Management of cardiac arrhythmias

Arrhythmias
Management
Dr. Sameh Ahmad Muhamad abdelghany
Lecturer Of Clinical Pharmacology
Mansura Faculty of medicine

2
Introduction
Normal Cardiac
Physiology
Pathogenesis & causes
Diagnosis
Treatment
CONTENTS

4
Introduction
 Definiton:
 a – “without” rhuthmos – “ryhtm” i.e it
means “without rhythm”.
 Also known as “ cardiac dysrhythmia”
 Cardiac arrhythmias are a group of
conditions in which the heart beats with an
irregular or abnormal rhythm.
 Arrhythmia /dysrhythmia: abnormality in
the site of origin of impulse, rate, or
conduction

5
Introduction
 Arrhythmia affects millions of people.
 Atrial fibrillation and atrial flutter resulted in 112,000 deaths
in 2013, up from 29,000 in 1990.
 Sudden cardiac death is the cause of about half of deaths due
to cardiovascular disease or about 15% of all deaths
globally.
 About 80% of sudden cardiac death is the result of
ventricular arrhythmias.
 Arrhythmias may occur at any age but are more common
among older people.

NORMAL CARDIAC
ELECTROPHYSIOLOGY

7
Normal cardiac rhythm
 Heart rate should be between 60 and 100
per minute.
 All the cardiac impulses should originate
from the SA node of the heart.
 The impulse should conduct through the
normal conduction pathway.
 The impulse should pass through
conducting pathways with normal velocity

8
Normal Electrical Conduction
System
 SA node
 Inter-nodal
pathways
 AV node
 Bundle of his
 Left & Right
bundle branches
 Purkinje fibers

9
Electrical Conduction System
EKG Waveforms
 One complete cardiac cycle = P, Q, R, S, (QRS
complex), and T wave
o P wave : Atrial depolarization (contraction)
o QRS Complex: Ventricular depolarization, atrial
repolarization
o T wave: Ventricular repolarization (resting phase)

10
Electrical Conduction System
EKG Waveforms

11
Electrophysiology - resting potential
 A transmembrane electrical gradient (potential) is
maintained, with the interior of the cell negative with
respect to outside the cell
 Caused by unequal distribution of ions inside vs. outside
cell
o Na+ higher outside than inside cell
o Ca+ much higher “ “ “ “
o K+ higher inside cell than outside
 Maintenance by ion selective channels, active pumps and
exchangers

12
Cardiac action potential
 Divided into five phases (0,1,2,3,4)
 Phase 4 : resting phase (resting membrane
potential)
o Phase cardiac cells remain in until stimulated
o Associated with diastole portion of heart cycle

13
 Addition of current into cardiac muscle (stimulation)
causes
 Phase 0 :opening of fast Na channels and rapid
depolarization
o Drives Na+ into cell (inward current), changing membrane
potential
o Transient outward current due to movement of Cl- and K+
 Phase 1 : initial rapid repolarization
o Closure of the fast Na+ channels
 Phase 0 and 1 together correspond to the R and S waves of
the ECG

14
 Phase 2 : plateau phase
o sustained by the balance between the inward movement of
Ca+ and outward movement of K +
o Has a long duration compared to other nerve and muscle
tissue
o Normally blocks any premature stimulator signals (other
muscle tissue can accept additional stimulation and
increase contractility in a summation effect)
o Corresponds to ST segment of the ECG.

15
 Phase 3 (repolarization)
o K+ channels remain open
o Allows K+ to build up outside the cell, causing the cell to
repolarize
o K + channels finally close when membrane potential
reaches certain level
o Corresponds to T wave on the ECG

17
 Differences between nonpacemaker and pacemaker cell
action potentials
o Thera are only 3 phases:0,3,4
o Pacemaker cells: Slow, continuous depolarization during
rest
o Continuously moves potential towards threshold for a new
action potential (called a phase 4 depolarization)

18
 Differences between non pacemaker and pacemaker
cell action potentials
o Pacemaker cells: Slow, continuous depolarization during
rest
o Continuously moves potential towards threshold for a new
action potential (called a phase 4 depolarization)

19
Cardiac action potential in
Pace maker cells

22
Arrhythmia pathogenesis
 Disorder of impulse formation:
 Automaticity.
 Triggered Activity.
o Early after depolarization.
o Delayed after depolarization.
 Disorder of impulse conduction:
 Impulse Block
 Re - entry phenomena

