General Features

Normal ECG

• ✓ Normal rate (60-100 beats/min in adults), sinus rhythm, and normal axes


• ✓ P wave: normal axis (0° to +75°, upright in I and II, inverted in aVR) and same morphology


• ✓ PR interval: 120-200 ms


• ✓ QRS complex: normal axis (-30° to +110°) and duration (<120 ms)


• ✓ ST segment: typically isoelectric with <1 mm of elevation or depression in limb leads


• ✓ T wave: upright in I, II, and V3-V6 with normal asymmetric morphology

Borderline normal ECG or normal variant

• ✓ Early repolarization: normal healthy individuals can have some ST-T segment elevation that is characterized by a distinct notch in the down stroke of the R wave with an elevated concave upward takeoff of the ST-segment at the J-point of the QRS complex; often seen in V2-V5


• ✓ Juvenile T waves: negative T-waves in V1-V3 that are typically not deep or symmetrical


• ✓ S waves in I, II, and III: seen in 20% of healthy adults


• ✓ Incomplete right bundle branch block: rSR’ in V1 with a narrow QRS interval (<120 ms), r wave amplitude <7 mm, and an R’ wave amplitude less than r or S wave amplitude

Incorrect electrode placement

• ✓ Right and left limb lead reversal: negative P wave and QRS complex in I and aVL, upright P wave and QRS complex in aVR


• ✓ Right arm-right leg lead reversal: consider if there is little to no voltage in II


• ✓ Left arm-left leg reversal: difficult to tell without prior tracing to compare; consider if lead I has a greater voltage than other limb leads and lead aVF has less voltage than other leads


• ✓ Reversal of two precordial leads: sudden decrease in R wave progression with a marked return in the R wave amplitude in the subsequent precordial lead


• ✓ Note: Limb lead reversal can mimic dextrocardia, although dextrocardia cannot exist if normal R wave progression is present in the precordial leads (i.e. dextrocardia causes reverse R wave progression in the precordial leads)

Artifact

• ✓ Physiologic tremor: often mimics an atrial rate of about 500 beats/min


• ✓ Parkinson tremor: can give appearance of atrial flutter with an atrial rate of about 300 beats/min


• ✓ Skeletal muscle fasciculations or movements (e.g. shivering), surgical electrocautery, or equipment malfunction

P Wave Abnormalities

Right atrial abnormality/enlargement

• ✓ II, III, or aVF: P wave amplitude >2.5 mm (P-pulmonale)


• ✓ V1 or V2: P wave amplitude >1.5 mm; if biphasic, initial P wave amplitude >1.5 mm


• ✓ Associated conditions: chronic obstructive pulmonary disease, congenital heart disease (e.g. Tetralogy of Fallot, pulmonic stenosis, tricuspid atresia, Eisenmenger’s physiology), pulmonary embolism, normal variant (e.g. small body habitus, vertical heart), secondary to left atrial enlargement (30%; look for left atrial enlargement)

Left atrial abnormality/enlargement

• ✓ II, III, or aVF: notched P wave with 40 ms between each peak and total P wave duration >120 ms (P-mitrale)


• ✓ V1: terminal portion of biphasic P wave >1 mm deep and 40 ms wide (e.g. 1 mm wide and 1 mm deep on standard 25 mm/s tracing)


• ✓ Associated conditions: left atrial dilation/hypertrophy, intra-atrial conduction delay

Biatrial abnormality/enlargement

• ✓ Criteria met for both left and right atrial enlargement

Atrial Rhythms

Sinus rhythm

• ✓ Default rhythm of the heart, whereby pacemaking impulses arise from the sinus (sinoatrial, SA) node and are transmitted to the ventricles via the AV node and His-Purkinje system


• ✓ P wave: normal axis (0° to +75°, upright in I and II +/- aVF and V4-V6, inverted in aVR) and same morphology


• ✓ Atrial rate (adults): 60-100 beats/min (age-specific: newborn 110-150 beats/min, 2 years 85-125 beats/min, 4 years 75-115 beats/min, 6+ years 60-100 beats/min)

Sinus arrhythmia

• ✓ Sinus rhythm with beat-to-beat variation in the P-P interval (i.e. time between successive P waves), resulting in an irregular ventricular rate


• ✓ P wave: normal axis (0° to +75°, upright in I and II, inverted in aVR) and same morphology


