History and exam
Key diagnostic factors
common
pulse rate <50 bpm
Palpation of peripheral pulse or cardiac auscultation may reveal a slow, regular heart beat of <50 bpm or an irregular pulse of varying intensity. Slow pulse may be due to other causes such as frequent ventricular ectopy.
While some consider bradycardia to be a heart rate <60 bpm, this is in dispute and most consider rates of <50 bpm to represent bradycardia.
age >70 years
Older patients present frequently with bradycardia owing to disease in the sinus node, the atrioventricular (AV) node, or the His-Purkinje system. In the AV conduction system, age-related fibrosis and sclerosis (Lenegre-Lev disease) account for AV block in almost half of the cases.
Older patients are also more likely to present with bradycardia induced by medications with AV-node blocking properties.
use of known causative medications
These are primarily medications that have atrioventricular-node-blocking properties, such as beta-blockers, calcium-channel blockers, and digoxin.
presence of known underlying cause
A history of infection, infiltrative diseases, increased intracranial pressure, electrolyte disorders, exposure to toxins, surgery, heart transplant, sleep-disordered breathing, or myocardial infarction may be present.
Sinus bradycardia is usually noted in patients with significant hypothyroidism, whether or not they have other symptoms of the disease.
Asymptomatic or symptomatic sinus bradycardia may occur in association with hypothermia.
dizziness/lightheadedness
Occurs owing to bradycardia-induced cerebral hypoperfusion, especially in the setting of left ventricular dysfunction.
syncope
Syncope is possible with long sinus nodal pauses or very slow heart rates due to AV block.
Occurs owing to bradycardia-induced cerebral hypoperfusion, especially in the setting of left ventricular dysfunction.
Common in patients with complete heart block and a very slow ventricular escape rhythm with left ventricular dysfunction and in patients with second-degree atrioventricular block.
fatigue
Many patients complain of worsening fatigue. This should also prompt evaluation for sleep-disordered breathing or hypothyroidism as a potential cause of bradycardia.
exercise intolerance
May be owing to sinus node, atrioventricular node, or His-Purkinje system disease.
shortness of breath
May be owing to sinus node, atrioventricular node, or His-Purkinje system disease.
cannon a-waves in jugular venous pulse
Patients with bradycardia secondary to complete heart block can have intermittent cannon a-waves in their jugular venous pulse noted, owing to atrial contraction against a closed tricuspid valve. Similarly, there may be a variable S1 during complete atrioventricular block.
During a junctional or ventricular rhythm with 1:1 V-to-A conduction, there may be cannon a-waves for each heart beat.
jugular venous distension
Owing to heart failure caused by bradycardia, or severe pulmonary hypertension from longstanding untreated sleep-disordered breathing.
Other diagnostic factors
common
increased intracranial pressure
Sinus bradycardia can be noted as part of the Cushing triad (hypertension, bradycardia, and irregular respirations) related to elevated intracranial pressure.
uncommon
abnormal heart sounds
Because bradycardia can contribute to heart failure, patients may have a third heart sound and rales.
abdominal or lower extremity edema
Owing to heart failure caused by bradycardia.
hypotension
Manifestation of poor cardiac output owing to bradycardia.
mental status changes
Manifestation of poor cardiac output owing to bradycardia.
pallor
Manifestation of poor cardiac output owing to bradycardia.
extremities cool to touch
Manifestation of poor cardiac output owing to bradycardia.
hypothermia
Asymptomatic or symptomatic sinus bradycardia may occur in association with hypothermia.
chest pain
Rare presentation of bradycardia.
rashes
Erythema migrans, or bull's eye rash, should prompt an investigation of Lyme disease as a potential cause of atrioventricular nodal dysfunction.
thyroid goiter
Sinus bradycardia is often noted in patients with hypothyroidism.
Risk factors
strong
use of known causative medications
Cardiac medications that can cause or accentuate bradycardia include: (1) antihypertensives: beta-blockers, topical ophthalmic beta-blockers, clonidine, methyldopa, non-dihydropyridine calcium-channel blockers (e.g., verapamil, diltiazem), reserpine; (2) anti-arrhythmics: class I anti-arrhythmic drugs (sodium-channel blockers such as quinidine, disopyramide, lidocaine, procainamide, flecainide, propafenone), class III anti-arrhythmic drugs (potassium-channel blockers such as amiodarone, sotalol, dronedarone), adenosine, and digoxin.[3][20] The effect is often dose- and drug-level dependent, which, in turn, will depend on factors affecting drug metabolism, such as patient age, renal function, and hepatic function. Ivabradine, a selective inhibitor of a sodium-potassium channel expressed in the sino-atrial node, slows the sinus rate and is used specifically for this purpose. It can cause sinus bradycardia.
Other non-cardiac medications that can cause bradycardia include: (1) psychoactive agents: cholinesterase inhibitors (e,g., donepezil), phenothiazine anti-emetic drugs (e.g., prochlorperazine, chlorpromazine), lithium, phenytoin, tricyclic antidepressants, selective serotonin reuptake inhibitors; (2) others: calcium chloride, calcium gluconate, opioids (e.g., fentanyl, alfentanil, sufentanil), cannabinoids, anticholinergic agents (e.g., benztropine), chemotherapy agents (e.g., paclitaxel), cimetidine, thalidomide, organophosphates (e.g., dimethyl sulfoxide), topical ophthalmic acetylcholine, sedatives (e.g., dexmedetomidine, propofol).
