Am. J. Respir. Crit. Care Med., Vol 152, No. 1, 07 1995, 142-147.
Effect of CPAP on pericardial pressure and respiratory system mechanics in pigs
SI Huberfeld, J Genovese, A Tarasiuk and SM Scharf
Division of Pulmonary and Critical Care Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine, New Hyde Park, New York 11042, USA.
It has been postulated that increased cardiac surface pressure with
continuous positive airway pressure (CPAP) results in decreased left-
ventricular (LV) transmural pressure. We tested this hypothesis in seven
sedated, unanesthetized, and previously instrumented pigs. We measured
pericardial (Pperi), LV, airway (P(aw)), and esophageal (Pes) pressures at
CPAP values of 0, 4, 8, and 12 cm H2O before and after blood-volume
expansion. With normovolemia, CPAP resulted in an increase in Pperi (from
-2.0 +/- 7.6 mm Hg at CPAP 0 to 2.3 +/- 5.6 mmHg at CPAP 12, p < 0.05).
Baseline end-diastolic Pperi rose with volume expansion from -2.0 +/- 7.6
mm Hg to 5.4 +/- 5.4 mm Hg, p < 0.05. With hypervolemia, CPAP was
associated with a decrease in Pperi (from 5.42 +/- 5.4 mm Hg to 2.3 +/- 5.6
mm Hg, p < 0.05). By contrast, Pes rose equally under both conditions
with CPAP. LV transmural end-diastolic pressure (TMEDP) fell significantly
under normovolemic conditions (from 16.5 +/- 7.4 mm Hg at CPAP 0 to 13.6
+/- 9.0 mm Hg at CPAP 12). The changes in FRC (pneumotachometry) with CPAP
were similar under both conditions. We conclude that the CPAP-induced
decrease in LV volume under hypervolemic conditions cannot be explained by
an increase in cardiac surface pressure. We present a model to explain the
decrease in cardiac surface pressure with CPAP.
