CASE CONFERENCES Sleep Fragments Section Editors: Shirin Shafazand, M.D. and Mihaela Teodorescu, M.D.

Sleep Rhythms Vinod Aiyappan1, Prashanthan Sanders2, Doug McEvoy1, and Nick A. Antic1 1

Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, Adelaide, South Australia, Australia; and 2Centre for Heart Rhythm Disorder, University of Adelaide and Royal Adelaide Hospital, Adelaide, South Australia, Australia

Keywords: sleep apnea syndromes; arrhythmias, cardiac; ectopic atrial tachycardia; continuous positive airway pressure; obstructive sleep apnea

A 76-year-old woman was referred for evaluation of snoring, witnessed apneic episodes, and daytime tiredness. She was otherwise well except for hypertension, for which she took telmisartan 80 mg daily. The patient underwent a split-night laboratory sleep study (baseline sleep evaluation followed by continuous positive airway pressure [CPAP] titration during one night of study). She took no sedating drugs and consumed no caffeinated beverages on the day before the overnight study. A representative sample of her polysomnography (PSG; 30-sec epoch for ECG and EEG and 5-min epoch for saturation trace, nasal pressure trace, thoracic and abdominal band traces) recorded during the diagnostic phase of the sleep study (Figure 1) is shown below.

Question What abnormalities were recorded on the polysomnogram (Figure 1)?

Discussion The diagnostic phase of the sleep study showed evidence of severe OSA with an apnea-hypopnea index of 33.7 and mild oxygen desaturation with a nadir of 87%. The respiratory flow disturbances, oxygen

desaturations, and runs of supraventricular tachycardia were largely abolished during the CPAP phase of the split-night study. The supraventricular tachycardia noted during the patient’s PSG is a long RP (interval between the R wave and the P wave of the next cycle) tachycardia. The arrhythmia, although asymptomatic, was paroxysmal and frequent during the diagnostic phase of the study and occurred in association with respiratory events. The heart rate rose to 110/min during the arrhythmia from a baseline heart rate of 60/min. A total of 92 episodes of paroxysmal atrial tachycardia were recorded during the diagnostic phase of the study (159.5 min), each lasting from 15 seconds up to 2 minutes. The CPAP titration portion showed only two short episodes of tachycardia. A long RP tachycardia of sudden onset and termination with recurrent short bursts is characteristic of a focal atrial tachycardia. Other possibilities that could result in a long RP tachycardia include sinus tachycardia (which would have a more gradual onset and termination), accessory pathway–related atrioventricular (AV) reentrant tachycardia, or AV junctional reentrant tachycardia (the latter two usually being more sustained). Although the tachycardia features are discernible on a single rhythm strip, prediction of the origin of the tachycardia focus is not possible without more ECG vectors.

The prevalence of OSA is increasing in the community (1). The Sleep Heart Health Study (SHHS) demonstrated a higher prevalence of cardiac arrhythmias in patients with sleep-disordered breathing (SDB) (2). The relative risk of an arrhythmia is markedly higher after a respiratory disturbance during sleep, although the absolute arrhythmia rate is low (3). Cardiac arrhythmias associated with OSA include bradycardia, tachycardia, AV block, increased atrial and ventricular ectopy, and supraventricular/ventricular tachyarrhythmias. There are several possible mechanisms by which OSA predisposes to cardiac arrhythmias. The acute obstructive respiratory event in OSA results in repeated inspiratory effort against a closed glottis and produces negative intrathoracic pressures, which increases left ventricular afterload and results in both direct and indirect stretch of the myocardium. Myocardial stretch is a potent stimulant for automatic activity resulting in development of an increased ectopy burden and sustained automatic tachycardias (such as atrial tachycardias). This effect may be amplified by the profound fluctuations in autonomic stimulation and blood pressure that have been observed with acute obstructive events. In patients with an established abnormal atrial or ventricular substrate, such an increase in trigger burden may potentially initiate atrial fibrillation (AF) or ventricular tachycardia, respectively.

