Increased Transmural Pressure Pulmonary Edema (“Cardiogenic” Pulmonary Edema)

Increased Transmural Pressure Pulmonary Edema (“Cardiogenic” Pulmonary Edema)

Significantly increased πc′ can increase extravascu-lar lung water and result in pulmonary edema. As can be seen from the Starling equation, a decrease in πc′ may accentuate the effects of any increase in πc′. Two major mechanisms increase πc′; namely, pulmonary venous hypertension and a markedly increased pulmonary blood flow. Any elevation of pulmonary venous pressure is transmitted passively backward to the pulmonary capillaries and second-arily increases πc′. Pulmonary venous hypertension usually results from left ventricular failure, mitral stenosis, or left atrial obstruction. Increases in pul-monary blood flow that exceed the capacity of the pulmonary vasculature will also raise πc′. Marked increases in pulmonary blood flow can be the result of large left-to-right cardiac or peripheral shunts, hypervolemia (fluid overload), or extremes of ane-mia or exercise.

Treatment

Management of cardiogenic pulmonary edema involves decreasing the pressure in the pulmo-nary capillaries. Generally, this includes mea-sures to improve left ventricular function, correct fluid overload with diuretics, or reduce pulmonary blood flow. Pharmacological treat-ment of acute cardiogenic pulmonary edema has included oxygen, morphine, diuretics (especially loop diuretics), vasodilators such as nitrates or angiotensin-converting enzyme (ACE) inhibitors (although these decrease both preload and after-load), and inotropes such as dobutamine or mil-rinone. Vasodilators, particularly nitrates, have proved useful. By reducing preload, pulmonary congestion is relieved; by reducing afterload, car-diac output may be improved. Positive airway pres-sure therapy is also a useful adjunct for improving oxygenation. When pulmonary edema is a conse-quence of acute coronary ischemia and left ventric-ular failure, intraaortic balloon counterpulsation or other assist devices may be used.