Conducting system of heart and ventriculr arrhythmias

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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