Speculations on neurogenic pulmonary edema (NPE)

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Theodore J and Robin ED (1976) Speculations on neurogenic pulmonary edema (NPE). Am Rev Respir Dis 113:4 405–11.

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Abstract: Evidence suggests the following pathogenesis for neurogenic pulmonary edema. The initial phase results from a centrally mediated, massive, sympathetic discharge. This produces intense, generalized, but transient, vasoconstriction with a resultant shift of blood from the high-resistance systemic circulation to the lowresistance pulmonary circulation. Marked increases in pulmonary vascular pressures and marked increases in pulmonary blood volume then produce pulmonary edema because of the hydrostatic effect of increased pulmonary capillary pressure. In addition, pulmonary hypertension and hypervolemia injure pulmonary blood vessels, altering pulmonary capillary permeability and producing lung hemorrhage. After the transient systemic and pulmonary vascular hypertension subside, the patient is left with abnormal pulmonary capillary permeability, so that pulmonary edema persists in the face of normal hemodynamics and normal cardia function.

Context

  • Suggests a pathogenetic mechanism for neurogenic pulmonary edema: massive sympathetic activation → increased systemic vascular resistance → increase in volume and pressure in pulmonary circulation → pulmonary edema secondary to elevated hydrostatic pressure and increased vascular permeability secondary to damage. Measurement of serum catecholamine levels immediately after seizure would permit testing of the hypothesis of seizure-induced sympathetic hyperactivation; this was found after GTCS by Simon et al.

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