Circulatory shock describes a state of tissue hypoperfusion. In the setting of an acute ischemic event (usually myocardial infarction) the "shock" state may arise from cardiogenic or noncardiogenic mechanisms. Noncardiogenic causes occurring in the setting of myocardial infarction include adverse effects of pharmacologic agents such as nitrates, angiotensin-converting enzyme inhibitors, and other vasodilator drugs. Hypotension may also arise during the infusion of thrombolytic agents such as streptokinase. Hem-orrhagic shock may occur secondary to gastrointestinal or occult retroperitoneal bleeding as most patients receive anticoagulant and/or thrombolytic agents. Massive pulmonary emboli can result in circulatory shock. A tension pneumothorax may result from mechanical ventilation or after cardiac arrest. Hypovolemia should always be considered as a result of diaphoresis, vomiting, and overdiuresis. Sepsis can result in a shock state in patients with other comorbid illnesses.
Cardiogenic etiologies of shock may occur in the setting of myocardial infarction independent of myocardial damage. Tachyarrhythmias such as ventricular tachycardia and rapid atrial fibrillation require prompt correction in the setting of hypotension. Hypotension may not only arise from direct effects of thrombolytic agents but have also resulted from hemopericardium with tamponade without identifiable rupture (7). Ascending aortic dissection can lead to the complex of pericardial tamponade and myocardial infarction. Associated cardiac conditions such as significant aortic stenosis, may importantly contribute to the development of shock. Excessive vagal tone can result in hypotension in the early phase of infarction commonly in association with bradycar-dia although isolated hypotension can occur from this accentuated cardiac reflex (8).
Direct myocardial damage may lead to a heterogeneous group of derangements resulting in circulatory shock. Pump failure from extensive left ventricular damage is the primary cause of cardiogenic shock. Mechanical defects as a direct result of myocardial injury occur less commonly and include papillary muscle dysfunction/rupture, ventricular septal defect, and free wall myocardial rupture with tamponade. Right ventricular infarction with an accompanying left ventricular infarction may also lead to shock.
Clinical recognition of circulatory shock includes identifying manifestations of a low cardiac output such cyanosis, cool extremities, altered mental status, and oliguria in the setting of hypotension. These findings with concomitant pulmonary edema establish relatively confirmatory evidence for cardiogenic shock. However, hemodynamic monitoring allows diagnostic confirmation and can guide management decisions. The hemodynamic manifestations of cardiogenic shock include a systolic blood pressure <90 mmHg (or >30 mmHg below basal levels), an elevated pulmonary capillary wedge pressure >15 mmHg, and a reduced cardiac index <2.2 L/min/m2 .
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