Bradycardia and pacemakers

Abstract

Bradyarrhythmias are frequently encountered in primary care; they comprise various rhythm disturbances including sinoatrial node and atrioventricular conduction disorders. Clinical presentation varies from a wide range of symptomatic presentations including dizziness, syncope, dyspnoea, fatigue and heart failure symptoms to the asymptomatic, incidental finding. Diagnosing patients correctly including a symptom–rhythm correlation is important, especially as some carry a risk of sudden death. In this article we will discuss disease states, diagnosis, referral and an essential guide to cardiac pacemakers, the primary lifelong treatment option for selected patients without reversible causes.

Clinical case scenario

Cornelius is a 72-year-old overweight gentleman with hypertension and type 2 diabetes. He currently takes ramipril 10 mg once daily, atorvastatin 20 mg once daily and metformin 1 g twice daily and has never smoked. He presents with fatigue and shortness of breath on exertion over the last 2–3 weeks. He does not feel dizzy, complain of chest pain and has never passed out. Recent laboratory investigations show normal electrolytes, haemoglobin and thyroid studies. The rhythm strip from his electrocardiogram (ECG) is shown in Fig. 1.

Figure 1.

Case rhythm strip.

Background

Bradycardia is defined as a heart rate of less than 50–60 beats per minute (bpm) and can be a normal variant, especially in younger patients and athletes (Olshansky et al., 2020). Bradyarrhythmias can arise as a result of various disease states (Table 1) due to pathology in the sino-atrial (SA) node, atrio-ventricular (AV) node or the specialised bundle of His. The prevalence increases with age, due to fibrosis of the conduction tissues and can be as high as 1.26% in those aged above 66 years (Khurshid et al., 2018). Diagnosis is important, as some bradyarrhythmias carry a risk of sudden death. Pacemakers (PMs) offer an effective means of lifelong treatment by re-establishing a more appropriate heart rate or heart rate response, thus restoring a haemodynamically stable circulation. However, there is large variability in the prevalence of PM implantation for bradyarrhythmias, which likely represents varying practices, demographics and prevalence of disease states (Brignole et al., 2013). Indications for pacing have been published by the European Society for Cardiology (Brignole et al., 2013) and also the joint American College of Cardiology, American Heart Association Task Force on Clinical Practice Guidelines and Heart Rhythm Society (Kusumoto et al., 2019).

Table 1.

Causes of bradyarrhythmias.

Type	Cause
Intrinsic	• Age-related fibrosis of the conduction system • Myocardial ischaemia • Iatrogenic injury (cardiac surgery, valve replacement or ablation) • Cardiomyopathy • Congenital heart disease • Infection (Lyme’s disease, endocarditis, myocarditis) • Infiltrative heart disease (amyloidosis, sarcoid, haemochromatosis) • Autoimmune (lupus, systemic sclerosis)
Extrinsic	• Medication (beta-blockers, digoxin, non-dihydropyridine calcium channel blockers, other antiarrhythmic medications and some psychoactive drugs) • Autonomic (neurally-mediated, carotid sinus hypersensitivity, situational) • Hypothyroidism • Electrolyte disturbance • Obstructive sleep apnoea

Presentation

Initial assessment

Bradycardia may be an incidental finding or present with dizziness, syncope, fatigue, chest pain, exertional dyspnoea or symptoms of heart failure. In those presenting with symptoms, especially transient loss of consciousness (TLoC), it is essential to undertake a detailed history (including a collateral and family history) and comprehensive examination. This should include a postural blood pressure and a neurological examination to ensure other differential diagnoses for TLoC can be excluded. The guidance from the National Institute for Health and Care Excellence (NICE) on TLoC provides an excellent framework for initial assessment and workup of patients (NICE, 2010). For patients that have chest pain or show haemodynamic compromise, urgent admission may be required. Additional features that should raise concern and warrant urgent specialist assessment include ongoing syncope (especially without prodromal features or on exertion), dizziness and specific rhythm abnormalities outlined later.

