Antiarrythmics

Front 1

Class I Antiarrhythmics

Back 1

block Na+

Front 2

Class II Antiarrhythmics

Back 2

Beta blockade

Front 3

Class III Antiarrhythmics

Back 3

block K+ channels

Front 4

Class IV Antiarrhythmics

Back 4

block Ca2+ channels

Front 5

Class Ia Antiarrhythmics do what?

Back 5

inhibit Na+ and K+ channels
slow conduction time
increase refractoriness/prolonged repolarization
decrease automaticity
lengthen action potential
useful for supraventricular and ventricular arrythmias

Front 6

Quinidine

Back 6

Class IA antiarrhythmic
blocks Na+ channels, delayed K+ channels,
alpha-adrenergic receptor blocker
alkaloid of cinchona bark
Adverse affects: anticholinergic, cinchonism (headache, dizzy, tinnitus), torsade de points (long QT)
metabolism via Cyp 3A4
Decreases clearance of digoxin

Front 7

Procainamide

Back 7

Class IA antiarrhythmic
blocks Na+ channels, delayed K+ channels
Adverse effects: lupus-like syndrome w/antinuclear Ab, joint pain and rash; Torsade

Front 8

Disopyramide

Back 8

Class Ia antiarrhythmic
blocks Na+ channels, delayed K+ channels
Adverse effects: pronounced anticholinergic effects: dry mouth, constipation, urinary retention, precipitate glaucoma; Torsade

Front 9

Class Ib antiarrythmics do what?

Back 9

Inhibit Na+ channels
decrease automaticity
increase threshold for excitability
slow conduction time
no effect or shortened action potential
frequency-dependent blockade = prefers activated and inactivated Na+ (not resting) => greater effect on ischemic and rapidly driven tissues (Purkinje and ventricular cells)

Front 10

Lidocaine

Back 10

Class Ib antiarrhythmic
acute IV therapy
rapidly blocks activated and inactivated (but not resting) Na+ channels so greater effect on ischemic and rapidly-driven tissues
Good for ventricular arrythmias and fibrillation; NOT atrial arrythmias

Front 11

Mexilitine

Back 11

Class IB antiarrhythmic
orally active lidocaine
ventricular arrythmias; NOT atrial arrythmias

Front 12

Phenytoin

Back 12

Class IB antiarrhythmic
second line antiarrythmic
used as anticonvulsant in epilepsy (Dilantin)
effective against digitalis-induced disrhythmias

Front 13

Class Ic antiarrythmics do what?

Back 13

Strong inhibition of Na+ channels
markedly depresses slope of phase 0 in fast tissues
slows conduction in fast tissues
no effect on A.P. duration

Front 14

Flecainide

Back 14

Class IC antiarrhythmic
blocks Na+ in all parts of heart
decreases conduction speed
used for sinus rhythm in supraventricular arrythmias in patients *without* structural heart disease
adverse effects: rarely used due to increased mortality

Front 15

Propafenone

Back 15

Class Ic antiarrhythmic
oral therapy for life-threatening ventricular arrythmias
adverse effects: dizziness, taste disturbances, blurred vision

Front 16

Moricizine

Back 16

Class IC antiarrhythmic
for ventricular arrythmias
Adverse effects: don't use in those with MI due to increased mortality

Front 17

What ion is responsible for Phase 0 in a non-pacemaker cell?

Back 17

Na+ channels open (depolarization)

Front 18

What ion is responsible for Phase 1 in a non-pacemaker cell?

Back 18

N+ channels close, K+ open (initial rapid repolarization)

Front 19

What ion is responsible for Phase 2 in a non-pacemaker cell?

Back 19

Decreased K+ conductance, Ca2+ movement into cell (plateau)

Front 20

What ion is responsible for Phase 3 in a non-pacemaker cell?

Back 20

Voltage-activated Ca2+ channels close, leaving K+ open (repolarization)

Front 21

What ion is responsible for Phase 4 in a non-pacemaker cell?

Back 21

None--resting state

Front 22

What ion is responsible for Phase 0 in a pacemaker cell?

Back 22

Ca2+ (depolarization)

Front 23

What ion is responsible for Phase 3 in a pacemaker cell?

Back 23

K+ (repolarization)

Front 24

What ion is responsible for Phase 4 in a pacemaker cell?

