RCES CERTIFICATION EXAMINATION TEST
2026 COMPLETE QUESTIONS WITH
ANSWERS
⩥ Describe the sub-classes of Vaughan-Williams Class 1 drugs. Answer:
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? Answer:
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? Answer: 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) Answer: 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) Answer: 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) Answer: 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).
2026 COMPLETE QUESTIONS WITH
ANSWERS
⩥ Describe the sub-classes of Vaughan-Williams Class 1 drugs. Answer:
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? Answer:
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? Answer: 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) Answer: 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) Answer: 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) Answer: 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).
