Pulmonary edema is an abnormal build up of fluid in the air sacs of the lungs, which leads to shortness of breath
Lung congestion; Lung water; Pulmonary congestion
Causes, incidence, and risk factors:
Pulmonary edema is usually caused by heart failure. As the heart fails, pressure in the veins going through the lungs starts to rise.
As the heart fails, pressure in the veins going through the lungs starts to rise. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs. This fluid interrupts normal oxygen movement through the lungs, resulting in shortness of breath.
Pulmonary edema may be caused by damage directly to the lung, such as that caused by poisonous gas or severe infection, as a side effect of medications, or the result of major trauma. Lung damage with a buildup of body fluid is also seen in kidney failure. Exercising at very high altitudes can also cause pulmonary edema
Pulmonary edema may also be a complication of a heart attack , leaking or narrowed heart valves (mitral or aortic valves), or any disease of the heart that results in weakening or stiffening of the heart muscle (cardiomyopathy ).
Additional symptoms that may be associated with this condition:
Signs and tests:
The health care provider will perform a physical exam and use a stethoscope to listen to the lungs and heart. The following may be detected:
- Crackles in the lungs, called rales
- Abnormal heart sounds
- Increased heart rate (tachycardia)
- Pale or blue skin color (pallor or cyanosis)
- Rapid breathing (tachypnea)
Possible tests include:
- Complete blood count (CBC) to check for anemia and reduced red cell count
- Other blood tests to measure blood chemistries and kidney function
- Blood oxygen levels (oximetry or arterial blood gases) -- low in patients with pulmonary edema
- Chest x-ray may reveal fluid in or around the lung space or an enlarged heart
- Electrocardiogram (ECG ) to detect abnormal heart rhythm or evidence of a heart attack
- Ultrasound of the heart (echocardiogram ) to see if there is a weak heart muscle, leaky or narrow heart valves, or fluid surrounding the heart
Oxygen is given through a face mask or tiny plastic tubes (prongs) placed in the nose. A breathing tube may be placed into the windpipe (trachea). A breathing machine (ventilator) may be needed.
The cause of the edema should be rapidly identified and treated. For example, if a heart attack has caused the condition, the heart must be treated and stabilized.
Water pills (diuretics) such as furosemide (Lasix) may be given to help excess water leave the body. Medications to strengthen the heart muscle, control its rhythm, or to relieve pressure on the heart, may also be given.
Some patients may need to use a breathing machine for a long time, which may lead to damage to lung tissue.
Kidney failure and damage to other major organs may occur if blood and oxygen flow are not restored promptly. If not treated, this condition can be fatal.
Some patients may need to use a breathing machine for a long time. If not treated, this condition can be fatal.
Calling your health care provider:
Go to the emergency room or call 911 if you have breathing problems.
If you have a disease that can lead to pulmonary edema or a weakened heart muscle, take all prescription medications as instructed. Following a healthy diet, one low in salt and fat, can significantly reduce the risk of developing this condition.
Hess OM, Carroll JD. Clinical assessment of heart failure. In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, Pa; Saunders Elsevier; 2007: chap 23.
American College of Cardiology/American Heart Association. ACC/AHA Task Force on Practice Guidelines. Update to the 2001 Guidelines for the Evaluation and Management of Heart Failure. J Am Coll Cardiol. 2005;46(6):e1-82.
Irwin RS, Rippe JM. Management of advanced heart failure. In: Irwin RS, Rippe JM, eds. Irwin and Rippe's Intensive Care Medicine. 6th ed. Baltimore, Md; Lippincott Williams & Wilkins; 2008:chap 33.