Although the diagnosis of cardiogenic shock can be suspected from the initial history and physical examination, ancillary tests are essential for confirmation, to define the specific causes, and to direct therapy. Findings of an AMI on the standard 12-lead electrocardiograph (ECG) support the diagnosis of cardiogenic shock. In cases of an inferior wall infarction, patients at risk to develop cardiogenic shock will have ST-segment elevation in the right-sided precordial leads, ST-segment depression in the left precordial leads, or third-degree heart block. Diffuse ST-T changes can be seen with acute myocarditis. The absence of ECG changes consistent with AMI suggests alternate causes of shock, such as aortic dissection, pulmonary embolus, pericardial tamponade, acute valvular insufficiency, hemorrhage, or sepsis.
The chest radiograph (usually an anteroposterior view obtained with a portable machine) should be inspected for evidence of pulmonary vascular congestion: Kerley-B lines, cephalization, interstitial edema, or frank pulmonary edema. A large heart size suggests prior CHF, and a globular cardiac shape provides a clue for chronic pericardial effusion. A wide mediastinum may indicate aortic dissection.
Baseline laboratory studies are of little immediate diagnostic value but provide a hematologic and metabolic assessment of the patient. The severity of tissue hypoperfusion is reflected in the degree of metabolic acidosis, as measured by arterial blood gases, serum bicarbonate, or serum lactate. Serum markers of myocardial injury support the clinical and ECG evidence: CK-MB, troponin I, and troponin T.
The best bedside diagnostic tool available for differentiating the causes of cardiogenic shock is the two-dimensional transthoracic echocardiogram (TTE). This imaging modality can reveal signs of myocardial pump failure by detecting regional hypokinetic, akinetic, or dyskinetic abnormalities. The TTE can detect early signs of distress by visualizing lack of compensatory hyperkinesis in uninvolved segments, which can alert the clinician to take steps to prevent further loss of myocardium, initiate inotropic support, and consult the invasive cardiologist. The TTE also can evaluate other causes of decreased cardiac output. The presence of acute RV dilatation, tricuspid insufficiency, paradoxical systolic septal motion, and high estimated pulmonary artery and right ventricular pressures suggest pulmonary hypertension, often seen with acute pulmonary embolus. Loss of RV contractility, RV dilatation, and normal estimated pulmonary pressures are observed more commonly with RV infarction. Use of the color flow Doppler can easily diagnose acute valvular stenosis or insufficiency, as well as septal and free wall rupture. Pericardial effusion with collapse of the right atrium or diastolic right ventricle collapse indicates cardiac tamponade. Although not the best imaging modality for aortic dissection, TTE sometimes can visualize dissection of the aortic root.
Although more often done in the intensive care unit than in the emergency department, invasive hemodynamic monitoring with a pulmonary artery catheter can provide confirmatory information and guide treatment. As noted earlier, patients with cardiogenic shock have decreased cardiac output (defined as a cardiac index <2.2 L/min/m2) and elevated LV preload (defined as a pulmonary artery occlusion or wedge pressure >18 mmHg). Because of impaired tissue oxygen delivery with continued metabolic need, there is an elevated oxygen extraction (arterial-venous oxygen content difference >5.5 mL/dL), and blood returning back to the heart is low in oxygen (pulmonary artery oxygen saturation <60 percent or partial pressure less than 30 mmHg). Continuous hemodynamic monitoring and treatment are facilitated by using both (1) a balloon-tipped pulmonary artery catheter with continuous oximetry and cardiac output monitoring and (2) an arterial catheter for pressure measurements. There is a fair correlation between clinical and hemodynamic assessments of cardiac output and LV preload during an AMI, but the overlaps between the different classes limit therapy based solely on clinical criteria.
Noninvasive hemodynamic monitoring by a variety of techniques shows promise, but the currently available devices lack sufficient accuracy for clinical use where important therapeutic decisions require precise measurement.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...