Approach to bradyarrhythmia.

Presenter = kuba.A (IMR3).

Moderator = Dr Duffera. (Internist and interventional

cardiologist).
 Outlines
• Introduction
• Approach to bradyarrhythmia's
• Sinus node dysfunction
• A-V Block
• Acute and chronic management
• Introduction to pacemaker therapy.
 Introduction
• Bradycardia is a commonly observed arrhythmia and a frequent occasion for cardiac
consultation.

• Defined as a heart rate of less than 50–60 bpm, bradycardia can be observed as a normal
phenomenon in young athletic individuals, and in patients as part of normal aging or
disease

• Pathology that produces bradycardia may occur within the sinus node, atrioventricular
(AV) nodal tissue, and the specialized His-Purkinje conduction system.

• Given the overlap of heart rate ranges with non-pathologic changes, assessment of
symptoms is a critical component in the evaluation and management of bradycardia.

• Treatment should rarely be prescribed solely on the basis of a heart rate lower than an
arbitrary cutoff or a pause above certain duration,
 Cont…
• SND is most common in individuals who are in their 70s or 80s

• The intrinsic sinus and A-V nodal diseases present in a similar clinical manner to
extrinsic/secondary processes that can injure the sinus node, atrioventricular node or
conduction system tissues.

• Multiple pathophysiologic processes individually or in combination, can

compromise impulse initiation and propagation.

• Whether intrinsic or extrinsic, the clinical manifestations of these pathologies can be

identical.
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Evaluation of the patient with suspected or documented
bradycardia or conduction system disease
 History
• Common symptoms of bradycardia
– syncope,
– presyncope,
– transient dizziness or lightheadedness
– fatigue, dyspnea on exertion
– heart failure symptoms
– confusion resulting from cerebral hypoperfusion.

• As part of the initial evaluation, a careful search for reversible causes should be
conducted with a comprehensive history and physical with review of medications.
 History
• frequency, timing, duration, severity, longevity, circumstances, triggers and
alleviating factors,
• The relationship of the symptoms to medications, meals, medical interventions,
emotional distress, physical exertion, positional changes, and triggers .
• review of both prescription and over-the-counter medications is essential.
• Bradycardia and conduction tissue disorders can be the first manifestation of a
systemic illness or heart disease .
• A complete history should include comprehensive cardiovascular risk assessment,
family history, travel history, and review of systems.
 Physical examination.
• correlate slow radial pulses with precordial auscultation or carotid
pulse.
• orthostatic changes in heart rate and blood pressure can be helpful.
• Carotid sinus massage can be helpful in patients with symptoms
suggestive of carotid sinus hypersensitivity syndrome (syncope or
near syncope elicited by tight collars, shaving, or turning the head).
• Carotid sinus massage should be performed in both the supine and
upright position in a safe environment with careful blood pressure
and electrocardiographic monitoring.
• Look for signs of underlying systemic illness and cardiac
auscultation.
• It is essential to differentiate reversible from non-reversible causes of
bradycardia.

• In a study including 277 patients referred to the emergency department

with bradycardia, electrolyte disorders were the underlying cause in 4%,
intoxication in 6%, acute MI in 14%, and adverse drug effects in 21%.
•
• In the case of non-reversible pathological causes of slow heart rate, the
presence and severity of symptoms play an essential role in the
consideration for permanent anti bradycardia pacemaker therapy.

• This may be challenging in patients with competing mechanisms for

their symptoms.
 Noninvasive Evaluation

• Resting ECG

• timed ECG during a symptomatic episode may provide a

definitive diagnosis
• a 12-lead ECG is useful to confirm;
– Rhythm and rate
– The nature and extent of conduction disturbance
– To document other abnormalities suggestive of structural heart
or systemic disease
• Inpatients presenting with syncope, the initial ECG
provides a diagnosis in only approximately 5%.
 Exercise ECG Testing

• diagnosis of chronotropic incompetence.

• In patients with exercise-related symptoms.

