IBHRE CEPS EVALUATION EXAMS 2026
QUESTIONS AND ANSWERS SURE A+
✔✔PVC localization: inferior leads (II, III, avF)
(+)
(-) - ✔✔(+) coming from up high
(-) coming from lower
✔✔PVC localization: precordial transition
-before v3
-after v3 or no transition (all positive) - ✔✔Transition before v3: left sided
Transition after v3: right sided
✔✔PVC localization: notching on inferior leads - ✔✔Freewall RVOT
✔✔PVC localization: notching v1 & v2 w/ (-) infeirors - ✔✔Pap muscle
✔✔PVC localization: inferior leads opposite - ✔✔Para Hisian
✔✔Fasicular VT
-drug sensitivity
-demographics
-most common variety
,-ablation target - ✔✔Verapamil sensitive
Young pts w/o heart disease
Left posterior fasicular: RBBB & superior axis
Ablation mid-septum guided by a diastolic purkinje potential or at the VT exit site guided
by a fused pre-systolic purkinje potential
✔✔Superior Axis - ✔✔Coming from lower moving up
Inferior leads (-)
✔✔Inferior Axis - ✔✔Coming from top moving down
Inferior leads (+)
✔✔BBR-VT
-demographics
-mechanism
-ECG pattern - ✔✔Patients have idiopathic dilated cardiomyopathy
PVC occurs and conducts to RBB & LBB. Typically the RBB has a longer refractory;
impulse can travel retrograde up LBB to HIS and down RBB
LBBB morphology
✔✔X-Ray damage
-bone marrow
-GI tract
-CNS - ✔✔-bone marrow 2-10 Gy
-GI tract 1-100 Gy
-CNS >100 Gy
✔✔Fluoro safety acronym - ✔✔ALARA: as low as reasonably achievable
✔✔Blood supply to SA and AV nodes - ✔✔RCA
(conus branch in particular feeds SA)
✔✔SA node shape & innervated by - ✔✔Looks like a comma
-head: sympathetic tone
-tail: parasympathetic
*epicardial structure
✔✔Fast pathway - ✔✔anterior/superior aspect of TVA; close to HIS
✔✔Slow pathway - ✔✔posterior/inferior
✔✔Function of CS - ✔✔Conduit to return deoxygenated coronary blood to RA
,✔✔Fibrous skeleton of the heart - ✔✔Annuli of Tricuspid, Mitral, Aortic, & Pulmonary
valves
✔✔Koch Triangle - ✔✔Tendon of Todaro, CS os, septal leaflet of TV
✔✔Wheatstone Bridge - ✔✔Resistor/transducer that detects pressure changes in the
cardiovascular system
✔✔Atrial pressure waveform
-average pressure - ✔✔0-5 mmHg
✔✔Right ventricular pressure waveform
-average pressure - ✔✔systole: 17-32 mmHg
diastole: 0-5 mmHg
✔✔Pulmonary artery pressure waveform - ✔✔systole: 17-32 mmHg
diastole: 8-15 mmHg
✔✔Mean LA pressure - ✔✔5-12 mmHg
✔✔Left ventricular pressure - ✔✔systole:90-120 mmHg
diastole: 5-12 mmHg
✔✔Aortic & Arterial pressure - ✔✔systole: 90-120 mmHg
diastole: 60-90 mmHg
✔✔Stroke volume - ✔✔The volume of blood pumped from a ventricle of the heart in one
beat (mL/beat)
normal=60-100 mL/beat
✔✔Cardiac Output - ✔✔CO=HR x SV
normal=4-8 L/min
✔✔Normal EF - ✔✔55-70%
✔✔Preload - ✔✔Volume of blood in ventricles at end of diastole
✔✔Afterload - ✔✔The amount of resistance to ejection of blood from the ventricle
✔✔Frank-Starling Law - ✔✔The greater the stretch, the stronger is the heart's
contraction. This increased contractility results in an increased volume of blood ejected
(Increased SV)... until a certain physiologic point at which contractility declines
✔✔Isovolumetric contraction - ✔✔Time from MV closure to opening of Aortic valve
, ✔✔Class 1a drugs - ✔✔Quinidine
Procainamide
Disopyramide
✔✔Class 1a action - ✔✔increase ERP; increase AP
sodium channel blocking (also block potassium currents)
✔✔Class 1b drugs - ✔✔Lidocaine
Mexiletine
Phenytoin
Tocainide
✔✔Class 1b action - ✔✔decrease ERP; decrease AP
Block fast sodium current which slows rate of depolarization and reduces conduction
velocity
✔✔Class 1c drugs - ✔✔Flecainide
Propafenone
Moricizine
✔✔Class 1c action - ✔✔significantly slows conduction but does not prolong ERP or AP
✔✔Class II drugs - ✔✔Beta blockers:
Atenolol
Esmolol
Metaprolol
Propranolol
✔✔Beta blocker action - ✔✔Decrease BP and pulse by blocking sympathetic
stimulation
-in ischemia: reduces MVO2
-in SVT: slows AVN conduction
-in Afib: slows V rate
-in heart failure: decreases HR & MVO2
✔✔Class III drugs - ✔✔Amiodarone
Sotalol
Ibutilide
Dofetilide
✔✔Class III action - ✔✔Lengthen AP and ERP by blocking potassium currents
✔✔Class IV drugs - ✔✔Verapamil
