Pacemaker syndrome
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2] Mahshid Mir, M.D. [3] Tayebah Chaudhry[4]
Overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2] Tayebah Chaudhry[3]
Overview
Pacemaker syndrome is a condition that represents the clinical consequences of suboptimal atrioventricular (AV) synchrony or AV dyssynchrony, regardless of the pacing mode, after pacemaker plantation. It is an iatrogenic disease that is often underdiagnosed.
In general, the symptoms of the syndrome are a combination of decreased cardiac output, loss of atrial contribution to ventricular filling, loss of total peripheral resistance response, and nonphysiologic pressure waves.
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.
- Decrease cardiac effect causes signs and symptoms of Pacemaker syndrome which includes:
- Shortness of breath
- Fatigue
- Chest pain
- Choking sensation
- Anxiety
- Dizziness
- Confusion
- Palpitations.
- 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.[4]
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/or AV dissociation.
Treatment
Surgery
- Sometimes surgical intervention is needed.
- After consulting an electrophysiologist, an additional pacemaker lead placement might be needed, which eventually relieves 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 and very low incidence of pacemaker syndrome than those with suboptimal AV synchronization.
- References
- ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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.
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Historical Perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2] Raviteja Guddeti, M.B.B.S. [3] Mohammed Salih, MD. [4] Tayebah Chaudhry[5]
Overview
Since the implantation of artificial pacemaker in 1958, cases of decreased cardiac output due to ventricular pacing have been reported. The majority of the patients had increased total peripheral resistance due to aortic and carotid reflexes activity resulting from the reduced cardiac output.
Historical Perspective
- Pacemaker syndrome was first described in 1969 by Mitsui et al. as a collection of symptoms associated with right ventricular pacing.[1][2]
- Since its first discovery, there have been many definitions of pacemaker syndrome but the understanding of the cause of pacemaker syndrome still under investigation.
- In a general sense, pacemaker syndrome can be defined as the symptoms associated with right ventricular pacing relieved with the return of A-V and V-V synchrony.
- In 1994 Furman redefined pacemaker syndrome to include loss of AV synchrony, retrograde ventriculoatrial conduction, and absence of rate response to the general physiologic requirement.
References
- ↑ 1.0 1.1 Travill CM, Sutton R (1992). “Pacemaker syndrome: an iatrogenic condition”. British Heart Journal. 68 (2): 163–6. doi:10.1136/hrt.68.8.163. PMC 1025005. PMID 1389730. Retrieved 2009-06-19. Unknown parameter
|month=ignored (help) - ↑ 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.
- ↑ 2 Erbel R. Pacemaker syndrome. AmJ Cardiol 1979;44:771-2.
Pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2] Raviteja Guddeti, M.B.B.S. [3] Tayebah Chaudhry[4]
Overview
The loss of physiologic timing of atrial and ventricular contractions, or sometimes called AV dyssynchrony, leads to different mechanisms of symptoms production. This altered ventricular contraction will decrease cardiac output, and in turn, will lead to systemic hypotensive reflex response with varying symptoms.
Pathophysiology
Pacemaker Syndrome Mechanisms:
AV dyssynchrony leads to various symptoms with different mechanisms of symptom production.
- Loss of AV synchrony
- Valvular incompetence
- Asynchronous ventricular contractions
- Ventriculoatrial conduction
- Echo beats
- Arrhythmias
Loss of Atrial Contraction
Inappropriate pacing in patients with decreased ventricular compliance, which may be caused by diseases such as:
All of the above causes result in loss of atrial contraction and significantly reduces cardiac output because in such cases the atria are required to provide 50% of cardiac output, which is normally only 15% – 25%.[1][2]
Cannon A Waves
- Atrial contraction against a closed tricuspid valve can cause pulsation in the neck and abdomen, headache, cough, and jaw pain.[1][3]
Increased Atrial Pressure
- Ventricular pacing is associated with dyssynchrony between the atria and ventricles causing an elevated right and left atrial pressures, as well as elevated pulmonary venous and pulmonary arterial pressures, which can in turn lead to symptomatic pulmonary and hepatic congestion.
Increased Production of Natriuretic Peptides
- Patients with pacemaker syndrome exhibit increased plasma levels of ANP. That’s due to increase in left atrial pressure and left ventricular filling pressure, which is due to decreased cardiac output caused by dyssynchrony in atrial and ventricular contraction in ventricle paced rhythms.
