Anti-Arrhythmics Flashcards

1
Q

What are the three requirements of reentry circuit?

A

Partial depolarization of the pathway. Unidirectional Block. Circuit takes longer than effective refractory period.

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2
Q

What are Class Ia drugs according to the Vaughan-Williams Classification? What is the prototype? What are the main effects?

A

Class Ia are sodium channel blockers with intermediate dissociation kinetics. Procainamide is the prototype. They decrease conduction velocity and automaticity while increasing refractoriness.

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3
Q

What are Class Ib drugs according to the Vaughan-Williams Classification? What is the prototype? What are its main effects?

A

Class Ib are sodium channel blockers with rapid dissociation kinetics. Lidocaine is the prototype. They have NO EFFECT on conduciton velocity, but may decrease refractoriness.

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4
Q

What are Class Ic drugs according to the Vaughan-Williams Classification? What is the prototype? What are its main effects?

A

Class Ic are sodium channel blockers with slow dissociation kinetics. The prototype is flecainide. They have NO EFFECT on refractoriness, but decrease conduction velocity.

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5
Q

What is procainamide? What are its effects on electrical conduction?

A

Procainamide is a Class Ia anti-arrhythmic. It slows action potential upstroke prolonging action potential. Also, prolongs conduction velocity and QRS.

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6
Q

What are the therapeutic uses and extra-cardiac effects of procainamide?

A

Used in atrial and ventricular arrhythmias. Also acts as a ganglion-blocker causing decreased PVR.

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7
Q

What is a key metabolite of procainamide? What are its toxic effects (4)?

A
N-acetylprocainamide is a metobalite produced by the liver. It acts as a class III anti-arrhythmic and can cause torsades des pointes.
Toxic effects include prolongation of action potential, prolongation of QT interval, hypotension, and lupus-like syndrome.
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8
Q

What can class Ib drugs not be used to treat?

A

atrial arrhythmias

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9
Q

What is the effect of lidocaine on electrical conduction? What are its therapeutic uses?

A

Causes shortened action potential by increasing the rate of phase 3.
Used to treat ventricular tachycardia and ventricular fibrillation after cardioversion.

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10
Q

Describe the metabolism of lidocaine and its route of administration. In what situation would an increased dose and decreased dose be required? What are the toxic effects of lidocaine?

A

Lidocaine is heavily metabolized by the liver and must be given by IV.
In MI or acute illness, an increase dose may be required due to the presence of alpha1 acid glycoprotein.
In congestive heart failure a decreased dose may be needed due to low volume of distribution and low clearance.
Toxicity will result in hypertension, tremors, and parasthesias.

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11
Q

What is a major contraindication for class Ic drugs?

A

These drugs cannot be used in structural heart disease due to high incidence of drug-induced arrhythmias.

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12
Q

What are the effects on electrical conduction, therapeutic uses, and toxic effects of flecainide?

A

Slows conduciton velocity by decreasing the rate of phase 0. Used to treat supraventricular arrhythmias. Exacerbation of arrhythmias.

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13
Q

What are the effects on electrical conduction and therapeutic uses of beta-blockers?

A

Beta-blockers decrease heart rate, conductivity, oxygen demand, and automaticity. The therapeutic uses are tachyarrhythmias, atrial fibrillations, atrial flutter, and hypertension.

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14
Q

What are the prototype potassium channel blockers and its effects on electrical conduction?

A

Amiodarone and sotalol are the prototypes. It prolongs phase 3, increasing the duration of action potentials and effective refractory periods.

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15
Q

What are the effects of amiodarone on other channels/receptors and its therapeutic uses?

A

Strongly blocks sodium channels, and weakly blocks calcium channels and adrenergic receptors. Therapeutic uses include atrial fibrillation, ventricular tachycardia, and adjunct to implantable cardioverter defibrillator.

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16
Q

How long can the effects of amiodarone be maintained after discontinuation?

A

1-3 months

17
Q

What are the toxic effects of amiodarone?

A

Causes bradycardia and AV block. Accumulation in the tissues can also lead to hyper/hypothyroidism, pulmonary fibrosis, and gray-blue skin discolorations.

18
Q

Describe the drug interaction of amiodarone with respect to CYP3A4 and drugs it may potentiate.

A

CYP3A4 blockers (cimetidine) can increase the levels of amiodarone, while CYP3A4 inducers (rifampin) can decreases levels. Amiodarone can potentiate digoxin, warfarin, and statins. So, these drugs may need to be reduced by 33-50%.

19
Q

What other receptors may soltalol operate on? What are its therapeutic uses? What are its toxic effects?

A

Soltalol operates as a non-selective beta-blocker in addition to being a potassium channel blocker. Its therapeutic uses include ventricular tachycardia and atrial fibrillation. Its toxic effect is torsades des pointes.

20
Q

What are the prototype calcium channel blockers and their effects on electrical conduction?

A

Verapamil and diltiazem are the prototypes. They slow calcium current delaying phase 4 and AV node conduction.

21
Q

What are the therapeutic uses and toxic effects of verapamil?

A

Therapeutic uses - SVT, slowing ventricular rate in atrial fibrillation/flutter, angina, and hypertension (due to extra-cardiac effects)
Toxic effects - AV block, progression of V tach to V fib, and constipation

22
Q

What are the therapeutic uses and toxic effects of diltiazem?

A

Therapeutic uses - SVT, angina, hypertension

Toxic effects - hypotension, bradycardia, AV block, headache, and edema

23
Q

What are the effects of adenosine on electrical conduction?

A

Activates the potassium channels and inhibits the calcium current. Causes hyperpolarization and increased refractory period.

24
Q

What are the therapeutic uses and pharmacokinetics of adenosine?

A

Therapeutic use - cardioversion in SVT

Adenosine is metabolized in the blood and tissues to hypoxanthine with a half-life of 10 seconds

25
Q

What are the toxic effects and drug interactions of adenosine?

A

Toxic effects include atrial fibrillation and high grade AV block. Adenosine can be inhibited by adenosine receptor blockers (caffeine) and potentiated by adenosine uptake inhibitors (dipyridamole).

26
Q

What is the mechanism of action, therapeutic uses, and toxic effects of atropine?

A

Blocks the action of acetycholine at cholinergic receptors. Used to reverse neuromuscular blockade, treat bradycardia, and prevent cholinergic poisoning. The toxic effects include dizziness, arrhythmias, tachycardia, urine retention, and constipation.

27
Q

What are the therapeutic uses of magnesium?

A

digoxin induced arrhythmias and torsades des pointes