23
Abnormal automaticity
 The SA node is the heart’s natural pacemaker
 Any impulses fired from elsewhere in the heart before
or concurrently with SA node firing can lead to
premature heartbeats or sustained abnormal
heartbeats.
 Problems associated are
o sinus tachyarrhythmia
o sinus bradyarrhythmia
o Abnormality in site of impulse generation ,ectopic loci
o Escape rhythms

24
Triggered automaticity
 This is an abnormal secondary upstroke which occur
only after a normal initial or “triggering “ upstroke or
action potential.
 These secondary upstrokes are called after --
depolarization's
 This may be of two types
o Early after depolarization
o Delayed after depolarization

25
Triggered automaticity
Early After depolarization Delayed After depolarization

26
Abnormal impulse conduction
 Conduction block may occur due to depression of
impulse conduction at AV node & bundle of His, due
to vagal influence or ischaemia .
 Types :
 1st degree heart block – slowed conduction
 2nd degree block – some supraventricular complex not
conducted
 3rd degree block – no supraventricular complex are
conducted

27
Re-entry phenomena
 It can be of two types
I. Anatomically defined re-entry
o E.g Wolf ParkinsonWhite syndrome(wpw)
II. Functionally defined re-entry
o Mostly seen in patients with ischemic heart disease

28
Re-entry phenomena(anatomical)

30
Two features of arrhythmias
 Site of origin
 Atria
 Atrioventricular node (AV node)
 Ventricles
 Affect on heart rate
 Too slow heart rate (bradycardia)
 Too fast heart rate(tachycardia)

31
Classification of arrhythmias
 Abnormal heart pulse formation
 Sinus arrhythmia
 Atrial arrhythmia
 Atrioventricular junctional arrhythmia
 Ventricular arrhythmia
 Abnormal heart pulse conduction
 Sinus-atrial block
 Intra-atrial block
 Atrio-ventricular block
 Intra-ventricular block
 Abnormal heart pulse formation and conduction

33
Causes
 Coronary artery disease.
 Electrolyte imbalances in your blood (such as sodium
or potassium).
 Structural changes of the heart
 Scarring of the heart, often the result of a heart attack
 Healing process after heart surgery.
 Hypertension (high blood pressure)

34
Causes
 Diabetes
 Drug abuse
 Excessive coffee consumption
 Hyperthyroidism (an overactive thyroid gland)
 Mental stress
 Smoking
 Some dietary supplements &some herbal treatments
 Some medications

36
Symptoms of tachycardia
 breathlessness (dyspnea)
 dizziness
 syncope (fainting, or nearly fainting)
 fluttering in the chest
 chest pain
 lightheadedness
 sudden weakness

37
Symptoms of bradycardia
 angina (chest pain)
 trouble concentrating
 confusion
 difficulties when exercising
 dizziness
 fatigue (tiredness)
 lightheadedness
 palpitations
 shortness of breath
 syncope (fainting or nearly fainting)
 diaphoresis, or sweating

39
Investigations
 blood and urine tests
 EKG (electrocardiogram)
 Holtermonitor - a wearable device that records the
heart for 1-2 days
 echocardiogram
 chest X-ray
 heart catheterization

42
Management of
arrhythmias
 Pharmacological therapy.
 Cardio version.
 Pacemaker therapy.
 Surgical therapy
 Interventional therapy

43
Pharmacologic Rationale & Goals
 The ultimate goal of antiarrhythmic drug therapy:
 Restore normal sinus rhythm and conduction
 Prevent more serious and possibly lethal arrhythmias
from occurring.
 Antiarrhythmic drugs are used to:
 decrease conduction velocity
 change the duration of the effective refractory period
(ERP)
 suppress abnormal automaticity

44
Mechanisms of
Anti-arrhythmic drugs
 To suppress automaticity
 ↓ Rate of phase 0
 ↓ Slope of phase 0
 ↑ Duration of ERP(effective refractory period)
 Resting membrane potential more negative
 Abolishing reentry
 Slow conduction
 ↑ ERP

45
Anti arrhythmic drugs
 Anti-tachycardia agents
 Anti-bradycardia agents

46
Anti-tachycardia agents
 Vaugham Williams classification
 Class I : Natrium channel blocker
 Class II : ß-receptor blocker
 Class III : Potassium channel blocker
 Class IV : Calcium channel blocker
 Others: Adenosine, Digitalis

47
Class I – Na+ channel blockers
 The primary action of these class of drugs is
o To limit the conductance of Na+ across the cell
membrane
o Reduce the rate of phase 4 depolarization
 They are further divide into three subclasses
o Subclass IA
o Subclass IB
o Subclass IC

