Heart block during sleep has been described in up to 10% of patients with obstructive sleep apnoea. The aim of this study was to determine the relationship between sleep stage, oxygen desaturation and apnoea-associated bradyarrhythmias as well as the effect of nasal continuous positive airway pressure (nCPAP)/nasal bi-level positive airway pressure (nBiPAP) therapy on these arrhythmias in patients without electrophysiological abnormalities. Sixteen patients (14 males and two females, mean age 49.6+/-10.4 yrs) with sleep apnoea and nocturnal heart block underwent polysomnography after exclusion of electrophysiological abnormalities of the sinus node function and atrioventricular (AV) conduction system by invasive electrophysiological evaluation. During sleep, 651 episodes of heart block were recorded, 572 (87.9%) occurred during rapid eye movement (REM) sleep and 79 (12.1%) during nonrapid eye movement (NREM) sleep stages 1 and 2. During REM sleep, the frequency of heart block was significantly higher than during NREM sleep: 0.69+/-0.99 versus 0.02+/-0.04 episodes of heart block x min(-1) of the respective sleep stage (p<0.001). During apnoeas or hypopnoeas, 609 bradyarrhythmias (93.5%) occurred with a desaturation of at least 4%. With nCPAP/ nBiPAP therapy, apnoea/hypopnoea index (AHI) decreased from 75.5+/-39.6 x h(-1) to 3.0+/-6.6 x h(-1) (p<0.01) and the number of arrhythmias from 651 to 72 (p<0.01). We conclude that: 1) 87.9% of apnoea-associated bradyarrhythmias occur during rapid eye movement sleep; 2) the vast majority of heart block episodes occur during a desaturation of at least 4% without a previously described threshold value of 72%; and 3) nasal continuous positive airway pressure or nasal bi-level positive airway pressure is the therapy of choice in patients with apnoea-associated bradyarrhythmias.

Prevalence of bradycardic arrhythmias in sleep apnoeaIn the early days of sleep research it was thought that heart block (second and third degree atrioventricular block), sinus arrest, or sinoatrial block were frequent findings in patients with sleep apnoea. Tilkian and co-workers 1 reported that more than 50% of patients with sleep apnoea develop episodes of heart block during sleep. In 400 patients studied by Guilleminault et al 2 bradycardic arrhythmias were reported in almost 18% of the patients and later studies found heart block in 9-13% of patients with sleep apnoea.3 4 Due to ventricular asystoles of up to 13 seconds in duration it was hypothesised that heart block might lead to an increased mortality risk in these patients.2 A recent publication challenged previous results in that no increased prevalence of bradycardic arrhythmias was seen in patients with sleep apnoea compared with those without sleep apnoea. 5To examine these seemingly discrepant results further we performed Holter monitoring in 239 consecutive patients diagnosed as having sleep apnoea (apnoea/hypopnoea index >10/h) using a validated ambulatory recording device based on the measurement of heart rate, SaO 2 , snoring sound, and body position. Episodes of second and third degree atrioventricular (AV) block and/or sinus arrest of more than two seconds in duration occurred in 17 of the 239 patients. 6 There was no significant difference in age between patients with and without heart block (mean (SD) 50.7 (12.8) versus 52.1 (9.8) years), but those with heart block were significantly more obese (38.7 (7.3) versus 30.7 (4.6)).Twelve of the 17 patients (70.6%) had arterial hypertension, seven (41.1%) suVered from heart failure (NYHA II-III), and four (23.5%) had pulmonary hypertension. None of the patients reported a myocardial infarction in their medical history, and in only one (5.9%) exercise testing showed signs of coronary heart disease. Ten of the 17 patients received no medication at all. Treatment with digoxin in two patients and with a blocker in one patient was discontinued one week prior to the study. Diuretic therapy in four patients and ACE inhibitors in two patients were continued unchanged.Standard polysomnography and a repeat 24 hour Holter monitoring were then performed. Severe sleep apnoea (mean (SD) AHI 90 (36)/h, range 59.6-158) was found in the 17 patients and in all of them episodes of heart block during sleep could again be demonstrated. In two of these patients clusters of sinus arrest and second degree AV block could be demonstrated during the daytime as well.Both patients reported that they were sleeping at the times when heart block had occurred.A total of 10 368 apnoeas and hypopnoeas were recorded, 81.8% of which were obstructive and mixed apnoeas, 17% were obstructive hypopnoeas, and only 1.2% were central apnoeas. Bradycardic arrhythmias exclusively occurred during apnoeas and hypopnoeas and were not found during hyperventilation.The occurrence of bradycardic arrhythmias was clearly linked to apnoea severity: no...

