GROUP MEMBERS
 Anum Aslam Khan
 Bushra Rubab
 Farah Ali Khan
 Javeria Rahat
 Najaf Farooq
 Nameera Ahmed
 Nida Ashraf
 Rabia Khalid Nadeem
 Urooba Iqbal

ARRHYTHMIA
Abnormality in the origin, rate, rhythm,
conduction velocity and sequence of heart
activation. It may cause sudden death or syncope,
heart failure, dizzines, palpitations, or no
symptoms at all.

Normal Physiology of Heart
 The cardiac muscles are
specialised tissue with
unique properties like
excitability, contractility
and automatcity
 The myocardium has 2
types of cells,
contracting and
conducting cell.
 The contracting cells
participate in the
pumping action of the
heart, and the have the
charachteristic
property of
Automaticity.

 Automaticity is the ability of the cell to
generate electrical impulses spontaneously.
 SA,AV and His-purkinje system comprises
the conduction tissue system of heart.
Normally the SA node act as a pace maker
of the heart.
 Excitability is the ability of the cell to undergo
depolarization in response to a stimulus.
 Contractility is he ability of he myocardium
to adequately contract ad pump the blood
out of the heart.

Cardiac Action Potential
When the stimulus reach the cardiac cell, specific
ions moves into and out of the eliciting the
action potential cell. Such movement of ions is
divided into following or phases:

Phases of Cardiac Action
Potential

 Phase 0: rapid depolarization of cell
membrane during which theirs is fast entry
of Na ions into the cells through Na
channels, this is followed by repolarization.
 Phase 1: is short initial rapid repolarization
due to Ka efflux
 Phase 2:prolonged plateue phase due to
slow Ca influx
 Phases 3: rapid repolarization with Ka efflux
 Phase 4: resting phase during which Ka ions
return into the cell while Na and Ka move
out of it and resting membrane potential is
stored

Mechanism of Arrhythmia
Abnormal heart
pulse formation
 Sinus pulse
 Ectopic pulse
 Triggered activity
Abnormal heart
pulse
 Reentry
 Conduction block

Two Main Features of Arrhythmia
Site of origin
 Atria
 Atrioventricle node (AV node)h
 Ventricles
Affect on heart rate
 Too slow heart rate (bradycardia : >60
beats/min)
 Too fast heart rate (tachycardia : < 80
beats per min)

Classification of
Arrhythmia
Abnormal heart
pulse formation
Sinus arrythmia
Atrial arythmia
Atrio vetricular
juctional
arrythmia
Ventricular
arrythmia
Abnormal heart
pulse
conduction
Sinus-atrial
block
Intra-atrial block
Atrio-
ventricular
block
Intra-ventricular
block

NAJAF FAROOQ
CLASS I(A) ANTI ARRHYTHMIC
DRUGS

CLASS I ANTI ARRHYTHMIC
DRUGS
 It is largest class of Anti arrhythmic drugs.
 Class I anti arrhythmic drugs act by blocking voltage-
sensitive sodium (Na+) channels.These drugs bind to
sodium channels when the channels are open and in
activated state and dissociate when the channels are in
resting phase.
 Inhibition of sodium channel decrease rate of rise of
phase 0 of cardiac membrane action potential and a
slowing of conduction velocity.
 They also block K channels (class IA) thus, slows the
repolarization in ventricular tissue.
 These drugs have local anesthetic activity and may
suppress myocardial contractile force, these affects are
observed at a higher plasma concentration.

USE DEPENDENCE:
 Class I drugs bind more rapidly to open or
inactivated sodium channels than to channels that
are fully repolarized following recovery from the
previous depolarization cycle. Therefore, these
drugs show a greater degree of blockade in
tissues that are frequently depolarizing (for
example, during tachycardia, when the sodium
channels open often). This property is called use-
dependence (or state-dependence) and it enables
these drugs to block cells that are discharging at
an abnormally high frequency, without interfering
with the normal, low-frequency beating of the
heart.

