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Pacemaker Syndrome Medication

  • Author: Daniel M Beyerbach, MD, PhD; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Nov 24, 2014
 

Medication Summary

No specific drugs are used to treat pacemaker syndrome directly because treatment consists of upgrading or reprogramming the pacemaker.

When lead or device implantation is required, wound infection prophylaxis with IV cefazolin for 24 hours is recommended; if the patient has a beta-lactam allergy, vancomycin is a reasonable alternative.[41]

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Antibiotics

Class Summary

Therapy must be comprehensive and cover all likely pathogens in the context of the clinical setting.

Cefazolin (Ancef, Kefzol, Zolicef)

 

First-line agent for wound prophylaxis. First-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth. Primarily active against skin flora, including Staphylococcus aureus. Typically used alone for skin and skin structure coverage.

IV and IM dosing regimens are similar.

Vancomycin (Vancocin)

 

Second-line agent for patients with beta-lactam allergy. Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci.

To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use CrCl to adjust dose in patients diagnosed renal impairment. Used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients undergoing GI or genitourinary procedures.

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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 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.

References
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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[27] 1838 18-47 0-17* 3.75 4.8-12.5 0-4.5*
Sutton and Kenny[28] 1061 22 3.9   AAI: 2.75



VVI: 3.25



6.77 1.42  
Hesselson[29] 8827 14-57 0-23   AAI: 1-8



VVI: 3-8



Cannot be determined
Hesselson[29] 950 38 7   7 5.43 1.00  
Santini[30] 339 48 3.7 13 5 9.6 0.74 2.6
Sasaki[31] 75 41 2* AAI: 3.25



VVI: 5.17



7.9 0.62*
Rosenqvist[32] 168 47 6.7   4 11.8 1.68  
*Combined AAI and DDD
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