01Approach to the Critical Patient/attcp51

Immediate stabilization

›ABC priorities

›Airway and breathing

›SpO2 target >= 94%

›Supplemental oxygen for hypoxemia

›IV access

›Two large-bore peripheral IVs

›Antecubital preferred for transvenous pacing access

›Continuous telemetry and ECG monitoring

›12-lead ECG immediately

›Defibrillator and transcutaneous pacing pads applied

›Hemodynamic assessment

›Hypotension threshold

›SBP < 90 mmHg or MAP < 65 mmHg

›Altered mental status

›Signs of end-organ hypoperfusion

›Ventricular escape rate characterization

›Rate < 40 bpm as high-risk marker

›Wide QRS escape indicates infra-Hisian origin

›Narrow QRS escape indicates junctional origin — more reliable

›Immediate interventions

›Transcutaneous pacing for hemodynamic instability

›Pads in anterior-posterior position

›Rate 60-80 bpm

›Current titrated to capture (usually 50-100 mA)

›Atropine 0.5-1.0 mg IV for AV nodal block

›Narrow QRS escape rhythm indicates likely AV nodal block

›Avoid or use cautiously with wide QRS escape

02History/hx90

Presenting symptoms

›Syncope and presyncope

›Most common presenting symptom

›Sudden loss of consciousness

›Prodromal lightheadedness

›Near-falls or unexplained falls

›Stokes-Adams attacks

›Seizure-like activity without true seizure

›Rapid recovery of consciousness

›Cardiac and exertional symptoms

›Exertional dyspnea

›Inability to augment heart rate with exertion

›Exercise intolerance

›Palpitations

›Awareness of slow or irregular rhythm

›Thumping quality from cannon A waves

›Chest pain

›Ischemic etiology concern

›Inferior or anterior MI as precipitant

Onset and temporal pattern

›Acute onset

›Ischemic cause

›Inferior MI — AV nodal block, often transient

›Anterior MI — infranodal block, worse prognosis

›Drug toxicity onset

›Recent initiation or dose change of AV nodal blocking agents

›Beta-blockers, verapamil, diltiazem, digoxin

›Insidious onset

›Degenerative conduction disease

›Lev disease — fibrosis of left side conduction system

›Lenegre disease — idiopathic sclerodegenerative disease

›Infiltrative disease

›Sarcoidosis — AV block in 23-30% of cardiac sarcoidosis

›Amyloidosis

Etiologic history

›Medication history

›AV nodal blocking agents

›Beta-blockers

›Calcium channel blockers — verapamil, diltiazem

›Digoxin

›Antiarrhythmics

›Class I — flecainide, propafenone

›Class III — amiodarone, sotalol

›Nutraceuticals

›Lily of the valley

›Infectious exposures

›Lyme disease risk

›Tick exposure in endemic areas

›Erythema migrans rash

›Lyme carditis resolves within 1-2 weeks of antibiotics

›Chagas disease

›Travel to Central or South America

›Endemic region residence

›Cardiac history

›Prior conduction abnormalities

›First-degree AV block

›Bundle branch block — strongest ECG predictor

›Prior cardiac interventions

›Cardiac surgery — especially valve surgery

›Catheter ablation

›TAVR — transcatheter aortic valve replacement

Risk factors

›Independent risk factors for AV block

›Advanced age

›Degenerative fibrosis — Lev/Lenegre disease

›Most common cause in developed countries

›Hypertension and elevated systolic blood pressure

›Identified by JAMA Network Open population study 2019

›Diabetes mellitus

›Elevated fasting glucose association

›Pre-existing bundle branch block

›RBBB or LBBB — strongest ECG predictors

›Structural and systemic conditions

›Coronary artery disease and prior MI

›Structural heart disease — valvular, cardiomyopathy

›Infiltrative diseases

›Sarcoidosis

›Amyloidosis

›Neuromuscular diseases

›Myotonic dystrophy

›Kearns-Sayre syndrome

›Autoimmune conditions

›SLE — anti-Ro/La antibodies

›Rheumatoid arthritis

Family and genetic history

›Familial risk

›Sudden cardiac death

›First-degree relatives

›Age of onset

›Congenital heart block

›Maternal SLE or anti-Ro/La antibodies

