1. The document discusses antiarrhythmic drugs and their classification and mechanisms of action. It focuses on Class I drugs that work by blocking sodium channels. 2. Class IA drugs like quinidine and procainamide have a moderate effect on sodium channels and are used for supraventricular and ventricular arrhythmias. They can cause side effects like QT prolongation. 3. Class IB drugs like lidocaine have a weak effect on sodium channels and are the drugs of choice for ventricular arrhythmias. They are used for ventricular arrhythmias due to ischemia or digoxin toxicity.

1. Dr Neelkant
MODERATOR : Dr S Mastan Saheb
ANTI- ARRHYTHMIC DRUGS

2. OUTLINE:
• ANATOMY OF THE CONDUCTION SYSTEM
(ELECTROPHYSIOLOGY OF THE HEART)
• ELECTRICAL PROPERTIES OF THE HEART
• MECHANISM/ PATHOLOGY, CAUSES AND TYPES OF ARRHYTHMIAS
• ANTI-ARRHYTHMIC DRUGS
• PERIOPERATIVE ARRHYTHMIAS

3. ELECTRICAL PROPERTIES OF THE HEART
• EXCITABIITY – BATHMOTROPISM
• AUTO-RHYTHMICITY –
CHRONOTROPISM
• CONDUCTIVITY – DROMOTROPISM
• CONTRACTILITY – IONOTROPISM
• RELAXATION – LUSITROPISM

4. Normal conduction pathway:
AV NODAL DELAY
Diminshed number of gap junctions in
the conducting pathway
PURKINJE – fast -1.5 to 4 m/s – highly
permeable and has high gap junctions
Penetrate 1/3 into the ventricular
muscle

5. CONTROL OF EXCITATION & CONDUCTION
• Normal pacemaker – sino- atrial node FASTER DISCHARGE RATE
AND BEFORE THE AVNODE OR PURKINJE FIBRES REACH THRESHOLDS
• AV nodal fibres – if not stimulated - 40 to 60 / min
• Purkinje fibres- 15-40/min
• ABNORMAL PACEMAKER – ANY part which discharges faster the SA node
• ECTOPIC – pacemaker other than the sinus node
• WHY PURKINJE SYSTEM IS IMPORTANT
Rapid conduction -> cardiac impulse arrives at all portions of ventricles
within a narrow span of time

6. Action potential of the heart:
PACEMAKER MUSCLE
-40 (TP) -65(TP)
3 phases 5 phases
Calcium sodium
0.05m/s 1-4m/s

7. N.B. The slope of phase 0 = conduction velocity
Also the peak of phase 0 = Vmax

8. It is also called absolute refractory period (ARP)
:
•In this period the cell can’t be excited
•Takes place between phase 0 and 3

9. Pathology
•Injury –
pacemaker or
conduction
pathway
•Automaticity
•Re-entry
•Ectopic /
irritable foci
•Ion channel
mutations
SA NODE
• Sinus arrhythmia
• Sinus bradycardia
• Sinus tachycardia
• Sick sinus syndrome
ARTIAL MUSCLE
• Atrial ectopics
• Atrial tachycardia
• Atrial flutter
• Atrial fibrillation
• Multifocal atrial tachycardia
AV NODE
• Junctional bradycardia
• Junctional tachycardia
• PSVT
• SVT
VENTRICULAR MUSCLE
• Ventricular ectopics
• Ventricular tachycardia
• Ventricular flutter
• Ventricular fibrillation
• Torsade-de-pointes
• Asystole

10. Mechnisms of Arrhythmogenesis
1- Abnormal
impulse
generation
Automatic
rhythms
Ectopic focus
Enhanced
normal
automaticity
Triggered
rhythms
Delayed
afterdepolarization
Early
afterdepolarization
↑AP from SA node
AP arises from sites
other than SA node
Early phase 4
Due to increased
Ca overload
ISCHEMIA
DIGOXIN TOXICITY
Phase 3
AP is prolonged
in outward K
ischemia, K channel
blockers

11. 2-Abnormal
conduction
Conduction
block
1st degree 2nd degree 3rd degree
Reentry
Circus
movement
1-This pathway
is blocked
2-The impulse from
this pathway travels
in a retrograde
fashion (backward)
3-So the cells here will be
reexcited (first by the
original pathway and the
other from the retrograde)

