Effect of positive end-expiratory pressure on central venous pressure in the closed and open thorax.

Objective. The magnitude and mechanism of the rise of central venous pressure (CVP) after positive end-expiratory pressure (PEEP) among patients with cardiac disease is poorly understood. Therefore, the study aimed to compare the magnitude of change in CVP after PEEP in patients with TR (tricuspid regurgitation), high CVP, and high PCWP (pulmonary capillary wedge pressure) and in those with no TR, low CVP, and low PCWP. Additionally, we hypothesized that PEEP in the open thorax would also lead to a rise in CVP. Approach. This prospective, quasi-experimental study was conducted in patients undergoing cardiac surgery. Three consecutive readings of variables were obtained at 1 min intervals after PEEP (5 and 10 cm H 2 O) application in the closed and open thorax. Patients were stratified a priori into low CVP (<10 cm H2O) and high CVP (≥10 cm H2O), no TR and TR, and low PCWP (<15 mm Hg) and high PCWP (≥15 mm Hg) in the closed and open thorax. Main Results. Sixty-two patients were eligible for final analysis. The mean difference (MD) in ΔCVP (CVP 10 cm H2O of PEEP -CVP zero end-expiratory pressure ) was 2.33 ± 1.13 (95% CI, 2.04-2.62, P = 0.000) and 1.02 ± 0.77 (95% CI, 0.82-1.22, P = 0.000) in the closed and open thorax, respectively. The increase in CVP was higher among patients who had a lower CVP (2.64 ± 0.9 mm Hg versus 1.45 ± 1.17 mm Hg; p=0.000), in patients without TR (2.64 ± 0.97 mm Hg versus 2.14 ± 1.2 mm Hg, p=0.09) and in patients with a lower PCWP (2.4 ± 0.9 mm Hg versus 2.3 ± 1.4 mm Hg, p=0.67) at 10 cm H 2 O PEEP in the closed thorax. Significance. The rise in CVP was higher among patients without TR, low CVP, and low PCWP. Zero intrathoracic pressure in the open thorax did not abolish the effect of PEEP on CVP rise altogether.