FPGEE REVIEWED STUDY
GUIDE QUESTIONS AND
CORRECT ANSWERS
GRADED A+ 2025-2026
In FAST response fibers - Electrolyte involved in phase 0 - ANS-Na+ influx
In FAST response fibers - Electrolyte involved in phase 2 - ANS-Ca+ influx, K+ outflux
plateau
In FAST response fibers - Electrolyte involved in phase 3 - ANS-K+ outflux (Ca+ drops
off) rapid repolarization
In SLOW response fibers - Electrolyte involved in phase 0 - ANS-Ca+(few Na+ channels
in Nodal fibers)
In SLOW response fibers - Electrolyte involved in phase 3 - ANS-K+ outflux
repolarization
In SLOW response fibers - Electrolyte involved in phase 4 - ANS-"Mainly Na+ (This is the
pacemaker current) aarapim. "
Ectopic rhythm can result from - ANS-ischemia, electrolyte abnormalities, or
heightened sympathetic tone
If an early afterdepolarization is sustained - ANS-torades de pointes (QRS complexes of
varying amplitudes)
,ECG of a patient with an accessory pathway (bundle of Kent) - ANS-"Wide QRS
complexes, early ventricular upstroke (also predisposed to re-entry loops) (Wolff
Parkinson White (WPW) syndrome) wolff-parkinson-white-accessory-bundle-bundle-of-
Kent "
MOA of quinidine - ANS-Blocks (open-activated) Na+ channels: In SA Nodal tissue -
Shift to a more positive threshold and decrease the pacemaker slope (phase 4), In
Ventricular tissue - Decreases the phase 0 slope (depolarization) and block K+ channels
prolongs repolarization (longer refractory period protected from reentry currents):
Anticholanergic (vagolytic effect faster conduction through AV node)
Indications of quinidine - ANS-"atrial flutter or fibrillation maintain normal sinus
rhythm,Paroxysmal supraventricular tachycardia, Premature atrial or ventricular
contractions, paroxysmal AV junctional rhythm 9"
When taking this drug patients must be monitored for lupus (with ANA) - ANS-
Procainamide
Take with quinidine to prevent rapid ventricular response in patient with atrial flutter -
ANS-β-blocker or Ca2+ channel blocker
Which 1A antiarrhythmic for a patient on digoxin - ANS-Procainamide (doesn't alter
digoxin levels)
MOA of Lidocaine and Phenytoin - ANS-( 1B) block of voltage-gated Na+ in ventricular
myocytes (decrease phase 0 upstroke)
MOA of Encainide, Flecainide, Moricizine, Propafenone - ANS-( 1C) block of voltage-
gated Na+ channelsin ventricular myocytes
MOA of Propranolol, Atenolol, Metoprolol... - ANS-( ) block β1-adrenergic receptors
SLOW SA and AV nodal activity,(decreases phase 4 slope)
,MOA of Ibutilide, Dofetilide, Sotalol, Amiodarone - ANS-( I) Block K+ channels longer
action potential plateau and prolonged repolarization
MOA of Verapamil, Diltiazem - ANS-( IV) Ca2+ channel blocker slows action potential
upstroke in SA and AV nodes
This 1A drug is associated with the development of Lupus, hematotoxicity, but less
likely to cause torsades - ANS-procainamide
Antiarrhythmics of choice for post ischemic insults - ANS-1B
Drug used for Supraventricular tachycardias, and post-MI prophylaxis - ANS-
antiarrhythmics (β-blockers)
What does Quinidine do to AV node - ANS-increases conduction velocity (via
anticholinergic effects)
This 1A drug is meolized to a meolite with a pure I effect (prolonging refractory,
lengthening QT interval) - ANS-Procainamide
DOC or ventricular arrhythmias in ER situations (like in MI) - ANS-Lidocaine
LidocaineMexiletine should be (increased or decreased) in patients with drug inducible
P0 - ANS-increased
Moderate Na+ channel block decrease phase 0, and prolonged repolarization ( 1A, 1B
or 1C) - ANS-1A
Mild Na+ channel block slight pahse 0 slope decrease, shortened repolarization( 1A, 1B
or 1C) - ANS-1B
Marked Na+ channel block severe decreased in phase 0 slope, No change in
repolarization ( 1A, 1B or 1C) - ANS-1C
, This drug can worsen the arrhythmia in patients with pre-existing ventricular
tachyarrythmias and those with a history of MI - ANS-Flecainide (a 1C)
Drug used when other measure fail to help life threatening paroxysmal
supraventricular or vventricular arrhythmias - ANS-Flecainide (a 1C)
MOA of β1-blockers - ANS-block sympathetic input to AV (and SA nodes) decrease the
rate of phase 4 depolarization (pacemaker current), prolong repolarization
Non-selective β1 and β2 blockers that DO NOT prolong repolarization - ANS-First
generation β-blockers (Propranolol, Nadolol, Timolol) and carvedilol and labetalol
Β-blocker also used for glaucoma - ANS-Timolol
This β-blocker can cause liver damage - ANS-labetalol
These β-blockers cause vasodilationvia α1-blockage - ANS-Carvedilol and labetalol
Selective β1-blocker with a very short half-life - ANS-Esmolol
Used in ER treatment to block β in thyroid storm - ANS-esmolol
A selective β1-blocker and selective β2-agonist - ANS-celiprolol
MOA of K+ channel blockers - ANS-I antiarrhythmics lengthen the plateau (phase 2)
and prolong repolarization
Lengthening the plateau phase does what (in I) - ANS-increases the refractory period
(prevents re-entry), On the bad side: increases likely-hood of afterdepolarizations and
