GMS 6530 MODULE 4 ANTIARRHYTHMICS EXAM QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST UPDATE

GMS 6530 MODULE 4 ANTIARRHYTHMICS EXAM QUESTIONS

AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST

UPDATE


IK-ACH

in SA/AV nodes and atrial cells, functions like IKI channel when activated, activated by

PNS during rapid repolarization and diastole, GPCR, ligand gated

IK-ATP

ligand gated

INa

voltage gated, phase 0

ICa

voltage gated

Ito1

transient outward current 1: efflux of K+, open during phase 1 in fast response

myocardial cells

Ito2

transient outward current 1: influx of Ca2+, open during phase 1 in fast response

myocardial cells

IKur

atrial potassium current

IKs

, voltage gated, ventricular potassium current, class 1A affects this channel,, class III

increases IKr amplitude, ischemia has reduced IKr expression

IKr

voltage gated, ventricular potassium current, class 1A affects this channel, class III

increases IKr amplitude, ischemia has reduced IKr expression

Inward-rectifier K+ currents

IKI maintain baseline in myocytes (NOT SA/AVN)

Class 1A

Na blockers, Quinidine and Procainamide, increase QRS & QT

Class 1B

Lidocaine high affinity for open & inactive channels, rapid unbinding during diastole,

direct effects: phase 0 depolarization, decr Vmax at high HR, AP dur slightly decr, no

change in ERP at normal HR, side eff dizziness, seizures, used for vtach, AMI, digitalis

induced arrhythmias decrease QT

Class 1C

Flecainide increase QRS duration

Class II

beta blockers - propranolol and esmolol

Class III

Dofetilide & Amiodarone



K+ blockers: incr APD → incr ERP → suppress reentry, wide spectrum antiarrhythmic,

decr conduction (suppress reentry) and decr automaticity (decr ectopy), EC K+