L. A. Engel

Cardiorespiratory consequences of expiratory chest wall compression during mechanical ventilation and severe hyperinflation.

To measure and compare the effects of manual expiratory compression of either the rib cage or abdomen on cardiac output, end-expiratory lung volume, and other cardiorespiratory variables in an animal model that mimics the severe pulmonary hyperinflation and hemodynamic impairment occurring in patients with severe acute asthma during mechanical ventilation. Design:Prospective, randomized, crossover trial. Setting:Research laboratory. Subjects:Seven cross-bred, anesthetized, supine dogs. Interventions:The following sequence was employed: a) spontaneous breathing without pulmonary hyperinflation; b) positive-pressure ventilation with severe pulmonary hyperinflation (produced by an external variable expiratory flow resistor); c) ∼7 mins of manual expiratory compression of either the rib cage or abdomen during positive-pressure ventilation-hyperinflation. This sequence was then repeated, incorporating the alternative type of expiratory compression. Measurements and Main Results:Cardiac output (measured by thermodilution), aortic pressure, pleural (esophageal) pressure, and changes in end-expiratory lung volume were measured. The decrease in cardiac output due to mechanical ventilation with pulmonary hyperinflation was exacerbated by rib cage compression (p < .001; spontaneous breathing 2.9 ± 0.2 L/min, hyperinflation 1.5 ± 0.1 L/min, and rib cage compression 1.0 ± 0.1 [SEM] L/min). However, the positive-pressure ventilation-hyperinflation-induced decrease in cardiac output was attenuated by abdominal compression (p < .001; spontaneous breathing 3.3 ± 0.2 L/min, hyperinflation 1.4 ± 0.1 L/min, and abdominal compression 2.1 ± 0.1 L/min). Mean aortic pressure returned to prehyperinflation levels during abdominal compression (p < .001; spontaneous breathing 126 ± 2 mm Hg, hyperinflation 75 ± 5 mm Hg, and abdominal compression 120 ± 3 mm Hg). Both types of compression were similarly effective (p > .75) in increasing mean expiratory pleural pressure, so that end-expiratory lung volume ‘was similarly (p > .25) reduced (0.45 ± 0.05 and 0.40 ± 0.05 L for rib cage and abdominal compressions, respectively) in this non-air flow, limiting animal model. Conclusions:The cardiorespiratory effects of manually compressing the rib cage or abdomen during expiration in this animal study suggest that these techniques should be carefully evaluated in mechanically ventilated patients with severe acute asthma. (Crit Care Med 1993; 21: 1908–1914)