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