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BradycardiaHighlights

Summary

Overview

Basics

Definition

EpidemiologyAetiology

Pathophysiology

Classification

Prevention

Screening

Secondary

Diagnosis

History & examination

Tests

Differential

Step-by-step

GuidelinesCase history

Treatment

Details

Step-by-step

Guidelines

Follow Up

Recommendations

Complications

Prognosis

Resources

References

Images

Patient leaflets

Credits

Email

Print

Feedback

Share

Add to Portfolio

Bookmark

Add notes

History & exam

Key factors

presence of risk factors

pulse rate below 50 bpm

dizziness/lightheadedness

syncope

fatigue
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exercise intolerance

shortness of breath

cannon a-waves in jugular venous pulse

jugular venous distension

Other diagnostic factors

increased intracranial pressure

abnormal heart sounds

abdominal or lower extremity oedema

hypotension

mental status changes

pallor

extremities cool to touch

hypothermia

chest pain

History & exam details

Diagnostic tests

1st tests to order

12-lead ECG

Holter monitoring

event monitor

exercise testing

carotid sinus massage

echocardiogram

thyroid function tests

basic metabolic panel

cardiac markers

serum digoxin level

serum creatinine

Tests to consider

implantable-loop recorder

tilt-table testing

electrophysiology testing

Diagnostic tests details

Treatment details
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Acute

haemodynamically unstable

pharmacotherapy

temporary pacing

haemodynamically stable: sinus node dysfunction

reversible cause: asymptomatic or mild symptoms

o treatment of underlying cause

o theophylline

reversible cause: severe symptoms

o treatment of underlying cause + temporary pacing

irreversible cause: asymptomatic or mild symptoms

o reassurance

irreversible cause: severe symptoms

o permanent pacing

haemodynamically stable: acquired AV block

reversible cause: asymptomatic without indications for pacing

o treatment of underlying cause

reversible cause: symptomatic or indications for pacing

o treatment of underlying cause + temporary pacing

irreversible cause: asymptomatic without indications for pacing

o reassurance

irreversible cause: symptomatic or indications for pacing

o permanent pacing

hemodynamically stable: congenital AV block

asymptomatic without indications for pacing

o reassurance

symptomatic or indications for pacing

o permanent pacing

haemodynamically stable: vagally mediated bradycardia

carotid hypersensitivity syndrome

o permanent pacing

neurocardiogenic or vasovagal syncope

o lifestyle modifications

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o pharmacotherapy

o permanent pacing

Treatment details

Summary

Any heart rhythm slower than 50 bpm, even if transient, owing to sinus node dysfunction and/or

atrioventricular (AV) conduction abnormalities.

Causes include intrinsic sinus node and AV nodal disease, or extrinsic influences, which may be

reversible.

Common symptoms include syncope, fatigue, and dizziness; however, the patient may be

asymptomatic.

Evaluation involves determining the association of symptoms with heart rate and an assessment of

underlying cardiovascular conditions. ECG is the diagnostic test of choice.

Patients with a reversible cause may not require long-term therapy; however, patients with non-

reversible causes may require an implantable pacemaker with or without a defibrillator. Urgent treatment may

include temporary pacing and drug interventions.

Potentially life-threatening complications, including cardiovascular collapse and death, may occur.

DefinitionWhile some consider bradycardia to be a heart rate

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tissue inflammation or infiltration, infections (e.g., typhoid fever, diphtheria,tuberculosis, toxoplasmosis, rheumatic fever, or viral myocarditis), orabnormal autonomic effects. Extrinsic causes include exposure to toxins(e.g., lead, black widow spider venom, or tricyclic antidepressant overdose),drugs (e.g., digoxin, beta-blockers, calcium-channel blockers, or class I or III

antiarrhythmics), or electrolyte abnormalities.[3] [16]Some causes, such ashypothyroidism, electrolyte disorders, and those that are drug-induced, arereversible. Inferior wall myocardial infarction and increased intracranialpressure can also cause various types of bradycardia.

High vagal tone in an otherwise healthy young adult is a common cause ofsinus bradycardia and Mobitz I (rarely Mobitz II) atrioventricular (AV) block.This may even manifest during sleep and may be exacerbated by sleepapnoea.

Generalised conduction system disease related to calcification and fibrosis iscalled Lev's disease (or Lenegre-Lev syndrome) and is a cause of acquiredcomplete heart block. Lev's disease is seen most commonly in older peopleand is often described as senile degeneration of the conduction system.

PathophysiologyThe cellular mechanisms are complex and interrelated. Failure of any one of these mechanisms can have an

effect on heart rate. Normal cardiac electrical activation requires normal sinus node automaticity and effective

AV node and His-Purkinje conduction. Anything that causes sinus node automaticity or conduction through the

AV node and/or His-Purkinje system can cause bradycardia.

Classification

Clinical classification

Bradycardia can be classified as asymptomatic or symptomatic.Asymptomatic patients often do not require treatment.

