Bradycardia

Description

Bradycardia is defined as a heart rate of <60 beats per minute (bpm). It can be secondary to:
- Organic disease
- Medications
- Vagal tone
- Healthy, well-conditioned heart
Perioperatively, treatment may consist of a temporary or permanent pacemaker for organic disease, or medications for other causes. Treatment is only indicated when the heart rate is affecting the cardiac output.

Epidemiology

Incidence

Third-degree atrioventricular (AV) block is highest in people >70 years of age (approximately 5–10% of patients with heart disease).

Prevalence

At 20 years of age, the PR interval may exceed 0.20 seconds in 0.5–2% of healthy people. At age 60 years, >5% of healthy individuals have PR intervals exceeding 0.20 seconds.
Approximately 5% of patients with heart disease have first-degree AV block, and about 2% have second-degree AV block.

Morbidity

Low heart rate observed in third-degree or Mobitz II AV block may lead to syncopal episodes with major injuries (e.g., head trauma, hip fracture), exacerbation of congestive heart failure, or exacerbation of ischemic heart disease symptoms due to low cardiac output.

Mortality

The mortality of patients with sick sinus syndrome is significant and not always due to cardiac causes.

Etiology/Risk Factors

Intrinsic causes:
- Sinus node disease
- AV node disease
- Idiopathic degeneration (aging)
- Infarction or ischemia (coronary artery disease and/or myocardial infarction [MI])
- Hypertension
- Hypoxemia
- Obstructive sleep apnea
- Myxedema
- Infiltrative diseases
- Surgical trauma
- Heart transplantation
Extrinsic causes:
- Autonomically mediated syndromes
- Vasovagal syncope
- Pressure on the carotid sinus or carotid sinus sensitivity
- Vomiting or coughing
- Bezold–Jarisch reflex
- Hypothermia
- Increased intracranial pressure (Cushing reflex)
- Electrolyte imbalance (hypokalemia, hyperkalemia)
Drugs:
- Sympatholytic drugs: Beta-blockers, clonidine, neostigmine
- Digoxin
- Non-dihydropyridine calcium channel blockers
- Antiarrhythmic agents (amiodarone, propafenone)
- Lithium
- Anesthetic drug overdose: succinylcholine, induction agents, neostigmine, opioids.

Physiology/Pathophysiology

Sinus bradycardia is defined as a sinus rhythm with a rate <60 bpm. It is caused by an increase in vagal tone or a reduction in sympathetic tone. It is seen in:
- The absence of heart disease and can occur in 25–35% of asymptomatic individuals <25 years of age as well as well-conditioned athletes and some elderly patients.
- Sleep: In young and healthy patients, rates of 30 bpm and pauses of up to 2 seconds are not uncommon.
Sick sinus syndrome is chronic sinoatrial (SA) nodal dysfunction that can result from a variety of causes. It is characterized by chronic, inappropriate, and often severe bradycardia, sinus pauses, arrest, and exit block with or without appropriate atrial and junctional escape rhythms. The failure of escape pacemakers may lead to symptomatic bradycardia. Additionally, atrial tachyarrhythmias have been seen in >50% of cases.
- Sinus node fibrosis: The replacement of sinus node tissue by fibrous tissue may be accompanied by degeneration and fibrosis of other parts of the conduction system including the AV node.
- SA nodal artery disease: The artery may be narrowed by atherosclerosis, inflammatory processes, or emboli.
- Tachycardia–bradycardia syndrome: Atrial fibrillation (AF) is the most common atrial tachyarrhythmia, and prolonged symptomatic pauses can occur after termination of AF that may result from tachycardia-mediated remodeling of the sinus node.
- Infiltrative diseases: The SA node may be affected by amyloidosis, scleroderma, hemochromatosis, and rarely tumor.
- Epicardial and pericardial disease: The SA node is located near the epicardium. As a result, diseases that involve the epicardium or pericardium (such as pericarditis and tumors) may affect the SA nodal function.
- Inflammatory diseases: Rheumatic fever, pericarditis, diphtheria, Chagas disease, Lyme disease, and other disorders may depress SA nodal function.
- Trauma: Cardiac trauma may affect either the SA node directly or its blood supply.
AV blocks describe a delay or interruption in the transmission of an impulse from the atria to the ventricles due to an anatomic or functional impairment in the conduction system. The conduction disturbance can be transient or permanent; conduction can be delayed, intermittent, or absent.
- First-degree AV block is slowed conduction without missed beats and results from a PR interval >200 ms (>210 ms at slow heart rates).
- Second-degree AV block is divided into 2 types:
  - Mobitz type I: The block is within the AV node and there is progressive PR interval prolongation, preceded by a nonconducted P wave. It is often transient and asymptomatic.
  - Mobitz type II: The block is usually below the AV node, within the His-Purkinje system. During normal conduction, the PR interval remains unchanged prior to the P wave. However, there is paroxysmal failed conduction to the ventricles. This block is often symptomatic, with the potential to progress to complete (third-degree) AV block.
- Third-degree or complete AV block may occur at the AV node, bundle of His, or bundle branches. When third-degree AV block is present, no impulses pass between the atria and ventricles.
- Idiopathic progressive cardiac conduction disease (i.e., fibrosis and sclerosis of the conduction system) accounts for approximately 50% of AV blocks.
- Ischemic heart disease accounts for about 40% of cases of AV block.
- Cardiomyopathy and myocarditis can result from hypertrophic obstructive cardiomyopathy and infiltrative processes such as amyloidosis and sarcoidosis. Causes of myopathy include: rheumatic fever, Lyme disease, diphtheria, viruses, systemic lupus erythematosus, toxoplasmosis, bacterial endocarditis, and syphilis.
- Congenital heart disease
- Iatrogenic AV block
  - Drugs: Digitalis, calcium channel blockers (especially verapamil and to a lesser extent diltiazem), amiodarone, adenosine, and beta-blockers
  - Cardiac surgery
  - Transcatheter closure of VSD
  - Alcohol (ethanol) septal ablation

