IBHRE CEPS cheat sheet

Normal conduction intervals: PR 120-200 ms, QRS <120 ms, QTc 350-450 ms (men) / 350-460 ms (women); AH 50-120 ms and HV 35-55 ms at baseline electrophysiology study.

Transmembrane ionic currents: phase 0 = fast Na+ (I_Na); phase 1 = transient outward K+ (I_to); phase 2 = L-type Ca2+ (I_Ca-L) balanced by I_Kr/I_Ks; phase 3 = delayed rectifier K+; phase 4 = I_f and I_K1 in nodal cells.

Effective refractory period vs relative refractory period: ERP is the longest coupling interval failing to propagate; RRP is the interval in which conduction is slowed but possible.

Atrial flutter: typical (counterclockwise) flutter uses the cavotricuspid isthmus, shows negative sawtooth F waves in inferior leads, and has an atrial cycle length near 200-260 ms.

AV nodal reentry (AVNRT): dual AV nodal physiology with jump in AH interval >50 ms on programmed atrial extrastimulus; slow pathway is the ablation target.

Orthodromic AVRT uses the AV node antegrade and the accessory pathway retrograde; antidromic AVRT uses the pathway antegrade and produces a pre-excited wide-complex tachycardia.

Ashman phenomenon: a wide QRS beat after a short coupling interval that follows a long cycle represents aberrant conduction, not ventricular ectopy.

QT interval correction: Bazett QTc = QT/√RR; prolonged QTc (>500 ms) raises torsades de pointes risk, and T-U wave alternans suggests imminent arrhythmia.

Differential pacing distinguishes AVNRT from AVRT: in AVNRT the atrial-His difference stays constant; in orthodromic AVRT the atrial signal moves with the ventricle.

Radiofrequency lesion size depends on power, contact force, duration, and catheter-to-tissue contact; impedance drop of 10-20 ohms indicates adequate heating, while an abrupt rise signals coagulum or steam pop risk.

Cryoablation for AVNRT uses a -30 °C cryomapping step to test lesion effect before reaching -70 to -80 °C for a durable lesion.

Cavotricuspid isthmus ablation for typical flutter: bidirectional block confirmed by pacing from the coronary sinus and lateral right atrium with a >130 ms trans-isthmus conduction delay.

Pulmonary vein isolation is the cornerstone of atrial fibrillation ablation; entry and exit block of each vein confirm electrical isolation.

Contact-force targets for radiofrequency pulmonary vein isolation are typically 10-40 g with a force-time integral of roughly 400 g·s per lesion.

Phrenic nerve injury is a recognized risk of right-sided pulmonary vein and superior vena cava ablation; pacing the phrenic nerve during lesion delivery allows monitoring of diaphragmatic capture.

Coronary artery injury risk is highest for ablation near the coronary sinus ostium, the cavotricuspid isthmus, and the left ventricular outflow tract; coronary angiography may be needed if chest pain follows ablation.

Esophageal injury after posterior left atrial ablation ranges from thermal lesions to atrial-esophageal fistula; luminal temperature monitoring and reduced posterior wall power or duration lower risk.

Ventricular tachycardia substrate ablation targets scar and abnormal electrograms, using entrainment mapping for hemodynamically tolerated VT and substrate modification for unstable VT.

NBG pacing codes: first letter chamber paced, second chamber sensed, third response (I inhibit, T trigger, D dual), fourth rate modulation, fifth multisite pacing.

Pacemaker timing: lower rate interval = 60,000/rate in ms; the AV delay follows an atrial event, and the total atrial refractory period (AV delay + PVARP) sets the upper rate limit in DDD mode.

Mode switch in dual-chamber devices converts to DDI or VDI during atrial tachyarrhythmia to avoid tracking rapid atrial rates.

ICD defibrillation threshold testing confirms adequate safety margin; a 10 J margin below maximum output is a common acceptance criterion.

Tachycardia detection uses rate plus duration or number of intervals; SVT discriminators include sudden-onset, stability, and morphology criteria.

Lead impedance trends: a sudden rise suggests fracture or dislodgement, while a gradual fall suggests insulation failure or fluid ingress.

Magnet application: pacemakers switch to asynchronous pacing (DOO/VOO) at the magnet rate; ICDs suspend tachyarrhythmia detection while the magnet is applied.

