Pulmonary edema is a condition in which fluid accumulates in the lungs, usually because the heart's left ventricle does not pump adequately.
The build-up of fluid in the spaces outside the blood vessels of the lungs is called pulmonary edema. Pulmonary edema is a common complication of heart disorders, and most cases of the condition are associated with heart failure. Pulmonary edema can be a chronic condition, or it can develop suddenly and quickly become life threatening. The life-threatening type of pulmonary edema occurs when a large amount of fluid suddenly shifts from the pulmonary blood vessels into the lung, due to lung problems, heart attack, trauma, or toxic chemicals. It can also be the first sign of coronary heart disease.
In heart-related pulmonary edema, the heart's main chamber, the left ventricle, is weakened and does not function properly. The ventricle does not completely eject its contents, causing blood to back up and cardiac output to drop. The body responds by increasing blood pressure and fluid volume to compensate for the reduced cardiac output. This, in turn, increases the force against which the ventricle must expel blood. Blood backs up, forming a pool in the pulmonary blood vessels. Fluid leaks into the spaces between the tissues of the lungs and begins to accumulate. This process makes it more difficult for the lungs to expand. It also impedes the exchange of air and gases between the lungs and blood moving through lung blood vessels.
Causes and symptoms
Most cases of pulmonary edema are caused by failure of the heart's main chamber, the left ventricle. It can be brought on by an acute heart attack, severe ischemia, volume overload of the heart's left ventricle, and mitral stenosis. Non-heart-related pulmonary edema is caused by lung problems like pneumonia, an excess of intravenous fluids, some types of kidney disease, bad burns, liver disease, nutritional problems, and Hodgkin's disease. Non-heart-related pulmonary edema can also be caused by other conditions where the lungs do not drain properly, and conditions where the respiratory veins are blocked.
Early symptoms of pulmonary edema include:
- shortness of breath upon exertion
- sudden respiratory distress after sleep
- difficulty breathing, except when sitting upright
In cases of severe pulmonary edema, these symptoms will worsen to:
- labored and rapid breathing
- frothy, bloody fluid containing pus coughed from the lungs (sputum)
- a fast pulse and possibly serious disturbances in the heart's rhythm (atrial fibrillation, for example)
- cold, clammy, sweaty, and bluish skin
- a drop in blood pressure resulting in a thready pulse
A doctor can usually diagnose pulmonary edema based on the patient's symptoms and a physical exam. Patients with pulmonary edema will have a rapid pulse, rapid breathing, abnormal breath and heart sounds, and enlarged neck veins. A chest x ray is often used to confirm the diagnosis. Arterial blood gas testing may be done. Sometimes pulmonary artery catheterization is performed to confirm that the patient has pulmonary edema and not a disease with similar symptoms (called adult respiratory distress syndrome or "noncardiogenic pulmonary edema").
Pulmonary edema requires immediate emergency treatment. Treatment includes: placing the patient in a sitting position, oxygen, assisted or mechanical ventilation (in some cases), and drug therapy. The goal of treatment is to reduce the amount of fluid in the lungs, improve gas exchange and heart function, and, where possible, to correct the underlying disease.
To help the patient breathe better, he/she is placed in a sitting position. High concentrations of oxygen are administered. In cases where respiratory distress is severe, a mechanical ventilator and a tube down the throat (tracheal intubation) will be used to improve the delivery of oxygen. Non-invasive pressure support ventilation is a new treatment for pulmonary edema in which the patient breathes against a continuous flow of positive airway pressure, delivered through a face or nasal mask. Non-invasive pressure support ventilation decreases the effort required to breath, enhances oxygen and carbon dioxide exchange, and increases cardiac output.
Edema— Swelling caused by accumulation of fluid in body tissues.
Ischemia— A condition in which the heart muscle receives an insufficient supply of blood and slowly starves.
Left ventricle— The large chamber on the lower left side of the heart. The left ventricle sends blood to the aorta and the rest of the body.
Mitral stenosis— Narrowing or constricting of the mitral valve, which separates the left atrium from the left ventricle.
Pulmonary— Referring to the lungs and respiratory system.
Drug therapy could include morphine, nitroglycerin, diuretics, angiotensin-converting enzyme (ACE) inhibitors, and vasodilators. Vasopressors are used for cardiogenic shock. Morphine is very effective in reducing the patient's anxiety, easing breathing, and improving blood flow. Nitroglycerin reduces pulmonary blood flow and decreases the volume of fluid entering the overloaded blood vessels. Diuretics, like furosemide (Lasix), promote the elimination of fluids through urination, helping to reduce pressure and fluids in the blood vessels. ACE inhibitors reduce the pressure against which the left ventricle must expel blood. In patients who have severe hypertension, a vasodilator such as nitroprusside sodium (Nipride) may be used. For cardiogenic shock, an adrenergic agent (like dopamine hydrochloride [Intropin], dobutamine hydrochloride [Dobutrex], or epinephrine) or a bipyridine (like amrinone lactate [Inocor] or milrinone lactate [Primacor]) are given.
Most patients with pulmonary edema who seek immediate treatment can be treated quickly and effectively.
Cardiogenic pulmonary edema can sometimes be prevented by treating the underlying heart disease. These treatments, can including maintaining a healthy diet, taking appropriate medications correctly, and avoiding excess alcohol and salt.
Sacchetti, Alfred D., and Russel H. Harris. "Acute Cardiogenic Pulmonary Edema: What's the Latest in Emergency Treatment?" Postgraduate Medicine 103, no. 2 (February 1998): 145-166.