CARDIAC

ARRHYTHMIA
Electrocardiogram (ECG)
 It is used to assess cardiac rhythm and conduction.
 The base of ECG recording is that electrical
depolarization of myocardial tissue produces a
small current which can be detected by electrolode
pairs on the body surface.
 The normal heart rate and rhythm are determined
by the sino-atrial node (SA) in the right atrium,
which acts as the pacemaker for the heart.
 During sinus rhythm, SA node triggers atrial
depolarization, producing a P wave.
 Depolarization proceeds slowly through the AV
node.
Electrocardiogram
 The bundle of His, bundle branches, and
purkinje fibers are then activated , initiating
ventricular depolarization , which produces
QRS complex.
 The muscle mass of the ventricle is much
larger than that of the atrium so, the QRS
complex is larger than the P wave.
 The interval between the onset of P wave
and the onset of QRS is termed ‘PR interval’
and reflects the duration of AV nodal
conduction (120-200 ms, 3-5 small squares).
Electrocardiogram
 Atrial repolarization dose not cause a
detectable signal.
 Ventricular repolarization produces the T
wave.
 The QT interval represents the total
duration of ventricular depolarization and
repolarization.
Conduction system
Normal ECG
Normal ECG
Arrhythmia
 There are 2 major types of arrhythmias:
 Tachycardias (the heartbeat is too fast:

>100 beats/minute).
 Bradycardia (the heartbeat is too slow: <

60 beats/minute).
 Arrhythmia is a common problem, occurring
in up to 25% of patients treated with digoxin,
50% of anesthetized and 80% in patients
with acute MI.
Arrhythmia
 Arrhythmias can be life-threatening if they
cause a severe decrease in the pumping
function of the heart.
 When the pumping function is severely
decreased for more than a few seconds,
blood circulation is essentially stopped, and
organ damage may occur within a few
minutes.
Types of arrhythmia
 Life-threatening arrhythmias include: ventricular
tachycardia and ventricular fibrillation.
 Arrhythmias are identified by where they occur
in the heart (atria or ventricles) and by what
happens to the heart's rhythm when they occur.
 Arrhythmias that start in the atria are called
‘atrial or supraventricular’ (above the ventricles)
arrhythmias.
 Ventricular arrhythmias begin in the ventricles.
Ventricular arrhythmias are usually caused by
heart disease and are very serious.
Sinus rhythm
Sinus bradycardia
 A sinus rate <60/min.

 May occur in healthy people at rest.

 Some pathological conditions may present: (MI,

hypothermia, hypothyroidism, and drugs (beta

blockers, verapamil, digoxin).
 Asymptomatic sinus bradycardia requires no

treatment.
 Symptomatic acute sinus bradycardia responds to i.v

atropine 0.6-1.2 mg.

 Patients with recurrent or persistent symptomatic

sinus bradycardia should be considered for

pacemaker implantation.
Sinus rhythm

Sinus tachycardia
 Sinus rate >100/min.

 Usually due to increase in sympathetic

activity associated with exercise, emotion,

pregnancy, or pathology.
 Young adults can produce a rapid sinus

rate, up to 200/min during exercise.

Atrial tachyarrhythmia

Atrial tachycardia
 May be a manifestation of increased atrial

automaticity, sinoatrial disease, or digoxin

toxicity.
 Produces narrow complex tachycardia with

abnormal P-wave morphology.

 Sometimes associated with AV block if atrial

rate is rapid.
 May respond to class II ( β-blockers) or class I

(Na channel blockers) or III (amiodarone,

sotalol) anti-arrhythmic drugs.
Atrial tachyarrhythmia
 Common in healthy people, and may be
triggered or increased by stress, caffeine,
and smoking.
 ECG shows a premature, but otherwise
normal QRS.
 Treatment is rarely necessary, but β-
blockers can be used if symptoms intrusive.
Atrial tachyarrhythmia

Atrial flutter (AFL):

 AFL occurs when an abnormal conduction circuit

develops inside the right atrium, allowing the
atria to beat excessively fast >300/min and is
associated with 2:1, 3:1 or 4:1 AV block.
 ECG showed saw-toothed flutter waves.
 AFL can come and go(paroxysmal AFL). Less
often it can be more permanent ( persistent
AFL).
Atrial tachyarrhythmia

Atrial flutter (AFL):

 Digoxin, β-blockers, or verapamil can be

used to control the ventricular rate.