Cardiac resynchronization therapy criteria include left bundle branch block with QRS ≥150 ms, ejection fraction ≤35%, and NYHA class II-IV symptoms despite optimal medical therapy.

MRI-conditional systems require specific leads and generator combinations plus a programmed MRI mode; legacy devices may be scanned under strict protocol at some centers.

Vaughan-Williams classification: class I = Na+ channel blockers (IA quinidine, IB lidocaine, IC flecainide); class II = beta-blockers; class III = K+ channel blockers (amiodarone, sotalol, dofetilide); class IV = non-dihydropyridine Ca2+ channel blockers.

Amiodarone monitoring: baseline TSH, liver enzymes, pulmonary function tests, and ophthalmologic exam; annual thyroid and hepatic testing, and chest imaging if pulmonary symptoms develop.

Dofetilide requires initiation in a monitored setting with QTc checks after each dose; it is contraindicated when baseline QTc exceeds 440 ms (500 ms if QRS is wide).

Flecainide and propafenone are contraindicated in structural heart disease (coronary disease, reduced ejection fraction, significant hypertrophy) due to proarrhythmia risk.

Anticoagulation for atrial fibrillation: CHA2DS2-VASc score ≥2 in men or ≥3 in women supports oral anticoagulation; DOACs are preferred over warfarin except with mechanical valves or moderate-severe mitral stenosis.

Sotalol prolongs QT and requires renal dose adjustment; initiation with QTc monitoring is required, and it should be stopped if QTc exceeds 500 ms.

Digoxin inhibits the Na+/K+ ATPase, increases vagal tone, and slows AV nodal conduction; toxicity is worsened by hypokalemia, hypomagnesemia, and renal impairment.

Adenosine transiently blocks the AV node with a half-life under 10 seconds; it terminates AV nodal reentrant tachycardias and unmasks atrial activity in wide-complex tachycardia.

Ivabradine lowers sinus rate by inhibiting the I_f current; it is used in symptomatic heart failure with reduced ejection fraction and sinus rhythm above 70 bpm on maximally tolerated beta-blocker.

Normal conduction intervals: PR 120-200 ms, QRS <120 ms, QTc 350-450 ms (men) / 350-460 ms (women); AH 50-120 ms and HV 35-55 ms at baseline electrophysiology study.

Transmembrane ionic currents: phase 0 = fast Na+ (I_Na); phase 1 = transient outward K+ (I_to); phase 2 = L-type Ca2+ (I_Ca-L) balanced by I_Kr/I_Ks; phase 3 = delayed rectifier K+; phase 4 = I_f and I_K1 in nodal cells.

Effective refractory period vs relative refractory period: ERP is the longest coupling interval failing to propagate; RRP is the interval in which conduction is slowed but possible.

Atrial flutter: typical (counterclockwise) flutter uses the cavotricuspid isthmus, shows negative sawtooth F waves in inferior leads, and has an atrial cycle length near 200-260 ms.

AV nodal reentry (AVNRT): dual AV nodal physiology with jump in AH interval >50 ms on programmed atrial extrastimulus; slow pathway is the ablation target.

Orthodromic AVRT uses the AV node antegrade and the accessory pathway retrograde; antidromic AVRT uses the pathway antegrade and produces a pre-excited wide-complex tachycardia.

Ashman phenomenon: a wide QRS beat after a short coupling interval that follows a long cycle represents aberrant conduction, not ventricular ectopy.

QT interval correction: Bazett QTc = QT/√RR; prolonged QTc (>500 ms) raises torsades de pointes risk, and T-U wave alternans suggests imminent arrhythmia.

Differential pacing distinguishes AVNRT from AVRT: in AVNRT the atrial-His difference stays constant; in orthodromic AVRT the atrial signal moves with the ventricle.

Radiofrequency lesion size depends on power, contact force, duration, and catheter-to-tissue contact; impedance drop of 10-20 ohms indicates adequate heating, while an abrupt rise signals coagulum or steam pop risk.

Cryoablation for AVNRT uses a -30 °C cryomapping step to test lesion effect before reaching -70 to -80 °C for a durable lesion.

