CARDIOGENIC SHOCK

The initial development of coronary care units and rapid cardioversion or defibrillation of life-threatening ventricular arrhythmias, followed by risk-factor modification and such major advances as thrombolytic therapy and emergency revascularization, have contributed significantly to the successful care of the acute myocardial infarction patient. To understand the reasons for the continued high mortality rates in cardiogenic shock patients, it is important to understand the pathophysiology of cardiogenic shock and to examine the optimal treatment strategies that may improve mortality rates. In a strict sense, cardiogenic shock syndrome develops as a result of cardiac muscle failure (either right or left ventricle) that causes inadequate cardiac output. The cardiovascular system can contribute in a number of other ways to the development of shock: hypovolemia, mechanical problems, nonischemic valve lesions, arrhythmias, and abnormalities of diastolic filling. Although the primary focus of this chapter is cardiogenic shock that is due to muscle failure, there is also some discussion of other mechanical causes associated with acute myocardial infarction.
A number of definitions have been proposed; although they differ in some ways, there is general agreement that both hemodynamic and clinical parameters should be included. The hemodynamic criteria include a systolic blood pressure less than 80 mm Hg (less than 90 mm Hg if the patient is on pressors, inotropic agents, or intraaortic balloon pumping) and cardiac index less than 2.2 L/min/m2. Clinical criteria require that signs of decreased peripheral perfusion be present, including cool clammy skin, cyanosis, altered mental status, and diminished urine output (less than 30 mL/h). The common denominator of the clinical findings is that they reflect a failure of tissue perfusion. Oxygen delivery is insufficient to sustain aerobic metabolism and therefore lactic acidosis is a metabolic consequence, regardless of the cause.
Using a combination of clinical and hemodynamic measurements means that fewer patients with only some symptoms (eg, low blood pressure but no signs of diminished tissue perfusion, or normal blood pressure with altered mental status or diminished urine output) are given an inappropriate diagnosis of shock.
Etiology
The most common cause of cardiogenic shock is acute myocardial infarction and is due to the loss of a large amount of myocardium. The incidence of shock in acute myocardial infarction is between 5% and 10%, and the mortality rate is extremely high in medically treated patients, ranging between 70% and 100%, a figure unchanged over the last several decades. Cardiogenic shock may occur in a patient with a massive first infarction, or it may occur with a smaller, recurrent infarction in a patient with an already substantially infarcted myocardium.
Mechanical complications of acute myocardial infarction can cause shock; ventricular septal rupture, papillary muscle rupture or dysfunction, and myocardial rupture are all associated with cardiogenic shock. Right ventricular infarction in the absence of significant left ventricular infarction or dysfunction can cause shock. Hypovolemia or hypovolemic shock, although distinct from cardiogenic shock by definition, may be an important contributor to the development of shock in acute myocardial infarction.
Refractory tachyarrhythmias or bradyarrhythmias, usually in the setting of left ventricular dysfunction, are occasionally a cause of shock, which can occur with either ventricular or supraventricular arrhythmias.
Cardiogenic shock may occur as the end-stage, final common pathway for any progressive myocardial dysfunction, including ischemic heart disease and idiopathic, hypertrophic, and restrictive cardiomyopathies.
Pathophysiology
In cardiogenic shock resulting from acute myocardial infarction, dysfunction of a large enough quantity of myocardium (if in the left ventricle, approximately 40% must be infarcted) occurs to prevent the heart from meeting its minimum work requirements as a pump. The initial event is obstruction of a coronary artery, usually the left anterior descending coronary artery in first infarctions, but it can be any artery when previous infarctions have caused significant cumulative myocardial damage. The obstruction decreases the oxygen supply, resulting in myocardial ischemia, which in turn leads to diminished myocardial contractility and impaired left ventricular function. The ensuing drop in cardiac output and blood pressure leads to decreased coronary perfusion, resulting in further ischemia and additional deterioration in left ventricular function. This process of ischemia leading to myocardial dysfunction leading to further ischemia and so on has been appropriately termed a vicious cycle. Prolonged serum enzyme elevations, rather than the characteristic rise and fall seen in acute myocardial infarction, also suggest a protracted, stuttering course. Evidence for this vicious cycle is also found in autopsy studies that show infarct extension at the edges of an infarct in addition to discrete, remote infarctions throughout the ventricle.
The majority of patients with shock in acute myocardial infarction have extensive coronary disease. In patients dying of cardiogenic shock, more than two thirds have severe three-vessel coronary artery disease.
Early studies of acute myocardial infarction identified clinical and hemodynamic subsets that had prognostic significance. The Killip classification is based on clinical subsets, as shown in Table 6–1. The Forrester classification uses hemodynamic instead of clinical subsets (Table 6–2). Although the Killip and Forrester subsets have somewhat different definitions, they very clearly establish the point that progressive worsening of left ventricular function, whether measured by clinical or by hemodynamic parameters, is associated with a poorer prognosis. The pathophysiology of cardiogenic shock in acute infarction complicated by mechanical problems is somewhat different. Acute severe mitral regurgitation from papillary muscle or chordal rupture markedly diminishes cardiac output, leading to pulmonary edema. The sympathetic nervous system response to cardiac failure results in increased afterload and a further increase in the regurgitant fraction, another example of a disastrous vicious cycle causing cardiogenic shock.