 In many cases it is preferable to try
restoring sinus rhythm by using i.v.
amiodarone or direct current cardioversion
(DC).
 Amiodarone and β-blockers can be used as
prophylactic.
Atrial tachyarrhythmia

Atrial flutter circuit:

Atrial tachyarrhythmia

Atrial fibrillation (AF):

 The most common sustained arrhythmia.

 Initiated by rapid bursts of ectopic beats arising

from diseased atrial tissues.

 Becomes sustained because of initiation of re-

entrant conduction within the atrium because of

continuous ectopic firing.
 In AF, the atria beat rapidly, but in an

uncoordinated and ineffective manner.

 The ventricles are activated irregularly, at a rate

determined by conduction through AV node.

Atrial tachyarrhythmia
Atrial fibrillation (AF):

 ECG characterized by irregularly irregular pulse.

 There are no P waves.
 AF may be the first manifestation of many forms of
heart diseases particularly those associated with
enlargement or dilatation of the atria.
 Alcohol, hyperthyroidism and chronic lung disease
are common causes of AF.
 AF causes palpitation, breathlessness and fatigue
and associated with significant morbidity and
mortality.
Atrial tachyarrhythmia

Atrial fibrillation circuit:

Atrial tachyarrhythmia
Management of AF:
Paroxysmal AF:
 Occasional attacks that are well tolerated and do not

necessarily require treatment.

 β-blockers used as first line if symptoms are

troublesome.
 Class Ic drugs (propafenone, flecainide)are also

effective.
 Amiodarone is the most effective for preventing AF,

but it is use is restricted due to its ADRs.

 Catheter ablation can be considered if β-blockers and

Class Ic failed or cause intolerable ADRs.

Atrial tachyarrhythmia

Persistent AF:
 There are two options for treating persistent

AF:
 Rhythm control: restoring and

maintaining sinus rhythm.

 Rate control: Control ventricular rate and

prevent embolic complications.

Atrial tachyarrhythmia
 Rhythm control:
 Electrical cardioversion is successful in three
quarters of patients but relapse is frequent.
 i.v. Flecainide is a safe alternative to DC.
 Anticoagulation should be maintained for at
least 3 months following cardioversion.
 If relapse occurs, a second or third
cardioversion may be appropriate.
 Concomitant therapy with amiodarone or β-
blockers may reduce risk of recurrence.
Atrial tachyarrhythmia

Rate control:
 If sinus rhythm can not be restored,

treatment should be directed at maintaining

an appropriate heart rate.
 Digoxin, β-blockers or rate-limiting CCBs

reduce ventricular rate by increasing the

degree of AV blocking.
 Combination therapy is often advisable

(digoxin+atenolol).
 In exceptional cases, poorly controlled

patients can be treated by complete AV

block with catheter ablation with permanent
Supraventricular tachycardia
 SVT is used to describe a range of regular
tachycardias that have similar appearance
on ECG.
 The term SVT is misleading as in many
cases the ventricles also form part of re-
entry circuit.
Supraventricular tachycardia
 Patient is usually aware of fast heart beat
and may feel faint or breathless.
 Treatment is not always necessary,
however, i.v adenosine or verapamil restore
sinus rhythm in most cases.
 Alternatives include β-blockers or flecainide.
 If episodes are frequent, prophylactic with
oral β-blockers or verapamil may be
indicated.
Supraventricular tachycardia
Wolff-Parkinson-White syndrome
 It is a heart condition in which there is an

abnormal extra electrical pathway of the heart.

