RCES Exam | Questions with 100% Correct
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Terms in this set (72)
Catecholaminergic polymorphic (also known as familial polymorphic VT) is a rare
ventricular tachycardia/fibrillation and highly arrhythmogenic INHERITED
(CPVF) is .....? 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. ↑ ERP. (AFib,
Vaughan-Williams Class 1 drugs. 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 slope
Class 1 drugs affect? 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 AV block;
can cause Bronchoconstriction in patients with
asthma or chronic obstructive pulmonary disease.
Isoproterenol (Isuprel) Nonselective beta-agonist (synthetic
catecholamine)
Action- causes increase in HR and cardiac
contractility.
Dose- IV: 2-10 mcg/min titrated to the desired
effect
Use- Bradycardia, provocation of syncope during
tilt table testing. Used to induce arrhythmias in
patients with history of arrhythmias. Increases
sympathetic tone and mimics autonomic responses
(exercise state).
Answers | Verified | Latest Update 2026
Save
Terms in this set (72)
Catecholaminergic polymorphic (also known as familial polymorphic VT) is a rare
ventricular tachycardia/fibrillation and highly arrhythmogenic INHERITED
(CPVF) is .....? 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. ↑ ERP. (AFib,
Vaughan-Williams Class 1 drugs. 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 slope
Class 1 drugs affect? 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 AV block;
can cause Bronchoconstriction in patients with
asthma or chronic obstructive pulmonary disease.
Isoproterenol (Isuprel) Nonselective beta-agonist (synthetic
catecholamine)
Action- causes increase in HR and cardiac
contractility.
Dose- IV: 2-10 mcg/min titrated to the desired
effect
Use- Bradycardia, provocation of syncope during
tilt table testing. Used to induce arrhythmias in
patients with history of arrhythmias. Increases
sympathetic tone and mimics autonomic responses
(exercise state).
