Download AV node disease

ARRHYTHMIAS
• TACHYCARDIA
• BRADYCARDIA
• CARDIAC ARREST
Electrical activity
– Chaotic
VF
– Absent
asystole
>100/min
<50/min
Action potential
0
-60
Propagating action potential
0
-60
Propagating action potential
0
-60
Propagating action potential
0
-60
Propagating action potential
0
-60
Propagating action potential
TREATMENT STRATEGY
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PROLONG ACTION POTENTIAL
MODIFY CONDUCTION
STABILISE AUTOMATICITY
INTERRUPT REENTRY
– PHARMACOLOGICAL
– PHYSICAL
• ELECTRICAL STIMULATION
– ATP/SHOCK TACHY
– PACE BRADY
DEPOL
Inward 
REPOL
outward
Propagating action potential
TREATMENT STRATEGY
•
•
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•
PROLONG ACTION POTENTIAL
MODIFY CONDUCTION
STABILISE AUTOMATICITY
INTERRUPT REENTRY
– PHARMACOLOGICAL
– PHYSICAL
• ELECTRICAL STIMULATION
– ATP/SHOCK TACHY
– PACE BRADY
DEPOL
Inward 
REPOL
outward
DEPOL
Inward 
REPOL
outward
AUTOMATICITY
Physiological: Sinus node
Pathological: Reduction/depolarisation of resting membrane potential (e.g. Ischaemia)
TREATMENT STRATEGY
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•
PROLONG ACTION POTENTIAL
MODIFY CONDUCTION
STABILISE AUTOMATICITY
INTERRUPT REENTRY
– PHARMACOLOGICAL
– PHYSICAL
• ELECTRICAL STIMULATION
– ATP/SHOCK TACHY
– PACE BRADY
Tachyarrhythmias
• Antiarrhythmic drugs
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Vaughan-Williams Classification
Drugs divided according to EP effects on cells
All are negatively inotropic
Can also be pro-arrhythmic
Tachyarrhythmias
• Class I
– Impede Na transport across cell membrane
– Ia increase AP duration eg quinidine,
disopyramide, procainamide
– Ib shorten AP duration eg lignocaine,
mexilitene, propafenone
– Ic little effect on AP eg flecainide
Tachyarrhythmias
• Class II
– Interfere with effects of SNS on the heart eg
beta blockers
• Class III
– Prolong AP duration but do not effect initial Na
dependent phase eg sotalol, amiodarone
• Class IV
– Antagonise Ca transport across cell membrane
– SA and AV node particularly susceptible eg
verapamil, diltiazem
TREATMENT STRATEGY
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•
PROLONG ACTION POTENTIAL
MODIFY CONDUCTION
STABILISE AUTOMATICITY
INTERRUPT REENTRY
– PHARMACOLOGICAL
– PHYSICAL
• ELECTRICAL STIMULATION
– ATP/SHOCK TACHY
– PACE BRADY
AV Nodal block
• [Class II
– Interfere with effects of SNS on the heart eg beta
blockers]
• Class III
– Prolong AP duration but do not effect initial Na
dependent phase eg sotalol, amiodarone
• Class IV
– Antagonise Ca transport across cell membrane
– SA and AV node particularly susceptible eg verapamil,
diltiazem
• Adenosine
– Specific AV nodal block
EP study: standard fixed wires
EP study: standard fixed wires
RADIOFREQUENCY ABLATION
TREATMENT STRATEGY
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STABILISE AUTOMATICITY
PROLONG ACTION POTENTIAL
SLOW CONDUCTION
INTERRUPT REENTRY
– PHARMACOLOGICAL
– PHYSICAL
• ELECTRICAL STIMULATION
– ATP/SHOCK TACHY
– PACE BRADY
RFA: success rates
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AVJ
98%
AVNRT
97%
AP
93% (L 95%, R 89%)
AFl
95%
Infarct VT
60-90%, long term 50%
Idiopathic VT 90%
Focal AF
60%
RFA: treatment of choice
• AVJ
98%
• AVNRT
97%
• AP
93% (L 95%, R 89%)
• AFl
95%
• Idiopathic VT 90%
______________________________
? Infarct VT
60-90%, long term 50%
? Focal AF
60%
Atrial flutter
Atrial Flutter: RFA vs AA drugs
JACC2000;35:1898 prospective, randomised – 61 pts
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SR at 21 months: 36%AAD vs 80% RFA
Rehospitalised:
63% AAD vs 22% RFA
AF:
53% AAD vs 29% RFA
QOL:
no change AAD
improvement RFA
TREATMENT STRATEGY
•
•
•
•
PROLONG ACTION POTENTIAL
MODIFY CONDUCTION
STABILISE AUTOMATICITY
INTERRUPT REENTRY
– PHARMACOLOGICAL
– PHYSICAL
• ELECTRICAL STIMULATION
– ATP/SHOCK TACHY
– PACE BRADY
Concepts of AF: 1900-2000
MULTIPLE WAVELETS
Ines, Garrey
MOTHER WAVE
Lewis
HYPEREXCITABILITY
Engelmann, Winterberg
WPW syndrome
AV re-entry tachycardia
TREATMENT STRATEGY
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PROLONG ACTION POTENTIAL
MODIFY CONDUCTION
STABILISE AUTOMATICITY
INTERRUPT REENTRY
– PHARMACOLOGICAL
– PHYSICAL
• ELECTRICAL STIMULATION
– ATP/SHOCK TACHY
– PACE BRADY
Ventricular tachycardia
Ventricular tachycardia
TREATMENT STRATEGY
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PROLONG ACTION POTENTIAL
MODIFY CONDUCTION
STABILISE AUTOMATICITY
INTERRUPT REENTRY
– PHARMACOLOGICAL
– PHYSICAL
• ELECTRICAL STIMULATION
– ATP/SHOCK TACHY
– PACE BRADY
Rhythm Strip During Episode of Sudden Death
TREATMENT STRATEGY
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PROLONG ACTION POTENTIAL
MODIFY CONDUCTION
STABILISE AUTOMATICITY
INTERRUPT REENTRY
– PHARMACOLOGICAL
– PHYSICAL
• ELECTRICAL STIMULATION
– ATP/SHOCK TACHY
– PACE BRADY
Implanatable defibrillators
Medtronic Implantable Defibrillators (1989-1997)
209 cc
113 cc
80 cc
80 cc
72 cc
54 cc
71 mm x 58 mm x 16 mm
2 4/5 in x 2 1/3 in x 2/3 in
Implanatable defibrillator in-situ
Sinus node disease
AV node disease
1st degree heart block
2nd degree heart block (2:1)
AV node disease
Complete (3rd degree) heart block
Bradyarrhythmias
• AV node disease
– 1st degree; prolonged PR interval
– 2nd degree; Mobitz type I (Wenckebach); increasing PR
interval then non-conducted P wave
– 2nd degree; Mobitz type II; non-conducted P waves
– 2nd degree; 2:1 or 3:1 AV node block
– 3rd degree; complete heart block
• AV block usually caused by idiopathic fibrosis;
other causes include MI, drugs and congenital block
TREATMENT STRATEGY
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PROLONG ACTION POTENTIAL
MODIFY CONDUCTION
STABILISE AUTOMATICITY
INTERRUPT REENTRY
– PHARMACOLOGICAL
– PHYSICAL
• ELECTRICAL STIMULATION
– ATP/SHOCK TACHY
– PACE BRADY
Bradyarrhythmias
• Treatment of symptomatic bradyarrhythmias
often consists of pacing
• In the short-term drugs may be used to augment
conduction eg atropine, isoprenaline