›Genetic conditions — SCN5A, lamin A/C, TRPM4 mutations

›Inherited cardiomyopathies

›Neuromuscular disease in family

›Inherited channelopathies

03Physical Exam/exam49

Vital signs

›Cardiovascular vitals

›Heart rate

›Typically 25-50 bpm in complete heart block

›Ventricular escape rate independent of atrial rate

›Blood pressure

›Hypotension from reduced cardiac output

›Wide pulse pressure from compensatory stroke volume increase

›Respiratory rate

›Tachypnea from pulmonary edema or poor perfusion

Cardiovascular exam

›Jugular venous pulsations

›Cannon A waves

›Irregular giant A waves in JVP — hallmark finding

›Atrial contraction against closed tricuspid valve

›Occur intermittently when P wave coincides with QRS

›Auscultation

›Varying intensity of S1

›Hallmark of AV dissociation

›Due to changing PR relationship and mitral valve position at closure

›Variable pulse volume

›Beat-to-beat variation in stroke volume

›S3 or S4 gallop

›Heart failure evidence

›Reduced ventricular compliance

Heart failure and perfusion signs

›Volume overload signs

›Elevated JVP

04Differential Diagnosis/ddx57

Life-threatening causes

›Acute myocardial infarction

›Inferior MI — AV nodal block

›ICD-10 I21.1

›Often transient, resolves with revascularization

›RCA occlusion affects AV nodal artery

›Anterior MI — infranodal block

›ICD-10 I21.0

›Indicates extensive septal necrosis

›Worse prognosis than inferior MI

›Drug toxicity

›Digoxin toxicity

›ICD-10 T46.0X1

›Hypokalemia and hypomagnesemia increase risk

›Beta-blocker overdose

›Glucagon as antidote

›High-dose insulin euglycemic therapy

›Calcium channel blocker overdose

›Calcium chloride and glucagon

›Lipid emulsion therapy

Conduction mimics

›Isorhythmic AV dissociation

›Atrial and ventricular rates similar but independent

›No true block — conduction is intact

›No treatment required

›Key differentiator from complete heart block

›High-grade second-degree AV block

›Two or more consecutive non-conducted P waves

05Laboratory Tests/lt55

Cardiac biomarkers

›Troponin

›High-sensitivity troponin I or T

›Rule out acute MI as precipitant

›Serial at 0 and 3 hours

›Elevation suggests ischemic etiology

›CK-MB

›Supplemental to troponin if MI suspected

›BNP or NT-proBNP

›Heart failure assessment

›BNP > 100 pg/mL suggests heart failure

›NT-proBNP age-adjusted cutoffs

›Elevated from reduced cardiac output

Electrolyte and metabolic panel

›Potassium

›Hyperkalemia as AV block precipitant or exacerbator

›K+ > 6.0 mmol/L associated with conduction block

›Hypokalemia increases digoxin toxicity risk

›Magnesium

›Hypomagnesemia increases digoxin toxicity risk

›Supplementation for electrolyte repletion

›Renal function

›Creatinine and eGFR

›Digoxin dosing adjustment

›Contrast nephropathy risk stratification

›Calcium

›Hypercalcemia increases digoxin toxicity risk

›Hypocalcemia as rare conduction disturbance cause

06Diagnostic Tests/dt78

Scoring Systems

›ACEP guideline recommendations for bradycardia evaluation

›Clinical risk stratification

›Symptomatic vs. asymptomatic presentation

›Hemodynamically stable vs. unstable

›Reversible vs. irreversible etiology

›Indications for urgent pacing per ACC/AHA/HRS 2018

›Class I: Third-degree AV block with symptoms or hemodynamic compromise

›Class I: Asystolic pauses >= 3 seconds while awake

›Class I: Ventricular escape rate < 40 bpm with symptoms

›Lyme carditis severity scoring

›PR interval > 300 ms

›High-degree AV block risk marker

›Hospitalization recommended

›Complete heart block

›Temporary pacing consideration

›Ceftriaxone preferred over oral antibiotics

MRI

›Cardiac MRI indications

›Primary indication: suspected infiltrative or inflammatory etiology

›Sarcoidosis workup — gold standard imaging

›Myocarditis evaluation

›Amyloidosis characterization

›Late gadolinium enhancement

›Patchy midwall or subepicardial enhancement in sarcoidosis

