Bradycardia - Prof Budi S. Pikir, MD, PHD, FIHA PDF

Bradyarrhythmia Management
in Emergency Setting
Budi Susetyo Pikir
Nadya Luthfah
CARDIOVASCULAR EMERGENCIES COURSE
Bumi Surabaya Hotel, November 7-8th, 2015
1. Asymptomatic Bradycardia
2. Symptomatic Bradycardia
1. Hemodynamically Stable Bradycardia
2. Hemodynamically Unstable Bradycardia
1. Cardiac Etiologies
2. Extra-Cardiac Etiologies
BRADYCARDIA
any rhythm disorder with a heart rate less than 60 bpm
(usually less than 50 bpm)
Asymptomatic
Symptomatic :
elicit sign and symptoms
Unstable
Stable
Immediate Intervention
PATHOPHYSIOLOGY
Impulse Formation
Impulse Conduction
Sinus Node Dysfunction
Atrioventricular &
Intraventricular Conduction
Abnormality

EXTRINSIC CAUSES
INTRINSIC CAUSES
Idiopathic Degenerative Disorder
Coronary Artery Disease
Hypertensive heart disease
Cardiomyopathy
Trauma
Surgery for Congenital Heart Dis.
Inflammation
Infection
Neuromuscular Disorder
Familial Disorder
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

MANIFESTATIONS
a.
a. Sinus Bradycardia
b. Sinus Pause/Arrest
c. Sinoatrial Exit Block
b.
c.
d. Tachycardia-Bradycardia Syndrome
e. Chronotropic Incompetence
d.
Atrioventricular Conduction
Abnormality
PERMANENT CAUSES
Idiopathic Fibrosis
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
Infection
Metabolic Electrolyte Imbalance
Traumatic
Atrioventricular Conduction
Abnormality
MANIFESTATIONS
a. First-degree AV block
a.
b.
b. Second-degree AV block
Mobitz type I (Wenkebach)
Mobitz type I
4 : 3 atrioventricular block
c. High-grade AV block .
Second-degree AV block
Mobitz type II
d. Third-degree AV block
Junctional Escape Rhythm
Ventricular Escape Rhythm
c.
d.
e. Atrioventricular Dissociation
Intraventricular Conduction
Abnormality
MANIFESTATIONS
Left Bundle Branch Block
Right Bundle Branch Block
Left Anterior & Posterior Hemiblock
Bifascicular/Trifascicular Block
Nonspesific Intraventricular
Conduction Defect
STEP-BY-STEP DIAGNOSTIC APPROACH
HISTORY
Symptoms due to Bradycardia
Etiology and Trigerring Factors

Age
Asymptomatic
History of disease
Symptomatic
History of medication (blockers, CCB, and digoxin)
Dizziness, light-headedness,vertigo
Pre-syncope, syncope
Easy fatigability,
reduced exercise capacity
Irritability, apathy, forgetfulness,
inability to concentrate
Angina, dyspnea
How Often ?
Suddenly
Continuously/Daily
Intermittent
Heart Failure symptomps

PHYSICAL EXAMINATION
Additional Sign secondary to :
Palpation of peripheral pulse/

cardiac auscultation
Complete Heart Block

Cannon a-waves in JVP
a slow and regular heart beat of <50 bpm

an irregular pulse of varying intensity
Heart Failure
Third heart sound, rales,
Jugular venous distension
Lower extremity oedema
Hypothiroidism
Dry or coarse skin or hair
Facial oedema
Poor Cardiac Output
Hypotension
Low peripheral perfusion
Mental status changes
DIAGNOSTIC TEST
12-lead ECG
the first test in the diagnosis of bradycardia
Laboratory test to aid identification of the

underlying cause
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

DIAGNOSTIC TEST
Further Investigations for diagnosing
bradyarrhytmias after the initial evaluation
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
TREATMENT
Bradycardia Algorithm
(with Pulse)
Assess appropriateness for clinical condition.
Heart rate typically <50/min if bradyarrhythmia.
Identify and treat underlying cause

Maintain patent airway; assist breathing as necessary
Oxygen (if hypoxemic)
Cardiac monitor to identify rhythm; monitor blood pressure and oximetry
IV access
12-lead ECG if available; dont delay therapy
Bradycardia Algorithm (with Pulse) cont.

No
Monitor and Observe
Persistent bradyarrhythmia causing :

Hypotension ?
Acutely altered mental status ?
Signs of shock ?
Ischemic chest discomfort ?
Acute heart failure ?
Yes
Atropine
If atropine ineffective :
Transcutaneous pacing
OR
Dopamine infusion
OR
Epinephrine infusion
Doses/Details
Atropine IV Dose:
First Dose : 0.5 mg bolus
Repeat every 3-5 minutes
Maximum : 3 mg
Dopamine IV infusion
2-10 mcg/kg per minute
Consider :
Expert consultation
Transvenous pacing
Epinephrine IV infusion
2-10 mcg per minute
MEDICATION
Anticholinergic drug :
- Adrenergic Agonist :
Atropine Sulfate
Epinephrine,Dopamine, Isoproterenol
First-line drug for acute

symptomatic bradycardia
Second-line drug for acute

blocking the action of the vagus

nerve on the heart resulting in an
increased heart rate
used as infusions in the bradycardia

algorithm if atropine is ineffective or
contraindication
should be avoided in hypothermic

bradycardia
an equally effective alternative to

transcutaneous pacing
not effective for Mobitz type II Second Degree AV Block and

