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Immediate management goals include adequate oxygenation and preload reduction to relieve pulmonary congestion. Because of sympathetic stimulation, the blood pressure should be elevated in the presence of pulmonary edema. Patients with this appropriate response can typically tolerate the required medications, all of which lower blood pressure.

If acute pulmonary edema is not associated with elevation of the systemic blood pressure, impending cardiogenic shock must be suspected. If pulmonary edema is associated with hypotension, cardiogenic shock is diagnosed. Those patients often need circulatory support with inotropic and vasopressor agents and/or intra-aortic balloon counterpulsation to relieve pulmonary congestion and maintain adequate perfusion.

Pulmonary edema may occur as an acute event with the onset of STEMI or reinfarction or as the culmination of slowly progressive CHF, and in the latter case is often associated with hypervolemia.

Management includes the use of agents that acutely reduce preload (i.e., nitrates, morphine sulfate, and diuretics), and avoidance of acute administration of negative inotropic agents (i.e., beta-blockers and calcium channel antagonists).

Nitrates are initially administered by sublingual tablets or spray nitroglycerin followed by intravenous nitroglycerin. Intravenous nitroglycerin is a venodilator that acutely reduces ventricular filling pressures. At high doses, it dilates arterioles. It is effective at relieving pulmonary congestion and ischemia and may be used in patients who have normal or elevated systemic arterial pressure. A 10- to 20-mcg bolus should be administered, followed by 10 mcg per minute, increased by 5 to 10 mcg per minute every 5 to 10 minutes until dyspnea is relieved, the mean arterial pressure is lowered by 10% in normotensive patients or 30% in hypertensive patients, or until the heart rate increases by more than 10 bpm.

Loop diuretics (furosemide, torsemide, or bumetanide) should be initiated in low to intermediate doses only in patients with associated hypervolemia. Low doses should be used unless there is renal insufficiency, chronic diuretic use, or the presence of chronic CHF and hypervolemia as described above. Typical furosemide doses range from 20 to 80 mg IV (0.5 to 1.0 mg/kg).

Angiotensin converting enzyme inhibitors are indicated for patients with pulmonary congestion. Oral ACE inhibitors, preferably a short-acting agent such as captopril, beginning with 1 to 6.25 mg, should be instituted early in normotensive or hypertensive patients. The dosage may be doubled with each subsequent dose as tolerated up to 25 to 50 mg every 8 hours, then changed to a long-acting agent. ACE inhibitors are the only adjunctive medication (beyond aspirin and reperfusion therapy) demonstrated to reduce 30-day mortality when CHF complicates STEMI. Therefore, if blood pressure limits use of vasodilators, ACE inhibitors are preferred.

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