›Basal septal involvement typical in cardiac sarcoidosis

›T1 mapping for amyloid infiltration

›Cardiac MRI sequences

07Disposition/dispo33

Admission criteria

›All patients with third-degree AV block require admission

›Continuous telemetry monitoring mandatory

›AHA 2017 scientific statement on ECG monitoring

›Continuous monitoring until etiology established and pacing secured

›ICU or CCU level care

›Hemodynamic instability

›Requiring temporary pacing

›Associated with acute MI

›Wide complex escape rhythm — infra-Hisian block risk of sudden failure

›Telemetry floor

›Hemodynamically stable

›Reliable narrow QRS junctional escape rhythm

›Awaiting permanent pacemaker implantation

Transfer criteria

›Transfer to cardiac care center

›No electrophysiology capability at receiving facility

›Transcutaneous pacing during transport

›ALS-level transport

›Acute MI requiring revascularization

›Primary PCI center transfer

›Time-sensitive — door-to-balloon target 90 minutes

Discharge criteria

›Permanent pacemaker implanted

›Device threshold testing satisfactory

›Sensing and pacing thresholds within normal limits

›Wound hemostasis confirmed

›No lead dislodgement or pneumothorax

08Treatment/t120

Immediate pharmacologic treatment

›Atropine for AV nodal block

›Atropine 0.5-1.0 mg IV

›Repeat every 3-5 minutes as needed

›Maximum total dose 3 mg

›Effective for supranodal block with narrow QRS escape

›Caution with wide QRS escape

›May paradoxically worsen infranodal block

›Accelerates atrial rate without improving ventricular rate

›Chronotropic infusions

›Epinephrine infusion

›2-10 mcg/min IV continuous infusion

›Push-dose 10-20 mcg IV boluses for acute hemodynamic support

›Titrate to SBP > 90 mmHg and HR > 40 bpm

›Dopamine infusion

›5-20 mcg/kg/min IV continuous infusion

›Titrate to hemodynamic response

›Wean as transcutaneous pacing established

›Isoproterenol

›2-10 mcg/min IV

›Enhances both nodal and His-Purkinje conduction

›Consider for infranodal block unresponsive to atropine

Transcutaneous pacing

›Transcutaneous pacing initiation

›Indication: symptomatic or hemodynamically unstable complete heart block

›Bridge to transvenous pacing

›AHA 2025 ACLS guideline recommendation

›Pad placement

›Anterior-posterior placement preferred

›Anterior pad: left precordium

›Posterior pad: left infrascapular region

›Settings

›Rate 60-80 bpm

›Output titrated from 50 mA upward until capture

›Confirm electrical capture on monitor and mechanical capture by pulse

›Patient comfort

›Analgesia and sedation required

›Morphine 2-4 mg IV or fentanyl 25-50 mcg IV

›Midazolam 1-2 mg IV

Temporary transvenous pacing

›Transvenous pacing indications

›Failed transcutaneous pacing

›Class I recommendation per ACC/AHA/HRS 2018

›Prolonged need for pacing before permanent device

›High-risk escape rhythm

›Wide QRS escape rate < 40 bpm

›Asystolic pauses

›Transvenous pacing procedure

›Access site

›Right internal jugular preferred — direct path to RV apex

›Right subclavian or femoral alternatives

›Lead placement

›RV apex or RV outflow tract

›Fluoroscopy or echocardiographic guidance

›Settings

›Rate 60-80 bpm

›Output 2x threshold (typically 3-5 mA)

›Sensitivity 2-5 mV

›Complication monitoring

›Lead dislodgement

›Perforation and tamponade

›Infection risk with prolonged use

Permanent pacemaker implantation

›Indications per ACC/AHA/HRS 2018 guideline

›Class I: Acquired third-degree AV block not attributable to reversible cause

›Regardless of symptoms

›Kusumoto FM et al., JACC 2019

›Class I: Third-degree AV block with associated ventricular dysfunction

›Cardiac resynchronization therapy consideration

›Reversible cause management

›Treat underlying cause first with temporary pacing support

›Permanent pacing if block fails to resolve

›Device selection

›Dual-chamber pacemaker (DDD)