12. Here is an
accessory pathway
in the heart called
Bundle of Kent
•Present only in small populations
•Lead to reexcitation  Wolf-Parkinson-White
Syndrome (WPW)
Abnormal anatomic conduction
TRIAD OF DELTA WAVES SHORT PR INTERVAL AND WIDE QRS
RE-ENTRY
Verapamil, digoxin
CONTRAINDICATED

13. SINUS ARRHYTHMIA – alteration of
heart rate with respiration
TYPES OF ARRHYTHMIAS

14. SINUS BRADYCARDIA – sinus rhythm with normal PQRST complexes, BUT
with a rate<60/min
beta blocker or CAD – 50/min
• Treat the reversible cause FIRST
• Atropine - 20µg/kg or Glycopyrrolate
10µg/kg
• Resistant -> known to take beta-
blockers -> Adrenaline / Isoprenaline
(0.5 to 10µg/kg)
• Resistant - > Temporary pacing for
emergency surgeries
• Vagal stimulation –
Anal/genito cervical
dilatation
MI, Sick sinus syndrome,
• Non-cardiac –
hypothermia,
Intracranial
hypertension,
hypothyroidism,
• DRUGS – Digoxin,
Halothane, Neostigmine
• ASYMPTO – NO Rx
• SYMPTOMATIC -
+hypotension
• Dopamine infusion 5 to
20µg/min

15. ATRIAL ECTOPIC BEATS
-
• Exclude reversible causes
• Treatment is usually unnecessary
Sinus Tachycardia: high sinus rate of 100-180 beats/min,
due to increased SA nodal firing rate with normal PQRST
complexes. IHD with ST changes – prevent ischemia
• Light depth of
anaesthesia
• Shock
• Ischemia
• Sepsis
• Light depth
of
anaesthesia
• Hypovolemia
• Pain
• Surgical
stimulation
• Blood loss

16. ✓Atrial Tachycardia: a series of 3 or more consecutive atrial
premature beats occurring at a frequency >100/min
✓P waves > QRS complexes
✓Fall in cardiac output
✓No Rx is required usually
✓ Carotid sinus massage / Verapamil
MULTI FOCAL TACHYCARDIA – 3 or more different P wave
morphologies with irregular QR complexes

17. ✓SUPRAVENTRICULAR AND JUNCTIONAL TACHYCARDIA – SVT is any
tachycardia originating above the ventricles
✓SVTs must be differentiated from potentially more problematic VT
✓MGMT –
Anaesthetised + hemodynamically unstable - > Synch DC cardioversion
with 200 J - > 2 shocks of 360J
Non anaesthetized - > sedation, then synchronized cardioversion
STABLE –
Carotid sinus massage
Valsalva manouvre
Drugs
✓Atrial Flutter: sinus rate of 250-350 beats/min rhythm
disturbance
Re-entry of electrical impulse into the atria
Saw tooth waves
ACUTE PAROXYSM – cardioversion

18. Both flutter and atrial tachycardia, the atria contract at >150bpm due to an ectopic
focus
P waves – superimposed on T waves
Both carry the same thromboembolic risk as atrial fibrillation

19. ✓Atrial Fibrillation: uncoordinated atrial depolarizations (90% of perioperative
arrhythmias)
✓R Right atrial pressure, mass, fibrosis, inflammation
Management depends on its onset - <48 hrs>
ACUTE – Rate control – beta blockers > CCB
DC cardioversion in hemodynamically unstable
embolization – systemic / PTE
Digoxin – chronic AF
Echocardiogram prior to surgery
Longer than 48 hrs - > Risk of atrial clot formation
AV blocks
A conduction block within the AV node , occasionally in the bundle of His, that impairs
impulse conduction from the atria to the ventricles
CAUSES –
1. Ischemia – most common cause
2. Sepsis
3. Dyselectrolytemia – hypoMg / hypo K
4. Hypertension, heart failure
5. Thoracic surgery

20. monitor
No pacing
->av block

21. ✓Ventricular Premature Beats
(VPBs): caused by ectopic
ventricular foci; characterized
by widened QRS.
✓Anaesthetized + CAD
Ventricular Arrhythmias
✓Ventricular Tachycardia (VT): high
ventricular rate caused by abnormal
ventricular automaticity or by
intraventricular reentry; can be
sustained or non-sustained
(paroxysmal); characterized by
widened QRS; rates of 100 to 200
beats/min; life-threatening.
Rx – underlying abnormalities
>5bpm multifocal + unstable
hemodynamics - > treat
Lidocaine 1.5mg/kg f/b 1-4mg/min