The condition can lead to episodes of rapid heart
rate.
 Caused by the presence of an abnormal
accessory electrical conduction pathway between
the atria and the ventricles.
 Electrical signals travelling down this abnormal
pathway may stimulate the ventricles to contract
prematurely.
 Premature activation of ventricles produces short
PR interval and delta wave.
Supraventricular tachycardia

Wolff-Parkinson-white syndrome
Ventricular tachyarrhythmia
Ventricular ectopic beats (VEBs)

 QRS complexes are premature, broad, and bizarre

because ventricles are activated one after another
rather than simultaneously.
 Ectopic beats produce a low stroke volume, because
contraction occurs before complete filling.
 Patients usually asymptomatic but may complain of
irregular heart beat, missed beats or abnormally strong
beats (due to increased output of post-ectopic sinus
beat).
Ventricular tachyarrhythmia
 The significance of VEBs depends on presence or
absence of underlying heart disease.
 Frequently found in healthy people.
 Treatment is not necessary unless the patient is
highly symptomatic, in which case β-blockers can
be used.
 It may be a manifestation of otherwise subclinical
heart disease, particularly CAD.
 Frequent VEBs often occur during MI, and in HF,
but need no treatment.
 VEBs are also a feature of digoxin toxicity.
Ventricular tachyarrhythmia

Ventricular tachycardia (VT)

 The common causes include MI, and chronic IHD.

 Caused by abnormal automaticity or triggered

activity in ischemic tissues.

 ECG shows tachycardia with broad, abnormal

QRS, with a rate>120/min.

 Prompt action to restore sinus rhythm is

required, and should be followed by prophylactic

therapy.
 Synchronized DC cardioversion is the treatment

of choice if systolic BP is <90mmHg.

Ventricular tachyarrhythmia

Ventricular tachycardia (VT)

 I.V amiodarone as bolus followed by continuous

infusion may be given.

 β-blockers are effective in preventing VT by

reducing automaticity and by blocking

conduction in scar reentry circuit.
 Amiodarone can be added if additional control

is needed.
 Class Ic anti-arrhythmic drugs should not be

used in patients with IHD or HF because they

depress myocardial function.
Sinoatrial disease (sick sinus syndrome)

 Can occur in any age, but most common in

elderly.
 Pathology involves fibrosis, degenerative
changes or ischemia of the SA node.
 Characterized by a variety of arrhythmias
(bradycardia, SA block, paroxysmal atrial
tachycardia, paroxysmal AF, AV block).
 Permanent pacing improves symptoms, but
not indicated in patients who are
asymptomatic.
Atrioventricular and bundle branch block

AV block
First-degree AV block:
 AV conduction is delayed, PR interval is

prolonged, and rarely cause symptoms.

Second-degree AV block:
 Dropped beats occur because some
impulses from the atria fail to conduct to the
ventricle.
Third-degree AV block:
 When AV conduction fails completely; the
atria and ventricle beats independently (AV
Atrioventricular and bundle branch block

 Complete AV block produces a slow 25-

50/min regular pulse.
 Patients with symptomatic bradyarrythmias
should receive permanent pacemaker.
 Asymptomatic first-degree or second-
degree does not require treatment.
 Some patients with second-degree or third
degree should receive permanent
pacemaker because of the risk of asystole
and sudden death.
 Atrioventricular and bundle branch block

AV block
First degree

Second degree
Atrioventricular and bundle branch block

Bundle branch block

 Conduction block in the right or left bundle

branch can occur due to HTN, IHD or

cardiomyopathy.
 Depolarization proceeds through slow

myocardial route rather than the rapidly

conducting purkinje tissues.
 This causes delayed conduction into the LV or

RV, broadens QRS complex.

Anti-arrhythmic drugs
 Arrhythmia may require treatment because it
can reduce cardiac output.
 Some arrhythmia can cause fatal rhythm
disturbances (ventricular fibrillation).
 The hazards of antiarrhythmic drugs (in
particular they can precipitate lethal
arrhythmia), led to re-evaluation of their
relative risks and benefits.
 In general, treatment of asymptomatic or
minimally symptomatic arrhythmia should be
avoided.
Ionic basis of membrane electrical activity

Nodal cell
Non-nodal Cell Action Potentials

 Phase 0: Rapid depolarization

- increased Na+ and decreased K conductance
 Phase 1: Initial repolarization
- decreased Na+ and increased K conductance
 Phase 2: Plateau phase
- increased Ca++ conductance
 Phase 3: Repolarization
- increased K+ and decreased Ca++conductance
 Phase 4: Resting potential
- increased K+ and decreased Na+ and
decreased Ca++ conductance
Nodal Cell Action Potentials

