Hemodynamic effects of negative-pressure ventilation in patients with COPD

In order to evaluate the hemodynamic effects of INPV, eight patients with COPD (FEV₁/FVC, 54 ± 6 percent; mean ± SD), respiratory failure (PaO₂, 52 ± 6 mm Hg; PaCO₂, 56 ± 4 mm Hg), and clinical signs of inspiratory muscle fatigue underwent right cardiac catheterization while performing 20 minutes of INPV by a cuirass ventilator at a pressure (-20 to -40 cm H₂O) able to reduce the diaphragmatic electromyographic activity. Patients showed a mild basal pulmonary artery hypertension. During INPV, no changes in the mean values of HR (from 79 ± 20 to 80 ± 18 beats per minute), systolic BP (141 ± 19 to 139 ± 16 mm Hg), CO (5.2 ± 0.8 to 5.1 ± 1.3 L/min), mean PAP (23.8 ± 3.8 to 23.9 ± 4.4 mm Hg), RAP (4.3 ± 2.6 to 5.5 ± 2.5 mm Hg), PWP (10.3 ± 4.5 to 9.4 ± 2.9 mm Hg), TPR (369 ± 76 to 392 ± 124 dynes·s·cm^-5), and PVR (199 ± 51 to 233 ± 94 dynes·s·cm^-5) were observed. Direct systemic BP monitoring could be performed in six patients. During INPV, three patients showed 'pulsus paradoxus', as assessed by an inspiratory fall in systolic BP of 11, 13, and 20 mm Hg, respectively. We conclude that INPV by cuirass ventilator does not induce adverse hemodynamic effects in patients with COPD who have pulmonary artery hypertension.