B.22 Bradyarrhythmia

Question 1

B.22 Bradyarrhythmia

definition

Answer 1

HR below 60 bpm

Relative bradycardia - a HR above 60 bpm but is still considered low due to the current medical status of the patient

Question 2

B.22 Bradyarrhythmia

Cardiac Causes of Brady Cardia

Answer 2

Acute or Chronic Ischemic Heart Disease

Coronary Artery Disease

Valvular Heart Disease

Degenerative Primary electrical Disease

Sick Sinus Syndrome

Question 3

B.22 Bradyarrhythmia

Extracardiac Causes

Answer 3

Hypothyroidism

Electrolyte Imbalance - Hyperkalemia

Autonomic/Neuorgenic Causes

Autoimmunity

Drugs

Drug Abuse

Question 4

B.22 Bradyarrhythmia

Pathomechanism

Answer 4

depressed automactity of the heart

conduction block

escape rhytms

Question 5

B.22 Bradyarrhythmia

List the Atrial Origin bradyarrhythmias

Answer 5

Respiratory Sinus Arrhythmia

Sinus Bradycardia

Sinus Pause or Arrest

Tachycardia-bradycardia Syndrome

Question 6

B.22 Bradyarrhythmia

Respiratory Sinus Arrhytmia

Answer 6

physiological, usually seen in youths - A natural variation of the heart rate during respiration; caused by changes in vagal tone, as well as changes in venous blood flow to the heart during inspiration and expiration

ECG:
minor changes in RR interval
- inspiration –> decreased RR —> increased HR

• expiration –> increased RR –> decreased HR

Question 7

B.22 Bradyarrhythmia

Sinus Bradycardia

Answer 7

can be physiological in altheletes

caused by sinus node dysfunction - SSS
hypothyroidism
hypothermia

Drugs: BB, CBB

ECG
< 60 bpm
Normal P wave before every QRS

Question 8

B.22 Bradyarrhythmia

Sinus Pause or arrest

Answer 8

Sinus Pause or Arrest - The SA node consists of pacemaking P cells in the center and transitioning T cells in the outer layer. SA node dysfunction can result from P cells that fail to generate an impulse (i.e., sinus pause or sinus arrest) or T cells that do not transmit the impulse (sinoatrial exit block).

May occurs in healthy individuals

Underlying cardiovascular disease - SSS

ECG
- Transient (sinus pause) or complete (sinus arrest) absence of the P wave - usually lasts 2 seconds to a few minutes

• Often with an escape rhythm (with variable origin)

Question 9

B.22 Bradyarrhythmia

Tachycardia-bradycardia syndrome

Answer 9

Tachycardia-bradycardia syndrome - A subtype of sinus node dysfunction in which there are alternating periods of bradyarrhythmia (e.g., sinus bradycardia, sinus pauses, sinoatrial exit block) with supraventricular tachyarrhythmia (e.g., atrial tachycardia, atrial flutter, atrial fibrillation).

Abnormal supraventricular impulse generation and conduction - sick sinus syndrome for details

ECG
Intermittent tachyarrhythmias and bradyarrhythmia

Question 10

B.22 Bradyarrhythmia

List AV node Origin bradyarrythmias

Answer 10

AV Block - An arrhythmia characterized by interrupted or delayed conduction between the atria and the ventricles. Divided into three different degrees depending on the extent of the interruption or delay.

• first degree
• second degree
• third degree

Question 11

B.22 Bradyarrhythmia

First Degree AV block

Answer 11

Physiological response
Increased vagal tone
Drugs: beta blocker or calcium channel blocker

ECG
PR interval > 200 m

Question 12

B.22 Bradyarrhythmia

Second Degree AV Block

Answer 12

Drugs: digoxin, beta blocker, calcium channel blocker
Increased vagal tone
Sinoatrial conduction disease
Right coronary infarction

ECG
Mobitz type I/Wenckebach: progressive lengthening of the PR interval until a beat is dropped - Regular atrial impulse does not reach the ventricles (a normal P wave is not followed by a QRS complex)

Mobitz type II: irregular dropped beat - Single or intermittent non-conducted P waves without QRS complexes with constant PR intervals

Question 13

B.22 Bradyarrhythmia

Third Degree

Answer 13

Complete block: no communication between the atria and ventricles - Atrial and ventricular contraction occur independently without organized electrical transmission through AV node.

