RCES Exam Review Questions with Verified
Correct Answers
Catecholaminergic polymorphic ventricular tachycardia/fibrillation (CPVF) is .....?
(also known as familial polymorphic VT) is a rare 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 Vaughan-Williams Class 1 drugs.
1A: Moderate NA+-channel blocker. ↑ 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 Class 1 drugs affect?
Sodium-channel blocker. Reduce phase 0 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 Class 2 drugs affects?
Drugs that bind to beta-adrenoceptors and 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).
Adenosine (Adenocard)
Naturally occurring chemical in all human cells.
Action- Decrease HR and reduces conduction velocity, especially at the AV node, which can
produce AV block. Shortens atrial action potential duration and refractoriness.
Dose- 6 mg rapid IVP, then 12mg IV q1-2 min x2.
Use- Symptomatic SVT. Adenosine can also hyperpolarize dormany pulmonary vein myocytes
and increase excitability, as well as trigger pulmonary vein ectopy (AF triggers).
Procainamide (Pronestyl)
Cassification: Antiarrhythmic, class lA
Action: Blocks influx of sodium through membrane pores, consequently suppresses
atrial and ventricular arrhythmias by slowing conduction in myocardial tissue. Prolongs the
action potential duration and the effective refractory period (ERP).
Indications: Alternative to amiodarone for stable monomorphic VT with normal QT
interval and preserved ventricular function, reentry SVT if uncontrolled by adenosine
Correct Answers
Catecholaminergic polymorphic ventricular tachycardia/fibrillation (CPVF) is .....?
(also known as familial polymorphic VT) is a rare 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 Vaughan-Williams Class 1 drugs.
1A: Moderate NA+-channel blocker. ↑ 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 Class 1 drugs affect?
Sodium-channel blocker. Reduce phase 0 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 Class 2 drugs affects?
Drugs that bind to beta-adrenoceptors and 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).
Adenosine (Adenocard)
Naturally occurring chemical in all human cells.
Action- Decrease HR and reduces conduction velocity, especially at the AV node, which can
produce AV block. Shortens atrial action potential duration and refractoriness.
Dose- 6 mg rapid IVP, then 12mg IV q1-2 min x2.
Use- Symptomatic SVT. Adenosine can also hyperpolarize dormany pulmonary vein myocytes
and increase excitability, as well as trigger pulmonary vein ectopy (AF triggers).
Procainamide (Pronestyl)
Cassification: Antiarrhythmic, class lA
Action: Blocks influx of sodium through membrane pores, consequently suppresses
atrial and ventricular arrhythmias by slowing conduction in myocardial tissue. Prolongs the
action potential duration and the effective refractory period (ERP).
Indications: Alternative to amiodarone for stable monomorphic VT with normal QT
interval and preserved ventricular function, reentry SVT if uncontrolled by adenosine
