Phosgene Poisoning as an Example of Neuroparalytic Acute Pulmonary Edema: The Sympathetic Vasomotor Reflex Involved

¹ Department of Pharmacology, University of California School of Medicine, San Francisco

Conditions of acute pulmonary edema are classified into two great groups, according to certain empirically useful anatomic, physiologic, pharmacologic, clinical and radiologic criteria. The hyperactive-sympathetic group is characterized by diffuse lung hyperemia, pulmonary hypertension, amelioration by sympatholytic agents, systemic hypertension and uniformly dense lung fields; it includes epinephrine toxicity and brainstem irritation. The hypoactive-sympathetic or neuroparalytic group is characterized by patchy lung hyperemia, pulmonary normo- or hypotension, non-amelioration by sympatholytic agents, systemic normo- or hypotension and generalized reticulogranular images in the lung fields; it includes vagal section, so-called high altitude pneumonia, hyaline membrane disease, explosive recompression, probably paroxysmal nocturnal dyspnea, and phosgene poisoning.

The basic assumption of this classification, specifically in relation to the neuroparalytic group, is tested by direct assay of total electrical activity of the right cervical sympathetic nerve in the rabbit before and after a lethal dose of phosgene. An immediate abrupt marked drop in systemic sympathetic outflow which precedes the lung changes occurs upon phosgene poisoning in the rabbit.

Other data are marshalled to establish that the sympathetic neuroparalysis of phosgene poisoning is reflex in nature and associated with vasoconstriction of the lung vascular bed, such pulmonary shutdown being essentially a post-capillary phenomenon.

The autonomic sensorimotor negative feedback reflex thus identified as controlling the vascular dynamics of the lung is presented as coursing afferently with the vagus, synapsing at the bulbar reticular formation, and coursing efferently with the upper thoracic sympathetics.