22. Ventricular Flutter -
ventricular depolarizations
>200/min
No mechanical effect – no
cardiac output
Ischemia / electrolytes / drugs
• Rx – CPR
• Defibrillation – 260-360 J
Ventricular Fibrillation - uncoordinated
ventricular depolarizations

23. Pharmacologic Rationale & Goals
❑ The ultimate goal of antiarrhythmic drug therapy:
o Restore normal sinus rhythm and conduction
o Prevent more serious and possibly lethal arrhythmias from occurring.
❑ Antiarrhythmic drugs are used to:
✓ decrease conduction velocity (phase 0)
✓ change the duration of the effective refractory period (ERP)
✓ suppress abnormal automaticity
✓ Better at terminating an attack than preventing a recurrence
✓ SELECTION – type of arrhythmia, urgency, short / longerm
With increased doses they become pro-arrhythmic as they start to effect
the normal tissues, or when ventricular function is impaired

24. Antyarrhythmic drugs
class mechanism action notes
I Na+ channel blocker
Change the slope of phase
0
Can abolish
tachyarrhythmia
caused by reentry
circuit
II β blocker
↓heart rate and
conduction velocity
Can indirectly alter K
and Ca conductance
III K+ channel blocker
1. ↑action potential
duration (APD) or
effective refractory
period (ERP).
2. Delay repolarization.
Inhibit reentry
tachycardia
IV Ca++ channel blocker
Slowing the rate of rise in
phase 4 of SA node(slide
12)
↓conduction velocity
in SA and AV node
•Most antiarrhythmic drugs are pro-arrhythmic (promote arrhythmia)
•They are classified according to Vaughan William into four classes according to their effects on
the cardiac action potential

27. Acts by blocking the If
IVABRADINE (class 0)

28. INDICATIONS
1. Heart failure in patients whose HR remains elevated
despite beta blocker therapy
2. Stable angina
3. Inappropriate sinus tachycardia
ADVERSE EFFECTS
1. Sinus bradycardia/ Sinus arrest
2. Increased risk of atrial fibrillation
3. Phosphenes

29. HEART FAILURE:
✓Initially, 5 mg twice daily.
✓After 2 weeks, adjust dose to achieve a resting HR between 50 to
60 bpm.
✓Maximum dose: 7.5 mg BD
Based on resting HR:
▪ If HR is >60 bpm :- Increase dose by 2.5 mg BD
▪ If HR is 50-60 bpm :- Maintain dose
▪ If HR is <50 bpm or hemodynamic compromise due to bradycardia
present :- Decrease dose by 2.5 mg BD
▪ Negative chronotropic actions and no other hemodynamic effects
▪ Single dose - > attenuates heart rate response to intubation and
skin incision without causing hypotension
IVABRADINE: DOSE

30. Class I

32. •Slowing of the rate of rise in
phase 0  ↓conduction
velocity
•Membrane- depressants
•↓of Vmax of the cardiac action
potential
•They prolong muscle action
potential & ventricular (ERP)
•They ↓ the slope of Phase 4
spontaneous depolarization (SA
node)  decrease enhanced
normal automaticity
Class IA
Quinidine Procainamide
They make the
slope more
horizontal

33. Class IA Drugs
⦿They possess intermediate rate of association and
dissociation (moderate effect) with sodium channels.
Pharmacokinetics:
procainamide
Good oral
bioavailability
Metabolised
(excretion) in
kidney
quinidine
Good oral
bioavailability
Metabolized
in the liver
Procainamide metabolized into N-acetylprocainamide (NAPA) (active class III)
which is cleared by the kidney (avoid in renal failure)

34. Class IA Drugs Uses
⦿ Supraventricular and ventricular arrhythmias
⦿ Quinidine is rarely used for supraventricular arrhythmias
⦿ Oral quinidine/procainamide are used with class III drugs
in refractory ventricular tachycardia patients with
implantable defibrillator
⦿ IV procainamide used for hemodynamically stable
ventricular tachycardia
⦿ VT – unresponsive to lidocaine –
IV procainamide 10-15mg/kg loading dose f/b 2-6mg/min
⦿ IV procainamide is used for acute conversion of atrial
fibrillation including Wolff-Parkinson-White Syndrome
(WPWS)

