Effects of hypoxia on diaphragm activity in anesthetized rats

Hypoxia is one of the most common conditions observed by PACU nurses after surgery. It may be caused by a reduced functional residual capacity, hypoventilation, and/or ventilation-perfusion mismatch. Hypoxia can also affect diaphragm contractility, making it difficult to wean postoperative patients from mechanical ventilation. Clinically, however, there is no method to directly measure diaphragm contractility; therefore, indicators of intrathoracic pressure such as tidal volume are used. The purpose of this study was to directly measure the effects of diaphragm shortening in 12 anesthetized Sprague-Dawley rats before, during, and after induced hypoxia. A miniaturized ultrasonic sensor was used to measure changes in diaphragm thickness as an index of diaphragm shortening. A stainless steel electrode was attached adjacent to the ultrasonic sensor and used to measure the electromyogram (EMG) of the diaphragm. After normoxic measurements were recorded, hypoxia was initiated by connecting the tracheal cannula to a latex balloon containing 7.4% oxygen in nitrogen. During the first 5 minutes of hypoxia, diaphragm shortening, EMG, and intrathoracic pressure increased. Over the next 30 to 100 minutes, EMG and intrathoracic pressure remained elevated, whereas diaphragm shortening decreased to 50% of control, which was defined as diaphragm fatigue. The mean time for hypoxia-induced diaphragm fatigue to occur was 63 minutes. These results indicate that hypoxia-induced decline in diaphragm shortening was not caused by a decrease in muscle excitation as measured by EMG. These data suggest that impairment in mechanical-chemical coupling (diaphragm shortening) could be a result of decreased oxygen availability associated with the lower arterial blood oxygen content. Thus, the increase in intrathoracic pressure throughout hypoxia suggests that intrathoracic pressure is not always a consistent index of the contractile state of the diaphragm.