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A 56-year-old man with past medical history of hypertension and hyperlipidemia presents to the emergency department with 1 hour of substernal chest pain and shortness of breath. On arrival, patient is lethargic, in respiratory distress and is emergently intubated. Vital signs on presentation are temperature, 100°F; heart rate, 110 bpm; blood pressure, 80/50 mm Hg; respiratory rate, 12 per minute; and oxygen saturation, 96% on assist control-volume control mechanical ventilation. On physical examination, the patient has elevated jugular venous distention, decreased breath sounds bilaterally, tachycardia without any audible murmurs, and cool extremities. An electrocardiogram (ECG) shows ST elevations in leads V1-V4 with ST depressions in leads II and III, and aVF (Figure 38-1). The troponin level is raised to 6 ng/mL (normal value < 0.01 ng/mL). He is given aspirin, 325 mg and started on a heparin drip.

Figure 38-1.

ECG of an anterolateral myocardial infarction. Note the ST elevations in the anterolateral leads (V2-V6, I, aVL) with reciprocal depressions in the inferior limb leads (II, III, aVF).

What are the initial steps in managing the care for this patient?

The clinical presentation of this case is consistent with a ST-segment elevation myocardial infarction (STEMI) complicated by cardiogenic shock (CS). Cardiogenic shock is defined as end-organ hypoperfusion due to cardiac failure. Hemodynamically, this manifests as persistent hypotension (systolic blood pressure < 90 mm Hg), severe reduction in cardiac index (< 1.8 L/min/m2), and adequate or elevated filling pressure (pulmonary capillary wedge pressure [PCWP] > 18 mm Hg). It is clinically diagnosed by the constellation of signs of hypoperfusion (decreased urine output, altered sensorium, and/or lactic acidosis), low cardiac output (CO; tachycardia, cool extremities), and congestion (jugular venous distention, pulmonary edema, and/or peripheral edema).1

The initial approach to the patient in cardiogenic shock should include fluid resuscitation unless pulmonary edema is present. Oxygenation and airway protection are critical; intubation and mechanical ventilation are often required, as was evident in this case. A 12-lead ECG and cardiac enzymes were appropriately and promptly obtained to identify the cause of chest pain and low blood pressure and initiate appropriate therapy for STEMI complicated by CS. The patient should be emergently taken to cardiac catheterization laboratory, and antithrombotic therapy in the form of aspirin and heparin should be administered, with possible withholding of clopidogrel until after angiography as these patients may require emergent coronary artery bypass graft (CABG) surgery based on angiography findings.2 An arterial catheter should be placed to continuously monitor the blood pressure. In addition, a central venous catheter should be placed to monitor central venous pressure and administer inotropic (dobutamine or milrinone) and/or vasopressor therapy. A transthoracic ECG should be obtained expeditiously to evaluate for etiologies of ventricular dysfunction and detect possible early mechanical complications of myocardial infarction. Lastly, patient monitoring in a cardiac intensive care unit (CICU) is essential given the high rates of morbidity and mortality associated with CS.1

The predominant cause of CS is ...

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