BRADY ARRHYTHMIA

Dr. Yonas N
Assistant professor,EMCC
February 2023
 Basics
 Arrhythmia/dysrhythmia = deviation from
physiologic heart rhythm
Measurements
Bradyarrhythmia

 INITIAL APPROACH TO THE STABLE

PATIENT
 The focused evaluation of the patient:
 Determining the presenting complaint(s)
 Obtaining the medical history
 Identifying medication use
 Performing a physical examination
 Initiating continuous cardiac rhythm monitoring,
reviewing the 12-lead ECG
 Analyzing the cardiac rhythm on the rhythm
monitor, a printer strip, or the ECG.
 Symptoms may include:
 palpitations

 lightheadedness

 Fatigue or weakness

 Ischemic symptoms:

-chest pain
-nausea
-dyspnea
-lightheadedness, may be due to dysrhythmia-induced
ischemia.
 INITIAL APPROACH TO THE UNSTABLE
PATIENT
 An unstable patient needs rapid assessment and
treatment to prevent cardiovascular collapse.
 Establish an IV line, initiate cardiac rhythm
monitoring, obtain an ECG, and be prepared for drug
or electrical therapy.
 Bradydysrhythmia describes rhythms with a ventricular rate
slower than 60 beats/min
 Bradydysrhythmias can be broadly categorized as
 Bradycardias and

 Atrioventricular (AV) blocks .

 The bradycardias include sinus bradycardia, junctional

rhythm, idioventricular rhythm, atrial fibrillation/flutter with a
slow ventricular response,
 Bradydysrhythmias due to AV blocks include second-degree
(usually type II) and third-degree AV bloc
 The most common bradycardia is sinus bradycardia, followed
by junctional rhythm and, less commonly, idioventricular
rhythm.
 These rhythms are found in both stable and unstable patients.
 Atrial fibrillation or flutter with slow ventricular response are
uncommon
 sick sinus syndrome

 AV nodal blocking agent

 If the patient is unstable, the vast majority of AV blocks are

third-degree heart block followed much less frequently by
second-degree AV block.
Mechanism of bradydysrhythmia

 Automaticity and refractoriness of cardiac cells as well as the

 Conduction of impulses abnormality

 About 80% of bradydysrhythmias caused by factors external

to the cardiac electrical system including
 acute coronary syndrome,

 drug effects or overdose, and

 hypoxia with cardiac hypoperfusion.

 Emergent treatment of bradydysrhythmia
 heart rate is slower than 50 to 60 beats/min
 Accompanied by hypotension or hypoperfusion and/or

 The bradydysrhythmia is due to structural disease of

the infranodal conduction system.
 Medications used to increase heart rate in
symptomatic bradycardias include:

Atropine, β-adrenergic agonists, and glucagon.

 Atropine- enhances the automaticity of the sinoatrial (SA) node
and potentiates conduction through the AV node by direct
vagolytic activity.
 β-Adrenergic agents- stimulate both chronotropic and inotropic
cardiac activity, as well as enhancing electrical conduction within
the AV node and infranodal system.
 Glucagon- stimulates inotropic and chronotropic cardiac activity
independent of the β-adrenergic receptors.

 Glucagon is primarily used for bradycardias due to cardiotoxicity

from β-blocker or calcium channel–blocker overdose.
 Atropine 0.5-milligram IV push, may repeat every 3–
5 min until desired heart rate is achieved or to total
dose of 3 milligrams (0.04 milligram/kg)
 Most effective for bradydysrhythmias due to sinus
and AV nodal disease.
 Dopamine IV infusion at rate 2–20 micrograms/kg
per min, titrate to desired heart rate
 May precipitate myocardial ischemia and ectopy
 Epinephrine IV infusion at rate 2–10
micrograms/min, titrate to desired heart rate
 May precipitate myocardial ischemia and ectopy
 Glucagon 3–10 milligrams IV infused over 1–2 min,
followed by an IV continuous infusion of 1–5
milligrams/h
 Used for cardiotoxicity associated with β-blocker and
calcium channel blocker overdose
 Nausea and vomiting are often limiting side effects
 Tachyphylaxis may develop during infusion
 Transcutaneous pacing can be applied quickly and
is the most appropriate pacing method for the acutely
symptomatic patient.
 Transvenous pacing requires physician expertise
and specialized equipment for insertion and proper
placement
 Disease-specific therapies for bradycardia:
 Treatment of hyperkalemia
 Treatment of toxicity from:
 calcium channel blockers
 β-blockers
 digitalis.
A 45 years old man who is on nifidipine 20mg PO
BID presented with chest pain.
PR=45/MIN BP=80/40MMHG, SPO2-95%WRA…

???
 SINUS BRADYCARDIA
 Clinical Significance
 represents a reduction of the SA node discharge rate.