• ✓ P-P interval varies by > 10% or 160 ms (0.16 seconds)

Sinus bradycardia (<60)

• ✓ Sinus rhythm with heart rate <60 beats/min in adults (or below the normal range for age in children)


• ✓ P wave: normal axis (0° to +75°, upright in I and II, inverted in aVR) and same morphology


• ✓ Atrial rate: <60 beats/min

Sinus tachycardia (>100)

• ✓ Sinus rhythm with heart rate >100 beats/min in adults (or above the normal range for age in children)


• ✓ P wave: normal axis (0° to +75°, upright in I and II, inverted in aVR) and same morphology


• ✓ Atrial rate: >100 beats/min

Sinus pause or arrest

• ✓ >2 second pause without a P wave


• ✓ Associated conditions: sinus arrhythmia (PP interval variability), sinoatrial exit block (failure of electrical impulse to leave sinus node, resulting in a pause duration that is a multiple of the P-P interval), non-conducted premature atrial complexes, sinus arrest

Sinoatrial exit block

• ✓ Failure of the sinus impulse to escape the sinoatrial (SA) node and enter the atrial conduction tissue; similar to atrioventricular (AV) blocks, there are four possible SA exit blocks


• ✓ First-degree: not detectable on surface ECG


• ✓ Second-degree Mobitz Type I: group beating, shortening PP interval with a constant PR interval, and a PP pause interval less than twice the usual PP interval


• ✓ Second-degree Mobitz Type II: constant PP interval with a PP pause interval being approximately a precise multiple (<100 ms) of the usual PP interval


• ✓ Third-degree: not debatable on surface ECG

Atrial premature complexes

• ✓ Also referred to as premature atrial complexes(PACs)


• ✓ Premature P wave, often with a non-sinus P wave morphology and normal appearing QRS complex


• ✓ Note: atrial premature complexes will often conduct back into the sinoatrial (SA) node, resetting the node and causing a temporary pause in sinus activity. In the event that an SA entrance block exists, thereby preventing conduction back into the SA node), the sinus node will not reset and therefore, an interpolated beat (extra QRS complex between otherwise constant RR intervals) or full compensatory pause will occur

Atrial tachycardia

• ✓ P waves with different (non-sinus) morphology


• ✓ Differs from atrial premature complexes as there are ≥3 beats in succession


• ✓ Atrial rate: 100-213 beats/min (often 100-180 beats/min)


• ✓ Typically normal QRS complexes (i.e. similar to sinus rhythm) following each P wave, unless the QRS complex is aberrantly conducted


• ✓ Can be present with a fixed or variable atrioventricular (AV) block

Atrial tachycardia, multifocal

• ✓ ≥3 different P wave morphologies with an atrial rate >100 beats/min


• ✓ Varying PP and PR intervals


• ✓ Associated conditions: lung disease (e.g. chronic obstructive lung disease, pulmonary edema, cor pulmonale, hypoxia)

Supraventricular tachycardia

• ✓ Regular rhythm with ventricular rate >100 beats/min


• ✓ Narrow QRS complexes unless aberrant conduction


• ✓ P waves buried in the QRS complex, immediately following a short RP interval (<90 ms) or long RP interval


• ✓ Note: ~90% of all supraventricular tachycardias associated with (1) AV nodal reentrant tachycardia (~60%) or (2) AV reentrant tachycardia (~30%)

Atrial flutter

• ✓ Organized macro-reentrant electrical activity in the atrium resulting in rapid, regular flutter (“F”) waves


• ✓ Flutter wave rate: 214-340 beats/min (often 240-340 beats/min)


• ✓ Ventricular rate can be irregular with coexisting variable AV block


• ✓ “Fixed” = constant RR intervals; “variable” = irregular RR intervals


• ✓ Typical (common) atrial flutter: sawtooth pattern with inverted flutter waves in lead II, III, and aVF + positive flutter waves in lead V1; due to counterclockwise reentry around the tricuspid annulus


• ✓ Atypical (uncommon) atrial flutter: sawtooth pattern with inverted flutter waves in V1 + positive flutter waves in leads II, III, and aVF (i.e. opposite pattern of typical); due to clockwise reentry in the right or left atria; may occur after ablation or following congenital/valvular cardiac surgery