Table 6–1. Killip classification.

Table 6–2. Forrester classification.

Rupture of the myocardial free wall resulting in shock, a rare complication of acute myocardial infarction, generally occurs within 4–7 days and may account for 10–30% of all deaths from acute infarction. Acute bleeding into a relatively nondistendible pericardial space leads rapidly to pericardial tamponade and cardiovascular collapse.
Rupture of the ventricular septum with formation of a ventricular septal defect has an incidence of 2–4% in acute myocardial infarction. A large ventricular septal defect causes significant left-to-right shunting and right ventricular volume overload. As with acute mitral regurgitation, the sympathetic nervous system response results in increased afterload, thereby shunting a larger fraction of the cardiac output across the interventricular septum. Pulmonary congestion develops as a consequence of the right ventricular volume and pressure overload. Diminished forward cardiac output from the left ventricle leads to depression of blood pressure and the diminished tissue perfusion characteristic of shock.
Right ventricular infarction occurs in 10–20% of patients with inferior myocardial infarctions and may be a cause of cardiogenic shock. The degree of left ventricular function is variable and shock can occur even in the absence of 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 (preload). Markedly diminished left ventricular filling pressure, even with normal left ventricular contractility, causes decreased systemic cardiac output.
As noted earlier, 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 are associated with both a greatly diminished time for ventricular filling in diastole and loss of the atrial contribution to diastolic filling. The diminished preload causes decreased volume available for forward output and, by the Frank-Starling relationship for ventricular performance, diminished contractility. These factors, superimposed on an already impaired left ventricle, may be enough to result in cardiogenic shock.
Bradyarrhythmias do not generally result in diastolic filling abnormalities, although (as with tachyarrhythmias) loss of atrial systole may be a factor. The major problem here is diminished forward cardiac output caused by the slow heart rate. Because total cardiac output is a function of heart rate and stroke volume, a markedly decreased heart rate, especially with left ventricular dysfunction and reduced stroke volume, may result in shock.
Many forms of heart disease can result in an end-stage dilated and congested cardiomyopathy. These include hypertensive heart disease; ischemic heart disease; restrictive, idiopathic, and toxic cardiomyopathies; and cardiomyopathy secondary to endocrine disease. In all cases, the inexorable progression of myocardial disease, accompanied by the effects of volume and pressure overload, can ultimately lead to inadequate cardiac output and shock.
Chatterjee K: Pathogenesis of low output in right ventricular infarction. Chest 1992;102(Suppl 2):590S.
Hollenberg SM, Kavinsky CJ, Parrillo JE: Cardiogenic Shock. Ann Intern Med 1999;131(1):47.
Clinical Findings
Approximately half the patients destined to develop shock will present initially with shock; the other half will develop cardiogenic shock after admission to the hospital.
A. HISTORY

