Anti-Arrythmics

Quinidine class

Class IA Na+ Channel Blocker

Procainamide class

Class IA Na+ Channel Blocker

Disopyramide class

Class IA Na+ Channel Blocker

Lidocaine class

Class IB Na+ Channel Blocker

Mexiletine class

Class IB Na+ Channel Blocker

Flecainide class

Class IC Na+ Channel Blocker

Propafenone class

Class IC Na+ Channel Blocker

Propranolol class

Class II Beta Blocker

Metoprolol class

Class II Beta Blocker

Amiodarone class

Class III K+ Channel Blocker

Dronedarone class

Class III K+ Channel Blocker

Sotalol class

Class III K+ Channel Blocker

Dofetilide class

Class III K+ Channel Blocker

Ibutilide class

Class III K+ Channel Blocker

Diltiazem class

Class IV Non-DHP Ca++ Channel Blockers

Verapamil class

Class IV Non-DHP Ca++ Channel Blockers

Digoxin class

Class V Na+/K+ ATPase inhibitor (and increases parasympathetic output to heart)

Adenosine class

Class V, A1 receptor agonist (and A2 receptor agonist)

Magnesium class

Class V (TdP treatment)

SAN and AVN are ___ fibers

slow

atria, his-purkinje, and ventricles are ___ fibers

fast

slow/funny Na+ channels affect phase ___ of slow fibers

4

LTCCs affect phase ___ of slow fibers

0

K+ channels affect phase ___ of slow fibers

3

fast/voltage gated Na+ channels affect phase ___ of fast fibers

0

LTCCs affect phase ___ of fast fibers

2

K+ channels affect phase ___ of fast fibers

3

Na+ channel blockers effect

decreased conduction velocity and decreased firing rate of myocytes

beta blockers effect

SAN: decreased firing rate

AVN: decreased conduction velocity, increased refractoriness

myocytes: decreased contractility

K+ channel blockers effect

increased refractoriness of myocytes

Ca++ channel blockers effect

SAN: decreased firing rate

AVN: decreased conduction velocity, increased refractoriness

myocytes: decreased contractility

type of arrhythmia and location of sinus bradycardia

supra-ventricular bradyarrhythmias

type of arrhythmia and location of AV blocks

supra-ventricular bradyarrhythmia

type of arrhythmia and location of bundle branch blocks

ventricular bradyarrhythmia

type of arrhythmia and location of sinus tachycardia

supra-ventricular tachyarrhythmia

type of arrhythmia and location of AF (atrial fib) and AFL (atrial flutter)

supra-ventricular tachyarrhythmia

type of arrhythmia and location of PSVT (Paroxysmal supraventricular tachycardia)

supra-ventricular tachyarrhythmia

type of arrhythmia and location of VT

ventricular tachyarrhythmia

type of arrhythmia and location of TdP

ventricular tachyarrhythmia

type of arrhythmia and location of VF (ventricular fib)

ventricular tachyarrhythmia

K+ channel blockers effect on QT, RR, and QTc

increases QT, RR stays the same, QTc increased

(QTc = QT / sqr (RR))

K+ channel blockers directly increase QT without affecting HR

beta blockers effect on QT, RR, QTc

QT increased, RR decreased, QTc stays the same

(QTc = QT / sqr (RR))

beta blockers indirectly increase QT by slowing HR

Ca++ channel blockers effect on QT, RR, QTc

QT increased, RR decreased, QTc stays the same

(QTc = QT / sqr (RR))

Ca++ channel blockers indirectly increase QT by slowing HR

MOA of Class IA drugs

moderate binding to Na+ channels → increases QRS

also block K+ channels → increases APD

also block ACh → anti-cholinergic effects

uses of Class IA drugs

rarely used because of toxicity (old school drugs)

formerly used for Afib, atrial flutter, PSVT, VT (almost everything)

what drug is a Class IA Na+ channel blocker that is rarely used due to multiple toxicities, can cause cinchonism (headache, dizziness, tinnitus), GI effects (N/V/D), has severe AEs of thombocytopenia, hepatitis, and autoimmune reactions

Quinidine

Quinidine is available as ___

PO or IV

what drug is a Class IA Na+ channel blocker that has autoimmune reactions and NAPA (an active metabolite, K+ blocker), can cause QTc prolongation

Procainamide

Procainamide is available as ___

IV only

what drug is a Class IA Na+ channel blocker that is highly anticholinergic

Disopyramide

Disopyramide is available as ___

PO only

Which is preferred out of the Class IA Na+ Channel Blockers?

