Anaesthetic management of patients with sleep apnoea syndrome

Purpose

Sleep apnoea syndrome (SAS) is a relatively common, potentially fatal, disorder. Patients with SAS exhibit repetitive, often prolonged episodes of apnoea during sleep, with serious nocturnal and diurnal physiologic derangements. Several anecdotal reports and clinical studies have documented anaesthetic-related occurrence of fatal and near-fatal respiratory complications in these patients. The purpose of this article is to outline the potential problems encountered in anaesthetic management of adult SAS patients, and to suggest a practical approach for anaesthesia both for incidental and specific procedures.

Principal findings

SASs have many implications for the anaesthetist. First, SAS patients are exquisitely sensitive to all central depressant drugs, with upper airway obstruction or respiratory arrest occurring even with minimal doses. Thus sedative and opioid premedication should be omitted as should the intra and postoperative use of opioids be limited or avoided. All anaesthetic drugs should be administered by titration to desired effect, preferably using short-acting drugs. When feasible, continuous regional anaesthesia using a catheter is the technique of choice. Where possible nonopioid analgesics or local anaesthetics should be used for postoperative analgesia. Perioperative monitoring for apnoea, desaturation, and dysrhythmias is essential. Secondly, SAS patients have a potentially difficult airway. Awake intubation is the safest approach to airway control. Extubation should only be tried in the fully conscious patient with intact upper airway function and under controlled situations. Thirdly, the cardiorespiratory complications of SAS and the presence of associated diseases can adversely influence anaesthetic management.

Conclusion

Perioperative risks attending SAS patients emphasize the importance of their detection, perioperative evaluation and planning.     

Pulmonary arterial hypertension in patients with sleep apnoea syndrome

BACKGROUND: Pulmonary arterial hypertension (PAH) in patients with sleep apnoea syndrome (SAS) is classically ascribed to associated chronic obstructive pulmonary disease (COPD). The aim of this retrospective study was to evaluate the possible occurrence of PAH as a complication of SAS in patients without COPD. METHODS: Right heart catheterisation was performed in 44 patients with SAS and without COPD confirmed by polysomnography (apnoea index >5/h) admitted for the administration of nasal continuous positive airway pressure (CPAP). RESULTS: Precapillary PAH, defined as mean pulmonary arterial pressure of >20 mm Hg with pulmonary capillary wedge pressure <15 mm Hg, was observed in 12/44 (27%) patients with SAS. There were no significant differences in apnoea index between patients with (PAH+) and those without PAH (PAH-) (42.6 (26.3) versus 35.8 (21.7) apnoeas/h). The PAH+ group differed significantly from the PAH- group in the following respects: lower daytime arterial oxygen tension (PaO(2)) (9.6 (1.1) versus 11.3 (1.5) kPa, p=0.0006); higher daytime arterial carbon dioxide tension (PaCO(2)) (5.8 (0.5) versus 5.3 (0.5) kPa, p=0.002); more severe nocturnal hypoxaemia with a higher percentage of total sleep time spent at SaO(2) <80% (32.2 (28.5)% versus 10.7 (18.8)%, p=0.005); and higher body mass index (BMI) (37.4 (6) versus 30.3 (6.7) kg/m(2), p=0.002). The PAH+ patients had significantly lower values of vital capacity (VC) (87 (14)% predicted versus 105 (20)% predicted, p=0.005), forced expiratory volume in one second (FEV(1)) (82 (14)% predicted versus 101 (17)% predicted, p=0.001), expiratory reserve volume (40 (16)% predicted versus 77 (41)% predicted, p=0.003), and total lung capacity (87 (13)% predicted versus 98 (18)% predicted, p=0.04). Stepwise multiple regression analysis showed that mean pulmonary artery pressure (PAPm) was positively correlated with BMI and negatively with PaO(2). CONCLUSION: Pulmonary arterial hypertension is frequently observed in patients with SAS, even when COPD is absent, and appears to be related to the severity of obesity and its respiratory mechanical consequences.     

Compliance with CPAP therapy in patients with the sleep apnoea/hypopnoea syndrome.

