Download arrhythmias

ARRHYTHMIAS
Jamil Mayet
Arrhythmias - learning objectives
– Mechanisms of action of antiarrhythmic drugs
– Diagnosis
• To differentiate the different types of SVTs on the ECG
• To diagnose ventricular tachyarrhythmias from the ECG
• To differentiate different bradyarrhythmias from the ECG
– Treatment
• Understand different options; drugs versus ablation; pacing
• Importance of anticoagulation in atrial fibrillation
• Appreciate increasing use of ICDs
Tachyarrhythmias
• Antiarrhythmic drugs
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Vaughn-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
Supraventricular arrhythmias
• Atrial fibrillation
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Rapid atrial discharge (350-600/min)
AV node cannot conduct all impulses
Cardioversion (electrical or drugs) can restore SR
Class Ia, Ic, III drugs may maintain SR
Px often rate control and stroke prevention
Rate control with digoxin, class II, III, IV drugs
Anticoagulation with warfarin in most cases
Causes include ht, ischaemia, rheumatic hd,
alcohol, thyrotoxicosis, cardiomyopathy, PTE,
thoracotomy, idiopathic (“lone”)
Atrial fibrillation
Supraventricular arrhythmias
• Atrial flutter
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Rapid atrial discharge (250-350/min)
Occasional 1:1 conduction
More often 2:1, 3:1, 4:1 conduction
Diagnosis aided by increasing block eg CSM, adenosine
Cardioversion (electrical or drugs) can restore SR
Class Ia, Ic, III drugs may maintain SR
Rate control with digoxin, class II, III, IV drugs
?Anticoagulation
Similar causes to atrial fibrillation
Atrial flutter
Atrial flutter with 2:1 block
Supraventricular arrhythmias
• Atrial tachycardia
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Atrial discharge slower (120-250/min)
Occasional 1:1 AV node conduction
More usually 2:1 conduction
With AV block often due to digitoxicity
Cardioversion (electrical or drug) can restore SR
Overdrive pacing is an alternative
Atrial tachycardia
Supraventricular arrhythmias
• AV nodal re-entry tachycardia
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Re-entry circuit within AV node
Rate usually 130-250/min
CSM or adenosine may terminate arrhythmia
Alternatives include cardioversion (electrical or
drug) and overdrive pacing
– Prophylaxis with class II, IV, III, Ia, Ic drugs
AV nodal re-entry tachycardia
Supraventricular arrhythmias
• Pre-excitation syndromes
– WPW syndrome due to accessory pathway (bundle
of Kent)
– 0.15% of population
– Accessory pathway allows rapid conduction
– Resting ECG shows short PR and delta wave
– May cause AV re-entry tachycardia
– A fib may be dangerous due to rapid conduction
Supraventricular arrhythmias
• Pre-excitation syndromes
– Digoxin/verapamil may increase conduction in bundle of
Kent and should be avoided
– Class Ia, Ic and III drugs slow ventricular rate and may
cardiovert to SR
– Electrical cardioversion especially in fast A fib
– Lown-Ganong-Levine syndrome: connection between
atria and His bundle; short PR; no delta wave
WPW syndrome
Ventricular arrhythmias
• Ventricular tachycardia
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Broad complex tachycardia
Independent atrial activity
Capture/fusion beats
Risk of degeneration to ventricular fibrillation
Cardioversion (electrical or drug) can restore SR
Overdrive pacing is an alternative
Idioventricular tachycardia; rate<120/min; often
related to reperfusion in AMI; Px often unnecessary
Ventricular tachycardia
Ventricular tachycardia
Ventricular arrhythmias
• Torsades de pointes
– Twisting pattern
– Precipitated by prolonged QT
– May be congenital, metabolic or drug induced
• Ventricular fibrillation
– Death
– Electrical cardioversion
Torsades de Pointes
Rhythm Strip During Episode of Sudden Death
VT versus SVT with aberrant conduction
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History of IHD (VT)
Age>60 (VT)
Independent P wave activity (VT)
Very broad QRS (>140ms) (VT)
Resting BBB of same morphology (SVT)
Concordant QRS direction (V1-V6) (VT)
If in doubt assume VT
EP studies and ablation therapy
• Diagnosis and curative treatment of AVNRT,
AVRT (eg WPW) atrial tachy and atrial flutter
• Potential curative treatment of VT
• Stratification of risk in patients with VT
– Guide need for implantable defibrillator insertion
– Guide antiarrhythmic drug treatment
• Potential for treatment of A fib
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
Bradyarrhythmias
• Sinus node disease
– Bradycardias usually caused by idiopathic
fibrosis, ischaemia or drugs
• Tachy-brady syndrome
– Combination of tachycardic and bradycardic
episodes
Sinus node disease
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
AV node disease
1st degree heart block
2nd degree heart block (2:1)
AV node disease
Complete (3rd degree) heart block
Bradyarrhythmias
• Treatment of symptomatic bradyarrhythmias
often consists of pacing
• In the short-term drugs may be used to augment
conduction eg atropine, isoprenaline