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MD Consult: Books: Goldman: Cecil Medicine: Chapter 108 – CARDIOGENIC SHOCK

Goldman: Cecil Medicine, 23rd ed.

Copyright © 2007 Saunders, An Imprint of Elsevier

Chapter 108 – CARDIOGENIC SHOCK

David R. Holmes Jr.

Definition

Cardiogenic shock describes tissue hypoperfusion as a result of an acute myocardial infarction (MI) or end-stage heart failure from any cause. Cardiogenic shock can be defined by clinical parameters alone ( Chapter 107 ), including the manifestations of a low–cardiac output state with peripheral hypoperfusion and cool, clammy extremities, cyanosis, oliguria, and altered central nervous system function. An obligate requirement is the presence of hypotension. The degree of hypotension required to fulfill the criteria for shock has varied but is usually a systolic blood pressure less than 90 mm Hg; an alternative definition is a systolic blood pressure more than 30 mm Hg below the patient’s basal level. A confounding variable is the requirement for and use of vasopressors to maintain blood pressure. A previously normotensive patient who now requires vasopressors to maintain a systolic blood pressure of 90 mm Hg is also typically characterized as having cardiogenic shock. Although the clinical manifestations of hypoperfusion and systolic blood pressure less than 90 mm Hg are the hallmarks of shock, other important hemodynamic manifestations include an elevated left ventricular (LV) filling pressure greater than 15 mm Hg and a reduction in cardiac index to less than approximately 2.2 L/min/m2. In addition, many patients with end-stage heart failure, especially if treated with afterload-reducing agents ( Chapter 58 ), may have blood pressure readings chronically less than 90 mm Hg but not be in shock.

Epidemiology

Acute Cardiogenic Shock

The incidence of cardiogenic shock after an acute MI has varied from 5 to 19%. The incidence may be underestimated because some reports may exclude patients with shock on admission or may not represent the full spectrum of those with both ST segment elevation and non–ST segment elevation MI. When compared with patients with ST segment elevation, those with ST segment depression have approximately half the incidence of cardiogenic shock. The incidence of cardiogenic shock has also varied over time; earlier recognition of the symptoms of MI, earlier initiation of medical care, and the administration of thrombolytic therapy may have reduced the incidence. Typically, only a minority of patients with shock (approximately 10 to 15%) have it on admission. Shock develops in most patients within the next 48 hours. In a multicenter, country-wide survey from Denmark, shock developed in about 60% of patients within 48 hours, but in 30%, shock developed more than 4 days after the MI. In another study, only about 30% of patients had cardiogenic shock on admission, whereas it developed in the remainder later. When cardiogenic shock develops in patients without ST segment elevation, it usually develops relatively later, commonly as a result of reinfarction. As might be expected, previous MI, older age, diabetes mellitus, female gender, and a history of angina pectoris, stroke, or peripheral vascular disease have been associated with an increased incidence of cardiogenic shock, but the predictive power of these factors in an individual patient is limited. In a registry of more than 24,000 patients with acute coronary syndrome from 14 countries between 1999 and 2002, the incidence of cardiogenic shock increased from 1.6% in patients younger than 45 years to 10% in those 85 years or older. Patients with preexisting LV dysfunction are also at higher risk. Occasionally, cardiogenic shock develops in patients with severe myocarditis, especially postpartum cardiomyopathy.

Refractory Chronic Heart Failure

Many of the chronic causes of refractory heart failure result in sudden death as often as or more often than they result in hospitalization or home treatment for refractory low-output heart failure. Essentially every cause of heart failure ( Chapter 57 ), however, can result in a refractory low-output state with congestion and systemic hypoperfusion.

Pathobiology

Acute Cardiogenic Shock

Acute cardiogenic shock is typically the result of an extensive MI associated with damage to 40% or more of the LV myocardium, but other causes include a wide range of cardiac conditions ( Table 108-1 ). It does not seem to matter whether this loss of LV myocardium is the result of a single ischemic insult, with occlusion of a single artery that supplies a large region of myocardium, or a series of multiple previous MIs. The sequence of ischemic insults (i.e., a single catastrophic event or a series of multiple previous infarctions) may affect the time course of the shock, however. A single catastrophic event may result either in early shock or in sudden death, in contrast to patients with multiple smaller previous infarctions, in whom shock may develop after hospital admission. Multiple clinical factors have been associated with the development or outcome of shock ( Table 108-2 ). Autopsy and angiographic studies have documented that multivessel coronary artery disease is almost universally present, particularly involving the left main and left anterior descending coronary artery.