Bradycardia classification

Bradycardia can be classified according to the site of the conductiondisturbance.[3]

Sinus node dysfunction

Sinus bradycardia: heart rate below 50 bpm. It can be a normal finding, especially during rest or sleep,

or can be abnormal and symptomatic.[4]

Sinus nodal pauses/arrest: episodic, abrupt termination of sinus rhythm generally lasting longer than 3

seconds. Episodes can last longer than 30 seconds. There can be haemodynamic collapse, loss of blood
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pressure, and/or loss of consciousness. The term sinus arrest is used generally for long sinus node pauses (i.e.,

>5 seconds).[5]

Sinus nodal exit block: sinus node continues to activate but electrical activation is delayed and either

blocked completely or incompletely between the sinus node and the atria. There can be various levels of block

(e.g., complete or intermittent block).[6]

Tachycardia-bradycardia syndrome: occurs when there are episodic periods of tachycardia (usually

atrial flutter, atrial fibrillation, or atrial tachycardia), followed by termination of the tachycardia leading to sinus

arrest or long sinus pauses, followed by sinus bradycardia.[7]

Chronotropic incompetence: a form of bradycardia in which the sinus rate does not accelerate

appropriately with exercise.[8]

Sick sinus syndrome: a condition in which sinus node dysfunction manifests as one of the above

abnormalities and there is evidence of slowing of sinus node function. Although this is generally not due to

autonomic abnormalities, they can contribute. Some patients have marked bradycardia owing to sinus node

dysfunction only after medicines that slow the sinus node are initiated. Sick sinus syndrome has been associated

with atrioventricular (AV) nodal conduction abnormalities and a high risk of systemic embolism.[9]AV conduction disturbance

AV block occurs when atrial depolarisation fails to reach the ventricles orwhen atrial depolarisation is conducted with a delay.

First-degree AV block: delay in AV conduction, such that the PR interval is over 0.2 seconds. During

first-degree AV block, there is one-to-one conduction but there is delay in AV nodal conduction.[10] It is not

necessarily associated with bradycardia but it may be associated with higher degrees of AV block and

subsequent bradycardia or sinus node dysfunction.

Second-degree AV block: periodic failure of conduction from the atria to the ventricles. This assumes

that the atrial rate is regular. A blocked premature atrial beat is not second-degree AV block. There are different

types:

o Mobitz I: grouped beating with a constant PP interval, lengthening in the PR interval and

changing (usually shortening) RR intervals with the cycle ending with a P-wave and not followed by a QRS

complex. As the PR interval gradually prolongs, the RR interval tends to stay the same or shorten.[11]Also

called Wenckebach AV block.

o Mobitz II: associated with single non-conducted P-waves with a constant PP interval and

constant PR intervals (no change in the PR above 0.025 seconds).[12]

o 2:1 block: only one PR interval to examine before the blocked P-wave and 2 P-waves for every

QRS complex. In most cases, it will change to Mobitz I or II. If there is an associated bundle branch block, this

suggests block in the His-Purkinje system.

o High-degree AV block: more than one sequentially blocked P-wave.[13]
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Third-degree AV block: occurs when there are no conducted impulses from the atria to the ventricles.

Also called complete AV block. This may occur with regular atrial activity without conduction or with an atrial

tachyarrhythmia.

Paroxysmal AV block: normal AV nodal conduction followed by sudden block of AV conduction

associated with a long pause and multiple blocked P-waves, with subsequent resumption of AV conduction. Thiscan be related to underlying AV nodal or His-Purkinje conduction anomalies or to abrupt parasympathetic

activation causing block in AV nodal conduction. In the latter instance, there is often slowing in sinus activation.

Vagotonic AV block: slowing of the sinus node with prolongation of the PR interval followed by AV block

owing to transient abrupt increase in parasympathetic tone.

Congenital complete heart block: usually associated with a narrow QRS complex escape rhythm arising

in the AV node.

Escape rhythms

When the sinus rate slows or there is AV block, other cardiac structures canactivate owing to their intrinsic automaticity. The AV nodal rate tends to be 40to 60 bpm and the ventricular rate tends to be 20 to 40 bpm.

Atrial rhythm: originates from atrial structures other than the sinus node during sinus bradycardia or

sinus arrest.

Junctional rhythm: escape rhythm when there is bradycardia or arrest of sinus node or atrial activation.

Activation of the junction may occur with or without AV block.[14]

Ventricular rhythm: an escape rhythm from the ventricles when there is AV block or sinus bradycardia.

AV dissociation

Atrial and ventricular activation occur from different pacemakers. Ventricular activation may be from

junctional or infranodal automaticity. AV dissociation can occur in the presence of intact AV conduction,

especially when rates of the pacemaker, either junctional or ventricular, exceed the atrial rate.

The atria and ventricles do not activate in a synchronous fashion but beat independent of each other.