BACKGROUND--Continuous positive airway pressure (CPAP) therapy is the treatment of choice for the sleep apnoea/hypopnoea syndrome. Compliance with this relatively obtrusive therapy has not been well studied. METHODS--Usage of CPAP was investigated in 54 patients with sleep apnoea/hypopnoea syndrome (median 36 (range 7-129) apnoeas + hypopnoeas/hour slept) over the first 1-3 months after starting CPAP therapy. In all cases CPAP usage was monitored by hidden time clocks that indicated for how long the machines were switched on--that is, the CPAP run time. In 32 patients the time at which the CPAP mask pressure was at the therapeutic level of CPAP pressure set for that patient--that is, the mask time--was also monitored. In all patients objective daytime sleepiness was assessed by multiple sleep latency before and after CPAP therapy. RESULTS--The mean (SE) nightly CPAP run time was 4.7 (0.4) hours. There was no correlation between run time and severity of the sleep apnoea/hypopnoea syndrome as assessed by apnoea + hypopnoea frequency or multiple sleep latency, and no correlation between CPAP usage and improvement in multiple sleep latency. Thirty two patients in whom mask time was recorded had therapeutic CPAP pressures for 89% (3%) of their CPAP run times. Patients who experienced side effects from CPAP used their CPAP machines significantly less than those who did not. CONCLUSIONS--Patients with sleep apnoea/hypopnoea syndrome used CPAP for less than five hours/night on average with no correlation between severity of sleep apnoea/hypopnoea syndrome and CPAP usage. Patients who complained of side effects used their CPAP therapy less. It is recommended that, as a minimum, CPAP run time should be regularly recorded in all patients receiving CPAP therapy.     

Postoperative management of patients with obstructive sleep apnoea syndrome

Editor—Patients with sleep apnoea are particularly atrisk from the respiratory depressant effects of inhaled anaesthetics,sedatives, and opioids after operation. Reduced upper airwaystone during deeper rapid eye movement (REM) sleep and     

Effects of posture on carbon dioxide responsiveness in patients with obstructive sleep apnoea.

BACKGROUND--It is well known that upper airway resistance increases with postural change from a sitting to supine position in patients with obstructive sleep apnoea (OSA). It is not known, however, how the postural change affects the ventilatory and occlusion pressure response to hypercapnia in patients with OSA when awake. METHODS--The responses of minute ventilation (VE) and mouth pressure 0.1 seconds after the onset of occluded inspiration (P0.1) to progressive hypercapnia (delta VE/delta PCO2, delta P0.1/delta PCO2) both in sitting and supine positions were measured in 20 patients with OSA. The ratio of the two (delta VE/delta P0.1) was obtained as an index of breathing efficiency. The postural changes in response to carbon dioxide (CO2) after uvulopalatopharyngoplasty (UPPP) were also compared in seven patients with OSA. RESULTS--There were no significant changes in the resting values of end tidal PCO2, P0.1, or VE between the two positions. During CO2 rebreathing, delta VE/delta PCO2 did not differ between the two positions, but delta P0.1/delta PCO2 was significantly higher in the supine than in the sitting position (supine, mean 0.67 (SE 0.09) cm H2O/mm Hg; sitting, mean 0.57 (SE 0.08) cm H2O/mm Hg), and delta VE/delta P0.1 decreased significantly from the sitting to the supine position (sitting, 4.6 (0.4) l/min/cm H2O; supine, 3.9 (0.4) l/min/cm H2O). In seven patients with OSA who underwent UPPP, delta VE/delta P0.1 improved significantly in the supine position and postural change in delta VE/delta P0.1 was eliminated. CONCLUSIONS--These results suggest that in patients with OSA the inspiratory drive in the supine position increases to maintain the same level of ventilation as in the sitting position, and that the postural change from sitting to supine reduces breathing efficiency. Load compensation mechanisms of patients with OSA appear to be intact while awake in response to the rise in upper airway resistance.     

Obstructive sleep apnoea syndrome in children

Obstructive sleep apnoea syndrome in children is a complex disorder characterised by repeated nocturnal episodes of increased upper airway resistive load. It is most commonly associated with adenotonsillar hypertrophy and more children are now presenting for adenotonsillectomy. These children may pose different anaesthetic problems to those having surgery for recurrent infection alone and anaesthetic morbidity and mortality has been reported. In addition, due to the varied symptomatology of the condition, children with unrecognised obstructive sleep apnoea syndrome may present for incidental surgery. This is of importance as patients with undiagnosed obstructive sleep apnoea syndrome may experience additional peri-operative morbidity when undergoing incidental surgery. This article aims to review the aetiology, pathophysiology, clinical presentation and anaesthetic management of children with obstructive sleep apnoea syndrome.     

Uvulopalatopharyngoplasty in severe idiopathic obstructive sleep apnoea syndrome.

