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Quick Dx & Rx: Cardiology

Wandering Atrial Pacemaker

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Key features, clinical presentation, diagnostic evaluation, ongoing management.

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ESSENTIALS OF DIAGNOSIS

Progressive cyclic variation in P-wave morphology

Heart rate 60–100 bpm

Variation of P-wave morphology, P-P interval, and P-R interval

GENERAL CONSIDERATIONS

This rhythm is benign

This rhythm and multifocal atrial tachycardia are similar except for heart rate

The other possible explanation is that there is significant respiratory sinus arrhythmia, with uncovering of latent foci of pacemaker activity

Usually, it is associated with underlying lung disease

In the elderly, it may be a manifestation of sick sinus syndrome

In the young and athletic heart, it may represent enhanced vagal tone

SYMPTOMS AND SIGNS

Usually causes no symptoms and is incidentally discovered

Occasional patient may feel skipped beats

PHYSICAL EXAM FINDINGS

Variable S 1

DIFFERENTIAL DIAGNOSIS

Multifocal atrial tachycardia (heart rate > 100 bpm)

Frequent premature atrial complexes and atrial bigeminy

LABORATORY TESTS

None specific

ELECTROCARDIOGRAPHY

ECG to document rhythm

CARDIOLOGY REFERRAL

Not required

MEDICATIONS

No specific treatment

Monitor and treat the underlying cause, such as sick sinus syndrome or lung disease

DIET AND ACTIVITY

No restrictions

General healthy lifestyle

Once a year if sinus node abnormality is suspected; otherwise when symptoms arise

COMPLICATIONS

May progress to sick sinus syndrome

This condition by itself is benign

PRACTICE GUIDELINES

Indications for pacemaker:

– If part of sick sinus syndrome

– If associated with documented symptomatic bradycardia

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wandering atrial pacemaker and syncope

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Ectopic Supraventricular Arrhythmias

, MD, Libin Cardiovascular Institute of Alberta, University of Calgary

  • 3D Models (0)
  • Calculators (0)

Various rhythms result from supraventricular foci (usually in the atria). Diagnosis is by electrocardiography. Many are asymptomatic and require no treatment.

Overview of Arrhythmias

Ectopic supraventricular rhythms include

Atrial premature beats

Atrial tachycardia, multifocal atrial tachycardia, nonparoxysmal junctional tachycardia, wandering atrial pacemaker.

Chronic Obstructive Pulmonary Disease (COPD)

Atrial premature beat (APB)

APBs may be normally, aberrantly, or not conducted and are usually followed by a noncompensatory pause. Aberrantly conducted APBs (usually with right bundle branch block morphology) must be distinguished from premature beats of ventricular origin.

Atrial escape beats are ectopic atrial beats that emerge after long sinus pauses or sinus arrest. They may be single or multiple; escape beats from a single focus may produce a continuous rhythm (called ectopic atrial rhythm). Heart rate is typically slower, P wave morphology is typically different, and PR interval is slightly shorter than in sinus rhythm.

Atrioventricular Block

Symptoms are those of other tachycardias (eg, light-headedness, dizziness, palpitations, and rarely syncope).

True atrial tachycardia

Vagal maneuvers may be used to slow the heart rate, allowing visualization of P waves when they are hidden, but these maneuvers do not usually terminate the arrhythmia (demonstrating that the AV node is not an obligate part of the arrhythmia circuit).

Cardiac Pacemakers

Nonparoxysmal junctional tachycardia is caused by abnormal automaticity in the AV node or adjacent tissue, which typically follows open heart surgery, acute inferior myocardial infarction, myocarditis, or digitalis toxicity. Heart rate is 60 to 120 beats/minute; thus, symptoms are usually absent. ECG shows regular, normal-appearing QRS complexes without identifiable P waves or with retrograde P waves (inverted in the inferior leads) that occur shortly before ( < 0.1 second) or after the QRS complex. The rhythm is distinguished from paroxysmal supraventricular tachycardia by the lower heart rate and gradual onset and offset. Treatment is directed at causes.

Wandering atrial pacemaker (multifocal atrial rhythm) is an irregularly irregular rhythm caused by the random discharge of multiple ectopic atrial foci. By definition, heart rate is ≤ 100 beats/minute. Except for the rate, features are the same as those of multifocal atrial tachycardia. Treatment is directed at causes.

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wandering atrial pacemaker and syncope

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Figures & Tables

Syncope in Patients with Pacemakers

Richard Sutton

Views: 2437

Downloads: 6

Citations: 12

Syncope in a pacemaker patient is a serious symptom but it is rarely due a pacemaker system malfunction. Syncope occurs in about 5 % of patients paced for atrioventricular (AV) block in 5 years, 18% in those paced for sinus node disease in 10 years, 20 % of those paced for carotid sinus syndrome in 5 years and 5–55 % of those older patients paced for vasovagal syncope in 2 years. The vastly different results in vasovagal syncope depend on the results of tilt testing, where those with negative tests approach results in pacing for AV block and those with a positive tilt test show no better results than with no pacemaker. The implication of tilt results is that a hypotensive tendency is clearly demonstrated by tilt positivity pointing to syncope recurrence with hypotension. This problem may be addressed by treatment with vasoconstrictor drugs in those who are suited or, more commonly, a reduction or cessation of hypotensive therapy in hypertensive patients. Other causes of syncope such as tachyarrhythmias are rare. The clinical approach to patients who report syncope is detailed.

Syncope , pacemaker , pacemaker malfunction , atrioventricular block , sinus node disease , carotid sinus syndrome , vasovagal syncope , tilt testing ,

Disclosure: The author has no relevant conflicts of interest.

Received: 21 August 2015

Accepted: 03 November 2015

Citation: Arrhythmia & Electrophysiology Review 2015;4(3):189–92.

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DOI: https://doi.org/10.15420/aer.2015.4.3.189

Correspondence Details: Richard Sutton, ICCH Building, St Mary’s Hospital Campus, 59–61 North Wharf Road, London W2 1LA, UK. E: [email protected]

The copyright in this work belongs to Radcliffe Medical Media. Only articles clearly marked with the CC BY-NC logo are published with the Creative Commons by Attribution Licence. The CC BY-NC option was not available for Radcliffe journals before 1 January 2019. Articles marked ‘Open Access’ but not marked ‘CC BY-NC’ are made freely accessible at the time of publication but are subject to standard copyright law regarding reproduction and distribution. Permission is required for reuse of this content.

Syncope in a patient with a pacemaker commands urgent action to ascertain its cause and provide appropriate treatment. This is a well accepted statement but the field has evolved in recent years and, strangely, has received little attention.

Many considerations bear on this issue. First, syncope in pacemaker patients is not common but may be more so than generally considered. The lack of frequency may be attributed to better technology and greater expertise amongst practitioners but it should be modulated by the fact that more patients today receive pacemakers for other indications than syncope, rendering them unlikely to sustain syncope even if their pacemaker system fails. Second, we now live in an era of telemedicine where remote monitoring not only provides an opportunity to identify technological or arrhythmic causes of syncope in a pacemaker patient but also a chance for the patient very readily to report such an episode to hospital carers. 1 Third, more patients today receive pacemakers for reflex syncope where the device is not expected to achieve the results in syncope prevention that pertain in atrioventricular block (AVB). 2,3 Included with this aspect of syncope in pacemaker patients must also now be the realisation that syncope may be reflex in the largest group of patients worldwide that receive pacemakers, those with sino-atrial node disease. 4

It is in these contexts that a review of this serious clinical problem is due.