Class I anti arrhythmic drugs are classified
into three sub classes:
Class IA
• Quinidine
• Procainamide
• Disopyramide
Class IB
• Lidocaine
• Mexiletine
• Tocainide
Class IC
• Flecanide
• Propafenone
Classification:

CLASS IA
Blocking of the fast sodium channel interferes with rapid
depolarization and decreases conduction velocity.
This will increases the duration of the cardiac action potential .
These drugs decrease rate of rise of phase 0
Block Na channels preferentially in open state ,so decrease the no.
of available Na channels for membrane depolarization.
Increase APD, and ERP

In addition to blocking the fast sodium
channel (Phase 0) some class I agents also
block the potassium channel (Phase 3)
Potassium channel blockade directly affects
the duration of the cardiac action potential
and the effective refractory period
All drugs have same effects but they differ
in pharmacokinetics and adverse effect.

QUINIDINE
• Quinidine is d-isomer of quinine obtained from cinchona tree.
• Quinidine binds with sodium channel and prevent sodium influx,
thus slowing the rapid upstroke during phase 0
• It also decreases the slope of phase 4 depolarization
and inhibits potassium channels. Because of these
action it decreases conduction velocity and increases
refractoriness.
• Additionally It has anti cholinergic activity (M receptor block) on
SA and AV NODE which increases HR and AV conduction.
• Inc: PR,QRS,QT interval

Therapeutic uses:
 Quinidine is used in the treatment of a
wide variety of arrhythmias, including:
 atrial,AV-junctional, and ventricular
tachyarrhythmias.
 Quinidine is used to maintain sinus rhythm
after direct-current cardioversion of atrial
flutter or fibrillation and to prevent
frequent ventricular tachycardia.

Adverse effects:
 nausea, vomiting, diarrhoea.
 large doses may produce cinchonism( tinnitus,
ocular dysfunction, CNS excitation). hypotension,
 prolongation of QRS and increase in QT interval
associated with syncope( which is due to
ventricular arrhythmia induced by quinidine),
 Torsade de pointes.
 Thrombocytopenia that disappear on drug
withdrawal.
 Enhances digoxin toxicity.

PROCAINAMIDE
• It is a derivative of local anesthetic procaine.
• Less M receptor blockade than quinidine, but
more cardio depressant.
• Orally effective, often substitution of quinidine.
• Increase PR,QRS,QT interval
• It Decreases re-entry by causing bidirectional
block.

Indications:
 effective in premature atrial contractions, PSVT,Atrial fibrillation.
 It converts atrial flutter or atrial fibrillation to sinus rhythm although
it has value in preventing reoccurrence of these arrhythmias once
they have been terminated by DC cardio version.
 Majority of patient of ventricular tachycardia respond to
procainamide.
Adverse effects:
With chronic use, procainamide causes a high incidence of side effects,
including
 a reversible lupus erythematosus–like syndrome that develops in
25 to 30 percent of patients..

 Toxic concentrations of procainamide may cause asystole
or induction of ventricular arrhythmias.
 Central nervous system (CNS) side effects include
depression, hallucination, and psychosis. With this drug,
gastrointestinal intolerance is less frequent than with
quinidine

DISOPYRAMIDE
• It produces a negative ionotropic effect that is greater
than the weak effect exerted by quinidine and
procainamide, and unlike the latter drugs, disopyramide
causes peripheral vasoconstriction
• The drug may produce a clinically important decrease in
myocardial contractility in patients with pre existing
impairment of left ventricular function.
• Disopyramide is used in the treatment of ventricular
arrhythmias as an alternative to procainamide or
quinidine.

Adverse effects:
 Disopyramide shows effects of anticholinergic
activity (for example, dry mouth, urinary
retention, blurred vision, and constipation).

31
ELECTROPHYSIOLOGICAL
EFFECTS OF CLASS I A DRUGS
DRUG CLASS ATRIA SA
NOD
E
AV –
NODE
C-RP
HIS
PURKINJ
E
C-RP
VENT
MUSCLE
C-RP
APD ERP
Quinidine I A DEC - D-0/I D-I DEC INC INC
procainamide IA DEC - DEC DEC DEC INC INC
Disopyramide
IA DEC - DEC DEC DEC INC INC

UROOBA IQBAL
CLASS I(B) ANTIARRHYTHMIC
DRUGS

CLASS IB ANTIARRHYTHMIC
DRUGS
 These drugs have minimal effect on rate of
depolarization and
 They decrease APD and ERP. of purkinje
fibers.
 They block inactivated channels.
 Examples are: Lidocaine, mexiletine, tocainide

LIDOCAINE
 Lidocaine (xylocaine,
or lignocaine ) is a common local
anesthetic & a class IB anti arrhythmic
drug.
 It is used intravenously for the treatment
of ventricular arrhythmias (for acute
myocardial infarction, digoxin
poisoning, cardioversion or cardiac
catheterization).

