Pacemaker Syndrome Treatment & Management

  • Author: Daniel M Beyerbach, MD, PhD; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Jan 4, 2012
 

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, 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.
Next

Surgical Care

Consultation with an electrophysiologist determines the possible need for additional pacemaker lead placement.

Previous
Next

Consultations

Electrophysiology should be consulted for specialized care related to the pacemaker and for procedures to aid in diagnosis and treatment of pacemaker syndrome.

Previous
Next

Diet

  • 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.
Previous
Next

Activity

Patients may engage in activities as tolerated.

Previous
Proceed to Medication
 
 
Contributor Information and Disclosures
Author

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.

Coauthor(s)

Christopher Cadman, MD  Director of Arrhythmia Service, Assistant Professor, Department of Internal Medicine, Division of Cardiology, University of New Mexico

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

Disclosure: Nothing to disclose.

Specialty Editor Board

Hanumant Deshmukh, MD †  Former Chief of Cardiology, Veterans Affairs Medical Center; Former Associate Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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

Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

References
  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. Jul 1978;42(1):137-42. [Medline].

  3. Erbel R. Pacemaker syndrome. Am J Cardiol. Oct 1979;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. Sep 1984;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). Jul-Aug 1971;20(4):371-9. [Medline].

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

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

  9. Gross JN, Keltz TN, Cooper JA, et al. Profound "pacemaker syndrome" in hypertrophic cardiomyopathy. Am J Cardiol. Dec 1 1992;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. May 27 2008;51(21):e1-62. [Medline].

  11. 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. Apr 16 1998;338(16):1097-104. [Medline].

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

  13. 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. Oct 1995;74(4):397-402. [Medline].

  14. 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. Apr 1991;65(4):188-93. [Medline].

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

  16. 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. Nov 1992;13(11):1477-81. [Medline].

  17. 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. Feb 1 1997;79(3):366-70. [Medline].

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

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

  20. 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. Dec 7 2004;44(11):2157-65. [Medline].

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

  22. 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. Jun 2 2004;43(11):2066-71. [Medline].

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

  24. 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. Jan 1992;67(1):57-64. [Medline].

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

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

  27. 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. Jun 1992;19(7):1542-9. [Medline].

  28. 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. Mar 15 1990;65(11):729-35. [Medline].

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

  30. 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. Jul 1988;116(1 Pt 1):16-22. [Medline].

  31. 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. Oct 25 1997;350(9086):1210-6. [Medline].

  32. 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. Jul 1989;12(7 Pt 1):1065-9. [Medline].

  33. 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. Apr 1986;7(4):925-32. [Medline].

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

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

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

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

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

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

Previous
Next
 
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



(number)



Total Incidence



(%)



Follow-up



(years)



Annual Incidence



(%)



VVI AAI DDD VVI AAI DDD
Frielingsdorf[25] 1838 18-47 0-17* 3.75 4.8-12.5 0-4.5*
Sutton and Kenny[26] 1061 22 3.9 AAI: 2.75



VVI: 3.25



6.77 1.42
Hesselson[27] 8827 14-57 0-23 AAI: 1-8



VVI: 3-8



Cannot be determined
Hesselson[27] 950 38 7 7 5.43 1.00
Santini[28] 339 48 3.7 13 5 9.6 0.74 2.6
Sasaki[29] 75 41 2* AAI: 3.25



VVI: 5.17



7.9 0.62*
Rosenqvist[30] 168 47 6.7 4 11.8 1.68
*Combined AAI and DDD
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.