• the development or progression of A-V block may occasionally b
the underlying cause
• defining the site of A-V block when unclear by ambulatory ECG
monitoring.
 Imaging
• Echocardiography

– excluding associated structural heart disease

– can be prognostic
• Cardiac MRI and computed tomography

– In diagnosing infiltrative processes.

– superior information regarding calcification of
cardiac structures.
Laboratory Testing
 Sleep Apnea Evaluation and Treatment

• Estimated rates of profound nocturnal sinus bradycardia

range from 7.2% to 40%.

• Rates of second- or third-degree A-V block range from

1.3% to 13.3%, and rates of sinus pauses range from 3.3%
to 33% .
• treatment of sleep apnea dramatically reduces the
frequency of these arrhythmias.
 Invasive Testing ICM
• Several RCTs have demonstrated the diagnostic value of ICM in
patients presenting with unexplained syncope or presyncope.

• Compared with investigation by conventional testing modalities

such as 24-hour ambulatory ECG monitoring, 12-lead ECG, and
treadmill stress test, the strategy of long-term rhythm monitoring
with ICM was more effective in obtaining a clinical diagnosis.
 Electrophysiology

• Used to identify the presence of abnormal sinus node function or

A-V conduction, and the anatomic location of any conduction
disorder.

• Pharmacologic drugs are sometimes administered during an EPS as

apart of study protocol to modulate the autonomic tone or to
“stress” the sinus node or A-V conduction, and intraventricular
conduction.

• The diagnostic yield of EPS in symptomatic patients with suspected

bradycardia has been shown to vary widely (range, 12%–80%),
depending on the patient population studied.
• Sinus node dysfunction

• A-V block and Conduction disturbance

 SND = inability of the SA node to generate a heart rate that meets the physiologic needs
of an individual.

Sinus bradycardia
● Sinus pauses
● Sinus arrest
● SA nodal exit block
● (chronotropic incompetence)
 Sinus Bradycardia
• Physiologic( well trained athletes and during sleep).
• Pathological( SND) &Mostly benign and asymptomatic
• Caused by either excessive vagal or decreased sympathetic tone,
• ECG findings
– Rate < 50 beats/min
– P waves have a normal contour,and are usually upright in leads I,II,and aVF,and
occur before each QRS complex,
– constant PR interval longer than 120 msec.
 SINUS PAUSE OR SINUS ARREST

• Sinus pause or sinus arrest is recognized by a pause in the sinus rhythm .

• The P- P interval delimiting the pause does not equal a multiple of the basic P-P
interval.
• can also result in ventricular asystole if escape beats do not occur.
 SINOATRIAL EXIT BLOCK

• Diagnosed by ECG by a pause resulting from absence of the normally expected P

wave
• The duration of the pause is a multiple of the basic P-P interval.
• An interval without P waves that equals approximately two, three, or four times the
normal P-P cycle characterizes type II second-degree SA exit block.
• During type I (Wenckebach) 2nd -degree SA exit block, the P-P interval
progressively shortens before the pause, and the duration of the pause is less than two
P- P cycles.
• First-degree SA exit block cannot be recognized on the ECG).
• Third-degree SA exit block can be manifested as a complete absence of P waves and
is difficult to diagnose with certainty without sinus node electrograms.
 Tachycardia-Bradycardia Syndrome
• occurs when a patient has tachyarrhythmias and bradyarrhythmias closely associated
in time.
• That can occur when a tachyarrhythmia, terminates,with a resultant excessive post-
conversion pause .

• TBS can also occur during atrial fibrillation when periods of atrial fibrillation with
rapid ventricular rates alternate with periods of excessive bradycardia (due to high-
grade AV block) during AF.

• typically occurs as a result of treatment with beta blockers or CCBs. 

 Chronotropic Incompetence
• Chronotropic incompetence (CI) is diagnosed when the heart rate does not increase
appropriately in the setting of increased physio-logic demand

• Defined as failure to obtain 80% or 85% of either maximal expected heart rate,or of
inadequate heart rate reserve (the difference between resting heart rate and age
predicted maximal heart rate).