Usually, the ventricular rate is the same or faster than the atrial rate. When the atrial rate is faster and the atria

and ventricles are beating independently, complete heart block is present.

AV dissociation can be complete or incomplete. When incomplete, some P-waves conduct and capture

the ventricles but, if they do not, it is complete. Complete AV dissociation mimics AV block and has to do with P-

wave timing in relation to independent ventricular activation.

There are 2 types
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o Isorhythmic: when the atrial rate is the same (or nearly the same) as the ventricular rate but the

P-wave is not conducted.

o Interference: when P-waves and QRS rates are similar but, occasionally, the atria conduct to the

ventricles.

ScreeningScreening for bradycardia is not carried out normally because treatment is usually administered for symptomatic

patients only.

Patients may present with conditions that potentially predispose to bradycardia during routine clinic visits and

these can be identified easily based on a review of the patient's medical history (e.g., hypothyroidism, medicines,

and history of myocardial infarction). Treatment is not offered unless the vital signs (hypotension and

bradycardia) suggest that the patient is, or may be at risk of, lightheadedness, syncope, or other complications.

Screening ECGs and Holter monitoring may be considered for special patient populations, such as those with

muscular dystrophies (e.g., myotonic dystrophy, Kearns-Sayre's syndrome, peronoeal muscular dystrophy, or

limb-girdle muscular dystrophy), which affect the conduction system of the heart specifically. Findings of bundle-

branch block and fascicular block with bradycardia in these patients, even though asymptomatic, should be

followed-up aggressively because these patients can have unpredictable progression to complete heart block

and sudden death.[35]

Secondary preventionRegular evaluation and examinations are necessary, and patient reporting of

suspicious symptoms is the best way to diagnose problems with bradycardia.Patients should guide practitioners regarding their symptoms and medicinesthat may be associated with bradycardia.

History & examinationKey diagnostic factorshide allpresence of risk factors (common)

Key risk factors include history of taking medicines known to cause bradycardia, age over 70 years,

previous myocardial infarction, surgery, hypothyroidism, sleep apnoea, exposure to toxins,

infections, infiltrative diseases, and electrolyte disorders.pulse rate below 50 bpm (common)

Palpation of peripheral pulse or cardiac auscultation may reveal a slow, regular heart beat of below

50 bpm or an irregular pulse of varying intensity.dizziness/lightheadedness (common)

Occurs owing to bradycardia-induced cerebral hypoperfusion, especially in the setting of left

ventricular dysfunction.syncope (common)
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Syncope is possible with long sinus nodal pauses or very slow heart rates.

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 (AV) block.fatigue (common)

Many patients complain of worsening fatigue.

exercise intolerance (common)

May be owing to sinus node, AV node, or His-Purkinje system disease.

shortness of breath (common)

May be owing to sinus node, AV node, or His-Purkinje system disease.

cannon a-waves in jugular venous pulse (common)

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 AV 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 (common)

Owing to heart failure caused by bradycardia.

Other diagnostic factorshide allincreased intracranial pressure (common)

Sinus bradycardia can be noted as part of Cushing's triad (hypertension, bradycardia, and irregular

respirations) related to raised intracranial pressure.

abnormal heart sounds (uncommon)

Because bradycardia can contribute to heart failure, patients may have a third heart sound and

rales.abdominal or lower extremity oedema (uncommon)

Owing to heart failure caused by bradycardia.

hypotension (uncommon)

Manifestation of poor cardiac output owing to bradycardia.

mental status changes (uncommon)


pallor(uncommon)


extremities cool to touch (uncommon)


hypothermia (uncommon)

Asymptomatic or symptomatic sinus bradycardia may occur in association with hypothermia.

chest pain (uncommon)

Rare presentation of bradycardia.

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Risk factorshide all

Strong

use of known causative medications

Class I antiarrythmics (sodium channel blockers such as quinidine, disopyramide, lidocaine,

phenytoin, fleicanide, propafenone), class III antiarrhythmics (potassium channel blockers such as

amiodarone, sotalol, dofetilide), digoxin, beta-blockers, and calcium-channel blockers can cause

bradycardia.[3] 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.

Other non-cardiac medicines that can cause bradycardia include: clonidine, calcium chloride,

calcium gluconate, lithium, reserpine, methyldopa, opioids, benzatropine, paclitaxel, topical

ophthalmic beta-blockers, phenytoin, cimetidine, thalidomide, dimethyl sulphoxide, topical

ophthalmic acetylcholine, fentanyl, alfentanil, sufentanil, and cholinesterase inhibitors.

Drugs that contribute to atrioventricular (AV) block and/or sinus node dysfunction may only be

uncovering an underlying 'occult' problem.[17]age over 70 years

Older patients are at greater risk for developing sinus node dysfunction and AV nodal disease,

which are the major causes of bradycardia in this patient cohort.