Where We Were

In the late 1980s and early 1990s, we had already achieved a high standard of implant techniques and devices were well constructed with rare failure. 2,3 Langenfeld et al. found a 3.5 % recurrence of syncope in AVB (Second and Third Degree) in 5 years; a question of reflex syncope did not arise. 2

However, by 1991, Pavlovic et al., in a detailed analysis of 46 VVI- paced patients with recurrent syncope, found only two with exit block and an additional patient with sensing failure, which was unlikely to have been the cause of syncope. 3 Thus, 4.3 % had pacing failure as the cause of syncope, while at the same time 8.6 % had orthostatic hypotension and 36.9 % were tilt positive. These tilt findings were invoked as explaining the syncope sustained by these patients but no explanation was found in another 30.4 %. They concluded that reflex syncope may be the most common cause of recurrent syncope in paced patients, with pacing hardware failure being quite rare.

This theme was reiterated by Sgarbossa et al. in a large series of 507 sick sinus syndrome patients from the Cleveland Clinic. 4 In 62 ± 38 months of follow-up, they found syncope recurrence in 3 % at 1 year, 8 % at 5 years and 13 % predicted at 10 years. Their analysis of the causes of syncope indicated lead or pacemaker failure in 6.5 %, vasovagal in 18 %, orthostatic hypotension in 25.5 %, unexplained in 29.5 %, atrial tachyarrhythmias in 11.5 % and ventricular tachyarrhythmias in 5 %. They concluded that autonomic disturbances were the main contributors to syncope recurrence and pacing hardware failure was uncommon. Such conclusion was reached at a time when syncope in sick sinus syndrome was considered to be sinus arrest without effective escape mechanism rather than reflex in origin. However, Sgarbossa et al. noted that syncope prior to implant was the only reliable predictor of syncope post-implant.

Helguera et al. focused on endocardial lead malfunction with a broad definition including exit block in 1,474 patients from the Cleveland Clinic. 5 In 33 ± 32 months follow-up, only 54 patients had lead malfunction and 37 % had either syncope in 7 or pre-syncope in 13 patients. These symptomatic lead malfunctions were more common in ventricular leads and in those who had severe symptoms pre-implant. No deaths were attributed to lead malfunction. The authors recommended closest attention to those patients with severe presenting symptoms and pacemaker dependency.

A PubMed search shows that little has been published on these issues between the mid-1990s and the recent past.

Where We Are Now

New information on patients with sick sinus syndrome emerged from the DANPACE study, in which 1,415 patients were followed for 5.4 years. 6 Syncope occurred in 17.5 % of patients after pacing; of those with AAIR pacing, 19 % had syncope whereas the figure was 15.8 % in DDDR-paced patients. Predictors for syncope were: for age 0–39 years, hazard ratio (HR) 2.9; >80 years, HR 1.4; and syncope pre-implant, HR 1.8. Patients with syncope after pacing suffered a higher mortality (HR 1.6). The authors of this highly regarded trial concluded that syncope after pacing in sick sinus syndrome is common, carries an increased mortality and is multifactorial. It would appear that reflex syncope may have been an important factor because syncope in the general population and in their paced group share a bimodal distribution curve with respect to age. Given the longer follow-up in these patients, they have confirmed the earlier findings in much smaller populations. The increased mortality raises some anxiety, but may be explained by comorbidities rather than by a direct effect of syncope itself.

It is well known that vasovagal syncope recurs and risk of recurrence increases with more historical attacks, approaching 50 % after six lifetime events. 7 It is therefore likely that a patient who has experienced many attacks in the past will have recurrences after pacing, even if the clear indication for pacing was not reflex syncope. Further, if the indication for pacing is reflex syncope, recurrence is highly likely. Much more has been learned recently in the latter group of patients. It is also necessary to restate, in this context, that reflex syncope has two components, bradycardia/asystole and vasodepression. The former of these may be well treated by a pacemaker but vasodepression is uninfluenced by pacing. Thus, the blood pressure may fall profoundly with a maintained heart rate by a pacemaker.

The ISSUE-3 study was to the first to demonstrate that pacing is significantly effective in older vasovagal syncope patients. 8 However, the results were tempered by the recurrence of syncope within 2 years of 25 % in those paced versus 57 % in those unpaced (P< 0.04). Reassurance was garnered from the nearly 18 % syncope recurrence in sinus node disease reported from Denmark. 6 Once the ISSUE-3 randomised controlled trial data were combined with the ISSUE-3 registry including patients (or physicians on their behalf) who refused pacing or the concept of randomisation at the point of randomisation, the importance of the tilt result was seen to be in terms of the outcome. 9 Tilt-negative patients (with implantable loop recorder (ILR) showing asystole in a spontaneous attack and otherwise clinically identical to those who were tilt positive with the same ILR findings) did well with pacing – 5 % recurrence of syncope in 21 months. Tilt-positive patients did no better than if they had no pacemaker, with 55 % recurrence rate of syncope. 9

This finding at first appeared counter-intuitive, but analysis of the reported results of tilt testing over 28 years since the test was introduced for diagnosis of syncope pointed to an explanation. 10,11

The hypothesis suggests that tilt testing merely reveals a hypotensive or vasodepressive tendency and no longer should be termed diagnostic because this tendency is hidden by severe cardioinhibition. So a tilt-positive patient with severe cardioinhibition will not readily reveal accompanying vasodepression. Once paced, the pacemaker is expected to prevent cardioinhibition but cannot combat vasodepression, rendering recurrence of syncope likely. The argument was strengthened by the literature on carotid sinus syndrome (CSS), a similar reflex syncope, where those CSS patients with a positive tilt test had 2.7 times the recurrence rate of those who were tilt negative. 12 These data have been further supported by a later report from the same group, with more patients showing very similar findings. 13 The Italian SUP-2 study, including 10 Italian centres, recently reported a decision algorithm for older patients presenting clinically likely reflex syncope. 14 The decision-tree demanded carotid sinus massage (CSM) according to the ‘method of symptoms’ as a first test. Those who had positive CSM were paced, those negative proceeded to a tilt test and, if positive with asystole, were also paced. Those who were tilt negative proceeded to ILR and, if positive with asystole in a spontaneous attack, were then paced. This algorithm permitted assessment of those who were tilt negative and ILR positive and it has been shown separately from the ISSUE-3 study that these patients do well with pacing with a very low syncope recurrence rate in 13 months of follow-up.

Thus, in reflex syncope, both vasovagal and CSS, recurrence of syncope can be predicted after pacing by the tilt test result. The hypothesis also addressed the frequent question in this age group of hypertension and its treatment. 11 Hypertension in these patients is often aggressively treated, producing side effects of episodes of orthostatic hypotension. It is considered likely that some of these patients, as a result, start to experience vasovagal syncope or it recurs (patients having sustained a few attacks in youth). Great care in administering hypotensive medication must now be the norm for these patients and randomised controlled trials are indicated. This group of patients should be considered at risk for syncope recurrence similarly to those who are tilt positive as in the ISSUE-38,9 and SUP-214 studies.

Syncope in paced patients has become much more clear now. It is either rarely due to pacing hardware malfunction or much more commonly due to reflex syncope occurring spontaneously or favoured by hypotensive treatment of hypertension.

How should Paced Patients who Report Syncope be Approached?

