cardiovascular disorders
Complications of Acute Coronary Syndromes
Hypotension and Cardiogenic Shock
Hypotension may be due to Decreased ventricular filling Loss of contractile force secondary to massive myocardial infarction 90 mm Hg) with tachycardia and symptoms of end-organ hypoperfusion (reduced urine output, mental confusion, diaphoresis, cold extremities) is termed Cardiogenic and obstructive shock . Pulmonary congestion develops rapidly in cardiogenic shock. is most often caused by reduced venous return secondary to hypovolemia, especially in patients receiving intensive loop diuretic therapy, but it may reflect Infarct location . Marked pulmonary congestion suggests loss of left ventricular contractile force (left ventricular failure) as the cause. Treatment depends on the cause. In some patients, determining the cause requires use of a pulmonary artery catheter to measure intracardiac pressures. If pulmonary artery occlusion pressure is<18 mm Hg, decreased filling, usually due to hypovolemia, is likely; if pressure is>18 mm Hg, left ventricular failure is likely. For hypotension due to hypovolemia, cautious fluid replacement with 0.9% saline is usually possible without left heart overload (excessive rise in left atrial pressure). However, sometimes left ventricular function is so compromised that adequate fluid replacement sharply increases pulmonary artery occlusion pressure to levels associated with pulmonary edema (>25 mm Hg). If left atrial pressure is high, hypotension is probably due to left ventricular failure, and if diuretics are ineffective, inotropic therapy or circulatory support may be required. Approximately 5 to 10% of patients with acute myocardial infarction have cardiogenic shock. In cardiogenic shock, an alpha-agonist or beta-agonist may be temporarily effective.Dopamine, a catecholamine with alpha and beta 1 effects, is given IV at 0.5 to 1 mcg/kg/minute, increased until response is satisfactory or the dose is about 10 mcg/kg/minute. Higher doses induce vasoconstriction and atrial and ventricular arrhythmias. Dobutamine, a beta-agonist, may be given IV at 2.5 to 10 mcg/kg/minute or in higher doses. It often causes or exacerbates hypotension; it is most effective when hypotension is secondary to low cardiac output with increased peripheral vascular resistance.Dopamineis more effective thandobutaminewhen a vasopressor effect is also required. In refractory cases of cardiogenic shock,dobutamineanddopaminemay be combined. The combination ofdobutamineplus a drug with more alpha-adrenergic effects (phenylephrine,norepinephrine) may be effective without causing excessive arrhythmias. An intraortic counterpulsation balloon pump may often temporarily support the patient, but recent evidence indicates no short-term or long-term benefit to this approach. Alternatives include a percutaneous or surgically implanted left ventricular assist device and occasionally heart transplantation. Definitive treatment for postinfarction cardiogenic shock is Revascularization for Acute Coronary Syndromes by thrombolysis of the clot, angioplasty, or emergency coronary artery bypass grafting. Revascularization usually greatly improves ventricular function. If coronary anatomy is suitable, percutaneous coronary intervention or coronary artery bypass grafting may be considered for persistent ischemia, refractory ventricular arrhythmia, hemodynamic instability, or shock. 