ANTIARRHYTHMIC

DRUGS

Moderator: Prof G.P. Singh

Presented by: Dr Rajesh Raman
& Dr Ravi Prakash
 Mechanism of arrhythmias

circulation of
an activation
wave around
an inexcitable
obstacle

2 0 depolarization
Abnormal originate during
generation of phase 2 or 3 of the
reduced (more
impulses action potential
positive) resting
membrane
potential bringing originating from
Ischemia phase 4
it closer to the and
threshold potential electrolyte
imbalances
 Types of Cardiac Arrhythmias

 Supraventricular arrhythmias
 Sinus arrhythmia (cyclic changes in heart rate during breathing)
 Sinus tachycardia (the SA node emits impulses faster than normal)
 Sick sinus syndrome (the SA node fires improperly)
 Premature supraventricular contractions (a premature impulse initiation in the atria
causes the heart to beat prior to the time of the next normal heartbeat)
 Supraventricular tachycardia (early impulse generation in the atria speed up the heart rate)
 Atrial flutter (rapid firing of signals in the atria cause atrial myocardial cells to contract
quickly, leading to a fast and steady heartbeat)
 Atrial fibrillation (electrical impulses in the atria are fired in a fast and uncontrolled manner,
and arrive in the ventricles in an irregular fashion)
 Wolff-parkinson-white syndrome (abnormal conduction paths between the atria and
ventricles cause electrical signals to arrive in the ventricles too early, and subsequently reenter the
atria)
…Types of Cardiac Arrhythmias
Ventricular arrhythmias
 Premature ventricular complexes (electrical signals
from the ventricles cause an early heartbeat, after which the
heart seems to pause before the next normal contraction of the
ventricles occurs);
 Ventricular tachycardia (increased heart rate due to
ectopic signals from the ventricles);
 Ventricular fibrillation (electrical impulses in the
ventricles are fired in a fast and uncontrolled manner, causing
the heart to quiver).
 Vaughan Williams'
Class Electrophysiology Examples
I. Na-Channel Blockers
Ia.  phase 0 quinidine
 conduction v disopyramide
 repolarisation procainamide
 APD
Ib.  phase 0 lignocaine
 conduction v phenytoin
 repolarisation tocainide, mexiletine
 APD
Ic.  phase 0 flecanide
 conduction v ecainide, lorcainide
 repolarisation
 APD
II. blockers propranolol
atenolol, esmolol
III. Prolong Repolarisation  repolarisation amiodarone
(us ua lly by K+ channe l block) bretylium, sotalol
IV. Calcium Entry verapamil
Blockers diltiazem

 Outflow of k+ ions Ca++
++ channel blockers

Slow inflow of Ca++

outflow of K+

K++ channel blockers

Fast outflow of K+
fast inflow of
Na+ ions

fully repolarised state

Na++ channel blocker

β-blockers
Antiarrhythmic Drug Actions
 Most of anti arrhythmic drugs have actions which can be
attributed to more than one class
Drugs unclassified in the Vaughan Williams system
CLASS I SODIUM CHANNEL BLOCKERS
 Bind to sodium channels and inhibit or block sodium
conductance
 Decrease in the rate of rise of phase 0 of the cardiac
membrane action potential and a slowing of the conduction
velocity
 Suppress both normal purkinje fiber and his bundle
automaticity in addition to abnormal automaticity resulting
from myocardial damage
 Bind more rapidly to open or inactivated sodium channels
than to channels that are fully repolarized
 Greater degree of blockade in tissues that are frequently
depolarizing
 ERP of fast-response fibers is prolonged
 These can depress myocardium at high doses
Reduce rate of phase 4 depolarization in automatic cells
Classification
 These have been divided into 3 classes on basis of
quantitative rates of drug binding to, and
dissociation from, sodium ion channels
• IB : interact rapidly with Na
channel
• IC: interact slowly
• IA: intermediate
 Class IA agents
 Include Quinidine, procainamide IA
and disopyramide
 Intermediate kinetics of binding
and dissociation
 Combined sodium and potassium channel blockade
 Moderate phase 0 depression and conduction slowing, prolonging
of action potential duration by blocking outward K+ current
 Blockade is greater in cells with greater frequency of
depolrization