• The normal heart rate increase with exercise and rapid decline with cessation of
activity results from an exquisite balance of inputs from the sympathetic and
parasympathetic nervous system to the sinus node.
 Acute management
• Depends on
– Hemodynamic stability
– Severity of symptoms
• Most patients with SND present with chronic complaints that does not require acute
treatment.
• In addition, most causes of SND are chronic and irreversible.
• If reversible causes are identified , treat the cause.
 Atropine and Beta Agonists for Bradycardia Attributable to SND

• Atropine - sinoatrial conduction and increases sinus node automaticity (0.5 to 2

mg).
– AVOID atropine in heart transplant patients.
• Isoproterenol- is a nonselective beta agonist with both chronotropic and inotropic
effects .
• Dopamine -is a catecholamine with mixed alpha-adrenergic, beta-adrenergic, and
dopaminergic effects that depend on dosage, distribution, and metabolism.
– 1 to 2 mcg/kg/min, vasodilatory,
– 5 to 20 mcg/kg/min, enhanced chronotropy and inotropy predominate.
• Epinephrine- is a catecholamine with strong alpha-adrenergic and beta-adrenergic.
– 2 to 10 mcg/min with titration to hemodynamic response
 Therapy of Beta Blocker and Calcium Channel Blocker Mediated Bradycardia
Attributable to SND

• Cardiovascular effects of beta-blocker and CCCBs toxicity are systemic and can be
fatal.
• The evidence base and specific treatment considerations for beta-blocker and
calcium channel blocker mediated bradycardia are the same for SND and
atrioventricular block.
• calcium chloride and calcium gluconate can be used.
• Glucagon (bolus of 3 to 10 mg/ 3 to 5 minutes. infusion of 3 to 5 mg/h is followed.
• High-dose insulin therapy-(bolus of 1 unit/kg followed by an infusion of 0.5
units/kg/h.
 Therapy of Digoxin Mediated Bradycardia Attributable to either SND or
Atrioventricular Block

• Digoxin-specific antibody (Fab) is a monovalent immunoglobulin.

• Each vial of 40 mg of digoxin Fab binds approximately 0.5 mg of digoxin.
• response rates to digoxin Fab are as high as 80% to 90%, particularly in the acute
setting.
• Use of any treatment directed specifically to digoxin toxicity will depend primarily
on the presence or likelihood of developing significant toxicity .

• digoxin is only slightly dialyzable.

 4. Aminophylline or Theophylline for Bradycardia Attributable to SND

• The methylxanthines theophylline and aminophylline( inhibit adenosine).

• Effective in spinal cord injury or post heart transplantation.

Temporary Pacing for Bradycardia Attributable to SND

• Temporary pacing is used to acutely treat bradycardia .

– prolonged and symptomatic pauses
– life-threatening ventricular arrhythmias mediated by bradycardia,
– severe symptomatic bradycardia attributable to a reversible cause

• Temporary pacing can be implemented

– Transcutaneously,transesophageal approach
– by insertion of a transvenous pacing electrode
– pulmonary-arterial pacing catheter .

• Emergency temporary pacing - pacing the right ventricle (RV)is preferred.

• In rare cases, temporary pacing of the right atrium (alone or in conjunction with
ventricular pacing) is used when maintenance of atrioventricular synchrony is critical
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Temporary pacing cont..
 Chronic Therapy/Management of Bradycardia Attributable to SND

• The goal of anti-bradycardia therapy in SND is to increase the heart rate so that
cardiac output is normalized,
• Identifying physiologic conditions and reversible conditions is very important.
• For other patients with symptomatic sinus bradycardia attributable to an intrinsic
pathology of sinus node, permanent pacing may be necessary.
• Complications associated with PPM implantation range from 3% to 7% and there
are significant long-term implications for pacing systems that use transvenous leads
.
 Permanent Pacing for Chronic Therapy/Management of Bradycardia
Attributable to SND

• Permanent cardiac pacing is indicated to alleviate the symptoms of cerebral

hypoperfusion attributable to bradycardia when other potential treatable or
reversible etiologies have been excluded.

