Antiarrhythmic drugs Flashcards by Emily Harrison

What are the prototypes of Class III drug

Amiodarone, Sotalol, Dofetilide

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Pharmacokinetics of amiodarone

extensively tissue bound, long half life up to 100 days

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MOA of Amiodarone

K+ , Na+, Ca++ channel blockade, alpha and beta adrenergic blockade, Jack of all trades

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Adverse effects of amiodarone

concentrates in tissues, yellow brown corneal microdeposits, photosensitivity, blue-gray skin
Gastrointestinal, constipation, loss of appetite, nausea, vomiting
Neurological, neuropathy, fatigue, motor
hypotension due to ca++ effects
Life threatening pulmonary toxicity (10-15%)
Hepatotoxicity
Thyroid dysfunctions

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Drug interactions for amiodarone

increases plasma levels of many antiarrhythmia drugs
amiodarone plus beta blockers of Ca2+ chanel antagonists can cause sinus arrest or AV block, worsen congestive heart failure
long lasting interaction possibility

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Summary of amiodarone

highly effective due to many targets, also has many adverse effects for the same reason

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Sotalol MOA

L-isomer is beta adrenergic receptor blocker

D-isomer is a K+ channel blocker

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Therapeutic use of Sotalol

atrial flutter and fibrillation, ventricular tachyarrhythmias

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Adverse effects of Sotalol

Torsades de pointes

Beta blocker effects

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MOA of Dofetilide

Selective blocker of CARDIAC K+ channels

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Adverse effects of Dofetilide

Torsades de pointes (2%)

few extracardiac effects

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Therapeutic use of dofetilide

typically only used in hospital settings with specially trained physicians due to high risk of torsades de pointes

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Class IV anti-arrhythmia drugs

verapamil and diltiazem

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MOA of verapamil and diltiazem

Blocks Ca+ channels, direct action on SA nodal cells generally slows heart rate

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Therapeutic use of verapamil and diltiazem

first choice with adenosine for supraventricular tachycardia due to AV nodal reentry
reduce ventricular rate in atrial flutter

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Adverse effects of verapamil and diltiazem

Cardiac, ventricular fibrillation and hypotension, AV block, decreased contractillity
Extracardiac, constipation, peripheral edema, CNS effects

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Drug interactions with verapamil and diltiazem

Bradycardia or AV block when administered with beta blockers or digoxin

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Pharmacokinetics of verapamil

short half live, can be removed from body quickly

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Non-classified drugs

Adenosine

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Adenosine MOA

Activates adenosine receptors, activates K+ channels which hyperpolarizes AV nodal tissue

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Therapeutic use of adenosine

IV bolus terminates paroxysmal supraventricular tachycardia, can even cause complete cardiac block. Very short time of action (sec) makes it safer than verapamil

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Effect of antiarrhythmic drugs on ECG

P-R interval prolonged by CA++ channel blockers
QRS complex is prolonged by Na+ channel blockers
QT interval is prolonged by K+ channels

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Do atrial or ventricular fast tissues have a longer plateau

ventricular

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What are the slow tissues and how are they different from the fast tissues

Study These Flashcards

SA and AV nodes. They do not have sodium channels. Instead they have voltage activated calcium channels

What is a common consequence of K+ channel blockers

Early after-depolarization (Torsades des pointes)

What is the common cause of delayed after-depolarization

digoxin through Ca+ overload

What is a common cause of ectopic pacemaker arrhythmias

ischemia due to dysfunction of the loss of Na+/K+ ATPase

How do you treat a reentry arrhythmia

lengthen the effective refractory period (ERP) by inhibiting K+ channels

What is PR interval

the time for the impulse to pass through AV node

What is the QT interval

length of ventricular action potential

What is the definition of Tachycardia

Rapid beating of atria or ventricles (100-200 bpm)

What causes tachycardia

reentry arrhythmia or ectopic pacemaker

Supraventricular tachycardias can be caused by...

AV nodal reentry | Wolff-Parkinsons-White syndrome due to bundle of Kent

What are paroxysmal tachycardias

rapid abnormal beats with sudden onset and offset

How is a flutter defined

rapid regular contractions 200-350 bpm that are self sustaining. Usually due to reentry. Can degenerate into fibrillation

Which type of fibrillation is lethal

ventricular

MOA of Class 1a drugs

block both K+ and Na+ channels

Prototype Class 1a drugs

Quinidine and procainamide

Therapeutic use of class 1a drugs

beneficial for arrhythmias of fast tissue.

Quinidine side effects

cardiac: Torsade de pointes extracardiac: GI, tinnitus, dizziness, blurred vision and headaches at hich doses Rare: thrombocytopenia, hepatitis, angioedema, fever

General pharmacokinetic profile of antiarrhythmics

metabolized in liver and/or kidney, plasma bound, half life of hours

Therapeutic use of quinidine

not first line due to side effects, supraventircular arrhythmias and ventricular tachycardia

Metabolism of procainamide

metabolized to NAPA in liver, excreted in kidney | slow and fast acetylators

Side effects of procainamide

Cardiac: torsade de pointes less common than with quinidine, but increased in fast acetylators hypotension Extracardiac: Lupus, nausea, diarrhea, hepatitis, rash, fever, agranulocytosis

Theapeutic use of procainamide

atrial and ventricular arrhythmias, not for long term therapy due to lupus.

Class 1b drugs

Na+ channel block, lidocaine

Moa of lidocaine

use-dependent blockade of Na+ channels

Pharmacokinetics of lidocaine

first pass metabolism in liver, IV or IM | half life 1-2 hrs

Side effects of lidocaine

fewer cardiac side effects that 1a or 1c CNS: parasthesis, drowsiness, tinnitus, blurred vision Toxic: tremors, convulsions, hearing disturvances, unconsiousness, respiratory arrest

Therapeutic use of lidocaine

suppressing ventricular tachycardias and arrhythmias in depolarized tissue

Class 1c MOA

block of healthy Na+ channels

Class 1c prototype

flecainide

Therapeutic use of flecainide

supraventricular arrhythmias in patients with otherwise normal hearts

Side effects of flecainide

significantly proarrhythmic, prolonged use decreases survival

Class II MOA

block calcium channels by blocking beta-adrenergic receptor stimulation

Class II prototype

propranalol

Cardiac action of propranalol

negative ionotropic and chronotropic effect. Decreases excitability and slows conduction velocity.

Therapeutic use of propranalol

ventricular arrhythmias due to exercise or emotion, after MI to prevent recurrent infarction. long-term survival benefit. Supraventricular arrhythmias

Side effects of propranalol

SA and AV block, withdrawl symptoms, dyspnea

Antiarrhythmic drugs Flashcards

(59 cards)