Medscape is available in 5 Language Editions – Choose your Edition here.


Pacemaker Syndrome Treatment & Management

  • Author: Daniel M Beyerbach, MD, PhD; Chief Editor: Jeffrey N Rottman, MD  more...
Updated: Aug 01, 2016

Approach Considerations

Patients with ventricular pacemakers and pacemaker syndrome may need placement of an additional pacemaker lead. Hospitalize and monitor patients undergoing device or lead implantation for 24 hours after placement surgery.

Administer intravenous antibiotics (cefazolin, or vancomycin in patients with beta-lactam allergy) for prophylaxis against skin wound infections. Do not continue intravenous antibiotic therapy for more than 24 hours. If infection develops around the device, it is better detected early in the course in case device explantation is necessary.


Because diagnosis and treatment require interrogation and reprogramming of pacemaker, patients must be seen in either a clinical or hospital setting in which the appropriate interrogation equipment is available. Each pacemaker manufacturer produces an interrogation computer for its own devices. A major institution will have interrogation computers from several different manufacturers available for use.

Some pacemaker manufacturers provide courtesy interrogation services involving site visits for rural populations without easy access to functional facilities.


Medical Care

For ventricularly paced patients, addition of an atrial lead and institution of AV synchronous pacing usually resolves symptoms.

In patients with other pacing modes, symptoms usually resolve after interrogation and reprogramming of pacemaker parameters, such as AV delay, postventricular atrial refractory period, sensing level, and pacing threshold voltage. In many cases, optimal parameter values may be obtained experimentally with successive reprogramming and measurement of pertinent parameters, such as blood pressure, cardiac output (see the Cardiac Output calculator), and total peripheral resistance, as well as observations of symptomatology.

In rare instances, using hysteresis to help maintain AV synchrony can help alleviate symptoms in patients with VVI pacemakers and intact sinus node function. For example, if pacing rate is 60 beats per minute (bpm), the hysteresis rate can be programmed to be 50 bpm; in this way, pacing is not instituted until the native ventricular rate falls below 50 bpm, but when pacing is instituted, the pacemaker rate is 60 bpm. Hysteresis effects a reduction in the amount of time spent in pacing mode, which can alleviate symptoms, particularly when the pacing mode, such as VVI, is generating AV dyssynchrony.

Additional treatment modalities include replacing the pacemaker pulse generator and revision of medication regimen.

Medical care includes supportive care in relation to possible heart failure, hypotension, tachycardia, tachypnea, and oxygenation deficit.


Diet and Activity

A low-salt diet is indicated for patients with heart failure.

For patients with autonomic insufficiency, a high-salt diet may be appropriate.

For patients with dehydration, oral fluid rehydration is needed.

Patients may engage in activities as tolerated.


Surgical Care

Consultation with an electrophysiologist determines the possible need for additional pacemaker lead placement and the care related to the pacemaker and for procedures to aid in diagnosis and treatment of pacemaker syndrome.



Because most cases of pacemaker syndrome occur in the setting of ventricular pacing, institute atrial pacing whenever it is not contraindicated. This includes AAI pacing for most cases of sinus node disease with intact AV nodal conduction. Alternatively, a dual-chamber system can be programmed to a long AV interval to promote intrinsic conduction, provided that the PR interval is not markedly prolonged.

Baseline studies by echocardiogram can assess change in cardiac output, stroke volume, and left atrial total emptying fraction in response to ventricular pacing. Examination of these parameters may guide the decision to institute dual-chamber pacing.

At the time of device implantation, optimize pacing parameters, such as AV delay, PVARP, and rate response slope, for physiologic timing of atrial and ventricular contractions.


Long-Term Monitoring

Schedule follow-up visits after device or lead implantation as follows:

  • 1-2 weeks for wound check
  • 1 month for pacemaker interrogation
  • 3 months for pacemaker interrogation
  • Every 6 months thereafter for pacemaker interrogation
Contributor Information and Disclosures

Daniel M Beyerbach, MD, PhD Medical Director, Cardiac Rhythm Program, The Christ Hospital; Affiliate Clinical Assistant Professor of Biomedical Science, Florida Atlantic University

Daniel M Beyerbach, MD, PhD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.