• Symptomatic SND is the most common indication for permanent pacing, followed
closely by atrioventricular block.

• Often the best response to pacing therapy is demonstrated when an unequivocal

correlation has been established between symptoms and bradycardia.

• The benefit of pacing in SND is mainly QOL Improvement

 Permanent Pacing Techniques and Methods .

• Atrial-based pacing modes (AAI and DDD) have been compared with ventricular-
based pacing mode (VVI)

• in 4 major RCTs and reviewed in a recent expert consensus document

• Results were inconsistent across the studies and the reconciliation of findings can be
challenging.

• However atrial-based pacing modes appeared to confer advantage over ventricular-

based pacing mode with respect to a lower incidence of AF.
• The impact of atrial-based pacing modes on the prevention of heart failure or
stroke, and improvement in QOL is less clear
 Indication for permanent pacing
• direct evidence of symptom correlating with sinus bradycardia or pauses

• BBs have a wide range of guideline-directed indications For patients who also
have symptomatic sinus bradycardia some should be managed with permanent
cardiac pacing.

• Tachy-brady syndrome describes a subset of symptomatic SND

• Chronotropic incompetence

• In patients who are unwilling to undergo PPM implantation or who are not
candidates for permanent pacing, oral theophylline could be considered for
treatment of symptomatic SND.
 A-V block
• Classified anatomically in to AV, intra-Hisian (within the His bundle
itself), and infra-Hisian (below the His bundle).

• The site of block may be clinically important and can be determined by

invasive EPS when not apparent from the ECG and clinical circumstance,
• Based on degree of Av block
– First-degree atrioventricular delay.
– Second-degree atrioventricular block
– Mobitz I (Wenckebach conduction) and Mobitz II.
– High-grade, high-degree, or advanced atrioventricular block
– Complete Av block
 Determining Level of block
• Surface ECG – The ECG is usually of limited value.

• A PR interval duration of 300 ms or greater with a normal QRS

complex.
•First-degree AV block coupled with a wide QRS complex can be due to
infr anodal disease,

• Vagal maneuver
• Atropine
• EPS
 First- Degree A-V Block

• every atrial impulse is conducted to the ventricles and a regular ventricular rate is
produced.
• the PR interval > 0.20 second in adults.
• If the QRS complex on the ECG is normal in contour and duration, the AV delay
almost always resides in the AV node .
• If the QRS complex shows a BBB pattern, the conduction delay may be within the AV
node or the His Purkinje system
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 Second- Degree Atrioventricular Block

• Blocking of some atrial impulses conducted to the ventricle).

• The non conducted P wave can be intermittent or frequent, can occur at regular or
irregular intervals.

• the association of P with QRS is not random.

• Type I second degree AV block- is characterized by progressive PR prolongation

culminating in a non conducted P wave

• Type II second- degree AV block- the PR interval remains constant before the
blocked P wave ,
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 Acute Medical Therapy for Bradycardia Attributable to Atrioventricular
Block

• timely identification and removal of potential causative factors as well as medical

therapy.
• Atropine
• Aminophylline and glucagon have a possible role in treatment of atrioventricular
block in the setting of acute MI and beta-blocker toxicity, respectively, but data are
sparse.
 Temporary Pacing

• The cause of atrioventricular block must be taken into account when considering
the timing and necessity of temporary pacing.

• For example, in the setting of an MI, initial focus on primary reperfusion rather
than temporary pacing for rate support may be associated with improved outcomes.
 Permanent pacing
• The presence or absence of symptoms is a major determinant on whether permanent
pacing will be required,

• the site of atrioventricular block is critical because patients with infra nodal disease
who then later develop complete heart block will be dependent on unreliable
ventricular escape rhythms.

