Cardiogenic shock occurs when there is insufficient cardiac output to meet the metabolic demands of the tissues. It is most commonly caused by an acute myocardial infarction (AMI) with extensive cardiac tissue damage, impaired right ventricular cardiac contractility, or subsequent rupture of a papillary muscle. Other potential causes of cardiogenic shock include cardiotoxic drug effects, infection such as myopericarditis or endocarditis, and mechanical cardiac dysfunction caused by valvular disease, pulmonary embolism, cardiac tamponade, or myocardial contusion. Early treatment and stabilization of patients suffering from cardiogenic shock are important, as mortality approaches 50% for an AMI that is complicated by cardiogenic shock.
A hallmark of all types of shock is tissue hypoperfusion and the resulting end-organ manifestations of this lack of adequate blood supply. Cardiogenic shock generally presents with hypotension (systolic blood pressure [SBP] <90 mm Hg), although SBP may be greater than 90 mm Hg in some patients such as those with preexisting and uncontrolled hypertension. Sinus tachycardia is frequently seen, but may be absent particularly when patients are taking medications that can inhibit an appropriate tachycardic response, such as β-blockers. Evidence of end-organ tissue hypoperfusion in cardiogenic shock may include cool or mottled skin, oliguria, or altered mental status. Left ventricular failure can present with findings concerning for acute pulmonary edema, such as tachypnea, rales, wheezing, and frothy sputum. Patients with hypotension who have jugular venous distention without pulmonary edema may be suffering from right ventricular failure due to infarction, cardiac tamponade, or pulmonary embolism. The presence of a new heart murmur on cardiac auscultation may represent a ventricular septal defect or an acute valvular dysfunction from papillary muscle dysfunction or chordae tendineae rupture that can manifest clinically as cardiogenic shock.
DIAGNOSIS AND DIFFERENTIAL
Once the diagnosis of shock has been made, a key task for the clinician is to differentiate cardiogenic shock from shock that is caused by other disease processes, such as hypovolemia, overwhelming sepsis, or neurogenic shock. Evaluation of a hypotensive patient for signs of gastrointestinal bleeding, severe dehydration, potential sources of significant infection, or the presence of new neurologic deficits may help to establish an alternate diagnosis.
When cardiogenic shock is suspected, an electrocardiogram (ECG) is appropriate to assist in the detection of acute cardiac ischemia or infarction, arrhythmias, electrolyte abnormalities, or signs of drug toxicity with cardiac manifestations. ST-segment depression in the lateral leads of the ECG may be suggestive of a right ventricular infarction, which is associated with increased mortality and may not manifest itself with ST-segment elevation in a standard twelve lead ECG. Look for pulmonary edema, widened mediastinum, enlarged cardiac silhouette, or other alternative diagnoses such as pneumonia or pneumothorax on chest radiograph.
Bedside echocardiography, while not a substitute for emergent formal transthoracic echocardiography when clinically indicated, can rapidly exclude other causes of hypotension, identify some mechanical precipitants of shock, and help guide therapy. Visualization of the inferior cava can help to determine volume status when considering hypovolemic shock. A pericardial effusion can be diagnosed using limited bedside echocardiography and along with findings such as diastolic collapse of the right atrium and ventricle can be diagnostic for cardiac tamponade. Left ventricular function and cardiac contractility can also be evaluated with bedside testing and may support the clinician's impression of cardiogenic shock when decreased from normal cardiac function.
There is no single laboratory test that is diagnostic for cardiogenic shock. Obtain a complete blood count and chemistries (including liver function tests) to evaluate for anemia, potential signs of infection, and some components of end organ dysfunction. In the absence of ST-segment elevation that is diagnostic for an acute MI, elevations of cardiac markers such as troponin can establish the diagnosis of non-ST-segment elevation MI (NSTEMI). In addition, these markers may add prognostic value ...