Syncope in the paced patient must be regarded as a serious symptom and be promptly investigated. The first consideration should be: was the correct diagnosis of the original syncope made? It is possible that syncope was reflex rather than conduction tissue disease. The second thought should be: are drugs playing a part? If the patient is hypertensive and on hypotensive treatment, this may be the cause of orthostatic hypotension or a rekindling of vasovagal syncope of youth. The third matter to consider is whether the pacing mode is correct. Patients with VVI pacing may have bouts of retrograde AV conduction that can precipitate syncope or, rarely, AAI mode has been selected for a patient with AVB. The fourth matter for thought is whether a tachyarrhythmia could be responsible for recurrence of syncope. In this instance, telemonitoring is extremely valuable for defining the arrhythmia. In such cases, assessment of left ventricular function by echocardiography may be helpful in showing deterioration of function that might be compatible with ventricular arrhythmias. Also, in the less likely possibility that atrial fibrillation is responsible for syncope, echocardiographic assessment of left atrial size is indicated.

Patients paced for AVB presenting syncope represent the most likely to have a pacing hardware fault as they are likely to be pacemaker dependent. First, it is necessary to make sure that the device is appropriate for the implanting indication and then consider the possibility of a technical fault. Always, it must be borne in mind that such faults may be difficult to identify in the clinic. In this instance, telemonitoring is much more effective. 1

Early after implantation, the technical fault might be lead displacement or perforation or incomplete connection at the lead–pulse generator interface. Exit block may present early but also after the first month of implantation. The term ‘exit block’ implies that there is an excessive reaction by the endocardium at the site of the electrode, which has raised the stimulation threshold to a level above the output of the pacemaker. The pacemaker then fails to capture the heart. Some devices now measure the stimulation threshold and adjust output to address this problem. Later problems include lead insulation failure causing failure to capture heralded by low lead impedance, lead conductor fracture heralded by high lead impedance and possibly by oversensing. While these late problems are mostly lead related there could also be a pulse generator problem including normal or early battery depletion. Again, in all of these problems, telemonitoring is very important and must now be considered the standard of care. 15

In patients with indications for pacing other than AVB, technical faults are also possible and must be excluded – telemonitoring is also ideal for this. After such a fault is considered very unlikely, a tilt test is advised to reveal a possible hypotensive tendency. If present, this may be the explanation for the patient’s problems but if absent hypotension could be considered unlikely. It should be borne in mind that a tilt test should no longer be taken as diagnostic but as a risk-of- syncope-recurrence stratification tool. 11

The patient needs to be seen and, if known to be pacemaker dependent, perhaps directly admitted to hospital (see Figure 1 ). In clinic, the usual assessments must be made, also including deep respiration and movement of the pulse generator to attempt to expose evidence of lead damage. A 12-lead ECG must be taken, which is something often not done in the pacemaker clinic. The pattern of depolarisation may have changed from that after implant, implying lead displacement. A chest X-ray may be needed and may show evidence of lead displacement, lead damage or twiddler’s syndrome. The evidence from remote monitoring must be set against the data collected in the clinic. Is the pacing mode and programme correct? The initial assessment for syncope, as in the European Society of Cardiology Guidelines, 16 should be undertaken as this may not have been done at implant. Last, the patient should be considered for admission to hospital – usually necessary for pacemaker-dependent patients, but unlikely to be necessary for patients not pacemaker dependent. For the non-dependent patient, remote monitoring should immediately be established if not already done. If remote monitoring is unavailable, prolonged Holter monitoring will often be required. Hospital admission is usually undertaken when a reoperation is needed rather than attempting therapy as a day case. It should be noted that diagnostic reoperation is now most unlikely to be needed because telemonitoring is so much more effective.

Management of Patients with a Pacemaker Reporting Syncope

Article image

Patient management after diagnosis of the cause of syncope may be reoperation to correct the identified fault, lead repositioning, lead replacement, generator change or upgrading of the pacemaker system. In less serious problems, reprogramming may be sufficient. In reflex syncope cases, use of a rate-drop response type of pacemaker algorithm may help, especially making use of data from tilt testing to tune the program. A closed-loop pacemaker may be more effective than others in reflex syncope but no trial proof of this is currently available. For those who are tilt positive, attempting vasoconstrictor therapy with a drug such as midodrine may help. When it appears that sinus tachycardia is the trigger for syncope, antagonism of this by ivabradine or beta-blocker may help. These patients always need much reassurance because recurrence of pre-pacing symptoms does so much to undermine confidence.

In conclusion, syncope in a pacemaker patient is a serious symptom requiring action. It is quite rare for its explanation to be pacemaker hardware malfunction (around 5 % of cases) and it is much more commonly due to reflex syncope involving vasodepression, which may be iatrogenic by excessive hypotensive therapy. Syncope in pacemaker patients is not as rare as often thought, occurring in 18 % of sinus node disease patients in 10 years and 55 % of tilt positive vasovagal patients in 2 years.

  • Varma N. Automatic home monitoring of patients with cardiac implantable electronic devices – the setting of a new standard. Europace 2013; 15: Suppl 1. Crossref | PubMed
  • Langenfeld H, Grimm W, Maisch B, et al. Course of symptoms and spontaneous ECG in pacemaker patients: a 5-year follow-up study. Pacing Clin Electrophysiol 1988; 11: 2198– 206. Crossref | PubMed
  • Pavlovic SU, Kocovic D, Djordjevic M, et al. The etiology of syncope in pacemaker patients. Pacing Clin Electrophysiol 1991; 14: 2086–91. Crossref | PubMed
  • Sgarbossa EB, Pinski SL, Jaeger FJ, et al. Incidence and predictors of syncope in paced patients with sick sinus syndrome. Pacing Clin Electrophysiol 1992; 15: 2055–60. Crossref | PubMed
  • Helguera ME, Maloney JD, Fahy GJ, et al. Clinical presentation of endocardial lead malfunction. Am J Cardiol 1996; 78: 1297–9. Crossref | PubMed
  • Chuen NK, Kirkfeldt RE, Andersen HR, et al. Syncope in paced patients with sick sinus syndrome from the DANPACE trial: incidence, predictors and prognostic implication. Heart 2014; 100: 842–7. Crossref | PubMed
  • Rose MS, Koshman ML, Spreng S, et al. The relationship between health-related quality of life and the frequency of spells in patients with syncope. J Clin Epidemiol 2000; 53: 1209–16. Crossref | PubMed
  • Brignole M, Menozzi C, Moya A, et al. Pacemaker therapy in patients with neurally-mediated syncope and documented asystole. Third international study on syncope of unknown etiology (ISSUE-3): a randomized trial. Circulation 2012; 125: 2566–71. Crossref | PubMed
  • Brignole M, Donateo P, Tomaino M, et al. The benefit of pacemaker therapy in patients with presumed neurally- mediated syncope and documented asystole is greater when tilt test is negative. An analysis from the third international study on syncope of uncertain etiology (ISSUE 3). Circ Arrhythm Electrophysiol 2014; 7: 10–6. Crossref | PubMed
  • Kenny RA, Ingram A, Bayliss J, et al. Head-up tilt: a useful test for investigating unexplained syncope. Lancet 1986; 1: 1352–5. Crossref | PubMed
  • Sutton R, Brignole M. Twenty-eight years of research permit reinterpretation of tilt-testing: hypotensive susceptibility rather than diagnosis. Eur Heart J 2014; 35: 2211–2. Crossref | PubMed
  • Gaggioli G, Brignole M, Menozzi C, et al. Reappraisal of the vasodepressor reflex in carotid sinus syndrome. Am J Cardiol 1995; 75: 518–21. Crossref | PubMed
  • Solari D, Maggi R, Oddone D, et al. Clinical context and outcome of carotid sinus symdrome diagnosed by means of the ‘method of symptoms’. Europace 2014; 16: 928–34. Crossref | PubMed
  • Brignole M, Ammirati F, Arabia F, et al. Assessment of a standardized algorithm for cardiac pacing in older patients affected by severe unpredictable reflex syncopes. Eur Heart J 2015; 36: 1529–35. Crossref | PubMed
  • Sutton R. Remote monitoring as a key innovation in the management of cardiac patients including those with implantable electronic devices. Europace 2013; 15: i3–i5. Crossref | PubMed
  • Moya, A, Sutton R, Ammirati F, et al. The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009; 30: 2631–71. Crossref | PubMed

