Bradyarrhythmias are abnormal heart rhythms with a pulse rate of <60 beats per minute (bpm). This can be due to a variety of causes, including sinus node disease, atrioventricular disease, or toxins.
Although the definition of bradyarrhythmia (brady- = slow, arrhythmia = abnormal rhythm) is defined as a heart rate (HR) <60bpm, many patients remain asymptomatic until the HR falls well below this rate.
A bradyarrhythmia can either be physiological or pathological.
*Throughout this article, bradycardia (brady- = slow, cardia = heart) will be used synonymously and interchangeably with bradyarrhythmia.
In the normal heart, the resting heart rate (HR) ranges from 60-100 bpm, and this is determined by the pacemaker cells of the sinoatrial node (SAN), and the confluence of the sympathetic and the parasympathetic nervous systems – therefore, in normal physiology, an increase in vagal tone, or a decrease in sympathetic outflow, will cause a drive towards sinus bradycardia (a HR <60 bpm that is determined by the SAN).
Examples of physiological causes of an increase in vagal tone include:
• The diving reflex
• Athlete’s heart
• Vagal manoeuvres
• Valsalva manoeuvre
• Respiratory-induced sinus arrhythmia (expiration phase)
Aside from physiological causes of bradycardia, there are multiple pathological causes of bradycardia – these can be subdivided into cardiac, and non-cardiac causes.
Cardiac causes of bradyarrhythmias are usually inherent to abnormalities with impulse generation (i.e., sinus arrest) or signal conduction (i.e., complete heart block). The cardiac causes below will be explored in more detail in future articles, but the general risk factors for both SAN and AVN disease include cardiac ischaemia, myocarditis, and idiopathic fibrosis / sclerosis1.
|Sinoatrial node causes
|Atrioventricular node causes
|Sinus pause / arrest
|Second degree AV block – Mobitz I
|Sinoatrial exit block
|Second degree AV block – Mobitz II
|Sick sinus syndrome
|Third-degree AV block
|Idiopathic fibrosis / sclerosis
|AV block in the context of atrial arrhythmia (i.e., atrial flutter with variable AV block)
There is a range of non-cardiac causes of bradycardia, and, although not exhaustive, the mnemonic below can be used as a useful memory tool:
|Systemic lupus erythematosus2
|Bisoprolol, Esmolol, Atenolol, Metoprolol, Propanolol
|Non-dihydropyridines – verapamil, diltiazem
|Digoxin, alpha-2 agonists, amiodarone, GABA-receptor agonists / modulators
|Funny current inhibitors
|Hyperkalaemia, hypokalaemia, hypoxia, hypothermia
|Lyme disease, Salmonella typhi, Legionnaire’s disease
|Raised intracranial pressure (Cushing’s reflex)
When taking a history, it is important to be comprehensive and to proceed in a structured manner, asking through the presenting complaint to the systems review. Focused features to always include in any cardiac history include:
• Chest pain*
• Shortness of breath*
• Dizziness / syncope / light-headedness*
• Smoking and alcohol
*The above symptoms would be more concerning for cardiac disease if they occurred in conjunction with exercise.
Physiological bradycardia does not always cause symptoms, and patients are commonly asymptomatic. In pathological states, bradycardia alone is unlikely to be a patient’s presenting complaint, and is likely to be manifest as a sign of another underlying issue – however, if a patient is inappropriately bradycardic, there is the risk of under perfusing muscle groups and vital organs, and we could expect this to present as a variety of symptoms:
• Dizziness and light-headedness
• Difficulty thinking/memory deficit
• Chest pain/tightness
• Dyspnoea and shortness of breath
Examination – Signs
Examination of a patient with bradycardia should bear in the mind the concerns related to reduced cardiac output, and potential precipitating causes. Signs elicited may coincide with the symptoms a patient is experiencing. Common signs may include3:
• Raised jugular venous pressure
• Cannon-a waves in the jugular venous pulse (JVP)
• Peripheral cyanosis / Pallor
• Thyroid mass/goitre
• Features of increased intracranial pressure (associated with Cushing’s Triad)
Diagnostic investigations for bradycardia, alongside a focused history and examination, should include4:
|1st line investigations
|12 lead ECG
|Event recorder / loop recorder
|Full blood screen*
|24hr Holter monitor
|Tilt table testing
|Lyme titres and urinary antigen test
*In this context, a full blood screen would include an FBC, U+E, CRP, TFT, troponin, magnesium, glucose, and toxicology screens and drug levels (where suspected, i.e., digoxin)
The management of bradycardia should first be determined by the clinical status of the patient. In any patient with haemodynamically instability, they should be managed as part of the Resuscitation Council UK’s guidelines5, as seen further below under ‘Life-threatening bradyarrhythmias’.
If a patient is haemodynamically stable, it should be remembered that bradycardia is usually a symptom of an underlying condition, and treatment will usually be guided by the underlying aetiology, where a pathological or iatrogenic cause is suspected (i.e., negatively chronotropic drugs). For example, if a patient appears to be bradycardic secondary to hypothyroidism in the absence of other causes, replacing thyroid hormones would be expected to normalise the heart rate. Alternatively, if a patient becomes bradycardic intraoperatively, secondary to sedation and anaesthesia, they can be treated with glycopyrrolate.
It is important to involve senior support early in patient management, especially if a cardiac cause is suspected, as this would need to be escalated to cardiology.
The Resuscitation Council UK Guidelines 2021 highlight that the management of bradycardia should be determined by ‘evidence of life-threatening signs’ (shock, syncope, myocardial ischemia, or heart failure), and also the ‘risk of asystole’.
As with any patient examination, an A to E approach should be used when assessing the patient with bradycardia – this will help identify any concerning features, and thus determine the appropriate management. The Resuscitation Council UK’s algorithm for managing life-threatening bradycardia can be seen below:
- Life in the Fast Lane: Sinus Node Dysfunction (Sick Sinus Syndrome)
- BMJ Best Practice: Bradycardia
- Patient UK: Bradycardia
- Resuscitation Council UK: 2021 Resuscitation Guidelines
Author: Dr Steven Scholfield (FY2)
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