›Maintains AV synchrony

›Preferred over single-chamber ventricular pacing

›Avoids pacemaker syndrome

›Cardiac resynchronization therapy

›If LV EF <= 35% and expected high ventricular pacing burden

›Class IIa recommendation

›ICD capability

›Cardiac sarcoidosis with LV dysfunction

›Neuromuscular disease with cardiomyopathy

›Conduction system pacing consideration

›His-bundle pacing

›Preserves physiologic activation pattern

›Avoids pacing-induced cardiomyopathy

›Left bundle branch area pacing

›Alternative to His-bundle pacing

›More stable thresholds

Etiology-specific treatment

›Lyme carditis

›Ceftriaxone 2 g IV daily

›For high-degree AV block or hospitalized patients

›Continue until clinical improvement

›Transition to oral doxycycline 100 mg twice daily for 14-21 days

›No permanent pacemaker until resolution confirmed

›AV block typically resolves within 6 days (median)

›Monitor for up to 42 days

›Drug-induced AV block

›Discontinue offending agent

›Beta-blockers: wean if possible, may need abrupt discontinuation

›Digoxin: hold and measure level

›Digoxin-specific Fab fragments for toxicity

›Beta-blocker toxicity

›Glucagon 5-10 mg IV bolus then 2-5 mg/hr infusion

›High-dose insulin 1 unit/kg/hr with glucose supplementation

›Calcium channel blocker toxicity

›Calcium chloride 1 g IV bolus

›High-dose insulin euglycemic therapy

›Lipid emulsion therapy 1.5 mL/kg IV bolus

›Inferior MI with AV block

›Urgent revascularization

›Primary PCI if STEMI with door-to-balloon < 90 minutes

›Temporary pacing as bridge

›AV block often resolves after reperfusion

›Permanent pacing only if block persists post-revascularization

›Cardiac sarcoidosis

›Permanent pacemaker implantation

›Class I recommendation

›ICD consideration for LV dysfunction or NSVT

›Corticosteroids

›Prednisone 40-60 mg daily

›May improve AV block in active inflammatory phase

›Not a substitute for device therapy

09Special Populations/sp86

Pregnancy

›Physiologic considerations

›Increased cardiac output in pregnancy

›30-50% increase by third trimester

›Heart rate physiologically increases 10-15 bpm

›Complete heart block impairs appropriate HR augmentation

›Hemodynamic risks

›Supine hypotension from IVC compression

›Left lateral decubitus position for pacing procedures

›Congenital complete heart block in neonates

›Maternal anti-Ro/La antibody mediated

›Occurs in 1-3% of anti-Ro positive mothers

›Antibody transfer causes fetal cardiac injury

›In utero management

›Fetal echocardiography monitoring

›Maternal hydroxychloroquine may reduce risk

›Fetal hydrops as severe complication

›Neonatal pacing

›Epicardial pacing in neonates — venous access too small for transvenous

›Rate thresholds for pacing: < 55 bpm with good ventricular function

›Acquired AV block in pregnancy

›Transcutaneous pacing as bridge

›Radiation avoidance preferred

›Echocardiographic guidance for transvenous pacing

›Permanent pacemaker implantation

›Can be performed safely in pregnancy

›Lead-based fluoroscopy shielded when possible

›Preferably after first trimester

Geriatric

›Epidemiology and etiology

›Degenerative fibrosis — most common cause in older adults

›Lev and Lenegre disease predominate

›Gradual progressive conduction system fibrosis

›High comorbidity burden

›CAD, hypertension, diabetes, cardiomyopathy

›Polypharmacy — multiple AV nodal blocking agents

›Modified assessment

›Atypical presentations

›Falls instead of syncope

›Confusion and delirium as primary symptom

›Fatigue and functional decline without classic symptoms

›Frailty assessment

›Increases procedural risk

›Affects device management decisions

›Shared decision-making priority

›Drug considerations in older adults

›Polypharmacy review essential

›Beta-blockers, CCBs, digoxin common in older patients

›Renal clearance reduction increases drug accumulation

›Digoxin toxicity at lower levels with age-related renal decline

›Atropine response reduced in older adults

›Vagolytic effect less predictable

›Lower threshold for transcutaneous pacing

›Pacemaker outcomes in geriatric patients

›Permanent pacemaker well tolerated

›High procedural success rate regardless of age

›Improved quality of life and syncope prevention

›ICD decision-making

›Life expectancy and functional status primary factors

›Shared decision-making with patient and family

Pediatrics

›Congenital complete heart block

›Prevalence 1 in 15,000-22,000 live births

›Structural heart disease in 50% — congenitally corrected TGA, AV septal defects

›Immune-mediated in 50% — maternal anti-Ro/La antibodies

›Prognosis

›Structural heart disease associated — higher mortality

›Isolated immune-mediated — better prognosis with pacing

›Pacing indications in pediatrics — 2021 PACES consensus

›Class I: Symptomatic bradycardia — syncope, presyncope, poor feeding

›Class I: LV dysfunction or structural disease

›Class I: Ventricular rate < 55 bpm in neonate

›Class I: Wide complex escape rhythm

›Acquired complete heart block in children

›Lyme carditis — most common reversible cause in endemic areas

›Ceftriaxone 50-75 mg/kg/day IV (max 2 g/day)

