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Pulmonary Edema

  • Pulmonary Edema is an anatomical subtype of edema characterized by abnormal collection of fluid within the lung interstitium. Pulmonary edema is always secondary to an underlying disease process and thus the ability to distinguish the cause of excess interstitial lung fluid is critical for its treatment. Below we discuss the basic pathogenesis of pulmonary edema along with possible etiologies and then detail the important clinical consequences of this pathology.
  • Overview
    • The basic development of pulmonary edema is no different than that of any other type of edema, and is thus the result of an imbalance between the rate at which fluid leaks out of the pulmonary vasculature and into the interstitium compared with the rate at which interstitial fluid is carried away by the pulmonary lymphatics. Although the basic pathogenesis is similar to other forms of edema, the possible causes of pulmonary edema are more limited. In general, lymphatic drainage of the pulmonary interstitium is rarely compromised and so pulmonary edema is typically caused by an excess in the rate of fluid leakage out of the pulmonary vasculature, a process controlled by Starling Forces. Excess starling leakage from the pulmonary vasculature is typically caused by only two basic types derangements within the lung: Excess vascular permeability or excess vascular hydorstatic pressure (See: Starling Forces). Importantly, reduced vascular oncotic pressure due to hypoalbuminemia typically does not result in pulmonary edema on its own.
  • Excess Vascular Permeability
    • Increases in pulmonary vascular permeability can occur due to a wide variety insults to the pulmonary capillaries. When such injuries occur, not only is permeability toward fluid leakage increased but plasma proteins are also able to leak into the interstitium across the injured capillary membrane. Leakage of plasma proteins results in increased interstitial oncotic pressure, further deranging starling forces, and thus yielding enhanced outward fluid movement.
  • Increased Hydrostatic Pressure
    • Increased hydrostatic pressure in the pulmonary capillaries will result in a larger net outward Starling Force]] for fluid movement into the interstitium. Increases in pulmonary capillary hydrostatic pressures are typically caused by pressures retrogradely transmitted from elevated left atrial pressures. Consequently, this basic mechanism for pulmonary edema is typically initiated by dysfunction of the heart.
  • As described above, the pathogenesis of pulmonary edema can result from either an increase in vascular permeability or an increase in vascular hydrostatic pressure. Increases in vascular permeability are typically caused by direct or indirect damage to the pulmonary vasculature and are thus categorized as "Non-cardiogenic" causes of pulmonary edema. Examples of Non-cardiogenic eiologies include, aspiration, chest trauma, ARDS, sepsis, and pulmonary embolism. In contrast, increases in pulmonary vascular hydrostatic pressure are typically caused by defects in cardiac function and are thus categorized as "Cardiogenic" causes of pulmonary edema. Any defect of the heart which results in chronically increased left atrial pressures can cause pulmonary edema and the reader is referred to the interlinks of this page.
  • The morphology of pulmonary edema typically progresses over two basic stages. Initially, edematous fluid remains within the pulmonary interstitium and any excess is siphoned off by the pulmonary lymphatics. However, once lymphatics are overloaded, edema fluid leaks into alveoli which can become filled. This flooding of the alveoli likely results in damage to the alveolar membrane and in many cases can yield leakage of proteins and blood from the pulmonary capillaries into the alveolar space. Over time, alveolar macrophages take up the leaked red blood cells, become laden with hemosiderin, and in so doing are sometimes termed "Heart Failure" cells when pulmonary edema is cardiogenic in etiology.
Clinical Consequences
  • Pulmonary edema typically results in dyspnea. When edematous fluid is large in volume it can redistribute when an individual lies supine, affecting more lung tissue and thus worsening dyspnea, a phenomenon known as orthopnea. In some patients, extreme edema may result in paroxysmal nocturnal dyspnea, although the pathogenesis of this conditions is not well-understood. Initially, pulmonary edema may cause a dry cough; however, when edema progresses to the point that alveoli are flooded, the cough can become productive, characterized by a pinkish sputum. Beyond these symptoms, pulmonary edema can cause serious derangements in pulmonary function. As alveoli become fluid-filled, they can no longer be ventilated effectively, resulting in the development of ventilation-perfusion defects and in extreme cases overt right-left shunts. Together, these defects in alveolar ventilation can yield clinically significant hypoxemia.