Clinical signs of cardiogenic shock include evidence of poor cardiac output with tissue hypoperfusion (hypotension, mental status changes, cool mottled skin) and evidence of volume overload (dyspnea, rales, jugular venous distention). Hemodynamic criteria for cardiogenic shock include (1) sustained hypotension (systolic blood pressure <90 mm Hg), (2) reduced cardiac index (<2.2 L/min/m2), and (3) an elevated (>18 mm Hg) pulmonary artery occlusion pressure. The causes and differential diagnosis of cardiogenic shock are listed in Tables 2 and 3.
There are no laboratory markers specific for the diagnosis of cardiogenic shock. Cardiac biomarkers (primarily troponin) may not be elevated upon initial presentation from an acute myocardial ischemic triggering event, but will eventually elevate. A CBC excludes anemia, which can contribute to cardiac ischemia. The clinical presentation guides the need for specific drug levels (e.g., digoxin, ethanol, or illicit drugs). Hypoperfusion commonly results in an elevated serum lactate, so checking serum lactate may aid diagnosis when overt hypotension is absent. Serum electrolytes and renal and hepatic studies can identify end-organ dysfunction.
The level of serum B-type natriuretic peptide (BNP) is an indicator of left ventricular dysfunction. Because of its high negative predictive value, a normal BNP level (<100 picograms/mL) eliminates cardiogenic shock as the cause of hypoperfusion unless very early after onset or with isolated right heart failure. Conversely, an elevated BNP does not diagnose cardiogenic shock.25,26
Although elevated inflammatory markers such as C-reactive protein have some prognostic value, these are rarely needed in the acute phase of care.27 Arterial blood gas measurements help identify those at risk of carbon dioxide retention, quantify the presence and severity of acidosis, and determine the contribution of metabolic or respiratory components to acidosis.
Imaging and Ancillary Studies
The ECG helps detect ischemia or STEMI, evaluates for rhythm abnormalities, and provides evidence of electrolytic abnormalities (e.g., hypokalemia) or drug toxicity (e.g., digoxin).
It is important to assess for right ventricle (RV) involvement whenever ischemia is considered because RV infarction is associated with an increased risk for cardiogenic shock and death.28 RV infarction is best evaluated by obtaining right-sided ECG leads (usually V4R and V5R) (Figure 1). RV infarction complicating inferior myocardial infarction is detected by ST elevation in lead V1 with depression in V2.
Right-sided leads demonstrating right ventricular infarction associated with inferior wall myocardial infarction. Right sided leads have replaced the normal left-sided V leads. In this example, the ST-segment elevation is prominent in leads VR3-6.
Obtain a portable chest radiograph in all patients. Chest x-ray typically shows pulmonary congestion or edema, alveolar infiltrates, and pleural effusion. These findings may lag by hours, so their absence does not exclude cardiogenic shock. Another confounder to interpreting the chest radiograph is underlying preexisting cardiopulmonary disease; pulmonary edema is difficult to detect on chest radiography in patients with severe chronic obstructive lung disease or interstitial lung disease. Cardiomegaly is the end result of long-standing myocardial remodeling, and its presence may not explain the acute symptoms. The chest radiograph can suggest alternative or confounding diagnoses, such as pneumonia, pneumothorax, aortic dissection, or progressive pericardial effusion (globular cardiac shape).
In the setting of cardiogenic shock, emergency bedside echocardiography can help exclude alternative etiologies of shock, identify some mechanical complications, and guide therapy. Assessment should include evaluation of the inferior vena cava (IVC) to determine volume status and estimate right atrial pressure. A subcostal four-chamber view is helpful to visualize pericardial effusion and identify cardiac tamponade. When tamponade is present, there is a pericardial effusion with associated dilation of the IVC and diastolic collapse of the RV with systolic collapse of the right atrium. When cardiac rupture has occurred, there may be a visible clot in the pericardial space. Subcostal, parasternal, and apical views together can help estimate EF and cardiac contractility. An aortic root measurement greater than 3 cm is concerning for ascending aortic dissection, especially when associated with a pericardial effusion. Also assess mitral valve morphology and motion. Apical four-chamber views are helpful for evaluating chamber size. In cases of acute right heart failure due to ischemia, the RV will be dilated and the left ventricle (LV) will appear to be smaller than expected due to low filling pressures. In left heart failure there will be dilation of the LV secondary to decreased cardiac output and increased filling pressure.
Bedside echocardiography is not a substitute for emergent formal transthoracic echocardiography. Formal echocardiography is better able to use color and spectral Doppler to identify mechanical complications and to characterize the nature of cardiac impairment. Echocardiography can detect regional wall motion abnormalities and identify a lack of compensatory hyperkinesis in uninvolved cardiac segments. Loss of RV contractility, RV dilatation, and normal estimated pulmonary pressures occur more commonly with RV infarction.
Color flow Doppler transthoracic echocardiography can identify mechanical causes of cardiogenic shock, such as acute mitral regurgitation or ventricular septal defect. Echocardiography can detect other causes of decreased cardiac output, notably pulmonary embolism. Acute RV dilatation, tricuspid insufficiency, paradoxical systolic septal motion, and high estimated pulmonary artery and RV pressures suggest pulmonary hypertension from an acute pulmonary embolus.
Mechanical Catastrophe Diagnosis
If mechanical catastrophe is suspected, consult cardiothoracic surgery immediately while obtaining a bedside echocardiogram. In the case of myocardial free wall rupture, death is probable unless a pseudoaneurysm forms. Pseudoaneurysm is detected as an acute pericardial effusion on echocardiography. An acute ventricular septal defect is confirmed by color Doppler echocardiography or right heart catheterization demonstrating oxygen saturation step-up from the right atrium to the RV. Acute mitral regurgitation, from papillary muscle rupture or dysfunction, can complicate AMI.
Patients in cardiogenic shock typically have low cardiac index (<2.2 L/min/m2) and elevated LV end-diastolic pressure (pulmonary artery occlusion pressure >18 mm Hg).29 Invasive hemodynamic monitoring with a pulmonary artery catheter can provide data and guide treatment but is unavailable in most EDs.29 Central venous pressure measurements can help guide fluid resuscitation, with the trend in venous pressures being more important than absolute values. Most patients will require continuous blood pressure monitoring, often with an indwelling catheter.