EFFECTS OF POSITIVE END-EXPIRATORY PRESSURE AND BODY POSITION ON PRESSURE IN THE THORACIC GREAT VEINS

Citation
He. Fessler et al., EFFECTS OF POSITIVE END-EXPIRATORY PRESSURE AND BODY POSITION ON PRESSURE IN THE THORACIC GREAT VEINS, The American review of respiratory disease, 148(6), 1993, pp. 1657-1664
Citations number
20
Categorie Soggetti
Respiratory System
ISSN journal
00030805
Volume
148
Issue
6
Year of publication
1993
Pages
1657 - 1664
Database
ISI
SICI code
0003-0805(1993)148:6<1657:EOPEPA>2.0.ZU;2-1
Abstract
Positive end-expiratory pressure (PEEP) commonly decreases cardiac out put. The major cause of this is believed to be decreased venous return due to increased right atrial pressure. We hypothesized that when the lungs were hyperinflated they could also restrict venous return by di rectly compressing the thoracic vena cavae. We measured the longitudin al distribution of pressure in the thoracic vena cavae of 10 dogs on a nd off 10 mm Hg PEEP, in the supine (S), prone (P), right lateral (RL) , and left lateral decubitus (LL) positions. In the superior vena cava (SVC) both on and off PEEP, and in the inferior vena cava (IVC) off P EEP, pressure fell uniformly from the thoracic inlet to the right atri um. However, in the IVC on PEEP, intravascular pressure fell abruptly by up to 5 mm Hg. This pressure drop occurred in a discrete (1 to 2-cm ) segment of the IVC, suggesting a localized increase in extravascular surface pressure. When this pressure inflection was present, changes in right atrial pressure had no effect on pressure in the IVC upstream of the inflection, consistent with a ''vascular waterfall''. These ob servations were most prominent in the LL, least common in the RL, and variably present in the P and S positions. Occlusion of the right bron chus intermedius prior to PEEP (preventing right lower, middle, and ac cessory lobe inflation) prevented the appearance of the pressure infle ction during PEEP in the LL but not in the S or P positions. We conclu de that PEEP impedes venous return partly by direct compression of the IVC, predominantly in positions in which the IVC is non-dependent. Th is may be due to hyperinflation of lobes of the right lung.