Anti-Arrhythmic Management and Pharmacology Flashcards
What are the three phases of Cardiac Pacemaker cell cycle and what channels are open at these times?
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
Name the class Ia antiarrhythmics.
Quinidine - prom queen, Procainamide - prom king, disopyramide - disappears
Name the class Ib antiarrhythmics.
Lidocaine - You lied
Mexiletine - Mexican flag
Phenytoin - Tow truck guy with crane
Name the class Ic antiarrhythmics.
Flecainide - Corn flakes
Propafenone - Purple phone
What is the usage of the class Ia drugs? What is the scariest potential side effect?
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
Which of the class I antiarrhythmics should be avoided in heart failure?
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
Which of the class I antiarrhythmics can cause a lupus-like syndrome? What is one additional side effect not mentioned in sketchy?
Procainamide - Lupus wolf in prom king’s room
Additional side effect: Anticholinergic effects
What is the primary usefulness of class Ib antiarrhythmics? Why?
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.
What is the primary toxicity of concern with class Ib antiarrhythmics?
Brain hat on the trucker -> neurologic issues
Lowers the seizure threshold, tremor, slurred speech, convulsions
What is the primary interval on ECG which class IC drugs will prolongate? What is their use?
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)
What are the contraindications of IC antiarrhythmics?
- HFrEF -> negative inotropic effect
- Structural heart disease -> too much depolarization, will lead to overacting / binding, healthy hearts only please! - remember flecainide trial
What is the clinical indication for Class II antiarrhythmics?
Rate control of AF or atrial flutter -> great for SVTs. Think of the rhythm control metronome
What are the heart rate targets for symptomatic vs asymptomatic ventricular rate control in AF? Who do you achieve this?
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.
What is the clinical use of Class III antiarrhythmics? Which can cause TdP?
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
What are the Class III antiarrhythmics other than amiodarone / dronedarone?
Sotalol, Dofetilide, Ibutilide (IV for cardioversion)
Soda, and Til I die
What are the indications for stopping sotalol / dofetilide?
QTc > 500 ms during treatment.
Do not even start if QTc > 400 msec
What is the primary use of amiodarone, and what are its drug interactions / half life?
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.
What are the side effects of Amiodarone treatment?
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
Why might Dronedarone be preferred to amiodarone, and when should it be avoided?
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)
What are Class IV antiarrhythmics used for and when are they contraindicated?
Used for rate control in AFib - kid hanging on light
Prolong the PR interval -> avoid in HFrEF due to negative inotropic effect (contraindication)
What are the Class IV antiarrhythmics?
Non-DHP CCBs - Verapamil / Diltiazem
What is the clinical use of digoxin as an antiarrhythmic, and its mechanism? Its main advantage?
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
What should the drug levels of digoxin be in HFrEF and AF?
HFrEF: 0.5-1 ng/mL
AF: 1-2 ng/mL
Higher than this is toxic
Should rhythm or rate controlled be used as a first line treatment approach to Afib and why?
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)