Block Na channel  conduction   QRS duration 

Block K channel  action potential duration   QT interval  effective refractory period
Quinidine
 Prototype class IA drug.
 Slows the rapid upstroke during phase 0 and
decreases the slope of phase 4 spontaneous
depolarization.
 In circuit loops in purkinje fibres, quinidine
frequently converts one-way conduction block into
two-way block, thus abolishing the reentry circuit
Electrocardiographic Changes

 Quinidine prolongs the PR, the QRS, and the QT intervals

Hemodynamic Effects

 In patients with compromised myocardial function, quinidine

may depress cardiac contractility sufficiently to result in a
decrease in cardiac output, a significant rise in left ventricular
end-diastolic pressure, and overt heart failure.
 Can relax vascular smooth muscle directly as well as
indirectly
Quinidine produces adrenergic receptor blockade and vagal
inhibition. Thus the intravenous use of quinidine is associated
with marked hypotension and sinus tachycardia
 Clinical Uses

(1)Abolition of premature complexes that have an atrial,

A-V junctional, or ventricular origin;
(2)Restoration of normal sinus rhythm in atrial flutter and
atrial fibrillation after controlling the ventricular rate with
digitalis;
(3)Maintenance of normal sinus rhythm after electrical conversion
of atrial arrhythmias;
(4)Prophylaxis against arrhythmias associated with electrical
countershock;
(5) Termination of ventricular tachycardia; and
(6) Suppression of repetitive tachycardia associated with wolff-
parkinson-white (WPW) syndrome.
 Because of the high incidence of ventricular
proarrhythmia associated with its use and
numerous other equally efficacious agents,
quinidine is now used sparingly
Procainamide
 Derivative of the local anaesthetic procaine
 Longer half-life, does not cause CNS toxicity at
therapeutic plasma concentrations, and is effective
orally
 Slows phase 0 & impulse conduction
 Increased ERP, APD, QRS and QT interval
 Procainamide is a particularly useful antiarrhythmic
drug, effective in the treatment of supraventricular,
ventricular, and digitalis-induced arrhythmias
Adverse effects
 With chronic use, it causes a reversible lupus
erythematosus-like syndrome
 CNS side effects include depression, hallucination and
psychosis.
 Gastrointestinal intolerance is less frequent than with
quinidine.
 Toxic concentrations of procainamide may cause
asystole or induction of ventricular arrhythmias.
 The intravenous route is rarely used because
hypotension occurs if the drug is too rapidly infused.
USES
 Terminate monomorphic VT
 Prevent recurrence of VF but is rarely used for
chronic therapy due to high incidence of lupus like
syndrome
Disopyramide
 Negative inotropic effect that is greater than the weak effect
exerted by quinidine and procainamide, and unlike the latter
drugs, disopyramide causes peripheral vasoconstriction.
 No effect on sinus rate
 Less prolonged PR & QRS broadening
 Used for treatment of ventricular arrhythmias as an
alternative to procainamide or quinidine.
 2nd line drug for prevention of recurance of VT/VF
 Maintaince therapy after cardioversion of AF/AFl
 Disopyramide shows effects of anticholinergic activity, for
example, dry mouth, urinary retention, blurred vision, and
constipation.
 CLASS IB
 Lidocaine, mexiletine, tocainide, phenytoin
 Pure sodium channel blockers
 Decrease the duration of action potential and ERP of
purkinje fibres
 Minimal effect on the rate of depolarization
 Minimal effect on conduction velocity in ventricular
myocardium
Ib
 Associate and dissociate rapidly within the timeframe of
the normal heartbeat with channel recovery time < 1
second
 Binds to open channels during phase 0 of the action
potential (affecting the rate of rise very little, but
leaving many of the channels blocked by the time the
action potential reaches its peak)
 Dissociation occurs in time for the next action potential
 A premature beat, however, will be aborted because the
channels are still blocked
 Bind selectively to refractory channels and thus block
preferentially when the cells are depolarised, for
example in ischaemia.
 Lignocaine
 Unlike quinidine or procainamide, most of its effects on the
heart are by direct action
 No important interactions with the ANS
 Causes suppression of automaticity of ectopic foci but SA node