Christopher Cadman, MD Decatur Memorial Hospital Heart and Lung Institute

Christopher Cadman, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Brian Olshansky, MD Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society, Cardiac Electrophysiology Society, American Heart Association

Disclosure: Received honoraria from Guidant/Boston Scientific for speaking and teaching; Received honoraria from Medtronic for speaking and teaching; Received consulting fee from Guidant/Boston Scientific for consulting; Received consulting fee from BioControl for consulting; Received consulting fee from Boehringer Ingelheim for consulting; Received consulting fee from Amarin for review panel membership; Received consulting fee from sanofi aventis for review panel membership.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

  1. McWilliam JA. Electrical stimulation of the heart in man. Br Med J. 1889. 1:348-350.

  2. Alicandri C, Fouad FM, Tarazi RC, et al. Three cases of hypotension and syncope with ventricular pacing: possible role of atrial reflexes. Am J Cardiol. 1978 Jul. 42(1):137-42. [Medline].

  3. Erbel R. Pacemaker syndrome. Am J Cardiol. 1979 Oct. 44(4):771-2. [Medline].

  4. Erlebacher JA, Danner RL, Stelzer PE. Hypotension with ventricular pacing: an atria vasodepressor reflex in human beings. J Am Coll Cardiol. 1984 Sep. 4(3):550-5. [Medline].

  5. Mitsui T, Hori M, Suma K, et al. The "pacemaking syndrome." In: Jacobs JE, ed. Proceedings of the 8th Annual International Conference on Medical and Biological Engineering. Chicago, IL: Association for the Advancement of Medical Instrumentation;. 1969. 29-3.

  6. Mitsui T, Mizuno A, Hasegawa T, et al. Atrial rate as an indicator for optimal pacing rate and the pacemaking syndrome. Ann Cardiol Angeiol (Paris). 1971 Jul-Aug. 20(4):371-9. [Medline].

  7. Furman S. Pacemaker syndrome. Pacing Clin Electrophysiol. 1994 Jan. 17(1):1-5. [Medline].

  8. Ellenbogen KA, Gilligan DM, Wood MA, et al. The pacemaker syndrome -- a matter of definition. Am J Cardiol. 1997 May 1. 79(9):1226-9. [Medline].

  9. Gross JN, Keltz TN, Cooper JA, et al. Profound "pacemaker syndrome" in hypertrophic cardiomyopathy. Am J Cardiol. 1992 Dec 1. 70(18):1507-11. [Medline].

  10. [Guideline] Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA 3rd, Freedman RA, Gettes LS. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008 May 27. 51(21):e1-62. [Medline].

  11. [Guideline] Tracy CM, Epstein AE, Darbar D, DiMarco JP, Dunbar SB, Estes NA 3rd, et al. 2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. [corrected]. Circulation. 2012 Oct 2. 126(14):1784-800. [Medline].

  12. Lamas GA, Orav EJ, Stambler BS, et al. Quality of life and clinical outcomes in elderly patients treated with ventricular pacing as compared with dual-chamber pacing. Pacemaker Selection in the Elderly Investigators. N Engl J Med. 1998 Apr 16. 338(16):1097-104. [Medline].

  13. Sulke N, Chambers J, Dritsas A, Sowton E. A randomized double-blind crossover comparison of four rate-responsive pacing modes. J Am Coll Cardiol. 1991 Mar 1. 17(3):696-706. [Medline].

  14. Hargreaves MR, Channon KM, Cripps TR, et al. Comparison of dual chamber and ventricular rate responsive pacing in patients over 75 with complete heart block. Br Heart J. 1995 Oct. 74(4):397-402. [Medline].

  15. Oldroyd KG, Rae AP, Carter R, et al. Double blind crossover comparison of the effects of dual chamber pacing (DDD) and ventricular rate adaptive (VVIR) pacing on neuroendocrine variables, exercise performance, and symptoms in complete heart block. Br Heart J. 1991 Apr. 65(4):188-93. [Medline].

  16. Lee TM, Su SF, Lin YJ, et al. Role of transesophageal echocardiography in the evaluation of patients with clinical pacemaker syndrome. Am Heart J. 1998 Apr. 135(4):634-40. [Medline].

  17. Theodorakis GN, Kremastinos DT, Markianos M, et al. Total sympathetic activity and atrial natriuretic factor levels in VVI and DDD pacing with different atrioventricular delays during daily activity and exercise. Eur Heart J. 1992 Nov. 13(11):1477-81. [Medline].

  18. Theodorakis GN, Panou F, Markianos M, et al. Left atrial function and atrial natriuretic factor/cyclic guanosine monophosphate changes in DDD and VVI pacing modes. Am J Cardiol. 1997 Feb 1. 79(3):366-70. [Medline].

  19. Nishimura RA, Gersh BJ, Vlietstra RE, et al. Hemodynamic and symptomatic consequences of ventricular pacing. Pacing Clin Electrophysiol. 1982 Nov. 5(6):903-10. [Medline].

