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Bradyarrhythmia Management
in Emergency Setting
Budi Susetyo PikirNadya Luthfah
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1. Cardiac Etiologies
2. Extra-Cardiac Etiologies
1. Hemodynamically Stable Bradycardia2. Hemodynamically Unstable Bradycardia
1. Asymptomatic Bradycardia2. Symptomatic Bradycardia
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any rhythm disorder with a heart rate less than 60 bpm
(usually less than 50 bpm)
BRADYCARDIA
Asymptomatic
Symptomatic :
elicit sign and symptoms
Unstable Stable
Immediate Intervention
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PATHOPHYSIOLOGY
Impulse Formation Impulse Conduction
Sinus Node Dysfunction Atrioventricular &
Intraventricular Conduction
Abnormality
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Sinus Node Dysfunction
INTRINSIC CAUSES
Idiopathic Degenerative Disorder
Coronary Artery Disease
Hypertensive heart disease
Cardiomyopathy
Trauma
Surgery for Congenital Heart Dis.
Inflammation
Infection
Neuromuscular Disorder
Familial Disorder
EXTRINSIC CAUSES
Medication
Anti-Arrhythmic Drugs
Cardiac Glycosides
Anti-Hypertensive Agents
Anti-Psychotic Agents
Autonomically mediated
Vasovagal syncope (cardioinhibitory)
Carotid sinus hypersensitivity
Hypothyroidism
Intracranial Hypertension
Hypothermia
Electrolyte Imbalance
Hypoxia
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Sinus Node Dysfunction
MANIFESTATIONS
a. Sinus Bradycardia
b. Sinus Pause/Arrest
c. Sinoatrial Exit Block
d. Tachycardia-Bradycardia Syndromee. Chronotropic Incompetence
a.
b.
c.
d.
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Atrioventricular Conduction
AbnormalityPERMANENT CAUSES
Idiopathic Fibrosis
Coronary Artery Disease
Congenital Heart disease
Cardiomyopathy
Infiltrative Disease
Trauma and Surgery
Autoimmune Disease
Inflammation
Infection
Neuromuscular Disorder
Tumors
REVERSIBLE CAUSES
Medication
anti-Arrhythmic Drugs
Cardiac Glycosides
anti-Hypertensive Agents
anti-Psychotic Agents
Autonomically mediated
Neurocardiogenic syncope
Carotid sinus hypersensitivity
Heightened Vagal Tone
Coronary Artery Disease
Infection
Metabolic Electrolyte Imbalance
Traumatic
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Atrioventricular Conduction
Abnormality
MANIFESTATIONS
a. First-degree AV block
b. Second-degree AV block
Mobitz type I (Wenkebach)
Mobitz type I
4 : 3 atrioventricular block
3 : 1 atrioventricular block
c. High-grade AV block .
Second-degree AV block
Mobitz type II
2 : 1 atrioventricular block
d. Third-degree AV block
Junctional Escape RhythmVentricular Escape Rhythm
e. Atrioventricular Dissociation
a.
b.
c.
d.
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Intraventricular Conduction
Abnormality
MANIFESTATIONS
Left Bundle Branch Block
Right Bundle Branch Block
Left Anterior & Posterior Hemiblock
Bifascicular/Trifascicular Block
Nonspesific Intraventricular
Conduction Defect
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STEP-BY-STEP DIAGNOSTIC APPROACH
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HISTORY
Symptomatic
Dizziness, light-headedness,vertigo
Pre-syncope, syncope
Easy fatigability,
reduced exercise capacity
Irritability, apathy, forgetfulness,
inability to concentrate
Angina, dyspnea
Heart Failure symptomps
Asymptomatic
Etiology and Trigerring Factors
Age
History of disease
History of medication (β-
blockers, CCB, and digoxin)
Symptoms due to Bradycardia
How Often ?• Suddenly
• Continuously/Daily
• Intermittent
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PHYSICAL EXAMINATION
Additional Sign secondary to :
Complete Heart Block
Cannon a-waves in JVP
Heart Failure
Third heart sound, rales,
Jugular venous distensionLower extremity oedema
Hypothiroidism
Dry or coarse skin or hair
Facial oedema
Poor Cardiac Output
HypotensionLow peripheral perfusion
Mental status changes
Palpation of peripheral pulse/
cardiac auscultation
a slow and regular heart beat of
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12-lead ECG
• the first test in the diagnosis of bradycardia
Laboratory test – to aid identification of the
underlying cause
DIAGNOSTIC TEST
Underlying Disease Laboratory Investigations
Electrolyte Imbalance Potassium, Calcium, Magnesium
Myocardial Ischaemia or infarction Cardiac Enzyme
Metabolic Cause Renal Function Test
Thyroid Function test
Medication Intoxication Serum Digoxin level
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Further Investigations for diagnosing
bradyarrhytmias after the initial evaluation
DIAGNOSTIC TEST
Prolonged ECG Monitoring
Strategy
Provocative Test Strategy
Holter Carotid Sinus Massage
External loop recorder Tilt table test
Remote at-home telemetry Electrophysiological study
Implantable loop recorder Exercise Test
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TREATMENT
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Bradycardia Algorithm
(with Pulse)
Assess appropriateness for clinical condition.