›Transition to oral amoxicillin or doxycycline when improving

›Post-cardiac surgery

›Temporary epicardial wires placed intraoperatively

›Permanent pacing if block persists > 7-10 days

›Autoimmune myocarditis

›Immunosuppression consideration

›Pacemaker implantation technique in children

›Weight-based approach

›Epicardial pacing for infants < 10-15 kg

›Transvenous pacing when adequate venous access possible

›Lead selection

›Active fixation leads for older children

›Growth allowance for lead length

10Background/b103

Epidemiology

›Incidence and prevalence

›AV block incidence increases with age

›Incidence 0.04% per year in general population

›Prevalence 1-2% in adults over 60 years

›Strong age-dependent increase — Kerola T, JAMA Network Open 2019

›Sex distribution

›Slight male predominance in acquired forms

›Congenital heart block more common with maternal anti-Ro antibodies

›Geographic variation

›Lyme carditis endemic in northeastern United States

›Chagas disease in Latin America

›Causes by frequency

›Degenerative fibrosis — most common in developed countries

›CAD and ischemia — second most common

›Post-surgical or post-procedural

›TAVR-associated AV block 10-30%

›Higher risk with pre-existing RBBB

›Drug-induced — common and underrecognized

›Infiltrative — sarcoidosis, amyloidosis

›Infectious — Lyme, Chagas, myocarditis

›Mortality and morbidity

›Untreated complete heart block

›High risk of syncope and sudden cardiac death

›Ventricular escape rhythm may abruptly fail

›Anterior MI with complete heart block

›In-hospital mortality significantly higher than inferior MI

›Indicates extensive septal necrosis

›With permanent pacemaker

›Excellent long-term outcomes

›Syncope prevention rate > 95%

Pathophysiology

›Normal conduction system

›AV node — located at Triangle of Koch

›Receives dual blood supply from RCA and circumflex

›Delays AV conduction — rate 40-60 bpm as escape pacemaker

›His bundle

›Common bundle through fibrous septum

›Single blood supply from LAD and posterior septal perforators

›More vulnerable than AV node

›Bundle branches and Purkinje fibers

›Left and right bundle branches

›Ventricular escape rate 20-40 bpm if infranodal block

›Mechanisms of third-degree AV block

›Supranodal block

›Block within or near AV node

›Junctional escape rhythm 40-60 bpm — narrow QRS

›Responds to atropine and catecholamines

›Infra-Hisian block

›Block below His bundle

›Ventricular escape rhythm 20-40 bpm — wide QRS

›Unreliable — may fail abruptly

›Does not respond to atropine

›Degenerative fibrosis mechanism

›Progressive replacement of conduction tissue by fibrosis

›Begins in peripheral bundle branches

›Advances proximally to main bundles and His bundle

›Eventually involves AV node

›Calcification of AV annuli and mitral or aortic valve rings

›Anatomic proximity to conduction system

›Ischemic mechanism

›RCA occlusion — AV nodal artery supply

›Reversible in most cases of inferior MI

›Proximal RCA more likely to cause AV block

›LAD occlusion — His bundle and bundle branches

›Indicates massive anterior infarction

›Associated with cardiogenic shock

›Less likely to resolve spontaneously

Therapeutic Considerations

›Reversibility assessment governs treatment pathway

›Reversible causes

›Lyme carditis — antibiotics with expected resolution

›Drug toxicity — discontinue offending agent

›Post-cardiac surgery — temporary pacing, observe

›Inferior MI — revascularization, temporary pacing

›Irreversible causes

›Permanent pacemaker implantation — Class I

›Degenerative fibrosis, sarcoidosis, anterior MI

›Atropine response as diagnostic tool

›Response implies AV nodal or supranodal level

›Improvement with atropine supports nodal mechanism