ECG
AV dissociation: no relationship between P waves and QRS complexes

Question 14

B.22 Bradyarrhythmia

Sick Sinus Syndrome
Definition

Answer 14

Sinus node dysfunction (SND), previously called sick sinus syndrome, is an abnormality in sinoatrial (SA) node action potential generation or conduction

Question 15

B.22 Bradyarrhythmia

SSS Risk Factors

Answer 15

Coronary artery disease
Hypertension
Diabetes mellitus
Obesity
Right bundle branch block

Question 16

B.22 Bradyarrhythmia

SSS Etiology Intrinsic Factors

Answer 16

Intrinsic factors :
Conditions that alter the structure or function of the SA node
- Degeneration, ischemia, infiltration , or fibrosis of the SA node and surrounding myocardium
inflitration can be caused by due to hemochromatosis, sarcoidosis, or amyloidosis

• Cardiac intervention (e.g., repair of a septal defect)

Question 17

B.22 Bradyarrhythmia

SSS Etiology Extrinsic Factors

Answer 17

Factors external to the SA node that affect sinoatrial conduction:

Medications such as β-blockers, digoxin, and nondihydropyridine calcium channel blockers (verapamil, diltiazem)

Excessive vagal tone (e.g., athletes)

Electrolyte abnormalities

Question 18

B.22 Bradyarrhythmia

How does β-blockers cause bradyarrthymia

Answer 18

Beta-blockers cause bradyarrhythmia by blocking β1-adrenergic receptors in the heart, which reduces sympathetic stimulation of the SA and AV nodes. This leads to decreased automaticity of the SA node and slowed conduction through the AV node, resulting in sinus bradycardia or AV block, especially in patients with underlying conduction system disease.

Question 19

B.22 Bradyarrhythmia

How does digoxin cause bradyarrthymia

Answer 19

Digoxin causes bradyarrhythmia by enhancing vagal (parasympathetic) tone, which slows SA node firing and AV node conduction, leading to sinus bradycardia or various degrees of AV block. At toxic levels, digoxin can also trigger ectopic atrial or junctional rhythms and promote dangerous ventricular arrhythmias by increasing intracellular calcium and triggering afterdepolarizations.

Question 20

B.22 Bradyarrhythmia

How does nondihydropyridine calcium channel blockers (verapamil, diltiazem) cause bradyarrthymia

Answer 20

Non-dihydropyridine calcium channel blockers (verapamil, diltiazem) cause bradyarrhythmia by blocking L-type calcium channels in the SA and AV nodes, which depend on calcium influx for depolarization. This leads to decreased SA node automaticity and slowed AV nodal conduction, resulting in sinus bradycardia and potentially AV block, especially when combined with other rate-lowering drugs or in patients with conduction system disease.

Question 21

B.22 Bradyarrhythmia

mechanism of SSS

Answer 21

↓ SA node automaticity

SA exit block (impulses generated but not transmitted to atria)

Alternating suppression and bursts of tachyarrhythmia (tachy-brady syndrome)

Question 22

B.22 Bradyarrhythmia

clinical features of SSS

Answer 22

Symptoms of bradycardia (features of end-organ hypoperfusion)

Fatigue
Dizziness or lightheadedness, syncope, presyncope, TIA (seen in ∼ 50% of patients)
Decreased physical activity tolerance - Heart rate does not increase appropriately during physical activity. 
Stokes-Adams attacks - A sudden loss of consciousness, usually without warning and lasting for a few seconds, due to an abnormal heart rhythm (especially complete atrioventricular block).
Dyspnea on exertion
Angina, palpitations
Oliguria

Patients with tachycardia-bradycardia syndrome will also present with symptoms of tachycardia, including palpitations.