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  • Wandering atrial pacemaker
  • 2 Clinical Features
  • 3.1 Palpitations
  • 4.2 Diagnosis
  • 5 Management
  • 6 Disposition
  • 8 External Links
  • 9 References
  • Three or more ectopic foci within the atrial myocardium serve as the pacemaker
  • Rate is less than 100bpm (in contrast to MAT )
  • Is irregularly irregular therefore sometimes confused with atrial fibrillation and sinus arrhythmia
  • Intrinsic cardiac or pulmonary disease
  • Metabolic derangements
  • Drug toxicity (including Digoxin )

Clinical Features

  • Often seen in the extremes of age and in athletes
  • Rarely causes symptoms

Differential Diagnosis

Palpitations.

  • Narrow-complex tachycardias
  • Wide-complex tachycardias
  • Second Degree AV Block Type I (Wenckeback)
  • Second Degree AV Block Type II
  • Third Degree AV Block
  • Premature atrial contraction
  • Premature junctional contraction
  • Premature ventricular contraction
  • Sick sinus syndrome
  • Acute coronary syndrome
  • Cardiomyopathy
  • Congenital heart disease
  • Congestive heart failure (CHF)
  • Mitral valve prolapse
  • Pacemaker complication
  • Pericarditis
  • Myocarditis
  • Valvular disease
  • Panic attack
  • Somatic Symptom Disorder
  • Drugs of abuse (e.g. cocaine )
  • Medications (e.g. digoxin , theophylline )
  • Thyroid storm
  • Pulmonary embolism
  • Dehydration
  • Pheochromocytoma

Wandering atrial pacemaker.JPG

  • ECG should show three distinct P wave morphologies with a ventricular rate <100bpm
  • Rarely requires treatment

Disposition

  • Outpatient management
  • Multifocal atrial tachycardia
  • Dysrhythmia

External Links

  • Richard Cunningham
  • fardis tavangary
  • Ross Donaldson
  • Privacy policy
  • Disclaimers

wandering atrial pacemaker and syncope

Enter search terms to find related medical topics, multimedia and more.

Advanced Search:

  • Use “ “ for exact phrases.
  • For example: “pediatric abdominal pain”
  • Use – to remove results with certain keywords.
  • For example: abdominal pain -pediatric
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  • For example: teenager OR adolescent

Ectopic Supraventricular Arrhythmias

, MD, Libin Cardiovascular Institute of Alberta, University of Calgary

  • 3D Models (0)
  • Calculators (0)

Various rhythms result from supraventricular foci (usually in the atria). Diagnosis is by electrocardiography. Many are asymptomatic and require no treatment.

Overview of Arrhythmias

Ectopic supraventricular rhythms include

Atrial premature beats

Atrial tachycardia, multifocal atrial tachycardia, nonparoxysmal junctional tachycardia, wandering atrial pacemaker.

Chronic Obstructive Pulmonary Disease (COPD)

Atrial premature beat (APB)

APBs may be normally, aberrantly, or not conducted and are usually followed by a noncompensatory pause. Aberrantly conducted APBs (usually with right bundle branch block morphology) must be distinguished from premature beats of ventricular origin.

Atrial escape beats are ectopic atrial beats that emerge after long sinus pauses or sinus arrest. They may be single or multiple; escape beats from a single focus may produce a continuous rhythm (called ectopic atrial rhythm). Heart rate is typically slower, P wave morphology is typically different, and PR interval is slightly shorter than in sinus rhythm.

Atrioventricular Block

Symptoms are those of other tachycardias (eg, light-headedness, dizziness, palpitations, and rarely syncope).

True atrial tachycardia

Vagal maneuvers may be used to slow the heart rate, allowing visualization of P waves when they are hidden, but these maneuvers do not usually terminate the arrhythmia (demonstrating that the AV node is not an obligate part of the arrhythmia circuit).

Cardiac Pacemakers

Nonparoxysmal junctional tachycardia is caused by abnormal automaticity in the AV node or adjacent tissue, which typically follows open heart surgery, acute inferior myocardial infarction, myocarditis, or digitalis toxicity. Heart rate is 60 to 120 beats/minute; thus, symptoms are usually absent. ECG shows regular, normal-appearing QRS complexes without identifiable P waves or with retrograde P waves (inverted in the inferior leads) that occur shortly before ( < 0.1 second) or after the QRS complex. The rhythm is distinguished from paroxysmal supraventricular tachycardia by the lower heart rate and gradual onset and offset. Treatment is directed at causes.

Wandering atrial pacemaker (multifocal atrial rhythm) is an irregularly irregular rhythm caused by the random discharge of multiple ectopic atrial foci. By definition, heart rate is ≤ 100 beats/minute. Except for the rate, features are the same as those of multifocal atrial tachycardia. Treatment is directed at causes.

wandering atrial pacemaker and syncope

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MATTHEW KENDALL HAWKS, MD, MADISON L.B. PAUL, MD, AND OMOJO ODIHI MALU, MD, MSc

Am Fam Physician. 2021;104(2):179-185

Author disclosure: No relevant financial affiliations.

Sinus node dysfunction, previously known as sick sinus syndrome, describes disorders related to abnormal conduction and propagation of electrical impulses at the sinoatrial node. An abnormal atrial rate may result in the inability to meet physiologic demands, especially during periods of stress or physical activity. Sinus node dysfunction may occur at any age, but is usually more common in older persons. The causes of sinus node dysfunction are intrinsic (e.g., degenerative idiopathic fibrosis, cardiac remodeling) or extrinsic (e.g., medications, metabolic abnormalities) to the sinoatrial node. Many extrinsic causes are reversible. Electrocardiography findings include sinus bradycardia, sinus pauses or arrest, sinoatrial exit block, chronotropic incompetence, or alternating bradycardia and tachycardia (i.e., bradycardia-tachycardia syndrome). Clinical symptoms result from the hypoperfusion of end organs. About 50% of patients present with cerebral hypoperfusion (e.g., syncope, presyncope, lightheadedness, cerebrovascular accident). Other symptoms include palpitations, decreased physical activity tolerance, angina, muscular fatigue, or oliguria. A diagnosis is made by directly correlating symptoms with a bradyarrhythmia and eliminating potentially reversible extrinsic causes. Heart rate monitoring using electrocardiography or ambulatory cardiac event monitoring is performed based on the frequency of symptoms. An exercise stress test should be performed when symptoms are associated with exertion. The patient's inability to reach a heart rate of at least 80% of their predicted maximum (220 beats per minute – age) may indicate chronotropic incompetence, which is present in 50% of patients with sinus node dysfunction. First-line treatment for patients with confirmed sinus node dysfunction is permanent pacemaker placement with atrial-based pacing and limited ventricular pacing when necessary.

