Respiratory muscle fatigue: a cause of ventilatory failure in septic shock

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Abstract
The effect of endotoxic shock on the respiratory muscle performance was studied in spontaneously breathing dogs given Escherichia coli endotoxin (10 mg/kg). Diaphragmatic (Edi) and parasternal intercostal (Eic) electromyograms were recorded using fishhook electrodes. The recorded signals were then rectified and electrically integrated. Pleural, abdominal and transdiaphragmatic (Pdi) pressures were recorded by a balloon-catheter system. After a short control period, the endotoxin was administered slowly i.v. (within 5 min). Death was secondary to respiratory arrest in all animals. All animals died within 150-270 min after the onset of endotoxic shock. Within 45-80 min of the endotoxin administration, mean blood pressure and cardiac output dropped to 42.1 .+-. 4.1 and 40.1 .+-. 6.0% (mean .+-. SE)of control values, respectively, with little change afterward. Mean inspiratory flow rate and Pdi increased from control values of 0.27 .+-. 0.03 l .cntdot. s-1 and 5.75 .+-. 0.7 cmH2O to mean values of 0.44 .+-. 0.3 l .cntdot. s-1 and 8.70 .+-. 1.05 cmH2O, and then decreased to 0.17 .+-. 0.03 l .cntdot. s-1 and 3.90 .+-. 0.30 cmH2O before the death of the animals. There were no major changes in the mechanics of the respiratory system. Edi and Eic increased progressively to mean values of 360 .+-. 21 and 263 .+-. 22% of control, respectively, before the death of the animals. None of the dogs were hypoxic. Arterial PCO2 decreased from a control value of 42.9 .+-. 1.7 Torr to a mean value of 29.9 .+-. 2.8 Torr, and then increased to 51 .+-. 4.3 Torr before the death of the animals. The ventilatory failure of E. coli endotoxic shock was due to fatigue of the respiratory muscles.

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