Effects of the components of positive airway pressure on work of breathing during bronchospasm

INTRODUCTION: Partial assist ventilation reduces work of breathing in patients with bronchospasm; however, it is not clear which components of the ventilatory cycle contribute to this process. Theoretically, expiratory positive airway pressure (EPAP), by reducing expiratory breaking, may be as important as inspiratory positive airway pressure (IPAP) in reducing work of breathing during acute bronchospasm. METHOD: We compared the effects of 10 cmH(2)O of IPAP, EPAP, and continuous positive airwaypressure (CPAP) on inspiratory work of breathing and end-expiratory lung volume (EELV) in a canine model of methacholine-induced bronchospasm. RESULTS: Methacholine infusion increased airway resistance and work of breathing. During bronchospasm IPAP and CPAP reduced work of breathing primarily through reductions in transdiaphragmatic pressure per tidal volume (from 69.4 ± 10.8 cmH(2)O/l to 45.6 ± 5.9 cmH(2)O/l and to 36.9 ± 4.6 cmH(2)O/l, respectively; P < 0.05) and in diaphragmatic pressure–time product (from 306 ± 31 to 268 ± 25 and to 224 ± 23, respectively; P < 0.05). Pleural pressure indices of work of breathing were not reduced by IPAP and CPAP. EPAP significantly increased all pleural and transdiaphragmatic work of breathing indices. CPAP and EPAP similarly increased EELV above control by 93 ± 16 ml and 69 ± 12 ml, respectively. The increase in EELV by IPAP of 48 ± 8 ml (P < 0.01) was significantly less than that by CPAP and EPAP. CONCLUSION: The reduction in work of breathing during bronchospasm is primarily induced by the IPAP component, and that for the same reduction in work of breathing by CPAP, EELV increases more

Airflow–volume tidal expiratory curves shifted to allow airflow comparisons under isovolumic conditions in three randomly selected animals

<p><b>Copyright information:</b></p><p>Taken from "Effects of the components of positive airway pressure on work of breathing during bronchospasm"</p><p>Critical Care 2004;8(2):R72-R81.</p><p>Published online 9 Feb 2004</p><p>PMCID:PMC420031.</p><p>Copyright © 2004 Miro et al., licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.</p> Inspiratory positive airway pressure (IPAP) and continuous positive airway pressure (CPAP) produced a leftward parallel shift in the expiratory curves, which is indicative of increases in end-expiratory lung volume (EELV) without changes in expiratory resistance compared with control conditions. Functional residual capacity (FRC) was defined as the EELV during spontaneous breathing (no positive airway pressure). Relative volume represents the increases in EELV above FRC, as defined above

Tracheal gas insufflation. Limits of efficacy in adults with acute respiratory distress syndrome.

In mechanically ventilated adults with acute respiratory distress syndrome (ARDS), peak airway pressures (Paw(peak)) above 35 cm H(2)O may increase the risk of barotrauma or volutrauma. Tracheal gas insufflation (TGI), an adjunctive ventilatory technique, may facilitate a reduction in set inspiratory pressure in these patients, and thereby in the tidal volume (VT) and Paw(peak) used in their ventilation, without a consequent increase in arterial carbon dioxide tension (PaCO(2)). The purpose of this study was to: (1) assess the limits of efficacy of continuous TGI at two levels of decreased mechanical ventilatory support; and (2) determine an appropriate time interval after initiation of TGI at which to evaluate response. We prospectively studied eight adults with ARDS and increased airway pressures (40.2 +/- 2.7 cm H(2)O) who were managed with pressure-control ventilation (PCV). After obtaining baseline ventilatory and hemodynamic measures, we initiated TGI at 10 L/min, adjusting ventilator positive-end expiratory pressure (PEEP) to maintain baseline VT, and decreased the set inspiratory pressure by 5 cm H(2)O. Data were obtained after 30 and 60 min. Set inspiratory pressure was then decreased by an additional 5 cm H(2)O (total: 10 cm H(2)O), and data were again obtained after 30 min. Baseline (zero TGI) measures were then again recorded. Thirty minutes after decreasing the set inspiratory pressure by 5 cm H(2)O with TGI at 10 L/min, there was a 15% decrease in Paw(peak) and a 16% decrease in VT as compared with their baseline values. However, Pa(CO(2)) remained constant (59 +/- 10 mm Hg versus 57 +/- 6 mm Hg) (p = NS). There was no change in Pa(O(2)) or in hemodynamic variables, and no differences between variables, at 30 min versus 60 min in seven subjects. The remaining subject did not tolerate the reduction in set inspiratory pressure for 60 min. Thirty minutes after the set inspiratory pressure was decreased by 10 cm H(2)O with TGI at 10 L/min, there was a 26% decrease in Paw(peak) and a 26% decrease in VT. However, Pa(CO(2)) increased by 19% and Pa(O(2)) decreased by 13%. Six subjects completed this phase of the protocol for 30 min, and one subject completed it for 60 min. TGI can be used to rapidly facilitate a 5 cm H(2)O reduction in set inspiratory pressure without an increase in Pa(CO(2)). The ability to achieve a 5 cm H(2)O reduction in set inspiratory pressure without adverse physiologic effects was evident within 30 min. Attempts to further reduce set inspiratory pressure were not successful