is not depressed
 Enhanced phase 4 depol. in partially depol. purkinje fibers and
delayed after depolarizations are antagonized
 Almost no change in the APD of normal specialised atrial fibres
 Substantially decreases APD in purkinje fibres and ventricular
muscle
 The ERP is also shortened but not to the same degree as the
APD, \­'s ERP:APD ratio
Lignocaine and Reentry
 Can abolish ventricular reentry, either by,
 Establishing 2-way conduction blockade
 Eg. Ischemia
 Improving conduction
 Eg. Low [k]o
 Much less effective than quinidine or procainamide in
slowing the atrial rate in AF or flutter, or in
converting these to SR
 In keeping with minimal effects on atrial tissue
Lignocaine & ECG
 In striking contrast to quinidine or procainamide,
lignocaine causes little or no change in the ECG
 The Q-T interval may shorten, but the QRS does not
widen
 Usually no change in the refractory period of the AV
node
 This may be shortened in some patients, who show an
increased ventricular rate in AF
 In patients with bundle branch disease, lignocaine may cause
complete AV block within the H-P system
Lignocaine: Kinetics
 Well absorbed after oral administration
 Subject to extensive first pass metabolism
 ® Bioavailability ~ 33%
 Almost completely absorbed after IM administration
 Kinetics after IV administration follow a two compartment
model
 Distribution half-life t½a ~ 8 mins
 Elimination half-life t½b ~ 100 mins
Lignocaine: Interactions
 Negative inotropic action may be potentiated by,
 Disturbances of acid-base, or electrolyte balance
 Hypoxia
 Other myocardial depressant drugs
 Pre-existing myocardial disease
Uses
 Treating ventricular arrhythmias arising during
myocardial ischemia
 Drug of choice for treatment of the electrical
manifestations of digitalis intoxication
 Used prophylactically in MI to prevent VF
Adverse effects
 One of the least toxic antiarrhythmic
 Mainly due to its actions on the central nervous
system and include drowsiness, disorientation and
convulsions
Tocainide.
 Analogue of lidocaine
 Mechanism of action that is similar to lidocaine
 It is orally active
 Used to prevent or treat ventricular tachycardias
 Tocainide can lead to pulmonary fibrosis.
Mexiletine.
 Resembles lidocaine and tocainide
 Orally active
 Effects on cardiac electrophysiology are similar to
that of lidocaine
 Used in the treatment of ventricular arrhythmias,
however, due to proarrhythmic side effects; it is
generally not used with less severe arrhythmias
 Effective in post MI ventricular arrhythmias as
alternative to lidocaine resistant cases
Class IC
 Associate and dissociate with sodium channels Ic much
more slowly
 Most potent sodium channel blockers
 They reach a steady-state level of block that does not vary
appreciably during the cardiac cycle; they also show only a
marginal preference for refractory channels, so are not specific for
damaged myocardium.
 Cause a rather general reduction in excitability and do not
discriminate particularly against occasional premature beats
 Significantly prolong the refractory period within the AV node and
in accessory bypass tracts
 Have minimal effects on the APD
 Used to prevent supraventricular arrhythmias in patients who
have otherwise structurally normal hearts
 High pro-arrhythmic potential
Propafenone
 Its major electrophysiological effect is to slow
conduction in fast-response tissues
 Propafenone prolongs PR and QRS durations
 Like other Na+ channel blockers, it also can be used in
ventricular arrhythmias, but with only modest efficacy.
 It has β-blocking properties and can aggravate congestive
heart failure and
 Chronic therapy with oral propafenone is used to
maintain sinus rhythm in patients with
supraventricular tachycardias, including atrial
fibrillation
FLECAINIDE
 Potent blocker of sodium and potassium channels
with slow unblocking kinetics
 Used for patients with otherwise normal hearts who
have supraventricular arrhythmias.
 Flecainide has a negative inotropic effect and can
aggravate congestive heart failure.
 It is used orally to suppress and prevent the
recurrent of documented life-threatening ventricular
arrhythmias and supraventricular tachyarrhythmias
in patients not associated with CHF
Encainide
 Used orally to suppress and prevent recurrence of
documented life-threatening ventricular