Assessment should include a 12-lead ECG, which can also suggest the possibility of structural heart disease. Correlation between symptoms and rhythm is essential, and is particularly important when selecting candidates for a PM in secondary care. There are different forms of rhythm monitoring, which can be selected depending on symptom frequency as detailed in Table 2. Within primary care, clinicians are likely to request 24–48 hours ambulatory ECG monitoring using event monitors with short duration (usually 5 to 10 days) or if accessible smart phone devices such as the AliveCor® KardiaMobile. Alternatively, it is appropriate to refer patients to a cardiology specialist for this procedure. Where nocturnal bradycardia or pauses are found, consideration should be given to the possibility of obstructive sleep apnoea where risk factors are present.

Table 2.

Types of rhythm monitoring.

Device	Description	Symptom frequency
Ambulatory ECG monitor	• Continuous monitoring for 1 to 5 days	Daily or every 2 to 3 days
External event monitors (CardioMemo)	• These can vary in type and are typically used for between 5 days and 4 weeks. Some can be lead-free and placed on the chest during symptoms • Others can be attached with two or three leads and the recorders memory runs on a loop so that the heart rhythm before and after activation can be stored. They can also be set to record automatically if they detect certain heart rhythms	Weekly to every month
Smartphone devices	• These provide a single lead (usually lead I) recording which the patient activates using purchasable devices such as the Apple Watch or the AliveCor® KardiaMobile.	Daily to every month
Implantable loop recorders (Reveal device)	• A subcutaneous implantable device that can be triggered or auto-record certain rhythm abnormalities for approximately 3 years	Less than every month

Potential reversible causes can also be identified through a review of the patient’s medication and organising laboratory investigations including thyroid function tests, electrolytes and where indicated Lyme’s serology. Echocardiography or cardiac magnetic resonance imaging (MRI) may also be required during specialist assessment, especially as quantifying left ventricular function can influence the choice of PM.

Driving considerations

Upon completion of a comprehensive history, a patient’s fitness to drive must be taken into account and documented. Patients should be informed at the end of the consultation, as alluding to this earlier may influence the history a patient gives. The Driver and Vehicle Licensing Agency (DLVA) can provide guidance to professionals on fitness to drive. Where syncope has occurred, patients will only need to be informed to stop driving pending formal cardiological opinion and investigation. Additionally, where a bradyarrhythmia has been noted on ECG (sinoatrial disease, significant atrioventricular conduction defect or atrial flutter/fibrillation), patients must not drive if incapacity has/or is likely to occur. For group 1 licence holders this is until the underlying cause for arrhythmia has been identified and controlled for 4 weeks. Where there is uncertainty despite DVLA guidance or to discuss specific cases, the DVLA offers an email (medadviser@dvla.gsi.gov.uk) and telephone (01792 782337) advice line for professionals.

Types of conduction abnormality

SA node disease/sick sinus syndrome

SA node disease (also known as sick sinus syndrome) is a broad range of conditions relating to the SA node that can result from a variety of causes, including age-related fibrosis, ischaemia, medication and infiltrative disease. PMs are an indicated in the context of symptom–bradycardia correlation. These may include:

Sinus bradycardia

Daytime sinus pauses (Fig. 2) longer than 3 seconds or nocturnal pauses of 5 seconds or more (although if patients are young and asymptomatic PMs are not usually inserted)

Chronotropic incompetence, which is defined as an impaired heart rate response to exercise or demand (Brubaker and Kitzman, 2011)

Tachy-brady syndrome, which is an alternation between tachycardia (most frequently as a result of atrial fibrillation) and bradycardia (Fig. 2)

Atrial fibrillation with slow ventricular response

Carotid sinus hypersensitivity with syncope can also be included in this heading. This is defined as syncope with carotid sinus massage yielding either asystole of 3 seconds or greater or a fall in systolic blood pressure of 50 mmHg or greater (Brignole et al., 2013). It is a benign condition, but a PM may be indicated to prevent traumatic injury

Figure 2.

