From the Guidelines
Acute pulmonary edema is a life-threatening condition characterized by the accumulation of fluid in the lungs, requiring immediate medical attention. The condition can be caused by various factors, including heart failure, high altitude, and fluid overload 1.
Key Characteristics
- Acute onset of symptoms, such as shortness of breath and coughing up pink, frothy mucus
- Hypoxia and respiratory acidosis, which can lead to respiratory failure if left untreated 1
- Often associated with cardiogenic shock, which requires prompt intervention to stabilize the patient
Treatment Options
- Nitroglycerin (0.4 to 0.6 mg sublingually, repeated every 5 to 10 minutes as needed) is effective in reducing symptoms and improving oxygenation 1
- Furosemide (20 to 80 mg intravenously) can help reduce fluid overload and alleviate symptoms 1
- Morphine sulfate (3 to 5 mg intravenously) can be used to ameliorate symptoms, but should be administered with caution in patients with chronic pulmonary insufficiency or respiratory acidosis 1
- In severe cases, intraaortic balloon counterpulsation or mechanical ventilation may be necessary to stabilize the patient 1
From the FDA Drug Label
Acute Pulmonary Edema The usual initial dose of furosemide is 40 mg injected slowly intravenously (over 1 to 2 minutes). If a satisfactory response does not occur within 1 hour, the dose may be increased to 80 mg injected slowly intravenously (over 1 to 2 minutes). Acute pulmonary edema is not explicitly defined in the provided text, but it is mentioned as an indication for the use of furosemide, with a specified dosage regimen 2.
- The provided text does not give a definition of acute pulmonary edema, it only provides treatment guidelines.
From the Research
Definition of Acute Pulmonary Edema
Acute pulmonary edema is a life-threatening condition that can occur in various forms, including high-altitude pulmonary edema (HAPE) [ 3, 4, 5, 6, 7 ].
Characteristics of High-Altitude Pulmonary Edema
HAPE is a noncardiogenic form of pulmonary edema that occurs after rapid ascent to high altitude above 2500 m [ 3 ]. The main early-stage presentations of HAPE include:
- Fatigue
- Headache
- Low-grade fever
- Dyspnea
- Cough [ 4 ] X-ray and computed tomography (CT) images show pulmonary shadows and patches, which may be localized or generalized to the bilateral lung base [ 4 ].
Pathogenesis of High-Altitude Pulmonary Edema
The pathogenesis of HAPE is related to:
- Increased sympathetic tone
- Exaggerated hypoxic pulmonary vasoconstriction
- Uneven hypoxic pulmonary vasoconstriction with overperfusion of some regions of the pulmonary vascular bed
- Increased pulmonary capillary pressure
- Stress failure of pulmonary capillaries
- Alveolar fluid leak across capillary endothelium resulting in interstitial and alveolar edema [ 3 ] Impaired pulmonary endothelial and epithelial NO synthesis and/or bioavailability may represent a central underlying defect predisposing to exaggerated hypoxic pulmonary vasoconstriction and, in turn, capillary stress failure and alveolar fluid flooding [ 6 ].
Treatment and Prevention of High-Altitude Pulmonary Edema
The most effective and reliable treatment of established HAPE is:
- Immediate descent
- Adequate flow supplemental oxygen to maintain arterial saturation above 90%
- Rest from strenuous physical activity [ 3, 4, 5, 7 ] Prevention of HAPE can be achieved by:
- Gradual ascent with time for acclimatization
- Pharmacologic options such as nifedipine, tadalafil, or dexamethasone [ 3, 7 ]