arrhythmias
Class
II β-adrenoceptor antagonists
drugs:
β-adrenoceptor antagonists
 Ventricular dysrhythmias following myocardial infarction are partly the result
of increased sympathetic activity, providing a rationale for using β-
adrenoceptor antagonists in this setting
 AV conduction depends critically on sympathetic activity; β-adrenoceptor
antagonists increase the refractory period of the AV node and can therefore
prevent recurrent attacks of SVT
 These decrease slope of phase 4 depolrization and automaticity in SA node,
Purkinje fibers & other ectopic foci, only when this has been increased under
adrenergic action
 The β-adrenoceptor antagonists are used to prevent paroxysmal attacks of atrial
fibrillation when these occur in the setting of sympathetic activation.
 Also frequently used to slow the ventricular rate in atrial flutter and fibrillation
by impairing conduction and increasing the refractoriness of the AV node
 The β -blockers must be tapered off gradually for 1 week.
Propranolol
 Propranolol is a non-selective β-antagonist
 Effective in attenuating supraventricular cardiac
arrhythmias but are generally not effective against
ventricular arrhythmias (except those induced by
exercise)
 Propranolol reduces the incidence of sudden
arrhythmic death after myocardial infarction
 Adverse effects include: Bronchoconstriction,
hypoglycemia, Na+ retention, Sexual impairment
Uses
 Sinus Tachycardia
 Atrial & nodal extrasystole evoked by
exercise/emotion
 PSVT
 Control ventricular rate in AF/A Fl
 Reduces digitalis induced tachyarrhythmias
 Arrhythmias associated with Pheochromocytoma
and halothane anaesthesia
Esmolol
 Short-acting β blocker used primarily as an
antiarrhythmic drug for intraoperative and other acute
arrhythmias
 Preferentially blocks the β1 receptors
 Esmolol’s electrophysiological actions are similar to those
of propranolol.
 Esmolol decreases arterial pressure, heart rate, ventricular
contractility, and pulmonary vascular resistance.
 Treatment of supraventricular tachyarrhythmias for
rapid control of ventricular rate and reduction of
myocardial oxygen consumption
CLAS
S III Agents Prolonging Repolarisation
CLASS III
 These drugs substantially prolong the cardiac action
potential usually by K+ channel block
 Action potential prolongation is least marked at fast rates
(where it is desirable) and most marked at slow rates
 Action potential prolongation increases the refractory
period(tissue remains refractory even after full
repolarization) , accounting for powerful and varied
antidysrhythmic activity, for example by interrupting re-
entrant tachycardias and suppressing ectopic activity
 Can cause torsade de pointes
AMIODARONE
Amiodarone
 Class III antiarrhythmic agent effective orally & IV in
the treatment of ventricular and atrial arrhythmias
 Analogue of thyroid hormone
 Prolongs APD and ERP, of atrial, nodal and
ventricular tissues
 Explains its broad spectrum of activity
 Decreases automaticity in the SA node by reducing the
slow phase 4 depolarization
 Inhibits myocardial Ca++ channels and has β blocking
properties
….Amiodarone
 The ERP of atrial fibres is responsible for its
effectiveness in SVTs
 Decreases the conduction velocity and increases the
ERP of the AV node, both anterograde and
retrograde, making it particularly useful for reentry
phenomena
  ERP of His Purkinje and myocardial fibres
 Minimal effect on SA node
…..Amiodarone
 Oral absorption is incomplete and erratic,
bioavailability ~ 22-86%
 Half life is long: t½b ~ 14-59 days
 Drug accumulates in adipose and highly perfused
tissues
 Pharmakokinetics after IV administration differ
markedly
 Removal being relatively rapid, t½ ~ 20 hrs, due to
redistribution
Amiodarone Toxicity
 N & V - rarely constipation
 abnormal LFT's
 abnormal TFT's
 ¯'s peripheral conversion T4 ® T3
 ¯'s conversion in the pituitary ® TSH levels
 both hyper & hypothyroidism may occur and the onset may be abrupt
 cardiovascular effects : *usually minimal
 atypical VT - Torsade de pointes
 bradycardia
 rarely exacerbation of CCF
 photosensitive skin rashes
 corneal micro-deposits
 pneumonitis & interstitial pulmonary fibrosis
Amiodarone - Drug Interactions
 Digoxin - potential severe bradycardia
 B-blockers - potential severe bradycardia
 Ca-antagonists- potential severe bradycardia