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][18] [19] [20]recent myocardial infarction

Acute myocardial infarction can cause bradycardia by causing conduction block in the AV node

(inferior infarction) or the His-Purkinje system (anterior infarction).[3] [21] [22] [23] 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. Generally, the bradycardia caused by AV block in the His-Purkinje system

owing to anterior wall myocardial infarction does not resolve.

Acute thrombosis of a coronary artery supplying the sinus or AV node can cause bradycardia,

although permanent AV block is generally caused by anterior infarction affecting the bundle of His.

Common causes for sinus bradycardia and AV block in the setting of acute myocardial infarction

include the use of beta-blockers, calcium-channel blockers, antiarrhythmics, and morphine; high

levels of pain; increased vagal tone (especially following inferior infarction); and atrial ischaemia.surgery

Sinus bradycardia is common intra-operatively owing to manoeuvres 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.
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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.

AV block can occur after mitral valve and/or aortic valve surgery and after ventricular septal defect

repair.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

Hyperkalaemia, hypokalaemia, hypercalcaemia, and hypocalcaemia can cause bradycardia.

Hyperkalaemia tends to be the most common abnormality seen; it causes bradycardia by causing a

sinoventricular rhythm or AV block.[3]

Should be screened for in all patients with bradycardia because they are easily correctable.

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.infiltrative diseases

Infiltrative disease, such as amyloidosis, Chagas' disease, or haemochromatosis, may also affect

the conduction system of the heart, causing bradycardia.sleep apnoea

Sinus node arrest, sinus bradycardia, and second-degree AV block are all manifestations of sleep

apnoea.

Diagnostic tests1st tests to ordershow all

Test Result

12-lead ECG may show sinus bradycardia with or without sinu

block with junctional or ventricular escape, His-and AV block in a setting of myocardial infarcti

precordium indicative of a neurological event m

bradycardia

Holter monitoring sinus pauses; sinus arrest; second- or third-degrewith symptoms

event monitor sinus pauses; sinus arrest; second- or third-degrewith symptoms
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exercise testing exercise-induced AV block; chronotropic incom

carotid sinus massage pause of over 3 seconds with symptoms suggestof carotid sinus hypersensitivity

echocardiogram underlying structural heart disease, such as ventrdisease

thyroid function tests elevated TSH in hypothyroidism

basic metabolic panel hypokalaemia or hyperkalaemia; hypocalcaemia

cardiac markers elevation of CK, CK-MB, and troponin in myoc

serum digoxin level depends on dose and drug-metabolism factors; m

serum creatinine elevated

Tests to considerhide all

Test

implantable-loop recorder

Subcutaneous monitoring device used for the detection of cardiac arrhythmias.

Typically implanted in the left parasternal or pectoral region.

Useful modality if a patient has intermittent symptoms suspected to be secondary to a bradyarrhythmia b

ECG abnormalities and negative Holter and/or event monitoring. Safe and efficacious in these settings.

Device is implanted by an electrophysiologist and can be used for monitoring for up to 18 months.

Stores recorded ECG strips either when the device is activated by the patient or when activated automa

according to programmed threshold criteria. Periodic interrogation of the device can retrieve this informa

Also useful to rule out bradyarrhythmia as a cause of the patient's symptoms by identifying normal sinus

time of a symptom event of interest.

Reduce/prevent recurrent symptoms.[29]

May be used if severe sinus node dysfunction (e.g., sinus exit block, sinus pauses, sinus arrest, or tachy

syndrome) is suspected but cannot be documented.

Particularly useful in diagnosing Mobitz I AV block.

tilt-table testing

Used to evaluate the adequacy of the autonomic system, especially when there is suspicion of neurocar

syncope. Commonly used method is head-upright tilting, which causes dependent venous pooling and th

provokes the autonomic response.
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electrophysiology testing

Recommended when symptoms cannot be correlated clearly and when significant bradyarrhythmias are

cannot be diagnosed by non-invasive modalities.

Testing can be useful in patients with AV block and no clear symptom association; in patients with symp

bradycardia and in whom AV block is suspected but not documented; and when the site of AV block candetermined reliably by surface tracings.

His-ventricle interval of >100 milliseconds in a patient with bradycardia, even in the absence of symptom

risk finding.[31] [32]

Overall, the role of electrophysiological testing for bradycardia is limited, owing to low sensitivity and spe

Positive findings may not be the reason for symptoms.[33] [34]

May be used if severe sinus node dysfunction (e.g., sinus exit block, sinus pauses, sinus arrest, or tachy

syndrome) is suspected but cannot be documented.

Atrial pacing progressively shorter cycle lengths during an electrophysiology study can manifest Mobitz t

subjects with normal or abnormal AV node conduction.

Asymptomatic patients with Mobitz II AV block may benefit from this test to localise the site of block and

therapy.

Useful to demonstrate the location of the block (i.e., AV node versus His-Purkinje system) in 2:1 and hig

block.