TABLE 108-1   — 
CARDIOGENIC SHOCK

   Acute myocardial infarction

   Pump failure
   Mechanical complication

   Ventricular septal defect
   Mitral regurgitation
   Ventricular rupture
   Tachyarrhythmia
   Valvular heart disease

   Acute mitral regurgitation
   Acute aortic regurgitation
   Aortic or mitral stenosis and acute comorbid condition, e.g., infection, anemia, tachyarrhythmia
   Prosthetic valve dysfunction
   Traumatic cardiac injury—penetrating or blunt
   Myocarditis
   Orthotopic transplant rejection
   Peripartum cardiomyopathy
   Pericardial disease with effusion
   End-stage low-output heart failure

TABLE 108-2   — 
RISK FACTORS FOR CARDIOGENIC SHOCK COMPLICATING ACUTE MYOCARDIAL INFARCTION

Factors Associated with the Development of Shock Factors Associated with Increased Mortality from Shock
Older age Older age
Diabetes mellitus Previous infarction
History of previous MI, stroke, or peripheral vascular disease Altered sensorium
  Peripheral vasoconstriction
  Baseline systolic blood pressure
Female gender Lower cardiac output
Reinfarction Higher heart rate
Initial EF <35%  
Lack of compensatory hyperkinesis in remote segments  

EF = ejection fraction; MI = myocardial infarction.

Infarct extension or reinfarction is common in patients with shock and is often the mechanism responsible for shock. Among the multiple factors that may be involved in infarct extension or expansion are impaired collateral flow, increased myocardial oxygen consumption, thrombus propagation or embolization, and passive collapse or vasoconstriction at a second site within the coronary circulation as a result of low coronary perfusion pressure during diastole. In patients with hypertensive cardiovascular disease and LV hypertrophy or aortic stenosis, the hypotension and elevated LV end-diastolic pressure may cause or aggravate diffuse subendocardial ischemia. Other important factors that can aggravate shock include anemia, poor oxygenation, and in some patients, inappropriately decreased peripheral arterial resistance.

The mechanical complications of mitral regurgitation, ventricular septal defect (VSD), or rupture of the LV myocardium account for 15 to 25% of cases of acute cardiogenic shock. The underlying MI may be only small or moderate in size but can involve crucial structures, such as the interventricular septum or papillary muscle. Free wall rupture accounts for 10% of all deaths from MI and is typically associated with an ST segment elevation anterior MI. In this setting, shock may develop abruptly and be followed by circulatory collapse with electromechanical dissociation. Rupture of the interventricular septum may result in a single direct perforation or many complex serpentine tracts; this defect is also seen with ST segment elevation anterior MI. Partial or complete rupture of one of the papillary muscles may result in severe mitral regurgitation; the posteromedial papillary muscle is involved more frequently than the anterolateral papillary muscle because the former usually receives its blood supply from just one source, the posterior descending coronary artery. Cardiogenic shock is a distinct and well-recognized complication of a right ventricular MI, which is always associated with posterobasal infarction of the left ventricle. With occlusion of the proximal right coronary artery, right ventricular pump function decreases and the right ventricle dilates, thereby leading to a decrease in LV preload and subsequent hypotension.

Refractory Chronic Heart Failure

End-stage refractory heart failure can be the final stage of any of the diseases that cause chronic heart failure ( Chapter 57 ). In these patients, key issues include evaluation of the underlying disease process, the development of new comorbid conditions, compliance with medication, and the adequacy of long-term therapy ( Table 108-3 ).


TABLE 108-3   — 
REASONS WHY CHRONIC HEART FAILURE MAY DECOMPENSATE WITH CARDIOGENIC SHOCK

   Development of new comorbid condition

   Infection/sepsis
   Renal insufficiency
   Uncontrolled diabetes
   Anemia
   Pulmonary embolism
   Hypothyroidism/hyperthyroidism
   Cardiac rhythm disorders—atrial fibrillation, bradycardia
   Progression of underlying disease

   Myocardial ischemia
   Chronic renal insufficiency
   Uncontrolled hypertension
   Patient compliance

   Poor compliance with the drug therapy regimen
   Dietary indiscretion
   Alcohol
   Drug therapy

   Inadequate doses of beneficial drugs
   Failure to prescribe beneficial drugs
   Over- or under-diuresis
   Sudden alteration in drug therapy
   Drug interactions
   Cardiotoxic medications
Clinical Manifestations

Cardiogenic shock is manifested as tissue hypoperfusion. Hypotension is usually defined as systolic blood pressure less than 90 mm Hg or more than a 30–mm Hg decrease in systolic blood pressure from baseline, although the latter criterion includes a larger group of patients who may not have shock or who have a milder form of shock. The term preshock has been used to define some of these patients. The prognosis of patients with preshock may be substantially better than that of patients with full-blown shock. Hypoperfusion is recognized by altered sensorium, cyanosis, oliguria, and cool, clammy extremities. Attendant dyspnea and ongoing ischemic chest pain may be present.