Drugs that contribute to atrioventricular (AV) block and/or sinus node dysfunction may only be uncovering an underlying "occult" problem.[31]
age >70 years
Older patients are at greater risk for developing sinus node dysfunction and atrioventricular nodal disease, which are the major causes of bradycardia in this patient cohort. Older patients also have an increased use of rate-limiting drugs; this increases the risk of drug-related bradycardia, particularly in those with atrial fibrillation.[21]
In general, bradycardia is related to degeneration of the conduction system and the sinus node and changes in autonomic tone, which tends to worsen with age.[9][32][33][34]
recent myocardial infarction
Acute myocardial infarction can cause bradycardia. An inferior infarction from right coronary artery occlusion could lead to conduction block in the atrioventricular (AV) node. The AV node is supplied by the AV nodal artery, which branches from the proximal portion of the posterior descending artery, which arises from the right coronary artery 80% of the time, the circumflex 10%, and both 10%. Sinus bradycardia and AV block owing to inferior infarction is often caused by the Bezold-Jarisch reflex (i.e., a transient increased vagal activation). Consequently, bradycardia following inferior infarction often resolves. However, permanent AV block is generally caused by an anterior myocardial infarction affecting the bundle of His or His-Purkinje system. The sinus node receives its blood supply from the sinus node artery, which originates from the proximal right coronary artery 65% of the time, circumflex artery 25%, and both 10%. Infarct or ischemia to any of these arteries may lead to sinus node dysfunction.
Common causes for sinus bradycardia and AV block in the setting of acute myocardial infarction can also be iatrogenic and include the use of beta-blockers, calcium-channel blockers, anti-arrhythmics, and morphine; high levels of pain; increased vagal tone; and atrial ischemia.[3][35][36][37]
surgery
Sinus bradycardia is common intraoperatively owing to maneuvers that increase vagal tone, such as intubation. If intra-operative hypothermia is planned, sinus bradycardia will almost certainly occur. It may also occur after hydrogen peroxide irrigation during neurosurgery.
Sinus bradycardia is also common postoperatively, mainly owing to pain, use of opioids, or the effects of the surgery itself.
Bradycardia can be due to injury to the sinus node during heart-transplant surgery. Sinus node disease can become apparent after a Mustard procedure for transposition of the great arteries and repair of an atrial septal defect.
Atrioventricular (AV) block can occur after mitral valve, tricuspid valve, and/or aortic valve surgery, and after ventricular septal defect repair.
percutaneous valve replacement procedures
Conduction abnormalities are a well-known complication of transcatheter aortic valve replacement (TAVR). It is hypothesized that injury to the conduction tissues occurs due to direct trauma from surgery, hemorrhage, compression, ischemia, or infarction. It is estimated that 8.8% of post-TAVR patients develop conduction delays or even complete heart block and require pacemaker placement after 30 days. About half of these patients remain pacemaker dependent; the other half are thought to have paroxysmal conduction delays. Pre-existing right bundle branch block, larger prosthesis to left ventricular outflow tract diameter ratio, and smaller left ventricular end-diastolic diameter have been found to be predictors of pacemaker placement. In post-operative patients who underwent mitral valve repair or replacement and develop new sinus node dysfunction or AV block associated with persistent symptoms or hemodynamic instability, permanent pacing is recommended prior to hospital discharge. Additionally, in post-operative patients who underwent TAVR and develop new AV block with persistent symptoms or hemodynamic instability, permanent pacing is also recommended prior to hospital discharge. [38][39]
hypothyroidism
Sinus bradycardia is usually noted in patients with significant hypothyroidism, whether or not they have other symptoms of the disease, including signs and symptoms of congestive heart failure.[3]
electrolyte disorders
Hyperkalemia, hypokalemia, hypercalcemia, and/or hypocalcemia can cause bradycardia.
Hyperkalemia tends to be the most common abnormality seen; it causes bradycardia by causing a sinoventricular rhythm or atrioventricular block.[3]
Electrolyte disorders should be screened for in all patients with bradycardia because this is easily correctable.
acidosis
Acidosis has been shown to have profound effects on the conduction pathways, particularly the atrioventricular node. Acidosis can lead to slowed nodal conduction, prolonged refractory period, and even complete heart block. Acidosis could be the result of myocardial infarction or other insult.[40]
infections
Typhoid fever, diphtheria, tuberculosis, toxoplasmosis, rheumatic fever, viral myocarditis, and Lyme disease have all been associated with bradycardia.
exposure to toxins
Lead exposure, black widow spider venom, and tricyclic antidepressant overdose have all been associated with bradycardia.
hypothermia
Hypothermia can lead to bradycardia. This can be seen with environmental exposures, during surgery, or as part of cooling protocols after cardiac arrest.
infiltrative diseases
Infiltrative disease, such as amyloidosis, Chagas disease, sarcoidosis, or hemochromatosis, may also affect the conduction system of the heart, causing bradycardia. Rheumatologic conditions such as collagen vascular disease or systemic lupus erythematosus can also cause bradycardia.
sleep-disordered breathing
Sinus node arrest, sinus bradycardia, and second-degree atrioventricular block are all manifestations of sleep-disordered breathing (SDB), comprising obstructive sleep apnea, central sleep apnea, and Cheyne-Stokes breathing. Nocturnal bradyarrhythmias should prompt an investigation for SBD.[25]
weak
epilepsy
Rarely, bradycardia may be associated with seemingly unrelated clinical conditions. Bradycardia can be rarely associated with epilepsy, and should be considered in patients with unusual presentations of syncope or in patients with a history suggestive of both epilepsy and syncope. Ictal bradycardia and ictal asystole predominantly occur in association with focal seizures, with loss of awareness in people with mainly left lateralized temporal lobe seizures, and are associated with electroencephalogram signs of brain ischemia during these episodes.[30]
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