This document provides an overview of the anatomy, physiology, and pathophysiology of the heart's conductive system and ventricular arrhythmias. It begins with a description of the anatomy of the heart's conductive system, including the sinoatrial node, atrioventricular node, bundle of His, bundle branches, and Purkinje fibers. It then discusses the physiology of cardiac conduction, including the properties of cardiac muscle cells and the differences between slow-response and fast-response action potentials. Finally, it covers the pathophysiologic bases of arrhythmias and various types of ventricular arrhythmias such as premature ventricular contractions, accelerated idioventricular rhythm, ventricular tachycardia, torsades de pointes,

1. Conducting system of heart and ventricular
arrhythmias.
Dr. Debashis Priyadarshan Sahoo
PGT, First year
Department of General medicine
NEIGRIHMS

2. Contents:
1. Anatomy of conductive system of heart
2. Physiology of conductive system of heart
3. Pathophysiologic basis of arrhythmia
4. Different types of Ventricular arrhythmias.
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3. Anatomy of conducting system of heart:
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SA Node
Internodal fibers
AV Node
Bundle of His
Left bundle branch
Right bundle branch
Purkinje fiber
(Fig. 1)
(Conduction Pathways)

4. Physiology of conduction:
• Properties of heart muscles:
1. Excitability
2. Contractility
3. Auto rhythmicity
4. Long refractory period
5. Gap junctions forming syncytium
6. Intercalated discs
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ICD
Syncytium
(Fig. 2)
(Histological structure of cardiac muscle)

5. Action potentials:
Slow response type
1. SA Node
2. AV node
• Long depolarization period and
short repolarization period.
• RMP: -55 to -65mv
Fast response type
1. Bundle of His, Bundle
branches
2. Purkinje fibers,
3. Ventricular fibers
• Short depolarization period and
long repolarization period.
• RMP: -90mv
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6. Slow response action potential Fast response action potential
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Fig. 3 Fig. 4
(Source : Ganong’s review of Medical Physiology.)

7. Rate of depolarization
• Determines speed of impulse
conduction.
Rate of repolarization
• Determines rhythmicity of heart.
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Part Speed (m/s)
SA Node 0.05-1
AV node 0.05-1 (slowest)
Bundle of his 1
Purkinje 1.5-4 (fastest)
Part Rhythmicity
SA Node 80-100/min
AV node 60/min
Bundle of his 25-40/min
Purkinje 15-40/min
(Table. 1) (Table. 2)

8. Pathophysiologic basis of arrhythmias:
1. Enhanced abnormal automaticity
(ischemia/hypoxia)
2. Re-entry and circus movements.
(slowed conduction velocity,
dilation of heart, damage to
purkinje system)
3. Triggered activity (after
depolarization: early/late)
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(Fig. 5)

9. Ventricular Arrhythmias:
1. Ventricular Premature complexes
2. Accelerated idioventricular rhythm
3. Ventricular tachycardia
4. Ventricular fibrillation
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10. Ventricular premature complexes:
• Origin: Site distal to purkinje network.
• Slow ventricular activation and a wide QRS complexes.
• Causes:
1. Increasing age
2. During acute MI or Post MI
3. Heart failure
4. Digoxin toxicity
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(Fig. 6)

11. • Commonly associated with fully compensatory pause. So duration
between QRS complexes before and after is twice the sinus rate.
• Generally does not conduct to atrium, if conducts, it falls in refractory
period.
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(Fig. 7)

12. Accelerated Idioventricular rhythm:
• Benign rhythm.
• Increased ventricular automaticity.
• Brief self limiting arrhythmia.
• Seen in absence of any structural heart disease
• Cause:
1. Increased automaticity in bundle branch or
2. Ventricular purkinje system fasciculation.
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13. • ECG:
1. Rate slightly above normal sinus rate but less than 120.
2. Abnormal QRS morphology
3. No preceding sinus P wave
• It reflects reperfusion of the infract territory and is a good sign.
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(Fig. 8)

