The relation of ventilatory failure to pulmonary, respiratory muscle and central nervous system disturbances in calves with an experimentally produced pneumonia.

To explore the pathophysiology of respiratory failure in an experimental pneumonia, a Pasteurella haemolytica broth culture was injected intratracheally into 12 calves, which were then studied over a period of 10 h. Measurements were made of inspired minute ventilation (VE), ventilatory pattern [inspiratory time (TI), expiratory time (TE), respiratory rate (RR) and tidal volume (VT)], transdiaphragmatic pressure (Pdi), occlusion pressure at the airway opening 100 milliseconds after onset of inspiration (Pawo100ms), arterial blood gas tensions and pH and recorded diaphragmatic electromyogram (EMGdi) and rectal temperature (Tr). On and after the third hour after inoculation, the animals varied in respect of clinical signs, Tr, RR, VE, Pawo100ms/EMGdi, and arterial gases and pH. In benign cases, diminished alertness, laboured respiration and fall of arterial oxygen pressure (PaO2) worsened up to 7 h after inoculation, but then progressively improved, VE being maintained at approximately 150% baseline throughout the study (10 h). Neither arterial carbon dioxide pressure (PaCO2) nor pH was altered. Moderate cases resembled benign cases in respect of laboured respiration, VE, PaO2 and PaCO2; however, pH was at first maintained at preinoculation levels, but declined thereafter. In severe cases, the animals were drowsy between hours 3 and 7, and became comatose between hours 8 and 10; in contrast to both benign and moderate cases: (1) RR was reduced by hour 5, (2) there was no trend towards recovery of PaO2 and pH, (3) VE, Pdi, Pawo100ms and Pawo100ms/EMGdi were severely decreased, and (4) PaCO2 increased. These results suggest that pneumonia does not alter ventilatory neuromuscular pump function in calves, unless concomitant cardiovascular collapse occurs. It is not clear whether fatal ventilatory failure is caused mainly by deterioration in ventilatory muscle fibre processes or structures, altered central nervous system adjustment of ventilatory timing, or cardiovascular dysfunction. However, inspiratory pressures fall when excitation to the diaphragm is still growing, which suggests peripheral respiratory muscle fatigue.