Bradycardia - Prof Budi S. Pikir, MD, PhD, FIHA.pdf

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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    Bradyarrhythmia Management

    in Emergency Setting

    Budi Susetyo PikirNadya Luthfah

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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    1. Cardiac Etiologies

    2. Extra-Cardiac Etiologies

    1. Hemodynamically Stable Bradycardia2. Hemodynamically Unstable Bradycardia

    1.  Asymptomatic Bradycardia2. Symptomatic Bradycardia

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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    PATHOPHYSIOLOGY

    Impulse Formation Impulse Conduction

    Sinus Node Dysfunction Atrioventricular &

    Intraventricular Conduction

     Abnormality

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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

     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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

     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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    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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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    Be aware of TOXIC BRADYCARDIA

    due to Drug Toxicities or MetabolicAbnormalities

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    CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015

    Thank You