Differential diagnosisCondition

Differentiating

signs/symptoms Differentiating tests

Ventricular bigeminy Post-

premature

ventricular

contraction

(PVC)

potentiation

not present

during sinus

rhythm

without PVCs.

Cannon a-

waves seen in

ECG and rhythm strip correlated with pulse show a

each normal beat.

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the jugular

venous pulse.

Frequent premature ventricular

contractions (PVCs) Non-perfused

ventricularectopy

causing

apparent

sinus

bradycardia.

Patients are

usually

asymptomatic

.

Cannon a-

waves may be

seen in the

jugular

venous pulse.

ECG and rhythm strip correlated with pulse. Specif

cause. However, ventricular beats occur earlier tha

Atrial fibrillation Apical versus

peripheral

pulse.

Irregular pulse

rate.

ECG shows absent P waves, presence of fibrillator

complexes. Rhythm strip may be useful.

Blocked premature atrial

contractions (PACs) Atrial rate is

fast but

ventricular

rate is slow.

ECG shows slight notching on preceding T-wave.

Ventricular tachycardia A-waves,

variable S1,

and variable

pulse seen in

ECG shows atrioventricular (AV) dissociation with c
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jugular

venous

pressure.

Cardiac tamponade

Muffled heartsounds.

Sinus

tachycardia.

Pulsus

paradoxus

(usually below

10 mmHg).

Elevated

jugular

venous

pressure.

ECG shows low voltage, QRS, or total electrical alt

Echocardiogram shows large pericardial effusion o

respiratory variation of ventricular filling.

Step-by-step diagnostic approachA diagnosis of bradycardia is simple and is generally made on an ECG or

telemetry monitor when there is slowing of the heart rhythm to below 50 bpm,even if only transient. The challenge is determining the aetiology of thebradycardia and determining the site at which there is reduction in impulsegeneration or propagation. The primary use of testing is to correlatesymptoms with bradycardia and/or to establish a potentially dangerouscondition as the cause of bradycardia, even though the patient may beasymptomatic.

History

The most important diagnostic factor is age. Older patients present frequentlywith bradycardia owing to disease in the sinus node, the atrioventricular (AV)node, or the His-Purkinje system. In the AV conduction system, age-relatedfibrosis and sclerosis (Lenegre-Lev's disease) account for AV block in almosthalf of the cases. Older patients in particular may also present withbradycardia associated with medicines that have AV-node-blockingproperties, such as beta-blockers, calcium-channel blockers, and digoxin;therefore, a detailed drug history should be taken.
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A history of infection, infiltrative diseases, increased intracranial pressure,electrolyte disorders, exposure to toxins, surgery, heart transplant, sleepapnoea, or myocardial infarction may be present. Sinus bradycardia is usuallynoted in patients with significant hypothyroidism, whether or not they haveother symptoms of the disease. Asymptomatic or symptomatic sinus

bradycardia may occur in association with hypothermia.

One of the most common symptoms associated with bradycardia is dizzinessor lightheadedness. Many patients also complain of worsening fatigue.Syncope is possible with long pauses or slow heart rates, especially inpatients with complete heart block and a slow ventricular escape rhythm withleft ventricular dysfunction or in patients with second-degree AV block. Thesesymptoms generally occur owing to bradycardia-induced cerebralhypoperfusion, especially in the setting of left ventricular dysfunction.Exercise intolerance and shortness of breath is also common and may bedue to sinus node, AV node, or His-Purkinje system disease. Chest pain is arare presentation. Bradycardia can be asymptomatic, especially in youngerindividuals.

Physical examinationExamination is usually non-specific. Palpation of peripheral pulse or cardiacauscultation may reveal a slow, regular heart beat of below 50 bpm or anirregular pulse of varying intensity.

Patients with bradycardia secondary to complete heart block can haveintermittent cannon a-waves in their jugular venous pulse (JVP) owing toatrial contraction against a closed tricuspid valve. Similarly, there may be avariable S1 during complete AV block. During a junctional or ventricularrhythm with 1:1 V-to-A conduction, there may be cannon a-waves for eachheart beat.

Because bradycardia can contribute to heart failure, patients may have a thirdheart sound, rales, jugular venous distension, and abdominal and lower

extremity oedema. Signs of hypothyroidism should be assessed (e.g., dry orcoarse skin or hair, facial oedema). Poor cardiac output due to bradycardiamay be manifest as hypotension, mental status changes, and/or pallor; theextremities may be cool to the touch.

ECG

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A 12-lead ECG is the first test in the diagnosis of bradycardia, regardless ofthe suspected cause. It is simple and easy to perform and providesdiagnostic information. ECG also offers important clues regarding underlyingconditions that could have caused the bradycardia; however, it only gives asnapshot in time that may not be helpful for diagnosis if bradycardia or

symptoms are intermittent. In this situation, ambulatory monitoring is neededto correlate symptoms to bradycardia. ECG result depends on the cause ofbradycardia.