The symptoms and signs that precede the development of cardiogenic shock depend on the cause. Patients with acute myocardial infarction will generally have the typical history of acute-onset chest pain, possibly in the setting of known coronary artery disease. The mechanical complications of acute myocardial infarction all tend to occur several days to a week following the infarction. They may be heralded by chest pain, but they more commonly present abruptly as acute pulmonary edema or cardiac arrest. Patients with arrhythmias may have a history of symptoms, such as palpitations, presyncope, syncope, or a sensation of skipped beats, that suggest this cause. The patient may appear obtunded and lethargic as a result of decreased central nervous system perfusion. Regardless of the cause, however, by the time shock develops, the patient may be unable to give any useful history. Family members may be able to help by identifying any previous history of heart disease and providing the history of the present illness.
B. PHYSICAL EXAMINATION

1. Vital signs— Blood pressure is less than 90 mm Hg systolic in patients on pressors and less than 80 mm Hg in the untreated patient. Heart rate is commonly elevated from sympathetic stimulation, and the respiratory rate is generally increased as a result of pulmonary congestion.
2. Chest— The chest examination in most cases shows diffuse rales. Patients with right ventricular infarction or those who are hypovolemic may have less evidence of pulmonary congestion.
3. Cardiovascular system— Neck veins are commonly elevated, although they may be normal in hypovolemic patients. The apical impulse is displaced in patients with dilated cardiomyopathy, and the intensity of heart sounds is diminished in pericardial effusion or tamponade. A gallop rhythm, especially a third heart sound suggesting significant left ventricular dysfunction, may be present. A mitral regurgitation or ventricular septal defect murmur can help in establishing these causes. Patients with significant right heart failure may have such signs (on abdominal examination) as liver enlargement, a pulsatile liver in the presence of significant tricuspid regurgitation, or ascites in long-standing right heart failure.
4. Extremities— Peripheral pulses will be diminished, and peripheral edema may be present. Cyanosis and cool extremities are indicative of diminished tissue perfusion. Profound peripheral vasoconstriction can result in livido reticularis on the abdomen.
C. DIAGNOSTIC STUDIES

The diagnosis of cardiogenic shock is a clinical diagnosis based on hypotension and evidence of peripheral hypoperfusion. Information gathered from history, physical examination, and laboratory data—especially hemodynamic monitoring—will corroborate the diagnosis and give valuable information as to its cause. It must be stressed, however, that shock in general and cardiogenic shock in particular are clinical syndromes that are diagnosed by clinical criteria.
1. Electrocardiography— The electrocardiogram (ECG) is often helpful in distinguishing between causes of cardiogenic shock. Patients with coronary disease and acute myocardial infarction may show evidence of both old and new infarctions. Right-sided chest leads in patients with inferior myocardial infarctions can detect the presence of right ventricular infarction (ST elevation in V4R). Although the ECG readily aids in the diagnosis of arrhythmias contributing to cardiogenic shock, it is often not precise when shock is caused by problems other than acute infarction or arrhythmia.
2. Chest radiograph— The chest radiograph shows cardiomegaly and evidence of pulmonary congestion or edema in patients with severe left ventricular failure. Ventricular septal defect or mitral regurgitation associated with acute infarction will lead to pulmonary congestion but not necessarily cardiomegaly, however, particularly in patients suffering a first infarction. Findings of pulmonary congestion may be less prominent—or absent—in the case of predominantly right ventricular failure or hypovolemia.
3. Echocardiography— The noninvasive nature and ready availability of two-dimensional and Doppler echocardiography make these techniques suitable for immediate assessment of the patient in shock and a tremendous benefit in the bedside diagnosis and treatment of many types of heart disease. Information obtained by echocardiography includes assessment of right and left ventricular function (global as well as segmental), valvular function (stenosis or regurgitation), right ventricular pressures; and detection of shunts (eg, ventricular septal defect with left-to-right shunting), pericardial fluid, or tamponade. The echocardiogram is especially helpful in diagnosing the mechanical complications of myocardial infarction.
4. Hemodynamic monitoring— The use of Swan-Ganz catheters to measure pulmonary artery and pulmonary capillary wedge pressure (PCWP) is generally very useful, if not essential, in establishing the diagnosis and cause of cardiogenic shock and in planning and monitoring therapy. Patients with cardiogenic shock as a result of severe left ventricular failure have, by definition, elevation of the PCWP. The presence of a wedge pressure higher than 18 mm Hg in a patient with acute myocardial infarction indicates adequate intravascular volume. Patients with primarily right ventricular failure or significant hypovolemia may have normal or reduced PCWP. The presence of a large v wave on the PCWP tracing implies significant mitral regurgitation.
The value of hemodynamic monitoring lies in its ability to assist in optimizing the ventricular function and thereby tissue perfusion. The Frank-Starling relationship of cardiac performance (measured by cardiac output, stroke work, or stroke volume) as a function of filling pressure demonstrates that the performance of the heart will increase as filling pressure increases—up to a point. In the failing heart, this point is eventually reached where no further increases in performance are gained by additional increases in preload—the “flat” part of the curve. Serial measurements of cardiac performance and left ventricular filling pressure indicate the optimal preload (ie, the lowest preload at which cardiac work is optimized).
Monitoring of hemodynamic parameters also allows calculation of the afterload (systemic vascular resistance [SVR]), defined by the following equation:

