Management of Arrhythmia

Question 1

What are some ways to approach managing bradyarrhythmia?

Answer 1

• look for reversible causes and treat those

- pacemaker

Question 2

What are some ways to approach managing tachyarrythmia?

Answer 2

• ablation therapy - cut off slow pathway
• antiarrhythmic agents
• implantable defibrillator

Question 3

What is the proposed mechanism of the origin of atrial fibrillation and how is it fixed?

Answer 3

• firing from pulmonary veins in left atrium (cardiac muscle sleeve)
• electrically isolate with ablation

Question 4

Compare and contrast using ablation therapy vs. using antiarrhythmic therapy

Answer 4

• ablation: definite, potential for cure, invasive, substrate oriented
• antiarrhythmic: indefinite, risk for breakthrough or proarrhythmia (blocks all over heart, not just atria), non invasive, modifies the substrate

Question 5

What are the ideal characteristics of an antiarrhythmic?

Answer 5

• safe, does not generate pro-arrhythmia
• effective
• no negative inotropic effect, interference with other drugs, or end organ toxicity

Question 6

What are the Vaughn Williams class Ia drugs and how do they work?

Answer 6

• quinidine, procainamide, disopyramide
• block fast Na channels
• increase action potential duration and effective refractory period
• also blocks K channel
• quinidine also blocks muscarinic and a-adrenergic receptors

Question 7

Quinidine used to be used primarily for _____ but has fallen out of favor due to side effects. Now, it is primarily used for _____.

Answer 7

A) atrial fibrillation

B) Brugada’s syndrome, short QT syndrome

Question 8

Procainamide is a class Ia drug. What is its active metabolite, and what class does this fall under?

Answer 8

• N-acetyl procainamide (NAPA), a class III drug

- blocks delayed K rectifier current

Question 9

What is unique about disopyramide?

Answer 9

induces vagal block

Question 10

What are the class Ib drugs and how do they work?

Answer 10

• lidocaine and mexiletine
• block inactivated fast Na channels, and have a preference for tissues that are partly depolarized, such as in ischemia
• this results in less excitability of hypoxic heart muscle
• decrease the action potential duration

Question 11

What are the class Ic drugs and how do they work?

Answer 11

• flecainide, propafenone
• block fast Na channels, especially in His-Purkinje tissue
• no effect on action potential duration

Question 12

What are contraindications of use of class Ic drugs?

Answer 12

• structurally abnormal heart
• long QRS
• heart failure
• ischemia
• history of CAD or hypertrophy

Question 13

What are the class II drugs and how do they work?

Answer 13

• beta blockers
• decrease SA and AV node activity
• decrease slope of phase 4
• increase refractory period
• negative inotropic actions

Question 14

What are the class III drugs and how do they work?

Answer 14

• sotalol, dofetilide, amiodarone, ibutilide, droniderone
• block delayed rectifier K channels, slowing phase 3 of AP
• increase action potential duration and effective refractory period

Question 15

What additional properties does sotalol have?

Answer 15

• non selective beta blocker (+ K channel block)

- renal excretion - monitor serum K, Mg, and renal function

Question 16

What additional properties does amiodarone have?

Answer 16

• Na and Ca channel blocker, beta blocker (+ K channel block)
• half life is 80 days, so takes forever to reach steady state and be eliminated
• iodine based med, with end organ toxicity to lung, liver, thyroid, and skin –> this brought about dronedarone, which is amiodarone without the iodine and with a half life of 24 hrs

Question 17

What are the class IV drugs and how do they work?

Answer 17

• L-type Ca channel blockers
• decrease phase 0
• decrease phase 4
• non dihydropyridines - verapamil, diltiazem
• used for supraventricular tachycardias

Question 18

How does adenosine work?

Answer 18

• activates adenosine receptors, causing a decrease in cAMP

- decreases SA and AV node activity