(Received in original form April 1, 2013; accepted in final form July 28, 2013 ) Correspondence and requests for reprints should be addressed to Vinod Aiyappan, M.B.B.S., M.D., M.R.C.P., F.R.A.C.P., Consultant Respiratory and Sleep Physician, Adelaide Institute for Sleep Health, Repatriation General Hospital, Daws Road, Daw Park, SA, Australia. E-mail: [email protected] Ann Am Thorac Soc Vol 10, No 5, pp 531–533, Oct 2013 Copyright © 2013 by the American Thoracic Society DOI: 10.1513/AnnalsATS.201304-073SF Internet address: www.atsjournals.org

Case Conferences: Sleep Fragments

531

CASE CONFERENCES

Figure 1. Representative recording from the diagnostic phase of the patient’s split night laboratory polysomnogram.

Our recent work demonstrates that patients with chronic repetitive obstruction may progress to electrical and structural remodelling of the atria to create this substrate for atrial fibrillation (5). Thus, in the patient with OSA, the acute obstructive episode may provide the milieu to trigger AF, whereas persistent and untreated OSA may result in chronic

substrate contributing to the maintenance of AF, which over time may contribute to mechanical and electrical remodeling (5). In addition to acute and chronic remodelling of the atria, there is repetitive and chronic sympathetic activation, which also contributes to the development of arrhythmia (4, 5, 13). Others have highlighted the relative contributions of the fluctuations

in hypoxia and hypercarbia to the development of the acute electrical milieu predisposing to arrhythmia due to obstruction (10). The bradyarrhythmias associated with OSA are attributed to the vagotonic effect of hypoxia on the carotid body (11). In addition to these mechanisms, atrial remodelling and the

Figure 2. Expanded view of the ECG tracing from Figure 1 showing abrupt onset of a focal atrial tachycardia (arrow). Note the long RP interval.

532

AnnalsATS Volume 10 Number 5 | October 2013

CASE CONFERENCES desaturation-resaturation cycle may activate atrial catecholamine-sensitive ion channels causing focal abnormal electric discharges contributing to the development of atrial arrhythmias (4, 5, 11, 12). There is high prevalence of sleep apnea (up to 87%) in patients with cardiac arrhythmias (14). An earlier study demonstrated resolution of cardiac arrhythmias (AV block, sinus arrest, ventricular tachycardia, atrial flutter, and atrial fibrillation) associated with SDB after treatment with tracheostomy (6). CPAP is an effective therapy for OSA, and withdrawal of CPAP is associated with prolongation of cardiac repolarization, which could predispose to cardiac arrhythmias (7). Although a prospective study demonstrated that CPAP treatment is effective in controlling cardiac arrhythmias associated with OSA (8), and observational

studies have suggested a reduced recurrence of atrial fibrillation after treating OSA with CPAP, a randomized controlled trial did not find any reduction in arrhythmias among patients with OSA using CPAP, when compared with placebo (9). In summary, OSA is associated with increased risk of cardiac arrhythmias. The ECG of patients undergoing PSG should therefore be scrutinized for cardiac arrhythmias. Patients with cardiac arrhythmias should be assessed for symptoms and clinical features of underlying SDB and referred for sleep studies, when appropriate.

Follow-Up

Answer

The patient’s thyroid function test results were normal. An echocardiogram did not reveal any structural cardiac abnormalities. Her symptoms resolved after initiation of nocturnal CPAP therapy. n

The diagnostic PSG shows obstructive sleep apnea (OSA)/hypopnea with associated

Author disclosures are available with the text of this article at www.atsjournals.org.

