Arrhythmias

T D Chawana
 Aetiology
Congenital abnormalities of structure (eg
accessory AV connection)
Congenital abnormalities of function (eg
hereditary ion channelopathies)
Electrolyte imbalances- hypokalaemia,
hypomagnaesemia
Hypoxia
Hormonal imbalances- hypo- or hyperthyroidism
Drugs and toxins- alcohol, caffeine
 Anatomy
SAN- at the junction of SVC and high lateral
right atrium
-a cluster of cells that generates the initial
electrical impulse of each heart beat
Generated impulse propagated and
transmitted in an orderly fashion
SANadjacent cellsatrial myocytes and
specialised internodal tractsAVN
 Cont.
AVN- on the right side of the inter-atrial septum
Slower conduction velocity, therefore delays
impulse transmission
AVNodal transmission is dependant on heart rate,
autonomic tone and circulating catecholamines
Annulus fibrosus electrically insulates atria from
ventricles except in the anteroseptal region
AVNbundle of HISinterventricular
septumright and left bundle
branchesPurkinje fibresetc
 Physiology
Fast channel tissues-working atrial and
ventricular myocytes, His-Purkinje system
Slow channel tissues- SA and AV nodes
Normal heart rate- 60-100 beats/min
Sinus bradycardia- during sleep, young people,
athletes
Sinus tachycardia- exercise, emotion, illness,
pyrexia
 Types of arrhythmias
Tachycardia- heart going too fast
->100 beats per minute

Bradycardia- heart going too slow

-<60 beats per minute

Irregular heart beat

 Classification
By site- atria or ventricles
In atria- atrial or supraventricular arryhthmias
In ventricules- ventricular arrhythmias

By what happens to the heart rhythm when

they occur
Tachycardia
Bradycardia
 Classification
Those resulting from an abnormality in impulse
generation (aka autonomic arrhythmias)

Those resulting from an abnormality in impulse

conduction (reentrant arrhythmias)
 Signs and symptoms
May be asymptomatic
Palpitations- sensation of missed, rapid or
forceful beats
Symptoms of hemodynamic compromise-
dyspnea, chest discomfort, presyncope,
syncope
Cardiac arrest
Polyuria occassionally
 Atrial arrhythmias
Ectopic beats
Atrial fibrillation
Atrial flutter
Supraventricular tacchycardia
Wolf-Parkinson-White syndrome
Sick sinus syndrome
 Ectopic beats
Premature or extra beats
Often benign
Reassure patient
Require pharmacological treatment
infrequently
 Atrial fibrillation
Paroxysmal/intermittent- come and go,
resolve spontaneously within 7 days
Persistent- episodes that last beyond 7 days,
require medical intervention to terminate
Longstanding persistent- continuous
fibrillations for >1 year
Permanent
 Atrial fibrillation
Atria quiver like a bag of worms
Inefficient or no contraction at all
Treatment- pharmacological and surgery
 Atrial flutter
Rapid but coordinated electrical stimulation of
the atria
Leads to a rapid pulse
Atria are stimulated so fast that they do not
effectively empty blood
Due to a loop of impulse in the atria
Treatment- surgery
 Supraventricular tachycardias
Fast atrial rhythm
Due to extra connections btwn atria and
ventricles
Difficult to control with drugs
Treatment often surgery
 Wolff-Parkinsonism-White syndrome
A type of supraventricular tachychardia
Consists of tachycardia that is caused by extra
connection between the atria and ventricules
 Sick sinus syndrome
Reduced firing by SAN
Results in bradycardia
Can have alternating bradycardia and
tachycardia
Common in the elderly
Due to degenerative changes
 Other.
Sinus arrhythmia- cyclic changes in heart rate
during breathing, can be found in healthy
individuals

Sinus tacchycardia- SAN fires rapidly resulting in

tachycardia, a normal response to exercise

Multifocal atrial tachycardia- multiple locations

within the atria fire, heart beat 100-250/min,
common in >50yrs, and patients often with lung
disease
 Ventricular arrhythmias
Ectopic beats

Ventricular fibrillation

Ventricular tachycardia
 Ectopic beats
As for atria
 Ventricular fibrillation
Rapid firing of electrical impulse in the
ventricles
Cause ventricles to quiver and not completely
empty blood
Requires prompt treatment
If not, there is reduced perfusion in heart and
brain, and death
Survivors should have a defibrillator (ICD)
implanted
 Ventricular tachycardia
Rapid, regular heart beat arising in the
ventricules
Usually fatal
Requires prompt action
 Diagnosis
History- positive family hx, palpitations,

Examination

Tests- Electrocardiogram (ECG), Holter

monitor (ECG for 24-48 hours), implantable
heart monitoring, echocardiogram, heart scan,
coronary angiogram, exercise stress tests
(treadmill tests)
 Management
Non- surgical

Surgical (the CryoMaze procedure)

 Non-surgical treatment
Pharmacologic- anti-arrhythmic drugs

Ablation- destroying affected tissue by

radiation or cold

Implantation of permanent pacemaker (to

provide a reliable heartbeat) OR internal
cardioverter defibrillator (ICD) (for those at
risk of life-threatening ventricular arrhythmias