35. Class IA Drugs Toxicity
quinidine
AV block
Torsades de
pointes
arrhythmia
because it ↑ ERP
(QT interval)
Shortens A-V nodal
refractoriness (↑AV
conduction) by
antimuscarinic like
effect
↑digoxin
concentration by :
1- displace from
tissue binding sites
2- ↓renal clearance
Ventricular
tachycardia
procainamide
Asystole or
ventricular
arrhythmia
Hypersensitivity
: fever,
agranulocytosis
Systemic lupus erythromatosus (SLE)-like
symptoms: arthralgia, fever, pleural-pericardial
inflammation.
Symptoms are dose and time dependent
Common in patients with slow hepatic
acetylation

36. Torsades de pointes: twisting of the point . Type of
tachycardia that gives special characteristics on ECG
At large dosesof quinidine  cinchonism occurs:blurred vision, tinnitus, headache, psychosis and
gastrointestinal upset
Quinidine induced syncope
TdP -> VF
IV Mg
Stop anti arrhythmic drugs
Increase heart rate to 100/min by pacing

37. Class IB Drugs
• They shorten Phase 3 repolarization
• ↓ the duration of the cardiac action
potential
• They suppress arrhythmias caused by
abnormal automaticity
❑They show rapid association &
dissociation (weak effect) with Na+
channels with appreciable degree of
use-dependence - > most Na channels
are ready for the next AP
❑No effect on conduction velocity
Class IB
lidocaine
mexiletin
e
tocainide

38. Agents of Class IB
Lidocaine
⦿ Used IV because of extensive 1st pass
metabolism
⦿ Lidocaine is the drug of choice in
emergency treatment of ventricular
arrhythmias VT +hemodynamically stable
-> 50-100mg IV f/b infusion (2-4mg/min)
⦿ VPB 1.5mg/kg f/b 1-4 mg/min
⦿ Has CNS effects: drowsiness, numbness,
convulsion, and nystagmus
Mexiletine
⦿ These are the oral analogs of lidocaine
⦿ Mexiletine is used for chronic treatment of
ventricular arrhythmias associated with
previous myocardial infarction
Uses
✓They are used in the treatment of ventricular arrhythmias arising during myocardial ischemia
or due to digoxin toxicity
✓They have little effect on atrial or AV junction arrhythmias (because they don’t act on
conduction velocity)
Adverse effects:
1- neurological effects
2- negative inotropic activity

39. Class IC Drugs
⦿ They markedly slow Phase 0 fast
depolarization
⦿ They markedly slow conduction in the
myocardial tissue
⦿ They possess slow rate of association
and dissociation (strong effect) with
sodium channels
⦿ They only have minor effects on the
duration of action potential and
refractoriness
⦿ They reduce automaticity by increasing
the threshold potential rather than
decreasing the slope of Phase 4
spontaneous depolarization
Class IC
flecainide propafenone
Flecainide –also blocks the
delayed rectifier K channels
Prevents Atrial fibrillation but
C/I in reduced ventricular
function
ORAL - 100 mg BD
IV – 1-2 mg/kg over 10 min

40. Uses:
➢ Ventricular tachyarrhythmias – attributable to re-entry – AF, A Flutter, PVC,
VT
➢ Refractory ventricular arrhythmias, Ventricular ectopics
➢ Flecainide is a particularly potent suppressant of premature ventricular
contractions (beats), WPW syndrome
Long half life – 16 hrs
Narrow therapeutic range
Toxicity and Cautions for Class IC Drugs:
➢ They are severe proarrhythmogenic drugs causing:
1. severe worsening of a preexisting arrhythmia
2. de novo occurrence of life-threatening ventricular tachycardia /
➢ In patients with frequent premature ventricular contraction (PVC) following
MI, flecainide increased mortality compared to placebo.
➢ Difficult to achieve a therapeutic dose without adverse effects
Notice: Class 1C drugs are particularly of low safety and have shown even
increase mortality when used chronically after MI
CONTRA-INDICATIONS( negative ionotropic action)
Heart failure with myocardial damage
Known CAD

41. Compare between class IA, IB, and IC drugs as regards
effect on Na+ channel & ERP
⦿ Sodium channel blockade:
IC > IA > IB
⦿ Increasing the ERP:
IA>IC>IB (lowered) Because of K+
blockade

42. • Piperazine derivative
• Chemical structure similar to Lidocaine
• Acts by binding at the local anaesthetic binding site of voltage
gated sodium channels
• Slight prolongation of AP - > Reduces refractoriness, and
reducing intracellular Calcium
• Noted to have efficacy in the treatment of atrial arrhythmias
and suppression of sustained ventricular tachycardia
• C/I in patients with creatinine clearance <30ml/min
RANOLAZINE – Class Id