Cavotricuspid isthmus ablation for typical flutter: bidirectional block confirmed by pacing from the coronary sinus and lateral right atrium with a >130 ms trans-isthmus conduction delay.

Pulmonary vein isolation is the cornerstone of atrial fibrillation ablation; entry and exit block of each vein confirm electrical isolation.

Contact-force targets for radiofrequency pulmonary vein isolation are typically 10-40 g with a force-time integral of roughly 400 g·s per lesion.

Phrenic nerve injury is a recognized risk of right-sided pulmonary vein and superior vena cava ablation; pacing the phrenic nerve during lesion delivery allows monitoring of diaphragmatic capture.

Coronary artery injury risk is highest for ablation near the coronary sinus ostium, the cavotricuspid isthmus, and the left ventricular outflow tract; coronary angiography may be needed if chest pain follows ablation.

Esophageal injury after posterior left atrial ablation ranges from thermal lesions to atrial-esophageal fistula; luminal temperature monitoring and reduced posterior wall power or duration lower risk.

Ventricular tachycardia substrate ablation targets scar and abnormal electrograms, using entrainment mapping for hemodynamically tolerated VT and substrate modification for unstable VT.

NBG pacing codes: first letter chamber paced, second chamber sensed, third response (I inhibit, T trigger, D dual), fourth rate modulation, fifth multisite pacing.

Pacemaker timing: lower rate interval = 60,000/rate in ms; the AV delay follows an atrial event, and the total atrial refractory period (AV delay + PVARP) sets the upper rate limit in DDD mode.

Mode switch in dual-chamber devices converts to DDI or VDI during atrial tachyarrhythmia to avoid tracking rapid atrial rates.

ICD defibrillation threshold testing confirms adequate safety margin; a 10 J margin below maximum output is a common acceptance criterion.

Tachycardia detection uses rate plus duration or number of intervals; SVT discriminators include sudden-onset, stability, and morphology criteria.

Lead impedance trends: a sudden rise suggests fracture or dislodgement, while a gradual fall suggests insulation failure or fluid ingress.

Magnet application: pacemakers switch to asynchronous pacing (DOO/VOO) at the magnet rate; ICDs suspend tachyarrhythmia detection while the magnet is applied.

Cardiac resynchronization therapy criteria include left bundle branch block with QRS ≥150 ms, ejection fraction ≤35%, and NYHA class II-IV symptoms despite optimal medical therapy.

MRI-conditional systems require specific leads and generator combinations plus a programmed MRI mode; legacy devices may be scanned under strict protocol at some centers.

Vaughan-Williams classification: class I = Na+ channel blockers (IA quinidine, IB lidocaine, IC flecainide); class II = beta-blockers; class III = K+ channel blockers (amiodarone, sotalol, dofetilide); class IV = non-dihydropyridine Ca2+ channel blockers.

Amiodarone monitoring: baseline TSH, liver enzymes, pulmonary function tests, and ophthalmologic exam; annual thyroid and hepatic testing, and chest imaging if pulmonary symptoms develop.

Dofetilide requires initiation in a monitored setting with QTc checks after each dose; it is contraindicated when baseline QTc exceeds 440 ms (500 ms if QRS is wide).

Flecainide and propafenone are contraindicated in structural heart disease (coronary disease, reduced ejection fraction, significant hypertrophy) due to proarrhythmia risk.

Anticoagulation for atrial fibrillation: CHA2DS2-VASc score ≥2 in men or ≥3 in women supports oral anticoagulation; DOACs are preferred over warfarin except with mechanical valves or moderate-severe mitral stenosis.

Sotalol prolongs QT and requires renal dose adjustment; initiation with QTc monitoring is required, and it should be stopped if QTc exceeds 500 ms.

Digoxin inhibits the Na+/K+ ATPase, increases vagal tone, and slows AV nodal conduction; toxicity is worsened by hypokalemia, hypomagnesemia, and renal impairment.

Adenosine transiently blocks the AV node with a half-life under 10 seconds; it terminates AV nodal reentrant tachycardias and unmasks atrial activity in wide-complex tachycardia.

Ivabradine lowers sinus rate by inhibiting the I_f current; it is used in symptomatic heart failure with reduced ejection fraction and sinus rhythm above 70 bpm on maximally tolerated beta-blocker.

