Diagnostic Considerations
Conditions to consider in the differential diagnosis of cardiogenic shock include the following:
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Systemic inflammatory response syndrome (SIRS)
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Acute coronary syndrome (ACS)
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Aortic regurgitation
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Dilated cardiomyopathy
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Restrictive cardiomyopathy
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Congestive heart failure (CHF) and pulmonary edema
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Mitral regurgitation
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Pericarditis and cardiac tamponade
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Hypovolemic shock
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Papillary muscle rupture
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Acute valvular dysfunction
Right ventricular infarction
Right ventricular (RV) infarction occurs in up to 30% of patients with inferior myocardial infarction (MI) and becomes hemodynamically unstable in 10% of these patients. The diagnosis is made by identifying an ST-segment elevation in the right precordial leads (V3 or V4 R) and/or typical hemodynamic findings after right heart catheterization. These are elevated right atrial (RA) and RV end-diastolic pressures with normal to low pulmonary artery wedge pressure and low cardiac output.
Echocardiography findings can also be very helpful in the diagnosis of RV infarction. Patients with cardiogenic shock due to this condition have a better prognosis than do patients when compared to those with cardiogenic shock due to left ventricular (LV) systolic failure.
Regarding the management of cardiogenic shock due to RV infarction, supportive therapy begins with the restoration and maintenance of RV preload with fluid administration. However, excessive fluid resuscitation may compromise LV filling by introducing an interventricular septal shift.
Inotropic therapy with dobutamine may be effective in increasing cardiac output in patients with RV infarction. Maintenance of systemic arterial pressure in order to maintain adequate coronary artery perfusion may require vasoconstricting agents, such as norepinephrine. In unstable patients, an intra-aortic balloon pump (IABP) may be useful for ensuring adequate blood supply to the already compromised RV.
Revascularization of the occluded coronary artery, preferably by means of percutaneous transluminal coronary angioplasty (PTCA), is crucial for management and has been shown to improve outcome dramatically.
Acute mitral regurgitation
Acute mitral regurgitation is usually associated with inferior MI due to ischemia or infarction of the papillary muscle. It occurs in approximately 1% of MIs, and posteromedial papillary muscle is involved more frequently than anterolateral muscle. Acute mitral regurgitation usually happens 2-7 days following acute MI and manifests with an abrupt onset of pulmonary edema, hypotension, and cardiogenic shock.
Echocardiography findings are extremely useful in making a diagnosis. The two-dimensional (2D) echocardiographic image shows the malfunctioning mitral valve, and findings from a Doppler study can be used to document the severity of mitral regurgitation. Right-heart catheterization is often required for stabilizing the patient. Tall V waves identified on pulmonary arterial and wedge pressure waveforms indicate acute mitral regurgitation. However, the diagnosis must be confirmed by means of echocardiography or left ventriculography before definitive therapy or surgery is initiated.
Hemodynamic stabilization by reducing afterload, either with nitroprusside or with an IABP, is often instituted. Definitive therapy requires revascularization, if ischemia is present, and/or surgical valve repair or replacement, if a structural valvular lesion is present. The mortality rate in the presurgical era was 50% in the first 24 hours, with a 2-month survival rate of 6%.
Cardiac rupture
Rupture of the free wall of the left ventricle occurs within 2 weeks of the MI and may occur within the first 24 hours. The rupture may involve the anterior, posterior, or lateral wall of the ventricle.
Cardiac rupture often presents as sudden cardiac death. Antemortem symptoms include chest pain, agitation, tachycardia, and hypotension. This diagnosis should be considered in patients with electromechanical dissociation who have a history of anginal pain. Patients rarely, if ever, survive cardiac rupture.
Ventricular septal rupture
Approximately 1-3% of acute MIs are associated with ventricular septal rupture. Most septal ruptures occur within the week following MI. Patients with acute ventricular septal rupture develop acute heart failure and/or cardiogenic shock, with physical findings of a harsh holosystolic murmur and left parasternal thrill.
A left-to-right intracardiac shunt, as demonstrated by a step-up (>5% increase in oxygen saturation) between the RA and the RV, confirms the diagnosis. Alternatively, 2D and Doppler echocardiographic findings can be used to identify the location and severity of the left-to-right shunt.
Rapid stabilization using an IABP and pharmacologic measures, followed by emergency surgical repair, is lifesaving. The timing of surgical intervention is controversial, but most experts suggest operative repair within 48 hours of the rupture.
Ventricular septal rupture portends a poor prognosis unless management is aggressive. Immediate surgical repair of patients with ventricular septal rupture is reported to be associated with survival rates of 42-75%; therefore, prompt surgical therapy is imperative as soon as possible after the diagnosis of ventricular septal rupture is confirmed.
Reversible myocardial dysfunction
Other causes of severe, reversible myocardial dysfunction are sepsis-associated myocardial depression, myocardial depression following cardiopulmonary bypass, and inflammatory myocarditis. In older literature, this presentation is often referred to as cold septic shock. In these situations, myocardial dysfunction occurs from the effects of inflammatory cytokines, such as tumor necrosis factor (TNF) and interleukin (IL)-1.
Myocardial dysfunction may vary from mild to severe and may lead to cardiogenic shock. For patients in cardiogenic shock, cardiovascular support with inotropic agents may be required until recovery, which generally occurs after the underlying disease process resolves.
Differential Diagnoses
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Myocardial Ischemia
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Cardiogenic shock. This image was obtained from a patient with an acute anterolateral myocardial infarction who developed cardiogenic shock. Coronary angiography images showed severe stenosis of the left anterior descending coronary artery, which was dilated by percutaneous transluminal coronary angioplasty.
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Cardiogenic shock. This coronary angiogram from a patient with cardiogenic shock demonstrates severe stenosis of the right coronary artery.
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Cardiogenic shock. This coronary angiogram from a patient with cardiogenic shock reveals severe stenosis of the right coronary artery. Following angioplasty of the critical stenosis, coronary flow was reestablished. The patient recovered from cardiogenic shock.
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Cardiogenic shock. This electrocardiogram shows evidence of an extensive anterolateral myocardial infarction. The patient subsequently developed cardiogenic shock.
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Cardiogenic shock. The electrocardiogram tracing shows further evolutionary changes in a patient with cardiogenic shock.
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Cardiogenic shock. The electrocardiogram tracing was obtained from a patient who developed cardiogenic shock secondary to pericarditis and pericardial tamponade.
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Cardiogenic shock. A 63-year-old man was admitted to the emergency department with clinical features of cardiogenic shock. The electrocardiogram revealed findings indicative of wide-complex tachycardia, likely ventricular tachycardia. Following cardioversion, his shock state improved. Myocardial ischemia was the cause of the ventricular tachycardia.
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Cardiogenic shock. A short-axis view of the left ventricle demonstrates small pericardial effusion, low ejection fraction, and segmental wall motion abnormalities. Courtesy of Michael Stone, MD, RDMS.
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Cardiogenic shock. Pleural sliding in an intercostal space demonstrates increased lung comet artifacts suggestive of pulmonary edema. Courtesy of Michael Stone, MD, RDMS.
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Cardiogenic shock. HeartMate II Left Ventricular Assist Device. Reprinted with the permission of Thoratec Corporation.
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