Smarter Decisions,
Better Care

UpToDate synthesizes the most recent medical information into evidence-based practical recommendations clinicians trust to make the right point-of-care decisions.

  • Rigorous editorial process: Evidence-based treatment recommendations
  • World-Renowned physician authors: over 5,100 physician authors and editors around the globe
  • Innovative technology: integrates into the workflow; access from EMRs

Choose from the list below to learn more about subscriptions for a:


Subscribers log in here


Sinoatrial nodal pause, arrest, and exit block

INTRODUCTION

The sinoatrial (SA) node represents the integrated activity of pacemaker cells, sometimes called P cells, in a compact region at the junction of the high right atrium and the superior vena cava. Perinodal cells, sometimes called transitional or (T) cells, transmit the electrical impulse from the SA node to the right atrium. Each of these cell types has distinct expression profiles of ion channels and gap junctions.

Given the architecture of the SA node, SA nodal dysfunction typically results from either abnormalities in impulse generation by the P cells or abnormalities in conduction across the T cells. SA nodal dysfunction is more commonly an acquired condition, but in some patients it can be inherited, with gene mutations having been described in some forms of inherited SA nodal dysfunction [1]. Patients with SA nodal dysfunction may be asymptomatic or highly symptomatic as in cases of sick sinus syndrome.

Sinoatrial nodal pauses, arrest, and exit block will be discussed here. Additional details regarding the anatomy and electrophysiology of the SA node, as well as a discussion of the sick sinus syndrome, are presented separately. (See "Manifestations and causes of the sick sinus syndrome".)

ETIOLOGY

Sinus pause, arrest, and exit block may arise from ischemic, inflammatory, or infiltrative or fibrotic disease of the SA node, excessive vagal tone, sleep apnea, digitalis, and some antiarrhythmic and other drugs. The causes of sinus node dysfunction are discussed in detail elsewhere. (See "Manifestations and causes of the sick sinus syndrome", section on 'Etiology' and "Obstructive sleep apnea and cardiovascular disease", section on 'Other arrhythmias' and "Cardiac arrhythmias due to digoxin toxicity", section on 'Sinus bradycardia, tachycardia, block, and arrest'.)

TYPES OF SA NODAL DYSFUNCTION

Sinus pause or arrest — A sinus pause or arrest is defined as the transient absence of sinus P waves on the electrocardiogram (ECG) that may last from two seconds to several minutes (waveform 1). This abnormality is an alteration in discharge by the SA pacemaker; as a result, the duration of the pause has no arithmetical relationship to the basic sinus rate (ie, the cycle length of the pause is not a multiple of the basic sinus cycle length as would occur with 2:1 or 3:1 SA nodal block). The pause or arrest often allows escape beats or rhythms to occur, but lower pacemakers may be sluggish or even absent in the sick sinus syndrome.

        

Subscribers log in here

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you:
Literature review current through: Nov 2014. | This topic last updated: Aug 27, 2014.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2014 UpToDate, Inc.
References
Top
  1. Park DS, Fishman GI. The cardiac conduction system. Circulation 2011; 123:904.
  2. Hilgard J, Ezri MD, Denes P. Significance of ventricular pauses of three seconds or more detected on twenty-four-hour Holter recordings. Am J Cardiol 1985; 55:1005.
  3. Brodsky M, Wu D, Denes P, et al. Arrhythmias documented by 24 hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease. Am J Cardiol 1977; 39:390.
  4. Yamada T, Fukunami M, Shimonagata T, et al. Identification of sinus node dysfunction by use of P-wave signal-averaged electrocardiograms in paroxysmal atrial fibrillation: a prospective study. Am Heart J 2001; 142:286.
  5. Hombach V, Gil-Sanchez D, Zanker R, et al. An approach to direct detection of sinus nodal activity in man. J Electrocardiol 1979; 12:343.
  6. Hariman RJ, Krongrad E, Boxer RA, et al. Method for recording electrical activity of the sinoatrial node and automatic atrial foci during cardiac catheterization in human subjects. Am J Cardiol 1980; 45:775.
  7. Reiffel JA, Gang E, Gliklich J, et al. The human sinus node electrogram: a transvenous catheter technique and a comparison of directly measured and indirectly estimated sinoatrial conduction time in adults. Circulation 1980; 62:1324.
  8. Asseman P, Berzin B, Desry D, et al. Persistent sinus nodal electrograms during abnormally prolonged postpacing atrial pauses in sick sinus syndrome in humans: sinoatrial block vs overdrive suppression. Circulation 1983; 68:33.
  9. Gomes JA, Hariman RI, Chowdry IA. New application of direct sinus node recordings in man: assessment of sinus node recovery time. Circulation 1984; 70:663.
  10. Wu DL, Yeh SJ, Lin FC, et al. Sinus automaticity and sinoatrial conduction in severe symptomatic sick sinus syndrome. J Am Coll Cardiol 1992; 19:355.
  11. Sakai Y, Imai S, Sato Y, et al. Clinical and electrophysiological characteristics of binodal disease. Circ J 2006; 70:1580.