Minimizing afterload is important because increasing afterload mimics the effect of decreased contractility, resulting in diminished cardiac output.
Right-side filling pressures (central venous or right atrial pressure) are commonly normal, except in the case of right ventricular infarction, pericardial tamponade, or preexisting pulmonary disease.
Hemodynamic definitions of cardiogenic shock, as noted previously, include a cardiac index 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. Small patients may be incorrectly diagnosed with shock if cardiac output alone is used.
5. Oxygen saturation— Venous O2 saturation may be helpful in two ways. The arteriovenous difference in oxygen content, which is a useful indicator of cardiac output, increases as more oxygen is extracted from the blood in the setting of low cardiac output. Serial determinations are especially useful in monitoring a patient’s course and response to therapy.
Oxygen saturations obtained while placing the Swan-Ganz catheter may also be helpful in diagnosing a ventricular septal defect. The shunting of oxygenated blood from the left ventricle to the right ventricle results in an oxygen saturation step-up when comparing venous oxygen saturation from the venae cavae with that obtained in the pulmonary artery.
Treatment
A. GENERAL

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. It is clear that 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 life-saving treatment can be carried out only when the cause is known (Table 6–3).

Table 6–3. Management of cardiogenic shock.

B. MECHANICAL COMPLICATIONS

Acute mitral regurgitation secondary to papillary muscle dysfunction or rupture or to ventricular septal defect is a true emergency when associated with cardiogenic shock. The only effective therapy for these catastrophes is surgical repair. 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 intraaortic balloon pumping (see section “Circulatory support devices”) are useful as temporizing measures only and should not delay surgical treatment.
Patients with ventricular free-wall rupture rarely survive if the rupture is massive and results in shock and pericardial tamponade. As is true with the other major mechanical problems, emergency surgical correction is the only hope for survival.
C. RIGHT VENTRICULAR INFARCTION