 Disopyramide - long QT syndrome

 Quinidine - long QT syndrome & atypical VT
 Mexiletine - long QT syndrome

 Procainamide - serum levels significantly increased

 Warfarin - inhibits metabolism
Sotalol
 It is a nonselective β adrenergic receptor antagonist that also
prolongs cardiac action potentials by inhibiting K+ currents
 Sotalol prolongs action potential duration throughout the heart
and QT interval on the ECG
 It decreases automaticity, slows AV nodal conduction, and
prolongs AV refractoriness by blocking both K+ channels and
β adrenergic receptors, but it exerts no effect on conduction
velocity in fast-response tissue
 Sotalol is approved for use in patients with both ventricular
tachyarrhythmias and atrial fibrillation or flutter.
 The most serious side effect is torsade de pointe, the QTc
interval must be watched carefully for excess prolongation
Dofetilide
 Orally active
 Selectively blocks K+ current: pure class
antiarrhythmic
 Used to maintain and convert AF/Afl to sinus
Rhythm
Ibutilide
 Newer class III antiarrhythmic used to convert
AF/AFl to sinus rhythm
Class IV Ca2+ channel blockers
 Selective blockade of the slow L-type cardiac
calcium channels
 They are most potent in tissues in which the action
potential depends on calcium currents, such as the
SA and AV nodes
 Within nodal tissue, calcium channel blockade
elevates the threshold potential, decreases the rate of
rise of phase 0 depolarization and conduction
velocity, and lengthens the refractory period of the
AV node
 Clinical effects caused are:
 The heart rate slows;
 transmission of rapid atrial impulses through the AV node to the ventricles
decreases, thus slowing the ventricular rate in atrial fibrillation and atrial
flutter; and
 reentrant rhythms traveling through the AV node may terminate
 Used in treatment of reentrant PSVT, to slow the ventricular rate
in patients with atrial fibrillation or flutter.
Verapamil
Verapamil
 A derivative of papaverine and was first used as a
coronary vasodilator
 Produces Ca++-channel blockade in cardiac and
smooth muscle membranes
 Substantially slows the rate of impulse formation in
the SA node in vitro
 However, this is offset in vivo due to reflex SNS
activity resulting from arteriolar vasodilation
 Normally the rate slows ~ 10-15%
Verapamil
 No significant effects on intra-atrial conduction
  Rate of phase 4 depolarisation in H-P fibres
 Can block delayed ADP's and triggered activity resulting
from digitalis toxicity
 Most marked effect of verapamil is on the AV node
  conduction velocity &  ERP
 Results directly from ca++-channel blockade
 However is not seen at usual therapeutic concentrations of
other Ca++-channel blockers, eg. Nifedipine