Rhythm tracings.

First-degree AV block

First-degree AV block is defined as a PR interval greater than 200 milliseconds (ms). It does not normally cause symptoms, and can be observed as a normal variant in healthy individuals and athletes, due to increased vagal tone. In the elderly, it is usually as a result of fibrosis. However, where prolongation is significant (usually greater than 300 ms) the loss of atrial and ventricular synchrony can mimic ‘pacemaker syndrome’ and can be a non-urgent indication for a dual-chamber PM (Kusumoto et al., 2019). PM syndrome is discussed in more detail later. Additionally, in the context of syncope or recurrent pre-syncope where there is significant PR prolongation, PMs can be considered for assumed higher grade AV block after specialist assessment.

Mobitz type I second-degree AV block (Wenckebach)

Mobitz type I second-degree AV block is often a benign rhythm with reversible AV block and is not usually an indication for a PM. On ECG there is progressive prolongation of the PR interval over successive beats followed by a non-conducted P wave, which manifests as a dropped QRS (Fig. 2). Typically, the P-P interval remains unchanged. It can be a benign finding in younger individuals, especially athletes, but may suggest conduction disease in older age groups. Pacing is controversial, but can be considered in symptomatic patients after workup by a cardiology specialist (Brignole et al., 2013; Coumbe et al., 2012).

Mobitz type II second-degree AV block

Mobitz type II second-degree AV block is an indication for a PM, due to the significant risk of progression to complete heart block or asystole, which can cause syncope or sudden death, thus constituting an urgent referral. It can be caused by a variety of conditions including ischaemia, infarction, fibrosis and infiltrative diseases. The PR interval is stable, but P wave conduction is variable, usually resulting in a dropped QRS in a 2:1 or 3:1 pattern (Fig. 2).

Consideration in 2:1 block

Where every other QRS complex is dropped there is only one PR interval, and one cannot differentiate between type I and II second-degree AV block on ECG alone and further testing may be required. Due to the reversibility of the conduction block in Mobitz type I, one may find reduced block (e.g. reducing from 2:1 to 3:1) following carotid massage where slowing of AV conduction occurs or complete elimination of the block with exercise, due to its reversibility with enhanced AV node conduction.

Complete or third-degree AV block

Complete AV block is an urgent indication for pacing and may present as a medical emergency. Here both P waves and QRS complexes occur at regular intervals (slower rate with the latter) but with complete disassociation (Fig. 2). The block can occur just above the AV node or below. If this occurs just above the AV node, typically a junctional rhythm will take over with narrow QRS complexes at a rate between 40 and 55 bpm. If the block is below the AV node, then a ventricular PM takes over with a slower rate of between 15 and 40 bpm and broad QRS complexes (Da Costa et al., 2002).

Bundle branch block

Bundle branch block (BBB) alone is not usually an indication for a PM unless patients are symptomatic or where there is a history of syncope indicating possible transient complete heart block, especially in the context of left ventricular failure. Referral to a cardiology specialist is indicated for further investigation. For selected patients a PM may be suitable.

The exception to this is alternating BBB which implies significant conduction disease in all conduction fascicles and impending complete heart block (Brignole et al., 2013). This is where there is:

Documented ECGs showing LBBB (L = left) and RBBB (R = right) separately, or

Alternating bi-fascicular block (RBBB with left anterior fascicular block and RBBB with left posterior fascicular block on separate ECGs).

