Cardiology Antiarrhythmics

Question 1

Cardiac Glycosides

Answer 1

Digoxin

Question 2

Digoxin

Answer 2

Cardiac Glycoside = Direct inhibition of Na/k ATPase - indirectly inhibits Na/Ca exchanger to increase IC Ca - positive inotropy
Stimulates Vagus nerve - decreases HR
CU: HF, A-fib (decreased AV node conduction & SA node depression)
AE: Cholinergic (N/V, diarrhea, blurry vision, arrhythmias, AV block); HYPERkalemia (poor prognosis)

Question 3

Digoxin Toxicity - Risk Factors

Answer 3

Renal Failure (decreased excretion)
Hypokalemia (permissive for digoxin K-binding site on Na/K ATPase)
Drugs that displace it from tissue binding sites/decrease clearance (verapamil, amiodarone, quinidine)

Question 4

Digoxin Antidote

Answer 4

Slowly normalize K+
Cardiac pacer
Anti-digoxin Fab fragments
Mg2+

Question 5

Class I

Answer 5

Sodium Channel Blockers

Question 6

Class IA Drugs

Answer 6

Quinidine, Procainamide, Disopyramide
“A - Queen Proclaims Disco Pyramid”

Na Channel Blockers:
INCREASE AP duration & effective refractory period (ERP) in ventricular action potential.
Increase QT interval (can cause torsades de pointes)

Atrial & Ventricular arrythmias (esp re-entrant/ectopic SVT & VT)

AE: 
Cinchonism: HA/tinnitus (Quinidine)
Reversible SLE-like syndrome (Procainamide)
Heart Failure (Disopyramide)
Thrombocytopenia

Question 7

Class IB Drugs

Answer 7

Lidocaine, Mexiletine
“B - a Lid on the Mexican Tacos” …“please”
- sometimes Phenytoin can fall in this category

Na Channel Blockers:
DECREASE AP duration (AE = CV depression)
Preferentially affect ISCHEMIC or DEPOLARIZED Purkinje and ventricle tissue.

Best Post-MI (for acute ventricular arrythmias)
Digitalis-induced arrythmias

AE: CNS stimulation/depression
CV depression

Question 8

Class IC Drugs

Answer 8

Propafenone, Flecainide
“C - the Propane Flame”

Na Channel Blockers:
Significantly prolongs ERP in AV node and accessory bypass tracts.
No effect on Purkinje/ventricle tissue
Minimal effect on AP duration

SVT’s (a-fib)
Only for last resort in refractory VT.

AE’s:
Proarrhythmic esp post-MI (contraindicated!)
Contraindicated in structural & ischemic heart Dz

Question 9

Post-MI Antiarrhythmic

Answer 9

IB = Best

Lidocaine, Mexiletine

Question 10

SLE-like AE

Answer 10

Procainamide

Question 11

NEVER GIVE post-MI

Answer 11

IC = Contraindicated in structural & heart dz

C - the Propane Flame (Propafenone, Flecainade)

Question 12

Causes Heart Failure

Answer 12

Standing on top of the Disco Pyramids causes heart failure

Disopyramide

Question 13

Class II

Answer 13

Beta Blockers

Question 14

Beta Blocker Drugs

Answer 14

Metoprolol, Propanolol, Atenolol, Timolol, Carvedilol,

Esmolol (super short acting)

Question 15

Beta Blocker MOA

Answer 15

Decrease SA and AV node activity by decreasing cAMP and Ca currents.
Suppress ectopic (abnormal) pacemakers by decreasing slope of Phase 4 - prolongs repolarization.
Note: AV node extra sensitive to increase PR interval

Question 16

Beta Blocker CU

Answer 16

SVT–ventricular rate control for A-fib and A-flutter

Question 17

Beta Blocker AE

Answer 17

Impotence
Exacerbates COPD/asthma and CV effects (bradycardia, AV block, HF)
CNS effects (sedation, sleep changes)
May mask hypoglycemia signs

Metoprolol - dyslipidemia
Propranolol - exacerbates Prinzmetal angina vasospasms

If given alone for pheochromocytoma or cocaine toxicity, beta blockers cause unopposed alpha1-agonism (except the nonselective alpha and beta antagonists carvedilol and labetalol)

Question 18

Beta Blocker OD Treatment

Answer 18

Saline
Atropine (alpha-1 antagonist)
Glucagon

Question 19

Non-selective alpha and beta blockers

Answer 19

Carvedilol, Labetalol

CU: pheochromocytoma and cocaine toxicitiy

Question 20

Class III

Answer 20

Potassium Channel Blockers

Question 21

Class III Drugs

Answer 21

Potassium Channel Blockers
Amiodarone, Ibutilide, Dofetilide, Sotalol
“K, AIDS”

Increase AP duration, ERP and QT interval

CU: A-fib, A-flutter, 
ventricular tachycardia (amiodarone, sotalol)

Question 22

Amiodarone AE’s

Answer 22

Remember to check: PFTs, LFTs, and TFTs!
Pulmonary fibrosis
Hepatotoxic
Hypo/hyperthyroid (drug is 40% iodine)

Hapten (corneal deposits, blue/gray skin deposits - photodermatitis)
Neurologic effects, constipation, CV (bradycardia, HF, heart block)

Amiodarone = lipophilic - has class I, II, III and IV effects

Question 23

Class IV

Answer 23

Calcium Channel Blockers

Question 24

Class IV Drugs

Answer 24

Verapamil, Diltiazem
“Velociraptors Die”

Decrease Conduction Velocity
Increase ERP, PR interval

CU: prevention of nodal arrhythmias (SVT), A-fib rate control

AE: Constipation, flushing, edema, CV effects (HF, AV block, sinus node depression

Question 25

Ibutilide and Sotalol AE’s

Answer 25

Ibutilide - Torsades de pointes

Sotalol - Torsades de pointes, excessive B blockade

Question 26

Adenosine

Answer 26

Increases K flow out of cell - hyperpolarization - decreases IC Ca

Drug of choice to terminate certain SVTs - VERY short acting

Effects blunted by adenosine R antagonists (theophylline and caffeine)

AE: flushing, hypoTN, chest pain/sense of impending doom, bronchospasm

Question 27

Mg2+

Answer 27

Effective in Torsades de Pointes and Digoxin Toxicity

Question 28

Drug of choice in Torsades de Pointes

Answer 28

Mg+