Uses:
 To prevent recurrence of paroxysmal supraventricular
tachycardia (SVT)
 To reduce the ventricular rate in patients with atrial
fibrillation, provided they do not have wolff-
parkinson-white or a related disorder.
Diltiazem
 Similar to verapamil but has relatively more
smooth muscle-relaxing effect and produces less
bradycardia.
 Diltiazem is effective in controlling the ventricular
rate in patients with atrial flutter or atrial
fibrillation
OTHER
ANTIARRHYTHMICS
 CARDIAC GLYCOSIDES:
Digoxin
 Digoxin shortens the refractory period in atrial and
ventricular myocardial cells while prolonging the
effective refractory period and diminishing
conduction velocity in Purkinje fibers.
 bind specifically to the Na+/K+-ATP'ase, inhibit its
enzymatic activity
 Digoxin enhances the inotropic state by increasing
the intracellular calcium concentration
 Used to treat and prevent sinus and supraventricular
fibrillation, flutter, and tachycardia
Adenosine
 Most of the purine agents have acute vasodilating
properties in most vascular beds
 Adenosine is an important autocoid and endogenous
vasodilator in man
 Decreases conduction velocity, prolongs the
refractory period, and decreases automaticity in the
AV node.
 Adenosine has an extremely short duration of action
(about 15 seconds).
Adenosine - Actions
 Termination of PSVT
 Demonstrated safely and effectively in older children and adults
 Induced hypotension
 Direct negative inotropic effect
 Coronary blood flow increases
 Pulmonary vascular resistance decreases but not to the same
extent as SVR
 Decreased GFR in the kidney
Atropine
 Atropine shortens AV node ERP and increases
conduction velocity in bundle of his
 When A-V block is due to vagal overactivity, eg.
Digitalis toxicity, it can be overcome by atropine
Sympathomimetics
 Adrenaline and isoprenaline can overcome partial
heart block by facilitating AV Conduction and
shortening ERP of conducting tissues
SUMMARY: ANTIARRHYTHMIC DRUGS
Antiarrhythmic Therapy
 Patient-Specific Contraindications
CONDITION EXCLUDE/USE WITH CAUTION
CONDITION EXCLUDE/USE WITH CAUTION
Cardiac
Heart failure Disopyramide, flecainide Noncardiac
Sinus or AV node Digoxin, verapamil, dil- Diarrhea Quinidine
dysfunction tiazem, β adrenergic Prostatism, glaucoma Disopyramide
receptor antagonists, Arthritis Chronic procainamide
amiodarone
Lung disease Amiodarone
Wolff–Parkinson–White Digoxin, verapamil, Tremor Mexiletine, tocainide
syndrome (risk of diltiazem
extremely rapid rate Constipation Verapamil
if atrial fibrillation
develops) Asthma, peripheral vas- β Adrenergic blockers,
Infranodal conduction Na+ channel blockers, cular disease, propafenone
disease amiodarone hypoglycemia

