Pulmonary Edema

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Last modified 23/05/2015

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Pulmonary Edema

Anatomic Alterations of the Lungs

Pulmonary edema results from excessive movement of fluid from the pulmonary vascular system to the extravascular system and air spaces of the lungs. Fluid first seeps into the perivascular and peribronchial interstitial spaces; depending on the degree of severity, fluid may progressively move into the alveoli, bronchioles, and bronchi (see Figure 19-1).

As a consequence of this fluid movement, the alveolar walls and interstitial spaces swell. As the swelling intensifies, the alveolar surface tension increases and causes alveolar shrinkage and atelectasis. Moreover, much of the fluid that accumulates in the tracheobronchial tree is churned into a frothy white (sometimes blood-tinged or pink) sputum as a result of air moving in and out of the lungs. The abundance of fluid in the interstitial spaces causes the lymphatic vessels to widen and the lymph flow to increase.

Pulmonary edema is a restrictive pulmonary disorder. The major pathologic or structural changes of the lungs associated with pulmonary edema are as follows:

Etiology and Epidemiology

The causes of pulmonary edema can be divided into two major categories: cardiogenic and noncardiogenic.

Cardiogenic Pulmonary Edema

The most common cause of cardiac pulmonary edema is left-sided heart failure—commonly called congestive heart failure (CHF). According to the Centers for Disease Control and Prevention (CDC), about 5 million people in the United States have CHF—or about 1.7% of the overall population. Approximately 550,000 new cases of CHF are diagnosed annually. Heart failure is most common in people over age 65 and is more common in African-Americans. CHF is a leading cause of hospitalization in people over the age of 65 and is estimated to be a contributing factor to nearly 300,000 deaths annually. In 2008 the estimated annual direct and indirect costs associated with heart failure totaled nearly 35 billion dollars. As the median age of the U.S. population of “baby boomers” continues to grow older—between the present and 2040—the number of patients diagnosed with CHF, along with the direct and indirect costs associated with CHF, will undoubtedly continue to rise.

Cardiac pulmonary edema occurs when the left ventricle is not able to pump out all of the blood that it receives from the lungs. As a result, the blood pressure inside the pulmonary veins and capillaries increases. This action literally causes fluid to be pushed through the capillary walls and into the alveoli in the form of a transudate. The basic pathophysiologic mechanism for this action is described in the following sections.

Ordinarily, hydrostatic pressure of about 10 to 15 mm Hg tends to move fluid out of the pulmonary capillaries into the interstitial space. This force is normally offset by colloid osmotic forces of about 25 to 30 mm Hg that tend to keep fluid in the pulmonary capillaries. The colloid osmotic pressure is referred to as oncotic pressure and is produced by the albumin and globulin in the blood. The stability of fluid within the pulmonary capillaries is determined by the balance between hydrostatic and oncotic pressure. This relationship also maintains fluid stability in the interstitial compartments of the lung.

Movement of fluid in and out of the capillaries is expressed by Starling’s equation:

< ?xml:namespace prefix = "mml" />J=K(PcPi)(πcπi)

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where J is the net fluid movement out of the capillary, K is the capillary permeability factor, Pc and Pi are the hydrostatic pressures in the capillary and interstitial space, and πc and πi are the oncotic pressures in the capillary and interstitial space.

Although conceptually valuable, this equation has limited practical use. Of the four pressures, only the oncotic and hydrostatic pressures of blood in the pulmonary capillaries can be measured with any certainty. The oncotic and hydrostatic pressures within the interstitial compartments cannot be readily determined.

When the hydrostatic pressure within the pulmonary vascular system rises to more than 25 to 30 mm Hg, the oncotic pressure loses its holding force over the fluid within the pulmonary capillaries. Consequently fluid starts to spill into the interstitial and air spaces of the lungs (see Figure 19-1).

Clinically, the patient with left ventricular failure often has anxiety, delirium, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, fatigue, and adventitious breath sounds. Because of poor peripheral circulation, such patients often have cool skin, diaphoresis, cyanosis of the digits, and peripheral pallor. Increased pulmonary capillary hydrostatic pressure is the most common cause of pulmonary edema. Box 19-1 provides common causes of cardiogenic pulmonary edema. Box 19-2 provides common risk factors for coronary heart disease (CHD).

Noncardiogenic Pulmonary Edema

There are numerous noncardiogenic causes of pulmonary edema. In these conditions, fluid can readily flow from the pulmonary capillaries into the alveoli—even in the absence of the back pressure caused by an abnormal heart. The more common conditions include those discussed in the following paragraphs.