Cardiogenic shock may occur with right ventricular infarction and no or only minimal left ventricular dysfunction. The probability for long-term survival is excellent if the diagnosis is made promptly and appropriate treatment instituted. Hemodynamic data suggesting right ventricular dysfunction out of proportion to left ventricular dysfunction and ST elevation in lead V4R are most helpful in establishing the diagnosis. Initial treatment is 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 ventricle. Inotropic agents are usually necessary when the right ventricular failure is so profound that shock continues despite adequate volume administration. Vasodilators may be helpful in some circumstances, diminishing the right ventricular afterload, which would theoretically improve the cardiac output. Vasodilators such as nitroprusside, which affect both the arterial and venous systems, may actually decrease preload, however—to the point that right ventricular output is unchanged.
Patients with right ventricular infarction are dependent on atrial contraction. As a result, single-chamber ventricular pacing may be inadequate in patients who require pacing, and atrioventricular sequential pacing is required to improve cardiac output.
D. ARRHYTHMIAS

Arrhythmias contributing to cardiogenic shock are readily recognized with ECG monitoring and should be promptly treated. Tachyarrhythmias (ventricular tachycardia and supraventricular tachycardias) should be treated with electrical cardioversion. Bradyarrhythmias may respond to pharmacologic agents (atropine, isoproterenol) in some circumstances, but external or transvenous pacing may be required.
E. ACUTE MyOCARDIAL InFARCTION