 The characteristic of action potentials found in

the SA node and the AV node.
 Phase 0: Depolarization
- increased Ca++ and decreased K+
conductance
 Phase 3: Repolarization
- increased K+ and decreased Ca++
conductance
 Phase 4: Spontaneous depolarization
- increased Ca++ and decreased K+
conductance
Effective Refractory Period

 During phases 0, 1, 2, and part of phase 3,

the cell is refractory to the initiation of new
action potentials. This is termed the effective
refractory period (ERP).
 During the ERP, stimulation of the cell does
not produce new, propagated action
potentials.
 The reason for this is that the fast sodium
channels are not fully reactivated.
 Many antiarrhythmic drugs alter the ERP,
thereby altering cellular excitability.
Effective Refractory Period

 Drugs that block potassium channels (Class III

antiarrhythmic) retard phase 3 repolarization
and increase the action potential duration,
thereby increasing the ERP.
 Sodium-channel blockers (particularly Class
IA) also increase the ERP by prolonging the
inactivation state of fast-sodium channels.
 Drugs that increase the ERP can be
particularly effective in abolishing reentry
currents that lead to tachyarrhythmia.
Basic pharmacology of antiarrhythmic

 Arrhythmias are caused by:

1) abnormal pacemaker activity.
2) abnormal impulse propagation.
 The aim of therapy is to:
1) Reduce ectopic pacemaker activity.

2) Modify conduction or refractoriness in re-

entry circuits.
Basic pharmacology of antiarrhythmic

The major pharmacological mechanisms

currently
available to accomplish these goals are:
1) Sodium channel blockade.

2) Blockade of sympathetic effect in the

heart.
3) Prolongation of the refractory period.

4) Calcium channel blockade.

Vaughn Williams Classification

Class I: Sodium channel blockade:

 Act principally by suppressing excitability and
slowing conduction in atrial or ventricular
muscles by blocking sodium channels.
 There are several types of sodium channels in
the heart.
 Should generally be avoided in patients with
heart failure, because they depress cardiac
function.
 Class Ia and Ic are often pro-arrhythmic.
Vaughan Williams Classification

 Subclasses reflects effects on the action potential

duration (APD).
 Class 1A:
 prolong cardiac APD and increase tissue refractory
period.
 Used to prevent both atrial and ventricular
arrhythmias.
 Class 1B:
 Shortens APD and tissues refractory period.
 Act on channels found predominantly in ventricular
myocardium, so used to treat and prevent VT and
VF.
Vaughn Williams Classification

 Class 1C:
 Have minimal effect on the APD or
refractory period.
 Used mainly for prophylaxis of AF, but also
effective in prophylaxis and treatment of
supraventricular or ventricular arrhythmia.
 Block conduction in accessory pathway
(WPW syndrome).
Vaughn Williams Classification

 Class II: Action is sympatholytic.

 Class III: Action manifests as prolongation of APD
, most of drugs block the rapid component
delayed rectifier potassium channels I k+.
 Class IV: Blockade of the cardiac calcium current,
this slow conduction in the regions where the
action potential upstroke is calcium dependant
(SA&AV node).
 A given drug may have multiple classes of
actions, for example, amiodarone, shares all four
classes of actions.
 Adenosine does not fit into this scheme.
Class IA Sodium channel-blocking drugs

 Includes quinidine, disopyramide and Procainamide.

 Procainamide:
 It blocks sodium channels, thus slow upstroke of
action potential, slow conduction, and prolongs QRS
duration.
 Its cardiotoxic effects include excessive action
potential prolongation, and QT-interval prolongation.
 Excessive slowness of conduction may occur
(precipitating new arrhythmia).
 Long-term therapy may induce a syndrome resemble
lupus erythematosus (arthralgia and arthritis).
Class IA Sodium channel-blocking drugs

 Therapeutic uses:
 Effective against most atrial and ventricular
arrhythmia.
 Not preferred in long-term therapy because of
frequent dosing, and the occurrence of lupus-
related effects.
 Alternative to lidocain or amiodarone for
treatment of sustained ventricular arrhythmia
associated with acute MI.
 Can be administered by i.v or i.m and is well
absorbed orally.
Class IA Sodium channel-blocking drugs