Aortic/subaortic stenosis Bretylium

History of myocardial Flecainide
infarction
Prolonged QT interval Quinidine, procainamide,
disopyramide, sotalol,
dofetilide, ibutilide,
amiodarone
Cardiac transplant Adenosine
Sinus Bradycardia
 Heart rates lower than 40 beats/min are poorly
tolerated, even in healthy patients, and should be
evaluated on the basis of their effect on cardiac
output
 Treatment is recommended if hypotension,
ventricular arrhythmias, or signs of poor peripheral
perfusion are observed
 When treatment is deemed necessary, the following
approach may be considered
 atropine, 0.5 to 1.0 mg by intravenous bolus repeated
every 3 to 5 minutes, up to 0.04 mg/kg
 ephedrine, 5 to 25 mg by intravenous bolus;
 dopamine or dobutamine (if blood pressure is
adequate), 5 to 20 µg/kg/min by intravenous infusion;
 epinephrine, 2 to 10 µg/min by intravenous infusion;
 isoproterenol, 2 to 10 µg/min by intravenous infusion.
 Temporary transcutaneous or transvenous pacing may be
necessary for severe, drug-refractory sinus bradycardia
Sinus Tachycardia
 Prolonged tachycardia in patients with underlying heart
disease can precipitate MI and congestive heart failure
(CHF) as a result of the increased myocardial work
required and decreased myocardial oxygen supply
because of decreased diastolic coronary perfusion time
 The underlying disorder should be treated. Hypovolemia
and light anesthesia are the most common causes. In
patients with ischemic heart disease in whom tachycardia
develops, β-adrenergic blockers should be used
judiciously to prevent myocardial ischemia regardless of
whether ST-segment changes are present.
 Paroxysmal Supraventricular
Tachycardia
 When a patient is anesthetized, PSVT can be precipitated by changes in autonomic
nervous system tone, by drug effects, or by intravascular volume shifts and can
produce severe hemodynamic deterioration
 Vagal maneuvers
 Adenosine, which is the drug of choice
 Verapamil (2.5 to 10 mg given intravenously) terminates AV nodal reentry
successfully in about 90% of cases
 Amiodarone
 Esmolol
 Phenylephrine (100 µg by intravenous bolus) is administered if the patient is
hypotensive
 Intravenous digitalization is performed with one of the short-acting digitalis
preparations
 Synchronized cardioversion may be performed with incremental doses of energy
of 100, 200, 300, and 360 J,
Atrial Flutter
 Atrial flutter does not always indicate severe heart
disease. It can be seen in patients with CAD, mitral
valve disease, pulmonary embolism, hyperthyroidism,
cardiac trauma, cancer of the heart, and myocarditis.
 Initial treatment should consist of control of the
ventricular response rate with drugs that slow AV
node conduction:
 β-Blockers such as esmolol (1 mg/kg by intravenous
bolus) or propranolol.
 Calcium channel blockers such as verapamil (5 to
10 mg given intravenously) or diltiazem
 If the ventricular response is excessively rapid or hemodynamic
instability is present, or both, the following guidelines should be used:

  Synchronized DC cardioversion starting at a relatively high energy of 100 J

and gradually increasing to 360 J is indicated.   
 ibutilide (1 mg in 10 mL saline or 5% dextrose in water [D5W] infused slowly
intravenously over a 10-minute period) has been documented to convert atrial
flutter to sinus rhythm in most patients with relatively new-onset atrial flutter.
[42] This may be repeated once, and although it is highly effective, life-

