B.22 Bradyarrhythmia Flashcards
B.22 Bradyarrhythmia
definition
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
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Cardiac Causes of Brady Cardia
Acute or Chronic Ischemic Heart Disease
Coronary Artery Disease
Valvular Heart Disease
Degenerative Primary electrical Disease
Sick Sinus Syndrome
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Extracardiac Causes
Hypothyroidism
Electrolyte Imbalance - Hyperkalemia
Autonomic/Neuorgenic Causes
Autoimmunity
Drugs
Drug Abuse
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Pathomechanism
depressed automactity of the heart
conduction block
escape rhytms
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List the Atrial Origin bradyarrhythmias
Respiratory Sinus Arrhythmia
Sinus Bradycardia
Sinus Pause or Arrest
Tachycardia-bradycardia Syndrome
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Respiratory Sinus Arrhytmia
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
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Sinus Bradycardia
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
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Sinus Pause or arrest
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)
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Tachycardia-bradycardia syndrome
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
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List AV node Origin bradyarrythmias
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
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First Degree AV block
Physiological response
Increased vagal tone
Drugs: beta blocker or calcium channel blocker
ECG
PR interval > 200 m
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Second Degree AV Block
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
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Third Degree
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
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Sick Sinus Syndrome
Definition
Sinus node dysfunction (SND), previously called sick sinus syndrome, is an abnormality in sinoatrial (SA) node action potential generation or conduction
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SSS Risk Factors
Coronary artery disease
Hypertension
Diabetes mellitus
Obesity
Right bundle branch block
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SSS Etiology Intrinsic Factors
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)
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SSS Etiology Extrinsic Factors
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
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How does β-blockers cause bradyarrthymia
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.
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How does digoxin cause bradyarrthymia
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.
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How does nondihydropyridine calcium channel blockers (verapamil, diltiazem) cause bradyarrthymia
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.
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mechanism of SSS
↓ SA node automaticity
SA exit block (impulses generated but not transmitted to atria)
Alternating suppression and bursts of tachyarrhythmia (tachy-brady syndrome)
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clinical features of SSS
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.
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Management of SSS
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.
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ECG findings SSS
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
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What other tests and findings can be done for SSS
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
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SSS TX
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
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SSS indications for permanent pacemaker placement
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
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Definition Atrioventricular block (heart block)
AV block) is characterized by an interrupted or delayed conduction between the atria and the ventricles.
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AV block etiology
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
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Definition First Degree AV Block
PR interval > 200 ms
No interruption in atrial to ventricular conduction
Rate of SA node = heart rate
Often discovered incidentally on ECG
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First Degree AV Block Characteristics
may be found in healthy individuals e.g. athletes with increased vagal tone
usually asymptomatic
often discovered incidentally on ECG
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First Degree AV Block TX
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
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Second Degree AV Block - Mobitz type I Description
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
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Second Degree AV Block - Mobitz type I Clinical Findings
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
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Second Degree AV Block - Mobitz type I TX in asymptomatic pts
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.
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Second Degree AV Block - Mobitz type I TX in symptomatic pts
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.
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Second Degree AV Block - Mobitz type II Description
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
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Second Degree AV Block - Mobitz type II Clinical
Decreased Cardiac Output may lead to:
Fatigue
Dyspnea (shortness of breath)
Chest pain
Dizziness or syncope (fainting)
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Second Degree AV Block - Mobitz type II TX
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.
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Third Degree AV Block - Complete Heart Block description
A complete block with no conduction between the atria and ventricles, resulting in AV dissociation on ECG.
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Third Degree AV Block - Complete Heart Block Characteristics
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.
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Third Degree AV Block - Complete Heart Block Clinical Symptoms
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.
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Third Degree AV Block - Complete Heart Block TX
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.
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List the main types of bradyarrhythmia.
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)
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What’s the difference between Mobitz I and Mobitz II AV block?
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
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What is the treatment for symptomatic bradycardia?
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
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Patient has HR 40 bpm but is asymptomatic. Do they need treatment?
Not necessarily. If they’re asymptomatic (e.g., athlete), observe only.
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Patient with AF has HR of 38. Is this bradyarrhythmia?
Yes — AF with slow ventricular response due to AV nodal disease or over-medication.
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Patient with Lyme disease develops syncope. What kind of bradyarrhythmia should you suspect?
High-grade AV block — can fluctuate and progress quickly. Needs pacing.
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Why might atropine fail in Mobitz II or complete heart block?
Because these are below the AV node, where atropine (vagal blocker) has minimal effect.
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Patient is bradycardic on digoxin. Can you give atropine?
Yes — unless they have digoxin toxicity, in which case pacing or Digibind is preferred due to risk of ventricular arrhythmias.
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How does hyperkalemia cause bradyarrhythmia?”
Suppresses conduction → slows SA node and blocks AV node/His-Purkinje system → can cause sine-wave ECG, arrest, or escape rhythms.
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How do you differentiate between sinus arrest and SA block on ECG?”
SA block: Pause is a multiple of P–P interval (timed drop)
Sinus arrest: Pause is not a multiple of the basic rhythm
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When is a pacemaker indicated for bradycardia?”
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)