In patients with cardiogenic shock caused by a large amount of infarcted or stunned myocardium, it has become increasingly clear that the only treatment that can decrease mortality is revascularization, with either coronary angioplasty or coronary artery bypass surgery (discussed later). A number of pharmacologic and nonpharmacologic measures may be helpful in stabilizing the patient prior to cardiac catheterization or surgery.
1. Ventilation-oxygenation— Because respiratory failure usually accompanies cardiogenic shock, every effort should be made to ensure adequate ventilation and oxygenation. Adequate oxygenation is essential to avoid hypoxia and further deterioration of oxygen delivery to tissues. The majority of patients with cardiogenic shock require mechanical ventilation with supplemental oxygen. Hypoventilation can lead to respiratory acidosis, which could exacerbate the metabolic acidosis caused by tissue hypoperfusion. Acidosis worsens cardiac function; it also makes the heart less responsive to inotropic agents.
2. Fluid resuscitation— Although hypovolemia is not the primary defect in cardiogenic shock, a number of patients may be relatively hypovolemic when shock develops following myocardial infarction. The causes of decreased intravascular volume include increased hydrostatic pressure and the increased permeability of blood vessels. Note that the physical examination may not always be helpful in determining the adequacy of left ventricular filling pressure. Furthermore, because the central venous pressure correlates poorly with PCWP in shock, it may not be useful, especially with a single reading. These facts underscore the importance of hemodynamic monitoring with a pulmonary artery catheter for an accurate assessment of left ventricular filling pressure. The optimal filling pressure is higher in patients with shock because the left ventricle is operating on a depressed function curve (less stroke volume for any given filling pressure). Generally, 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 resuscitation, when indicated by low or normal PCWPs, should be undertaken in boluses of 200–300 mL saline, followed by reassessment of hemodynamic parameters, especially cardiac output and PCWP.
3. Inotropic agents— A variety of drugs are available for intravenous administration to increase the contractility of the heart. Because the heart is operating on a markedly depressed Frank-Starling curve, a positive inotropic agent may improve the hemodynamic status significantly.
a. Digoxin— Although digoxin benefits patients with chronic congestive heart failure, it is of less benefit in cardiogenic shock because of its delayed onset of action and relatively mild potency (compared with other available agents).
b. Beta-adrenergic agonists— Dopamine is an endogenous catecholamine with qualitatively different effects at varying doses. At low doses (less than 4 µg/kg/ min) it predominantly stimulates dopaminergic receptors that dilate various arterial beds, the most important being the renal vasculature. Intermediate doses of 4–6 µg/kg/min cause b1-receptor stimulation and enhanced myocardial contractility. Further increases in dosage lead to prominent a-receptor stimulation (peripheral vasoconstriction) in addition to continued b1 stimulation. Dopamine improves cardiac output, and its combination of cardiac stimulation and peripheral vasoconstriction may be especially 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 vasodilation, and it has a much stronger b2 (arteriolar vasodilation) effect. The vasodilatory effect may be deleterious in the hypotensive patients because a further drop in blood pressure may occur. On the other hand, many patients with cardiogenic shock experience excessive vasoconstriction and inappropriately elevated afterload as a result of the natural sympathetic discharge or of 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.
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 for bradyarrhythmias responsive to its chronotropic effect.
Norepinephrine has even stronger a and b1 effects than dopamine and may be beneficial when a patient continues to be hypotensive despite large doses of dopamine (more than 20 µg/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 cannot be used for any extended time unless plans are made for definitive treatment. Beta-adrenergic agonists, which are extremely useful agents for improving the circulatory state of patients with cardiogenic shock, can also have adverse effects. Their ability to increase cardiac output is accompanied by an increased oxygen demand from enhanced contractility, a faster heart rate, and increased blood pressure—which can be harmful to the already ischemic myocardium. In addition, b-agonists can precipitate serious ventricular or atrial tachyarrhythmias.
c. Phosphodiesterase inhibitors— The intracellular mediator of b-adrenergic-receptor stimulation is cyclic adenosine monophosphate (cAMP), produced by adenylate cyclase after stimulation of the receptor. Cyclic-AMP in turn increases calcium influx into the cell, thereby increasing contractility. The phosphodiesterase inhibitors, such as milrinone and amrinone, inhibit the breakdown of cAMP by phosphodiesterase, prolonging its effect on cardiac contractility. These agents also act on cAMP produced at sites of b2 stimulation to prolong the vasodilatory effects. Phosphodiesterase inhibitors appear to have no advantage over the b-agonists in patients with cardiogenic shock.
4. Vasodilators— Vasodilation (especially of the arterioles to reduce afterload) is often necessary because of the increased levels of catecholamines and resultant peripheral vasoconstriction. Vasodilators are also useful in patients who require the enhanced contractility of b1 stimulation by an adrenergic agonist, even though the associated vasoconstriction (especially with dopamine) may inappropriately increase the afterload. In addition, the preload may be inappropriately high in many patients; here, a venodilator will be beneficial in reducing filling pressure (preload).
a. Nitroprusside— Nitroprusside is a direct-acting vascular smooth muscle relaxant, with a balanced effect (vasodilation of both the arterial and venous beds). It is commonly used in combination with an inotropic agent. Doses begin as low as 0.25–0.5 µg/kg/min and may go as high as 8–10 µg/kg/min. Even though nitroprusside is a very short-acting drug, hypotension is a common side effect, and close arterial pressure monitoring is required.
b. Phentolamine— Phentolamine is an a-antagonist that acts predominantly on arterial a receptors to produce vasodilation. It is not commonly used because of the tachycardia induced by the release of cardiac norepinephrine stores.