We hypothesized that upper airway collapsibility is modulated dynamically throughout the respiratory cycle in sleeping humans by alterations in respiratory phase and/or airflow regimen. To test this hypothesis, critical pressures were derived from upper airway pressure-flow relationships in six tracheostomized patients with obstructive sleep apnea. Pressure-flow relationships were generated by varying the pressure at the trachea and nose during tracheostomy (inspiration and expiration) (comparison A) and nasal (inspiration only) breathing (comparison B), respectively. When a constant airflow regimen was maintained throughout the respiratory cycle (tracheostomy breathing), a small yet significant decrease in critical pressure was found at the inspiratory vs. end- and peak-expiratory time point [7.1 +/- 1.6 (SE) to 6.6 +/- 1.9 to 6.1 +/- 1.9 cmH(2)O, respectively; P < 0.05], indicating that phasic factors exerted only a modest influence on upper airway collapsibility. In contrast, we found that the inspiratory critical pressure fell markedly during nasal vs. tracheostomy breathing [1.1 +/- 1.5 (SE) vs. 6.1 +/- 1.9 cmH(2)O; P < 0.01], indicating that upper airway collapsibility is markedly influenced by differences in airflow regimen. Tracheostomy breathing was also associated with a reduction in both phasic and tonic genioglossal muscle activity during sleep. Our findings indicate that both phasic factors and airflow regimen modulate upper airway collapsibility dynamically and suggest that neuromuscular responses to alterations in airflow regimen can markedly lower upper airway collapsibility during inspiration.

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SUMMARY  The effect of nasal continuous positive airway pressure (nCPAP) and nasal bi‐level positive airway pressure (nBiPAP) on intrathoracic pressure and haemodynamics during wakefulness was studied in a group of nine patients with severe sleep apnoea. No patient took cardiovascular medication. Patients were studied with a Swan Ganz catheter, an arterial line and an oesophageal balloon. nCPAP and nBiPAP were applied in the following pressure sequence: 5, 10 and 15 cm H2O of CPAP and 10/5 and 15/10 cm H2O of nBiPAP. Measurements were made at the end of a 5‐min period at each pressure level. Intrathoracic pressure was noted to increase to a level of approximately 50% of the pressure delivered at the mask. At a CPAP of 10 cm H2O and above, as well as at BiPAP of 10/5 or higher, there was a decrease in cardiac output (CO) and cardiac index (CI). CI fell below the normal value in two of the patients. Transmural pulmonary artery pressure (PPAtm) decreased at a CPAP of 15 cm H2O and at both BiPAP levels. Transmural right atrial pressure (PRAtm) decreased at both BiPAP levels. There were no differences in CO, CI, PPAtm and PRAtm between nCPAP and nBiPAP at equal inspiratory pressures. SaO2 increased during BiPAP 15/10 cm H2O, whereas heart rate and arterial blood pressure did not change significantly. The data presented here are consistent with the literature on positive end‐expiratory pressure (PEEP) applied via intratracheal tube and are likely to be due to a reduced venous return. It is concluded that nasally applied positive pressure may have acute negative effects on cardiac function in patients with sleep apnoea.