- ANP and BNP are potent arterial and venous vasodilators that can override carotid and aortic baroreceptor reflexes attempting to compensate for decreased blood pressure.
- Usually patients with cannon a waves have higher plasma levels of ANP than those without cannon a waves.[4][5][6][7]
VA Conduction
- A major cause of AV dyssynchrony is VA conduction.
- VA conduction, sometimes referred to as retrograde conduction, leads to delayed, nonphysiologic timing of atrial contraction in relation to ventricular contraction.
- Nevertheless, many conditions other than VA conduction promote AV dyssynchrony.[4][1][3]
- Ventricular paced rhythms cause a reduction in cardiac output by causing a nonphysiologic depolarization of the ventricles.
- Depolarization patterns and contraction are altered when pacemaker leads are placed in the apex of the right ventricle.
- This will further decrease blood pressure and cause a secondary increase in ANP and BNP.[5][6]
- In patients with heart failure it has been shown that institution of biventricular pacing mode has been associated with a better cardiac output.
References
- ↑ 1.0 1.1 1.2 Petersen HH, Videbaek J (1992). “[The pacemaker syndrome]”. Ugeskr. Laeg. (in Danish). 154 (38): 2547–51. PMID 1413181. Unknown parameter
|month=ignored (help) - ↑ Gross JN, Keltz TN, Cooper JA, Breitbart S, Furman S (1992). “Profound “pacemaker syndrome” in hypertrophic cardiomyopathy”. Am. J. Cardiol. 70 (18): 1507–11. doi:10.1016/0002-9149(92)90313-N. PMID 1442632. Unknown parameter
|month=ignored (help) - ↑ 3.0 3.1 Schüller H, Brandt J (1991). “The pacemaker syndrome: old and new causes”. Clin Cardiol. 14 (4): 336–40. doi:10.1002/clc.4960140410. PMID 2032410. Unknown parameter
|month=ignored (help) - ↑ 4.0 4.1 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) - ↑ 5.0 5.1 Theodorakis GN, Panou F, Markianos M, Fragakis N, Livanis EG, Kremastinos DT (1997). “Left atrial function and atrial natriuretic factor/cyclic guanosine monophosphate changes in DDD and VVI pacing modes”. Am. J. Cardiol. 79 (3): 366–70. doi:10.1016/S0002-9149(97)89285-5. PMID 9036762. Unknown parameter
|month=ignored (help) - ↑ 6.0 6.1 Theodorakis GN, Kremastinos DT, Markianos M, Livanis E, Karavolias G, Toutouzas PK (1992). “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. 13 (11): 1477–81. PMID 1334465. Unknown parameter
|month=ignored (help) - ↑ Mollazadeh R, Mohimi L, Zeighami M, Fazelifar A, Haghjoo M (2012). “Hemodynamic effect of atrioventricular and interventricular dyssynchrony in patients with biventricular pacing: Implications for the pacemaker syndrome”. J Cardiovasc Dis Res. 3 (3): 200–3. doi:10.4103/0975-3583.98892. PMC 3425026. PMID 22923937. Unknown parameter
|month=ignored (help)
Differentiating Pacemaker syndrome from other Diseases
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2] Raviteja Guddeti, M.B.B.S. [3]
Overview
Patients with pacemaker syndrome present with varied symptoms resulting from dyssynchrony between atria and ventricles. Pacemaker syndrome should be differentiated from the following diseases:Acute coronary syndrome, failed pacemaker, hypothyroidism, cardiogenic pulmonary edema, arrhythmias (especially supraventricular tachycardias), hyperthyroidism, pulmonary embolism, and carotid sinus hypersensitivity.
Differentiating Pacemaker syndrome from other Diseases
Patients with pacemaker syndrome present with varied symptoms resulting from dyssynchrony between atria and ventricles.