43. Class II ANTIARRHYTHMIC DRUGS
(autonomic modulators )
Mechanism of action
⦿ Negative inotropic and
chronotropic action.
⦿ Prolong AV conduction
(delay)
⦿ Diminish phase 4
depolarization 
suppressing automaticity(of
ectopic focus)
⦿ DO NOT AP OF MYOCARDIAL
CELLS
Uses
⦿ Treatment of increased sympathetic
activity-induced arrhythmias such as
stress- and exercise-induced
arrhythmias
⦿ Atrial flutter and fibrillation (to reduce
the ventricular rate)
⦿ AV nodal tachycardia.
⦿ Reduce mortality in post-myocardial
infarction patients
⦿ Protection against sudden cardiac death
Beta-blockers
M2 receptor blockers
M2 receptor activators
A1 receptor activators

45. Class II ANTIARRHYTHMIC DRUGS
•Propranolol (nonselective): was proved to
reduce the incidence of sudden arrhythmic
death after myocardial infarction
•Metoprolol
➢reduce the risk of bronchospasm
•Esmolol:
➢Esmolol is a ultra short-acting β1-
adrenergic blocker that is used by
intravenous route in acute arrhythmias
occurring during surgery or emergencies
➢Rapid onset and offset - > perioperative
period
➢Loading dose – 0.5 – 1 mg/kg, 0.05 to 0.3
mg/kg infusion
➢Continuous use – metoprolol 5 to 10 mg
IV
selective

48. MUSCARNIC RECEPTOR BLOCKERS
• Atropine and Glycopyrrolate
• Bradyarrhythmias – common during perioperative period
• CAUSES – Decreased sympathetic tone, myocardial ischaemia
• Bradyarrhythmias +/- AV block - > severe haemodynamic instability
and can potentially evolve into TdP,
• Mechanism – Increase the automaticity in the SA node and increase
the conduction through the AV node
• Atrpoine – faster than glycopyrrolate

49. DIGOXIN: MECHANISM OF ACTION

51. • Digoxin also enhances vagal tone on the heart leading to
(MUSCARNIC RECEPTOR ACTIVATOR)
1. Decreased sinus rate
2. Increased duration of the AV nodal refractory period
3. Decreased AV nodal conduction velocity
INDICATIONS
1. Atrial fibrillation and atrial flutter with rapid ventricular
response
2. Heart failure with reduced ejection fraction

52. CARDIAC TOXICITY
• Arrhythmias:
➢ Atrial tachycardia with AV block
(avoided in WPW syndrome)
➢ Atrial fibrillation with slow
ventricular response or
complete heart block
➢ Bidirectional Ventricular
Tachycardia
➢ Hypokalemia, diuretics,
dehydration –add to toxicity
NON CARDIAC TOXICITY
• GI distress
• Dizziness
• Fatigue
• Depression
• Confusion
• Visual disturbances
Digoxin: toxicity

53. • SLOW ORAL DIGITALIZATION
➢LOADING DOSE: 0.125-0.5 mg/day. Steady state achieved
in 7-10 days
• RAPID ORAL DIGITALIZATION
➢LOADING DOSE: 10-15 mcg/kg total LD. Administer 50 %
initially, then 1/4th the LD Q6-8H
• RAPID IV LOADING:
➢0.25-0.5 mg IV over several minutes; followed by 0.25
mg every 6 hrs for a total LD of 0.75-1.5 mg
➢1 amp – 0.25mg/ml comes in 2ml vials 2ml=0.5mg
• MAINTENANCE DOSE: 3.4-5.1 mcg/kg/day or 0.125-0.5
mg/day, may increase dose every 2 weeks
DOSE

54. • Purine Nucleoside
MECHANISM OF ACTION:
Stimulates cardiac adenosine1
receptors  Increase K+ current 
Shortens AP duration and
Hyperpolarizes cardiac cell membranes
in the SA and AV node (supresses
pacemaker function)
A1 receptors – regulate myocardial
oxygen consumption & coronary blood
flow
Myocardial depression
ACTION:
• Suppresses AV nodal conduction
• Suppresses automaticity
• Dilates coronary arteries
• Highly effective in AVNRT
ADENOSINE – A1 receptor

55. • PHARMACOKINETICS:
• Effect short lived due to short elimination t1/2 (10s)
• Metabolism: To inosine by ADA
• Antagonised by theophylline and caffeine
❖Methylxanthines bind to Adenosine1 receptors and inhibits
action of adenosine
❖Dipyridamole inhibits adenosine uptake and potentiates action
of adenosine
❖Heart transplant patients and when administered by Central
line -> Prolonged asystole
ADENOSINE