  20. Rosenqvist M, Isaaz K, Botvinick EH, et al. Relative importance of activation sequence compared to atrioventricular synchrony in left ventricular function. Am J Cardiol. 1991 Jan 15. 67(2):148-56. [Medline].

  21. Bordachar P, Lafitte S, Reuter S, et al. Echocardiographic parameters of ventricular dyssynchrony validation in patients with heart failure using sequential biventricular pacing. J Am Coll Cardiol. 2004 Dec 7. 44(11):2157-65. [Medline].

  22. Mollazadeh R, Mohimi L, Zeighami M, et al. Hemodynamic effect of atrioventricular and interventricular dyssynchrony in patients with biventricular pacing: Implications for the pacemaker syndrome. J Cardiovasc Dis Res. 2012 Jul. 3(3):200-3. [Medline]. [Full Text].

  23. Poller WC, Dreger H, Schwerg M, Melzer C. Prevalence of E/A wave fusion and A wave truncation in DDD pacemaker patients with complete AV block under nominal AV intervals. PLoS One. 2015. 10 (2):e0116075. [Medline].

  24. Link MS, Hellkamp AS, Estes NA, et al. High incidence of pacemaker syndrome in patients with sinus node dysfunction treated with ventricular-based pacing in the Mode Selection Trial (MOST). J Am Coll Cardiol. 2004 Jun 2. 43(11):2066-71. [Medline].

  25. Schuller H, Brandt J. The pacemaker syndrome: old and new causes. Clin Cardiol. 1991 Apr. 14(4):336-40. [Medline].

  26. Torresani J, Ebagosti A, Allard-Latour G. Pacemaker syndrome with DDD pacing. Pacing Clin Electrophysiol. 1984 Nov. 7(6 Pt 2):1148-51. [Medline].

  27. Jais P, Barold S, Shah DC, et al. Pacemaker syndrome induced by the mode switching algorithm of a DDDR pacemaker. Pacing Clin Electrophysiol. 1999 Apr. 22(4 Pt 1):682-5. [Medline].

  28. Grant JD, Jensen GL, Tang C, et al. Radiotherapy-induced malfunction in contemporary cardiovascular implantable electronic devices: clinical incidence and predictors. JAMA Oncol. 2015 Aug. 1 (5):624-32. [Medline].

  29. Pascale P, Pruvot E, Graf D. Pacemaker syndrome during managed ventricular pacing mode: what is the mechanism?. J Cardiovasc Electrophysiol. 2009 May. 20(5):574-6. [Medline].

  30. Barold SS, Herweg B. The effect of hyperkalaemia on cardiac rhythm devices. Europace. 2014 Apr. 16 (4):467-76. [Medline].

  31. Ausubel K, Furman S. The pacemaker syndrome. Ann Intern Med. 1985 Sep. 103(3):420-9. [Medline].

  32. Heldman D, Mulvihill D, Nguyen H, et al. True incidence of pacemaker syndrome. Pacing Clin Electrophysiol. 1990 Dec. 13(12 Pt 2):1742-50. [Medline].

  33. Sulke N, Dritsas A, Bostock J, et al. "Subclinical" pacemaker syndrome: a randomised study of symptom free patients with ventricular demand (VVI) pacemakers upgraded to dual chamber devices. Br Heart J. 1992 Jan. 67(1):57-64. [Medline].

  34. Frielingsdorf J, Gerber AE, Hess OM. Importance of maintained atrio-ventricular synchrony in patients with pacemakers. Eur Heart J. 1994 Oct. 15(10):1431-40. [Medline].

  35. Sutton R, Kenny RA. The natural history of sick sinus syndrome. Pacing Clin Electrophysiol. 1986 Nov. 9(6 Pt 2):1110-4. [Medline].

  36. Hesselson AB, Parsonnet V, Bernstein AD, Bonavita GJ. Deleterious effects of long-term single-chamber ventricular pacing in patients with sick sinus syndrome: the hidden benefits of dual-chamber pacing. J Am Coll Cardiol. 1992 Jun. 19(7):1542-9. [Medline].

  37. Santini M, Alexidou G, Ansalone G, et al. Relation of prognosis in sick sinus syndrome to age, conduction defects and modes of permanent cardiac pacing. Am J Cardiol. 1990 Mar 15. 65(11):729-35. [Medline].

  38. Sasaki Y, Furihata A, Suyama K, et al. Comparison between ventricular inhibited pacing and physiologic pacing in sick sinus syndrome. Am J Cardiol. 1991 Apr 1. 67(8):771-4. [Medline].