48
Na+ channel blockers(subclass IA)
 Less use in clinic
 The anti arrhythmic drugs include
o quinidine
o procainamide.
 are open state Na+ channel blockers.
 This class of drugs moderately delay the channel
recovery.
 They suppress the AV conduction and prolong
refractoriness

49
Na+ channel blockers(subclass IB)
 block the Na+ channels more in inactivated than in open
state, but do not delay channel recovery.
 have little or no effect at slower heart rates, and more
effects at faster heart rates
 do not change or may decrease the action potential
duration.
 Class IB drugs tend to be more specific for voltage gated
Na channels than Ia
 E.g Lidocaine - Mexiletine
 Perfect to ventricular tachyarrhythmia

50
Na+ channel blockers(subclass IC)
 Most prominent action is on open state Na+ channels
and have the longest recovery time
 delay conduction and prolong the P-R interval,
broaden the QRS complex
 have minimal effect on action potential duration
 E.g Moricizine – Propafenone
 Can be used in ventricular and/or supra-ventricular
tachycardia and extrasystole.
 This class of drug has high proarrhythmic potential

52
Class II – adrenergic agents
 are conventional beta blockers
 act by blocking the effects of catecholamines at the
β1- adrenergic receptors, thereby decreasing
sympathetic activity on the heart.
 They decrease conduction through the AV node.
 They prolong PR interval, but no effects on QRS or
QT interval
 E.g. Propranolol - Metoprolol
 Perfect to hypertension and coronary artery disease
patients associated with tachyarrhythmia

53
Class III – K+ channel blockers
 acts by prolonging repolarization.
 Not affect the sodium channel, so conduction velocity
is not decreased.
 The prolongation of the action potential duration and
refractory period, combined with the maintenance of
normal conduction velocity, prevent re-entrant
arrhythmias.
 Class III agents have the potential to prolong the QT
interval of the ECG
 E.g Amiodarone - Bretylium

54
Class IV- calcium channel blockers
 The primary action of this class of drug is to inhibit Ca2+
mediated slow inward current.
 They decrease conduction through the AV node, and shorten
phase two (the plateau) of the cardiac action potential.
 As they reduce the contractility of the heart, so may be
inappropriate in heart failure.
 They slow sinus rhythm, prolong PR interval, no effect on
QRS complex
 E.g. Verapamil - Diltiazem
 used in supraventricular tachycardia

55
Others
 Adenosine
 be used in supraventricular tachycardia
 Digoaxin:
 Used to control ventricular rate in AF – AFL -PSVT

56
Adenosine
 Endogenously produced important chemical mediator used
in PSVT
 Mechanism:
 Activation of Ach sensitive K+ channel causes membrane
hyper polarization of SA node and results in
o depression of SA node
o slowing of AV conduction and shortening of action potential
in atrium
 indirectly reduces CA++ current in AV node with depression
of reentry in PSVT.

57
Anti-bradycardia agents
 ß-adrenic receptor activator:
 Isoprenaline
 Epinephrine
 M-cholinergic receptor blocker:
 Atropine
 Non-specific activator:
 Aminophylline

58
Proarrhythmic effect of
antiarrhythmic agents
 Class Ia, Ic : Prolong QT interval, will cause VT or VF
in coronary artery disease and heart failure patients
 Class III : Like Ia, Ic class agents
 Class II, IV : Bradycardia

59
New developments
 Agents Similar to Amiodarone
o Dronedarone, budiodarone, celivarone
 Others
o Ranolazine, vernaklant, ivabradine
 Nutritional alternatives
o Berberine, coenzymeQ10, taurine

60
Non-drug therapy
 Cardioversion:
 For tachycardia especially hemodynamic unstable
patient
 Radiofrequency catheter ablation (RFCA):
 For those tachycardia patients (SVT, VT, AF, AFL)
 Artificial cardiac pacing:
 For bradycardia, heart failure and malignant
ventricular arrhythmia patients.

62
Radiofrequency catheter ablation

Management of
different types
of arrythmia

65
Premature beats
 Premature beats are the most common type of
arrhythmia.
 Premature beats that occur in the atria are called
premature atrial contractions, or PACs and those that
occur in the ventricles are called premature ventricular
contractions
 PACs are common and may occur as the result of
stimulants such as coffee, tea, alcohol, cigarettes, or
medications.
 Treatment is rarely necessary

67
Sinus tachycardia
 Sinus tachycardia is a heart rhythm originating from the
SA node with an elevated rate of impulses, defined as a
rate greater than 100 beats/min in an average adult.
 Sinus tachycardia is usually a response to normal
physiological situations, such as exercise and an
increased sympathetic tone with increased catecholamine
release—stress, fright, flight,anger
 Treatment not required for physiologic sinus tachycardia.
 Underlying causes are treated if present.