Sinus node dysfunction, previously known as sick sinus syndrome, is characterized by abnormal initiation and propagation of electrical impulses from the sinoatrial node (SAN). The resulting abnormalities include bradycardia (less than 50 beats per minute [bpm]), sinus pause (more than three seconds), sinus arrest, and sinoatrial exit blocks, which are sometimes associated with supraventricular tachyarrhythmias in bradycardia-tachycardia syndrome 1 – 4 ( Table 1 5 – 11 ) . Bradycardia-tachycardia syndrome occurs in approximately 50% of patients with sinus node dysfunction and increases the risk of stroke and death. 5 , 12 Symptoms manifest as end-organ hypoperfusion, including palpitations, decreased physical activity tolerance, easy fatigability, dizziness, and syncope. 2 , 5 , 6 , 13 To diagnose sinus node dysfunction, a combination of symptoms and documented electrical abnormalities must be present. 5 , 7

Epidemiology

Sinus node dysfunction may occur at any age 7 , 14 ; however, increasing age is the most significant risk factor with the highest disease prevalence in patients 70 to 89 years of age. 2 , 7 , 8 , 14 The incidence of sinus node dysfunction is 0.8 per 1,000 person-years and is expected to double by 2060 due to the aging population. 15 Conditions associated with advanced age such as hypertension, chronic kidney disease, diabetes mellitus, and coronary heart disease are overlapping risk factors and potential causes of sinus node dysfunction. 2 , 15 Brugada syndrome, a rare inherited ion channel disorder that results in ventricular tachyarrhythmias and sudden cardiac death, is also associated with sinus node dysfunction. 5 , 16 , 17

Causes of sinus node dysfunction are generally categorized as intrinsic or extrinsic based on their effect on the SAN ( Table 2 2 , 5 – 8 , 18 ) . It is important to note that sinus node dysfunction is usually a progressive condition and most causes are chronic and irreversible. 5

INTRINSIC CAUSES

Intrinsic causes originate from structural or functional changes within the SAN. These changes can occur because of fibrosis, ischemia, cardiac remodeling, infiltrative disease, or ion channel dysfunction. 8 , 18 , 19 Degenerative idiopathic fibrosis of the SAN is the most common cause of sinus node dysfunction. 4 , 5 , 7 , 8 , 15 Elastic fiber and fatty and fibrous tissue buildup at the SAN and surrounding myocardial tissue increases with age and may lead to prolonged SAN refractory time and, therefore, a decreased intrinsic heart rate. 2 , 4 , 8 Ischemic heart disease and embolization of the sinus node artery may cause ischemic necrosis of the node, resulting in sinus node dysfunction. 8 Acute myocardial infarction may induce a transient sinus node dysfunction caused by autonomic disturbance and increased vagal tone. 2 , 12 Cardiac remodeling following myocardial infarction, congestive heart failure, or advanced age can result in structural changes that decrease cardiac tissue voltage transmission and ultimately delay or block the SAN and result in sinus node dysfunction. 3 , 8 , 14

Another result of this remodeling is the formation of bradycardia-tachycardia syndrome. It is unclear if a supraventricular tachycardia or sinus node dysfunction is the primary disorder in bradycardia-tachycardia syndrome. The etiology is further complicated by current contradictory evidence about the role of supraventricular tachycardia and atrial fibrillation as a cause of sinus node dysfunction. 3 At a minimum, it is clear that these diagnoses are associated even if the causal pathway is unclear.

Infiltrative diseases such as sarcoidosis, amyloidosis, hemochromatosis, and connective tissue diseases can disrupt the cardiac tissue and result in abnormal SAN function. 2 , 5 Similarly, sinus node dysfunction has been associated with cardiomyopathy from infection with Chagas disease, with which the arrhythmia may be permanent. 6 , 8 Rhythm abnormalities associated with myocarditis from infections such as diphtheria and typhoid and immune-mediated disorders such as rheumatic fever may cause sinus node dysfunction temporarily. 6 , 8

About 80% of patients younger than 21 years with sinus node dysfunction have a history of congenital heart malformations (e.g., atrial septal defect, transposition of the great arteries) that required surgical intervention. 18 , 20 Genetic mutations in genes responsible for coding ion channels, such as HCN4 and SCN5A , have also been identified as a cause of intrinsic sinus node dysfunction. 18

EXTRINSIC CAUSES

Extrinsic causes are related to external factors causing abnormal conduction at the SAN. These causes include medications, metabolic abnormalities, autonomic imbalances, toxins, and endocrine disorders ( Table 2 2 , 5 – 8 , 18 ) . Extrinsic causes may be reversible, such as electrolyte abnormalities, hypothyroidism, metabolic abnormalities, and certain medications. 2 , 8 Anesthesia (e.g., sympatholytic drugs) has been shown to induce autonomic imbalances that may mimic sinus node dysfunction or may reveal the underlying dysfunction in previously asymptomatic patients. 8 , 21 Other pharmacotherapies known to cause sinus node dysfunction include beta blockers, nondihydropyridine calcium channel blockers, digoxin, lithium, and antiarrhythmics. 5 , 7 , 8 Toxins such as nicotine and marijuana have also been implicated in sinus node dysfunction. 7 , 8 , 22

Patients with sinus node dysfunction typically present with end-organ hypoperfusion symptoms from decreased cardiac output caused by the underlying arrhythmia ( Table 1 5 – 11 ) . The most common symptoms of cerebral hypoperfusion are syncope, presyncope, lightheadedness, and cerebrovascular accidents, with syncope occurring in 50% of patients with sinus node dysfunction. 2 , 5 , 7 , 23 Cardiovascular hypoperfusion can present with palpitations, decreased physical activity tolerance, angina, or, less commonly, heart failure. Musculoskeletal hypoperfusion can present with muscle fatigue. Renal hypoperfusion can present as oliguria. 2 , 5 , 6 , 13 , 23 Correlation between symptoms and arrhythmias is considered the diagnostic standard (on electrocardiography [ECG] or other cardiac monitoring). 2 , 5 , 6

A definitive diagnosis of sinus node dysfunction is established when symptoms are directly associated with cardiac monitoring that demonstrates a bradyarrhythmia 2 , 6 ( Table 1 5 – 11 ) . The initial assessment should begin with a history and physical examination ( Figure 1 2 – 4 , 8 , 14 , 17 , 21 , 24 ) . Clinicians should focus their history by investigating the intrinsic and extrinsic causes of sinus node dysfunction ( Table 2 2 , 5 – 8 , 18 ) . It should include a medication review to assess for a potential extrinsic cause. Initial diagnostic evaluation should include 12-lead ECG, a basic chemical panel to assess for metabolic abnormalities, and any additional laboratory tests needed to rule out other extrinsic causes that were not excluded by the history or physical examination (i.e., thyroid-stimulating hormone to rule out hypothyroidism or A1C to rule out diabetic atrial myopathy). 5 , 6

wandering atrial pacemaker and syncope

Initial evaluation of sinus node dysfunction can be performed in an outpatient setting; patients with hemodynamic instability (i.e., systolic blood pressure less than 90 mm Hg, ventricular arrhythmias) or severe symptoms (i.e., recurrent syncope, anginal symptoms) should be hospitalized because these patients need urgent evaluation and may require temporary transcutaneous pacing for stabilization. 2 When a potential extrinsic factor is identified during the workup, further evaluation should focus on confirming the diagnosis followed by a trial of therapy. With successful treatment of the extrinsic factor (e.g., continuous positive airway pressure for confirmed sleep apnea or thyroid supplementation for hypothyroidism) and subsequent resolution of sinus node dysfunction, no further workup is indicated.

