2. Cardiac arrhythmia
• Abnormal cardiac rhythm usually involving a
change in rate or regularity.
• Synonym: dysrhythmia

4. Etiology
Physiological:
-sympathetic or parasympathetic control changes
eg. Stress , anxiety, exercise , smoking.
Hypothyroidism,
Hyperthyroidism
Hypoadrenalism
Hyperkalemia
hypokalemia and
other electrolyte changes.

5. Pathological:
Valvular heart disease.
Ischemic heart disease.----------MI causing death of
pacemaker cells or conducting tissue.
Hypertensive heart diseases.
Congenital heart disease.
Cardiomyopathies.
Carditis.
RV dysplasia.
Drug related.
Pericarditis.
Pulmonary diseases.
Others.

6. CLINICAL EVALUATION
I. PHYSICAL FINDINGS
Palpitation.
Dizziness.
Chest Pain.
Abnormal pulse rate , rhythm or amplitude
Dyspnea.
Anxiety and confusion (from reduced brain perfusion)
Fainting (syncope)
Skin pallor or cyanosis
Reduced blood pressure
Weakness
Convulsions
Decreased urinary output
Sudden cardiac death.

7. II. DIAGNOSTIC TEST RESULTS
ECG
electrophysiological (EP) testing
His bundle study
III. LAB FINDINGS:
hyperkalemia (>5mEq/L)
Hypocalcemia (<4.5mEq/L)
hypomagnesemia(<2.5mEq/L)

8. Mechanism of Arrhythmogensis
1. Disorder of impulse formation.
a) Automaticity.
b) Triggered Activity.
1) Early after depolarization.
2) Delayed after depolarization.
2. Disorder of impulse conduction.
a)
b)
Block – Reentry.
Reflection.
3. Combined disorder.

9. Nomenclature for describing
arrhythmias
• Rate
tachycardia
bradycardia
• Origin:
sinus
atrial
nodal
supraventricular
re-entrant
ventricular

10. • Pattern:
ectopic
Premature contraction
paroxysmal
flutter
fibrillation
block
torsades
electromechanical dissociation

11. Duration:
i) paroxysmal- self terminating
episodes upto 7 days
ii) persistent
-non self terminating more
than 7 days
iii) permanent - not responding to
cardioversion attempts
iv) recurrent: returning after once stopped.

12. Electrophysiological treatment
1) Cardioversion
2) Implantable Cardiac Defibrillator (ICD)
3) Pace maker
4) Lead extraction

13. Pharmacology of anti- arrhythmic drugs

15. Quinidine (Class IA prototype)
• Other examples: Procainamide, Disopyrimide
General properties:
a. D-isomer of quinine
b. As with most of the Class I agents
- moderate block of sodium channels
- decreases automaticity of pacemaker cells
- increases effective refractory period/AP
duration

16. Actions of quinidine
• Cardiac effects
a. ↓ automaticity, conduction velocity and excitability of
cardiac cells.
b. Preferentially blocks open Na channels
c. Recovery from block slow in depolarized tissue;
lengthens refractory period (RP)
d. All effects are potentiated in depolarized tissues
e. Increases action potential duration (APD) and
prolongs AP repolarization via block of K channels;
decreases reentry
f. Indirect action: anticholinergic effect (accelerates
heart), which can speed A-V conduction.

17. – Cardiac tissue:
•
•
•
•
•
Reduce automaticity
Reduce excitability
Reduce conductivity
Prolong refractory period
Reflex tachycardia
– Other action:
• Anti-malarial
• Anti-pyretic
• Decrease B.P (vasodilation)

18. Pharmacokinetics:
– Orally active; i.v. in emergency; i.m. painful
– 80% bound to plasma proteins
– Half-life: 4-6 hrs
– Metabolized by liver (75%)
– Excretion: unchanged fraction by kidney

20. Extracardiac
a. Blocks alpha-adrenoreceptors to yield vasodilatation.
b. Other strong antimuscarinic actions
Toxicity
- "Quinidine syncope"(fainting)- due to disorganized ventricular
tachycardia
- associated with greatly lengthened Q-T interval; can lead to
Torsades de Pointes (VT, precursor to ventricular fibrillation)
- negative inotropic action (decreases contractility)
- GI - diarrhea, nausea, vomiting
- CNS effects - headaches, dizziness, tinnitus (quinidine
“Cinchonism”)

21. • Adverse effects:
–
–
–
–
–
–
–
–
–
–
Heart block
Sinus arrest
Myocardial depression
Q-T prolongation
Ventricular fibrillation
Nausea
Vomiting
Diarrhoea
Rash
Oedema