69
Paroxysmal supraventricular
tachycardia
 Here the heart rate ranges from 160 – 250 beats per
min
 There are 2 common types
1) Atrio ventricular reciprocating tachycardia
2) AV nodal reentrant tachycardia

70
AV nodal Re-entrant Tachycardia
 AVNRT develops because of the presence of two electro
physiologically distinct pathways for conduction in the
complex the AV node.
 The fast pathway in the more superior part of the node
has a longer refractory period, whereas the pathway
lower in the AV node region conducts more slowly but
has a shorter refractory period.
 As a result of the inhomogeneities of conduction and
refractoriness, a reentrant circuit can develop in response
to premature stimulation.

71
AV Nodal Reciprocating Tachycardia
 Patients with AVRT have been born with an extra,
abnormal electrical connection in the heart.
 In AVRT, the extra connection, which is often called an
accessory pathway, joins one of the atria with one of the
ventricles
 In some patients with AVRT, the accessory pathway is
capable of conducting electrical impulses in both
directions while in other patients the accessory pathway
can only conduct electrical impulses in one direction or
the other

72
AV Nodal Reciprocating Tachycardia
 This difference turns out to be important. In most
patients with AVRT, the impulses can only go across the
accessory pathway from the ventricle to the atrium.
 Patients in whom the impulses can travel across the
accessory pathway in the other direction - from the
atrium to the ventricle - are said to have Wolff-
Parkinson-White (WPW) syndrome

73
Management of PSVT
 Acute Management
 If the patient is hemodynamically stable, vagal
maneuvers e.g carotid massage , can be successfully
employed.
 If not successful, the administration of IV adenosine
frequently does so.
 Intravenous beta blockade or calcium channel therapy
should be considered as second-line treatment.
 Patients with hemodynamic instability require emergency
cardioversion.

74
Management of PSVT
 Long-term management
 It includes ablation of the accessory pathway.
 Also, verapamil, diltiazem & β-blockers are effective in
60- 80% of patients.

75
Wolf Parkinson White Syndrome
 An abnormal band of atrial tissue connects the atria and
the ventricles and can electrically bypass the normal
conducting pathways
 A reentry circuit develops causing paroxysms of
tachycardia.
 Drug treatment : flecainide, amiodarone or
disopyramide
 Digoxin and verapamil are contraindicated
 Transvenous catheter radiofrequency ablation is the
treatment of choice

76
Wolf Parkinson White Syndrome

77
Atrial Flutter
 HR ranges between 200-350/min
 Here the electrical signals come from the atria at a fast but
even rate, often causing the ventricles to contract faster
and increase the heart rate.
 When the signals from the atria are coming at a faster rate
than the ventricles can respond to, the ECG pattern
develops a signature "sawtooth" pattern, showing two or
more flutter waves between each QRS complex

79
Atrial Flutter
 Treatment
 For acute paroxysm : Cardioversion
 Recurrent paroxysms may be prevented by class Ic and
class III agents
 The treatment of choice for patients with recurrent atrial
 flutter is radiofrequency catheter ablation

80
Atrial fibrillations
 Atrial fibrillation is the most common sustained
arrhythmia.
 It is marked by disorganized, rapid, and irregular atrial
activation. The ventricular response to the rapid atrial
activation is also irregular
 Typically the pulse rate will vary between 120 and 160
beats per minute
 The ECG shows normal but irregular QRS complexes,
fine oscillations of the baseline (so-called fibrillation or f
waves) and no P waves

82
Atrial fibrillations
 When atrial fibrillation is due to an acute precipitating
event the provoking cause should be treated.
 Acute management of AF
 Cardioversion rates delivered synchronously with the
QRS complex typically are >90%.
 Pharmacologic therapy to terminate AF is less reliable.
Oral and/or IV administration of amiodarone or
procainamide has only modest success.
 Patients are anticoagulated ( warfarin) for 4 weeks before
cardioversion

83
Ventricular tachycardia
 This is a potentially life-threatening arrhythmia because it
may lead to ventricular fibrillation, asystole, and sudden
death.
 A condition in which an electrical signal is sent from the
ventricles at a very fast but often regular rate.
 If the fast rhythm self-terminates within 30 seconds, it is
considered a non-sustained ventricular tachycardia.
 If the rhythm lasts more than 30 seconds, it is known as a
sustained ventricular tachycardia