Eleven patients with severe obstructive sleep apnoea syndrome, which was fully reversed by treatment with nasal continuous positive airways pressure, underwent uvulopalatopharyngoplasty. All patients were followed for at least 12 months after surgery. One patient with large tonsils was cured. Of the remaining 10 patients, two showed minimal objective improvement at 12 months and the rest were unchanged. Four patients subsequently developed cardiac failure due to obstructive sleep apnoea. Thus uvulopalatopharyngoplasty was not effective in these patients with severe idiopathic obstructive sleep apnoea syndrome.     

Effects of submental stimulation for several consecutive nights in patients with obstructive sleep apnoea.

BACKGROUND--It has previously been reported that short term submental stimulation can reduce the frequency of apnoea and improve sleep architecture in patients with obstructive sleep apnoea. The effects of submental stimulation during consecutive nights on apnoea or on daytime sleepiness have not, however, been studied. METHODS--Patients with obstructive sleep apnoea were studied by polysomnography on a control night, for five consecutive nights of submental stimulation, and on three following nights (n = 8). A multiple sleep latency test (MSLT) (n = 8) and measurement of the upper airway resistance (n = 5) were performed during the day after the polysomnographic study, on the control night, and on the fifth stimulation night. In an additional five patients with obstructive sleep apnoea, matched for age, sex, and weight, the effects of two nights of stimulation were examined for comparison. Submental stimulation began when an apnoea lasted for five seconds and stopped with the resumption of breathing as detected by oronasal flow. RESULTS--The apnoea index, the number of times per hour that SaO2 dropped below 85% (SaO2 < 85%/hour), and the total apnoea duration expressed as a percentage of total sleep time during stimulation nights decreased to approximately 50% of the corresponding values on the control night. This improvement persisted for at least two nights after the five consecutive stimulation nights, but not after the two consecutive stimulation nights. Sleep architecture and MSLT following the stimulation nights improved but upper airway resistance did not change. CONCLUSIONS--Submental stimulation for five consecutive nights in patients with obstructive sleep apnoea improved the breathing disturbance, sleep quality, and daytime sleepiness. The effect lasted for the following two nights, but did not completely abolish the sleep disordered breathing.     

Tetraplegic obstructive sleep apnoea patients dilate the airway similarly to able-bodied obstructive sleep apnoea patients

Context/objective: Obstructive sleep apnoea (OSA) develops soon after cervical spinal cord injury (SCI) at rates higher than the general population, but the mechanisms are not understood. This study aimed to determine whether OSA in SCI is associated with altered pharyngeal muscle dilatory mechanics during quiet breathing, as has been observed in the non-SCI injured with obstructive sleep apnoea.Design: Cross sectional imaging study.Setting: Medical research institute.Participants: Eight cervical SCI patients with OSA were recruited and compared to 13 able-bodied OSA patients and 12 able-bodied healthy controls of similar age and BMI.Interventions and outcome measures: 3T MRI scans of upper airway anatomy and tagged-MRI to characterize airway muscle motion during quiet breathing were collected for analysis.Results: Considerable variation in the patterns of inspiratory airway muscle motion was observed in the SCI group, with some participants exhibiting large inspiratory airway dilatory motions, and others exhibiting counterproductive narrowing during inspiration. These patterns were not dissimilar to those observed in the able-bodied OSA participants. The increase in airway cross-sectional area of able-bodied control participants was proportional to increase in BMI, and a similar, but not significant, relationship was present in all groups.Conclusion: Despite the limited sample size, these data suggest that SCI OSA patients have heterogeneous pharyngeal dilator muscle responses to the negative pressures occurring during inspiration but, as a group, appear to be more similar to able-bodied OSA patients than healthy controls of similar age and BMI. This may reflect altered pharyngeal pressure reflex responses in at least some people with SCI.     

Sleep. 5: Driving and automobile crashes in patients with obstructive sleep apnoea/hypopnoea syndrome

Driving is a complex task involving distinct cognitive, perceptual, motor, and decision making skills. After placing the vehicle on the road, the driver must constantly survey the ever changing roadway environment to keep the vehicle in the lane and moving at an appropriate safe speed. This surveillance involves two distinct visual tasks: estimating and responding to the oncoming curvature and controlling lane position. Driving is therefore a divided attention task involving speed and lane control as well as monitoring. To do this in a safe manner requires careful attention and alertness which can be problematic for patients with obstructive sleep apnoea/hypopnoea syndrome (OSAHS) or other sleep disorders.     

Atrial natriuretic peptide levels in the sleep apnoea/hypopnoea syndrome.