Indications:
 It is prescribed for ventricular
arrhythmias (particularly in patients with
Mayocardial Infarction).
Adverse effects:
 Drowsiness
 Confusion
 Irritability
 Convulsions.

TOCAINIDE (Tonocord)
 Tocainide (Tonocard) is a class
IB antiarrhythmic drug.
Mechanism of action:
 It decreases His-purkinjie conduction.
 Also it abolishes re-entry by causing bi-
directional block.

Indications:
 It is used in ventricular arrhythmia
refractory to more conventional therapy.
Adverse effects:
 Light headedness
 Dizziness
 Nausea

MEXILETINE (Mexitil)
 It is yet another class IB antiarrhythmic
drug.
 It is similar to lidocaine,tocainide in action
but it produces greater effect in normal
cardiac tissues than does lidocaine.

 It slows conduction in the heart and
makes the heart tissue less sensitive.
Indications:
 It is used to treat arrhythmias within the
heart or seriously irregular heart beats.

Adverse effects:
 Dizziness
 Heartburn
 Nausea
 Nervousness
 Trembling
 Unsteadiness
 Widening of QRS wave
 GI distress
 Chest pain (rare)

ELECTROPHYSIOLOGICAL
EFFECTS OF CLASS I B DRUGS
DRUG CLASS ATRIA SA
NODE
AV
NODE
C-RP
HIS –
PURKIN
JE
C-RP
VENTM
USCLE
C-RP
APD ERP
Lidocaine IB D - D-0/I D-I D DEC -
Tocainide IB - - D D D DEC -
Mexiletine IB - - D D D DEC DEC

FARAH ALI KHAN
CLASS I(C) ANTIARRHYTHMIC
DRUGS

CLASS IC ANTIARRHYTHMIC
DRUGS
Class IC antiarrhythmic medications are
proarrhythmic, and their use should be
limited to patients without structural
heart disease.
Class Ic does not significantly affect the
action potential .It dec: QT interval b/c
these drugs have less effect on K rectifier
current.
E.g. Moricizine, Flecainide, Propafenone

Potent blocker of Na & K channel with slow unblocking
kinetics.
Block K channel but does not prolong APD and QT
interval.
Slows conduction of the electrical impulse within the
heart.
Greatest effect is on the His-Purkinje system and
ventricular myocardium.
ventricular myocardium causes decreased contractility of
the muscle. decrease in the ejection fraction.
FLECAINIDE (TAMBOCOR):

Indication:
•After digoxin it is 2nd line drug in the treatment of fetal
arrhythmia, many types of supraventricular tachycardias,
including AV nodal re-entrant tachycardia (AVNRT)
and Wolff-Parkinson-White syndrome(WPW).This is
because of the action of flecainide on the His-Purkinje
system.
•It is also used in ventricular tachyarrhythmias.

Contraindications:
Flecainide is contraindicated in patients with pre-
existing second- or third-degree AV block, or with
right bundle branch block when associated with a
left hemiblock (bifascicular block), unless a
pacemaker is present to sustain the cardiac rhythm
should complete heart block occur. Flecainide is also
contraindicated in the presence of cardiogenic
shock or known hypersensitivity to the drug.

Adverse effects:
 visual disturbances, blurred vision, nausea,
headache, dyspnea. Inc:PR ,QRS are likely
to occur.
 dizziness, fainting, or lightheadedness
 fast, irregular, pounding, or racing
heartbeat or pulse
 tightness in the chest
 wheezing

PROPAFENONE (Rythamol)
Mechanism of Action:
 Slowing the influx of sodium ions into
the cardiac muscle cells, causing a
decrease in excitability of the cells. it has
additional activity as a beta-adrenergic
blocker which can cause bradycardia and
bronchospasm.

Indication:
Contraindication:
 hepatic or renal dysfunction
 Asthma
 CHF
 bradycardia.
 Life-threatening ventricular arrhythmias
atrial fibrillation (AF) or in patients
exclusively with atrial flutter

Adverse effects:
 Lupus-like syndrome
 Agranulocytosis
 CNS disturbances such as dizziness,
lightheadedness, gastrointestinal upset, a metallic
taste
 Bronchospasm
 About 20% of patients treated with RYTHMOL
have discontinued treatment because of adverse
reactions.