22. Indications :
1) Premature atrial contractions
2) Paroxysmal atrial fibrillation and flutter
3) Intra-atrial and A-V nodal reentrant dysrhythmias
4) Wolff-Parkinson-White tachycardias (SVT, A-V bypass)
5) Premature ventricular contractions (PVCs)
6) Useful in treating chronic dysrhythmias requiring
outpatient treatment
• Also as anti-malarial
• Anti-pyretic
• During digitalis therapy

23. • Contraindications:
– Quinidine intolerance
– Digitalis intoxication
– Heart failure
– Hypotension
– hypokalemia

24. Procainamide (Class 1A) also
Disopyrimide
Cardiac effects
a) Similar to quinidine, less muscarinic & alphaadrenergic blockade
b) Also has negative inotropic action .
Extracardiac effects
a) Ganglionic blocking reduces peripheral vascular
resistance
Toxicity
a) Cardiac: Similar to quinidine; cardiac depression
b) Noncardiac: Syndrome resembling lupus
erythematosus

25. Pharmacokinetics/therapeutics
a. Administered orally, i-v
b. Major metabolite in liver is N-acetylprocainamide
(NAPA), a weak Na channel blocker with class III activity.
Bimodal distribution in population of rapid acetylators,
who can accumulate high levels of NAPA.
c. T1/2 = 3-4 hours; necessitates frequent dosing; kidney
chief elimination path. NAPA has longer T1/2 and can
accumulate
d. Usually used short-term. Commonly used in CCUs for
ventricular dysrhythmias associated with acute
myocardial infarctions (MI)

26. Lidocaine (Class IB prototype)
Other examples: Mexiletine, Phenytoin, Tocainide
General
a). Commonly used antidysrhythmic agent in
emergency care (decreasing use)
b) Given i-v; widely used in ICU-critical care units
c)Low toxicity (especially cardiac, good
therapeutic index)
d) A local anesthetic, works on nerve at higher
doses

27. • Mechanism of anti-arrhythmic effect of
lignocaine:
– It has membrane stabilizing effect by blocking
both activated and inactivated sodium channels;
which in turn supresses SA node and also ectopic
beats.
– Shortens refractory period and action potential;
make uniform rhythm

29. Cardiac effects
a. Generally decreases APD, hastens AP repolarization, decreases
automaticity and increases refractory period in depolarized
cells.
b. Exclusively acts on Na channels in depolarized tissue by
blocking open and inactivated (mainly) Na channels
c. Potent suppresser of abnormal activity
d. Most Na channels of normal cells rapidly unblock from
lidocaine during diastole; few electrophysiological effects in
normal tissue
Toxicity: - least cardiotoxic, high dose can lead to hypotension
• - tremors, nausea, slurred speech, convulsions
– Bradycardia, Hypotension, Dizziness, Blurred vision,
Sleepiness, Confusion

30. • Pharmacokinetics
a. i-v, since extensive first pass hepatic metabolism
b. T1/2 = 0.5-4 hours
Indications
a) Effective in suppressing dysrhythmia associated with
depolarised.( Tissue ischemia; digitalis toxicity);
ineffective against dysrhythmias in normal tissue (atrial
flutter).
b) Suppresses ventricular tachycardia; prevents fibrillation
after acute MI; rarely used in supraventricular
dysrhythmias

31. Contraindications of lidocaine
• Heart block, second or third degree (without pacemaker)
• Severe sinoatrial block (without pacemaker)
• Serious adverse drug reaction to lidocaine or amide local
anaesthetics
• Concurrent treatment with quinidine, flecainide,
disopyramide, procainamide (Class I antiarrhythmic agents)
• Prior use of Amiodarone hydrochloride
• Hypotension not due to Arrhythmia
• Bradycardia
• Accelerated idioventricular rhythm
• Pacemaker
• Porphyria, especially acute porphyria (AIP)

32. Phenytoin
1. Non-sedative anticonvulsant used in treating epilepsy
('Dilantin')
2. Limited efficacy as antidysrhythmic (second line
antiarrythmic)
3. Suppresses ectopic activation by blocking Na and Ca
channels
4. Especially effective against digitalis-induced
dysrhythmias
5. T1/2 = 24 hr – metabolized in liver
6. Gingival hyperplasia (40%)

