INSIGHTS INTO THE INCREASED OXYGEN-DEMAND DURING CHEST PHYSIOTHERAPY

Objectives: To determine the mechanism responsible for the increase in oxygen consumption (Vo(2)) during chest physical therapy. Specificall y, to examine the hypothesis that muscular activity is the major contr ibutor to the increase in oxygen demand. Design: Prospective, observat ional study. Setting: University hospital surgical intensive care unit . Patients: Phase one included 13 patients who were mechanically venti lated after coronary artery bypass surgery. Phase two involved seven m echanically ventilated patients who had undergone major vascular or ab dominal surgery. Interventions: Phase one involved turning patients to the lateral decubitus position. During the second phase, patients wer e given midazolam (0.15 mu g/kg) 2 mins before an initial chest physio therapy session and midazolam plus vecuronium (0.7 mg/kg) before a sub sequent session. Physiologic measurements were made during the resting periods before and following each session, as well as at the completi on of the intervention. Measurements and Main Results: Turning patient s to the lateral position resulted in significant increases in oxygen uptake and CO2 elimination (Vco(2)), Vo(2) increased from 219 +/- 21 ( SD) mL/min at rest to 324 +/- 58 mL/min (p <.05) with turning. These i ncreases in oxygen demand were met by increases in both oxygen deliver y (852 +/- 238 mL/min at rest to 1116 +/- 430 mL/min, p<.05) and extra ction (0.27 +/- 0.7 at rest to 0.32 +/- 0.09, p <.05). There were asso ciated increases in hemodynamic and respiratory variables including he art rate and systolic blood pressure. The administration of vecuronium completely suppressed the 50% increases in Vo(2) and Vco(2) seen with out the use of a muscle relaxant. The increases in systolic blood pres sure were unaffected by vecuronium. The magnitude of the increase in P aco(2) (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 vecuroniu m (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 respi ratory rate. This change was due to the parallel suppression of Vco(2) . Conclusions: The increase in metabolic demand during chest physiothe rapy is the result of increased muscular activity as evidenced by the suppression of Vo(2) following the administration of the muscle relaxa nt and the observation that turning a patient into the lateral decubit us position produces similar increases in Vo(2). The increases in bloo d pressure and cardiac output are due to another mechanism, most likel y enhanced sympathetic output. The increase in physiologic activity pr oduced by chest physiotherapy is thus secondary to both exercise-like and stress-like responses.