LUNG AND CHEST-WALL MECHANICAL-PROPERTIES BEFORE AND AFTER CARDIAC-SURGERY WITH CARDIOPULMONARY BYPASS

Citation
Gm. Barnas et al., LUNG AND CHEST-WALL MECHANICAL-PROPERTIES BEFORE AND AFTER CARDIAC-SURGERY WITH CARDIOPULMONARY BYPASS, Journal of applied physiology, 76(1), 1994, pp. 166-175
Citations number
35
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
76
Issue
1
Year of publication
1994
Pages
166 - 175
Database
ISI
SICI code
8750-7587(1994)76:1<166:LACMBA>2.0.ZU;2-Z
Abstract
From measurements of airway and esophageal pressures and flow, we calc ulated the elastance and resistance of the total respiratory system (E rs and Rrs), chest wall (Ecw and Rcw), and lungs (EL and RL) in 11 ane sthetized-paralyzed patients immediately before cardiac surgery with c ardiopulmonary bypass and immediately after chest closure at the end o f surgery. Measurements were made during mechanical ventilation in the frequency and tidal volume ranges of normal breathing. Before surgery , frequency and tidal volume dependences of the elastances and resista nces were similar to those previously measured in awake seated subject s (An. Rev. Respir. Dis. 145: 110-113, 1992). After surgery, Ers and R rs increased as a result of increases in EL and RL (P < 0.05), whereas Ecw and Rcw did not change (P > 0.05). EL and RL exhibited nonlineari ties (i.e., decreases with increasing tidal volume) that were not seen before surgery, and RL showed a greater dependence on frequency than before surgery. The changes in RL or EL after surgery were not correla ted with the duration of surgery or cardiopulmonary bypass time (P > 0 .05). We conclude that 1) frequency and tidal volume dependences of re spiratory system properties are not affected by anesthesia, paralysis, and the supine posture, 2) open-chest surgery with cardiopulmonary by pass does not affect the mechanical properties of the chest, and 3) ca rdiac surgery involving cardiopulmonary bypass causes changes in the m echanical behavior of the lung that are generally consistent with thos e caused by pulmonary edema induced by oleic acid (J. Appl. Physiol. 7 3: 1040-1046, 1992) and decreases in lung volume.