  39. Rosenqvist M, Brandt J, Schuller H. Long-term pacing in sinus node disease: effects of stimulation mode on cardiovascular morbidity and mortality. Am Heart J. 1988 Jul. 116(1 Pt 1):16-22. [Medline].

  40. Andersen HR, Nielsen JC, Thomsen PE, et al. Long-term follow-up of patients from a randomised trial of atrial versus ventricular pacing for sick-sinus syndrome. Lancet. 1997 Oct 25. 350(9086):1210-6. [Medline].

  41. Zanini R, Facchinetti A, Gallo G, et al. Survival rates after pacemaker implantation: a study of patients paced for sick sinus syndrome and atrioventricular block. Pacing Clin Electrophysiol. 1989 Jul. 12(7 Pt 1):1065-9. [Medline].

  42. Alpert MA, Curtis JJ, Sanfelippo JF, et al. Comparative survival after permanent ventricular and dual chamber pacing for patients with chronic high degree atrioventricular block with and without preexistent congestive heart failure. J Am Coll Cardiol. 1986 Apr. 7(4):925-32. [Medline].

  43. Bush DE, Finucane TE. Permanent cardiac pacemakers in the elderly. J Am Geriatr Soc. 1994 Mar. 42(3):326-34. [Medline].

  44. Kastrup EK, Hebel SK, Olin BR. Drug Facts and Comparisons. 55th ed. 2001. 1275-1288.

  45. Sharma PS, Kaszala K, Tan AY, et al. Repetitive nonreentrant ventriculoatrial synchrony: An underrecognized cause of pacemaker-related arrhythmia. Heart Rhythm. 2016 Aug. 13 (8):1739-47. [Medline].

Pacemaker syndrome without pacemaker participation. Displayed are stored data from a dual-chamber pacemaker. The intracardiac tracings reveal atrial tachycardia with second-degree AV block that together created continuous atrioventricular (AV) dyssynchrony, leading to symptoms of pacemaker syndrome, including fatigue, lightheadedness, and exertional dyspnea. Notice that the pacemaker does not participate in creation of AV dyssynchrony. There are no paced events. Top tracing: atrial electrogram. Middle tracing: ventricular electrogram. Bottom tracing: channel markers. Ab = atrial sensed event in postventricular blanking period, AR = atrial sensed event in postventricular refractory period; VS – Ventricular sensed event.
Pronounced PR interval prolongation. The effect of this PR interval prolongation on AV dyssynchrony is demonstrated in this ECG image.
AV dyssynchrony resulting from severe PR interval prolongation in the setting of sinus rhythm. In this ECG, the PR interval is prolonged to the point that the P wave occurs coincident with the peak of the T wave. Compare to the prior image of the same patient with a slower sinus rate.
Accelerated idioventricular rhythm with retrogradely conducted P waves. This ECG demonstrates a mechanism of AV dyssynchrony that might lead to pseudopacemaker syndrome.
Junctional rhythm with retrogradely conducted P waves. If symptoms of pacemaker syndrome develop, increasing the lower rate limit for pacing may help to restore AV synchrony.
Retrogradely conducted P waves are visible directly following each ventricular-paced complex.
This is an ECG tracing of a patient with continuous atrioventricular synchronous (DDD) pacing prior to development of symptoms. Atrial stimulation (open arrows) is followed by visible P waves. Wide QRS complexes follow ventricular stimulation (solid arrows).
This is an ECG tracing of a patient with atrioventricular (AV) dissociation and resultant pacemaker syndrome. Native atrial depolarizations (arrows) move progressively closer to pacemaker-stimulated ventricular depolarizations. Ventricular pacemaker stimuli (arrowheads) are greater in amplitude than those visible in the previous image, consistent with mode reversion from AV synchronous (DDD) to ventricular inhibited (VVI), which includes a switch from bipolar pacing (low amplitude) to unipolar pacing (higher amplitude).
Table. Incidence of Atrial Fibrillation in Patients with Pacemakers
Study Patients


Total Incidence




Annual Incidence


Frielingsdorf[34] 1838 18-47 0-17* 3.75 4.8-12.5 0-4.5*
Sutton and Kenny[35] 1061 22 3.9   AAI: 2.75

VVI: 3.25

6.77 1.42  
Hesselson[36] 8827 14-57 0-23   AAI: 1-8

VVI: 3-8

Cannot be determined
Hesselson[36] 950 38 7   7 5.43 1.00  
Santini[37] 339 48 3.7 13 5 9.6 0.74 2.6
Sasaki[38] 75 41 2* AAI: 3.25

VVI: 5.17

7.9 0.62*
Rosenqvist[39] 168 47 6.7   4 11.8 1.68  
*Combined AAI and DDD
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.