56. • INDICATIONS:
1. Acute treatment of paroxysmal ventricular tachycardia
ADENOSINE

57. 2. Uncover hidden atrial activity in unknown SVT
ADENOSINE

58. • DOSE:
6 mg IV bolus as fast push f/b 20 ml of 0.9% saline flush
This blocks the AV node - > slows the ventricular rate - > cardioverting the rhythm
to sinus (chemical cardioversion)
repeat injection of 6 to 12 mg IV 3 minutes later
Effects last for 10 to 15 seconds
Beta blockers – esmolol 50 to 100 ug/kg or metaprolol 3 – 5 mg IV over 10 min
every 6 hrs
Verapamil – 5 -10 mg IV over 2 min, with a second dose of 5 mg after 10 min –every
6 hrs
AMIODARONE – CENTRAL LINE – 300 MG OVER 1 HR - if all the above measures
fail
• ADVERSE EFFECTS:
1. Facial flushing
2. Headache
3. Dyspnoea
4. Chest discomfort
5. Nausea
6. Transient AV Block
7. Bronchospasm
CONTRAINDICATED IN PATIENTS TAKING
DIPYRIDAMOLE - > potentiates side effects and risk of
severe myocardial depression (3mg)
ASHTMA – relative contraindication

59. Class III ANTIARRHYTHMIC DRUGS
K+ blockers
⦿Prolongation of phase 3
repolarization without altering
phase 0 upstroke or the resting
membrane potential
⦿ They prolong both the duration of the action
potential and ERP
⦿ Re-entry atrial and ventricular arrhythmias
⦿ Their mechanism of action is still not clear but it
is thought that they block potassium channels

60. Uses:
➢Ventricular arrhythmias, especially ventricular fibrillation or tachycardia –
refractory
➢Supra-ventricular tachycardia
➢Amiodarone usage is limited due to its wide range of side effects
Class III
sotalol amiodarone ibutilide

61. Sotalol (Sotacor)
• Sotalol also prolongs the duration of action potential and
refractoriness in all cardiac tissues (by action of K+ blockade)
• Sotalol suppresses Phase 4 spontaneous depolarization and possibly
producing severe sinus bradycardia (by β blockade action)
• The β-adrenergic blockade combined with prolonged action potential
duration may be of special efficacy in prevention of sustained
ventricular tachycardia
• It may induce the polymorphic torsades de pointes ventricular
tachycardia (because it increases ERP)
Ibutilide
❖Used in atrial fibrillation or flutter to normal sinus rhythm
❖IV administration
❖May lead to torsade de pointes
❖Only drug in class three that possess pure K+ blockade

62. Amiodarone (Cordarone)
• Amiodarone is a drug of multiple actions and is still not well understood
• It is extensively taken up by tissues, especially fatty tissues (extensive distribution)
• Potent P450 inhibitor / Elimination half life of 29 days, effects last for 60 days
• Amiodarone antiarrhythmic effect is complex comprising class I, II, III, and IV actions
• Dominant effect: Prolongation of action potential duration and refractoriness
• It slows cardiac conduction, works as Ca2+ channel blocker, and as a weak β-
adrenergic blocker
• DECREASES THE INCIDENCE OF AF POST CARDIAC SURGERY BY 50 TO 60%

63. • DOES NOT IMPAIR VENTRICULAR PERFORMANCE – can be given in heart
failure
• BOTH SUPRA VENTRICULAR AND VENTRICULAR ARRHYTHMIAS
• long half life – once daily regimen is enough
• Oral – delayed onset of action (3-7days)
• IV – effect is seen in 1 to 24 hrs
• VT – resistant to electrical cardioversion – 300mg over 10 min, f/b 900 mg
over 24 hrs

64. Toxicity
➢Most common include GI intolerance, tremors, ataxia, dizziness, and
hyper-or hypothyroidism
➢Short term – vasodilation and myocardial depression
➢Corneal microdeposits may be accompanied with disturbed night vision
➢Others: liver toxicity, photosensitivity, gray facial discoloration,
neuropathy, muscle weakness, and weight loss
➢The most dangerous side effect is pulmonary fibrosis which occurs in
2-5% of the patients
MULTI ION CHANNEL BLOCKER
Vernalakant - Blocks sodium, Potassium channels
Atria specific – so only causes mild QT prolongation without increasing
the risk of tdP
USE – Terminating acute AF