threatening torsades de pointes may occur hours after ibutilide administration,

thus making 4- to 8-hour monitoring after treatment highly desirable.   
 Procainamide (5 to 10 mg/kg for the intravenous loading dose, infused no
faster than 0.5 mg/kg/min) may rarely be used in an attempt to restore sinus
rhythm after the ventricular response has been adequately controlled. [43]   
 Amiodarone (150-mg intravenous loading dose infused over a 10-minute
period, followed by 1 mg/min intravenously for 6 hours, a 0.5-mg/min
intravenous infusion for 18 hours, and then a reduced intravenous dose or
switching to an oral dose) has recently been shown to be effective.
Atrial Fibrillation
 Atrial fibrillation is the most common
postoperative arrhythmia and has significant
consequences
 Numerous studies support the efficacy of β-
blockers in the prevention of postoperative atrial
fibrillation. Perioperative administration of
amiodarone, sotalol, nondihydropyridine calcium
channel blockers, and magnesium sulfate has also
been associated with a reduction in the
occurrence of atrial fibrillation
 Acute atrial fibrillation: Treatment of acute atrial
fibrillation is very similar to that for atrial flutter.
Primary attention should be focused on controlling
the ventricular response, especially with the
administration of diltiazem or esmolol
intravenously
Junctional Rhythms
 Junctional rhythms are common in patients under
anesthesia (about 20%), especially with halogenated
anesthetic agents. Junctional rhythms frequently decrease
blood pressure and cardiac output by about 15%, but
they can decrease it up to 30% in patients with heart
disease
 Usually, no treatment is required, and the rhythm reverts
spontaneously. If hypotension and poor perfusion are
associated with the rhythm, treatment is indicated.
Atropine, ephedrine, or isoproterenol can be used in an
effort to increase the activity of the SA node so that it will
take over as the pacemaker.
Ventricular Premature Beats
 VPBs are common during anesthesia, where they
account for 15% of observed arrhythmias. They are
much more common in anesthetized patients with
preexisting cardiac disease.
 VPBs result from ectopic pacemaker activity arising
below the AV junction
 The new onset of VPBs must be considered a
potentially serious event because the arrhythmia may
progress to VT or VF d/t coronary artery insufficiency,
MI, digitalis toxicity with hypokalemia, and
hypoxemia
 In most patients, VPBs (occurring as single, bigeminy, or
trigeminy but excluding nonsustained VT) do not need to be
treated, particularly if the patient does not have an acute
coronary syndrome, and treatment is generally dictated by the
presence of symptoms attributable to the VPBs
 First step in treatment is to correct any underlying
abnormalities such as decreased serum potassium or low
arterial oxygen tension.
 If the arrhythmia is of hemodynamic significance or if it is
believed to be a harbinger of worse arrhythmias, lidocaine is
the treatment of choice, with an initial bolus dose of
1.5 mg/kg. Recurrent VPBs can be treated with a lidocaine
infusion at 1 to 4 mg/min; additional therapy includes
esmolol, propranolol, procainamide, quinidine,
disopyramide, atropine, verapamil, or overdrive pacing.
Ventricular Tachycardia
 The presence of three or more sequential VPBs defines VT
 Acute onset is life threatening and requires immediate
treatment.
 If the patient is hemodynamically stable, amiodarone
administered as one or more intravenous doses of 150 mg in
100 mL saline or D5W over a period of 10 minutes, followed
by an intravenous infusion of 1 mg/min for 6 hours and
0.5 mg/min thereafter, is the recommended current treatment
(maximum intravenous dose, 2.2 g/24 hr)
 Lidocaine and procainamide have been used with varying
degrees of success to treat VT
 Synchronized cardioversion is the indicated
nonpharmacologic intervention in any wide-
complex tachycardia, whether monomorphic VT or
a wide-complex SVT.
 Polymorphic VT with a normal QT interval is
treated with amiodarone and cardioversion
 Polymorphic VT with a prolonged QT interval is a
more serious rhythm disturbance, and the
recommended current treatment is an intravenous
infusion of 1 g of magnesium administered over a 2-
to 3-minute period.
Ventricular Fibrillation
 Ventricular fibrillation is an irregular rhythm that results from a
rapid discharge of impulses from one or more ventricular foci
or from multiple wandering reentrant circuits in the ventricles
 There is no effective cardiac output, and life must be
sustained by artificial means, such as external cardiac
massage
 Cardiopulmonary resuscitation must be initiated immediately,
and then defibrillation must be performed as rapidly as
possible.
 Asynchronous external defibrillation should be performed with
a DC defibrillator using incremental energies in the range of
200 to 360 J.
 Early administration of 1 g of magnesium sulfate
may facilitate defibrillation. In some instances,
epinephrine has been used to facilitate
defibrillation. Vasopressin has been added as a
drug for the treatment of ventricular fibrillation
 Supportive pharmacologic therapy may include
lidocaine, amiodarone, bretylium, procainamide,
phenytoin, or esmolol.
Thank you