscitation, pharmacologic therapy as indicated, and rapid placement of an IABP to support coronary and systemic perfusion. Emergent revascularization with PCI or CABG is associated with improved long-term outcomes. VADs provide an important adjunct to revascularization by supporting circulation through the period of myocardial stunning and providing a bridge to transplantation, and potentially as destination therapy, when appropriate.