• ✓ Management: similar to atrial fibrillation (e.g. catheter ablation, antiarrhythmic agents, cardioversion), although rhythm control strategy is favored because rate control can be difficult to achieve and often requires high doses of >1 AV-nodal blocking agent; definitive treatment for typical atrial flutter = catheter ablation (high success [>95%] and low complication rates); oral anticoagulation approach is similar to atrial fibrillation; high risk of recurrent atrial flutter with antiarrhythmic therapy

Atrial fibrillation

• ✓ Indiscernible, absent P waves with an irregularly irregular ventricular rate


• ✓ Atrial activity is represented by fibrillatory (“f”) waves with no organized pattern


• ✓ Classification based on ventricular rate: <60 beats/min = slow ventricular rate (SVR), 60-100 beats/min = controlled ventricular rate (CVR), >100 beats/min = rapid ventricular rate (RVR)

AV Junctional Rhythms

AV junctional escape complexes

• ✓ Typically narrow QRS complex (<120 ms) following a previously conducted beat with a coupling interval that corresponds to a rate of 40-60 beats/min


• ✓ P wave is often absent and buried within QRS complex; if present, it will be seen immediately before or after QRS complex with a superior and leftward axis along with PR interval <110 ms


• ✓ Note: these are termed “escape” complexes because they act as a backup pacemaker of the heart in the setting of severe sinus node dysfunction, sinus pauses, or high-degree AV block

AV junctional rhythm/tachycardia

• ✓ Typically regular, narrow QRS complexes (<120 ms); QRS complexes can be wide in the presence of aberrancy or a pre-existing intraventricular conduction disturbance


• ✓ Ventricular rate dictates name of rhythm: <40 beats/min = AV junctional bradycardia, 40-60 beats/min = AV junctional rhythm, 60-100 beats/min = accelerated AV junctional rhythm, >100 beats/min = AV junctional tachycardia


• ✓ P waves are often absent and buried within QRS complexes; if present, they will be seen immediately before or after QRS complex with a superior and leftward axis


• ✓ Note: a regular RR interval with underlying atrial fibrillation/flutter can be seen with digitalis toxicity; this represents complete heart block with an accelerated AV junctional rhythm or AV junctional tachycardia

Ventricular Rhythms

Ventricular premature complex(es)

• ✓ Also known as a premature ventricular complex (PVC)


• ✓ Prematurely wide QRS complex (typically >120 ms) that is not preceded by a P wave (unless a non-conducted sinus P wave that occurs prior to the premature ventricular beat)

Interpolated ventricular premature complex(es)

• ✓ Ventricular premature complex that falls between two QRS complexes and does not interrupt the regularity of the R-R cycle.


• ✓ No compensatory pause is present

Fusion ventricular premature complex(es)

• ✓ Ventricular premature complex that occurs at the same time as the sinus node impulse produces a P wave

Ventricular parasystole

• ✓ Occurs when a ventricular focus stimulates premature ventricular complexes (PVCs) at a constant rate or a multiple of constant rate


• ✓ Results in the presence of sinus rhythm with a concomitant secondary rhythm of PVCs (i.e. ventricular parasystolic rhythm that is not suppressed by the intrinsic rhythm)


• ✓ An entrance block often exists at the origin of the parasystolic PVC, preventing sinus-stimulated ventricular depolarization from resetting the ectopic ventricular focus

Ventricular tachycardia (≥3 consecutive complexes)

• ✓ ≥3 consecutive, wide QRS complexes (≥120 ms) occurring at a rapid rate (>100 beats/min)


• ✓ Often an abrupt onset and termination


• ✓ RR interval is typically regular, but can be irregular

Torsades de pointes (TdP)

• ✓ Form of polymorphic ventricular tachycardia


• ✓ Rapid succession of ≥3 beats with a ventricular origin and rate >100 beats/min


• ✓ Noticeable change in the ventricular origin given the varying axis and morphology changes (“twisting of the points”)

Accelerated idioventricular rhythm (AIVR)

• ✓ Also known as accelerated ventricular rhythm


• ✓ Often occurs when the rate of an ectopic ventricular pacemaker exceeds that of the sinus node


• ✓ Proposed mechanism: enhanced automaticity of a ventricular pacemaker, although triggered activity may play a role (e.g. ischemia, digoxin toxicity)


• ✓ ECG findings: regular or mildly irregular ventricular rhythm with a rate of 40-100 beats/min; ≥3 wide QRS complexes (≥120 ms) with a morphology similar to premature ventricular complexes; fusion and capture beats may be present


• ✓ Associated conditions: reperfusion phase following an acute myocardial infarction (e.g. post-thrombolysis; most common); commonly associated with an increase in vagal tone and decrease in sympathetic tone (e.g. beta-sympathomimetics such as adrenaline or isoprenaline); drug toxicity (e.g. digoxin, cocaine, desflurane); electrolyte abnormalities; cardiomyopathy; congenital heart disease; myocarditis; return of spontaneous circulation (ROSC) following cardaic arrest; and athletic heart.