This constellation of findings may be noted at the initial evaluation for acute MI, but they more frequently develop later, 48 hours after the onset of MI. Either bradycardia, usually a manifestation of the Bezold-Jarisch reflex, or tachycardia may be present. Acute myocarditis with shock is also characterized by hypoperfusion; marked fluid retention may be prominent if the myocarditis has been present for several days to weeks. When accompanied by low blood pressure and systemic hypoperfusion, the clinical manifestations of refractory heart failure may be indistinguishable from those of acute cardiogenic shock.

Physical Examination

The physical examination should be focused on identification of hypoperfusion, volume status, and secondary causes of shock. Typically, venous pressure is elevated. The presence of low venous pressure identifies a group of patients who usually have hypovolemia rather than cardiogenic shock as a predominant cause; correction by fluid administration may lead to an improved outcome ( Chapter 107 ). Concomitant pulmonary edema ( Chapter 58 ) may be present, which in a hypotensive patient establishes the diagnosis of cardiogenic shock. In patients with a mechanical complication resulting in shock, the physical findings may not be typical of the underlying cause. Patients with acute mitral regurgitation may not have a systolic murmur because of equalization of pressure between the left ventricle and left atrium ( Chapter 75 ); in these patients, a high index of suspicion is required so that appropriate tests (e.g., LV angiography or echocardiography) can be performed to make the definitive diagnosis. In patients with a VSD, the systolic murmur may be at the lower left sternal border without a thrill. Patients with a free wall rupture commonly demonstrate electromechanical dissociation, which is almost uniformly fatal. In patients with myocarditis, a pericardial or pleuropericardial rub may be present.

Diagnosis

Noninvasive Evaluation

Electrocardiogram

In patients with circulatory collapse, an initial electrocardiogram (ECG) is essential. In acute cardiogenic shock caused by acute MI, ST segment elevation is the most common finding, although cardiogenic shock can occur without it. ST segment depression or nonspecific ST segment changes may occur in approximately 25% of patients. The ECG also provides information on previous MI and rhythm disorders. Isolated elevation of the ST segment in lead aVR in a patient with acute MI and shock suggests the possibility of left main coronary artery involvement. In patients in whom right ventricular MI is suspected, modified right precordial leads are helpful ( Chapter 52 ). In acute myocarditis, ECG abnormalities are usually diffuse. Tachyarrhythmias are common, especially sinus tachycardia or atrial fibrillation; in some patients, new intraventricular conduction defects may be seen. When cardiogenic shock complicates end-stage heart failure, the ECG may reflect extensive previous MI, interventricular conduction defects, or bundle branch blocks.

Echocardiography

Echocardiography ( Chapter 53 ) is extremely useful in the evaluation of a patient with shock ( Fig. 108-1 ). It can make the diagnosis of a mechanical complication, such as a ruptured papillary muscle or a VSD. In addition, echocardiography can assess overall LV function, including compensatory hyperkinesis of noninfarcted segments. Patients with cardiogenic shock from a large MI can be expected to have severe regional wall motion abnormalities. Severe diffuse hypokinesis may suggest cardiomyopathy as the cause of shock, whereas a flail mitral leaflet would suggest acute mitral regurgitation ( Chapter 75 ). Both short- and long-term mortality are associated with worse initial LV function and more mitral regurgitation as assessed by echocardiography. In patients in whom free wall rupture is suspected, echocardiography can document a pericardial effusion ( Chapter 77 ).

FIGURE 108-1  Role of echocardiography in assessing the cause of cardiogenic shock. AR = aortic regurgitation; AS = aortic stenosis; CHD = coronary heart disease; ECG = electrocardiogram; HOCM = hypertrophic obstructive cardiomyopathy; LVEF = left ventricular ejection fraction; MI = myocardial infarction; MR = mitral regurgitation; MS = mitral stenosis; PA = pulmonary artery; RV = right ventricle; VSD = ventricular septal defect.

