Pacemaker syndrome overview

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Pacemaker syndrome Microchapters

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Overview

Historical Perspective

Pathophysiology

Differentiating Pacemaker syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

Echocardiography

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]

Overview

Pacemaker syndrome is a disease that represents the clinical consequences of suboptimal atrioventricular (AV) synchrony or AV dyssynchrony, regardless of the pacing mode, after the pacemaker plantation.[1][2]. It is an iatrogenicdisease that is often underdiagnosed[1][3]. In general, the symptoms of the syndrome are a combination of decreased cardiac output, loss of atrial contribution toventricular filling, loss of total peripheral resistance response, and nonphysiologic pressure waves.[2][4][5]

Individuals with a low heart rate prior to pacemaker implantation are more at risk of developing pacemaker syndrome. Normally the first chamber of the heart (atrium) contracts as the second chamber (ventricle) is relaxed, allowing the ventricle to fill before it contracts and pumps blood out of the heart. When the timing between the two chambers goes out of synchronization, less blood is delivered on each beat. Patients who develop pacemaker syndrome may require adjustment of the pacemaker timing, or another lead fitted to regulate the timing of the chambers separately.

Historical Perspective

Since the implantation of artificial pacemaker in 1958, cases of decreased cardiac output due to ventricular pacing have been reported. Majority of the patients had increased total peripheral resistance due to aortic and carotid reflexes activity resulting from reduced cardiac output.

Pathophysiology

  • The loss of physiologic timing of atrial and ventricular contractions, or sometimes called AV dyssynchrony, leads to different mechanisms of symptoms production.
  • Due to loss of AV synchrony, there is no atrial kick, and thus cardiac output decreases.
  • This altered ventricular contraction will decrease cardiac output, and in turn will lead to systemic hypotensive reflex response with varying symptoms.[1]

Epidemiology and Demographics

  • The wide range of reported incidence is likely attributable to two factors which are the criteria used to define pacemaker syndrome and the therapy used to resolve that diagnosis.[8]

Diagnosis

Laboratory Findings

No laboratory tests are usually indicated in pacemaker syndrome. But levels of atrial natriuretic peptide and brain natriuretic peptide can be measured to define the level of cardiac functioning.

Electrocardiogram

Electrocardiographic findings in pacemaker syndrome may include prolonged PR interval, VA conduction due to dyssynchrony between atria and ventricles and/orAV dissociation.

Treatment

Surgery

Sometimes surgical intervention is needed. After consulting an electrophysiologist, possibly an additional pacemaker lead placement is needed, which eventually relieve some of the symptoms.

Prevention

At the time of pacemaker implantation, AV synchrony should be optimized to prevent the occurrence of pacemaker syndrome. Patients with optimized AV synchrony have shown great results of implantation and very low incidence of pacemaker syndrome than those with suboptimal AV synchronization.

References

  1. 1.0 1.1 1.2 Ellenbogen KA, Gilligan DM, Wood MA, Morillo C, Barold SS (1997). "The pacemaker syndrome -- a matter of definition". Am. J. Cardiol. 79 (9): 1226–9. doi:10.1016/S0002-9149(97)00085-4. PMID 9164889. Unknown parameter |month= ignored (help)
  2. 2.0 2.1 Chalvidan T, Deharo JC, Djiane P (2000). "[Pacemaker syndromes]". Ann Cardiol Angeiol (Paris) (in French). 49 (4): 224–9. PMID 12555483. Unknown parameter |month= ignored (help)
  3. Baumgartner, William A.; Yuh, David D.; Luca A. Vricella (2007). The Johns Hopkins manual of cardiothoracic surgery. New York: McGraw-Hill Medical Pub. ISBN 0-07-141652-8.
  4. Frielingsdorf J, Gerber AE, Hess OM (1994). "Importance of maintained atrio-ventricular synchrony in patients with pacemakers". Eur. Heart J. 15 (10): 1431–40. PMID 7821326. Unknown parameter |month= ignored (help)
  5. Furman S (1994). "Pacemaker syndrome". Pacing Clin Electrophysiol. 17 (1): 1–5. doi:10.1111/j.1540-8159.1994.tb01342.x. PMID 7511223. Unknown parameter |month= ignored (help)
  6. Andersen HR, Thuesen L, Bagger JP, Vesterlund T, Thomsen PE (1994). "Prospective randomised trial of atrial versus ventricular pacing in sick-sinus syndrome". Lancet. 344 (8936): 1523–8. doi:10.1016/S0140-6736(94)90347-6. PMID 7983951. Retrieved 2009-06-19. Unknown parameter |month= ignored (help)
  7. Heldman D, Mulvihill D, Nguyen H; et al. (1990). "True incidence of pacemaker syndrome". Pacing and Clinical Electrophysiology : PACE. 13 (12 Pt 2): 1742–50. doi:10.1111/j.1540-8159.1990.tb06883.x. PMID 1704534. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  8. Farmer DM, Estes NA, Link MS (2004). "New concepts in pacemaker syndrome". Indian Pacing and Electrophysiology Journal. 4 (4): 195–200. PMC 1502063. PMID 16943933. Retrieved 2009-06-19.

Template:WH Template:WS 9. [1]

  1. Van Orden Wallace CJ (2001). "Diagnosing and treating pacemaker syndrome". Crit Care Nurse. 21 (1): 24–31, 35, quiz 36-7. PMID 11858242.