Sinus node dysfunction

Sinus bradycardia: regular P-wave followed by QRS at a rate of below 50 bpm; ambulatory ECG

monitoring is helpful to correlate symptoms with heart rate.

Sinus nodal pauses or arrest: long RR cycle length, which is longer than the RR interval of the

underlying sinus rhythm. View image

Sinus nodal exit block: an absent P-wave and prolongation of the RR cycle length, usually twice the

underlying sinus RR interval.

Tachy-brady syndrome: episodic periods of tachycardia (usually atrial flutter, atrial fibrillation, or atrial

tachycardia), followed by termination of the tachycardia leading to sinus arrest or long sinus pauses, followed by

sinus bradycardia.View imageView imageView imageView image

AV conduction disturbance

First-degree AV block: fixed prolongation of the PR interval over 0.2 seconds.[10] View image Second-degree AV block:

o Mobitz I: grouped beating with a constant PP interval, lengthening in the PR interval and

changing (usually shortening) RR intervals with the cycle ending with a P-wave not followed by a QRS complex.

As the PR interval gradually prolongs, the RR interval tends to stay the same or shorten.[11] View imageView

imageView image

o Mobitz II: associated with single non-conducted P-waves with a constant PP interval and

constant PR intervals (no change in the PR of over 0.025 seconds).[12] View imageView image

o 2:1 AV block: only one PR interval to examine before the blocked P-wave and 2 P-waves for

every QRS complex.View imageView image Block can be at the level of the AV node or the His-Purkinje system.

If the QRS is narrow, the level of the block is probably in the AV node (which is more benign). If the QRS is wide

(owing to bundle branch block or other conduction delay), block in the AV node is still most common but block in

the His-Purkinje system is more frequent than when the QRS complex is narrow.

o High-degree: more than one sequentially blocked P-wave. Block can be at the level of the AV

node or the His-Purkinje system, as is the case with 2:1 AV block.
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Third-degree AV block: occurs when there are no conducted impulses from the atria to the ventricles;

shows no consistent PR relationship.View imageView image May occur with ventricular or junctional escape

rhythm.View imageView imageView image

Paroxysmal AV block: normal AV nodal conduction followed by sudden block of AV conduction

associated with a long pause and multiple blocked P-waves, with subsequent resumption of AV conduction.

Vagotonic AV block: slowing of the sinus node with prolongation of the PR interval followed by AV block

owing to transient abrupt increase in parasympathetic tone.

Congenital complete heart block: usually associated with a narrow QRS complex escape rhythm arising

in the AV node.

Escape rhythms may also occur in AV block, such as atrial (abnormal P-wave and decreased PR

interval), junctional (above the bundle of His, produces a rate of approximately 40 to 60 bpm and narrow QRS

complexes) View imageand ventricular rhythms (below the bundle of His, produces a slower rate of 20 to 40

bpm and wide QRS complexes).

AV dissociation

Independent activation of the atria and ventricles results in no fixedrelationship between the P-waves and the QRS complexes. The PR intervalsare variable in a random fashion. Ventricular rate is the same or faster thanthe atrial rate. There are 2 types:

Isorhythmic: when the atrial rate is the same (or nearly the same as the ventricular rate) but the P-wave

is not conducted.

Interference: when P-waves and QRS rates are similar but, occasionally, the atria conduct to the

ventricles.View imageView image

Laboratory investigationsThere are no specific laboratory investigations used to diagnose bradycardia;however, initial work-up should include thyroid function tests and a completemetabolic panel to rule out electrolyte disturbances, particularly

hyperkalaemia, hypokalaemia, hypercalcaemia, and hypocalcaemia. Cardiacenzymes should be obtained if bradycardia is associated with ECG changessuggestive of myocardial infarction or ischaemia. Patients who have

junctional bradycardia and who are prescribed digoxin should have theirserum digoxin level checked. Patients with chronic bradycardia may haveevidence of worsening renal function. Any additional laboratory testing shouldbe guided by information obtained by history and physical examination to aididentification of the underlying cause.
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Other initial investigationsHolter or event monitoring, exercise testing, carotid sinus massage, andechocardiogram all form part of the initial work-up in addition to the ECG andare especially useful for intermittent bradycardia or patients with symptoms. Ifpatients have sinus bradycardia, they should be further evaluated only if theyare symptomatic or show evidence of haemodynamic compromise.

Holter monitoring

Enables correlation of symptoms with episodes of bradycardia. Diagnostic clues are obtained in 50% to

70% of patients with bradycardia suspected on clinical grounds.[24] [25]However, events can be missed if

symptoms do not occur in the 24- to 48-hour monitoring period.

Asymptomatic bradycardia and pauses (especially nocturnal) are not uncommon in the normal heart and

are probably non-diagnostic.