 Quinidine:
 Has action similar to procainamide.
 It also prolongs action potential duration by blockade of
potassium channels.
 Its toxic effects include excessive QT-interval prolongation
and induction of torsades de pointes arrhythmia.
 git side effects observed in one third to one half of
patients.
 Cinchonism ( headache, dizziness, tinnitus) observed at
toxic levels.
 Rarely used because of cardiac and extra-cardiac adverse
effects.
Class IA Sodium channel-blocking drugs

 Disopyramide
 Similar mechanism of procainamide and
quinidine.
 Has more marked antimuscarinic effect compared
to quinidine.
 Accordingly, a drug that slows AV conduction
must be with disopyramide upon treating AFL or
AF.
 Has negative inotropic effect and may precipitate
HF in predisposed patients.
 Approved for treatment of ventricular arrhythmia.
Class IB Sodium channel-blocking drugs

 Lidocaine:
 Available only by i.v route.
 Has low incidence of toxicity and high degree
of effectiveness in arrhythmias associated
with acute MI.
 It is one of the least cardiotoxic sodium
blockers.
 Its most common adverse effects include
parathesaias, tremor, lightheadedness,
slurred speech and convulsion.
 Due to extensive first pass effect, it is given
parentally.
Class IB Sodium channel-blocking drugs

 Therapeutic uses:
 The agent of choice for termination of
ventricular tachycardia.
 Mexiletine:
 Orally active congener of lidocaine.
 Used for treatment of ventricular
arrhythmias.
Class IC Sodium channel-blocking drugs

Flecainide
 Potent blocker of sodium and potassium

channels.
 Used for patients with otherwise normal hearts

who have supraventricular arrhythmias.

 It may cause severe exacerbation of

arrhythmias in patients with preexisting VT

and those with a previous MI and ventricular
ectopy (CAST trial).
 The usual dose is 100-200 mg twice daily.
Class IC Sodium channel-blocking drugs

Propafenone:
 Has some structural similarities to propranolol

and posses weak β-blocking activity.

 It does not prolong the action potential.
 It is used primarily for supraventricular
arrhythmia.
 The usual daily dose is 450-900 mg/day in divided
doses.
 The most common adverse effects are metallic
taste, and constipation, arrhythmia exacerbation
may occur.
Class II β-blockers

 They reduce the rate of SA node depolarization and

cause relative block in the AV node.
 Useful for rate control in AFL and AF.
 Can be used to prevent supraventricular or
ventricular tachycardia.
 Their efficacy for suppression of ventricular ectopic
depolarization is lower than that of sodium channel
blockers.
 Involves non-selective, and cardioselective.
 Esmolol is a short-acting β-blocker used primarily as
an antiarrhythmic drug for intraoperative and other
acute arrhythmia.
Class III drugs

 Act by prolonging the plateau phase of the

action potential, thus lengthening the
refractory period.
 They prolong action potential by blocking
potassium channels or by enhancing inward
current.
 Most of the class cause QT prolongation, and
they tend to cause torsades de pointes.
 They are very effective in preventing atrial
and ventricular tachyarrhythmia.
Class III drugs

Amiodarone:
 It is a complex drug that has also class I, II, and IV activity.

 Amiodarone markedly prolongs action potential (and QT

interval) by blockade of K.
 It also significantly inactivate sodium channels.

 Has weak adrenergic and calcium channel-blocking

actions.
 As a result of its broad spectrum antiarrhythmic actions, it

is used extensively for a wide variety of arrhythmias.

 Approved as oral or i.v for treating serious ventricular

arrhythmias.
 Also effective for supraventricular arrhythmias such as AF.
Class III drugs

 Causes slowing of heart rate and AV nodal conduction.

 Variably absorbed with 35-65% bioavailability.
 It undergoes first pass metabolism, the major
metabolite (ethylamiodarone) is bioactive.
 Has many drug interactions, and all medications should
be reviewed when initiating amiodarone.
 Its level is altered by drugs that inhibits CYP3A4 liver
enzyme (cimetidine), or activate the enzyme
(rifampicin).
 It inhibits several cytochrome P450 enzymes results in
high level of many drugs (statins, digoxin, warfarin).
Class III drugs

 Low dose amiodarone (100-200mg/day) is

effective for patients with AF.
 It is effective for prevention of recurrent
ventricular tachycardia.
Class III drugs

Sotalol:
 A racemic mixture of two isomers with non-

selective β blocking and class III effects (action

potential prolongation).
 It is approved for treating life-threatening

ventricular arrhythmias and the maintenance of

sinus rhythm in patients with AF.
 Also approved for treatment of supraventricular

and ventricular arrhythmias in pediatric age group.

