arrhythmias
DESCRIPTION
ARRHYTHMIAS. TACHYCARDIA>100/min BRADYCARDIATRANSCRIPT
ARRHYTHMIAS
• TACHYCARDIA >100/min
• BRADYCARDIA <50/min
• CARDIAC ARRESTElectrical activity– Chaotic VF– Absent asystole
Action potential
-60
0
Propagating action potential
-60
0
Propagating action potential
-60
0
Propagating action potential
-60
0
Propagating action potential
-60
0
Propagating action potential
TREATMENT STRATEGY
• PROLONG ACTION POTENTIAL• MODIFY CONDUCTION• STABILISE AUTOMATICITY• INTERRUPT REENTRY
– PHARMACOLOGICAL– PHYSICAL
• ELECTRICAL STIMULATION– ATP/SHOCK TACHY– PACE BRADY
DEPOLInward
REPOLoutward
Propagating action potential
TREATMENT STRATEGY
• PROLONG ACTION POTENTIAL• MODIFY CONDUCTION• STABILISE AUTOMATICITY• INTERRUPT REENTRY
– PHARMACOLOGICAL– PHYSICAL
• ELECTRICAL STIMULATION– ATP/SHOCK TACHY– PACE BRADY
DEPOLInward
REPOLoutward
DEPOLInward
REPOLoutward
AUTOMATICITY
Physiological: Sinus nodePathological: Reduction/depolarisation of resting membrane potential (e.g. Ischaemia)
TREATMENT STRATEGY
• PROLONG ACTION POTENTIAL• MODIFY CONDUCTION• STABILISE AUTOMATICITY• INTERRUPT REENTRY
– PHARMACOLOGICAL– PHYSICAL
• ELECTRICAL STIMULATION– ATP/SHOCK TACHY– PACE BRADY
Tachyarrhythmias
• Antiarrhythmic drugs– 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
• 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
• STABILISE AUTOMATICITY• PROLONG ACTION POTENTIAL• SLOW CONDUCTION• INTERRUPT REENTRY
– PHARMACOLOGICAL– PHYSICAL
• ELECTRICAL STIMULATION– ATP/SHOCK TACHY– PACE BRADY
RFA: success rates
• 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 drugsJACC2000;35:1898 prospective, randomised – 61 pts
• 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 WAVELETSInes, Garrey
MOTHER WAVELewis
HYPEREXCITABILITYEngelmann, Winterberg
WPW syndrome
AV re-entry tachycardia
TREATMENT STRATEGY
• PROLONG ACTION POTENTIAL• MODIFY CONDUCTION• STABILISE AUTOMATICITY• INTERRUPT REENTRY
– PHARMACOLOGICAL– PHYSICAL
• ELECTRICAL STIMULATION– ATP/SHOCK TACHY– PACE BRADY
Ventricular tachycardia
Ventricular tachycardia
TREATMENT STRATEGY
• 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
• PROLONG ACTION POTENTIAL• MODIFY CONDUCTION• STABILISE AUTOMATICITY• INTERRUPT REENTRY
– PHARMACOLOGICAL– PHYSICAL
• ELECTRICAL STIMULATION– ATP/SHOCK TACHY– PACE BRADY
Medtronic Implantable Defibrillators (1989-1997)
209 cc 113 cc
80 cc 72 cc 54 cc71 mm x 58 mm x 16 mm2 4/5 in x 2 1/3 in x 2/3 in
80 cc
Implanatable defibrillators
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
• 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