Patients with history or physical examination findings for underlying structural defects such as a history of valvular disease, new cardiac murmur, bibasilar crackles, lower extremity edema, or concerning ECG findings (e.g., left bundle branch block, second-degree Mobitz type II block, third-degree atrioventricular block) should have transthoracic echocardiography. 2 If the results suggest a specific pathology, further workup and treatment should be initiated based on the suspected etiology. Abnormal results may be because of complications from sinus node dysfunction or an alternative diagnosis, and will require further workup and potential specialty referral for evaluation and treatment.

Chronotropic incompetence is associated with sinus node dysfunction, with 50% of patients diagnosed with sinus node dysfunction also meeting chronotropic incompetence criteria. 25 , 26 It is a separate diagnosis associated with an array of diseases, including sinus node dysfunction. Chronotropic incompetence is defined as the sinus node's inability to mount a heart rate high enough to meet physiologic demands during exertion, resulting in symptoms of central nervous system hypoperfusion similar to those found in sinus node dysfunction. 5 , 25 When symptoms are associated with exertion, the patient should have an exercise ECG test to assess chronotropic incompetence. A diagnosis of chronotropic incompetence is made if the patient is unable to meet 80% of the maximum heart rate (220 bpm – age) during exertion. 2 , 25 It is important to distinguish that chronotropic incompetence is a separate disease process and alone is not enough to diagnose sinus node dysfunction. Sinus node dysfunction and chronotropic incompetence follow the same treatment algorithm ( Figure 1 2 – 4 , 8 , 14 , 17 , 21 , 24 ) .

When initial 12-lead ECG is unable to confirm sinus node dysfunction by correlating symptoms with a definitive bradyarrhythmia ( Table 1 5 – 11 ) , further electrical monitoring is indicated. 2 , 5 , 9 There are multiple types of ambulatory monitoring available. These devices include continuous monitoring (e.g., Holter monitor, external patch recorder, ambulatory telemetry) and patient- or event-activated devices (e.g., event monitor, external loop recorder, implantable loop recorder). First-line devices include the original Holter monitor or the external patch recorder. 8 , 9 , 27 – 32 The external patch recorder is a smaller second-generation monitor that is water-resistant and can be worn for seven to 14 days. The external patch recorder detected more arrhythmias and was better tolerated by patients compared with the Holter monitor. 31 , 33 The frequency of symptoms, the patient's ability to use the device, and the need for continuous vs. intermittent monitoring should be considered when deciding the best form of monitoring for a patient. 9 Table 3 lists cardiac monitoring options with associated indications and pros and cons of use. 9 , 27 – 31 If sinus node dysfunction cannot be definitively established after ambulatory monitoring is completed, further evaluation for an alternative diagnosis and expert consultation should be considered.

Permanent pacemaker placement is the first-line treatment for patients with confirmed sinus node dysfunction , 2 , 5 , 34 – 36 accounting for 50% of pacemakers implanted in the United States. 5 , 7 , 12 Pacemaker therapy has been found to provide symptom relief and improve quality of life, but it is unclear if it provides a mortality benefit. 5 , 36 This treatment includes patients with chronotropic incompetence and patients with pharmacologically induced sinus node dysfunction where continued treatment is clinically necessary. Atrial-based pacing has been established as superior because right ventricular pacing has been associated with an increased risk of arrhythmias and decreased cardiac function. 2 , 37 , 38 A well-powered randomized controlled trial demonstrated no difference in mortality, stroke, heart failure, or atrial fibrillation hospitalizations when comparing single-chamber atrial pacing with dual-chamber atrial pacing. 21 However, over five years of follow-up, 3% to 35% of patients will transition from a single-chamber atrial device to a dual-chamber device with minimized ventricular pacing. 2 , 6 To minimize the risk of these additional procedures, patients with evidence of atrioventricular nodal or bundle branch conduction dysfunction should be considered for initial dual-chamber device placement. 2 It is common in the United States for patients to receive a dual-chamber device with right atrial pacing unless otherwise indicated. Overall, permanent pacemaker placement is relatively safe, with complications estimated at less than 1% to 6%. Most common complications include lead dislodgment (5.7% in left ventricular leads), hematomas (3.5%), venous thrombus/obstruction (2%), infections (1%), and pneumothorax (1%). 34

Medication control of sinus node dysfunction is a secondary option for patients who decline permanent pacemaker placement. Phosphodiesterase inhibitors (e.g., theophylline, cilostazol [Pletal]) have a positive chronotropic effect, resulting in symptom control for patients with sinus node dysfunction. However, the long-term impact of medication control on disease progression and mortality is unclear. 2 , 35 Other pharmaceuticals (e.g., atropine, dopamine, epinephrine, glucagon) used in advanced cardiac life support protocols for acutely unstable bradycardic patients are effective for short-term control of unstable patients but are not appropriate for long-term management of sinus node dysfunction because of significant adverse effect profiles. 2 , 35

The role of oral anticoagulation in patients with sinus node dysfunction is unclear. There is limited evidence to support its use in patients with sinus node dysfunction who do not have another indication for anticoagulation therapy. 2 , 37 , 39 Anticoagulation is currently not routinely recommended for the treatment of sinus node dysfunction.

This article updates previous articles on this topic by Semelka, et al. , 5 and by Adán and Crown . 7

Data Sources: We searched Essential Evidence, PubMed, and Google Scholar. Key words included sinus node dysfunction, sick sinus syndrome, causes, bradyarrhythmia, permanent pacemaker indications, chronotropic incompetence, loop recorders, ambulator cardiac monitoring. The search included practice guidelines, randomized controlled trials, a retrospective case control study, and review articles. Search dates: December 2019 to October 2020.

The opinions and assertions contained herein are those of the authors and are not to be construed as official or as reflecting the views of the Uniformed Services University, the U.S. Air Force Medical Department, the Air Force at large, the U.S. Army Medical Department, the Army at large, or the U.S. Department of Defense.

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Sanders P, Kistler PM, Morton JB, et al. Remodeling of sinus node function in patients with congestive heart failure: reduction in sinus node reserve. Circulation. 2004;110(8):897-903.

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Semelka M, Gera J, Usman S. Sick sinus syndrome: a review. Am Fam Physician. 2013;87(10):691-696. Accessed September 28, 2020. https://www.aafp.org/afp/2013/0515/p691.html

De Ponti R, Marazzato J, Bagliani G, et al. Sick sinus syndrome. Card Electrophysiol Clin. 2018;10(2):183-195.

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Kistler PM, Sanders P, Fynn SP, et al. Electrophysiologic and electro-anatomic changes in the human atrium associated with age. J Am Coll Cardiol. 2004;44(1):109-116.

Zimetbaum P, Goldman A. Ambulatory arrhythmia monitoring: choosing the right device. Circulation. 2010;122(16):1629-1636.

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Go AS, Mozaffarian D, Roger VL, et al.; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Executive summary: heart disease and stroke statistics—2013 update: a report from the American Heart Association. Circulation. 2013;127(1):143-152.

