Anti-Arrhythmic Management and Pharmacology

Question 1

What are the three phases of Cardiac Pacemaker cell cycle and what channels are open at these times?

Answer 1

Phase 4: Resting / slow diastolic depolarization -> Ifunny channel activated by hyperpolarization, some contribution from T-type calcium channels

Phase 0: Rapid depolarization - influx via L-type Ca+2 channels

Phase 3: Repolarization K+ efflux

Question 2

Name the class Ia antiarrhythmics.

Answer 2

Quinidine - prom queen, Procainamide - prom king, disopyramide - disappears

Question 3

Name the class Ib antiarrhythmics.

Answer 3

Lidocaine - You lied
Mexiletine - Mexican flag
Phenytoin - Tow truck guy with crane

Question 4

Name the class Ic antiarrhythmics.

Answer 4

Flecainide - Corn flakes

Propafenone - Purple phone

Question 5

What is the usage of the class Ia drugs? What is the scariest potential side effect?

Answer 5

Primarily used for AF rhythm control, but also decent for ventricular tachycardias

-> Intermediate Na+ blockade, prolong the QT interval with K+ channel blockade and can cause TdP

Question 6

Which of the class I antiarrhythmics should be avoided in heart failure?

Answer 6

Ia and Ic -> don’t want to block cardiac action potential conduction so much (negative inotropic effect), think of how closely they grip the peanut butter jars

Question 7

Which of the class I antiarrhythmics can cause a lupus-like syndrome? What is one additional side effect not mentioned in sketchy?

Answer 7

Procainamide - Lupus wolf in prom king’s room

Additional side effect: Anticholinergic effects

Question 8

What is the primary usefulness of class Ib antiarrhythmics? Why?

Answer 8

Usually used in ACLS, very good at terminating ventricular arrhythmias, especially Vfib or pulseless Vtach.

Low affinity for Na+ channels so it tends to have a more rapid onset. Works better in ischemic ventricular tissue which will be farther from resting potential and have more open or inactivated Na+ channels.

Question 9

What is the primary toxicity of concern with class Ib antiarrhythmics?

Answer 9

Brain hat on the trucker -> neurologic issues

Lowers the seizure threshold, tremor, slurred speech, convulsions

Question 10

What is the primary interval on ECG which class IC drugs will prolongate? What is their use?

Answer 10

Primarily the QRS interval -> strongly bind Na+ channels, leaving K+ channels untouched (curtain untouched) -> no QT effect really

Use: Atrial fibrillation rhythm control - guy sitting in bed changing channel on TV (2nd line to amiodarone)

Question 11

What are the contraindications of IC antiarrhythmics?

Answer 11

1. HFrEF -> negative inotropic effect
2. Structural heart disease -> too much depolarization, will lead to overacting / binding, healthy hearts only please! - remember flecainide trial

Question 12

What is the clinical indication for Class II antiarrhythmics?

Answer 12

Rate control of AF or atrial flutter -> great for SVTs. Think of the rhythm control metronome

Question 13

What are the heart rate targets for symptomatic vs asymptomatic ventricular rate control in AF? Who do you achieve this?

Answer 13

Asymptomatic: <110 bpm
Symptomatic: <80 bpm

Push current medication to maximum tolerated dose before adding another agent -> dual use of non-DHP CCB may cause 3rd degree heart block.

Question 14

What is the clinical use of Class III antiarrhythmics? Which can cause TdP?

Answer 14

Atrial fibrillation rhythm control -> think of the TV in corner

• > do so by prolonging the QT interval, beware of TdP
• > Less risk in amiodarone and dronedarone because of all 4 classes of antiarrhythmic properties

Question 15

What are the Class III antiarrhythmics other than amiodarone / dronedarone?

Answer 15

Sotalol, Dofetilide, Ibutilide (IV for cardioversion)

Soda, and Til I die

Question 16

What are the indications for stopping sotalol / dofetilide?

Answer 16

QTc > 500 ms during treatment.

Do not even start if QTc > 400 msec

Question 17

What is the primary use of amiodarone, and what are its drug interactions / half life?

Answer 17

Use - Most effective anti-arrhythmic for maintaining sinus rhythm in AF, as well as termination of ventricular tachycardias

• > Inhibits many CYP450s -> think of the CYP450 truck holding cow, especially warfarin problem
• > Half life ~60 days = need a huge loading dose.

Question 18

What are the side effects of Amiodarone treatment?

Answer 18

Thyroid: Hyper or hypothyroidism (bowties), inhibits conversion of T4->T3
Pulmonary function: Pulmonary fibrosis (vest)
Liver function: Hypersensitivity hepatitis (think of cow)
Skin: Photosensitivity, turn blue due to metHg
Eyes: Corneal deposits

Question 19

Why might Dronedarone be preferred to amiodarone, and when should it be avoided?

Answer 19

Has a shorter halflife due to lack of iodine moieties, good for non-permanent Afib (paroxysmal <7 days or persistent >7 days but cardiovertable)

Avoid: HFrEF, and PERMANENT Afib (dumb)

Question 20

What are Class IV antiarrhythmics used for and when are they contraindicated?

Answer 20

Used for rate control in AFib - kid hanging on light

Prolong the PR interval -> avoid in HFrEF due to negative inotropic effect (contraindication)

Question 21

What are the Class IV antiarrhythmics?

Answer 21

Non-DHP CCBs - Verapamil / Diltiazem

Question 22

What is the clinical use of digoxin as an antiarrhythmic, and its mechanism? Its main advantage?

Answer 22

Used in Afib rate control, like Class II and IV

• > directly stimulate the vagal nerve for parasympathetic output
• > advantage of II and IV -> safe in heart failure (does not negatively control intropy

Question 23

What should the drug levels of digoxin be in HFrEF and AF?

Answer 23

HFrEF: 0.5-1 ng/mL
AF: 1-2 ng/mL

Higher than this is toxic

Question 24

Should rhythm or rate controlled be used as a first line treatment approach to Afib and why?

Answer 24

Rate control - although there was no mortality difference between study groups, this group had significantly fewer adverse events (most due to drug side effects and cardiac events like TdP, cardiac arrest w/ Vtach, hospitalization)

Question 25

When can you or can you not simply directly electrically cardiovert a patient’s Atrial fibrillation / flutter? What is the protocol for when you cannot? Why?

Answer 25

<48 hours: Go for it
>48 hours: Must be anticoagulated for 3 weeks prior and 4 weeks post cardioversion for fear that a mural thrombus formed in atria from blood stasus

4 weeks post because there is myocardial stunning which occurs which may not directly restore sinus rhythm until months after the electrical cardioversion

Question 26

What drugs can be used for pharmacological cardioversion?

Answer 26

Class 1C = Flecainide, propafenone

Class 3 = Dofetilide, Ibutilide, amiodarone

Question 27

What is the first line treatment for Rate control in Afib with and without heart failure?

Answer 27

Afib w/ heart failure = Digoxin, add beta-blocker if needed

Afib w/o heart failure = non-DHP CCBs, add dogoxin if needed

Can consider Beta blockers for Afib w/o HF, but not calcium channel blockers in heart failure (think of guy holding balloon outside sketchy)