AR, a 47-year-old man, presented with new-onset atrial fibrillation and a heart rate of 130 beats per minute. He was given IV diltiazem which controlled his heart rate. After 24 hours on the IV diltiazem infusion without any issues, the medical team wants to transfer AR to a regular floor but needs to convert him to oral diltiazem first. The document discusses the classification of arrhythmias and antiarrhythmic drugs, specifically explaining the mechanism of action of diltiazem in treating atrial fibrillation and how to calculate the oral dose when converting from IV diltiazem. It also briefly mentions the role of cardioversion in restoring

1. CARDIOLOGY POSTING
Activity-1
by
V ARAVIYNDAN
4031628

2. CASE 1
• AR is a 47-year-old, 80-kg man who presents to the hospital
with new-onset atrial fibrillation (AF) and a heart rate of 130
beats/min. He is given a bolus of 20 mg (0.25 mg/kg)
intravenous (IV) diltiazem over 2 minutes and then is initiated
on a diltiazem drip of 10 mg/hr, which is ultimately titrated to a
rate of 15 mg/hr for heart rate control. As per the hospital’s
policy regarding patients receiving IV diltiazem, AR is receiving
care in the intermediate care unit (IMU). AR has received his
infusion of diltiazem for the past 24 hours and has not required
any supplemental bolus doses or dose adjustments. AR has
achieved a desirable heart rate and has no other medical
problems that would necessitate remaining in the IMU. The
team would like to transfer AR to a medical floor, but this
requires conversion of IV diltiazem to oral diltiazem.

3. 1. Classify arrhythmias
Bradycardia or
Bradyarrhythmias
• Sinus bradycardia
• Sinus pauses
• Sick sinus syndrome
• Bradycardia-tachycardia
syndrome
• Atrio-ventricular (AV) conduction
block
• Intraventricular conduction
abnormalities
Tachycardias or
Tachyarrhythmias
• Supraventricular
tachyarrhythmias
• Atrial tachycardia
• Atrial fibrillation (AF)
Ventricular tachyarrhythmias
• Ventricular extrasystoles
• Ventricular tachycardia (VT)
• Ventricular fibrillation (VF)

4. 2. Discuss the classification of antiarrhythmics
• ANTI-ARRYTHMIC DRUGS MOSTLY ACT ON ONE OF THE FOLLOWING PHASES

5. 2. Discuss the classification of antiarrhythmics
• Class I: Fast sodium (Na) channel blockers
Ia -Quinidine, procainamide, disopyramide (depress phase 0, prolonging
repolarization)
Ib -Lidocaine, phenytoin, mexiletine (depress phase 0 selectively in
abnormal/ischemic tissue, shorten repolarization)
Ic -Flecainide, propafenone, moricizine (markedly depress phase 0, minimal effect
on repolarization)
Side Effects and Contraindications
• The anticholinergic effects of IA drugs can produce tachycardia, dry mouth,
urinary retention, blurred vision and constipation. Diarrhea, nausea, headache
and dizziness are also common side effects of many Class I drugs. Quinidine
enhances digitalis toxicity, especially if hypokalemia is present.. Disopyramide is
contraindicated for patients with uncompensated heart failure because of its
negative inotropic actions; propafenone can also depress inotropy. IC compounds
can cause increased risk of sudden death in patients with a prior history of
myocardial infarction or sustained ventricular arrhythmias.

6. 2. Discuss the classification of antiarrhythmics
• Class II: Beta blockers- Propranolol, Esmolol,Timolol, Metoprolol, Atenolol (decreases
slope of phase 4)
Many of the side effects of beta-blockers are related to their cardiac mechanisms and
include bradycardia, reduced exercise capacity, heart failure, hypotension, and
atrioventicular (AV) nodal conduction block. Beta-blockers are therefore contraindicated in
patients with sinus bradycardia and partial AV block.
• Class III: Potassium (K) channel blockers- Amiodarone (prolongs phase 3; also acts on
phases 1, 2, and 4), Sotalol (prolongs phase 3, decreases slope of phase 4), Ibutilide
(prolongs phase 3), Dofetilide (prolongs phase 3)
Side effect of class III can cause bradycardia and atrioventricular block, and therefore is
contraindicated in patients with heart block, or sinoatrial node dysfunction.
• Class IV: Slow calcium (Ca) channel blockers -Verapamil (prolongs phase 2), Diltiazem
(prolongs phase 2)
non-dihydropyridines, should not be administered to patients being treated with a beta-
blocker because beta-blockers also depress cardiac electrical and mechanical activity and
therefore the addition of a CCB augments the effects of beta-blockade.

7. 3. Explain the mechanism of action of diltiazem and its role
in AF
• MOA- Diltiazem is a potent vasodilator, increasing blood flow
and variably decreasing the heart rate via strong depression of
A-V node conduction. It binds to the alpha-1 subunit of L-type
calcium channels causing negative inotropic, chronotropic
effects.
• ROLE IN AF- Diltiazem causes a decrease in heart muscle
contractility – how strong the beat is, lowering of heart rate –
due to slowing of the sinoatrial node, and a slowing of
conduction through the atrioventricular node – increasing the
time needed for each beat. Each of these effects results in
reducing symptoms of AF.

8. 4. As the pharmacist, how would you recommend the IV to
oral conversion of diltiazem to be done?
• For Diltiazem Oral dose (in mg per day) = [rate (mg/hr) x 3 + 3]
x 10 formula is used(University of Wisconsin).
• 15 mg/hr IV = 480 mg daily in 4 divided doses using IR dosage
forms would be recommended

9. 5. Explain the role of cardioversion in AF.
• used for atrial fibrillation in an attempt to restore sinus rhythm
and correct the electrophysiological abnormalities associated
with AF

10. THANK YOU