14. Ventricular tachycardia:
• Three or more consecutive PVCs at a rate exceeding 100 or more beats
per minute.
• AV dissociation with complete AV asynchrony.
• Common causes:
1. Acute myocardial infraction
2. Chronic coronary artery disease
3. Cardiomyopathy
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(Fig. 9)

15. Types of ventricular Tachycardia:
Monomorphic VT
• Single focus ectopic impulse
• QRS complexes of same heights.
• Causes:
Ischemic heart disease
Cardiomyopathies Etc.
Polymorphic VT
• Multiple focus ectopic impulses
• QRS complexes of different
heights.
• Most common cause is
myocardial infraction.
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(Fig. 10) (Fig. 11)

16. Sustained VT
• VT lasts more than 30s
• Mostly symptomatic
• Patients with myocardial
infraction and chronic coronary
artery diseases
Non sustained VT
• VT lasts less than 30s
• Mostly asymptomatic
• Patients in
Ischemic and nonischemic
heart diseases,
Electrolyte imbalances,
Drug toxicity etc.
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17. • Symptoms:
1. Palpitation
2. Symptoms of low cardiac output: Dizziness, dyspnea, syncope
• ECG Changes: It can start from left ventricle (RBBB morphology) or right ventricle
(LBBB morphology).
1. Tachycardia (>120/min)
2. Regular RR interval
3. Broad abnormal QRS complexes (>160ms)
4. Fusion beat
5. Capture beat
6. Positive and negative concordance (V1-V6)
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18. Fusion Beat
Capture beat
Broad QRS complexes
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(Fig. 12)

19. Management of Ventricular tachycardia:
• Non sustained VT:
1. Asymptomatic: No therapy
2. Symptomatic: Beta blockers, if not controlled CCB are used.
• Sustained VT:
1. Hemodynamically unstable: Biphasic Synchronized DC cardioversion is the treatment of
choice. Commonly 200J (100-360J).
2. Hemodynamically stable patient:
a) With good LV function: Procainamide
b) LV dysfunction: Amiodarone
c) VT in MI: Lignocaine
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20. Torsades de pointes:
• Complication of prolonged ventricular repolarization.
• Polymorphic VT triggered by prolonged QT interval.
• Non sustained, repetitive.
• Common in women.
• Can be congenital and acquired.
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(Fig. 13)

21. Causes:
• Electrolyte abnormality: Hypocalcemia, hypokalemia, hypomagnesemia
• Drugs:
1. Class Ia, Class III antiarrhythmics
2. Antibiotics (Macrolides, clindamycin), Antifungal (ketoconazole), Antiviral
(Amantadine)
3. Antipsychotics (Haloperidol and TCAs)
4. Antihistaminic (Terfenadine, astemizole and fexofenadine)
• Endocrine causes: Hypothyroidism, hyperparathyroidism
• Cardiac causes: MI
• CNS causes: CNS bleed/ infraction
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22. Treatment:
• Congenital: Beta blocker.
• Hemodynamically unstable: Defibrillation
• Conscious and hemodynamically stable:
a) IV magnesium sulfate
b) Temporary pacing
c) Implantable cardioverter defibrillator
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23. Ventricular fibrillation:
• Uncoordinated, very rapid, irregular and ineffective ventricular
contractions caused by many chaotic impulses.
• It may be preceded by VPCs, ST changes, pauses, QT prolongation,
VT.
• Terminal arrhythmia.
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(Fig. 14)

24. • Causes: Coronary artery disease, cardiomyopathies,
myocarditis, trauma, cardiac tamponade, electrolyte
imbalances, electric shock, drugs, seizures, CVA.
• ECG:
a) Chaotic irregular deflections of varying impulses.
b) Non identifiable P wave, QRS complexes and T wave.
c) Heart rate 150-500bpm
d) Amplitude gradually decreases from coarse to fine VF, resemble
asystole.
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(Fig. 15)

25. • Significance:
a) Ventricles unable to contract synchronously resulting in
immediate loss of cardiac output.
b) It proceed to a mechanical standstill of heart, where heart will be
unable to contract further.
• Treatment: Defibrillation.
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26. Thank You.
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