Acute Pulmonary Edema. Life-threatening, acute development of alveolar lung edema often due to:
• Elevation of hydrostatic pressure in the pulmonary capillaries (left heart failure, mitral stenosis)
• Specific precipitants (Table), resulting in cardiogenic pulmonary edema in pts with previously compensated CHF or without previous cardiac history
• Increased permeability of pulmonary alveolar-capillary membrane
• Elevation of hydrostatic pressure in the pulmonary capillaries (left heart failure, mitral stenosis)
• Specific precipitants (Table), resulting in cardiogenic pulmonary edema in pts with previously compensated CHF or without previous cardiac history
• Increased permeability of pulmonary alveolar-capillary membrane
Physical Findings
Patient appears severely ill, sitting bolt upright, tachypneic, dyspneic, with marked perspiration; cyanosis may be present. Bilateral pulmonary rales; third heart sound may be present. Frothy and blood-tinged sputum.
Laboratory
Early ABGs show reductions of both PaO2; and PaCO2
• Later, withprogressive respiratory failure, hypercapnia develops with progressive acidemia.
• CXR shows pulmonary vascular redistribution, diffuse haziness in lung fields withperih ilar “butterfly” appearance.
• Later, withprogressive respiratory failure, hypercapnia develops with progressive acidemia.
• CXR shows pulmonary vascular redistribution, diffuse haziness in lung fields withperih ilar “butterfly” appearance.
Treatment
Immediate, aggressive therapy is mandatory for survival. The following measures should be instituted nearly simultaneously:
• Seat pt upright to reduce venous return.
• Administer 100% O2 by mask to achieve PaO2 > 60 mmHg; in pts who 2 can tolerate it, continuous positive airway pressure (10 cmH2O pressure) by mask improves outcome. Assisted ventilation by mask or endotracheal tube is frequently necessary.
• Intravenous loop diuretic (furosemide, 40–100 mg, or bumetanide, 1 mg); use lower dose if pt does not take diuretics chronically.
• Morphine 2–4 mg IV (repetitively); assess frequently for hypotension or respiratory depression; naloxone should be available to reverse effects of morphine if necessary.
Additional therapy may be required if rapid improvement does not ensue:
• The precipitating cause of pulmonary edema (Table 16-1) should be sought and treated, particularly acute arrhythmias or infection.
• The precipitating cause of pulmonary edema (Table 16-1) should be sought and treated, particularly acute arrhythmias or infection.
• Several noncardiogenic conditions may result in pulmonary edema in the absence of left heart dysfunction; therapy is directed toward the primary condition.
• Inotropic agents, e.g., dobutamine, in cardiogenic pulmonary edema withsh ock.
• Reduce intravascular volume by phlebotomy (removal of ~250 mL through antecubital vein) if rapid diuresis does not follow diuretic administration.
• Nitroglycerin (sublingual 0.4 mg x 3 q5min) followed by 5 to 10 mug/min IV. Alternatively, nesiritide [2-mug/kg bolus IV followed by 0.01 (mug/kg)/min] may be used.
• For refractory pulmonary edema associated withpersistent cardiac ischemia, early coronary revascularization may be life-saving.
• Inotropic agents, e.g., dobutamine, in cardiogenic pulmonary edema withsh ock.
• Reduce intravascular volume by phlebotomy (removal of ~250 mL through antecubital vein) if rapid diuresis does not follow diuretic administration.
• Nitroglycerin (sublingual 0.4 mg x 3 q5min) followed by 5 to 10 mug/min IV. Alternatively, nesiritide [2-mug/kg bolus IV followed by 0.01 (mug/kg)/min] may be used.
• For refractory pulmonary edema associated withpersistent cardiac ischemia, early coronary revascularization may be life-saving.
Salam
source: Manual of Medicine
Image: eccpn.aibarra.org
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