BRADYARRHYTHMIAS

DR. ROSE TOM

Basics
• Arrhythmia/dysrhythmia = deviation from physiologic heart rhythm
• Bradycardia < 60/min. Tachycardia > 100/min.
Calculation
of HR
• The standard paper speed is
25mm/sec:
• 1 SMALL square (1mm) = 0.04 sec
(40ms)
• 5 SMALL squares (5mm) = 1
LARGE square = 0.2 sec (200ms)
• 5 LARGE squares = 1 second
Large square
method
• 300 large squares is equal to 1
minute at a paper speed of
25mm/sec.
• Useful for regular rhythm
Small square method
 R wave method

• Rate = Number of R waves

(rhythm strip) X 6

• (number of complexes (count R waves) on the

rhythm strip gives the average rate over a ten-second
period)

• Useful for slow and/or irregular

rhythms
 Physiology of heart rhythm
• Origin of depolarization
- sinoatrial (SA) node
• Transfer of depolarization
- Atrial
- Atrioventricular (AV) node
- Intraventricular Conduction system
 Non-pharmacological Pharmacological
Normal during sleep Beta-blockers

Increased vagal tone (e.g athletes) Calcium-channel blockers

Inferior myocardial infarction Digoxin

Sinus
Bradycardia Hypothyroidism,Hypothermia Opiates

Sinus rhythm with a resting heart Brainstem herniation – Cushing Amiodarone

rate of < 60 bpm in adults reflex
ECG- Each normal P wave followed Myocarditis Organophosphate poisoning
by normal QRS + HR< 60/min
I. Sinus Node Dysfunction (Sick Sinus
Syndrome)
• Sinus Bradycardia
• Sinus Arrhythmia — associated with sinus node dysfunction in the
elderly in the absence of respiratory pattern association ( Inspiration --
↑Heart rate by ↓ vagal tone; Expiration -↓ HR by ↑ vagal tone)
• Sinus Pause and Sinus Arrest
• Sinoatrial Exit Block
• Bradycardia – tachycardia syndrome
 Anatomical Basis
• The SA node consists of two main groups of cells:
- A central core of pacemaker cells (P cells) that produce the sinus
impulses
- An outer layer of transitional cells (T cells) that transmit the sinus
impulses out into the right atrium.
• Sinus node dysfunction can result from either:
- Failure of the P cells to produce an impulse  This leads to sinus
pauses and sinus arrest
- Failure of the T cells to transmit the impulse  This leads to Sino-
atrial exit block.
Sinus Node Dysfunction (Sick Sinus
Syndrome)
1. Sinus pause/ Sinus arrest:   Impulses are not produced.
Complete absence of P-waves that may last from 2 seconds to
several minutes. (Unless Lower pacemakers produce "escape"
rhythms)

2. Sinoatrial nodal exit block (SA exit block): P Cells working, T

cells not transmitting impulses.
Impulses are produced at regular interval , but not transmitted.
Sinoatrial nodal exit block (SA exit block)
• First Degree SA Block: Slowing of impulse exit. This cannot be
seen on the surface ECG 

• Second Degree SA Block

Neither P wave nor QRS is recorded
- Type I: (Wenckebach): progressively decreasing P-P intervals prior to a
pause; the pause has a duration ˂ 2 P-P cycles
- Type II: P-P interval is a multiple of the normal P-P intervals

• Third Degree SA Block: The impulse does not reach the

atrium at all ( Thus cannot be differentiated from sinus arrest on
the surface ECG)
Sinoatrial nodal exit block (SA exit block)
4. Bradycardia-tachycardia syndrome:
• Runs of tachycardia interspersed with long sinus pauses (up to 6 seconds).
• The sinus rate is extremely slow, varying from 40 bpm down to around 10
bpm in places.
• Sinus beats are followed by paroxysms of junctional tachycardia at around
140 bpm.
AV BLOCK
• Delay or interruption in conduction of atrial impulse through – AV
node and bundle of His.
 • Delay in conduction through system
• Prolonged PR interval > 0.2 seconds ( 5 small squares)
1st degree bloc • PR interval – Time taken for impulse to travel from SA node to AV node + Time
k taken for impulse to travel through AV node, bundle of His and bundle branches
to ventricles.
• SIGNIFICANCE : Associated with CAD, acute rheumatic carditis, digitalis, beta
blocker
• Treatment: not required
2nd degree AV block

• Intermittent failure or interruption of AV conduction.