c. Nitroglycerin— Nitroglycerin is primarily a venodilator, although it may have some arterial effects at high doses. Its benefits arise from a decrease in pulmonary congestion and, through its coronary vasodilatory effects, a decrease in myocardial ischemia. It is not commonly used in cardiogenic shock, however, unless coronary vasospasm is thought to be contributing to myocardial ischemia.
5. Circulatory support devices— Among the mechanical devices developed to assist the left ventricle until more definitive therapy can be undertaken, the intraaortic balloon pump (IABP) has been in use the longest and is the most well studied.
The IABP is placed in the descending aorta 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 (to a level higher than systolic pressure) increases coronary perfusion as well as that of other tissues. The balloon deflates at the end of diastole, immediately before left ventricular contraction, abruptly decreasing the afterload and improving left ventricular ejection.
Indications for use of the IABP include shock from severe ischemia, severe ventricular failure (especially when used as a bridge to cardiac transplant), ventricular septal rupture, and mitral regurgitation. In both ventricular septal rupture and mitral regurgitation, the principal benefit is caused by the decreased afterload as the balloon deflates. This results in a larger fraction of the left ventricular volume being ejected into the aorta rather than into the left atrium (mitral regurgitation) or the right ventricle (ventricular septal rupture).
The complication rate, especially vascular damage, is significant because of the large catheter size. As a result, the IABP is contraindicated in patients with significant peripheral vascular disease. In selected cases the balloon can be placed in the descending thoracic aorta from an axillary cut-down. It must be remembered that although these devices can clearly improve hemodynamics in the short term, they cannot improve survival by themselves, reaffirming the importance of definitive treatment.
A number of other circulatory support devices have been developed in recent years. A percutaneous cardiopulmonary bypass device with large-bore catheters placed in the right atrium and the femoral artery is capable of creating flow rates of 3–5 L/min. Prosthetic left ventricles and various surgically placed left ventricular assistance devices have also been used in patients with cardiogenic shock as a bridge to cardiac transplant. Although anecdotal reports of their benefits are encouraging, none has yet been subjected to controlled studies for comparison with IABP.
6. Revascularization— Revascularization is the only definitive therapy shown to decrease mortality in patients who develop cardiogenic shock following myocardial infarction. Early, primarily retrospective, studies of coronary angioplasty or coronary artery bypass graft surgery (CABG) reported survival rates of 60–80% in revascularized patients compared with 0–30% survival rate with medical therapy alone. More recently the multicenter, randomized SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) trial showed a trend toward improved survival at 30 days in patients randomized to revascularization (either angioplasty or CABG). The survival benefit for revascularization became significant at 6 months, a benefit that persisted at 1 year. Of note, patients 75 years of age and older had worse survival rates with revascularization, a finding that was also seen in earlier nonrandomized studies. Many experts believe that the SHOCK trial was underpowered to show a mortality difference at 30 days and, based on the 6 month and 1 year data, now recommend emergency revascularization for patients with cardiogenic shock complicating acute myocardial infarction.
a. Coronary angioplasty— Studies of coronary angioplasty in cardiogenic shock have consistently found that older patients (65 years of age or older) do not appear to benefit from coronary angioplasty. It is also noteworthy that although the likelihood of survival appears to be much improved in patients with successful coronary angioplasty, it remains very low—around 20%—in those with failed angioplasty. Whether these patients should be offered any further CABG surgery is unclear at this time. Future research will be aimed at identifying patients at high risk for failed coronary angioplasty and determining any preferable alternatives.
b. Coronary artery bypass graft surgery— Emergency CABG has also been studied in patients with cardiogenic shock caused by acute myocardial infarction. As with coronary angioplasty, the studies are generally retrospective but also show an improved survival rate (60–80%) over patients treated medically. These benefits appear to be more consistent in trials reflecting post-1980 improvements in surgical techniques. Again, as in coronary angioplasty, elderly patients do not appear to benefit from CABG.
7. Thrombolytic therapy— Thrombolytic therapy is considered a reperfusion strategy comparable to coronary angioplasty for decreasing mortality rates in acute myocardial infarction patients without cardiogenic shock. It would seem logical that patients in cardiogenic shock might also benefit from thrombolytic therapy. This benefit, however, has not been realized. Analysis of survival data for thrombolytic trials of patients with cardiogenic shock have consistently shown mortality rates in the 70–80% range—no different from those treated conservatively. Thrombolysis has been less successful in patients with cardiogenic shock; the rates of reperfusion are lower. It has been suggested that the low flow state present in shock may explain this lack of benefit in that adequate cardiac output appears to be necessary for successful thrombolysis. If the patient is not a candidate for angioplasty or CABG, however, or if revascularization is not immediately available, there appears to be no harm from thrombolytic therapy—and it may succeed in some cardiogenic shock patients.
8. Other medical therapies— Platelet IIb/IIIa inhibitors have been studied extensively in recent years in the setting of acute coronary syndromes and with percutaneous coronary interventions. A retrospective analysis of one such trial showed that patients randomized to the IIb/IIIa inhibitor eptifibatide had a significant 50% absolute risk reduction for mortality at 30 days. This finding will need to be verified in future trials designed to prospectively evaluate the efficacy of IIb/IIIa inhibitors in cardiogenic shock.