Back 24

Na+ (spontaneous depolarization)

Front 25

Beta-adrenergic stimulation of the heart is from what part of the autonomic nervous system?

Back 25

Sympathetic (Parasympathetic stimulates muscarinic)

Front 26

Beta-adrenergic stimulation of the heart causes

Back 26

Increased contractility
increased SA node automaticity
accelerated AV node conduction
accelerated HIS/Purkinje conduction

Front 27

Describe the process by which beta-adrenergic stimulation of the heart affects it in terms of ions, cellular products, and heart behavior

Back 27

receptor stimulation => increased cAMP => opens Ca2+ channels => increased intracellular Ca2+ => increased contractility

and

elevates phase 4 slope => increases SA node automaticity => increased heart rate

Front 28

What are Class II Beta-blocker effects on the action potential?

Back 28

Decrease automaticity!
Decrease AV node conduction (prolonged repolarization at AV node)
Prolong refractory period (decreased slope of phase 4 depolarization)

Antiarrythmic mainly by reducing automaticity of ectopic pacemakers and by slowing conduction in slow fibers

Front 29

What is the only antiarrhythmic found to decrease sudden cardiac death in patients with prior MI?

Back 29

Beta-adrenergic receptor blocker

Front 30

What are the adverse effects of Beta-blockers?

Back 30

fatigue
depression
impotence
hypotension
AV block

Front 31

Propranolol

Back 31

Class II antiarrhythmic: Beta-adrenergic receptor blocker
Useful for atrial and ventricular arrythmias; re-entrant arrythmias involving AV node; atrial flutter & fibrillation
Side effects: fatigue, depression, impotence, hypotension, AV block

Front 32

Acebutolol

Back 32

Class II antiarrhythmic: Beta-adrenergic receptor blocker
Useful for atrial and ventricular arrythmias; re-entrant arrythmias involving AV node; atrial flutter & fibrillation
Side effects: fatigue, depression, impotence, hypotension, AV block

Front 33

Esmolol

Back 33

Class II antiarrhythmic: Beta-adrenergic receptor blocker
IV only
Useful for atrial and ventricular arrythmias especially after cardiac surgery; re-entrant arrythmias involving AV node; atrial flutter & fibrillation
Side effects: fatigue, depression, impotence, hypotension, AV block

Front 34

How do Class III antiarrhythmics work?

Back 34

Class III antiarrhythmics block repolarizing K+ channels (phase 2) and prolonged repolarization (phase 3), leading to prolonged action potential

Front 35

Amiodarone

Back 35

Class III antiarrhythmic: K+ channel blocker
Blocks K+, Na+, Ca2+ channels and alpha and beta-adrenergic receptors
Used for: sustained ventricular tachycardia (IV), ventricular fibrillation (IV), and maintenance of normal sinus in atrial fib (oral)

Adverse effects: asymptomatic AV block; pulmonary fibrosis (dose-related) so monitor chest x-ray and pulmonary function tests; corneal microdeposits (often asymptomatic); hepatic dysfunction; photosensitivity; thyroid dysfunction (hypo- or hyper-)
PROFOUND drug interactions vi P450 3A4 and slow elimination (1/2 life 53 days)

Front 36

Sotalol

Back 36

Class III antiarrhythmic: non-selective Beta blocker and K+ channel blocker
(like a beta blocker class II and class III K+ channel, therefore decreases automaticity and increases refractoriness like a beta; prolongs action potential and QT interval like a K+ channel blocker)
Adverse effects: same as Beta blocker, torsade de pointes (from prolonged AP)
Not metabolized, renally eliminated
Used for life-threatening ventricular arrhythmias and maintenance of sinus rhythm in atrial fibrillation

Class II antiarrhythmic: Beta-adrenergic receptor blocker
(also blocks K+ channels)
Useful for atrial and ventricular arrythmias; re-entrant arrythmias involving AV node; atrial flutter & fibrillation
Side effects: fatigue, depression, impotence, hypotension, AV block

Front 37

Ibutilide

Back 37

Class III antiarrhythmic: K+ channel blocker
Used via rapid infusion for conversion of atrial fibrillation or flutter to sinus
Adverse effect: Torsade

Front 38

Dofetilide

Back 38

Class III antiarrhythmic: K+ channel blocker
PURE K+ channel blocker: slows AP and increases refractory period in atria and ventricle
Used for conversion of atrial fib/flutter to normal sinus rhythm & maintenance of normal sinus rhythm in atrial fibrillation
Adverse effect: prolonged QT and torsade (dose-related)

Front 39

How do Class IV antiarrhythmics work?

