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Abstract
Previous studies have shown that pulmonary edema occurs in half of all pre-hospital
cardiac arrest victims who cannot be successfully resuscitated and is a major cause
of hypoxemia and poor lung compliance during resuscitation. Pulmonary vascular hypertension
and elevation of pulmonary capillary wedge pressure have been observed during cardiac
resuscitation in humans. To further define the time course of the pulmonary hemodynamic
changes, pulmonary artery diastolic pressure (PAd) was measured on a computerized
trend recorder prior to, during, and immediately after arrest in three adult patients.
Prior to arrest, PADP was 20.9 ± 3.1 mm Hg. The PADP rose in all three patients by
an average of 30.6% after 5–10 minutes and 71.3% after 10–15 minutes of CPR. Peak
PADP reached 35.8 ± 5.1 mm Hg (difference from pre-arrest level significant, P < 0.001). In both patients who were resuscitated successfully, the PADP returned
to baseline within 5 minutes of effective spontaneous circulation. The finding that
such hemodynamic changes occur rapidly during resuscitation and can reverse quickly
with resumption of effective spontaneous circulation is consistent with the time course
for the early development of pulmonary edema. Development of pulmonary edema many
hours following successful resuscitation likely involves other mechanisms.
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Article Info
Publication History
Accepted:
October 31,
1984
Received:
April 13,
1984
Footnotes
☆Presented at the Fifth Purdue Conference on CPR and Defibrillation, West Lafayette, Indiana, September 25–26, 1984.
Identification
Copyright
© 1985 Published by Elsevier Inc.
