HEMODYNAMIC AND RESPIRATORY CONDITIONS DURING ALTERNATING AND SYNCHRONOUS VENTILATION OF BOTH LUNGS

Citation
A. Versprille et al., HEMODYNAMIC AND RESPIRATORY CONDITIONS DURING ALTERNATING AND SYNCHRONOUS VENTILATION OF BOTH LUNGS, Intensive care medicine, 22(8), 1996, pp. 813-817
Citations number
5
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
03424642
Volume
22
Issue
8
Year of publication
1996
Pages
813 - 817
Database
ISI
SICI code
0342-4642(1996)22:8<813:HARCDA>2.0.ZU;2-Z
Abstract
Objective: We tested the hypothesis that mean thoracic expansion (and mean lung volume) is lower during alternating Ventilation (AV), i.e. v entilation of both lungs with a phase shift of half a ventilatory cycl e, compared to synchronous ventilation (SV) of both lungs. As a conseq uence, intrathoracic pressure will be lower, causing lower, central ve nous pressure and higher cardiac output.Design: In eight anaesthetized and paralysed piglets, differential ventilation was established by fi xation of an endobronchial tube in the left main bronchus. SV and AV w ere sequentially applied for four and three periods, respectively, of 10 minutes each. Minute ventilation was the same during AV and SV and adapted to normocapnia. Two series of observations were performed: ser ies 1 with intact thorax and monitoring of oesophageal pressure; serie s 2 after perforation of the sternum, airtight closure of the thorax a nd monitoring of pericardial pressure. Results: In both series, mean l ung volume was 16 +/- 4% lower and central venous, oesophageal (series 1) and pericardial pressures (series 2) were 0.5-0.7 mmHg lower durin g AV compared to SV (all p < 0.001). In series 1, aortic pressure was 5 mmHg and cardiac output 8% higher (both p < 0.001). In series 2, car diac output was 5% higher during AV (p < 0.001), but aortic pressure d id not change (p = 0.07). Conclusion: Our data verified the hypothesis . The lower oesophageal (series 1), pericardial (series 2) and central venous pressures during AV compared to SV could be explained by the s maller thoracic expansion due to the lower mean lung volume, which was attributed to compression of the opposite lung by the expansion of th e inflated lung.