Presenting symptoms include:
- Dyspnea
- Edema
- Orthopnea
- Symptoms of low cardiac output like weakness, fatigue, lightheadedness and dyspnea on exertion
- Hypotension
- Shock
- Orthostatic changes
- Syncope
- Dizziness
- Right upper quadrant pain
- Headaches
- Palpitations
- Easy fatigability
Pacemaker syndrome should be differentiated from the following diseases:
- Consider Pacemaker Syndrome as a differential diagnosis in a patient with implanted ventricular pacemaker who develops new neurological or cardiovascular symptoms
- Acute coronary syndrome
- Failed pacemaker
- Hypothyroidism
- Cardiogenic pulmonary edema
- Arrhythmias (especially supraventricular tachycardias)
- Hyperthyroidism
- Pulmonary embolism
- Carotid sinus hypersensitivity
Differentiating [disease name] from other diseases on the basis of [symptom 1], [symptom 2], and [symptom 3]
On the basis [symptom 1], [symptom 2], and [symptom 3], [disease name] must be differentiated from [disease 1], [disease 2], [disease 3], [disease 4], [disease 5], and [disease 6].
| Diseases | Clinical manifestations | Para-clinical findings | Gold standard | Additional findings | |||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Symptoms | Physical examination | ||||||||||||||
| Lab Findings | Imaging | Histopathology | |||||||||||||
| Symptom 1 | Symptom 2 | Symptom 3 | Physical exam 1 | Physical exam 2 | Physical exam 3 | Lab 1 | Lab 2 | Lab 3 | Imaging 1 | Imaging 2 | Imaging 3 | ||||
| Differential Diagnosis 1 | |||||||||||||||
| Differential Diagnosis 2 | |||||||||||||||
| Differential Diagnosis 3 | |||||||||||||||
| Diseases | Symptom 1 | Symptom 2 | Symptom 3 | Physical exam 1 | Physical exam 2 | Physical exam 3 | Lab 1 | Lab 2 | Lab 3 | Imaging 1 | Imaging 2 | Imaging 3 | Histopathology | Gold standard | Additional findings |
| Differential Diagnosis 4 | |||||||||||||||
| Differential Diagnosis 5 | |||||||||||||||
| Differential Diagnosis 6 | |||||||||||||||
References
Epidemiology and Demographics
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2] Mohammed Salih, MD. [3] Tayebah Chaudhry[4]
Overview
Epidemiology
- The incidence of pacemaker syndrome varies from 2%[1] to 83%.[2] [3]
- 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.[3]
References
- ↑ 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) - ↑ 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) - ↑ 3.0 3.1 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.
Risk Factors
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2] Mohammed Salih, MD. [3]
Risk Factors
- People with the following conditions are at higher risk of developing Pacemaker Syndrome:
- Left ventricular disease
- Recipients of single-chamber ventricular pacemakers
- Retrograde conduction
- Decreased stroke volume
- Decreased cardiac output
- Decreased left atrial total emptying fraction
- Elderly people
- According to most trials the only two variables that predict the development of pacemaker syndrome in the pre-implantation period are low sinus rate, and a higher programmed lower rate limit. Similarly in the post-implantation period, an increased percentage of ventricular paced beats is the only variable that significantly predicts the development of pacemaker syndrome.
- One major risk factor for the development of pacemaker syndrome is the presence of an intact VA conduction (retrograde ventriculo-atrial conduction).
- Intact VA conduction is present in as many as 90% of patients with preserved AV conduction, and in about 30-40% of patients with complete AV block. VA conduction may develop at any time after implantation of the pacemaker and may not be apparent at the time of implantation of the device.
- Patients with cardiomyopathy (hypertensive, hypertrophic, restrictive) and elderly individuals are particularly sensitive to the development of pacemaker syndrome because of the presence of noncompliant ventricles and diastolic dysfunction which lead to loss of atrial contribution to ventricular filling and in turn to pacemaker syndrome.
References
- ↑ Van Orden Wallace CJ (2001). “Diagnosing and treating pacemaker syndrome”. Crit Care Nurse. 21 (1): 24–31, 35, quiz 36-7. PMID 11858242.
Natural History, Complications and Prognosis
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2] Mohammed Salih, MD. [3]
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Complications
Studies have shown that patients with pacemaker syndrome and/or with sick sinus syndrome are at higher risk of developing fatal complications that calls for the patients to be carefully monitored in the ICU. Complications include:
- Atrial fibrillation
- Thrombo-embolic events
- Heart failure
- Hypotension
- Cardiogenic shock
- Complications of treatment – when a new pacemaker is implanted or a new lead is placed the following complications may be seen:
Prognosis
Prognosis of pacemaker syndrome is usually excellent after correction of the pacing mode.
References
Diagnosis
Diagnosis
History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | Echocardiography | Other Imaging Findings | Other Diagnostic Studies
Treatment
Treatment
Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies
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