I Pulmonary edema
Definition
Pulmonary edema is the accumulation of excess fluid in the interstitial and air-filled spaces of the lung. The mechanisms responsible for its development include an increase in hydrostatic pressure within the pulmonary capillary system, an increase in the permeability of the alveolocapillary membrane, and a decrease in intravascular colloid oncotic pressure.
Pulmonary edema is classified as being either cardiogenic (high pressure, hydrostatic) or noncardiogenic (increased permeability).
Cardiogenic pulmonary edema
Cardiogenic pulmonary edema is initiated by some type of left-sided heart incompetence or failure. Left ventricular failure implies that there is a decrease in left ventricular contractility, which ultimately leads to a reduction in both stroke volume and cardiac output. Incomplete left ventricular emptying elevates left ventricular end-diastolic volume, which, in turn, elevates left ventricular end-diastolic pressure. Increased left ventricular end-diastolic pressure is “reflected back,” causing elevation of the left atrial, pulmonary venous, and pulmonary capillary pressures. When pulmonary capillary pressure reaches levels of 20 to 25 mmHg (normal range, 10–16 mmHg), the rate of fluid transudation often exceeds lymphatic drainage capacity, and alveolar flooding occurs.
Noncardiogenic pulmonary edema
Noncardiogenic pulmonary edema is associated with an increase in endothelial permeability caused by an insult that disrupts the barrier function of the blood–tissue interface. Noncardiogenic pulmonary edema is associated with the leakage of both fluid and protein from the vascular space. Because this respiratory membrane disruption cannot be easily or directly measured, noncardiogenic pulmonary edema is said to exist when suspicious chest radiographic evidence coexists with insufficient hemodynamic basis. The presence of pulmonary wedge pressure less than 12 mmHg and the absence of a significant history of cardiac disease generally suffice for exclusion of a hemodynamic mechanism.
Neurogenic pulmonary edema
Neurogenic pulmonary edema begins with a massive outpouring of sympathetic nervous system stimulation triggered by CNS insult. This centrally mediated CNS overactivity typically occurs in the hypothalamic area. Excessive sympathetic activation induces remarkable hemodynamic alterations, primarily systemic and pulmonary vasoconstriction. The left ventricle fails because of the inordinate pressure work imposed by the systemic hypertension, and pulmonary blood volume increases because of the functional imbalance between the failing left ventricle and the normal right ventricle. Although this sequence seems to parallel that of hemodynamic pulmonary edema, a permeability component exists, as evidenced by the high protein concentration found in the pulmonary secretions of these patients.
Uremic pulmonary edema
Uremic pulmonary edema is seen in those patients with renal insufficiency or failure. Overhydration and expansion of the circulating blood volume lead to increases in pulmonary capillary pressures. Again, a “leaky” component exists because of the metabolic abnormalities associated with uremia. Reducing the circulating blood volume of these patients by hemodialysis promotes the resolution of this type of pulmonary edema.
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