Shows sinus pauses, sinus arrest, second- or third-degree AV block, or severe sinus bradycardia with

symptoms. First-degree AV block or Mobitz type I AV block may be noted while patients are asleep owing to high

vagal tone.

May be used if severe sinus node dysfunction (e.g., sinus exit block, sinus pauses, sinus arrest, or

tachy-brady syndrome) is suspected but cannot be documented.

May help distinguish the location of the block (i.e., AV node versus His-Purkinje system) in 2:1 and high-

degree AV block. A long-monitored strip should be run because 2:1 AV block is unlikely to persist. The other

forms of AV block (Mobitz I or II) should then become apparent. Monitoring while the patient does some form of

exertion (e.g., arm exercise, standing, and walking) may also help to demonstrate the level of block. Block at the

level of the AV node should improve with the adrenergic stimulation but block below the AV node in the His-

Purkinje system may worsen as AV nodal conduction improves and increases the frequency of inputs to the His-

Purkinje system.

Event monitoring

Widely used in the diagnosis of symptomatic bradycardia and can be worn for up to 30 days.

Earlier designs were patient-triggered and so relied on the patient being able to recognise their

symptoms and activate the monitor in a timely manner. This issue has been corrected to some extent by newer-

generation monitors with auto-triggering capability and implantable loop recorders.

Shows sinus pauses, sinus arrest, second- or third-degree AV block, or severe sinus bradycardia with

symptoms. May be used if severe sinus node dysfunction (e.g., sinus exit block, sinus pauses, sinus arrest, or
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tachy-brady syndrome) is suspected but cannot be documented. Particularly useful in diagnosing Mobitz I AV

block.

Exercise testing

A sub-normal increase in heart rate after exercise (chronotropic incompetence) can be useful in

diagnosing sick sinus syndrome.[24] [26] However, sensitivity and specificity are unclear and the results

obtained may not be reproducible.[27] Even so, exercise-induced AV block, even if asymptomatic, can be

significant and suggests disease of the His-Purkinje system.

Identifying symptoms owing to sinus bradycardia can be difficult; however, exercise testing can be useful

to help determine sinus node dysfunction as the cause of symptoms.

Useful in determining level of block in Mobitz I.

Carotid sinus massage

Used during continuous ECG monitoring (after evaluating for the presence of carotid bruit by direct

auscultation) in the evaluation of carotid sinus hypersensitivity, which causes symptomatic bradycardia and is

associated with sick sinus syndrome.

Diagnostic yield of carotid sinus massage can be increased by performing this during head-up

tilting.[28]

A pause of over 3 seconds with symptoms is indicative of a cardio-inhibitory response from carotid sinus

hypersensitivity.

Can help diagnose Mobitz I and II AV block; it will accentuate Wenckebach in the AV node but will have

an opposite effect if the block is below the His bundle.

May help distinguish the location of the block (i.e., AV node versus His-Purkinje system) in 2:1 and high-

degree AV block. It may improve block in the His-Purkinje system by slowing the sinus and AV nodal inputs to

the His-Purkinje system, enabling the His-Purkinje system longer in which to recover between inputs.

Echocardiogram

Although it provides no direct diagnostic role for bradycardia, it provides valuable information regarding

underlying heart disease that can influence management and decision making.Patients with significantly reduced

left ventricular systolic function should be considered for an implantable cardioverter defibrillator if clinically

appropriate.

Further investigationsImplantable loop monitor

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A subcutaneous monitoring device used for the detection of cardiac arrhythmias. Typically implanted in

the left parasternal or pectoral region.

Useful modality if a patient has rare symptoms that are difficult to record with non-invasive tools such as

ECG, Holter monitors, and/or event monitors due to their infrequent nature, but are suspected to be secondary to

a bradyarrhythmia. Safe and efficacious in these settings.[29] [30] Also useful to rule out bradyarrhythmia as a cause of symptoms by identifying normal sinus rhythm at

the time of a symptom event of interest.

May show sinus pauses, sinus arrest, second- or third-degree AV block, or severe sinus bradycardia

with symptoms. May be used if severe sinus node dysfunction (e.g., sinus exit block, sinus pauses, sinus arrest,

or tachy-brady syndrome) is suspected but cannot be documented. Particularly useful in diagnosing Mobitz I AV

block.

Tilt-table testing

Used to evaluate adequacy of the autonomic system, especially when there is suspicion of

neurocardiogenic syncope.

A commonly used method is head-upright tilting, which causes dependent venous pooling and thereby

provokes the autonomic response.

Electrophysiological testing

Recommended when symptoms cannot be correlated clearly and when significant bradyarrhythmias are

suspected but cannot be diagnosed by non-invasive modalities.

Electrophysiological measurements of sinus node function serve only as an adjunct to clinical and non-

invasive parameters because these tests are based on assumptions that limit their validity and clinical utility.

