Download Pharmacology Objectives 11

Pharmacology
Lecture 11 Antiarrhythmic Drugs
1) Define cardiac arrhythmias. Arrhythmias are any abnormalities in heart rate,
rhythm or a change in the site of the cardiac pacemaker resulting from alterations in
the electrical activity of certain cardiac cells.
2) List the goals of antiarrhythmic therapy with drugs. The goal of antiarrhythmic
therapy is to restore normal cardiac function, alleviate symptoms and prevent sudden
cardiac death.
3) List three mechanisms of arrhythmogenesis.
Enhanced automaticy – the cardiac impulse originates in cells outside of the SA node
that are undergoing spontaneous depolarization at a rate faster than the SA node.
Triggered automaticy – is characterized by after depolarizations, depolarizations that
occur before or after full repolarization of the cell. After depolarizations can be early
(EAD) or delayed (DAD).
Re-entry – occurs when there is slower conduction down one branch of fibers than on
a neighboring branch such that the impulse on the normal branch depolarizes its cells
and comes back the wrong direction. This occurs with congenital bypass tracts
connecting atrium and ventricle, myocardial ischemia, and electrolyte imbalance. It
produces atrial and ventricular fibrillation.
4) For each of the drugs discussed in this section, describe: electrophysiologic
actions, antiarrhythmic actions, indications for use and adverse action both
cardiac and non-cardiac.
Drug
Electrophysiologic actions
Adenosine
↑K+ conductance and
cAMP-induced Ca2+ influx
is inhibited. Inhibits AV
nodal conduction and ↑AV
nodal refractory period
Threshold is increased and
impulse conduction is
slowed
Amiodarone
Antiarrhythmic
actions
Activates the
adenosine A1 receptor
resulting in A-V
nodal block
Indications for use
Adverse action
IV use in the emergent
treatment of proxysmal
supraventricular
tachycardia
Na+, K+, and Ca2+ ion
channel block
Acute ventricular
tachycardia and
fibrillation, and long-term
treatment of atrial
fibrillation
Atrial fibrillation, chronic
heart failure
Cardiac – risk of
transient AV block.
Flushing occurs
Ineffective with
antagonist theophylline
Corneal micro-deposits,
skin discoloration,
thyroid disfunction,
liver dysfunction,
pulmonary fibrosis
Cardiac – arrhythmias
Fatigue, anorexia,
N&V, altered vision
and confusion
Cardiac – least
cardiotoxic.
CNS stimulation
w/seizures
Cardiac – not used in
severe or unstable CHF.
Contraindicated –
asthma, COPD, severe
peripheral vascular
disease, diabetes
Cardiac – worsen CHF,
AV block with digoxin
or β blockers.
Hypotension
Digoxin
↓excitability, ↓automaticity,
↓conduction velocity and
↑refractory periods
Block Na+/K+ATPase
to ↓HR ↑contractility
Vagomimetic
Lidocaine
Suppresses electrical
activity in tissue causing
arrhythmias but not in
normal tissue
Decreases automaticity,
prolongs the refractory
period of the A-V node and
slows conduction through
the A-V node thus slowing
ventricular rate
Affects abnormal tissue
more, selectively depresses
frequently depolarizing
tissue, SA and AV nodal
conduction velocity is
slowed and the refractory
period is prolonged
Na+ channel block
Propranolol
Verapamil
β-Blockade
Ca2+ channel block
Ventricular ectopy and
tachycardia associated
with hemodynamic
instability
Atrial fibrillation to slow
ventricular rate, to
maintain sinus rhythem
post electrical conversion,
other supraventricular
tachycardias, and after MI
Reentrant supravenricular
tachycardia, also slows
the ventricular rate in
atrial fibrillation