Alonso A, Jensen PN, Lopez FL, et al. Association of sick sinus syndrome with incident cardiovascular disease and mortality: the Atherosclerosis Risk in Communities study and Cardiovascular Health Study. PLoS One. 2014;9(10):e109662.

Dobrzynski H, Boyett MR, Anderson RH. New insights into pacemaker activity: promoting understanding of sick sinus syndrome. Circulation. 2007;115(14):1921-1932.

Jensen PN, Gronroos NN, Chen LY, et al. Incidence of and risk factors for sick sinus syndrome in the general population. J Am Coll Cardiol. 2014;64(6):531-538.

Sarquella-Brugada G, Campuzano O, Arbelo E, et al. Brugada syndrome: clinical and genetic findings. Genet Med. 2016;18(1):3-12.

Mizusawa Y, Wilde AAM. Brugada syndrome. Circ Arrhythm Electrophysiol. 2012;5(3):606-616.

Benson DW, Wang DW, Dyment M, et al. Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A). J Clin Invest. 2003;112(7):1019-1028.

Bashour TT. Classification of sinus node dysfunction. Am Heart J. 1985;110(6):1251-1256.

Yabek SM, Swensson RE, Jarmakani JM. Electrocardiographic recognition of sinus node dysfunction in children and young adults. Circulation. 1977;56(2):235-239.

Khanna S, Sreedharan R, Trombetta C, et al. Sick sinus syndrome: sinus node dysfunction in the elderly. Anesthesiology. 2020;132(2):377-378.

Iqbal AM, Mubarik A, Cheetirala VG, et al. Marijuana induced sick sinus syndrome: a case report. Am J Case Rep. 2019;20:882-885.

Nielsen JC, Thomsen PEB, Højberg S, et al.; DANPACE Investigators. A comparison of single-lead atrial pacing with dual-chamber pacing in sick sinus syndrome. Eur Heart J. 2011;32(6):686-696.

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Melzer C, Witte J, Reibis R, et al. Predictors of chronotropic incompetence in the pacemaker patient population. Europace. 2006;8(1):70-75.

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Electrical Injury and Wandering Atrial Pacemaker

Ranjan k singh.

1 Internal Medicine, Anti-Retroviral Therapy Centre, District Hospital, Khagaria, IND

The supply of household electricity remains a low-voltage (110-220 V) energy source, and its effects on the human body depend on several factors, including the type of contact and duration of contact, among other things. In a significant number of cases, direct contact with household electricity causes reversible cardiac arrhythmia-ventricular fibrillation, ventricular premature beats, atrial tachycardia, and atrial fibrillation.

Wandering atrial pacemaker (WAP) is a benign atrial arrhythmia observed in elderly patients suffering from obstructive pulmonary diseases that result from an ischemic heart. This report discusses WAP as observed in a patient who suffered an electrical injury.

Introduction

The effects of electrical injury vary from skin burn to internal organ damage directed especially at the cardiovascular and nervous systems. The extent of electrical injury depends on the type of electricity source, i.e., direct current (DC) or alternating current (AC), the duration of contact with the source of electricity, the state of the body whether wet or dry, the presence of calluses over the palm, the route of electrical flow, and the level of voltage [ 1 ]. The severity of an electric shock depends on the current flow (I) measured in ampere (A). It is linked to the resistance of the conductor (R, unit: ohm ‘W’) and the potential difference between the two ends of a conductor (Volt; unit V), and is derived by applying the formula based on Ohm’s law: i.e., I = V/R. The severity of an electrical burn, by contrast, depends on the energy (Watt) and is derived from Joule’s formula W=I2 x R x T (duration of exposure with the source of current).

Household electrical supply is a low-voltage (220 V) AC at 60 Hz frequency. The physiological effects of contact with a low-frequency AC (60 Hz) current vary at different amperes. For example, 1mA (1/1000 A) is barely perceptible as numbness, whereas 20 mA can cause respiratory muscle paralysis, while 100 mA reaches a threshold for ventricular fibrillation [ 1 , 2 ]. The resulting cardiac arrhythmia may take the form of ventricular fibrillation, ventricular tachycardia, ventricular premature beats, atrial premature beats, atrial arrhythmia, and/or heart block [ 2 ].

Case presentation

A 40-year-old male patient was brought into the emergency ward after suffering an accidental electrical injury that involved an entry wound in the middle of his left hand and an exit wound in the back of his chest. He was holding the hanging rod for a ceiling fan when the connection was plugged in, resulting in electric shock. He lost consciousness and fell to the ground with the rod clenched in his hand for a minute and a half. The electricity source was disconnected and cardiopulmonary resuscitation was administered to the patient by his neighbors. The patient regained consciousness and complained of aching all over the body along with general weakness. 

He had a black hole in the middle of his left palm (Figure ​ (Figure1A) 1A ) and a linear burn on the back of his chest (Figure ​ (Figure1B 1B ).

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His pulse was irregularly irregular at 78/minute, and his blood pressure was 110/78 mm Hg. His total leucocyte count was 8600/cmm with neutrophils at 64%, and his hemoglobin was 13 gm/dL. Urinalysis did not show myoglobin. Serum sodium and potassium were 134 mEq/L and 4.2 mEq/L, respectively. Electrocardiography (ECG) showed occasional ventricular premature beat with wandering atrial pacemaker (Figures ​ (Figures2A 2A - ​ -2B). 2B ). Of note, the patient did not have any kind of cardiac ailment previously. The patient was hydrated with intravenous fluids and his wounds were treated with antiseptic dressings and antibiotics. He remained under observation for 48 hours and the ECG showed sinus rhythm (Figure ​ (Figure2C 2C ).

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Low voltage currents cause severe electrical burns to the skin as a result of high energy output from the current flow. Dry skin with callouses over palm (resistance of 500 W) and a long contact of palm with the source of electricity attribute to severe burn in this patient (Joule formula). Thereby, the electrical energy output is dissipated and there is less internal injury [ 3 , 4 ].

Low voltage currents travel through the body along low-resistance pathway nerves and blood vessels to cause severe cardiac injury. Also, the distance between the entry and exit wounds can determine the severity of the cardiac injury. The heart remains in the central location of the electrical current’s pathway between the left palm and back of the chest. Current spikes occur in the palm and fingers of an individual holding a metal rod that is suddenly connected to an electric source [ 5 ]. The electric shock causes depolarisation of cardiac muscles and increases membrane pores of the cells resulting in arrhythmias; sinus tachycardia, ventricular premature beats, ventricular tachycardia, and atrial fibrillation are common [ 6 , 7 ]. Wandering atrial pacemaker (WAP) is a benign atrial arrhythmia that has been observed in this case study. WAP and multifocal atrial tachycardia (MAT) differ only with the heart rate - WAP has a heart rate less than 100 bpm whereas MAT has a heart rate greater than 100 bpm. In the WAP rhythm, the pacemaker wanders with the impulses originating from the sinoatrial node to the atrium, and to the atrioventricular junction with a changing focus. Hence, the P waves on an ECG are presented in different configurations. WAP is differentiated from sinus arrhythmia by the fact that heart rate variability occurs from beat-to-beat, and is not phasic. Also, in sinus arrhythmia, the P-wave morphology and the P-R interval are constant [ 7 ]. Most of the arrhythmias occur soon after electric shock and are short-lived. However, delayed arrhythmias occurring 12 hours after electric shock have been reported, too [ 8 ].