Pacemakers

In primary care we commonly encounter implantable trans-venous PM systems, which constitute the bulk of contemporary PMs. The main component of these is the pulse generator (also known as the ‘box’). This is the battery component and brain of the pacemaker, which is typically subcutaneously implanted in a pre-pectoral position (the ‘pocket’). These can monitor and deliver electrical impulses to the myocardium through trans-venous electrodes (commonly referred to as ‘leads’) implanted percutaneously through the subclavian, axillary or cephalic vein. Most commonly, the leads are placed in the right atrium and right ventricle.

Pacemaker classification

Classification of PMss and their codes was standardised by both the North American Society of Pacing and Electrophysiology (NASPE) and the British Pacing and Electrophysiology Group (BPEG). The NASPE/BPEG Generic (NBG) Pacemaker Code was revised in 2002 and is expressed as five letters. The four most common codes are shown in Table 3.

Table 3.

NBG PM codes.

Position 1	Position 2	Position 3	Position 4
Chamber Paced	Chamber sensed	Response to sensing*	Rate modulation**
O = None	O = None	O = None	O = None
A = Atrium	A = Atrium	T = Triggered	R = Rate Modulation
V = Ventricle	V = Ventricle	I = Inhibited	R = Rate Modulation
D = Dual (A + V)	D = Dual (A + V)	D = Dual (T + I)

This refers to the PM’s action upon detecting native activity within the chamber of the heart. This can either trigger a pacing event (e.g. if a ventricular event is not sensed) or inhibit pacing where appropriate activity is detected.

The ability for the PM to alter heart rate for exercise demand using sensors monitoring respiratory rate and vibration. This is indicated where there is SA node disease, carotid sinus hypersensitivity or chronotropic incompetence.

Atrial pacemaker

Atrial PMs are single-lead devices (classified as AAI) indicated for SA node disease. They are not commonly used other than in specific subgroups, as 1–2% of patients with SA node disease go on to develop AV block annually, thereby requiring intervention to change to either ventricular or dual-chamber pacing (Healey et al., 2006).

Ventricular pacemaker

Ventricular PMs are usually indicated in bradycardia where patients have atrial fibrillation. These are usually in the form of VVI or VVI(R). Only the right ventricle is sensed and paced using a single lead with inhibition of output when intrinsic ventricular activity is detected. Due to the loss of atrial and ventricular synchrony for those in sinus rhythm, this may lead to PM syndrome which is discussed later.

Dual-chamber pacemaker

Dual-chamber PMs are able to pace and sense both the right atrium and the right ventricle, thus coming close to the normal physiological activity of the heart. The commonest pacing mode in these PMs is DDD or DDD(R). These PMs are most appropriate for a combination of SA and AV node dysfunction, but also for patients with independent SA or AV node dysfunction. Other indications include significant first-degree AV block with pseudo-PM syndrome and carotid sinus syncope. Essentially, through programmed settings and dual-chamber sensing there are four possible rhythms one can see in these modes:

Sinus rhythm: The PM is inhibited when there in normal sinus rhythm with normal AV conduction at a faster rate than programmed

Atrial pace, ventricular sense: When sinus bradycardia is sensed in the atrial lead, atrial pacing occurs with intrinsic conduction to the ventricles via the His–Purkinje system. Ventricular activity is sensed by the PM and ventricular pacing inhibited

Atrial pace, ventricular pace: Both the atrium and ventricle are paced when sinus bradycardia is detected in the atrium coupled with either delayed or absent AV conduction

Atrial sense, ventricular pace: The ventricle will be paced synchronously with the atrium if there is sinus activity sensed in the atrium but delayed or absent AV conduction to the ventricle

Cardiac re-synchronisation therapy

As right ventricular pacing does not utilise the His– Purkinje system, left ventricular activation is consequently delayed similar to LBBB. Cardiac re-synchronisation therapy (CRT) overcomes this by having an additional lead on the epicardial surface of the left ventricle. CRTs are also known as bi-ventricular PMs. There is evidence to support CRT in patients with left ventricle systolic dysfunction. The indications are as per ventricular or dual-chamber PMs, but specifically where there is likely to be a high burden of ventricular pacing, which can further deteriorate left ventricular function (e.g. third-degree AV block or Mobitz type II) (Curtis et al., 2013).

