• K Horiuchi, D Jordan, D Cohen, M C Kemper, and C Weissman.
• Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY, USA.
• Crit. Care Med. 1997 Aug 1; 25 (8): 1347-51.

ObjectivesTo determine the mechanism responsible for the increase in oxygen consumption (VO2) during chest physical therapy. Specifically, to examine the hypothesis that muscular activity is the major contributor to the increase in oxygen demand.DesignProspective, observational study.SettingUniversity hospital surgical intensive care unit.PatientsPhase one included 13 patients who were mechanically ventilated after coronary artery bypass surgery. Phase two involved seven mechanically ventilated patients who had undergone major vascular or abdominal surgery.InterventionsPhase one involved turning patients to the lateral decubitus position. During the second phase, patients were given midazolam (0.15 microg/kg) 2 mins before an initial chest physiotherapy session and midazolam plus vecuronium (0.7 mg/kg) before a subsequent session. Physiologic measurements were made during the resting periods before and following each session, as well as at the completion of the intervention.Measurements And Main ResultsTurning patients to the lateral position resulted in significant increases in oxygen uptake and CO2 elimination (VCO2). VO2 increased from 219 +/- 21 (SD) mL/min at rest to 324 +/- 58 mL/min (p <.05) with turning. These increases in oxygen demand were met by increases in both oxygen delivery (852 +/- 238 mL/min at rest to 1116 +/- 430 mL/min, p < .05) and extraction (0.27 +/- 0.7 at rest to 0.32 +/- 0.09, p < .05). There were associated increases in hemodynamic and respiratory variables including heart rate and systolic blood pressure. The administration of vecuronium completely suppressed the 50% increases in VO2 and VCO2 seen without the use of a muscle relaxant. The increases in systolic blood pressure were unaffected by vecuronium. The magnitude of the increase in PaCO2 (32 +/- 5 torr [4.3 +/- 0.7 kPa] at rest to 36 +/- 5 torr [4.8 +/- 0.7 kPa] during therapy, p < .05), was not accentuated by vecuronium (30 +/- 4 torr [4.0 +/- 0.5 kPa] to 35 +/- 6 torr [4.7 +/- 0.8 kPa], p < .05) despite a lack of any increase in minute ventilation or respiratory rate. This change was due to the parallel suppression of VCO2.ConclusionsThe increase in metabolic demand during chest physiotherapy is the result of increased muscular activity as evidenced by the suppression of VO2 following the administration of the muscle relaxant and the observation that turning a patient into the lateral decubitus position produces similar increases in VO2. The increases in blood pressure and cardiac output are due to another mechanism, most likely enhanced sympathetic output. The increase in physiologic activity produced by chest physiotherapy is thus secondary to both exercise-like and stress-like responses.

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