Diltiazem
QUESTIONS AND ANSWERS SURE A+
✔✔PVC localization: inferior leads (II, III, avF)
(+)
(-) - ✔✔(+) coming from up high
(-) coming from lower
✔✔PVC localization: precordial transition
-before v3
-after v3 or no transition (all positive) - ✔✔Transition before v3: left sided
Transition after v3: right sided
✔✔PVC localization: notching on inferior leads - ✔✔Freewall RVOT
✔✔PVC localization: notching v1 & v2 w/ (-) infeirors - ✔✔Pap muscle
✔✔PVC localization: inferior leads opposite - ✔✔Para Hisian
✔✔Fasicular VT
-drug sensitivity
-demographics
-most common variety
,-ablation target - ✔✔Verapamil sensitive
Young pts w/o heart disease
Left posterior fasicular: RBBB & superior axis
Ablation mid-septum guided by a diastolic purkinje potential or at the VT exit site guided
by a fused pre-systolic purkinje potential
✔✔Superior Axis - ✔✔Coming from lower moving up
Inferior leads (-)
✔✔Inferior Axis - ✔✔Coming from top moving down
Inferior leads (+)
✔✔BBR-VT
-demographics
-mechanism
-ECG pattern - ✔✔Patients have idiopathic dilated cardiomyopathy
PVC occurs and conducts to RBB & LBB. Typically the RBB has a longer refractory;
impulse can travel retrograde up LBB to HIS and down RBB
LBBB morphology
✔✔X-Ray damage
-bone marrow
-GI tract
-CNS - ✔✔-bone marrow 2-10 Gy
-GI tract 1-100 Gy
-CNS >100 Gy
✔✔Fluoro safety acronym - ✔✔ALARA: as low as reasonably achievable
✔✔Blood supply to SA and AV nodes - ✔✔RCA
(conus branch in particular feeds SA)
✔✔SA node shape & innervated by - ✔✔Looks like a comma
-head: sympathetic tone
-tail: parasympathetic
*epicardial structure
✔✔Fast pathway - ✔✔anterior/superior aspect of TVA; close to HIS
✔✔Slow pathway - ✔✔posterior/inferior
✔✔Function of CS - ✔✔Conduit to return deoxygenated coronary blood to RA
,✔✔Fibrous skeleton of the heart - ✔✔Annuli of Tricuspid, Mitral, Aortic, & Pulmonary
valves
✔✔Koch Triangle - ✔✔Tendon of Todaro, CS os, septal leaflet of TV
✔✔Wheatstone Bridge - ✔✔Resistor/transducer that detects pressure changes in the
cardiovascular system
✔✔Atrial pressure waveform
-average pressure - ✔✔0-5 mmHg
✔✔Right ventricular pressure waveform
-average pressure - ✔✔systole: 17-32 mmHg
diastole: 0-5 mmHg
✔✔Pulmonary artery pressure waveform - ✔✔systole: 17-32 mmHg
diastole: 8-15 mmHg
✔✔Mean LA pressure - ✔✔5-12 mmHg
✔✔Left ventricular pressure - ✔✔systole:90-120 mmHg
diastole: 5-12 mmHg
✔✔Aortic & Arterial pressure - ✔✔systole: 90-120 mmHg
diastole: 60-90 mmHg
✔✔Stroke volume - ✔✔The volume of blood pumped from a ventricle of the heart in one
beat (mL/beat)
normal=60-100 mL/beat
✔✔Cardiac Output - ✔✔CO=HR x SV
normal=4-8 L/min
✔✔Normal EF - ✔✔55-70%
✔✔Preload - ✔✔Volume of blood in ventricles at end of diastole
✔✔Afterload - ✔✔The amount of resistance to ejection of blood from the ventricle
✔✔Frank-Starling Law - ✔✔The greater the stretch, the stronger is the heart's
contraction. This increased contractility results in an increased volume of blood ejected
(Increased SV)... until a certain physiologic point at which contractility declines
✔✔Isovolumetric contraction - ✔✔Time from MV closure to opening of Aortic valve
, ✔✔Class 1a drugs - ✔✔Quinidine
Procainamide
Disopyramide
✔✔Class 1a action - ✔✔increase ERP; increase AP
sodium channel blocking (also block potassium currents)
✔✔Class 1b drugs - ✔✔Lidocaine
Mexiletine
Phenytoin
Tocainide
✔✔Class 1b action - ✔✔decrease ERP; decrease AP
Block fast sodium current which slows rate of depolarization and reduces conduction
velocity
✔✔Class 1c drugs - ✔✔Flecainide
Propafenone
Moricizine
✔✔Class 1c action - ✔✔significantly slows conduction but does not prolong ERP or AP
✔✔Class II drugs - ✔✔Beta blockers:
Atenolol
Esmolol
Metaprolol
Propranolol
✔✔Beta blocker action - ✔✔Decrease BP and pulse by blocking sympathetic
stimulation
-in ischemia: reduces MVO2
-in SVT: slows AVN conduction
-in Afib: slows V rate
-in heart failure: decreases HR & MVO2
✔✔Class III drugs - ✔✔Amiodarone
Sotalol
Ibutilide
Dofetilide
✔✔Class III action - ✔✔Lengthen AP and ERP by blocking potassium currents
✔✔Class IV drugs - ✔✔Verapamil
Diltiazem