Normal conduction intervals: PR 120-200 ms, QRS <120 ms, QTc 350-450 ms (men) / 350-460 ms (women); AH 50-120 ms and HV 35-55 ms at baseline electrophysiology study.

Transmembrane ionic currents: phase 0 = fast Na+ (I_Na); phase 1 = transient outward K+ (I_to); phase 2 = L-type Ca2+ (I_Ca-L) balanced by I_Kr/I_Ks; phase 3 = delayed rectifier K+; phase 4 = I_f and I_K1 in nodal cells.

Effective refractory period vs relative refractory period: ERP is the longest coupling interval failing to propagate; RRP is the interval in which conduction is slowed but possible.

Atrial flutter: typical (counterclockwise) flutter uses the cavotricuspid isthmus, shows negative sawtooth F waves in inferior leads, and has an atrial cycle length near 200-260 ms.

AV nodal reentry (AVNRT): dual AV nodal physiology with jump in AH interval >50 ms on programmed atrial extrastimulus; slow pathway is the ablation target.

Orthodromic AVRT uses the AV node antegrade and the accessory pathway retrograde; antidromic AVRT uses the pathway antegrade and produces a pre-excited wide-complex tachycardia.

Ashman phenomenon: a wide QRS beat after a short coupling interval that follows a long cycle represents aberrant conduction, not ventricular ectopy.

QT interval correction: Bazett QTc = QT/√RR; prolonged QTc (>500 ms) raises torsades de pointes risk, and T-U wave alternans suggests imminent arrhythmia.

Differential pacing distinguishes AVNRT from AVRT: in AVNRT the atrial-His difference stays constant; in orthodromic AVRT the atrial signal moves with the ventricle.

Radiofrequency lesion size depends on power, contact force, duration, and catheter-to-tissue contact; impedance drop of 10-20 ohms indicates adequate heating, while an abrupt rise signals coagulum or steam pop risk.

Cryoablation for AVNRT uses a -30 °C cryomapping step to test lesion effect before reaching -70 to -80 °C for a durable lesion.

Cavotricuspid isthmus ablation for typical flutter: bidirectional block confirmed by pacing from the coronary sinus and lateral right atrium with a >130 ms trans-isthmus conduction delay.

Pulmonary vein isolation is the cornerstone of atrial fibrillation ablation; entry and exit block of each vein confirm electrical isolation.

Contact-force targets for radiofrequency pulmonary vein isolation are typically 10-40 g with a force-time integral of roughly 400 g·s per lesion.

Phrenic nerve injury is a recognized risk of right-sided pulmonary vein and superior vena cava ablation; pacing the phrenic nerve during lesion delivery allows monitoring of diaphragmatic capture.

Coronary artery injury risk is highest for ablation near the coronary sinus ostium, the cavotricuspid isthmus, and the left ventricular outflow tract; coronary angiography may be needed if chest pain follows ablation.

Esophageal injury after posterior left atrial ablation ranges from thermal lesions to atrial-esophageal fistula; luminal temperature monitoring and reduced posterior wall power or duration lower risk.

Ventricular tachycardia substrate ablation targets scar and abnormal electrograms, using entrainment mapping for hemodynamically tolerated VT and substrate modification for unstable VT.

NBG pacing codes: first letter chamber paced, second chamber sensed, third response (I inhibit, T trigger, D dual), fourth rate modulation, fifth multisite pacing.

Pacemaker timing: lower rate interval = 60,000/rate in ms; the AV delay follows an atrial event, and the total atrial refractory period (AV delay + PVARP) sets the upper rate limit in DDD mode.

Mode switch in dual-chamber devices converts to DDI or VDI during atrial tachyarrhythmia to avoid tracking rapid atrial rates.

ICD defibrillation threshold testing confirms adequate safety margin; a 10 J margin below maximum output is a common acceptance criterion.

Tachycardia detection uses rate plus duration or number of intervals; SVT discriminators include sudden-onset, stability, and morphology criteria.

Lead impedance trends: a sudden rise suggests fracture or dislodgement, while a gradual fall suggests insulation failure or fluid ingress.

Magnet application: pacemakers switch to asynchronous pacing (DOO/VOO) at the magnet rate; ICDs suspend tachyarrhythmia detection while the magnet is applied.