MORICIZINE (Ethmozine)
Indication:
 Life threatening ventricular arrhythmias (eg,
sustained ventricular tachycardia).
 Used to treat irregular heartbeats (arrhythmias)
and maintain a normal heart rate.
Moricizine works by inhibiting the rapid inward sodium
current across myocardial cell membranes. Ethmozine
shortens Phase II and III repolarization, resulting in a
decreased action potential duration and effective
refractory period.

Contraindications:
Ethmozine® (moricizine hydrochloride) is
contraindicated in patients with pre-
existing second- or third-degree AV block
and in patients with right bundle branch
block when associated with left
hemiblock (bifascicular block) unless a
pacemaker is present. Ethmozine® is also
contraindicated in the presence of
cardiogenic shock or known
hypersensitivity to the drug.

Adverse effects:
 Cardiac arrest
 Heart failure
 Sinus node dysfunction
 Conduction block
 Dizziness
 Dyspnea
 Headache
 Visual disturbance

BUSHRA RUBAB
CLASS II ANTIARRHYTHMIC
DRUGS

CLASS II ANTIARRHYTHMIC
DRUGS
(BETA BLOCKERS)
 It reduce sympathetic tone
 Like propranolol exert anti arrhythmic effect
due to blackade of cardiac beta receptor
.They depress myocardial contractility
,automaticity and conduction velocity .

PROPRANOLOL
 BRAND NAME : INDERAL
 In all type of arrhythmias caused by enhance sympathetic stimulation
 In SVT andVT.
Mechanism of action :
DIMINISH PHASE 4 DEPOLARIZATION
DEPRESSED AUTOMATICITY GIVE NEGATIVE
INOTROPIC EFFECT ,HEART RATE , CARDIAC
OUTPUT CARDIAC AUTOMATICITY DECREASE
PROLONG AV CONDUCTION AND INC AV NODAL RP

Adverse effects:
 Bradycardia
 Bronchospasm
 Fatigue
 Insomnia

JAVERIA RAHAT
CLASS III ANTIARRHYTHMIC
DRUGS

CLASS III ANTIARRYTHMIC
DRUGS
General Pharmacology:
 The primary role of potassium
channels in cardiac action potentials
is cell repolarization.
 In non-nodal tissue (see figure),
action potentials are initiated when
a cell is depolarized to a threshold
potential by an adjacent cell.
 This leads rapid opening of fast
sodium channels and a slower
opening of L-type calcium channels
that permit calcium to enter the
cell (phase 0 and 2, respectively).

 As these channels become inactivated, potassium
channels open permitting potassium ions to leave the
cell (K+ out), which causes repolarization of the
membrane potential (phase 3). Potassium channels
remain open until the next action potential is triggered.
 There are also different potassium channels that are
responsible for the initial repolarization (phase 1) that
occurs as the fast sodium channels become inactivated.
Potassium channels are also responsible for repolarizing
slow-response action potentials in the sinoatrial and
atrioventricular nodes.

POTASSIUM CHANNEL BLOCKER
 Potassium-channel blockers comprise the Class III
antiarrhythmic compounds according to the Vaughan-
Williams classification scheme.
 These drugs bind to and block the potassium channels
that are responsible for phase 3 repolarization.
Therefore, blocking these channels slows (delays)
repolarization, which leads to an increase in action
potential duration and an increase in the effective
refractory period (ERP).

 On the electrocardiogram, this increases the Q-
T interval.This is the common effect of all Class
III antiarrhythmic drugs.The electrophysiological
changes prolong the period of time that the cell
is unexcitable (refractory) and therefore make
the cell less excitable.

 By increasing the ERP, these drugs are
very useful in suppressing
tachyarrhythmia's caused by reentry
mechanisms.
 Reentry occurs when an action
potential reemerges into normal
tissue when that tissue is no longer
refractory.
 When this happens, a new action
potential is generated prematurely
(before normal activation) and a
circular, repeating pattern of early
activation can develop, which leads to
a tachycardia. If the ERP of the normal
tissue is lengthened, then the
reemerging action potential may find
the normal tissue refractory and
premature activation will not occur.