References 1 Adams R, Appleton S, Vakulin A, Taylor A, Martin S, Catcheside P, Antic A, McEvoy D, Wittert G. High prevalence of undiagnosed OSA in a community sample of men aged 40 years and over. Sleep Biol Rhythms 2012;10:42. 2 Mehra R, Benjamin EJ, Shahar E, Gottlieb DJ, Nawabit R, Kirchner HL, Sahadevan J, Redline S; Sleep Heart Health Study. Association of nocturnal arrhythmias with sleep-disordered breathing: the Sleep Heart Health Study. Am J Respir Crit Care Med 2006;173:910–916. 3 Monahan K, Storfer-Isser A, Mehra R, Shahar E, Mittleman M, Rottman J, Punjabi N, Sanders M, Quan SF, Resnick H, et al. Triggering of nocturnal arrhythmias by sleep-disordered breathing events. J Am Coll Cardiol 2009;54:1797–1804. 4 Ludka O, Konecny T, Somers V. Sleep apnea, cardiac arrhythmias, and sudden death. Tex Heart Inst J 2011;38:340–343. 5 Dimitri H, Ng M, Brooks AG, Kuklik P, Stiles MK, Lau DH, Antic N, Thornton A, Saint DA, McEvoy D, et al. Atrial remodeling in obstructive sleep apnea: implications for atrial fibrillation. Heart Rhythm 2012;9:321–327. 6 Guilleminault C, Connolly SJ, Winkle RA. Cardiac arrhythmia and conduction disturbances during sleep in 400 patients with sleep apnea syndrome. Am J Cardiol 1983;52:490–494. 7 Rossi VA, Stoewhas AC, Camen G, Steffel J, Bloch KE, Stradling JR, Kohler M. The effects of continuous positive airway pressure therapy withdrawal on cardiac repolarization: data from a randomized controlled trial. Eur Heart J 2012;33:2206–2212.

Case Conferences: Sleep Fragments

oxygen desaturation. Figure 1 shows an additional abnormality that reinforces the importance of systematically reviewing all of the tracings included in a polysomnogram. The ECG recording shows abrupt onset of a narrow complex tachycardia associated with the respiratory event (Figure 2).

8 Harbison J, O’Reilly P, McNicholas WT. Cardiac rhythm disturbances in the obstructive sleep apnea syndrome: effects of nasal continuous positive airway pressure therapy. Chest 2000;118: 591–595. 9 Craig S, Pepperell JC, Kohler M, Crosthwaite N, Davies RJ, Stradling JR. Continuous positive airway pressure treatment for obstructive sleep apnoea reduces resting heart rate but does not affect dysrhythmias: a randomised controlled trial. J Sleep Res 2009;18: 329–336. 10 Stevenson IH, Roberts-Thomson KC, Kistler PM, Edwards GA, Spence S, Sanders P, Kalman JM. Atrial electrophysiology is altered by acute hypercapnia but not hypoxemia: implications for promotion of atrial fibrillation in pulmonary disease and sleep apnea. Heart Rhythm 2010;7:1263–1270. 11 Chen PS, Douglas P. Douglas P. Zipes Lecture. Neural mechanisms of atrial fibrillation. Heart Rhythm 2006;3:1373–1377. 12 Leung RS. Sleep-disordered breathing: autonomic mechanisms and arrhythmias. Prog Cardiovasc Dis 2009;51:324–338. 13 Pinto JM, Garpestad E, Weiss JW, Bergau DM, Kirby DA. Hemodynamic changes associated with obstructive sleep apnea followed by arousal in a porcine model. J Appl Physiol 1993;75: 1439–1443. 14 Hoyer FF, Lickfett LM, Mittmann-Braun E, Ruland C, Kreuz J, Pabst S, Schrickel J, Juergens U, Tasci S, Nickenig G, et al. High prevalence of obstructive sleep apnea in patients with resistant paroxysmal atrial fibrillation after pulmonary vein isolation. J Interv Card Electrophysiol 2010;29:37–41.

533

Sleep rhythms.

Sleep rhythms. - PDF Download Free
860KB Sizes 0 Downloads 0 Views