Cardiac resynchronization therapy criteria include left bundle branch block with QRS ≥150 ms, ejection fraction ≤35%, and NYHA class II-IV symptoms despite optimal medical therapy.

MRI-conditional systems require specific leads and generator combinations plus a programmed MRI mode; legacy devices may be scanned under strict protocol at some centers.

Vaughan-Williams classification: class I = Na+ channel blockers (IA quinidine, IB lidocaine, IC flecainide); class II = beta-blockers; class III = K+ channel blockers (amiodarone, sotalol, dofetilide); class IV = non-dihydropyridine Ca2+ channel blockers.

Amiodarone monitoring: baseline TSH, liver enzymes, pulmonary function tests, and ophthalmologic exam; annual thyroid and hepatic testing, and chest imaging if pulmonary symptoms develop.

Dofetilide requires initiation in a monitored setting with QTc checks after each dose; it is contraindicated when baseline QTc exceeds 440 ms (500 ms if QRS is wide).

Flecainide and propafenone are contraindicated in structural heart disease (coronary disease, reduced ejection fraction, significant hypertrophy) due to proarrhythmia risk.

Anticoagulation for atrial fibrillation: CHA2DS2-VASc score ≥2 in men or ≥3 in women supports oral anticoagulation; DOACs are preferred over warfarin except with mechanical valves or moderate-severe mitral stenosis.

Sotalol prolongs QT and requires renal dose adjustment; initiation with QTc monitoring is required, and it should be stopped if QTc exceeds 500 ms.

Digoxin inhibits the Na+/K+ ATPase, increases vagal tone, and slows AV nodal conduction; toxicity is worsened by hypokalemia, hypomagnesemia, and renal impairment.

Adenosine transiently blocks the AV node with a half-life under 10 seconds; it terminates AV nodal reentrant tachycardias and unmasks atrial activity in wide-complex tachycardia.

Ivabradine lowers sinus rate by inhibiting the I_f current; it is used in symptomatic heart failure with reduced ejection fraction and sinus rhythm above 70 bpm on maximally tolerated beta-blocker.

Normal conduction intervals: PR 120-200 ms, QRS <120 ms, QTc 350-450 ms (men) / 350-460 ms (women); AH 50-120 ms and HV 35-55 ms at baseline electrophysiology study.

Transmembrane ionic currents: phase 0 = fast Na+ (I_Na); phase 1 = transient outward K+ (I_to); phase 2 = L-type Ca2+ (I_Ca-L) balanced by I_Kr/I_Ks; phase 3 = delayed rectifier K+; phase 4 = I_f and I_K1 in nodal cells.

Effective refractory period vs relative refractory period: ERP is the longest coupling interval failing to propagate; RRP is the interval in which conduction is slowed but possible.

Atrial flutter: typical (counterclockwise) flutter uses the cavotricuspid isthmus, shows negative sawtooth F waves in inferior leads, and has an atrial cycle length near 200-260 ms.

AV nodal reentry (AVNRT): dual AV nodal physiology with jump in AH interval >50 ms on programmed atrial extrastimulus; slow pathway is the ablation target.

Orthodromic AVRT uses the AV node antegrade and the accessory pathway retrograde; antidromic AVRT uses the pathway antegrade and produces a pre-excited wide-complex tachycardia.

Ashman phenomenon: a wide QRS beat after a short coupling interval that follows a long cycle represents aberrant conduction, not ventricular ectopy.

QT interval correction: Bazett QTc = QT/√RR; prolonged QTc (>500 ms) raises torsades de pointes risk, and T-U wave alternans suggests imminent arrhythmia.

Differential pacing distinguishes AVNRT from AVRT: in AVNRT the atrial-His difference stays constant; in orthodromic AVRT the atrial signal moves with the ventricle.

Radiofrequency lesion size depends on power, contact force, duration, and catheter-to-tissue contact; impedance drop of 10-20 ohms indicates adequate heating, while an abrupt rise signals coagulum or steam pop risk.

Cryoablation for AVNRT uses a -30 °C cryomapping step to test lesion effect before reaching -70 to -80 °C for a durable lesion.