Question 23

B.22 Bradyarrhythmia

Management of SSS

Answer 23

Assess patients for clinical features of unstable bradycardia.

Hemodynamically unstable patients
  -   Initiate immediate treatment for unstable bradycardia (e.g., IV atropine, temporary cardiac pacing). 

Hemodynamically stable patients
    Severe symptoms (e.g., angina, recurrent syncope) OR SBP < 90 mm Hg: Manage as an inpatient with continuous telemetry.

No severe symptoms AND SBP ≥ 90 mm Hg: Diagnostic evaluation can be performed on an outpatient basis.

Identify and treat the underlying cause.

Question 24

B.22 Bradyarrhythmia

ECG findings SSS

Answer 24

Preferred initial diagnostic study: 12-lead ECG
Second line : ambulatory cardiac monitoring (typically in the following order) Holter monitor or external patch recorder
Event monitor or mobile cardiovascular telemetry

ECG
- non-respiratory sinus arrythmia, bradycardia, sinus arrest, sinoatrial pauses or SA Block

• in cases of tachycardia-bradycardia syndrome - atrial tachycardia, artial flutter, or artial fibrillation
• Holter monitor - detects bradycardic episodes and sinus pauses

Question 25

B.22 Bradyarrhythmia What other tests and findings can be done for SSS

Answer 25

Exercise stress testing - shows an inadequate increasing heart rate during physical exercise - i.e chronotropic incompetence Atropine Challenge Test - shows an inadequate increasing heart rate after administration of atropine Electrophysiology studies - may show prolonged sinus node recovery time

Question 26

B.22 Bradyarrhythmia SSS TX

Answer 26

Asymptomatic patients: observation Symptomatic patients Manage reversible causes of SSS. Severe and/or frequent symptoms of bradycardia due to irreversible causes First-line (after patient stabilization): permanent pacemaker placement Alternative: phosphodiesterase inhibitors

Question 27

B.22 Bradyarrhythmia SSS indications for permanent pacemaker placement

Answer 27

Permanent pacing decreases symptom frequency and improves quality of life. Indications First-line management for symptomatic SND caused by intrinsic or irreversible extrinsic factors Symptomatic SND caused by essential medications that cannot be stopped Symptomatic SND with chronotropic incompetence Important considerations: Permanent pacing is not routinely recommended in the following circumstances Asymptomatic or minimally symptomatic SND Symptoms in the absence of rhythm abnormalities of SND Nocturnal SND

Question 28

B.22 Bradyarrhythmia Definition Atrioventricular block (heart block)

Answer 28

AV block) is characterized by an interrupted or delayed conduction between the atria and the ventricles.

Question 29

B.22 Bradyarrhythmia AV block etiology

Answer 29

physiological: increased vagal tone Pathophysiological - idiopathic fibrosis of the conduction system - ischemic heart disease - cardiomyopathy - infections - Lyms, bacterial endocarditis - Hyperkalemia > 6.3 mEq/L Itrogenic - side effect of certain drugs - e.g. BB, CCB, digitalis - cardiac interventions e.g. alochol spetal ablation

Question 30

B.22 Bradyarrhythmia Definition First Degree AV Block

Answer 30

PR interval > 200 ms No interruption in atrial to ventricular conduction Rate of SA node = heart rate Often discovered incidentally on ECG

Question 31

B.22 Bradyarrhythmia First Degree AV Block Characteristics

Answer 31

may be found in healthy individuals e.g. athletes with increased vagal tone usually asymptomatic often discovered incidentally on ECG

Question 32

B.22 Bradyarrhythmia First Degree AV Block TX

Answer 32

clinical assessment for underlying disease e.g. structural heart abnormailty, electrolyte imbalance usually no speicifc tx pacemaker IF the patient also exhibits wide QRS complex on ECG --- identify the level of the AV block, within or below the bundle of HIS using intracardiac electrogram --- if conduction time form the bundle of His to the ventricles is > 100 ms - PACEMAKER PLACEMENT