Although echocardiography is a vital tool, it must be performed expeditiously, particularly in the setting of an acute ischemic event. Other procedures, most importantly urgent cardiac catheterization in patients with acute MI ( Chapter 56 ), should not be delayed excessively while echocardiography is being considered or performed. LV angiography can yield extremely important data on ventricular and valvular function.

Invasive Evaluation

Pulmonary Artery Catheterization

Right heart catheterization with flow-directed catheters can sometimes be useful by documenting low LV filling pressure in patients with hypovolemic shock or right ventricular infarction, giant v waves in patients with unsuspected severe mitral regurgitation, or an oxygen saturation gradient in a patient with a VSD.

Differential Diagnosis

Acute Cardiogenic Shock

In the acute setting, cardiogenic causes of shock must be distinguished from septic and other causes of shock (see Fig. 107-2 ). Even in cardiac patients, shock can be due to noncardiogenic causes, including hypotension caused by medications such as nitrates, angiotensin-converting enzyme inhibitors, other vasodilators, or streptokinase; hemorrhage from anticoagulant or thrombolytic drugs; pulmonary embolism ( Chapter 99 ); or hypovolemia. The diverse causes of cardiogenic shock must be kept in mind (see Table 108-1 ). Although the classic cause is pump failure secondary to extensive LV damage, right ventricular infarction can also lead to cardiogenic shock if associated posterior LV infarction is present ( Chapter 72 ). In addition, the differential diagnosis of acute cardiogenic shock includes the mechanical causes of mitral regurgitation from papillary muscle rupture or dysfunction, rupture of the LV free wall, and VSD. In a large registry, acute shock was due to predominantly LV failure in 74.5% of patients but was related to acute severe mitral regurgitation in 8.3%, ventricular septal rupture in 4.6%, and isolated right ventricular shock in 3.4%. Cardiogenic shock may also result from other cardiac conditions, such as aortic stenosis ( Chapter 75 ) or pericardial tamponade ( Chapter 77 ), the latter of which may be the result of an ascending aortic dissection ( Chapter 78 ) that propagates in retrograde fashion, with shearing of the right coronary artery and then creation of a rupture into the pericardium. Cardiac arrhythmias, such as atrial fibrillation with a rapid ventricular response ( Chapter 63 ) or ventricular tachycardia ( Chapter 64 ), may contribute to hypotension. Myocarditis ( Chapter 59 ) can also result in shock.

The clinical circumstances and time course of shock often provide important clues to specific causes. Given the diverse number of disease states that may cause shock ( Chapter 107 ), identifying the specific cause is important because it may mandate a different treatment strategy and may affect the prognosis.

Refractory Chronic Heart Failure

Patients with end-stage refractory heart failure ( Chapters 57 and 58 ) may also have severe hypoperfusion, but in general, shock develops more slowly than in patients with acute MI. In patients with chronic heart failure, blood pressure may be less than 90 mm Hg in the absence of shock, especially if aggressive afterload reduction therapy is being administered; in these individuals, fluid overload may precipitate cardiogenic shock.

Treatment

Medical Therapy

The prognosis of patients with cardiogenic shock is poor. Supportive measures, such as maintenance of adequate oxygenation and treatment of arrhythmias, are essential, and documentation of volume status is important. Attempts to improve blood pressure are crucial to break the vicious cycle of progressive hypotension leading to further myocardial ischemia. If LV filling pressure is elevated as assessed by either hemodynamic monitoring or the presence of pulmonary edema, further volume expansion is not beneficial and may be harmful. If volume status is uncertain, a trial of volume expansion is warranted with careful monitoring. Monitoring of left-sided heart pressure with periodic wedge recordings can help optimize filling pressure during the initial attempts at stabilization. Hemodynamic monitoring is also extremely useful for initiating aggressive afterload reduction. Nevertheless, routine use of pulmonary artery catheters to guide therapy does not improve the outcome.[1] Furthermore, in some patients the relationship between central venous pressure and pulmonary capillary wedge pressure may be sufficiently consistent to allow the physician to monitor only central venous pressure. Urine output should also be monitored.