Complete AV Block
TEMPORARY PACEMAKER
Trans-Cutaneous/TCP
Treatment of choice for
with sign of poor perfusion
which doesnt respond to
atropin
Temporizing measure,
painful in conscious patients
Contraindicated for
hypotermia and not
recommended for asystole
Trans-Venous
indicated if the patient does not
respond to chronotropic drugs
should be limited to cases of :

high-degree AV block without
escape rhythm
Life threatening
bradyarrhythmias, such as
during interventional procedures
acute settings (acute myocardial
infarction, drug toxicity,
concomitant systemic infection)
Transcutaneous Cardiac Pacing
Cardiac Arrest ?
PERMANENT PACEMAKER
Indications for Pacing in patients with Persistent Bradycardia
Recommendations
Class
Level
Sinus Node Disease

1. Pacing is indicated when symptoms can clearly be attributed to bradycardia.
2. Pacing may be indicated when symptoms are likely to be due to bradycardia,

even if the evidence is not conclusive
IIb
3. Pacing is not indicated in patients with sinus bradycardia which is

asymptomatic or due to reversible causes.
III
Acquired Atrioventricular (AV) Block

1. Pacing is indicated in patients with third- or second-degree type 2 AV block
irrespective of symptoms
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 at
electrophysiological study
IIa
3. Pacing is not indicated in patients with AV block which is due to reversible

causes.
III
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?
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?
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 and
suspect an overdose. They left the bottles behind.
What medications cause bradycardia?
TOXIC BRADYCARDIA
due to Medication
Beta Blockers
Cardiac glycosides (digoxin)
Cholinergic agents
Clonidine/Imidazolines (alpha2 agonists)
Opioids/Sedative Hypnotics
Phenylpropanolamine (alpha1 agonists)
Sodium channel blockers
THE BIG FOUR

Beta 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
Introduction
Maybe put in some physiology and table 17.11 page

393 of lilly
TOXIC BRADYCARDIA
due to Metabolic Abnormalities
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
Effects of hyperkalaemia on the

ECG
Serum 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 and
bradycardia:
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
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-sparing
diuretics and potassium supplements.
For an excellent review of the management of

hyperkalaemia, check out this podcast by Scott
Weingart.
Hyperkalaemia
Tall, symmetrically peaked T waves.
This patient had a serum K+ of 7.0.
Hyperkalaemia:
Slow junctional rhythm.
Intraventricular conduction delay.
Peaked T waves.
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.
Hyperkalaemia:
Sine wave appearance with severe hyperkalaemia (K+ 9.9 mEq/L).
Hyperkalaemia:
Broad complex rhythm with atypical LBBB morphology.
Left axis deviation.
Absent P waves.
Hyperkalaemia:
Huge peaked T waves.
Sine wave appearance.
This patient had severe hyperkalaemia (K+ 9.0 mEq/L) secondary to
rhabdomyolysis.
SUMMARY
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
A proper diagnosis including a symptom-rhythm
correlation is extremely important and is generally
established by noninvasive diagnostic studies (12lead 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
Be aware of TOXIC BRADYCARDIA

due to Drug Toxicities or Metabolic
Abnormalities
Thank You

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Bradyarrhythmia Management

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Bumi Surabaya Hotel, November 7-8th, 2015

Bumi Surabaya Hotel, November 7-8th, 2015

Sinus Node Dysfunction

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Sinus Node Dysfunction

Bumi Surabaya Hotel, November 7-8th, 2015

Sinus Node Dysfunction

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Bumi Surabaya Hotel, November 7-8th, 2015

Bumi Surabaya Hotel, November 7-8th, 2015

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

STEP-BY-STEP DIAGNOSTIC APPROACH

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Etiology and Trigerring Factors

History of medication (blockers, CCB, and digoxin)

Heart Failure symptomps

Bumi Surabaya Hotel, November 7-8th, 2015

Palpation of peripheral pulse/

Complete Heart Block

a slow and regular heart beat of <50 bpm

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Laboratory test to aid identification of the

Potassium, Calcium, Magnesium

Myocardial Ischaemia or infarction

Renal Function Test

Serum Digoxin level

Bumi Surabaya Hotel, November 7-8th, 2015

Prolonged ECG Monitoring

Provocative Test Strategy

Carotid Sinus Massage

External loop recorder

Tilt table test

Remote at-home telemetry

Implantable loop recorder

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Identify and treat underlying cause

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Bradycardia Algorithm (with Pulse) cont.

Persistent bradyarrhythmia causing :

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

First-line drug for acute

Second-line drug for acute

blocking the action of the vagus

used as infusions in the bradycardia

should be avoided in hypothermic

an equally effective alternative to

not effective for Mobitz type II Second Degree AV Block and

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015