BACKGROUND--Patients with the sleep apnoea/hypopnoea syndrome have increased salt and water excretion at night which has been reported to be associated with an increase in plasma levels of atrial natriuretic peptide (ANP). A study was performed to determine whether any rise in plasma ANP levels was related to nocturnal hypoxaemia. METHODS--Nine patients with sleep apnoea/hypopnoea syndrome were studied on two nights, one breathing air and the other 28% oxygen, the order being randomised. Venous levels of ANP, aldosterone, and renin activity were measured. RESULTS--No decrease in plasma ANP levels on oxygen was seen, and, indeed, there was no evidence of an overnight increase in ANP levels. CONCLUSION--Oxygen therapy does not diminish nocturnal plasma ANP levels in patients with sleep apnoea/hypopnoea syndrome.     

Postoperative episodic oxygen desaturation in the sleep apnoea syndrome

We describe a patient with sleep apnoea syndrome who showed severe episodic hypoxaemia in the late postoperative period. The sleep apnoea syndrome should be studied further to evaluate its significance as a surgical risk factor.     

Effects of nasal CPAP on simulated driving performance in patients with obstructive sleep apnoea

BACKGROUND: Many patients with obstructive sleep apnoea (OSA) have difficulty in driving and experience increased automobile accidents. It has previously been shown that patients with OSA perform poorly on a laboratory based divided attention driving test (DADT). METHODS: Seventeen men with OSA of mean (SD) age 49.7 (11.2) years and an initial apnoea/hypopnoea index (AHI) of 73.0 (28.9) were restudied from one to 12 (mean (SD) 9.2 (4.2)) months after initiating treatment with nasal continuous positive airway pressure (CPAP) to examine the effects of treatment on DADT performance. Eighteen age and sex matched controls were also retested 8.4 (3.4) months after their initial tests. Following a practice session, all subjects were given the DADT for 20 minutes before each daytime nap of the standard multiple sleep latency test (MSLT). RESULTS: Untreated patients with OSA, who performed much worse than controls in all measures, improved significantly on all measures of performance, particularly in tracking error which returned to the level of controls in all but one patient. Changes in performance were much greater for patients with OSA than for controls in tracking error (mean difference 106 (95% CI 75 to 135) cm), sleep latency/ MSLT (5.3 (95% CI 2.7 to 8.0) min), number of correct responses (1.2 (95% CI 0.4 to 1.9)), number of missed responses (1.7 (95% CI 0.9 to 2.3)), and number out of bounds (10.0 (95% CI 7.9 to 13.6)), but not for response time (0.1 (95% CI -0.3 to 0.2) s). Improvement in tracking error was highly correlated with improvement in sleepiness (r = 0.65). CONCLUSIONS: Impairment in laboratory driving performance skills in patients with OSA is reversed by successful treatment with nasal CPAP. Changes in daytime sleepiness account for some but not all of the improvement.


     

Effects of posture on flow-volume curves during normocapnia and hypercapnia in patients with obstructive sleep apnoea.

BACKGROUND: A high ratio of forced expiratory to forced inspiratory maximal flow at 50% of vital capacity (FEF50/FIF50) may identify upper airway dysfunction. Since hypercapnia increases the motor activity of airway dilating muscles its effects on the maximum expiratory and inspiratory flow-volume curves (MEIFV) in patients with obstructive sleep apnoea and in normal subjects in different postures was studied. METHODS: The effects of posture on the maximum expiratory and inspiratory flow-volume curves during the breathing of air and 7% carbon dioxide in 11 patients with obstructive sleep apnoea were compared with those in nine normal subjects. Measurements were made in the sitting, supine, and right lateral recumbent positions. Forced expiratory flow at 50% vital capacity (FEF50), forced inspiratory flow at 50% vital capacity (FIF50) and FEF50/FIF50 were determined. RESULTS: In the normal subjects FEF50, FIF50, and FEF50/FIF50 were not affected by change in posture or by breathing carbon dioxide. In the patients there was a fall in FIF50 and an increase in FEF50/FIF50 when breathing air in the supine position compared with values in the seated and lateral position. While they were breathing carbon dioxide there was a slight increase in FEF50 when patients were seated or in the lateral position compared with values during air breathing. Hypercapnia abolished the effects of posture on FEF50/FIF50. Values for FEF50/FIF50 in the supine position while they were breathing air correlated with the apnoeic index but not with other polysomnographic data. CONCLUSION: In patients with obstructive sleep apnoea the upper airway is prone to collapse during inspiration when the patient is supine, even when awake; this tendency can be reversed by breathing carbon dioxide.