Vasopressor therapy (see Table 107-5 ) is usually essential to improve cardiac performance and stabilize the patient; its risks include aggravation of arrhythmias and, even more importantly, an increase in myocardial oxygen demand. Dopamine, which is generally the initial drug given, can increase systemic pressure and cardiac output. Dobutamine may be used in combination with dopamine to augment cardiac output, but it does not usually increase arterial pressure further. Levosimendan, a calcium sensitizer, may be better than dobutamine in low-output heart failure.[2] In patients who have severe or resistant hypotension, norepinephrine is commonly given and may be effective. In general, myocardial oxygen demand can be minimized by titrating vasopressive agents to the lowest dose required to optimize blood pressure and maintain adequate cardiac output. Vasodilators, such as intravenous nitroglycerin or nitroprusside, are not generally used initially because they can aggravate hypotension; however, they may be given later in combination with vasopressors and inotropic agents. The effectiveness of all inotropic agents may diminish over time, so these drugs are not usually definitive therapies. Milrinone, a second-generation phosphodiesterase inhibitor, should not be used because of its substantial vasodilatory properties.

In patients with acute MI, aspirin and heparin are important and serve as baseline treatments. Thrombolytic drugs have been used widely for acute MI, but most trials have not included patients with preexisting cardiogenic shock. The benefit of thrombolysis has been equivocal, with some trials showing no benefit and others showing a small benefit. This equivocal benefit may be related to multiple factors, including (1) poor delivery or penetrance of lytic agents to the thrombus because of the hypotension and (2) impaired transformation of plasminogen to plasmin because of acidosis. To negate the effect of these factors as much as possible, thrombolytic therapy in patients with shock or preshock should be accompanied by vigorous attempts to augment blood pressure and treat acidosis. Thrombolysis may reduce the subsequent development of shock, perhaps because of a decrease in reinfarction or limitation of the size of the initial infarct.

Inhaled nitric oxide, 80 ppm, can result in a significant decrease in right atrial and mean pulmonary arterial pressure and an increase in the cardiac index. However, a large randomized trial showed that use of a nitrous oxide synthetase inhibitor was of no clinical benefit.

Mechanical Therapy

Insertion of an intra-aortic balloon pump (IABP) for counterpulsation increases diastolic coronary artery perfusion pressure, decreases LV afterload, improves cardiac output, and decreases myocardial oxygen demand. An IABP can stabilize hemodynamics and improve survival at 30 days and 1 year in acute cardiogenic shock complicating acute MI.[3] However, the currently available data suggest that IABP is underused.

A variety of percutaneous partial cardiopulmonary bypass techniques can be performed in the acute or chronic setting, but these devices are used only in specialized centers because of the need for special equipment. Partial LV assist devices decrease myocardial oxygen demand while maintaining or augmenting perfusion and may provide an important adjunct to myocardial salvage. In one randomized trial of patients with end-stage heart failure, an implantable LV assist device improved survival and quality of life.[4] Clinical trials are also under way to test whether devices that lower body temperature to approximately 33° C can improve outcome.

Surgical Therapy

Revascularization

Urgent percutaneous intervention (PCI) ( Chapter 73 ) has been advocated for cardiogenic shock in the setting of acute MI based on nonrandomized data and subset analysis of large randomized trials. In the one randomized trial that focused exclusively on cardiogenic shock in acute MI, early coronary revascularization within 6 hours was compared with medical stabilization and IABP followed by delayed coronary revascularization. The primary end point, 30-day mortality, was not significantly different in the two groups (46.7% in the early revascularization group vs. 56.0% in the initial medical stabilization group). At 6 months, however, mortality in the revascularization group was significantly lower (50.3 vs. 63.1%, P = .027), and the benefit was greatest in patients younger than 75 years.[5] Other nonrandomized data also suggest improved survival in patients older than 75 years.

In clinical trials and in clinical practice, PCI is generally combined with other adjunctive therapies, such as IABP, which is typically placed before treatment. Historically, only the infarct-related artery was treated at the initial PCI, unless the patient had multivessel disease with other critical lesions and was not helped by PCI of the infarct-related artery. With the advent of coronary stents ( Chapter 73 ), it may be possible to treat all significant stenoses and provide more complete revascularization. Adjunctive therapy with glycoprotein IIb/IIIa inhibitors may be helpful, although these drugs may complicate the situation by increasing the potential for bleeding in patients in whom surgery is subsequently required.

Coronary stents provide improved angiographic success for PCI, and this higher angiographic success rate has been associated with improved 30-day survival. The additional benefit, if any, of newer adjunctive pharmacologic agents and new devices that prevent distal embolization is unknown, but they are currently being tested.