65. Class IV ANTIARRHYTHMIC DRUGS
(Calcium Channel Blockers)
❖Calcium channel blockers decrease inward Ca2+ currents
resulting in a decrease of phase 4 spontaneous
depolarization (SA node)
❖They slow conductance in Ca2+ current-dependent tissues
like AV node.
❖Examples: verapamil & diltiazem
Because they act on the heart only and not on blood vessels.
❖Dihydropyridine family are not used
because they only act on blood vessels

66. • Verapamil (5 to 10 mg over 30-60 seconds ) - > slows the ventricular
response to Atrial Fibrillation and flutter
• ORAL – not that effective
• C/I as they cause negative ionotropic action
• Patients on beta blockers, hypotension

67. Mechanism of action
⦿ They bind only to depolarized (open) channels  prevention of repolarization
⦿ They prolong ERP of AV node  ↓conduction of impulses from the atria to the ventricles
So they act only in cases of arrhythmia because many Ca2+ channels
are depolarized while in normal rhythm many of them are at rest
• More effective in treatment of atrial than ventricular
arrhythmias.
• Treatment of supra-ventricular tachycardia preventing the
occurrence of ventricular arrhythmias
• Treatment of atrial flutter and fibrillation
Uses

68. ❑Contraindicated in patients with pre-existing depressed
heart because of their negative inotropic activity
❑DO NOT SUPRESS CONDUCTION VIA ACCCESSORY
PATHWAY - C/I in pre-excitation syndromes
Adverse effects
❑Cause bradycardia, and asystole especially when given in
combination with β-adrenergic blockers
❑DOSE – Verapamil for AVNRT – 5- 10 mg iv f/b infusion of
5µg/kg/min

69. MECHANISM INDICATIONS SIDE EFFECTS
ISOPROTERNOL /
ISOPRENALINE
β1 and β2 agonist Torsades de
Pointes (2nd or 3rd
line)
Symptomatic
Sinus Bradycardia
(Refractory)
• Hypotension
• Various
tachyarrhyth
mias
• Angina
• Restlessness/
Anxiety
• Tremor
ISOPROTERNOL
Structurally resembles Adrenaline
Cardiac arrest in heart blocks when pacemaker
is unavailable
Shock, Bronchospasm during anaesthesia
DOSE - 0.02-0.06 mg/ kg(1-3 mL of a
1:50,000 dilution), initially, THEN doses of
0.01-0.2 mg

70. MAGNESIUM
• Preventing and treating torsade de points
VT
• Mechanism – unknown as it does not
shorten the QT interval
• Membrane stabilising effect as a result of
blocking Ca and K channels
• Arrythmias associated with digoxin
toxicity
• 1-2 gm IV

71. PERIOPERATIVE ARRHYTHMIAS
• Adverse Events – occur rarely
• More common in cardiac surgeries compared to non cardiac Sx
• Elderly + comorbid - > single event can have long lasting implications
• Post-operative AF -> 2.3 times increased risk of stroke
• Factors increasing the risk of arrhythmias should be corrected
before surgery
• Increased Sympathetic Activity – hypoxemia, hypercarbia, acidosis
• Anaesthetic factors – Laryngoscopy, Drugs – ketamine, ephedrine,
adrenaline etc
• Already hypovolemia - > added effects of anaesthesia - > fatal
• Severe bradycardia – Intense vagal stimulation (laparoscopic
surgeries)
• Hypervolemia – due to IV fluids - > stretch the atria - > abnormal
rhythm

72. PATIENT- related factors
PRE-EXISTING
CONDITIONS
CNS DISEASE OLD AGE
MI – HIGHER
INCIDENCE OF
ARRHYTHMIA
SAH – QT
INTERVAL
CHANGES
Q WAVES
POST OPERATIVE
AF – ELERLY
UNDERGOING
THORACIC SX
AGEING ->
DEGENERATIVE
CHANGES IN
ATRIAL ANATOMY
INJURY TO THE
SYMPATHOMIME
TIC STRUCTURES
DURING Sx

73. • Myocardial ischemia / Infarction(most of
anaesthetic drugs) - cells are partially
depolarised -> Calcium is released from SR ->
triggers Na-K ATPase-> Delayed
Afterdepolarisation
CARDIAC SURGERY NON-CARDIAC
SURGERY
RELEASE OF AORTIC CROSS
CLAMP - > MYOCARDIUM IS
RECOVERING FROM ISCHAEMIC
INSULT
SURGICAL MANIPULATION ->
RETRACTION OF THE HEART IN
OFF-PUMP SX
SUTURES OVER THE ATRIUM
OPHTHALMIC – OCULO-
CARDIAC REFLEX
VAGAL STIMULATION –
TRACTION ON THE
PERITONEUM, DIRECT
PRESSURE ON THE VAGUS
NERVE DURING CAROTID
SURGERY

