Effects of noninvasive ventilation on pulmonary gas exchange and hemodynamics during acute hypercapnic exacerbations of chronic obstructive pulmonary disease

Abstract

Noninvasive positive pressure ventilation (NIPPV) can replace tracheal intubation in acute exacerbations of chronic obstructive pulmonary disease (COPD) with severe hypercapnic respiratory failure. However, the underlying mechanisms by which NIPPV improves pulmonary gas exchange are not known. We studied 10 male COPD patients (68 ± 8 [SD] yr) with acute severe hypercapnic respiratory failure within 36 h after hospital admission. Measurements of pulmonary gas exchange, hemodynamics, and respiratory mechanics were done: (1) breathing spontaneously (baseline); (2) after 15 and 30 min of NIPPV with pressure support (inspiratory pressure = 12 ± 2 cm H2O, PEEP = 3 ± 2 cm H2O); and (3) 15 min after NIPPV withdrawal. Patients were ventilated using a full face mask, keeping FI(O2) constant (0.23 ± 0.02) in all conditions. Compared with baseline, during NIPPV (15 min) we observed a moderate increase in Pa(O2) (from 50 ± 6 to 57 ± 9 mm Hg; p < 0.05), and a fall in Pa(CO2) (from 66 ± 10 to 59 ± 10 mm Hg; p < 0.0001), but AaP(O2) increased (from 39 ± 13 to 48 ± 13 mm Hg; p < 0.001). Breathing frequency decreased (from 26 ± 5 to 19 ± 3 breaths/min; p < 0.0001), tidal volume increased (from 311 ± 42 to 520 ± 133 ml; p < 0.0001), and minute ventilation increased (from 8.0 to 1.7 to 9.6 ± 2.0 L/min; p < 0.05). Cardiac output fell during NIPPV in all patients (from 6.7 ± 1.6 to 5.8 ± 1.3 L/min; p < 0.0025) with no impact on mixed venous P(O2). No substantial changes in V̇(A)/Q̇ mismatching (multiple inert gas elimination technique) were observed. While oxygen uptake showed a trend to decrease, the respiratory exchange ratio (R) increased (from 0.78 ± 0.17 to 0.90 ± 0.22; p < 0.001). The effects of NIPPV were unchanged at 30 min compared with 15 min and were reversed after 15 min of NIPPV withdrawal. We conclude that improvement in respiratory blood gases during NIPPV is essentially due to higher alveolar ventilation (p < 0.001) and not to improvement in V̇(A)/Q̇ relationships. The increase in AaP(O2) was explained by the rise in R due to an increased clearance of body stores of CO2 during NIPPV. Our results indicate that attainment of an efficient breathing pattern rather than high inspiratory pressures should be the primary goal to improve arterial blood gases during NIPPV in this type of patient.