torsades de pointes
GUIDE QUESTIONS AND
CORRECT ANSWERS
GRADED A+ 2025-2026
In FAST response fibers - Electrolyte involved in phase 0 - ANS-Na+ influx
In FAST response fibers - Electrolyte involved in phase 2 - ANS-Ca+ influx, K+ outflux
plateau
In FAST response fibers - Electrolyte involved in phase 3 - ANS-K+ outflux (Ca+ drops
off) rapid repolarization
In SLOW response fibers - Electrolyte involved in phase 0 - ANS-Ca+(few Na+ channels
in Nodal fibers)
In SLOW response fibers - Electrolyte involved in phase 3 - ANS-K+ outflux
repolarization
In SLOW response fibers - Electrolyte involved in phase 4 - ANS-"Mainly Na+ (This is the
pacemaker current) aarapim. "
Ectopic rhythm can result from - ANS-ischemia, electrolyte abnormalities, or
heightened sympathetic tone
If an early afterdepolarization is sustained - ANS-torades de pointes (QRS complexes of
varying amplitudes)
,ECG of a patient with an accessory pathway (bundle of Kent) - ANS-"Wide QRS
complexes, early ventricular upstroke (also predisposed to re-entry loops) (Wolff
Parkinson White (WPW) syndrome) wolff-parkinson-white-accessory-bundle-bundle-of-
Kent "
MOA of quinidine - ANS-Blocks (open-activated) Na+ channels: In SA Nodal tissue -
Shift to a more positive threshold and decrease the pacemaker slope (phase 4), In
Ventricular tissue - Decreases the phase 0 slope (depolarization) and block K+ channels
prolongs repolarization (longer refractory period protected from reentry currents):
Anticholanergic (vagolytic effect faster conduction through AV node)
Indications of quinidine - ANS-"atrial flutter or fibrillation maintain normal sinus
rhythm,Paroxysmal supraventricular tachycardia, Premature atrial or ventricular
contractions, paroxysmal AV junctional rhythm 9"
When taking this drug patients must be monitored for lupus (with ANA) - ANS-
Procainamide
Take with quinidine to prevent rapid ventricular response in patient with atrial flutter -
ANS-β-blocker or Ca2+ channel blocker
Which 1A antiarrhythmic for a patient on digoxin - ANS-Procainamide (doesn't alter
digoxin levels)
MOA of Lidocaine and Phenytoin - ANS-( 1B) block of voltage-gated Na+ in ventricular
myocytes (decrease phase 0 upstroke)
MOA of Encainide, Flecainide, Moricizine, Propafenone - ANS-( 1C) block of voltage-
gated Na+ channelsin ventricular myocytes
MOA of Propranolol, Atenolol, Metoprolol... - ANS-( ) block β1-adrenergic receptors
SLOW SA and AV nodal activity,(decreases phase 4 slope)
,MOA of Ibutilide, Dofetilide, Sotalol, Amiodarone - ANS-( I) Block K+ channels longer
action potential plateau and prolonged repolarization
MOA of Verapamil, Diltiazem - ANS-( IV) Ca2+ channel blocker slows action potential
upstroke in SA and AV nodes
This 1A drug is associated with the development of Lupus, hematotoxicity, but less
likely to cause torsades - ANS-procainamide
Antiarrhythmics of choice for post ischemic insults - ANS-1B
Drug used for Supraventricular tachycardias, and post-MI prophylaxis - ANS-
antiarrhythmics (β-blockers)
What does Quinidine do to AV node - ANS-increases conduction velocity (via
anticholinergic effects)
This 1A drug is meolized to a meolite with a pure I effect (prolonging refractory,
lengthening QT interval) - ANS-Procainamide
DOC or ventricular arrhythmias in ER situations (like in MI) - ANS-Lidocaine
LidocaineMexiletine should be (increased or decreased) in patients with drug inducible
P0 - ANS-increased
Moderate Na+ channel block decrease phase 0, and prolonged repolarization ( 1A, 1B
or 1C) - ANS-1A
Mild Na+ channel block slight pahse 0 slope decrease, shortened repolarization( 1A, 1B
or 1C) - ANS-1B
Marked Na+ channel block severe decreased in phase 0 slope, No change in
repolarization ( 1A, 1B or 1C) - ANS-1C
, This drug can worsen the arrhythmia in patients with pre-existing ventricular
tachyarrythmias and those with a history of MI - ANS-Flecainide (a 1C)
Drug used when other measure fail to help life threatening paroxysmal
supraventricular or vventricular arrhythmias - ANS-Flecainide (a 1C)
MOA of β1-blockers - ANS-block sympathetic input to AV (and SA nodes) decrease the
rate of phase 4 depolarization (pacemaker current), prolong repolarization
Non-selective β1 and β2 blockers that DO NOT prolong repolarization - ANS-First
generation β-blockers (Propranolol, Nadolol, Timolol) and carvedilol and labetalol
Β-blocker also used for glaucoma - ANS-Timolol
This β-blocker can cause liver damage - ANS-labetalol
These β-blockers cause vasodilationvia α1-blockage - ANS-Carvedilol and labetalol
Selective β1-blocker with a very short half-life - ANS-Esmolol
Used in ER treatment to block β in thyroid storm - ANS-esmolol
A selective β1-blocker and selective β2-agonist - ANS-celiprolol
MOA of K+ channel blockers - ANS-I antiarrhythmics lengthen the plateau (phase 2)
and prolong repolarization
Lengthening the plateau phase does what (in I) - ANS-increases the refractory period
(prevents re-entry), On the bad side: increases likely-hood of afterdepolarizations and
torsades de pointes