Conclusions

Household electric supply is low voltage AC of 60 Hz. It is the electric current that determines the pathophysiological effects in the body but the voltage does determine the outcome of electric shock. Even a low-voltage shock can cause ventricular fibrillation if resistance is low and current flow reaches a threshold of 100 mA. The severity of burn lesion is determined by the resistance of skin and duration of exposure with the source of current. Most cardiac arrhythmias are short-lived and do not require treatment.

The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

The authors have declared that no competing interests exist.

Human Ethics

Consent was obtained or waived by all participants in this study. NA issued approval NA. This is a case report.

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COMMENTS

  1. Syncope in Patients with Cardiac Pacemakers

    The study included 95 patients with pacemakers: 47 experienced syncope in the last 12 months and 48 did not. Of the 100 documented episodes of syncope, 48.9% were vasovagal syncopes, 17% had cardiac-related causes, 10.6% had unknown causes, and 8.5% had pacemaker failure.

  2. Wandering Atrial Pacemaker (WAP) ECG Review

    Wandering Atrial Pacemaker (WAP) ECG Review | Learn the Heart - Healio

  3. PDF Sinus Node Dysfunction

    pacemaker placement with atrial-based pacing and limited ventricular pacing when necessary. ... Wandering pacemaker: at least three distinct P waves ... with syncope occurring in 50% of patients with

  4. Wandering atrial pacemaker

    Wandering atrial pacemaker (WAP) is an atrial rhythm where the pacemaking activity of the heart originates from different locations within the atria. This is different from normal pacemaking activity, where the sinoatrial node (SA node) is responsible for each heartbeat and keeps a steady rate and rhythm. Causes of wandering atrial pacemaker are unclear, but there may be factors leading to its ...

  5. Management of Common Arrhythmias: Part I. Supraventricular ...

    Sometimes, however, the long pauses can cause dizziness or syncope. Treatment is usually unnecessary. ... With wandering atrial pacemaker, the ECG shows variable P-wave morphology and PR intervals ...

  6. Wandering Atrial Pacemaker

    This rhythm and multifocal atrial tachycardia are similar except for heart rate. The other possible explanation is that there is significant respiratory sinus arrhythmia, with uncovering of latent foci of pacemaker activity. Usually, it is associated with underlying lung disease. In the elderly, it may be a manifestation of sick sinus syndrome.

  7. Ectopic Supraventricular Arrhythmias

    Wandering atrial pacemaker (multifocal atrial rhythm) is an irregularly irregular rhythm caused by the random discharge of multiple ectopic atrial foci. By definition, heart rate is ≤ 100 beats/minute. Except for the rate, features are the same as those of multifocal atrial tachycardia. Treatment is directed at causes. Ectopic ...

  8. Wandering Atrial Pacemaker: What Is It?

    A wandering atrial pacemaker is a rare form of a condition called arrhythmia. That's a problem with your heartbeat. It can happen anytime, even when you're sleeping. It's usually nothing to ...

  9. Syncope triggered by atrial flutter in a patient with a pacemaker

    Introduction. In patients with a previously implanted permanent pacemaker who are admitted to the hospital with syncope, the working diagnosis is often a device malfunction until the pacemaker interrogation reveals it is functioning normally. 1 However, in the majority of cases, pacemaker malfunction is not the cause of syncope. 1, 2 Reflex syncope seems to be the most frequent diagnosis. 2 In ...

  10. Syncope in Patients with Pacemakers

    Abstract. Syncope in a pacemaker patient is a serious symptom but it is rarely due a pacemaker system malfunction. Syncope occurs in about 5 % of patients paced for atrioventricular (AV) block in 5 years, 18% in those paced for sinus node disease in 10 years, 20 % of those paced for carotid sinus syndrome in 5 years and 5-55 % of those older ...

  11. AHA Releases Recommendations on Cardiovascular Monitoring and ...

    Ectopic atrial rhythms; right atrial, left atrial, wandering atrial pacemaker at normal rates Low right atrial rhythms are common, usually are normal variants, and will rarely need further ...

  12. Prevention of Syncope Through Permanent Cardiac Pacing in Patients With

    Prevention of syncope through permanent cardiac pacing in patients with bifascicular block (PRESS) is a multicenter, prospective, randomized, single-blinded study designed to demonstrate a reduction in symptomatic events in patients with bifascicular block and syncope of undetermined origin implanted with permanent pacemaker.

  13. WAP vs. MAT on ECG: What's the difference?

    This results in at least three different P wave morphologies, and often the PR interval may vary due to this. If the heart rate is less than 100 BPM we call this a wandering atrial pacemaker, or WAP. If it's greater than 100 BPM we call it a multifocal atrial tachycardia, or MAT for short.

  14. Wandering atrial pacemaker

    Three or more ectopic foci within the atrial myocardium serve as the pacemaker; Rate is less than 100bpm (in contrast to MAT) Is irregularly irregular therefore sometimes confused with atrial fibrillation and sinus arrhythmia; Causes. Intrinsic cardiac or pulmonary disease; Metabolic derangements; Drug toxicity (including Digoxin) Clinical Features

  15. Heart Atrium Pacemaker

    Wandering atrial pacemaker (WAP) ( Fig. 3.12) is an atrial rhythm with multiple P-wave morphologies (three or more), often occurring in a repetitive pattern at a rate of less than 100 bpm. The pattern may be dependent on autonomic tone and the respiratory phase (with competing activation from the sinus node, AV node, and other areas in the atria).

  16. Ectopic Supraventricular Arrhythmias

    Wandering atrial pacemaker (multifocal atrial rhythm) is an irregularly irregular rhythm caused by the random discharge of multiple ectopic atrial foci. By definition, heart rate is ≤ 100 beats/minute. Except for the rate, features are the same as those of multifocal atrial tachycardia. Treatment is directed at causes.

  17. Wandering Pacemaker

    The patient was discharged without recurrence of symptoms of congestive heart failure or syncope. One month later, the patient came to the pacemaker clinic where an examination in the supine position revealed normal pacemaker function. ... Wandering pacemaker. in: Mandel WJ Cardiac arrhythmias. Their mechanisms, diagnosis and management. JB ...

  18. Sinus Node Dysfunction

    Sinus node dysfunction may occur at any age 7, 14; however, increasing age is the most significant risk factor with the highest disease prevalence in patients 70 to 89 years of age. 2, 7, 8, 14 ...

  19. Electrical Injury and Wandering Atrial Pacemaker

    Wandering atrial pacemaker (WAP) is a benign atrial arrhythmia observed in elderly patients suffering from obstructive pulmonary diseases that result from an ischemic heart. This report discusses WAP as observed in a patient who suffered an electrical injury. Keywords: wandering atrial pacemaker, voltage, electrical injury, arrhythmia, ampere.

  20. Association of Antiarrhythmic Drug Therapy With Syncope and Pacemaker

    Atrial fibrillation (AF) confers a major health care burden and has an overall prevalence of 1% to 2% in the general population, with even higher rates in older people. 1, 2 Major adverse cardiovascular events such as cardiovascular death, stroke, and heart failure are associated with AF. 3, 4, 5 Whether these complications of AF can be reduced by rhythm control therapy is a subject of debate.

  21. UC San Diego Health First in Region to Implant Dual Chamber, Leadless

    Approved by the U.S. Food and Drug Administration (FDA) in July 2023, a new leadless pacemaker system placed in both chambers of the heart and using a novel communication technology is now offering a more minimally invasive option for patients. UC San Diego Health implanted the pacemaker system in the first patient in February 2024.