• Sinus impulse from SA node → activate atria → P wave → blocked
within AV node.
• ECG- Each P will not be f/b QRS
2nd degree Mobitz type I (Wenckebach)
block
• Transmission through AV node become increasingly difficult until it
fails completely, and a beat is dropped.
• Progressive lengthening of PR interval until one atrial depolarization
is not conducted to ventricles
• Defect usually in AV node
• Progressive prolongation of the PR
interval culminating in a non-conducted P wave:
• PR interval is longest immediately before dropped
beat
• PR interval is shortest immediately after dropped
beat
• Causes:
• Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
• Increased vagal tone (eg. athletes)
• Inferior MI
• Myocarditis
• Following cardiac surgery (mitral valve repair, Tetralogy of Fallot
 repair)
Clinical Significance

• Mobitz I is usually a benign rhythm, causing minimal haemodynamic

disturbance and with low risk of progression to third degree heart block
• Treatment
• Asymptomatic patients do not require treatment.
• Symptomatic patients , with haemodynamic instability – Atropine and
temporary peacemaking.
• Symptomatic patients, hemodynamically stable – Continous monitoring
• Permanent pacing is rarely required
2nd degree Mobitz type II block

• PR intervals remain unchanged prior to a P wave that fails to conduct

to ventricles.

• Mechanism : due to failure of conduction at the level of the His-

Purkinje system
• intermittent non-conducted P waves without progressive prolongation of the PR
interval
Causes
• Anterior MI (due to septal infarction with necrosis of the bundle branches)
• Idiopathic fibrosis of the conducting system (Lenègre-Lev disease)
• Cardiac surgery, especially surgery occurring close to the septum e.g. mitral
valve repair
• Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease)
• Autoimmune (SLE, systemic sclerosis)
• Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis)
• Hyperkalaemia
• Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
Clinical Significance

• Most patients have symptoms – Fatigue, dyspnea, chest pain, syncope,

sudden cardiac death

• Mobitz II - more likely than Mobitz I to be associated with

haemodynamic compromise, severe bradycardia and progression to 3rd
degree heart block

• Mobitz II mandates immediate admission for cardiac monitoring,

backup temporary pacing and ultimately insertion of a permanent
pacemaker.
Treatment of Mobitz type 2

Unstable patient Stable patient

Urgent beta-adrenergic agents Continous monitoring
Temporary pacing Look for reversible cause

Permanent pacemaker if Permanent pacemaker if

cause not reversible cause not reversible
ECG
3rd degree block (complete heart block)

• In complete heart block, there is complete absence of AV conduction,

with none of the atrial impulses conducted to the ventricles.
• The perfusing rhythm is maintained by junctional or ventricular
 escape rhythm.
• Severe bradycardia due to absence of AV conduction
• The ECG demonstrates complete AV dissociation, with
independent atrial and ventricular rates (Wide QRS +
QRS independent of P)
Causes of complete heart block

• Inferior myocardial infarction

• AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-blockers
, digoxin)
• Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s
disease
• Amyloidosis, sarcoidosis
• Myocarditis, endocarditis
• Hyperkalemia
• Traumatic- post cardiac surgery
Clinical significance
• All the patients are symptomatic (fatigue, dyspnoea, chest pain, syncope,
sudden cardiac death)

• Patients with third degree heart block are at high risk of ventricular
standstill and sudden cardiac death

• They require urgent admission for cardiac monitoring, backup temporary

pacing and usually insertion of a permanent pacemaker
THANK YOU