6th March 2024

Bradycardias

Background 

Bradycardia is defined as a ventricular rate below 60 bpm and may be physiological in athletes or during sleep. Pathological bradycardia may be a consequence of SA node and or AV node dysfunction. In these cases, patients may present with fatigue, dizziness, syncope, vertigo, and hypotension. Causes for bradycardia include:

• Acute myocardial infarction and ischaemia
• Disease of SA node (Sick sinus syndrome)  
• AV node dysfunction
• Anorexia nervosa
• Hypothyroidism 
• Hypothermia 
• Electrolyte imbalances – hypo or hyperkalaemia.
• Raised intracranial pressure
• Increased vagal tone 
• Medications: beta blockers, digoxin, calcium channel blockers, ivabradine, lithium, clonidine.

Diagnosis

History and clinical examination are important in the initial assessment of any patient who presents with an arrhythmia. Their past medical history (e.g., Sarcoidosis causing complete heart block, a background of bipolar affective disorder requiring lithium therapy) is particularly relevant and may help reveal the underlying aetiology for the bradycardia. Observations, including temperature readings, may reveal hypothermia as the underlying culprit. Other baseline investigations include blood tests such as thyroid function, troponin in the event of accompanying chest pain or a suspicion of ischaemia, and venous blood gas to rule out acidosis.

The specific rhythm can be identified on a 12-lead ECG or through more prolonged monitoring if bradycardia is intermittent. An echocardiogram is recommended to rule out any structural causes for the underlying arrhythmia. Further imaging may be warranted, such as cardiac CT or MRI. Electrophysiology studies have a limited role in bradycardias and are usually reserved for measuring conduction delay in the His-Purkinje system in patients with suspected AV conduction abnormalities.

Management 

Reversible causes should be treated initially and further treatment guided by the underlying mechanism for the bradycardia. The specific therapies are included in their respective sections below. In certain arrhythmias e.g., sick sinus disease or 1st degree AV node block, asymptomatic patients are likely to be monitored and interventions only to be considered if symptoms – such as pre-syncope, syncope or dyspnoea from chronotropic incompetence – develop. 

In haemodynamic instability, the heart rate should be increased to promote cardiac output through pharmacological or electrical means. Atropine and or isoprenaline are typically used. Atropine, an antimuscarinic drug that reduces parasympathetic activity, while Isoprenaline is a non-selective beta adrenoreceptor agonist that targets beta receptors of the sympathetic nervous system; both influence the SA and AV to increase automaticity and conduction respectively. If this fails, temporary pacing may be achieved either transcutaneously with sedation and analgesia or transvenously if facilities are available.

Sick sinus syndrome/SA node disease

This is caused by dysfunction of the heart’s natural pacemaker and can manifest on an ECG as sinus bradycardia, SA exit block, or sinus pauses. Causes can be intrinsic or extrinsic. The most common intrinsic cause is idiopathic degenerative fibrosis of the SA node cells. Other causes include ischaemia due to right coronary artery occlusion. 

Extrinsic factors include negatively chronotropic medications such as digoxin or beta-blockers, hypothyroidism and electrolyte abnormalities. Treatment for symptomatic disease is with the implantation of a permanent pacemaker. A common manifestation of sinus node disease is termed tachy-brady syndrome. This is where an SVT such as atrial fibrillation, flutter or atrial tachycardia coincides with the presence of sick sinus disease, resulting in periods of tachycardia alongside periods of bradycardia, pauses, or escape rhythms. This is managed with pacemaker insertion.

Atrioventricular block  

This occurs due to impaired conduction between the atria and ventricles. This may be at the level of the AV node (intranodal) or within His-Purkinje system (infranodal). Causes are predominantly due to idiopathic fibrosis with increasing frequency in old age. Other causes include ischaemia, infiltration (e.g., amyloidosis, haemochromatosis), infections such as endocarditis and diphtheria, negative chronotropic and antiarrhythmic drugs. There are three types of intranodal AV blocks:

• 1st degree: prolongation of the PR interval (>200ms or 5 small squares on a standard ECG at 25mm/s)
• 2nd degree: dropped QRS complexes following non-conducted P waves. This is divided into:
  • Mobitz 1 (Wenckebach): PR interval gradually prolongs until a QRS complex is dropped.
  • Mobitz 2: characterised by a fixed block without PR prolongation; often two or three P waves precede a successfully conducted QRS complex (termed 2:1 or 3:1 block respectively).
• 3rd degree or complete block is where there is complete dissociation between the P waves and QRS complexes. Here, the P-P and R-R intervals are preserved, but the two are not associated with each other. The resulting heartbeat originates from an ectopic focus and is known as a junctional escape beat. 

In addition to the ECG changes in complete heart block, clinical examination may reveal a variable S1 due to the uncoordinated nature of atrial and ventricular contraction, resulting in changes in preload and blood flow from atria to ventricles in each cardiac cycle. Assessment of the JVP will reveal cannon a-waves caused by the atria contracting against a closed tricuspid valve. 

Management 

Those with asymptomatic first-degree blocks do not require pacemaker implantation. In the event of no reversible causes, 3rd degree block requires pacemaker implantation. Mobitz 2 blocks are treated with insertion of a pacemaker due to a high risk of progressing to complete block. Complete heart block following inferior MI is likely a result of right coronary artery disease, which typically supplies the AV node. This is likely to improve with conservative measures and if the patient is haemodynamically stable, pacemaker implantation is not required in the immediate setting.

References 

• Ginks MR, Lane DA, McGavigan AD, et al. Cardiac Arrhythmias. Oxford Textbook of Medicine. Oxford University Press. 2020 January. 3 (6th ed.): 179-218. Available at https://oxfordmedicine.com/view/10.1093/med/9780198746690.001.0001/med-9780198746690-chapter-346/ 
• Glikson M, Nielsen JC, Kronborg MB, et al. ESC Scientific Document Group. 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy: Developed by the Task Force on cardiac pacing and cardiac resynchronization therapy of the European Society of Cardiology (ESC) With the special contribution of the European Heart Rhythm Association (EHRA). European Heart Journal. 2021 September. 42(35): 3427–3520. Available at https://academic.oup.com/eurheartj/article/42/35/3427/6358547/ 
• Burns E, Buttner R. Sinus Node Dysfunction (Sick Sinus Syndrome). Life in the Fast Lane. Last updated December 23rd 2021. Available at https://litfl.com/sinus-node-dysfunction-sick-sinus-syndrome/
• Olshansky B, Saha S, Gopinathannair R. Bradycardia. BMJ Best Practice. Last updated November 18th 2021. Available at https://bestpractice.bmj.com/topics/en-gb/832/