33. Flecainide (Class IC prototype)
Other examples: Lorcainide, Propafenone, Indecainide, Moricizine
Depress rate of rise of AP without change in refractoriness or APD
1. Decreases automaticity, conduction in depolarized cells.
2. Marked block of open Na channels (decreases Ph. 0); no change
repolarization.
3. Used primarily for ventricular dysrhythmias but effective for atrial
too
4. No antimuscarinic action
5. Suppresses premature ventricular contractions (PVCs)
6. Associated with significant mortality; thus, use limited to last resort
applications like treating ventricular tachycardias
7. Significant negative inotropic effect

35. Propranolol (Class II, betaadrenoreceptor blockers)
• Other agents: Metoprolol, Esmolol (short acting), Sotalol (also Class
III), Acebutolol
• Propranolol as anti-arrhythmic drug:
– It blocks β-receptors in heart, thereby exerts
•
•
•
•
Negative inotropic effect
Negative chronotropic effect
Depress atrioventricular conduction
Depresses automaticity
– It has:
• Anti-arrhythmic effect
• Anti-hypertensive effect
• Anti-anginal-effect in CVS.
a. Slow A-V conduction
b. Prolong A-V refractory period

36. Cardiac effects (of propranolol), a non-selective
beta blocker
a. Main mechanism of action is blockade of beta
receptors; ↓ Ph 4 slope which decreases
automaticity under certain conditions
b. Some direct local anesthetic effect by block of Na
channels (membrane stabilization) at higher
doses
c. Increases refractory period in depolarized tissues
d. Increases A-V nodal refractory period
Non-cardiac: Hypotension

37. • Therapeutics
a. Blocks abnormal pacemakers in cells receiving
excess catecholamines (e.g. pheochromocytoma)
or up-regulated beta-receptors (ie.
hyperthyroidism)
b. Blocks A-V nodal reentrant tachycardias; inhibits
ectopic foci
c. Beta-blockers are used to treat supraventricular
tachydysrhythmias
d. Propranolol contraindicated in ventricular failure;
can lead to A-V block.

38. Amiodarone (Class III)
• others: Ibutilide, Bretylium, Sotalol, Dofetilide
• Dronedarone
• General
a. New DOC for ventricular dysrhythmias (Lidocaine, old DOC)
b. prolongs refractory period by blocking potassium channels
c. also member of Classes IA,II,III,IV since blocks Na, K, Ca
channels and alpha and beta adrenergic receptors
d. serious side effects (cardiac depression, pulmonary fibrosis,
thyroid)
e. effective against atrial, A-V and ventricular dysrhythmias
f. widely used, very long acting (>25 d)

40. Effects of amiodarone
Cardiac effects
a. Block Na channels (1A), but low affinity for open
channels; mainly blocks inactivated Na channels
b. Block is most pronounced in tissues with long action
potentials
c. Weak Ca channel blocker also (Class IV activity)
d. A powerful inhibitor of abnormal automaticity, decreases
conduction, increases refractory period and APD.
e. Has antianginal effects (blocks alpha/beta receptors and
Ca channels)
Extracardiac effects:
Vasodilation via block of Ca channels and alpha receptors

41. • B. Non-cardiac:
• i. Deposits into almost every organ
• ii. Reduces clearance of drugs like procainamide, flecainide,
digitalis,
• quinidine and diltiazem.
• iii. Thyroid dysfunction (hypo or hyperthyroidism)
• iv. Pulmonary fibrosis is most serious adverse effect
• v. Paresthesias (tingling, pricking, or numbness)
• vi. Photosensitivity
• vii. Corneal microdeposits and blurred vision
• viii. Ataxia, dizziness, tremor
• ix. Anorexia, nausea

42. Adverse effects of amiodarone
• A. Cardiac
• i. Sinus bradycardia, increase QT interval
↑risk TdP
• ii. Negative inotropic action due to block of Ca
channels and beta
• receptors; but can improve heart failure via
vasodilation.
• iii. A-V block, paradoxical VTs.

43. Verapamil (Class IV, Ca++ channel
blockers)
• Other example: Diltiazem - CCBs increasing use and
importance
a. Blocks active and inactivated Ca channels, prevents Ca
entry
b. More effective on depolarized tissue, tissue firing
frequently or areas where activity dependent on Ca
channels (SA node; A-V node)
c. Increases A-V conduction time and refractory period;
directly slows SA and A-V node automaticity
d. suppresses oscillatory depolarizing after
depolarizations due to digitalis
e. Dihydropyridine CCBs are generally poor antiarrythmics