›No improvement or worsening supports infranodal mechanism

›Narrow vs. wide QRS escape rhythm

›Most reliable predictor of block level

›Wide QRS mandates urgent pacing regardless of atropine response

›Pacing modality selection

›Transcutaneous pacing — first-line emergency bridge

›Widely available

›Painful — requires sedation and analgesia

›Transvenous pacing — definitive temporary therapy

›More reliable and comfortable

›Risk of perforation, infection, lead dislodgement

›Permanent pacemaker — definitive therapy for irreversible block

›Right ventricular pacing — standard

›Conduction system pacing — emerging preferred option

›Avoids pacing-induced cardiomyopathy from RV apical pacing

›Evidence base

›ACC/AHA/HRS 2018 guideline on bradycardia and conduction delay

›Kusumoto FM, Schoenfeld MH, Barrett C, et al.

›JACC 2019 — Class I recommendation for pacing in complete heart block

›AHA 2025 ACLS guidelines

›Wigginton JG, Agarwal S, Bartos JA, et al.

›Transcutaneous pacing as initial emergency treatment

›2021 PACES pediatric device consensus statement

›Shah MJ, Silka MJ, et al.

›Heart Rhythm 2021

11Patient Discharge Instructions/pdi39

copy discharge instructions

›Diagnosis and basic explanation

›Third-degree heart block diagnosis

›Complete block of electrical signals between heart chambers

›Heart depends on a slow backup rhythm

›Treatment depends on whether the cause is reversible

›Pacemaker post-implant instructions

›Activity restrictions

›Avoid raising the arm on the pacemaker side above shoulder level for 4-6 weeks

›No heavy lifting > 10 pounds for 4-6 weeks

›Driving restriction until cleared by cardiologist — typically 1 week

›Wound care

›Keep incision dry for 5-7 days

›No submersion in water until healed

›Wound check appointment in 1-2 weeks

›Electromagnetic interference

›Avoid strong magnets and MRI unless device is MRI-conditional

›Inform medical staff of pacemaker before any procedures

›Airport security — inform screeners and carry device ID card

›Device follow-up

›First device check at 2-12 weeks post-implant

›Every 6-12 months thereafter or per remote monitoring schedule

›Return to emergency department immediately

›Cardiac warning signs

›Syncope or loss of consciousness

›Near-fainting or severe dizziness

›Chest pain or pressure

›Palpitations or very slow heart rate

12References/r32

Guidelines and key sources

›ACC/AHA/HRS 2018 Guideline on Bradycardia and Cardiac Conduction Delay

›Kusumoto FM, Schoenfeld MH, Barrett C, et al.

›Journal of the American College of Cardiology. 2019

›Class I recommendation for permanent pacing in acquired third-degree AV block

›AHA 2025 ACLS Guidelines — Adult Advanced Life Support

›Wigginton JG, Agarwal S, Bartos JA, et al.

›Circulation. 2025

›Transcutaneous and transvenous pacing protocols for symptomatic bradycardia

›AHA 2017 Scientific Statement on ECG Monitoring

›Sandau KE, Funk M, Auerbach A, et al.

›Circulation. 2017

›Continuous telemetry monitoring standards for AV block

›2021 PACES Expert Consensus — Cardiovascular Devices in Pediatric Patients

›Shah MJ, Silka MJ, et al.

›Heart Rhythm. 2021

›Pacing indications and thresholds in congenital complete heart block

Landmark studies

›Risk Factors Associated With Atrioventricular Block

›Kerola T, Eranti A, Aro AL, et al.

›JAMA Network Open. 2019

›Population-based study identifying independent risk factors for AV block

›Etiology and device therapy in complete AV block in pediatric and young adult population

›Cioffi GM, Gasperetti A, Tersalvi G, et al.

›Journal of Cardiovascular Electrophysiology. 2021

›Contemporary review of congenital and acquired pediatric AV block

›Clinical Significance of Drug-Induced AV Block

›Sfairopoulos D, Bazoukis G, Sideris S, et al.

Evidence & Review