SEMINAR ON APPROACH TO

BRADYARRHYTHMIAS

Presenter: Dr.Nassir Miftah ,IMR3

Moderator: Dr. Duffera. (Internist and interventional cardiologist)

October 10 , 2022

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Outlines

• Introduction
• Etiology
• Clinical features
• Diagnosis
• Managements

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 Figure 1 : The electrical conduction pathway of the heart

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 Phase 4 spontaneous depolarization results
from if (funny) current, along with T- and L-type
calcium channels.
Phase 0 is the depolarization phase of the
action potential
Phase 3 repolarization, which results from the
outward directed hyperpolarizing K+ currents. if,
funny current; iCa-T, T-type calcium current; iCa-
L, L-type calcium current; iK, potassium current.

FIGURE 2. Cellular ion currents involved in

depolarization and automaticity of SA nodal
pacemaker cells.

10/26/2022 Harrisons 21st ed 4

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 Bradyarrhythmias

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Bradyarrhythmias

• The term arrhythmia refers to any disturbance in the rate, regularity, site of
origin, or conduction of the cardiac electrical impulse.

• Bradyarrhythmia is arbitrarily defined as a heart rate less than 60 beats/min.

• Bradyarrhythmias can be physiologic( athletes ,during sleep).

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10/26/2022 Uptodate 8
Bradyarrhythmias

Bradyarrhythmias can be categorized on the basis of the level of

disturbance in the hierarchy of the normal impulse generation and
conduction system.

1.Disorders of the Sinoatrial Node

2.AV-Blocks

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Disorders of the Sinoatrial Node

Sick sinus syndrome may be used interchangeably with SND

o Sinus bradycardia
o Sinoatrial exit block
o Sinus pause/arrest
o Tachycardia-bradycardia-syndrome

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The Sinoatrial Node

• The sinoatrial (SA) node serves as the natural pacemaker of the heart.
• Clusters of myocytes with pacemaker activity are surrounded by fibroblasts,
endothelial cells, and transitional cells.
• The sinus node is a small, flattened, ellipsoid strip of specialized cardiac muscle
about 3 mm wide, 15 mm long, and 1 mm thick.
• The SA nodal artery arises from the right coronary artery in 55–60% and the left
circumflex artery in 40–45% of persons.
• Parasympathetic and sympathetic innervation affects the SA node.

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Normal sinus rhythm (NSR)

• NSR - in adults if the heart rate is between 60 and 100 beats/min,

• The P wave on the ECG is normal, and the rate is largely regular.
• The P wave -an upright in leads I, II and aVL, and negative lead aVR.

10/26/2022 Uptodate online 12

 Sinus bradycardia

 By conventional definition, bradycardia indicates a heart rate less than 60

beats per minute with a normal P wave vector on the surface ECG.

10/26/2022 Uptodate 13
 Table . Common Potentially Reversible or Treatable Causes of SND

10/26/2022 2018 ACC/AHA/HRS Bradycardia Clinical Practice Guidelines 14

Medications potentially result in SSS

The most commonly used prescription medications which can potentially result in
SSS include :
• Beta blockers
• Non-dihydropyridine calcium channel blockers
• Digoxin
• Antiarrhythmic medications
• Donepezil and rivastigmine used in the treatment of Alzheimer's disease
• Methyldopa, clonidine, cimetidine, lithium, and ivabradine.

10/26/2022 Uptodate 15
Sinus pause or arrest

• A sinus pause or arrest is defined as the transient absence of sinus P waves on

the ECG) that may last from two seconds to several minutes.
• The pause or arrest often allows escape beats or rhythms to occur, but lower
pacemakers may be sluggish or even absent in the sick sinus syndrome.
• Does not necessarily indicate disease, it can occur in the normal heart.
• Can produce symptoms of dizziness, presyncope, syncope, and, rarely death.

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 Sinus arrest

Sinus arrest occurs after the fourth beat.

The fifth beat, restoring electrical activity to
the heart, is a junctional escape beat. Note
the absence of P waves.

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Only EKG Book You'll Ever Need, The, 5th Edition, Uptodate 17
Sinus Node Exit Block

• Sinoatrial exit block results from failure of sinus node activity to propagate to the
atrium.
• Sinoatrial exit block can have similar pattern characteristics of types of AV node
block.
• It can manifest as complete SA block.
• Type I SA block involves fixed delay out of the sinus node.
• Type II SA block can occur with either progressive delay and then intermittent
failure to propagate to the atrium (Mobitz I type) or fixed delay with intermittent
failure to conduct (Mobitz II).

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Sinus Node Exit Block cont….