Palpate the patient's pulse, assess EKG and pulse oximetry (strength of pulse)
Assess EKG to determine if sinus bradycardia (P wave preceded QRS complex) is present.
Review recent events: Vagal stimulation, medications, ischemic insult, hypoxemia, hypothermia
Consider checking labs:
- Electrolyte levels, magnesium, calcium
- Glucose level

Differential Diagnosis

EKG interference

Bradycardia may be well tolerated if it develops slowly or is >50 bpm. Acute onset of bradycardia is more likely to be symptomatic.
Treatment should be instituted independently of the heart rate when bradycardia becomes symptomatic. In most cases the treatment threshold lies between 30 and 40 bpm.
Cease vagal stimulation
- Oculocardiac reflex
- Carotid sinus stimulation
- Laparoscopic insufflation of the abdomen
- Bladder catheterization
- Electroconvulsive therapy (ECT)
Medications should be implemented when bradycardia is persistent and affecting the cardiac output.
- Atropine is the drug of choice irrespective of the etiology
  - Recommended dosing: 0.5 mg IV q 3–5 minutes to a maximum of 3 mg.
  - Paradoxical slowing of the heart rate may be seen with doses <0.5 mg
  - Paradoxical AV block may occur in patients s/p heart transplantation
  - Should not delay implementation of external pacing for patients with poor perfusion
  - Use cautiously in the presence of acute coronary ischemia or MI (increased myocardial oxygen demand)
- Glycopyrrolate
- Ephedrine
- Dopamine, epinephrine, isoproterenol
- Catecholamine infusion is an alternative for bradycardia treatment when a bradyarrhythmia is unresponsive to or inappropriate for treatment with atropine, or while awaiting pacemaker placement.
Transcutaneous (TCP) or transvenous pacing: Immediate pacing might be considered in unstable patients with high-degree AV block when IV access is not available. Additionally, if the patient does not respond to drugs or TCP, transvenous pacing is indicated.

Bradyarrhythmias that occur in the perioperative period are usually secondary to some other cause, such as certain medications, an electrolyte disturbance, hypoxemia, vagal stimulation, or ischemia.
Indications for permanent pacing, regardless of associated symptoms:
- Sinus bradycardia in which symptoms are clearly related to the bradycardia (usually in patients with a heart rate <40 bpm or frequent sinus pauses)
- Symptomatic chronotropic incompetence
- Complete (third-degree) AV block
- Advanced second-degree AV block (block of 2 consecutive P waves)
- Symptomatic Mobitz I or Mobitz II second-degree AV block
- Mobitz II second-degree AV block with a widened QRS or chronic bifascicular block, regardless of symptoms
- Intraventricular conduction delays, bifascicular or left bundle-branch block with or without first-degree AV block in the presence of syncope or a more advanced AV block.

Neumar RW , Otto CW , Link MS , et al. Part 8: Adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(Suppl 3):S729–S767.

Epstein AE , DiMarco JP , Ellenbogen KA , et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A report of the American College of Cardiology/American Heart Association Task force on Practice. J Am Coll Cardiol. 2008;51(21):e1–e62.

ICD9

426.0 Atrioventricular block, complete
426.11 First degree atrioventricular block
427.89 Other specified cardiac dysrhythmias
426.12 Mobitz (type) II atrioventricular block

ICD10

I44.0 Atrioventricular block, first degree
I44.2 Atrioventricular block, complete
R00.1 Bradycardia, unspecified
I44.1 Atrioventricular block, second degree

See Also (Topic, Algorithm, Electronic Media Element)

Sick Sinus Syndrome

Active bradyarrhythmias for which the patient should undergo evaluation and treatment before noncardiac surgery include:
- High-grade AV block
- Symptomatic bradycardia
- Third-degree AV heart block
- Mobitz II AV block
High-grade cardiac conduction abnormalities, such as complete AV block, if unanticipated, can increase operative risk and may necessitate temporary or permanent transvenous pacing.
Intraventricular conduction delays, in the presence of a left or right bundle-branch block, but lacking a history of advanced heart block or symptoms, rarely progress to complete heart block in the perioperative period.
Atropine is a drug of choice irrespective of the type of etiology of the bradycardia; ephedrine and glycopyrrolate are also commonly used.
Unstable patients require temporary or permanent pacing.
Severe bradycardia can complicate regional anesthesia (in particular, subarachnoid or epidural anesthesia, not necessarily with high block). Ensure volume loading, vasopressors (early epinephrine), airway support, and left uterine displacement (parturients).

Piotr K. Janicki , MD, PhD

Marek Postula , MD, PhD

section name header

Basics ⬇

Incidence

Prevalence

Morbidity

Mortality

Diagnosis ⬆ ⬇

Treatment ⬆ ⬇

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