OBJECTIVE: We tested the hypothesis that mean thoracic expansion (and mean lung volume) is lower during alternating ventilation (AV), i.e. ventilation of both lungs with a phase shift of half a ventilatory cycle, compared to synchronous ventilation (SV) of both lungs. As a consequence, intrathoracic pressure will be lower, causing lower, central venous pressure and higher cardiac output. DESIGN: In eight anaesthetized and paralysed piglets, differential ventilation was established by fixation of an endobronchial tube in the left main bronchus. SV and AV were 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: series 1 with intact thorax and monitoring of oesophageal pressure; series 2 after perforation of the sternum, airtight closure of the thorax and monitoring of pericardial pressure. RESULTS: In both series, mean lung volume was 16 +/- 4% lower and central venous, oesophageal (series 1) and pericardial pressures (series 2) were 0.5-0.7 mmHg lower during 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, cardiac output was 5% higher during AV (p < 0.001), but aortic pressure did 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 smaller thoracic expansion due to the lower mean lung volume, which was attributed to compression of the opposite lung by the, expansion of the inflated lung.
OBJECTIVE: We tested the hypothesis that mean thoracic expansion (and mean lung volume) is lower during alternating ventilation (AV), i.e. ventilation of both lungs with a phase shift of half a ventilatory cycle, compared to synchronous ventilation (SV) of both lungs. As a consequence, intrathoracic pressure will be lower, causing lower, central venous pressure and higher cardiac output. DESIGN: In eight anaesthetized and paralysed piglets, differential ventilation was established by fixation of an endobronchial tube in the left main bronchus. SV and AV were 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: series 1 with intact thorax and monitoring of oesophageal pressure; series 2 after perforation of the sternum, airtight closure of the thorax and monitoring of pericardial pressure. RESULTS: In both series, mean lung volume was 16 +/- 4% lower and central venous, oesophageal (series 1) and pericardial pressures (series 2) were 0.5-0.7 mmHg lower during 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, cardiac output was 5% higher during AV (p < 0.001), but aortic pressure did 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 smaller thoracic expansion due to the lower mean lung volume, which was attributed to compression of the opposite lung by the, expansion of the inflated lung.