Cavotricuspid isthmus ablation for typical flutter: bidirectional block confirmed by pacing from the coronary sinus and lateral right atrium with a >130 ms trans-isthmus conduction delay.

Pulmonary vein isolation is the cornerstone of atrial fibrillation ablation; entry and exit block of each vein confirm electrical isolation.

Contact-force targets for radiofrequency pulmonary vein isolation are typically 10-40 g with a force-time integral of roughly 400 g·s per lesion.

Phrenic nerve injury is a recognized risk of right-sided pulmonary vein and superior vena cava ablation; pacing the phrenic nerve during lesion delivery allows monitoring of diaphragmatic capture.

Coronary artery injury risk is highest for ablation near the coronary sinus ostium, the cavotricuspid isthmus, and the left ventricular outflow tract; coronary angiography may be needed if chest pain follows ablation.

Esophageal injury after posterior left atrial ablation ranges from thermal lesions to atrial-esophageal fistula; luminal temperature monitoring and reduced posterior wall power or duration lower risk.

Ventricular tachycardia substrate ablation targets scar and abnormal electrograms, using entrainment mapping for hemodynamically tolerated VT and substrate modification for unstable VT.

NBG pacing codes: first letter chamber paced, second chamber sensed, third response (I inhibit, T trigger, D dual), fourth rate modulation, fifth multisite pacing.

Pacemaker timing: lower rate interval = 60,000/rate in ms; the AV delay follows an atrial event, and the total atrial refractory period (AV delay + PVARP) sets the upper rate limit in DDD mode.

Mode switch in dual-chamber devices converts to DDI or VDI during atrial tachyarrhythmia to avoid tracking rapid atrial rates.

ICD defibrillation threshold testing confirms adequate safety margin; a 10 J margin below maximum output is a common acceptance criterion.

Tachycardia detection uses rate plus duration or number of intervals; SVT discriminators include sudden-onset, stability, and morphology criteria.

Lead impedance trends: a sudden rise suggests fracture or dislodgement, while a gradual fall suggests insulation failure or fluid ingress.

Magnet application: pacemakers switch to asynchronous pacing (DOO/VOO) at the magnet rate; ICDs suspend tachyarrhythmia detection while the magnet is applied.

Cardiac resynchronization therapy criteria include left bundle branch block with QRS ≥150 ms, ejection fraction ≤35%, and NYHA class II-IV symptoms despite optimal medical therapy.

MRI-conditional systems require specific leads and generator combinations plus a programmed MRI mode; legacy devices may be scanned under strict protocol at some centers.

Vaughan-Williams classification: class I = Na+ channel blockers (IA quinidine, IB lidocaine, IC flecainide); class II = beta-blockers; class III = K+ channel blockers (amiodarone, sotalol, dofetilide); class IV = non-dihydropyridine Ca2+ channel blockers.

Amiodarone monitoring: baseline TSH, liver enzymes, pulmonary function tests, and ophthalmologic exam; annual thyroid and hepatic testing, and chest imaging if pulmonary symptoms develop.

Dofetilide requires initiation in a monitored setting with QTc checks after each dose; it is contraindicated when baseline QTc exceeds 440 ms (500 ms if QRS is wide).

Flecainide and propafenone are contraindicated in structural heart disease (coronary disease, reduced ejection fraction, significant hypertrophy) due to proarrhythmia risk.

Anticoagulation for atrial fibrillation: CHA2DS2-VASc score ≥2 in men or ≥3 in women supports oral anticoagulation; DOACs are preferred over warfarin except with mechanical valves or moderate-severe mitral stenosis.

Sotalol prolongs QT and requires renal dose adjustment; initiation with QTc monitoring is required, and it should be stopped if QTc exceeds 500 ms.

Digoxin inhibits the Na+/K+ ATPase, increases vagal tone, and slows AV nodal conduction; toxicity is worsened by hypokalemia, hypomagnesemia, and renal impairment.

Adenosine transiently blocks the AV node with a half-life under 10 seconds; it terminates AV nodal reentrant tachycardias and unmasks atrial activity in wide-complex tachycardia.

Ivabradine lowers sinus rate by inhibiting the I_f current; it is used in symptomatic heart failure with reduced ejection fraction and sinus rhythm above 70 bpm on maximally tolerated beta-blocker.