 Pharmacological intervention
Arrhythmic patients should have treatment to:
Preventing clot formation
Thinning the blood
Reducing cholesterol
Lowering BP
Correcting arrhythmias
Improving heart function
Controlling heart failure
 Anti-arrhythmic drugs
Vaughan Williams classification
Class 1- Na channel blockers

Class 2- beta blockers

Class 3- K channel

Class 4- non-dihydropyridine Ca channel blockers

 Class 1 drugs
Slow conduction in fast channels
1a- intermediate kinetics, intermediate potency,
also block K channels directly- disopyramide,
procainamide, quinidine
1b-fast kinetics (hence used in fast heart rates),
not very potent, minimal effects on atrial tissue,
do not directly block K channels- lidocaine,
mexiletine
1c-slow kinetics, more potent, do not directly
block K channels- blockers-flecainide,
propafenone
 Indications for class 1 drugs
1a AND 1c - SVTs

1a, 1b and 1c- all VTs

 Adverse effects- Class 1
Proarrythmias- drug induced arrythmias,
worse than the arrythmias being treated
1a- torsades de pointes VT
1a and 1c may slow conduction to permit 1:1
AV conduction
1a, b and c may worsen the arrhythmias
Contra-indicated in structural heart disorders
 Class 1a
Procainamide, quinidine, and disopyramide.
Quinidine
Blocks Na channels thus slowing down action
potential upstroke, conduction and the QRS
duration on the ECG.
It also blocks the K channels.

Indications: atrial and ventricular arrhythmias.

 1a
A/E- Excessive action potential prolongation,
QT interval prolongation, torsade de pointes
arrhythmia and syncope, headache, dizziness,
tinnitus.

70-80% systemic bioavailability when given

orally, 80% bound to albumin, eliminated via
hepatic metabolism.
 1a
Procainamide- prolongs QRS duration of the
ECG by blocking sodium channels.

It also indirectly blocks K channels, but has

less prominent antimuscarinic effects than
quinidine.

Indications: atrial and ventricular arrhythmias

 1a
A/E: similar to quinidine, hypotension
(ganglion blocking effects), systemic lupus
erythematous (SLE), pleuritis, pericarditis.

Rarely used but can be administered IV or IM

with 75% systemic bioavailability when given
orally.
 1a
Disopyramide- effects similar to quinidine, with greater
antimuscarinic effects.

Thus should be administered with a drug that slows AV

conduction esp. when treating atrial flutter.

Only available for oral use

A/E: may precipitate heart failure in patients with

preexisting left ventricular depression, urinary retention,
dry mouth, blurred vision, constipation, worsening of
glaucoma.
 Class 1b
Lidocaine- inhibits fast sodium channels and
shortens APD inhibiting ectopic beats and
conduction in depolarized cells.

Least cardiotoxic of all the sodium channel

blockers.

Indications- suppression of ventricular

arrhythmias associated with MI, cardiac surgery
or other acute situations.
 1b
A/E: SA node arrest, worsening of impaired
conduction, vetricular arrhythmias, paresthesias,
tremor, nausea, slurred speech, lightheadedness,
convulsions.

Extensive 1st pass metabolism thus only 3% is

bioavailable, give parenterally (rapid/immediate
onset of action).

Mexiletine- resistant to 1st pass metabolism and

is effective by the oral route
 1c
Powerful sodium channel blockers, manifested by
QRS widening on the ECG, with little effect on the
QT interval.

They allow 1:1 conduction to the ventricles

causing marked acceleration in the ventricular
rate.

Thus in atrial flutter, they should only be used

with beta blockers or verapamil.
 1c
Flecainide- potent Na and K channel blocker with slow
unblocking kinetics (used for patients with otherwise
normal hearts who have supraventricular arrhythmias.)

Effective in suppressing premature ventricular

contractions.

Negative inotropic effects but no -blocking action.

A/E- may cause severe exacerbation of arrhythmia in

patients with preexisting tachycardia.
 1c
Propafenone- structurally similar to propranolol,
with weak -blocking properties.

Has negative inotropic effects with sodium

blocking linetics similar to those of flecainide.

Used for supraventricular arrhythmias.

A/E: metallic taste, constipation, exacerbation of

arrhythmias might occur.
 Class 2 drugs
Beta blockers
Acebutolol, atenolol, betaxolol, bisoprolol,
carvedilol, esmolol, propranolol, metoprolol,
nadolol, timolol
Act on slow channel tissue- SAN and AVN
Reduce rate of automacity, slow conduction
velocity, prolong refractoriness
 Indications for class 2 drugs
SVTs- sinus tachycardia, AV nodal reentry,
atrial flutter
VTs
 Adverse effects
Generally well tolerated
Lassitude, sleep disturbance, GI upset

Contraindicated in asthma
 Class 3 drugs
K channel blockers
Membrane stabilising drugs
Amiodarone, azimilide, bretylium, dofetilide,
dronedarone, ibutilide, sotalol
Prolong duration of action potential, and
refractoriness in slow and fast channel tissues
Indications- SVTs and VTs
Adverse effects- ventricular proarrhythmia
particularly torsades de pointes VT
 Class 4 drugs
Nondihydropyridine calcium channel blockers
Depress Ca channel blocker dependant Apsin
slow channel tissues
Reduce rate of automacity, slow conduction
velocity, prolong refractoriness
Diltiazem, verapamil
Indications- SVT