Question 33

B.22 Bradyarrhythmia Second Degree AV Block - Mobitz type I Description

Answer 33

Progressive lengthening of the PR interval until a beat is dropped, which means a regular atrial impulse does not reach the ventricles (a normal P wave is not followed by a QRS complex) Mostly regular rhythm separated by short pauses, which may lead to bradycardia (regularly irregular rhythm) Rate of SA node > heart rate

Question 34

B.22 Bradyarrhythmia Second Degree AV Block - Mobitz type I Clinical Findings

Answer 34

Asymptomatic: Many patients may not show any symptoms. Symptoms of Reduced Cardiac Output: Some may experience dizziness, syncope, or bradycardia due to hypoperfusion. Irregular Pulse: Patients may present with an irregular pulse on examination

Question 35

B.22 Bradyarrhythmia Second Degree AV Block - Mobitz type I TX in asymptomatic pts

Answer 35

Clinical Evaluation: Assess for any underlying conditions such as structural heart diseases or electrolyte imbalances. Treatment: Generally, no specific treatment is required. Monitoring: Regular follow-ups with ECG and cardiac monitoring to track the progression of the condition.

Question 36

B.22 Bradyarrhythmia Second Degree AV Block - Mobitz type I TX in symptomatic pts

Answer 36

Hemodynamically Stable: Monitor using transcutaneous pacing pads. If symptoms do not improve, consider the placement of a permanent pacemaker. Hemodynamically Unstable: Administer atropine. Consider temporary cardiac pacing if there is no response to atropine.

Question 37

B.22 Bradyarrhythmia Second Degree AV Block - Mobitz type II Description

Answer 37

Single or intermittent nonconducted P waves without QRS complexes The PR interval remains constant. The conduction of atrial impulses to the ventricles typically follows a regular pattern, e.g.: 3:2 block: regular AV block with 3 atrial depolarizations but only 2 atrial impulses that reach the ventricles (heart rate = ⅔ SA node rate) 4:3 block: regular AV block with 4 atrial depolarizations but only 3 atrial impulses that reach the ventricles (heart rate = ¾ SA node rate) While 2:1 block follows a regular pattern, it cannot be classified as Mobitz type I or II and is classified separately

Question 38

B.22 Bradyarrhythmia Second Degree AV Block - Mobitz type II Clinical

Answer 38

Decreased Cardiac Output may lead to: Fatigue Dyspnea (shortness of breath) Chest pain Dizziness or syncope (fainting)

Question 39

B.22 Bradyarrhythmia Second Degree AV Block - Mobitz type II TX

Answer 39

Hemodynamically Stable Patients: - Monitor using transcutaneous pacing pads. - Assess for underlying conditions (e.g., structural heart disease, electrolyte imbalances). - If symptoms are not reversible, consider placing a permanent pacemaker. Hemodynamically Unstable Patients: - Administer atropine. - Consider temporary cardiac pacing. Note: Second-degree AV block (Mobitz type I) may progress to a third-degree block, necessitating monitoring and treatment.

Question 40

B.22 Bradyarrhythmia Third Degree AV Block - Complete Heart Block description

Answer 40

A complete block with no conduction between the atria and ventricles, resulting in AV dissociation on ECG.

Question 41

B.22 Bradyarrhythmia Third Degree AV Block - Complete Heart Block Characteristics

Answer 41

P waves and QRS complexes have independent rhythms. Escape Mechanism: Generated by sites located near the AV node or below the bundle of His. Distance of the impulse generation: The slower the ventricular escape, the wider the QRS complex. Blocks closer to the bundle of His typically show narrow QRS complexes. Prognosis: Sudden onset can lead to Stokes-Adams attacks due to the ineffective escape mechanism.