Disopyramide

MOA of Class IB drugs

weak binding to Na+ channels which has no effect on QRS and decreases APD

Class IB drugs are used only for ___

ventricular arrhythmias

which class IB drug has a short half-life (IV bolus followed by infusion), levels can be monitored, and has neurological AEs (dizziness, tremor, confusion)

lidocaine

lidocaine is available as __

IV only

which class IB drug is orally absorbable and has gastric AEs (nausea, heartburn)?

Mexiletine

Mexiletine is available as ___

PO only

which of the class IB drugs could you use for AF?

none (ventricular arrhythmias only)

MOA of class IC drugs

strong binding to Na+ channels → INCREASES QRS interval

unchanged APD

may increase PR interval, decrease contractility

Class IC drug uses

ventricular and supraventricular arryhthmias

most commonly: Afib, atrial flutter

__ drugs have increased mortality in patients with CHF and CAD

Class IC (due to structural damage to heart)

which class IC drug is first line for AF in patients without structural heart disease (CHF, CAD) and has GI and CNS AEs of headache, dizziness, fatigure

Flecainide

Flecainide is available as ___

PO only

which class IC drug has beta blocker properties, is contraindicated in bronchospastic disease (asthma, COPD), and can have metallic taste

Propafenone

Propafenone is available as ___

PO only

this action potential graph represents Class ___ drugs due to ___

IA (moderate block)

increased QRS, increased APD

this action potential graph represents Class ___ drugs due to ___

IB (weak block)

unchanged QRS, decreased APD

this action potential graph represents Class ___ drugs due to ___

IC (strong block)

INCREASED QRS, unchanged APD

MOA of K+ channel blockers

increases APD, increases refractoriness

this graph represents effects of class ___ drugs

III (K+ channel blockers)

what is important to consider about K+ channel blockers?

QTc prolongation (increases QTc) → increased risk of Torsades de Pointes

which class III drug has properties of all four VW classes, serious AEs (pulm fibrosis, thyrotoxicity, neurotoxicity, hepatotoxicity), lots of DDIs, and long half-life

Amiodarone

Amiodarone is available as __

PO or IV

which class III drug increases QTc and requires inpatient initiation?

Dofetilide

Dofetilide is available as ___

PO only

which class III drug has beta blocker properties; contraindicated in decompensated CHF, asthma, and COPD; and increases QTc (requires inpatient initiation)?

Sotalol

Sotalol is available as ___

PO or IV

which class III drug is contraindicated in CHF, CAD, and permanent AF; and is FDA approved for AF/AFL only?

Dronedaone

Dronedarone is available as ___

PO only

which class III drug is inpatient use only and is not a maintenance treatment?

Ibutilide

Ibutilide is available as ___

IV only

For patients with h/o CAD and CHF, what drugs can be used for rhythm control?

K+ channel blockers (not Na+ channel blockers due to increased mortality)

a 60 y/o F with h/o CAD and CHF wants long-term reduction of AF, which is the least toxic option?

Dofetilide

what to use for rate control if BP is stable?

1. beta blockers

2. Ca+ channel blockers

what to use for rate control if BP is too low?

1. Amiodarone

2. Digoxin

which med/s is/are used for rate control of supraventricular arrhythmias in unstable patients?

Amiodarone, Digoxin

MOA of Amiodarone

has properties of all four VW classes, beta blockade is responsible for rate control properties

effect of Amiodarone on BP

doesn’t significantly lower BP if dosed by slow IV infusion

MOA of Digoxin

1. inhibits Na+/K+ ATPase

2. Increases intracellular Ca++

3. increases contractility

4. baroreceptor reflex (increases parasympathetic output to heart)

effect of Digoxin on SAN and AVN

SAN: decreases firing rate

AVN: decreases conduction velocity

which IV drug(s) can decrease ventricular rate without significantly lowering BP?

Amiodarone, Digoxin

paroxysmal supraventricular tachycardia is caused by

reentry circuits within AVN, or between atria and ventricles

Adenosine is used for

acute treatment of PSVT (also as coronary vasodilator)

Adenosine is available as __

IV only

MOA of Adenosine

binds adenosine A1 receptors in SAN and AVN

• A1 receptors → Gi coupled → decreases cAMP → increases K+ channels, decreases Ca++ channels

• SAN: decreases firing rate

• AVN: DECREASES conduction velocity

also binds A2 receptors in vascular SM

• A2 receptors → Gs coupled → increases cAMP → increases vasodilation

when Adenosine given as fast IV bolus, it ___

halts AVN conduction (~ 5 seconds)

• Adenosine rapidly eliminated from circulation by cellular uptake (T1/2 = seconds)

Torsades de Pointes is ___

early after depolarizations (EADs) due to increased QTc interval (K+ channel blockade, decreased K+, decreased HR) → ventricular tachyarrhythmia

often drug induced

__ is used as a treatment for TdP

Magnesium

antiarrhythmic drugs have a ___-dependent binding

state