Cardiopulmonary effects of permissive hypercapnia in the management of adult respiratory distress syndrome.

Abstract

Despite numerous advances, the mortality from adult respiratory distress syndrome (ARDS) remains high. Traditional ventilator management in ARDS has been to maintain normal PaCO2 by positive pressure ventilation (PPV). However, high levels of PPV may worsen the lung injury by alveolar overdistension. Permissive hypercapnia (PHC) has been proposed as an alternative method of ventilation, but hypercapnia may affect the hemodynamics of a hyperdynamic, critically ill patient. The purpose of this study was to determine the effect of PHC on ventilator requirement, arterial oxygenation, and hemodynamic performance in patients with severe ARDS. Ten men and 5 women with established ARDS (mean Murray lung injury score 3.42 +/- 0.1) were prospectively studied using an established protocol when the static pulmonary plateau pressure (Pplat) exceeded 40 cm H2O. The initial tidal volume (V(t)) was decreased to achieve a Pplat < 40 cm H2O or to a lower limit of 5 cc/kg. Arterial blood gas and hemodynamic data were obtained serially. The V(t) was reduced from 9.9 +/- 0.5 mL/kg to 7.7 +/- 0.5 mL/kg at 24 hours, p < 0.05. This reduction of V(t) produced a decrease in minute ventilation (Ve: 18.0 +/- 1.6 to 11.9 +/- 0.7 L/min, p < 0.05), peak airway pressure (PAP: 55 +/- 2 vs 45 +/- 3 cm H2O, p < 0.05), and Pplat (Pplat 45.4 +/- 1.5 vs. 36.7 +/- 1.9) at 24 hours. The PaCO2 rose from 37.9 +/- 1.3 to 56.7 +/- 3.0 mm Hg (p < 0.05), and the pH decreased from 7.41 +/- 0 to 7.31 +/- 0 (p < 0.05) at 24 hours. There were no significant changes in mean airway pressure, static compliance, arterial oxygenation, pulmonary vascular resistance, systemic vascular resistance, cardiac index, or systemic oxygen delivery and consumption. Permissive hypercapnia by V(t) reduction: (1) decreased Ve, PAP, and Pplat without a change in mean airway pressure, static compliance or arterial oxygenation; (2) caused a mild partially compensated acidosis; and (3) does not adversely affect pulmonary vascular resistance, systemic vascular resistance, cardiac index, or systemic oxygen delivery and consumption.