Heart rate typically
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Bradycardia Algorithm (with Pulse) cont.
Persistent bradyarrhythmia causing :
• Hypotension ?
• Acutely altered mental status ?• Signs of shock ?
• Ischemic chest discomfort ?
• Acute heart failure ?
AtropineIf atropine ineffective :
• Transcutaneous pacing
OR
• Dopamine infusion
OR
• Epinephrine infusion
Consider :
• Expert consultation
• Transvenous pacing
Monitor and Observe
Doses/DetailsAtropine IV Dose:First Dose : 0.5 mg bolus
Repeat every 3-5 minutes
Maximum : 3 mg
Dopamine IV infusion2-10 mcg/kg per minute
Epinephrine IV infusion2-10 mcg per minute
No
Yes
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TEMPORARY PACEMAKER
Trans-Cutaneous/TCP
Treatment of choice for
symptomatic bradycardia
with sign of poor perfusion
which doesn’t respond toatropin
Temporizing measure,
painful in conscious patients
Contraindicated for
hypotermia and notrecommended for asystole
Trans-Venous
indicated if the patient does notrespond to chronotropic drugs
should be limited to cases of :
high-degree AV block withoutescape rhythm
Life threateningbradyarrhythmias, such asduring interventional procedures
acute settings (acute myocardial
infarction, drug toxicity,concomitant systemic infection)
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Transcutaneous Cardiac Pacing
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Cardiac Arrest ?
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Indications for Pacing in patients with Persistent Bradycardia
PERMANENT PACEMAKER
Recommendations Class Level
Sinus Node Disease
1. Pacing is indicated when symptoms can clearly be attributed to bradycardia.I B
2. Pacing may be indicated when symptoms are likely to be due to bradycardia,
even if the evidence is not conclusiveIIb C
3. Pacing is not indicated in patients with sinus bradycardia which is
asymptomatic or due to reversible causes.III C
Acquired Atrioventricular (AV) Block
1. Pacing is indicated in patients with third- or second-degree type 2 AV block
irrespective of symptoms
I C
2. Pacing should be considered in patients with second-degree type 1 AV block
which causes symptoms or is found to be located at intra- or infra-His levels atelectrophysiological study IIa C
3. Pacing is not indicated in patients with AV block which is due to reversible
causes.III C
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TOXIC BRADYCARDIA
Beta Blockers
Calcium Channel Blockers
Cardiac glycosides (digoxin)
Cholinergic agents
Clonidine/Imidazolines (alpha2 agonists)
Opioids/Sedative Hypnotics
Phenylpropanolamine (alpha1 agonists)
Sodium channel blockers
Can we eliminate any of these based on clinical presentation?
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CASE It is 3:30 am when the paramedics patch to tell you
they are on scene with a man who has a pulse of 45 /
m and SBP of 80
What medical conditions could cause this?
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CASE CONTINUED… The patient arrives. Vitals are unchanged after 2 L N/S
and 2 mg of atropine. He is obtunded but breathing
spontaneously. His wife says he has a history or atrial
fibrillation, angina, hypertension and depression. The
paramedics found a lot of pill bottles beside him andsuspect an overdose. They left the bottles behind.
What medications cause bradycardia?