CLASS III ANTIARYTHMIC DRUGS
BRETYLIUM
AMIODARONE
SOTALOL

BRETYLIUM
 Bretylium (also bretylium tosylate) is
an antiarrhythmicagent.It blocks the release
of noradrenaline from nerve terminals.
 In effect, it decreases output from the
peripheralsympathetic nervous system.
 It also acts by blocking K+channels and is
considered a class III antiarrhythmic

 It is used in emergency medicine, cardiology, and
other specialties for the acute management
of ventricular tachycardia and ventricular
fibrillation.
 It is contraindicated in patients with AV
(atrioventricular)heart block or digoxin toxicity.
 Bretylium should be used only in an ICU or
Emergency Department setting and should not be
used elsewhere due to its dramatic actions and its
predominant side effect of hypotension.

Therapeutic uses:
 In life-threatening ventricular tachycardia and
fibrillation.
Adverse effects:
 nausea,
hypotension,
diarrhea
Indications:
 In treating life threatingVT, when lidocaine or
procainamide become in effective.

NIDA ASHRAF
CLASS III ANTIARRHYTHMIC
DRUGS (CONTD.)

 Amiodarone is an antiarrhythmic agent used for
various types of cardiac dysrhythmias, both
ventricular and atrial.
 Amiodarone is categorized as a class III
antiarrhythmic agent, and prolongs phase 3 of the
cardiac action potential, the repolarization phase
where there is normally decreased calcium
permeability and increased potassium permeability.
 It is similar to those of antiarrhythmic classes I a, II,
and IV.
AMIODARONE

Amiodarone shows beta blocker-like and potassium channel
blocker-like actions on the SA and AV nodes, increases the
refractory period via sodium- and potassium-channel
effects, and slows intra-cardiac conduction of the cardiac
action potential, via sodium-channel effects

Indication:
 tachyarrhythmia, including atrial fibrillation and
ventricular tachycardia
 patients at high risk of sudden cardiac death.
Although amiodarone is effective, it is not
generally recommended for minor rhythm
disturbances because of its toxicity.

Contraindications:
• Individuals who are pregnant or may become pregnant are
strongly advised to not take amiodarone.
• It is contraindicated in individuals with sinus nodal
bradycardia, atrioventricular block, and second or third degree
heart block who do not have an artificial pacemaker.
• Individuals with baseline depressed lung function should be
monitored closely if amiodarone therapy is to be initiated.

Adverse effects:
Most common side effects are:
 Cough
 Dizziness, lightheadedness, or fainting
 Fever (slight)
 numbness or tingling in the fingers or toes
 painful breathing
 trouble with walking

Less common side effects are:
 Blue-gray coloring of the skin on the face, neck, and
arms
 Blurred vision or blue-green halos seen around
objects
 Dry eyes
 Fast or irregular heartbeat
 Nervousness
 Sensitivity of the eyes to light
 Slow heartbeat
 Sweating
 Swelling of the feet or lower legs trouble with
sleeping

SOTALOL
• Sotalol is a drug used in individuals with rhythm
disturbances (cardiac arrhythmias) of the heart, and to
treat hypertension in some individuals.
• It is a non-selective competitive β-adrenergic receptor
blocker that also exhibits Class III antiarrhythmic
properties by its inhibition of potassium channels.
• Because of this dual action, Sotalol prolongs both the
PR interval and the QT interval.

Sotalol hydrochloride has
both beta-adrenoreceptor
blocking and cardiac
action potential duration
prolongation
antiarrhythmic properties.
Sotalol hydrochloride is a
racemic mixture of d- and
l-Sotalol.
Both isomers have
similar Class III
antiarrhythmic effects,
while the I-isomer is
responsible for virtually
all of the beta-blocking
activity.The beta-
blocking effect of Sotalol
is non-cardioselective.
Sotalol does not have
partial agonist or
membrane stabilizing
activity.
In children, a Class III
electro physiologic effect
can be seen at daily
doses of 210 mg/m2
body surface area (BSA).

Indications:
Ventricular arrhythmias
Like other beta-blockers, sotalol is an effective antihypertensive
agent and it is also suited for combinations with other
antihypertensive drugs.
Because of the risk of hypokalemia, a combination with diuretics
is better avoided

Adverse effects:
More common side effects are:
 Blurred vision
 chest pain or discomfort
 confusion
 Diarrhea
 lightheadedness, dizziness, or fainting
 nausea and vomiting
 shortness of breath
 sweating
 swelling of face, fingers, feet, or lower legs
 tightness in chest
 unusual tiredness or weakness
 wheezing

Less common side effects are:
 Abdominal pain or swelling
 back pain
 black, tarry stools
 blood in eyes
 blood in urine
 body aches or pain

NAMEERA AHMED
CLASS IV ANTIARRHYTHMIC
DRUGS:

CLASS IV ANTIARRHYTHMIC
DRUGS:
•Class IV drugs are calcium channel blockers.
•They decrease the inward current carried by Ca+2
resulting in a decreased rate of phase 4 spontaneous
depolarization.
•Also slow conduction in tissues that depend on
calcium currents , such as AV node.
•Major effect of CCBs is on vascular smooth muscles
& on heart.