There is little utility for electrophysiology testing in already-documented second- and third-degree AV

block. Testing can be useful in patients with AV block and no clear symptom association; in patients with

symptoms of bradycardia in whom AV block is suspected but not documented; and when the site of AV block

cannot be determined reliably by surface tracings.

His-ventricle interval of over 100 milliseconds in a patient with bradycardia, even in the absence of

symptoms, is a high-risk finding.[31] [32]

Overall, the role of electrophysiological testing for bradycardia is limited, owing to low sensitivity and

specificity. Positive findings may not be the reason for patient symptoms.[33][34]

May be used if severe sinus node dysfunction (e.g., sinus exit block, sinus pauses, sinus arrest, tachy-

brady syndrome) is suspected but cannot be documented.
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Atrial pacing at progressively shorter cycle lengths during an electrophysiology study can manifest

Mobitz type I in subjects with normal or abnormal AV node conduction.

Asymptomatic patients with Mobitz II AV block may benefit from this test to localise the site of block and

to guide therapy.

Useful to demonstrate the location of the block (i.e., AV node versus His-Purkinje system) in 2:1 and

high-degree AV block.

Click to view diagnostic guideline references. Case history #1An 85-year-old man presents with fatigue and episodes during which he feelshe is going to pass out. He has no known heart disease. His ECG showssinus bradycardia with a rate of 30 bpm and on a rhythm strip he has up to 5-second pauses.

Case history #2A 55-year-old man with hypertension and diabetes presents at theemergency department with complaints of dizziness and lightheadedness onexertion that has occurred gradually over the past month. He takesmetoprolol (a beta-blocker) for hypertension. He is hypotensive and has aheart rate of 45 bpm. The rhythm strip shows Mobitz type II atrioventricular(AV) block with Q waves in the inferior leads. There are no previous ECGs.

Other presentationsOther diagnostic features include exercise intolerance and chest pain.

Atypical presentations include elite athletes who present with sinusbradycardia, Mobitz I, or even Mobitz II atrioventricular (AV) block withoutsymptoms owing to a conditioned heart. The condition could also manifestshortly after taking a beta-blocker, calcium-channel blocker, or digoxin in apatient with conduction system disease. Adolescents may not have anysymptoms owing to preserved left-ventricular function; by contrast, older

people are more likely to manifest symptoms because of structural heartdisease.

Treatment Options
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Patient group

Treatment

line Treatmenthide all

haemodynamically unstable1st pharmacotherapy

In patients with systemic hypotension, signs of

cerebral hypoperfusion, progressive heart failure,

angina, or life-threatening ventricular

tachyarrhythmia, medical therapy should be

started immediately until temporary cardiac pacing

is initiated.

The most common medicines used to increase

ventricular rate are intravenous atropine,

epinephrine (adrenaline), or dopamine. All drugs

are only marginally effective in providing sustained

chronotropic support.

Their efficacy is limited to patients with sinus node

dysfunction or conduction abnormalities at the

level of the atrioventricular (AV) node. However,

patients with infranodal conduction system

disease may demonstrate further worsening

bradycardia.

Dopamine should not be used in patients with life-

threatening tachyarrhythmias and should be usedwith caution in patients with ischaemic heart

disease.

Primary Options

atropine: 0.5 to 1 mg intravenously as a bolus,

repeat every 3-5 minutes as needed, maximum 3

mg total dose

Secondary Options

epinephrine: 2-10 micrograms/min intravenous

infusion, titrate rate according to response

OR

dopamine : 2-10 micrograms/kg/min intravenous


2nd temporary pacing

Patients who are not responsive to medical
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Patient group

Treatment








is initiated.



epinephrine (adrenaline), or dopamine.All drugs








bradycardia.



disease.

Primary Options

atropine : 0.5 to 1 mg intravenously as a bolus,


mg total dose

Secondary Options

epinephrine : 2-10 micrograms/min intravenous


OR



haemodynamically stable: sinus
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Patient group

Treatment








is initiated.











bradycardia.



disease.

Primary Options



mg total dose

Secondary Options



OR



node dysfunction

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Patient group

Treatment








is initiated.











bradycardia.



disease.

Primary Options



mg total dose

Secondary Options



OR



reversible cause: asymptomatic or1st treatment of underlying cause

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Patient group

Treatment








is initiated.











bradycardia.



disease.

Primary Options



mg total dose

Secondary Options



OR



mild symptoms For mild symptoms or when sinus node

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Patient group

Treatment








is initiated.











bradycardia.



disease.

Primary Options



mg total dose

Secondary Options



OR



dysfunction is a result of a reversible or isolated

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Patient group

Treatment








is initiated.











bradycardia.



disease.

Primary Options



mg total dose

Secondary Options



OR



cause (e.g., specific medicine, electrolyte disorder,

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Patient group

Treatment








is initiated.











bradycardia.



disease.

Primary Options



mg total dose

Secondary Options



OR



or vasovagal event, such as taking blood),

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Patient group

Treatment


haemodynamically unstable1st pharmac

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