RCES Exam Questions and Answers with
Verified Solutions | Latest Updated 2026
Catecholaminergic polymorphic (also known as familial polymorphic VT) is
ventricular tachycardia/fibrillation a rare
(CPVF) is.....? and highly arrhythmogenic INHERITED
channelopathy. It is characterized as
exercise-
induced polymorphic VF in a structurally
normal
heart. The genetic mutation specifically
affects the
calcium RyR2 gene, which is responsible
for
calcium release (contraction).
Triggered:DELAYED
AFTERDEPOLARIZATION
(DAD) causing triggered activity is
responsible for
the ECG arrhythmia pattern (bidirectional
VT) of
the CPVF patient.
Treatments: ICD, cardiac ablation, left
cervicothoracic sympathectomy, and
pharmacologic (A non-selective beta
blocker,
sometimes combined with Flecanide, is
typically
prescribed for identified CPVF patients and
carriers of the genetic mutation.)
,Describe the sub-classes of 1A: Moderate NA+-channel blocker. ↑
Vaughan-Williams Class 1 drugs. ERP. (AFib,
Flutter, SVT/VT)
Quinidine= Anticholinergic (moderate).
Procainamide= "Antich-" (weak); relatively
short
half-life.
Disopyramide= "Antich-" (strong) negative
inotropic
effect.
1B: Weak NA+-channel blocker. ↓ ERP.
(VT)
Lidocaine= IV only; VT and PVCs. Good
efficacy in
ischemic myocardium
Tocainide= orally active lidocaine analog.
Can
cause pulmonary fibrosis
Mexiletine=orally active lidocaine analog.
Good
efficacy in ischemic myocardium.
1C: Strong NA+-channel blocker. →ERP.
(Life
threatening SVT and VT).
Flecainide=SVT; can induce VT.
Propafenone= SVT/VT; beta-blocking and
CA++
blocking activity can worsen HF.
Moricizine= VT
,According to Vaughan-Williams Sodium-channel blocker. Reduce phase 0
Class 1 drugs affect? slope
and the peak of the action potential.
They bind and block fast sodium channels
that are
responsible for the rapid depolarization
(phase 0).
Affects non-nodal cardiomyocytes. Nodal
cells do
not contain fast NA+ channels they
depend on
calcium channels.
, According to Vaughan-Williams Drugs that bind to beta-adrenoceptors and
Class 2 drugs affects? thereby block the binding of
norepinephrine/epinephrine to these
receptors.
this inhibits normal sympathetic effects.
Reduce
chronotropy (heart rate), inotropy
(contractility),
dromotropy (electrical conduction) and
isotropy
(relaxation). Beta-blockers can attenuate
these
sympathetic effects and thereby decrease
sinus
rate, decrease conduction velocity (which
can
block reentry mechanisms), and inhibit
aberrant
pacemaker activity. Beta-blockers also
affect non-
pacemaker action potentials by increasing
action
potential duration and the effective
refractory
period. This effect can play a major role in
blocking
arrhythmias caused by reentry.
Vascular Effects=smooth muscle
contraction (mild)
Used to treat hypertension, angina,
myocardial
infarction, arrhythmias and heart failure.
Drugs= Propranolol, Metoprolol, Atenolol
and
Esmolol (short half life)
Contraindicates= Bradycardia and partial
Verified Solutions | Latest Updated 2026
Catecholaminergic polymorphic (also known as familial polymorphic VT) is
ventricular tachycardia/fibrillation a rare
(CPVF) is.....? and highly arrhythmogenic INHERITED
channelopathy. It is characterized as
exercise-
induced polymorphic VF in a structurally
normal
heart. The genetic mutation specifically
affects the
calcium RyR2 gene, which is responsible
for
calcium release (contraction).
Triggered:DELAYED
AFTERDEPOLARIZATION
(DAD) causing triggered activity is
responsible for
the ECG arrhythmia pattern (bidirectional
VT) of
the CPVF patient.
Treatments: ICD, cardiac ablation, left
cervicothoracic sympathectomy, and
pharmacologic (A non-selective beta
blocker,
sometimes combined with Flecanide, is
typically
prescribed for identified CPVF patients and
carriers of the genetic mutation.)
,Describe the sub-classes of 1A: Moderate NA+-channel blocker. ↑
Vaughan-Williams Class 1 drugs. ERP. (AFib,
Flutter, SVT/VT)
Quinidine= Anticholinergic (moderate).
Procainamide= "Antich-" (weak); relatively
short
half-life.
Disopyramide= "Antich-" (strong) negative
inotropic
effect.
1B: Weak NA+-channel blocker. ↓ ERP.
(VT)
Lidocaine= IV only; VT and PVCs. Good
efficacy in
ischemic myocardium
Tocainide= orally active lidocaine analog.
Can
cause pulmonary fibrosis
Mexiletine=orally active lidocaine analog.
Good
efficacy in ischemic myocardium.
1C: Strong NA+-channel blocker. →ERP.
(Life
threatening SVT and VT).
Flecainide=SVT; can induce VT.
Propafenone= SVT/VT; beta-blocking and
CA++
blocking activity can worsen HF.
Moricizine= VT
,According to Vaughan-Williams Sodium-channel blocker. Reduce phase 0
Class 1 drugs affect? slope
and the peak of the action potential.
They bind and block fast sodium channels
that are
responsible for the rapid depolarization
(phase 0).
Affects non-nodal cardiomyocytes. Nodal
cells do
not contain fast NA+ channels they
depend on
calcium channels.
, According to Vaughan-Williams Drugs that bind to beta-adrenoceptors and
Class 2 drugs affects? thereby block the binding of
norepinephrine/epinephrine to these
receptors.
this inhibits normal sympathetic effects.
Reduce
chronotropy (heart rate), inotropy
(contractility),
dromotropy (electrical conduction) and
isotropy
(relaxation). Beta-blockers can attenuate
these
sympathetic effects and thereby decrease
sinus
rate, decrease conduction velocity (which
can
block reentry mechanisms), and inhibit
aberrant
pacemaker activity. Beta-blockers also
affect non-
pacemaker action potentials by increasing
action
potential duration and the effective
refractory
period. This effect can play a major role in
blocking
arrhythmias caused by reentry.
Vascular Effects=smooth muscle
contraction (mild)
Used to treat hypertension, angina,
myocardial
infarction, arrhythmias and heart failure.
Drugs= Propranolol, Metoprolol, Atenolol
and
Esmolol (short half life)
Contraindicates= Bradycardia and partial
