Premium
Postictal Pulmonary Edema Requires Pulmonary Vascular Pressure Increases
Author(s) -
Johnston S. Claiborne,
Darragh Teresa M.,
Simon Roger P.
Publication year - 1996
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1996.tb00587.x
Subject(s) - medicine , pulmonary edema , status epilepticus , anesthesia , pulmonary artery , edema , pulmonary hypertension , lung , cardiology , left atrial pressure , vascular resistance , epilepsy , hemodynamics , psychiatry
Summary: The pathogenesis of neurogenic pulmonary edema has been debated for many years. Whether cardiogenic mechanisms and increased pulmonary vascular pressures are primary or even necessary for the production of pulmonary edema has been argued. We used postictal pulmonary edema to study this problem in a sheep model of neurogenic pulmonary edema with bicucullin‐induced status epilepticus. Seizure‐induced increases in pulmonary vascular pressures were averted with a reservoir system to maintain left atrial pressure (LAP) and pulmonary artery pressure (PAP) at preseizure levels. No increase in lung lymph flow occurred during seizures, in contrast to the doubling of lung lymph flow that occurred during seizures when ictal pulmonary vascular hypertension was not blocked. These data support a primary role of pulmonary vascular pressure increases in the production of neurogenic pulmonary edema.