CRT can also be indicated for selected heart failure patients independently of bradyarrhythmia where there is QRS prolongation greater than 150 ms. In certain heart failure patients where ventricular tachyarrhythmias are a concern, CRT devices can be coupled with an implantable cardioverter defibrillator.

Risks and complications of pacemaker implantation

The rate of complications with PMs is not insignificant and highlights the importance of patient selection and close follow-up (Table 4). Early complication rates can be as high as 5% and late complications 2.7% (Trohman et al., 2004). Most early complications are picked up within 24 hours of implantation, with the exception of infection, which is also the most worrisome and occurs as both an early and late complication. It may be present with only superficial tissue involvement or extend deeper and present as a collection, endocarditis or sepsis. Superficial infections may respond to topical antibiotics, but cardiology review is always indicated. Anything more than superficial infection is likely to warrant complete device and lead removal.

Table 4.

Pacemaker complications.

Early	Late
Pneumothorax	Pocket erosion
Haemothorax	Heart failure
Air embolism	Venous thromboembolism
Cardiac perforation and tamponade	Infection (pocket, lead, endocarditis
Coronary sinus dissection	Lead failure/fracture
Pocket hematoma	Twiddler syndrome
Pacemaker malfunction	Cardiac perforation and tamponade
Lead dislodgment	Pacemaker syndrome
Infection (pocket, sepsis)	Pacemaker-mediated arrhythmias
Loose set screws	Pacemaker malfunction
Diaphragmatic stimulation	Pacemaker tachycardia
Death	Electromagnetic interference

Adapted from Shokry and Daoud (2018).

Late complications can be monitored during annual pacing checks, which are usually performed by physiologists. However, knowledge of pocket erosion, thromboembolism and that those with high ventricular pacing burden can go on to develop left ventricular dysfunction is important for primary care physicians.

Additionally, with single-lead ventricular pacemakers (VVI ± R), patients in sinus rhythm may develop PM syndrome where there is prolongation between atrial and ventricular systole similar to first-degree AV block. This results in atrial contraction poorly contributing to ventricular filling and cardiac output, thus mimicking symptoms of heart failure. If atrial systole is premature enough, it may occur against a closed valve or lead to mitral regurgitation, which increases pulmonary pressure and thus dyspnoea (Link, 2020). There also may be retrograde blood flow in the jugular veins with patients describing a feeling of fullness in the neck with heart beats.

Recent advances

The field of pacing is constantly evolving with the major advance being leadless PMs. These are a self-contained system with both pulse generator and electrode in one small unit placed into the right ventricle with the potential of a second companion device in the atrium wirelessly communicating to attain dual- chamber function where needed. These are thought to offer significant benefit to patients and have potentially lower complication rates (Roberts, 2018). Other advances include direct His bundle pacing (to try and achieve near-physiological pacing), battery-less PMs (relying on harvesting kinetic energy from the patient) and MRI-safe PMs.

KEY POINTS

Bradyarrhythimas can be incidental or present with dizziness, syncope, fatigue, chest pain, exertional dyspnoea or symptoms of heart failure

Evaluation must include a comprehensive history (including collateral and family history), both neurological and cardiovascular examination, and a 12-lead ECG

Symptom correlation with rhythm is essential using ambulatory/event monitoring in primary care or following referral to a cardiologist

PM implantation is indicated when symptoms can be attributed to certain bradyarrhythimas (SA node disease, heart bock or bundle branch block), Mobitz type II second-degree heart block or third-degree heart block

PM implantation can carry risks and complications; GPs need to be aware of complications including infection, thromboembolism, pocket erosion and the potential for secondary heart failure

Footnotes

ORCID iDs

Dr Mohammed Sohail Ahmed

Dr Tahir Shaheen

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