VERAPAMIL:
•Verapamil is a prototype drug.
•Shows greater action on heart than on vascular smooth muscle.
Cardiac effects:
•It usually slows the sinoatrial node by its direct action.
•But its hypotensive action may occasionally result in a
small reflex increase of sinoatrial nodal rate.
•It can suppress both early & delayed after
depolarizations & may antagonize slow responses
arising in severly depolarized tissue.Verapamil blocks
both activated & inactivated L-type calcium channels.

Extra-cardiac effects:
•Verapamil cause peripheral vasodilation ,which may be
beneficial in HTN & peripheral vasospastic disorders.
•Its effects on smooth muscle produce a no. of cardiac
effects.
•Supra ventricular tachycardia is the major arrhythmia
indication for verapamil.
•It preferred over older treatments (propranolol ,digoxin
,etc)for termination.
Therapeutic uses:

•Also reduce ventricular rate in atrial fibrillation or
flutter.
•Occasionally useful in ventricular arrhythmia.
•IV verapamil in a patient with sustained ventricular
tachycardia can cause hemodynamic collapse.
Adverse effects:
• Verapamil have –ve inotropic properties.
•May be contraindicated in patients with preexisting
depressed cardiac function.
• Verapamil can produce a decrease in BP b/c of peripheral
vasodilation –an effect that is actually beneficial in treating
HTN.

DILTIAZEM
It is a class III antianginal drug, and a class IV antiarrythmic.
 Diltiazem is a potent vasodilator, increasing blood flow and variably
decreasing the heart rate via strong depression of AV node
conduction. Its pharmacological activity is somewhat similar
to verapamil.
 It is a potent vasodilator of coronary and peripheral vessels, which
reduces peripheral resistance and afterload.
 Because of its negative inotropic effect, diltiazem causes a modest
decrease in heart muscle contractility and reduces myocardium
oxygen consumption. Its negative chronotropic effect results in a
modest lowering of heart rate, due to slowing of the sinoatrial
node. It results in reduced myocardium oxygen consumption.
 Because of its negative dromotropic effect, conduction through the
AV (atrioventricular) node is slowed, which increases the time
needed for each beat. This results in reduced myocardium oxygen
consumption.

Indications:
 Hypertension
 Angina pectoris
 Arrhythmia
Adverse effects:
 Hypotension
 Bradycardia
 dizziness
 flushing

Contraindications:
 CHF
 AV or Sa node disturbances
 Low blood pressure
 Bradycardia
 Impaired left ventricle function
 Peripheral artery occlusive disease
 Chronic obstructive pulmonary disease

Drug interactions:
 Beta blockers
 Quinidine
 Diltiazem inhibits hepatic
cytochromes CYP3A4, CYP2C9 and CYP2D6,
possibly resulting in drug interactions.

RABIA KHALID NADEEM
OTHER DRUGS

DIGOXIN
 Digoxin shortens the refractory period
in atrial & ventricular myocardial cells
while prolonging the ERF & diminishing
conduction velocity in the AV node.
 It is used to control the ventricular
response rate in atrial fibrillation & flutter.
OTHER DRUGS:-

Digoxin toxicity:
 At toxic conc. it causes ectopic
ventricular beats that may result in
ventricular tachycardia & fibrillation.
 [note: this arrhythmia is usually treated
with Lidocaine]

Indications:
 CHF
 Atrial arrhythmia
 Heart failure
Adverse effects:
 GI upset
 Yellow vision
 ECG will show increased RP interval
 ST scooping
 T-WAVE inversion

ADENOSINE
 It is a naturally occurring nucleoside, but
at high doses it decreases conduction
velocity, prolongs the refractory period, &
decreases automaticity in the AV node.
Toxicity:
 It has low toxicity, but causes flushing,
chest pain, & hypotension.

We hope you liked our presentation.
Thank you! 

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