44. Ca++ Channel Blockers - Actions
Extracardiac
a. Peripheral vasodilatation via effect on smooth muscle
b. Used as antianginal / antihypertensive
c. Hypotension may increase HR reflexively
Toxicity
a. Cardiac
- Too negative inotropic for damaged heart, depresses
contractility
- Can produce complete A-V block
b. Extracardiac
- Hypotension
- Constipation

45. Other antiarrythmics
A. Adenosine: i.v. (15 secs), activates P1 purinergic
receptors (A1) coupled to K channels, ↓CV, ↑refractory
period. SVT. Flushing, hypotension, burning sensation
B. Potassium ions (K+): Depress ectopic pacemakers
- can depress CV → reentrant dysrhythmia
C. Digoxin: used to treat atrial flutter and fibrillation
- AV node ↓conduction (vagal stimulation)
- myocardium ↓refractory period
- Purkinje fibers ↑refractory period, ↓conduction
D. Magnesium: used to treat Torsades de Pointes
E. Autonomic agents: used to treat A-V block
- β-agonists , anticholinergics (ie. atropine)
Anticoagulant therapy:
- prevent formation of systemic emboli & stroke

46. Life style changes
•
•
•
•
•
Eat heart-healthy foods.
Increase your physical activity.
Quit smoking.
Cut back on caffeine and alcohol.
Find ways to reduce the amount of stress in your
life.
• Avoid stimulant medications, such as medications
found in over-the-counter treatments for colds
and nasal congestion.

48. Arrythmia detected
yes
Is it life threatening?
emergency resuscitation
no
is it affecting cardiac output
Or threatening to do so
yes
Or unpleasant for the patient ?
monitor , check electrolytes and
possible causes.
yes
yes
is the rate slow?
Consider electrolyte pacing
no
correct elctrolyte abnormalities
choose a drug according to origin
Of arrhythmia
Algorithm for treatment of arrhythmia

49. Condition
Drug
Sinus tachycardia
Class II, IV
Atrial fibrillation/flutter
Class IA, IC, II,
III, IV
digitalis
adenosine
Paroxysmal supraventricular
tachycardia
Class IA, IC, II,
III, IV
adenosine
AV block
Atropine
Ventricular tachycardia
Class I, II, III
Premature ventricular complexes
Class II, IV
Mg++ salts
Digitalis toxicity
Class IB
Mg++ salts;
KCl

50. Diagnosis
Treatment
Avoid
Atrial Fibrillation
in Patient with
WPW Syndrome
Direct
Cardioversion+Lidocaine or
Procainamide Or Ibutilide
Digoxin
Amiodarone
Verapamil
WPW and
Pseudo-Inferior
MI
Betablocker
CCB
Quinidine
Flecainide
Pace-maker
Digoxin
Verapamil
Atrial Flutter
with 2:1 Av
Conduction
Digoxin 0.25
Esmolol 0.5 Mg/Kg
Amiodarone 150mg
Quinidine
Ventricular tachycardia
Magnesium-Sulphate
Procainamide Amiodarone Lidocaine
If failed:
Cardioversion
Verapamil
Adenosine
Atrial flutter
Digoxin 0.25
Esmolol 0.5 Mg/Kg
Amiodarone 150mg
Quinidine

51. Drug choice in treating chronic or
persistent atrial fibrillation
Associated factors
First choice
Second choice
Avoid
Acute systemic illness
Nothing or II
IV, II
I
II
Disopyramide
Sotalol/Amiodar
one
Sotalol, IC
Sotalo, IC
Digoxin
II
IC
Digoxin, IV
IA, III
Paroxysmal
exercise induced
vagal origin
elderly
Sustained AF
ventricular rate control
cardioversion
Respiratory disorders
II, IV, Digoxin
II, sotalol
IHD
Sotalol
Amiodarone
I
Heart failure
Amiodarone
Digoxin
I
Hypertension
Sotalol
Amiodarone

52. Drug classes in chronic
tachyarrythmias
SA node
Commonly
used
Also used
Atria
AV node
Accessory Ventricles
pathway
II
II
IV
IV for urgent
cardioversion
II
IC
II
III
Digoxin
III
IC
IA
Digoxin
IC
II
IA
I

58. Common therapeutic problems in the
management of arryhthmias
Problem
Management
Narrow therapeutic range of digoxin
Encourage compliance and perform TDM
Beta blockers contraindicated in bronchial
and peripheral vascular diseases
Consider verapamil or diltiazem
Verapamil induced constipation
Give regular laxatives
Pro-arrythmic actions of antiarrhytmics
Minimise requirements of drugs , else
switch to pacemaker or elctrical therapy
Amiodarone sun burn
Stay indoors , use sunblock