Moderate and prolonged hypercapnic acidosis may protect against ventilator-induced diaphragmatic dysfunction in healthy piglet: an in vivo study

Abstract

IntroductionProtective ventilation by using limited airway pressures and ventilation may result in moderate and prolonged hypercapnic acidosis, as often observed in critically ill patients. Because allowing moderate and prolonged hypercapnia may be considered protective measure for the lungs, we hypothesized that moderate and prolonged hypercapnic acidosis may protect the diaphragm against ventilator-induced diaphragmatic dysfunction (VIDD). The aim of our study was to evaluate the effects of moderate and prolonged (72 hours of mechanical ventilation) hypercapnic acidosis on in vivo diaphragmatic function.MethodsTwo groups of anesthetized piglets were ventilated during a 72-hour period. Piglets were assigned to the Normocapnia group (n = 6), ventilated in normocapnia, or to the Hypercapnia group (n = 6), ventilated with moderate hypercapnic acidosis (PaCO2 from 55 to 70 mm Hg) during the 72-hour period of the study. Every 12 hours, we measured transdiaphragmatic pressure (Pdi) after bilateral, supramaximal transjugular stimulation of the two phrenic nerves to assess in vivo diaphragmatic contractile force. Pressure/frequency curves were drawn after stimulation from 20 to 120 Hz of the phrenic nerves. The protocol was approved by our institutional animal-care committee.ResultsModerate and prolonged hypercapnic acidosis was well tolerated during the study period. The baseline pressure/frequency curves of the two groups were not significantly different (Pdi at 20 Hz, 32.7 ± 8.7 cm H2O, versus 34.4 ± 8.4 cm H2O; and at 120 Hz, 56.8 ± 8.7 cm H2O versus 60.8 ± 5.7 cm H2O, for Normocapnia and Hypercapnia groups, respectively). After 72 hours of ventilation, Pdi decreased by 25% of its baseline value in the Normocapnia group, whereas Pdi did not decrease in the Hypercapnia group.ConclusionsModerate and prolonged hypercapnic acidosis limited the occurrence of VIDD during controlled mechanical ventilation in a healthy piglet model. Consequences of moderate and prolonged hypercapnic acidosis should be better explored with further studies before being tested on patients.

Hypercapnia attenuates ventilator-induced diaphragm atrophy and modulates dysfunction

“…Very recently however, Jung et al . showed that hypercapnic acidosis protects against diaphragm dysfunction in piglets after 72 hours of mechanical ventilation [9]. In apparent contrast, we observed a decreased force in single fibers after 18 hours of hypercapnic mechanical ventilation.…”

Effects of acute hypercapnia with and without acidosis on lung inflammation and apoptosis in experimental acute lung injury

“…The proportion of alveolar collapse in non-ventilated animals was approximately 30% (Table 2), which is similar to that observed in previous experimental ALI studies (Rocco et al, 2001;Farias et al, 2005;Santiago et al, 2010). Carbon dioxide was increased with an inhaled gas mixture containing 5% CO 2 in air to maintain a PaCO 2 between 60 and 70 mmHg, which is defined as a moderate level of hypercapnia (Jung et al, 2013). This method allows increasing PaCO 2 without changes in RR or V T , since these changes may lead to ventilator-induced lung injury, and could add bias to the study design.…”

Ventilator-induced diaphragmatic dysfunction

“…In this regard, piglets ventilated with increased dead space to achieve moderate hypercapnic acidosis (pCO 2 55-70 mmHg) showed preserved diaphragmatic force production after 72 h of mechanical ventilation [49]. A similar level of hypercapnia induced by adding inspired CO 2 also attenuated several aspects of VIDD in rats [50].…”