Back 39

Ca2+ channel blockers.
Decrease slope of phase 0 of action potential on both SA and AV nodes, and prolong AV node repolarization. Both actions delay conduction through AV node => prevent re-entry

Front 40

What are the two subclasses of Ca2+ channel blockers?

Back 40

dihydropyridine (nifedipine)
nondihydropyridines (diltiazem and verapamil)

Front 41

Dihydropyridines are selective for what tissue type?

Back 41

Dihydropyridines=nifedipine
selective for vascular tissue

Front 42

Nondihydropyridines are selective for what tissue type?

Back 42

Nondihydropyridines = diltiazem and verapamil
selective for cardiac tissue

Front 43

Describe the Class III antiarrhythmic cardiac effects

Back 43

decreased contractility
reduced SA node impulse generation,
slowed AV node conduction

verapamil > diltiazem > nifedipine

Front 44

Describe the Class IV antiarrythmic vascular effects

Back 44

vasodilation

nifedipine > diltiazem > verapamil

Front 45

Tissue selectivity in Class III antiarrhythmics can result in opposite heart effects T or F? Explain.

Back 45

True
nifedipine increases HR; verapamil slows HR.
Nifedipine is most likely to cause reflex tach since it causes pronounced vasodilation without inhibiting SA/AV node conduction. Verapamil and diltiazem are not as likely since they have weaker vasodilation effects but they slow the heart by depressing SA and AV node function directly.

Front 46

Which calcium channel blocker increases heart rate?

Back 46

nifedipine (the dihydropyridine)

Front 47

Which calcium channel blocker slows SA/AV node conduction?

Back 47

nondihydropyridines (verapamil and diltiazem)

Front 48

Verapamil

Back 48

Class IV: Ca2+ channel blocker
Nondihydropyridine: targets cardiac tissue
Used for rate control: reduce ventricular rate in atrial fib/flutter.
Adverse effects: constipation; inhibits P450 3A4, so possible drug interactions; increases serum digoxin concentrations

Front 49

Diltiazem

Back 49

Class IV: Ca2+ channel blocker
Nondihydropyridine: targets cardiac tissue (in-between cardiac and vascular)
Used for rate control: reduce ventricular rate in atrial fib/flutter.
Adverse effects: constipation; inhibits P450 3A4, so possible drug interactions; increases serum digoxin concentrations

Front 50

Nifedipine
Amlodipine
Felodipine

Back 50

Class IV: Ca2+ channel blocker
dihydropyridine: blocks Ca2+ in vascular smooth muscle
NOT USEFUL IN TREATING ARRHYTHMIAS since cardiac effects are due to reflex sympathetic activation secondary to peripheral vasodilation.

Front 51

Adenosine

Back 51

Nonclassified antiarrhythmic
activates K+ channels in AV and SA node, hyperpolarizes atrial tissues.
Shortens refractory period.
Acute termination of re-entrant drug of choice for superventricular arrythmias which are AV node dependent.
IV only (t1/2 = 10 secs)
Adverse effects: proarrythmic effects but only lasts a few seconds

Front 52

Digoxin

Back 52

Cardiac Glycoside antiarrhythmic
Inhibits Na+/K+ ATPase => increased intracellular Na+ => inhibition of Na+/Ca2+ exchanger => increases intracellular Ca2+ => more Ca2+ released => more contraction = positive inotropic effect.
Decreased SA node automaticity and slowed AV node conduction as a result of enhancing parasympathetic and decreasing sympathetic regulation of heart = negative chronotrope.
Slows AV node conduction.
Used for heart failure (increased contractility) and atrial fibrillation (slows rate and conduction).
Do not use in patients with low EF.
Adverse effects: narrow therapeutic window; can stimulate almost any type of arrythmia; GI effects from toxicity including nausea, vomiting, diarrhea, and anorexia = digoxin toxicity; visual disturbances (yellow-green vision); electrolyte disturbances (esp. K+).
Drug interaction: amiodarone increases digoxin concentrations.
Counteract with Digibind.