Bradycardia

Bradycardia is defined as a heart rate below 50–60 beats per minute. The condition may be physiological in young, well-trained individuals, or part of normal aging and certain disease states¹. Heart rate follows a circadian pattern, with the lowest rate typically occurring between 04:00 and 06:00 and the highest between 14:00 and 17:00. During sleep, heart rate decreases by an average of 24 beats per minute in young adults and 14 beats per minute in people over 80 years of age. Women generally have a higher resting heart rate than men, with a difference of approximately 10 beats per minute in younger age groups².

Bradycardia and cardiac rhythm assessment

The Cardiac Conduction System and Regulation

Normal heart rhythm is controlled by the sinoatrial node (SA node), which functions as the heart's primary pacemaker. The SA node consists of specialized cardiomyocytes embedded in connective tissue and is closely connected to the right atrium through conduction pathways. These structures enable electrical transmission and regulate automatic impulse formation².

Several physiological systems influence heart rate:

• Autonomic nervous system activity (balance between sympathetic and parasympathetic activity)

• Baroreceptors and the Bainbridge reflex

• Intrinsic heart rate

• Hormones and metabolites

The SA node is particularly richly innervated by the autonomic nervous system, emphasizing its central role in rhythm regulation².

Main Types of Bradycardia

1. Sinus Bradycardia: Caused by increased vagal tone and often physiological in athletes³.

2. AV Block (Atrioventricular Block)
   

   • First Degree: Delayed conduction between the atria and ventricles, often caused by vagal stimulation or medications.

   • Second Degree
     

     • Mobitz Type I: Progressive prolongation of the PR interval before a dropped QRS complex.

     • Mobitz Type II: Sudden, unpredictable dropped QRS complexes.

   • Third Degree (Complete Heart Block): Complete dissociation between atrial and ventricular activity.

3. Sinus Node Dysfunction
   

   • Sinus Pause: Delayed impulse formation.

   • Sinus Arrest: Complete failure of impulse formation.

   • SA Nodal Exit Block: Failure of impulse transmission to the atrium³.

Causes of Bradycardia

Intrinsic causes:

• Aging: Fibrosis of the SA node increases with age and contributes to impaired conduction².

• Ischemic Heart Disease: Infarction involving regions that supply the SA or AV node can cause bradyarrhythmias.

• Infiltrative diseases, surgical procedures or genetic changes may also damage the conduction system.

Bradycardia in athletes is often physiological. Regular exercise increases stroke volume and lowers resting heart rate as an adaptation to more efficient circulation⁴.

Extrinsic causes:

• Medications
  

  • Beta-blockers (e.g. metoprolol), calcium-channel blockers (verapamil, diltiazem), digoxin and antiarrhythmic drugs.

  • Timolol eye drops used for glaucoma can cause systemic beta-blockade after absorption through mucous membranes².

  • Other medications such as corticosteroids, anesthetic agents, donepezil and certain antihypertensive drugs (clonidine, prazosin) can also cause a low heart rate.

• Metabolic and Systemic Conditions
  

  • Hypothyroidism, hypoglycemia, hypothermia, hypoxia

  • Electrolyte disturbances (e.g. hyperkalemia)

  • Infections (e.g. encephalitis, dengue fever)

  • Trauma to the cardiac conduction system²,⁵

Clinical Presentation

Bradycardia may be completely asymptomatic and discovered incidentally during routine examination, but some patients develop typical symptoms reflecting reduced perfusion of vital organs. Common symptoms include dizziness, light-headedness or confusion, reduced exercise tolerance, muscle weakness, fatigue, palpitations or signs of heart failure². In severe cases, syncope, chest pain or dyspnea may occur because of reduced cardiac output and cerebral hypoperfusion.