85
Ventricular tachycardia
 Treatment
 In hemodynamically compromised :emergency
asynchronous defibrillation is done
 If hemodynamically stable:
 intravenous therapy with class I drugs or amiodarone .
 VT in patients with structural heart disease is now almost
always treated with the implantation of an ICD to manage
anticipated VT recurrence

86
Ventricular fibrillation
 A condition in which many electrical signals are sent from
the ventricles at a very fast and erratic rate. As a result,
the ventricles are unable to fill with blood and pump.
 This rhythm is life-threatening because there is no pulse
and complete loss of consciousness.
 It requires prompt defibrillation to restore the normal
rhythm and function of the heart.

88
Ventricular fibrillation
 Basic and advanced cardiac life support is needed
Implantable cardioverter-defibrillators (ICDs) are first-
line therapy in the management of these patients

89
Torsades pointes
 This is a type of short duration tachycardia that reverts to
sinus rhythm spontaneously.
 It may be Congenital or due to Electrolyte disorders and
certain Drugs
 It may present with syncopal attacks and occasionally
ventricular fibrillation.
 QRS complexes are irregular and rapid that twist around
the baseline. In between the spells of tachycardia the ECG
show prolonged QT interval

91
Torsades pointes
 Treatment:
 correction of any electrolyte disturbances
 stopping of causative drug
 atrial or ventricular pacing
 Magnesium sulphate for acquired long QT interval
 IV isoprenaline in acquired cases
 B blockers in congenital types
 Patients who remain symptomatic despite conventional
therapy and those with a strong family history of sudden
death usually need ICD therapy

92
Sinus Bradycardia
 Physiological variant due to strong vagal tone or atheletic
training.
 Rate as low as 50 at rest and 40 during sleep.
 Common causes:
 Hypothermia, hypothyroidism, Drug therapy with
betablockers, digitalis and other antiarrhythmic drugs.
 Acute ischemia and infarction of the sinus node (as a
complication of acute myocardial infarction).

94
Sick sinus syndrome
 Sick sinus syndrome is a group of arrhythmias caused by
a malfunction of the sinus node
 A condition in which the sinus node sends out electrical
signals either too slowly or too fast. There may be
alternation between too-fast and too-slow rates.
 This condition may cause symptoms if the rate becomes
too slow or too fast for the body to tolerate.

95
Sick sinus syndrome
 Artificial pacemakers have been used in the treatment of
sick sinus syndrome.
 Bradyarrhythmias are well controlled with pacemakers,
while tachyarrhythmias respond well to medical therapy.
 However, because both bradyarrhythmias and
tachyarrhythmias may be present, drugs to control
tachyarrhythmia may exacerbate bradyarrhythmia.
Therefore, a pacemaker is implanted before drug therapy
is begun for the tachyarrhythmia

96
Atrio ventricular block
 First degree heart block
 PR interval is lengthened beyond 0.20 seconds.
 In first-degree AV block, the impulse conducting from
atria to ventricles through the AV node is delayed and
travels slower than normal
 Seldom of clinical significance, and unlikely to progress

98
 Second degree A-V Block
A- Mobitz type I (Wenckebach phenomenon):
 Gradually increasing P-R intervals culminating in an
omission.
 When isolated, usually physiological and due to increased
vagal tone and abolished by exercise and atropine.

99
 Second degree A-V Block
B- Mobitz type II:
 The P wave is sporadically not conducted.
 Occurs when a dropped QRS complex is not preceded by
progressive PR interval prolongation.
 Pacing is usually indicated in Mobitz II block, whereas
patients with Wenckebach AV block are usually
monitored

101
 Third degree A-V Block
 Common in elderly age groups due to idiopathic bundle
branch fibrosis.
 Other causes include coronary heart disease, calcification
from aortic valve, sarcoidosis or it may be congenital.
 ECG shows bradycardia, P wave continues which is
unrelated to regular slow idioventricular rhythm.
 Treatment is permanent pacing.

103
thanksF o r W a t c h i n g

Management of cardiac arrhythmias

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Management of cardiac arrhythmias

Similar to Management of cardiac arrhythmias (20)

More from Sameh Abdel-ghany

More from Sameh Abdel-ghany (20)

Recently uploaded

Recently uploaded (20)

Management of cardiac arrhythmias