Antiarrhythmic Agents

exam 1

SA and AV nodal cells

pacemaker cells

true resting potential

SA/AV nodal cells do not have a

spontaneous depolarization via funny Na+ current (if)

phase 4 SA/AV nodal cells

Ca+2 influx through l type Ca+2 channels

phase 0 (upstroke) SA/AV nodal cells

repolarization via K+ efflux

phase 3 SA/AV nodal cells

Ca2+

SA/AV nodal cells have a slower upstroke due to

non nodal myocytes

atrial/ventricular cells

non nodal myocytes

have a true resting membrane potential

rapid Na+ influx

phase 0 for nonnodal myocytes

brief repolarization (Na+ inactivation, K+ efflux)

phase 1 non nodal myocytes

Ca2+ influx via l type channels

phase 2 (plateu) of non nodal myocytes

repolarization via K+ efflux

phase 3 non nodal myocytes

resting potential

phase 4 non nodal myocytes

conduction pathway

Sa node → AV node→ bundle of HIS→ HIS-purkinje system

intrinsic rates ( fastest to slowest)

SA node > AV node > His-purkinje system

ECG correlation

p wave, QRS complex, and T wave =

atrial depolarization

P wave=

ventricular depolarization

QRS complex=

ventricular repolarization

T wave=

60-100bpm

normal sinus rhythm

SA node

normal sinus rhythm originates from the

Na+ channel blockers

class 1 vaughn williams of antiarrhythmics

B-blockers

class 2 vaughn williams of antiarrhythmics

K+ channel blockers

class 3 vaughn williams of antiarrhythmics

Ca2+ channel blockers

class 4 vaughn williams of antiarrhythmics

adenosine, digoxin, and magnesium

other classes of vaughn williams of antiarrhythmics

blocking open/inactivated Na+ channels

class 1 Na+ channel blocker work by

class 1 Na+ channel blockers

are use dependent and have more effect at faster HR

la class 1 Na+ channel blockers

increases AP duration and has intermediate dissociation

lb class 1 Na+ channel blockers

decrease or expand AP and have fast dissociation with ischemic tissue

lc class 1 Na+ channel blockers

expand AP with slow dissociation, and decreased conduction

class 2 beta blockers

• decrease SA node automaticity

• decrease AV nodal conduction

• increase PR interval

• decrease Ca2+ overload

class 3 K+ channel blockers

• block delayed rectifier K+ currents

• prolong refractory period

• increase QT interval = risk of TDP

class 4 Ca2+ channel blockers

• block L type Ca2+ channels

• affect nodal tissue

• decrease SA automaticity

• increase AV nodal refractoriness

proarrhythmic

statistically all antiarrhythmics are

antiarrhythmic

QT prolongation = torsade de pointes

class lc antiarrhythmics

structural heart disease limits use of

sotalol, dofetilide

in antirrhythmics renal function affects

amiodarone

antiarrhythmics have long half life and tissue accumulation with

class 4 agents

in antiarrhythmics heart failure contraindicates

anticholinergic effects and effect QT prolongation

class 1 la antiarrhythmics have

neurological toxicity

class 1 lb antiarrhythmics may cause

increase mortality in structural heart disease

class 1 lc antiarrhythmics may

bradycardia, heart block, broncospasm, CNS penetration (insomnia, fatigue, depression)

adverse effects of class 2 antiarrhythmics

TDP

adverse effects of class 3 antiarrhythmics

adverse effects of amiodarone (class 3)

pulmonary fibrosis, thyroid dysfunction, liver toxicity, corneal deposits

class 4 antiarrhythmics adverse effects

bradycardia, AV block, and worsening heart failure

dronedarone

less adverse effects reaction than aimiodarone (worse cv effects), less effective, no pulmonary fibrosis

flushing

adenosine may cause transient. asystole or

nausea, visual disturbances, arrhythmias

digoxin may cause adverse effects like

narrowing therapeutic index

magnesium may cause adverse effects like

n/v, cognitive dysfunction, blurred vision, bradyarrhythmia or tachyarryhthmia

signs of toxicity in magnesium

monitoring for antiarryhthmics

• ECG: PR, QRS, QT intervals

• electrolytes: K+, Mg2+

renal function

when on sotalol, dofetilide, or digoxin as antiarrhythmics monitor

LFTs and thyroid function and pulmonary function

when taking amiodarone as and antiarrhythmic monitor for

drug levels

when on digoxin monitor (goal 0.8-2.0 ng/mL, check >6 hrs post dose)