Question 42

B.22 Bradyarrhythmia Third Degree AV Block - Complete Heart Block Clinical Symptoms

Answer 42

Symptoms vary based on: Rate of Ventricular Escape Mechanism: - Bradycardia (< 40 bpm) can lead to cerebral hypoperfusion, causing symptoms like fatigue, irritability, apathy, dizziness, syncope, cognitive impairment, heart failure, and dyspnea. - Length of Asystole: -Symptoms may include nausea, dizziness, Stokes-Adams attacks, and potential cardiac arrest.

Question 43

B.22 Bradyarrhythmia Third Degree AV Block - Complete Heart Block TX

Answer 43

Hemodynamically Stable Patients: - Monitor using transcutaneous pacing pads. - Conduct a clinical assessment for underlying conditions (e.g., structural heart diseases, electrolyte imbalances). - If no reversible causes are found, place a permanent pacemaker. Hemodynamically Unstable Patients: - Administer Atropine. - Provide temporary transcutaneous or transvenous cardiac pacing. - For low blood pressure, administer dopamine. - For heart failure, administer dobutamine.

Question 44

B.22 Bradyarrhythmia List the main types of bradyarrhythmia.

Answer 44

Sinus bradycardia Sinus pause/arrest Sinoatrial (SA) exit block AV blocks: first-degree, Mobitz I (Wenckebach), Mobitz II, complete heart block Escape rhythms (junctional, ventricular)

Question 45

B.22 Bradyarrhythmia What’s the difference between Mobitz I and Mobitz II AV block?

Answer 45

Mobitz I PR interval - Progressively lengthens Dropped beats - After PR prolongation Location - AV node (usually) Stability - Often benign Mobitz II PR interval - Constant Dropped beats - Suddenly without warning Location - Below AV node (His–Purkinje) Stability - High risk — pacemaker needed

Question 46

B.22 Bradyarrhythmia What is the treatment for symptomatic bradycardia?

Answer 46

Atropine 0.5 mg IV, repeat q3–5 min (max 3 mg) If ineffective → transcutaneous pacing, dopamine or epinephrine infusion Long-term: Permanent pacemaker if chronic or irreversible cause

Question 47

B.22 Bradyarrhythmia Patient has HR 40 bpm but is asymptomatic. Do they need treatment?

Answer 47

Not necessarily. If they’re asymptomatic (e.g., athlete), observe only.

Question 48

B.22 Bradyarrhythmia Patient with AF has HR of 38. Is this bradyarrhythmia?

Answer 48

Yes — AF with slow ventricular response due to AV nodal disease or over-medication.

Question 49

B.22 Bradyarrhythmia Patient with Lyme disease develops syncope. What kind of bradyarrhythmia should you suspect?

Answer 49

High-grade AV block — can fluctuate and progress quickly. Needs pacing.

Question 50

B.22 Bradyarrhythmia Why might atropine fail in Mobitz II or complete heart block?

Answer 50

Because these are below the AV node, where atropine (vagal blocker) has minimal effect.

Question 51

B.22 Bradyarrhythmia Patient is bradycardic on digoxin. Can you give atropine?

Answer 51

Yes — unless they have digoxin toxicity, in which case pacing or Digibind is preferred due to risk of ventricular arrhythmias.

Question 52

B.22 Bradyarrhythmia How does hyperkalemia cause bradyarrhythmia?”

Answer 52

Suppresses conduction → slows SA node and blocks AV node/His-Purkinje system → can cause sine-wave ECG, arrest, or escape rhythms.

Question 53

B.22 Bradyarrhythmia How do you differentiate between sinus arrest and SA block on ECG?”

Answer 53

SA block: Pause is a multiple of P–P interval (timed drop) Sinus arrest: Pause is not a multiple of the basic rhythm

Question 54

B.22 Bradyarrhythmia When is a pacemaker indicated for bradycardia?”

Answer 54

Symptomatic sinus node disease Mobitz II or complete heart block Post-MI AV block that doesn’t resolve Post-ablation AV block Pause-dependent VT (e.g., long QT)