Cardiogenic Shock Differential Diagnoses
- Author: Xiushui (Mike) Ren, MD; Chief Editor: Henry H Ooi, MD, MRCPI more...
Diagnostic ConsiderationsRight ventricular infarctionAcute mitral regurgitationCardiac ruptureVentricular septal ruptureReversible myocardial dysfunction
Conditions to consider in the differential diagnosis of cardiogenic shock include the following:
Systemic inflammatory response syndrome
Acute coronary syndrome
Congestive heart failure and pulmonary edema
Pericarditis and cardiac tamponade
Papillary muscle rupture
Acute valvular dysfunction
Right ventricular 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 and right ventricular 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 right ventricular 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 systolic failure.
Regarding the management of cardiogenic shock due to right ventricular infarction, supportive therapy begins with the restoration and maintenance of right ventricular preload with fluid administration. However, excessive fluid resuscitation may compromise left ventricular filling by introducing an interventricular septal shift.
Inotropic therapy with dobutamine may be effective in increasing cardiac output in patients with right ventricular 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 right ventricle.
Revascularization of the occluded coronary artery, preferably by percutaneous transluminal coronary angioplasty (PTCA), is crucial for management and has shown to dramatically improve outcome.
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 2-dimensional (2-D) 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 based on echocardiography or left ventriculography findings before definitive therapy or surgery is initiated.
Hemodynamic stabilization by reducing afterload, either with nitroprusside or 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%.
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. Premortem 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.
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 right atrium and right ventricle, confirms the diagnosis. Alternatively, 2-D 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 emergent 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.
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 and interleukin 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.
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