Coronary artery bypass graft (CABG) surgery ( Chapter 74 ) has potential advantages, including the ability to achieve complete revascularization and the opportunity to vent the ventricle and cool the heart with cardioplegia to limit ongoing ischemia and reduce myocardial oxygen consumption. There are currently no randomized studies, however, comparing CABG surgery with PCI or medical therapy. Despite the likelihood that aggressive revascularization with either PCI or surgery will improve survival in cardiogenic shock, these approaches appear to be underused, particularly in older patients.

Other Surgical Procedures

In patients with mechanical complications, surgery often provides the only therapeutic approach. If possible, these patients should be stabilized before surgery, often with an IABP. In patients with a VSD or severe mitral regurgitation, surgery can improve the outcome dramatically despite high operative mortality rates. Free wall rupture is commonly accompanied by electromechanical dissociation and is almost always fatal. Subacute rupture with false aneurysm formation is rare, but it can be treated surgically with suture or patch closure when it is diagnosed in time. In patients with shock from mechanical causes not related to acute MI, such as ruptured chordae or severe acute aortic regurgitation, surgical approaches are required. In some patients (e.g., those with ruptured chordae), placement of an IABP may improve cardiac performance substantially and reduce the risk associated with surgery.

Recommended Current Approach

Acute Myocardial Infarction

At present, an aggressive approach seems to have the most potential to improve outcome ( Fig. 108-2 ). Management requires rapid evaluation of the multiple potential causes of shock in parallel with supportive therapy designed to improve perfusion and optimize right ventricular and LV pressure. An IABP and right heart catheterization are helpful for stabilization, management, and diagnosis. Catheterization can detect an increase in oxygen saturation in the right ventricle as found in a post-MI VSD ( Chapters 68 and 72 ). Revascularization with either emergency percutaneous transluminal coronary angioplasty or CABG surgery seems to confer early and longer-term survival benefits in eligible patients, although the problem of selection bias and its effect on outcome must be kept in mind.

Acute Myocardial Disease

General supportive measures ( Chapter 58 ) are the cornerstone of therapy for severe heart failure. If the patient is in shock despite supportive measures, circulatory support with either an IABP or LV or biventricular assist devices should be considered. Some patients may have spontaneous recovery of ventricular function; alternatively, circulatory support may be used as a bridge to heart transplantation ( Chapter 82 ). Specific therapies, such as steroids and cyclosporine or azathioprine, may be helpful in specific patient groups (e.g., those with idiopathic giant cell myocarditis or sarcoidosis), but not in patients with nonspecific myocarditis ( Chapter 59 ).

Refractory Chronic Heart Failure

In patients with refractory chronic heart failure, medical therapy is generally similar to therapy for acute cardiogenic shock. Mechanical and surgical interventions, including cardiac transplantation ( Chapter 82 ), can benefit selected patients ( Chapter 58 ).

FIGURE 108-2  Acute myocardial infarction with hypotension: an aggressive approach. ASA = acetylsalicylic acid (aspirin); CABG = coronary artery bypass graft; IABP = intra-aortic balloon pump; LV = left ventricular; MI = myocardial infarction; PTCA = percutaneous transluminal coronary angioplasty.

Prognosis

Acute Cardiogenic Shock

Cardiogenic shock now accounts for most deaths related to acute MI. Before the era of reperfusion, mortality from cardiogenic shock approximated 80%. In the larger thrombolytic trials, mortality rates remain at 51 to 70%. Although findings such as altered sensorium and peripheral vasoconstriction are important predictors of prognosis, cardiac output and wedge pressure measurements add essential independent information regarding prognosis and increase the ability to identify patients at greatest risk of dying of cardiogenic shock. Cardiac power, which is a function of the product of cardiac output times mean arterial pressure, measures the rate of energy input that the systemic vasculature receives from the heart and is also a strong predictor of outcome in cardiogenic shock.

In selected series of shock patients, an aggressive strategy consisting of placement of an IABP followed by revascularization, either by PCI or by CABG surgery, may reduce 30-day mortality to 30 to 40%. The outlook in patients who survive for 1 month is good; among 1-month survivors, 85 to 90% are alive at 1 year. This survival rate is better in patients who have undergone coronary revascularization.

The prognosis in patients with myocarditis and shock is variable and depends on the underlying cause ( Chapter 59 ). Some patients can be supported by a mechanical circulatory device until spontaneous recovery occurs or a heart transplant is available ( Chapter 82 ).

Refractory Chronic Heart Failure

Except in patients who may benefit from specific mechanical or surgical interventions, the prognosis of patients with refractory chronic heart failure is bleak ( Chapter 58 ).

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