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PHARMACOLOGY

What

are arrhythmias?

Normal

cardiac contraction originates at the


SA node at 60-100 bpm.

Spreads

through atria into the AV node


propagates over the His-Purkinje system to the
ventricles

Arrhythmia-

abnormal pacemaker activity or


abnormal impulse propagation.

Arrhythmia

activity is divided into two


general categories:

Those resulting from an abnormality in impulse


generation (aka autonomic arrhythmias)
Those resulting from an abnormality in impulse
conduction (reentrant arrhythmias)

When

an arrhythmia is present heart rate


may be:

Too slow (bradycardia)


Too quick (tachycardia)
Irregular

There

are many different types of


arrhythmias e.g.:

Atrial fibrillation or flutter


Atrioventricular nodal reentry tachycardia
(AVNRT)
Heart block or atrioventricular block
Multifocal atrial tachycardia
Paroxysmal supraventricular tachycardia
Sick sinus syndrome
Ventricular fibrillation
Ventricular tachycardia -- a fast heart rate that
originates in the lower chambers (ventricles)
Wolff-Parkinson-White syndrome

Risk

factors???

Possible

causes??

The

risk of getting a tachycardia or


bradycardia varies greatly, depending on:

Blood chemistry imbalances, such as abnormal


potassium levels
Cardiomyopathy -- a weakening of the heart
muscle or a change in the heart muscle
Heart failure
Overactive thyroid gland
Past heart attacks

Arrhythmias

may also be caused by some


substances or drugs, including:

Amphetamines
Caffeine
Cocaine
Beta blockers
Psychotropics
Sympathomimetics

Symptoms??

Arrhythmia

symptoms may be present all of the


time, they may come and go or may be
asymptomatic.
Common symptoms include:

Chest pain
Fainting
Fast or slow heartbeat (palpitations)
Light-headedness, dizziness
Paleness
Shortness of breath
Skipping beats - changes in the pattern of the pulse
Sweating

The

following tests may be performed to


identify arrhythmias:

Ambulatory cardiac monitoring


Coronary angiography
ECG
Echocardiogram
Electrophysiology study

Goals

for treatment:

Reduce ectopic pacemaker activity


Modify conduction.

Normal

conduction can be restored by:

Electrical "shock" therapy (defibrillation or


cardioversion)
Implanting a temporary pacemaker to interrupt
the arrhythmia
Medications given through a vein (intravenous)

How

would you prevent arrhythmias from


occuring?

To

prevent development of arrhythmias,


patients must be advised to take steps to
prevent coronary artery disease.

Eating a well-balanced, low fat & salt diet


Exercising regularly
Not smoking
Cut alcohol
Comply with treatment

Achieved

with:

Sodium channel blockers


Blocking sympathetic autonomic effects in the
heart
Prolonging the effective refractory period
Calcium channel blockers

Four classes:
Class 1- sodium channel blockade- (NB:

subclasses reflect effects on the APD and


the kinetics of Na blockade)

1A: prolong action potential duration (APD) and


dissociate from the Na channel with intermediate
kinetics.

1B: shorten APD and dissociate from the Na channel


with rapid kinetics.

1C: minimal effects on APD and dissociate from the


Na channel with slow kinetics.

Class

2 action is sympatholytic- drugs reduce


-adrenergic activity in the heart.

Class 3

action manifests as prolongation of the

APD.
Class

4 action is blockade of the cardiac Ca


current.

Procainamide,

quinidine, and disopyramide.

Quinidine
Blocks Na channels thus slowing down action
potential upstroke, conduction and the QRS
duration on the ECG.
It also blocks the K channels.
Indications: atrial and ventricular arrhythmias.

A/E-

Excessive action potential prolongation,


QT interval prolongation, torsade de pointes
arrhythmia and syncope, headache,
dizziness, tinnitus.

70-80%

systemic bioavailability when given


orally, 80% bound to albumin, eliminated via
hepatic metabolism.

twisting

the points-

Procainamide-

prolongs QRS duration of the


ECG by blocking sodium channels.

It

also indirectly blocks K channels, but has


less prominent antimuscarinic effects than
quinidine.