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TOXIC BRADYCARDIA
due to Medication
Beta Blockers
Calcium Channel Blockers
Cardiac glycosides (digoxin)
Cholinergic agents
Clonidine/Imidazolines (alpha2 agonists)
Opioids/Sedative Hypnotics
Phenylpropanolamine (alpha1 agonists)
Sodium channel blockers
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THE “BIG FOUR” Beta Blockers
Calcium Channel Blockers
Cardiac Glycosides
Sodium Channel Blockers :
Extracellullar : Alkaloid :
Saxitoxin Neosaxitoxin
Tetrodotoxin
Intracellular :
Class I antiarrhytmic agents
Class Ia : quinidine, procainamide & disopyramide
Class Ib : ;idocaone, ,exiletine, tocainnide, phemytoin
Class Ic : encainide, flecainide, moricizine, propafenone
Local Anesthesia
Various anticonvulsants
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Introduction
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Maybe put in some physiology and table 17.11 page
393 of lilly
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Definitions
Hyperkalaemia is defined as a potassium level > 5.5
mEq/L
Moderate hyperkalaemia is a serum potassium > 6.0
mEq/L
Severe hyperkalaemia is a serum potassium > 7.0 mE/L
TOXIC BRADYCARDIA
due to Metabolic Abnormalities
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Effects of hyperkalaemia on the
ECGSerum potassium > 5.5 mEq/L is associated with repolarization abnormalities:
• Peaked T waves (usually the earliest sign of hyperkalaemia)
Serum potassium > 6.5 mEq/L is associated with progressive paralysis of the atria:
• P wave widens and flattens
• PR segment lengthens
• P waves eventually disappear
Serum potassium > 7.0 mEq/L is associated with conduction abnormalities andbradycardia:
• Prolonged QRS interval with bizarre QRS morphology
• High-grade AV block with slow junctional and ventricular escape rhythms
• Any kind of conduction block (bundle branch blocks, fascicular blocks)
• Sinus bradycardia or slow AF
• Development of a sine wave appearance (a pre-terminal rhythm)
Serum potassium level of > 9.0 mEq/L causes cardiac arrest due to:• Asystole
• Ventricular fibrillation
• PEA with bizarre, wide complex rhythm
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Handy Tips
Suspect hyperkalaemia in any patient with a new
bradyarrhythmia or AV block, especially patients with
renal failure, on haemodialysis or taking any
combination of ACE inhibitors, potassium-sparingdiuretics and potassium supplements.
For an excellent review of the management of
hyperkalaemia, check out this podcast by Scott
Weingart.
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Hyperkalaemia
Tall, symmetrically peaked T waves.
This patient had a serum K+ of 7.0.
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Hyperkalaemia:
• Slow junctional rhythm.
• Intraventricular conduction delay.
• Peaked T waves.
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This ECG displays many of the features of
hyperkalaemia:
Prolonged PR interval.
Broad, bizarre QRS complexes — these merge with both
the preceding P wave and subsequent T wave. Peaked T waves.
This patient had a serum K+ of 9.2.
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Hyperkalaemia:
• Sine wave appearance with severe hyperkalaemia (K+ 9.9 mEq/L).
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Hyperkalaemia:
• Broad complex rhythm with atypical LBBB morphology.• Left axis deviation.
• Absent P waves.
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Hyperkalaemia:
• Huge peaked T waves.
• Sine wave appearance.
This patient had severe hyperkalaemia (K+ 9.0 mEq/L) secondary to
rhabdomyolysis.
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Bradyarrhythmias are defined as any rhythm
disorder with a heart rate less than 60 bpm (usually
less than 50 bpm)
Clinical presentation ranges from asymptomatic to
various symptoms due to the slow heart rate
Disorder to the impulse formation or conduction
system can be caused by intrinsic , extrinsic, or
combination of both factors
SUMMARY
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A proper diagnosis including a symptom-rhythm
correlation is extremely important and is generally
established by noninvasive diagnostic studies (12-
lead electrocardiogram, Holter electrocardiogram)
Atropine sulfate is the first-line treatment for Symptomatic bradycardia.
Sympatomimethic drugs and temporary pacemaker
implantation are used if atropine is ineffective or
contraindication
SUMMARY
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Be aware of TOXIC BRADYCARDIA
due to Drug Toxicities or MetabolicAbnormalities
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Thank You
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