[Diaphragmatic fatigue in hypovolemic shock]

A model of hemorrhagic shock (arterial mean pressure = 40 mmHg) terminated by death in all cases was developed in 21 dogs. The study was addressed to investigate the central respiratory response, development of diaphragmatic fatigue (FD) and the influence of the suppression of spontaneous rhythmic respiratory muscle activity by mechanical ventilation during shock. We measured diaphragmatic force: transdiaphragmatic pressure (Pdi), spontaneous and stimulated electrical activity of the diaphragm (integrated and rectified electromyogram: Edi) tracheal occlusion pressure (P 0, 1) cardiac output (Q) and survival, ventilatory variables were also measured. We constructed Pdi/Frequency and Pdi/Edi curves. The phrenic nerves were stimulated: 1) by bipolar electrodes at the 5th cervical roots or 2) by a bipolar electrode catheter introduced through the left jugular vein. The animals were divided in 3 groups: 1) during spontaneous breathing (light pentobarbital anesthesia and positive corneal reflex) Pdi/Frequency curves and Pdi response to single twitch were measured (n = 9); 2) evolution of Edi and Pdi/Edi curves during spontaneous breathing (n = 6); 3) Pdi/Frequency curves (n = 6) during mechanical ventilation (ARM). We found (groups 1, 2) initially compensated (increased P 0, 1 and hyperventilation: table 1) metabolic acidosis, followed by mixed acidosis after FD (fall in Pdi/Frequency: Fig. 1, and Pdi/Edi: Fig. 2, 3, table 3) and associated with falling respiratory frequency (Fr). During hyperventilation, central respiratory drive/minute: Edi.Ti.Fr (Ti = inspiratory time, sec) increased and fell later during FD, remaining however higher than basal.(ABSTRACT TRUNCATED AT 250 WORDS)