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.