74. Pharmacological factors
• IV anaesthetic drugs – Most drugs reduce
Sympathetic activity -> myocardial depression and
bradycardia
• Baroreceptor reflex is attenuated
• OPIOIDS – Marked hemodynamic instability Large
boluses -> severe sinus bradycardia and blunting
of sympathetic tone
• Anticholinesterases -> Neostigmine M2 receptors
activation -> bradycardia and AB conduction delay

75. ANAESTHETIC FACTORS
TRACHEAL
INTUBATION
GENERAL
ANAESTHETICS
LOCAL
ANAESTHESIA
ELECTROLYTE
ABNORMALAITIES
CENTRAL VENOUS
CANNULATION
MOST COMMON
CAUSE OF
ARRHYTHMIA
DURING
INDUCTION
DRUGS USED FOR
INDUCTION,
MAINTENANCE
AND REVERSAL –
NOT
ARRHYTHMOGENIC
SPINAL / EPIDURAL
- >
PHARMACOLOGICA
L
SYMPATHECTOMY
-> PNS
PREDOMINANCE
HYPERCARBIA
HYPPOXAEMIA
ELECTROLYTE
DISTURBANCES
STIMULATION OF
CAROTID SINUS
REFLEX
ASSOCIATED WITH
HAEMODYNAMIC
DISTURBANCES
BUT ARRHYTHMIA
– IN TRIGGERING
AGENTS AND
DURING HIGH
CATECHOLAMINES
BRADYARRHYTHMI
A
HYPO/HYPER
KALEMIA
HYPO/HYPER
CALCEMIA
HYPO/HYPER
MAGNESEMIA
LIGHT PLANES –
HYPERTENSION,
TACHYCARDIA
HYPOXAEMIA
HYPERCARBIA
HALOTHANE – RE-
ENTRANT
MECHANISM

76. • VASOCONSTRICTORS – Phenylephrine,
metaraminol, Noradrenaline – have no direct
proarrhythmic effects
• BUT they cause hypertension -> activation of
baroreceptors-> reflex bradycardia
• Drugs that increase the QT interval
• Antiarrhythmics
• Antibiotics – Azithromycin, Erythromycin
• Anti-emetics – Chlorpromazine, Droperidol

77. Oxygenation
Ventilation,
ETCO2
Depth
Drug error
Vagal stim
VAE
Hemorrhage
Sx manip

79. CARDIOVERSION
• Trans- thoracic and trans venous
• Except VF – shock delivery should be synchronised
with R wave of ECG
• Patient on pacemaker – place electrodes 15 cm
away
• Always check rhythm before cardioversion
• Complications – muscle damage, electrical burns,
embolization
• Elective – warfarin for 3 weeks
• Urgent – use TEE for monitoring + Heparin

80. INDICATIONS
• VENTRICULAR FIBRILLATION – immediate
cardioversion 150-200J (biphasic) -> further
200J (360 if monophasic)
• VETRICULAR TACHYCARDIA –Shock / arrest /
drug failure - > same energy levels as VF
• AF – 150-200J Antero- posterior placement of
electrodes in resistant cases
• A flutter – low energy shocks – 50J

81. TRANSVENOUS CARDIOVERSION
• Low energy shock (15-30J) between
transvenous electrodes positioned in right
atrium
• Success rate is higher

82. References
• https://journals.lww.com/ijaweb/pages/articleviewer.aspx?
year=2007&issue=51040&article=00006&type=Fulltext
• Millers 9th edition
• Bennet’s cardiac arrhythmias
• https://www.bjaed.org/article/S2058-5349(22)00141-
X/fulltext
• https://www.bjaed.org/article/S2058-5349(22)00147-
0/fulltext
• https://resources.wfsahq.org/atotw/peri-operative-cardiac-
arrhythmias-part-one-supraventricular-arrhythmias-
anaesthesia-tutorial-of-the-week-279/
• https://resources.wfsahq.org/atotw/peri-operative-cardiac-
arrhythmias-part-two-ventricular-dysrhythmias-
anaesthesia-tutorial-of-the-week-285/