• patients with atrioventricular block may have an associated systemic disease that
leads to progressive atrioventricular block or has additional risk for ventricular
arrhythmias
 Permanent Pacing

• Similar to SND, symptoms are an important factor when determining whether

permanent pacing is indicated.

• If the patient is symptomatic, regardless of the level of atrioventricular block and the
likelihood of future progression of atrioventricular block, permanent pacing is
indicated.

• However, unlike SND, infranodal atrioventricular block regardless of the presence or

absence of symptoms warrants a pacemaker because the patient could suffer from
sudden onset complete atrioventricular block resulting in syncope and subsequent
harm .
 1. Permanent Pacing Techniques and Methods for Chronic Therapy

• There are several RCTs that looked at the possible benefits of dual chamber pacing for
atrioventricular block compared with ventricular pacing but neither improvements in all-cause
mortality nor cardiovascular mortality were demonstrated .

• However, regardless of pacing technique, patients with atrioventricular block will require
ventricular pacing for rate support.

• Specialized pacing modalities, such as biventricular pacing or His bundle pacing may alleviate
the deleterious effects of right ventricular pacing in these patients.
• When determining the type of pacemaker (single, dual, biventricular), many patient
• factors should be considered including the projected percent of ventricular pacing and the
LVEF.
• biventricular pacing can be useful for the patient on guideline-directed management and
therapy who has an LVEF of ≤35% with an anticipated requirement for significant ventricular
pacing (>40%)
Special populations
Mitral Valve Surgery
 Management of Bradycardia in Patients With an Acute MI

• nonreversible injury to the A-V conduction system accounts for most pacing
indications.
• The transient nature of the effects conduction issues in this setting must be
considered.
• For example, SND and atrioventricular block in the setting of an inferior wall MI may
be attributable to a transient increase in vagal tone or decreased blood supply to the
atrioventricular node or less commonly the sinus node.
• The long-term prognosis for survivors of MI who have had A-V block is related
primarily to the extent of myocardial injury and the character of intraventricular
conduction disturbances rather than the atrioventricular block itself. .
Discontinuation of Pacemaker Therapy
 CIED
• Electrical therapy for cardiac arrhythmias includes

– low- voltage (typcally 1 to 5 V) pacing stimuli (pulses) and

– high- voltage (typically 500 to 1400 V) stimuli (shocks).
• Pacemakers deliver pacing pulses to treat bradycardia.

• ICDs deliver shocks to defibrillate ventricular fifibrillation (VF) or to cardiovert ventricular

tachycardia (VT).

• ICDs also have anti bradycardia pacing functions that can deliver pacing pulses to treat
bradycardia, as well as anti tachycardia pacing functions that can deliver sequences of rapid
pacing pulses to treat ventricular or atrial tachyarrhythmias.

• Cardiac resynchronization therapy (CRT) pacemakers (CRT- P) or ICDs (CRT- D) also provide
electrical therapy for heart failure in the form of pacing pulses that resynchronize the ventricular
contraction sequence.
Pacemaker components
 Types of pacemakers

• Transvenous systems-most common

• His bundle pacing- for A-V synchrony
• Left bundle branch pacing-more physiological
• Epicardial pacing –when transvenous system is
contraindicated
• Leadless pacing- less complications(only RV pacing).
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 Pacemaker syndrome —  is a phenomenon associated with the loss of AV
synchrony and is seen most commonly with single-chamber VVI pacing.

It is defined as the adverse hemodynamics associated with a normally

functioning pacing system, resulting in overt symptoms or limitation of the
patient's ability to achieve optimal functional status .

The development of the pacemaker syndrome with VVI pacing may require
upgrade from a VVI pacemaker to a dual-chamber system in some patients.

Symptoms most commonly include general malaise, easy fatigability, dyspnea,

orthopnea, cough, dizziness, atypical chest discomfort, and a sensation of throat
fullness and, less commonly, may result in pre-syncope or syncope.

Physical examination may reveal hypotension, rales, increased jugular venous

pressure with cannon A waves, peripheral edema, and murmurs of tricuspid
and/or mitral regurgitation

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