Indications:

arrhythmias

atrial and ventricular

A/E:

similar to quinidine, hypotension


(ganglion blocking effects), systemic lupus
erythematous (SLE), pleuritis, pericarditis.

Rarely

used but can be administered IV or IM


with 75% systemic bioavailability when given
orally.

Disopyamide-

effects similar to quinidine, with


greater antimuscarinic effects.

Thus

should be administered with a drug that


slows AV conduction esp. when treating atrial
flutter.

Only
A/E:

available for oral use

may precipitate heart failure in patients


with preexisting left ventricular depression,
urinary retention, dry mouth, blurred vision,
constipation, worsening of glaucoma.

Lidocaine-

inhibits fast sodium channels and


shortens APD inhibiting ectopic beats and
conduction in depolarized cells.

Least cardiotoxic

Indications-

of all the sodium channel blockers.

suppression of ventricular arrhythmias


associated with MI, cardiac surgery or other acute
situations.

A/E:

SA node arrest, worsening of impaired


conduction, vetricular arrhythmias,
paresthesias, tremor, nausea, slurred speech,
lightheadedness, convulsions.

Extensive

1st pass metabolism thus only 3% is


bioavailable, give parenterally
(rapid/immediate onset of action).

Mexiletine-

resistant to 1st pass metabolism


and is effective by the oral route

Powerful

sodium channel blockers,


manifested by QRS widening on the ECG,
with little effect on the QT interval.

They

allow 1:1 conduction to the ventricles


causing marked acceleration in the
ventricular rate.

Thus

in atrial flutter, they should only be


used with beta blockers or verapamil.

Flecainide-

potent Na and K channel blocker


with slow unblocking kinetics (used for patients
with otherwise normal hearts who have
supraventricular arrhythmias.)

Effective

in suppressing premature ventricular


contractions.

Negative

inotropic effects but no -blocking

action.
A/E-

may cause severe exacerbation of


arrhythmia in patients with preexisting
tachycardia.

Propafenone-

structurally similar to
propranolol, with weak -blocking properties.

Has

negative inotropic effects with sodium blocking


linetics similar to those of flecainide.

Used for

supraventricular arrhythmias.

A/E: metallic

taste, constipation, exacerbation of


arrhythmias might occur.

-blockers

like propranolol belong to this class due


to their -receptor blocking actions and direct
membrane effects.

Cardiac

1-receptor blockade, intrinsic


sympathomimetic activity, membrane effects
and prolonging cardiac AP.

Prolong

action potentials via K channel


blockade in the cardiac muscle.

Ultimately,

prolonging repolarisation
manifested as an increase in the QT interval
on the ECG.

Includes

amiodarone, dronedarone, sotalol.

Used

for prophylaxis and treatment of


supraventricular and ventricular arrhythmias.

A/E- torsades de pointes,


hyper/hypothyroidism, neurotoxicity,
photosensitivity, GI effects.

35-60%

bioavailability after hepatic


metabolism.

Sotalol-

has class 2 (-blocking) and class 3


properties (AP prolonging).

Used

in arrhythmias that fail to respond to blockers, in patients with high risk of


developing torsades de pointes.

100%

bioavailable (no hepatic metabolism


and no plasma binding).

Examples:

verapamil and diltiazem.

Verapamil-

blocks both activated and


inactivated L-type calcium channels and
slows SA node conduction.
Indicated for supraventricular tachycardia.
NB:

bulk up these notes, add dosages

VS

a 69-year-old retired teacher presents


with a 3-month history of palpitations,
intermittent shortness of breath, and
fatigue. She has a history of hypertension
and says she drinks at least 4 mugs of coffee
daily. An ECG shows an irregular heart rate.
The patient complains that she sweats a lot.
Upon physically examining the patient, you
also note that her paleness.

At

this stage, would you initiate treatment


with an antiarrhythmic drug to maintain
normal sinus rhythm?
What drug would you choose?
After initiating the patient on a class I
antiarrhythmic agent on a chronic basis, she
comes back complaining of fatigue, lowgrade fever and joint pain suggestive of
systemic lupus erythematosus (SLE). What
drug was issued?
How would you counsel this patient?