Mechanisms of breathing instability in patients with obstructive sleep apnea

The response to chemical stimuli (chemical responsiveness) and the increases in respiratory drive required for arousal (arousal threshold) and for opening the airway without arousal (effective recruitment threshold) are important determinants of ventilatory instability and, hence, severity of obstructive apnea. We measured these variables in 21 obstructive apnea patients (apnea-hypopnea index 91 ± 24 h−1) while on continuous-positive-airway pressure. During sleep, pressure was intermittently reduced (dial down) to induce severe hypopneas. Dial downs were done on room air and following ≈30 s of breathing hypercapneic and/or hypoxic mixtures, which induced a range of ventilatory stimulation before dial down. Ventilation just before dial down and flow during dial down were measured. Chemical responsiveness, estimated as the percent increase in ventilation during the 5th breath following administration of 6% CO2 combined with ≈4% desaturation, was large (187 ± 117%). Arousal threshold, estimated as the percent increase in ventilation associated with a 50% probability of arousal, ranged from 40% to >268% and was <120% in 12/21 patients, indicating that in many patients arousal occurs with modest changes in chemical drive. Effective recruitment threshold, estimated as percent increase in pre-dial-down ventilation associated with a significant increase in dial-down flow, ranged from zero to >174% and was <110% in 12/21 patients, indicating that in many patients reflex dilatation occurs with modest increases in drive. The two thresholds were not correlated. In most OSA patients, airway patency may be maintained with only modest increases in chemical drive, but instability results because of a low arousal threshold and a brisk increase in drive following brief reduction in alveolar ventilation.

The Oxygen Analyser: Applications and Limitations – An Analysis of 2000 Incident Reports

The first 2000 incidents reported to the Australian Incident Monitoring Study were analysed with respect to the role of the oxygen analyser; 27 (1%) were first detected by the oxygen analyser. All of these were amongst the 1256 incidents which occurred in association with general anaesthesia, of which 48% were “human detected” and 52% “monitor detected”. The oxygen analyser was ranked 7th and detected 4% of these monitor detected incidents. This figure would have been much higher had the oxygen analyser been correctly used on more occasions. The oxygen analyser detected 10 ventilator-driving-gas leaks into the circuit, 6 hypoxic mixtures due to rotameter settings, 3 inappropriate nitrous oxide concentrations, 2 disconnections and 1 leak at the common gas outlet, and 2 partial and 1 total failure of ventilation. In a theoretical analysis of these 1256 incidents it was considered that the oxygen analyser, used on its own, would have detected 114 (9%), had they been allowed to evolve (3% before any potential for organ damage). In 4 incidents an oxygen analyser gave faulty readings, in 3 caused a leak and in one a total circuit obstruction; 5 incidents were not detected because the alarm had been disabled. Despite the advent of piped gas supplies, failure of gas delivery or delivery of a “wrong” gas mixture still occurs surprisingly frequently in current anaesthetic practice; hypoxic mixtures were supplied on 16 occasions, other “wrong” mixtures on 23 and the oxygen supply failed on 7 occasions. Failure to use and improper use of the oxygen analyser is also surprisingly common; this is mainly due to a rule-based error encouraged by the poor design of the high alarm. It is highly recommended that a suitable, correctly sited, calibrated, tested oxygen analyser be used from before pre-oxygenation until the patient is no longer breathing gas from the anaesthetic machine or circuit.

Time course of phrenic activity and respiratory pressures during airway occlusion in cats

The morphology of integrated ("moving time average") phrenic electroneurograms (EPHR) and of tracheal (Ptr) and transdiaphragmatic (Pdi) pressure waves during occluded inspirations was studied in eight anesthetized cats breathing air and various hypercapnic and hypoxic mixtures. The shape of the rising part of EPR-, Ptr-, and Pdi-time profiles varied between animals (from convex to concave), but in each animal it remained virtually unchanged by hypoxia and hypercapnia. The shape of the Ptr and Pdi occlusion waves reflected the shape of EPHR. The relationship of EPHR to Pdi and Ptr did not change with chemical drive. It is concluded that central inspiratory activity (CIA) (as reflected by EPHR and its mechanical transforms Pdi and Ptr) increases in amplitude with stimulation of breathing but that the profile of CIA remains essentially unchanged. However, substantial differences in the time course development of phrenic activity, Pdi, and Ptr exist between cats. The fixed interrelationships among EPHR, Pdi, and Ptr indicate a proportional increase in activity among all inspiratory muscles with increased chemical drive.

Absence of effects of hypoxia on small airway function in humans

We measured the effects of sustained isocapnic hypoxia (PAO2 = 40--50 Torr; PACO2 = 38--42 Torr) on tests sensitive to small airway function in healthy human subjects. Maximum expiratory flow-volume curves on air, nitrogen-hypoxic, helium-normoxic, and helium-hypoxic mixtures as well as closing volumes while subjects breathed air and a hypoxic mixture were obtained. We then measured total lung capacity (TLC), both plethysmographically and by inert gas dilution, and used the nonplethysmographic method to measure the effects of hypoxia on TLC. In none of these tests were there any statistically significant changes when values obtained during hypoxia were compared with those during normoxia. It is suggested that previous reports that indicated that TLC was increased by hypoxia might have arisen from a plethysmographic artifact.

Hypoxia with a Third Flowmeter Tube on the Anaesthetic Machine

Hypoxic mixtures of oxygen and nitrous oxide were demonstrated with three anaesthesia machines which had cyclopropane flowmeters. In one machine the bobbin did not prevent back flow and the hypoxic mixture occurred when the cyclopropane flow control was left open. Two other machines only delivered hypoxic mixtures if the cyclopropane bobbins were removed from their seats and the flow controls opened. The vaporizer on one machine increased the hypoxia when turned on.