 [For dronedarone, vernakalant, dofetilide and

ibutilide refer to basic & clinical pharmacology]

Class IV CCBs

 They block ‘slow calcium channels’ which are important for

impulse generation and conduction in atrial and nodal tissues.
 Their main indications are prevention of SVT (by blocking AV

node) and rate control in AF.

 Verapamil and diltiazem have antiarrhythmic actions while

dihydropyridines do not.
Verapamil:
 Blocks both activated and inactivated L-type calcium

channels.
 Its effect is more marked in SA, and AV node.

 Indicated mainly for SVT.

 Can also reduce ventricular rate in AF and AFL.

 Occasionally useful in ventricular arrhythmia.

Class IV CCBs

 A common error has been to administer i.v verapamil to

a patient with ventricular tachycardia misdiagnosed as
supraventricular tachycardia. Hypotension and
ventricular fibrillation can occur.
 Its negative inotropic effect limits its use in diseased
heart.
 Can induce AV block when used in large doses or in
patients with AV nodal disease.

Diltiazem:
 Similar in efficacy to verapamil in the management of

supraventricular arrhythmias, including rate control in

AF.
Miscellaneous agents

Adenosine
 A nucleoside that occurs naturally throughout the

body.
 Its half life is <10 seconds.

 Its mechanism involves activation of inward K

current and inhibition of calcium current, results

in marked hyperpolarization and suppression of
calcium-dependant action potential.
 When given as bolus dose it inhibits AV nodal

conduction and increases AV nodal refractory.

 Has lesser effect on the SA node.
Miscellaneous agents

 It is the drug of choice prompt conversion of

paroxysmal supraventricular tachycardia.
 Given usually in bolus dose 6 mg followed if
necessary by a dose of 12 mg.
 Induction of high grade AV block may occur
but is very short-lived.
Miscellaneous agents

Atropine sulphate:
 Used as 0.6 mg, repeated if necessary to a

maximum of 3 mg.
 It increases the sinus rate and SA, AV node

conduction.
 Is the treatment of choice for severe bradycardia

or hypotension due to vagal overactivity and in

cardiac arrest due to asystole.
 Repeat dosing may be necessary because the

drug disappears rapidly from the circulation after

parenteral administration/
Therapeutic procedures

External defibrillation and cardioversion:

 The heart can be completely depolarized by

passing a large electrical current through it

from an external source.
 Electrical cardioversion:

 A termination of AF or VT with synchronized

shock usually under general anesthesia.

 Patients with AF, or AFL >47=8 hours are at

risk of systemic embolism after cardioversion

and should be adequately anticoagulated for 4
weeks before and after.
Therapeutic procedures

Defibrillation:
 Defibrillators deliver high-energy, short-

duration shock via two metal paddles.

 Delivery of unsynchronized shock during

cardiac arrest caused by VF.

 There is no need for an anesthetic as the

patient is unconscious.
Therapeutic procedures

Catheter ablation:
 The treatment of choice for many patients with

recurrent arrhythmias.
 A series of catheter electrolode inserted into the heart.

 Once the arrhythmia focus or circuit is identified, a

steerable catheter is placed into this critical zone and

the tissue is selectively ablated using heat or
sometimes by freezing.
 It is now the treatment of choice for AVNRT and AV re-

entrant (accessory pathway) tachyarrhythmia.

 Focal atrial tachycardia and AFL can also be eliminated,

but some patients experience episodes of AF.

Therapeutic procedures

 Temporary pacemakers:
 Indicated in the management of transient AV block and other
arrhythmias complicating acute MI, or cardiac surgery.
 Permanent pacemakers:
 Atrial pacing is appropriate for patients with SA disease
without AV block (external sinus node).
 Ventricular pacing is suitable for patients with continuous AF.
 Implantable cardiac defibrillators (ICDs):
 Have all the functions of a permenant pacemakers but can
also detect and terminate life threatening ventricular
tachyarrhythmia.
 Indicated for primary and secondary prevention of life-
threatening ventricular arrhythmias.