-Sinus bradycardia can be:

(1) physiologic (in well-conditioned athletes, during sleep, or
with vagal stimulation),
(2) pharmacologic (β-blockers, digoxin, opioids, calcium
channel blockers),
(3) pathologic (hypoxia, acute inferior wall myocardial ischemia
or infarction, increased intracranial pressure, carotid sinus
hypersensitivity, hypothyroidism).
 Treatment
 usually does not require specific treatment unless the
heart rate is slower than 50 beats/min and there is
evidence of hypoperfusion
 Correct underlying causes.
 Use atropine in the unstable patient, followed by
transcutaneous cardiac pacing and infusions of
dopamine or epinephrine if there is no response to
atropine.
 JUNCTIONAL RHYTHM
 If SA node discharges slow or fail to reach the AV node,
junctional escape beats will produce a rhythm usually at a rate
between 40 and 60 beats/min.
 If the junctional beats continue in sequence, then a junctional
rhythm is present.
 In most cases, junctional escape beats do not conduct
retrograde into the atria, so a QRS complex without a P wave
is usually seen.
 At times, enhanced AV nodal automaticity overrides the sinus
node and produces:
 Accelerated junctional rhythm with a rate of 60 to 100
beats/min or
 Junctional tachycardia with a rate greater than 100
beats/min.
 Usually, the enhanced junctional pacemaker captures both the
atria and ventricles.
 ??
 Rate?
 ??
 Rate?
 Clinical Significance
 Junctional escape beats may occur whenever

there is a long enough pause in the impulses reaching the AV

node, as with sinus bradycardia, slow phase of sinus arrhythmia,
or during the pause after premature beats
 Sustained junctional escape rhythms may

be seen with heart failure, myocarditis, hypokalemia, or digitalis

toxicity.
 Treatment Isolated, infrequent junctional escape beats
usually do not require specific treatment.
 If sustained junctional escape rhythms are producing
symptoms, the underlying cause should be treated.
 Atropine can be used to accelerate the SA node discharge rate
and enhance AV nodal conduction.
 Accelerated junctional rhythm and junctional tachycardia
usually do not produce significant symptoms.
 IDIOVENTRICULAR RHYTHMS
 Idioventricular rhythms are of ventricular origin manifesting
as regular widened QRS complexes without evidence of atrial
activity.
 An idioventricular rhythm has a ventricular rate of 30 to 50
beats/min, and the
 Accelerated idioventricular rhythm has a ventricular rate of
50 to 75 beats/min.
 Clinical Significance
 Most commonly seen in the setting of an ST-segment
elevation myocardial infarction.
 An accelerated idioventricular rhythm that appears
during successful fibrinolysis of an occluded coronary
artery is termed a reperfusion dysrhythmia.
 The slower versions, can produce dizziness, weakness,
syncope, chest pain, and dyspnea; profound
hypoperfusion may occur.
 Treatment
 If hypoperfuson, drugs to increase the heart rate are
appropriate.
 Atropine is recommended, although the likelihood of
successful treatment is low.
 Cardiac pacing is often needed, starting via the transcutaneous
route.
 In most cases of accelerated idioventricular rhythm, treatment
is not necessary.
 Heart blocks

 Clues for diagnoses are:

1) RR rate ,Rhythm
2) Is every QRS have preceding P , the PR interval?
3) Is there P without QRS?
4) The PR prolongation-prolonged and constant PR,or variably
prolonged until final one drop
5) The QRS width—in distal to bundle of HIS it is widened,
proximally to the bundle narrow.
 FIRST DEGREE A-V HEART BLOCK
 P wave: normal and QRS: normal Rhythm: regular
 Conduction: impulse originates in the SA node but has prolonged
conduction in the AV junction;
 P-R interval is > 0.20 seconds,and is the most common conduction
disturbance. Both healthy and diseased
 First degree AV block can be due to:
 inferior MI, digitalis toxicity ,hyperkalemia ,increased vagal
tone ,acute rheumatic fever ,myocarditis.
 Interventions include treating the underlying cause and observing
for progression to a more advanced AV block.
SECOND DEGREE A-V BLOCK MOBITZ TYPE I
(WENCKEBACK)

 Rate: irregular, QRS: normal Rhythm: irregular

 P wave: normal morphology
 Conduction: the P-R interval is progressively longer until one
P wave is blocked
 It occurs in the AV node above the Bundle of His.
 It is often transient and may be due to acute inferior MI or
digitalis toxicity.
 Treatment is usually not indicated as this rhythm usually
produces no symptoms.
 SECOND DEGREE A-V BLOCK
MOBITZ TYPE II
 Rate: variable,while P wave: normal with constant P-P
 QRS: usually widened , this is usually associated with BBB
 Conduction: P-R interval may be normal or prolonged, but it is
constant until one P wave is not conducted to the ventricles.
 Rhythm: usually regular
 This block usually occurs below the Bundle of His and may
progress into a higher degree block.
 It can occur after an acute anterior MI due to damage in the
bifurcation or the bundle branches.
 It is more serious than the type I block.
 Treatment is usually artificial pacing.
THIRD DEGREE (COMPLETE)
A-V BLOCK
 Rate: atrial rate is usually normal; ventricular rate is usually less than
70/bpm.
 P wave: normal with constant P-P intervals, but not followed by QRS
complexes,
 QRS: may be normal or widened depending on where the escape
pacemaker is located in the conduction system
 Complete block of the atrial impulses occurs at the A-V junction,
common bundle or bilateral bundle branches.
 Another pacemaker distal to the block takes over in order to activate the
ventricles
 May be caused by:digitalis toxicity ,acute infection ,MI and or
degeneration of the conductive tissue.
 Treatment modalities include: external pacing and atropine for acute,
symptomatic episodes and permanent pacing for chronic complete heart
block.
 Thank you


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