• The mass of the node is not large enough to have an appearance on the ECG.
• Instead, the P waves that result from atrial depolarization can provide
information that reflects the health of the sinus node.
• Other types of SA block require invasive EPS to decipher.
• The exercise of determining the type of SA block with invasive electrophysiology
testing is typically not necessary because it does not alter management.

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Tachy-Brady Syndrome

• Is a subset of sick sinus syndrome that consists of high heart rates (most
commonly atrial fibrillation) with alternating symptomatic bradycardia or offset
pauses.
• Medications that are needed for rate control of tachycardia exacerbate
bradycardia episodes, and thus the presence of tachy-brady syndrome is often a
reason to consider pacemaker implantation.

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Chronotropic Incompetence (CI)

• The inability of the heart to increase its rate commensurate with increased activity or
demand.
• Definition - Failure to attain 80% of expected heart rate reserve during exercise.
• Compared to an increase stroke volume, the increase in heart rate is a stronger contributor
to the increase in oxygen uptake during aerobic exercise.
• CI can be associated with severe exercise intolerance and increased cardiovascular events
and overall morality.
• Ambulatory heart rate monitoring along with a diary can be helpful to correlate symptoms
with abnormally slow heart rates.

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SA Nodal Ischemia and Infarction

• Sinus bradycardia is common in patients with acute inferior or posterior MI

• Can be exacerbated Bezold-Jarisch reflex or with the use of drugs such as
morphine and beta blockers.
• Ischemia of the SA nodal artery probably occurs in ACS more typically with
involvement with the right coronary artery.
• Even with infarction, the effect on SA node function most often is transient.
• There are rare cases where sinoatrial infarction can affect sinus node function.
• Ablation of atrial fibrillation - the inadvertent injury to the SA nodal artery .

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10/26/2022 Uptodate 25
Table Acute Medical Management of Bradycardia Attributable to SND or Atrioventricular Block

10/26/2022 2018 ACC/AHA/HRS Bradycardia Clinical Practice Guidelines 26

 Figure - Chronic SND management algorithm .

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10/26/2022 AHA-ACLS 2020 Guidelines 28
 Table Indications for Permanent Pacing in SND

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 AV-Blocks

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AV-node

• The AV node itself is a small region (∼1 × 3 × 5 mm) .

• Lies beneath the right atrial endocardium at the apex of the triangle of Koch.
• Cells located in the AV node sit at a relatively higher resting membrane potential
than surrounding atrial and ventricular myocytes.
• The AV node has the potential for pacemaker activity,
• The normal automaticity rate of AV-node is 20–60 beats/min, which is
overridden by the higher intrinsic rate of the SA node (60–100 beats/min).

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Blood supply and innervation …

• The AV node artery arises from the right coronary artery (80–90% of the time) or
the left circumflex (10%).
• The bundle branches- have a dual blood supply from the septal perforators of the
LAD coronary artery and branches of the posterior descending coronary artery.
• The AV node is highly innervated with postganglionic sympathetic and
parasympathetic nerves.
• The bundle of His and distal conducting system are minimally influenced by
autonomic tone.

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AV-Blocks

• First Degree
• Second Degree
- Mobitz1
- Mobitz2
- 2:1 Block
• Third Degree
• High Grade AV Block

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First degree AV block

• Involves a fixed prolongation of the PR interval >200 ms.

• Although the term block is a misnomer of sorts because electrical conduction is
delayed and not interrupted, it remains in use.
• Delay usually occurs within the AV node, although the atria, His bundle, and
Purkinje system may also be involved.

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Sites of conduction delay in 1st degree AV- block

• Atrium – endocardial cushion defects and Ebstein's anomaly of the tricuspid valve.
• AV node – Increased vagal tone, digoxin ,calcium channel blockers, and beta-
blockers.
• Bundle of His – Rare, (eg, quinidine, procainamide, and disopyramide)
• Infra-Hisian conduction system -Rare, most commonly due to drugs
(eg, quinidine, procainamide, and disopyramide).

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Causes of first-degree heart block

The most common causes of first-degree heart block are :

• AV nodal disease,
• Enhanced vagal tone ,
• Myocarditis, acute myocardial infarction,
• Electrolyte disturbances ,and
• Medication (calcium channel blockers, beta-blockers, cardiac glycosides, and
cholinesterase inhibitors).

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Clinical presentation and Dx of 1st degree AV-block  

• First degree AV block is almost universally benign.

• There are no signs or symptoms that are either sensitive or specific that are
related to first degree AV block.
• First degree AV block cannot be detected from history or physical examination
alone.
• May result in signs and symptoms similar to the pacemaker syndrome.
• The diagnosis of first degree AV block is typically confirmed using ECG.