Examination and Clinical Assessment

Pulse should be assessed during all consultations, and when bradycardia is suspected, a thorough history and physical examination are essential. Assessment should include:

• Symptoms: fatigue, syncope, dizziness, chest pain, dyspnea

• Triggering factors: physical activity, rest, sleep, medications (including eye drops)

• Medication review: particularly digitalis, beta-blockers, calcium-channel blockers and antiarrhythmic drugs

• Family and personal medical history: sudden death, cardiac arrhythmias or ischemic heart disease

• Signs of hypoperfusion: pallor, low blood pressure, cold extremities

• Signs of underlying causes: dry skin, thinning hair and enlarged thyroid gland (hypothyroidism)

Physiological testing includes observation of heart rate at rest and during light activity. When chronotropic incompetence is suspected, simple functional tests such as stair climbing or sit-to-stand testing can be used to observe the heart-rate response.

Diagnostic Procedures

• ECG: A standard 12-lead electrocardiogram is the first-line test for identifying the type of bradyarrhythmia and assessing structural or electrical changes in the heart, such as signs of previous infarction.

• Holter Monitoring: In intermittent bradycardia, continuous recording for 24–48 hours can provide valuable information.

• Event Recorder: When symptoms are infrequent, monitoring for 1–4 weeks may be used, with automatic or manual recording during events².

• Blood Tests: Electrolytes, glucose, thyroid function, toxicology screening and digoxin levels when relevant.

• Exercise Stress Test: Treadmill testing may reveal an inadequate increase in heart rate during exertion (chronotropic incompetence)⁷.

• Invasive Electrophysiological Study: May be considered to evaluate sinus-node dysfunction or AV block in complex cases.

Medical Treatment

• Atropine is the first-line medication for acute symptomatic bradycardia. It blocks vagal influence and increases heart rate by stimulating the SA and AV nodes². It should be regarded as a temporary measure and should not delay pacemaker implantation when pacing is indicated.

• If atropine is ineffective, intravenous sympathomimetic drugs such as dopamine, adrenaline or isoprenaline may be used. These can increase heart rate and cardiac output in severe hemodynamic compromise.

Pacemaker Treatment

• Temporary Pacing: Used in acute, unstable bradyarrhythmia or asystole that does not respond to medication. Transcutaneous pacing is often used first, but it may be painful and can require sedation.

• Permanent Pacemaker: Indicated in persistent symptomatic bradyarrhythmia, sinus-node dysfunction or high-grade AV block. The pacemaker electrically stimulates the myocardium and must be individually programmed according to the patient's needs⁵.

Relevance to Physiotherapy

Bradycardia and cardiac rhythm assessment

Bradycardia may be encountered during physiotherapy, particularly in cardiopulmonary settings. A multisystem assessment is therefore essential before treatment begins:

• Heart rate and blood pressure should be measured before, during and after treatment

• When monitoring is available, the physiotherapist should be able to recognize arrhythmias and warning symptoms

• When bradycardia is present, exercise intensity and duration must be adjusted appropriately

• In patients with an implanted pacemaker, the physiotherapist should know the pacemaker type and any restrictions relevant to exercise and equipment use

Interventions that increase vagal stimulation—such as Valsalva-like maneuvers, head-below-heart positions and certain mobilization techniques—should be used with caution. Exercise can be individualized with a focus on improving general physical capacity, pulmonary function and muscular endurance without excessive parasympathetic stimulation.

Sources:

1. Sidhu S, Marine JE. Evaluating and managing bradycardia. Trends in cardiovascular medicine. 2020 Jul 1;30(5):265-72.

2. Wung SF. Bradyarrhythmias: clinical presentation, diagnosis, and management. Critical Care Nursing Clinics. 2016 Sep 1;28(3):297-308.

3. Desai DS, Hajouli S. Arrhythmias. StatPearls [Internet]. 2020 Jun 25.

4. What is it? Bradycardia. Harvard Health Publishing.

5. Textbook of Cardiology.org.BradycardiaSébastien Krul, MD

6. John Hopkins Medicine, Health, Event Monitor. fromhttps://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/event-monitor

7. Brubaker PH, Kitzman DW. Chronotropic incompetence: causes, consequences, and management. Circulation. 2011 Mar 8;123(9):1010-20.

8. Pathmanathan N, Beaumont N, Gratrix A. Respiratory physiotherapy in the critical care unit. Continuing Education in Anaesthesia, Critical Care & Pain. 2015 Feb 1;15(1):20-5.