Early arterial blood gases show reductions of both PaO2 and PaCO2. With progressive respiratory failure, hypercapnia develops with acidemia. CXR shows pulmonary vascular redistribution, diffuse haziness in lung fields with perihilar “butterfly” appearance.
Treatment: Acute Pulmonary Edema Immediate, aggressive therapy is mandatory for survival. The following measures should be instituted as simultaneously as possible for cardiogenic pulmonary edema: - Administer 100% O2 by mask to achieve PaO2 >60 mmHg; if inadequate, use positive-pressure ventilation by face or nasal mask, and if necessary, proceed to endotracheal intubation.
- Reduce preload:
- Seat pt upright to reduce venous return, if not hypotensive.
- Intravenous loop diuretic (e.g., furosemide, initially 0.5-1.0 mg/kg); use lower dose if pt does not take diuretics chronically.
- Nitroglycerin (sublingual 0.4 mg × 3 q5min) followed by 5-20 µg/ min IV if needed.
- Morphine 2-4 mg IV; assess frequently for hypotension or respiratory depression; naloxone should be available to reverse effects of morphine if necessary.
- Consider ACE inhibitor if pt is hypertensive, or in setting of acute MI with heart failure.
- Consider nesiritide (2-µg/kg bolus IV followed by 0.01 µg/kg per min) for refractory symptoms—do not use in acute MI or cardiogenic shock.
- Inotropic agents are indicated in cardiogenic pulmonary edema and severe LV dysfunction: dopamine, dobutamine, milrinone (Chap. 11. Shock).
- The precipitating cause of cardiogenic pulmonary edema (Table 13-1) should be sought and treated, particularly acute arrhythmias or infection. For refractory pulmonary edema associated with persistent cardiac ischemia, early coronary revascularization may be life-saving. For noncardiac pulmonary edema, identify and treat/remove cause (Table 13-2).
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For a more detailed discussion, see Schwartzstein RM: Dyspnea, Chap. 47e; and Hochman JS, Ingbar DH: Cardiogenic Shock and Pulmonary Edema, Chap. 326, p. 1759, in HPIM-19. |