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Second-degree atrioventricular block

Second-degree atrioventricular block: P waves with a constant rate (<100 bpm)

where atrioventricular conduction is present but not 1:1
• Mobitz type I: P waves with a constant rate (<100 bpm) with a periodic single non
conducted P wave associated with P waves before and after the non conducted P
wave with inconstant PR intervals
• Mobitz type II: P waves with a constant rate (< 100 bpm) with a periodic single
non conducted P wave associated with other P waves before and after the non
conducted P wave with constant PR intervals (excluding 2:1 atrioventricular
block)

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 Mobitz type I second-degree AV block
(Wenckebach block). The PR intervals
become progressively longer until one
QRS complex is dropped.

Mobitz type II second-degree AV block. On

the EKG, every third P wave is not followed
by a QRS complex (dropped beat).

Only EKG Book You'll Ever Need, The, 5th Edition

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Is this ECG Shows Mobitz type I or Mobitz type II ???

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Third-degree atrioventricular block

• Complete failure of conduction from atrium to ventricle

• The block is most often distal to the AV node.
• The level of the block.
– In the absence of a preexisting BBB, a wide QRS escape rhythm distal His
or bundle branches;
– narrow QRS -AV node or proximal His and an escape rhythm originating in
the AV junction.
• There is AV dissociation.

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 Third-degree AV block. The P waves appear at
regular intervals, as do the QRS complexes, but they
have nothing to do with one another. The QRS
complexes are wide, implying a ventricular origin.

Only EKG Book You'll Ever Need, The, 5th Edition

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AV Block in the setting of myocardial ischemia

• AV conduction abnormalities may be caused by either direct ischemia to the

conduction system or enhanced autonomic tone
• Bezold-Jarisch reflex.
• Coronary artery disease may produce transient or persistent AV block.
• In the setting of coronary spasm, ischemia, particularly in the
right coronary artery distribution, may produce transient AV block.
• In acute MI, AV block transiently develops in 10– 25% of patients.
• Second degree and higher-grade AV block tends to occur more often in
inferior than in anterior acute M.

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AV Block in the setting of MI cont…

• Conduction abnormalities can be considered based on infarct location.

• The infarct location predicts which conduction abnormalities may be reversible.
• High-grade AV block associated with inferior MI is often located proximal to the His bundle in
90% of patients.
- AV block is often reversible and successfully managed with pharmacologic therapy.

• High-grade AV block in the setting of anterior MI is typically indicative of extensive infarction.

- Is more often distal to the AV node, and is associated with a high mortality rate.
- Temporary pacing in this circumstance is typically indicated.

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Congenital heart block

The etiologies of congenital CHB include the following :

• Autoimmune antibodies
• Structural heart abnormalities due to congenital heart disease .
• Idiopathic familial congenital CHB

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Evaluation of patients with symptoms suggestive of
bradycardia

• Together with the history and physical examination, the resting ECG
is an essential component of the initial evaluation of patients with
documented or suspected bradycardia.
• A 12-lead ECG or a rhythm strip during the symptomatic episode provides the
definitive diagnosis.
• For those in whom physical examination suggests a bradycardia, a
12-lead ECG is useful to confirm the rhythm, rate, nature, and extent
of conduction disturbance .
• An ECG may provide information about structural heart or systemic illness that
predict adverse outcomes in symptomatic patients.

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 Table . Acute Medical Management of Bradycardia Attributable to SND or AV Block

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 Table - Choice of ambulatory electrocardiographic monitoring
depending on symptom frequency

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 Cardiac implantable electrical devices (CIED)

• Electrical therapy for cardiac arrhythmias includes

• low- voltage (typically 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 fibrillation or to cardiovert VT.
• 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.

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Artificial Pacemaker

Parts of Artificial Pacemaker

o Generators
o Leads
o Electrodes

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Pacemaker Mode and Timing Cycles

Pacing modes describe which chambers are sensed and paced and are characterized
by a four-letter code.
• The first letter indicates the chamber paced: A for atrium, V for ventricle, and D for
dual— both atrium and ventricle.
• The second letter denotes the chamber sensed.
• The third letter describes pacemaker function: I for inhibition, T for triggered, and D
for dual—tracking of atrial activity but inhibited by ventricular activity, “O” indicates
absence of any of these functions.
• The fourth letter is R, for rate-adaptive 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.
• 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 .
• 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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References
• Harrison’s 21st ed.
• Braunwald’s heart disease 11th ed.
• 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy.
• 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients
With Bradycardia and Cardiac Conduction Delay.
• Only EKG Book You'll Ever Need, The, 5th Edition.
• ACLS –AHA2020 guidelines.
• Uptodate online.

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 Thank you

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