• ✓ Prognosis: usually well tolerated, benign, and self-limited

Ventricular escape complexes or rhythm

• ✓ Regular or mildly irregular ventricular rhythm with a rate of 20-40 beats/min


• ✓ Wide QRS complexes (≥120 ms) with a morphology similar to premature ventricular complexes

Ventricular fibrillation

• ✓ Rapid, chaotic, irregular ventricular rhythm


• ✓ Electrical deflections of varying amplitude and contour with no recognizable P waves, QRS complexes, or T waves

AV block, first degree

• ✓ Constant PR interval >200 ms (0.2 seconds)


• ✓ Each P wave is followed appropriately by a QRS complex


• ✓ Note: prolonged PR interval represents delay from the onset of atrial conduction to ventricular conduction; does not evaluate the time for the sinoatrial node to atrial tissue; hence, a prolonged PR interval with a narrow QRS complex localized the site of the block to the atrioventricular (AV) node

AV block, second degree, Mobitz type I (Wenckebach)

• ✓ Progressive prolongation of the PR interval until a P wave is blocked (“longer, longer, longer drop that’s a sign of Wenckebach”)


• ✓ RR interval of non-conducted beat must be less than two times the PP interval (otherwise, a higher degree of AV block exists)


• ✓ Can give the appearance of grouped beating

AV block, second degree, Mobitz type II

• ✓ Regular sinus or atrial rhythm with intermittent non-conducted P waves and no evidence of premature atrial contractions


• ✓ Constant PR interval with all conducted beats


• ✓ RR interval of non-conducted beat is equal to two PP intervals


• ✓ Note: Often results from a block below the bundle of His and therefore, has a wide QRS complex (>120 ms)

AV block, 2:1

• ✓ Regular sinus or atrial rhythm with two P waves for every QRS complex (i.e. every other P wave is conducted)


• ✓ May be secondary to second-degree AV block Mobitz Type I or II

AV block, high grade

• ✓ Regular P-P and R-R intervals with a constant PR interval with conducted beats


• ✓ 3 P waves for every QRS complex (3 Pw : 1 QRS) with a loss in conduction with every other beat


• ✓ Sometimes used if AV block cannot be 100% determined to be 2nd- or 3rd-degree


• ✓ “High-grade” suggests an “upper” AV block (i.e. 2nd-/3rd-degree AV block)

AV block, third degree (complete)

• ✓ Complete failure of atrial impulses to pass through the AV node and stimulate ventricular activity


• ✓ Constant PP and RR intervals, but atrial and ventricular rhythm are independent of each other


• ✓ Atrial rate is typically faster than ventricular rate, as the ventricular rate is driven by either a junctional rhythm, ventricular escape complex, or a ventricular pacemaker


• ✓ Associated conditions: degenerative conduction system disease (e.g. Lev’s, Lenegre’s), infiltration disease (e.g. amyloidosis, sarcoidosis), myocardial infarction, digitalis toxicity, endocarditis, marked hyperkalemia, Lyme disease, myocardial confuse, acute rheumatic fever, severe valvular disease

Wolff-Parkinson-White (WPW) pattern

• ✓ Short PR interval (<120 ms during sinus rhythm in adults, <90 ms during sinus rhythm in children)


• ✓ Slurring of the initial portion of the QRS complex (delta wave), resulting in a prolonged QRS interval (≥120 ms in adults, >90 ms in children); wide QRS complex results from fusion of the two electrical impulses – one through the atrioventricular (AV) bypass tract and the other through the normal AV node


• ✓ Secondary ST-T wave changes may be present (i.e. ST-T segment deviation opposite in direction [discordant] to the main QRS deflection)


• ✓ Note: Wolff-Parkinson-White (WPW) syndrome exists due to an abnormal muscular network of conduction tissue that connects the atrium to the ventricle, thereby bypassing the AV node. Most patients do not have structural heart disease, but the syndrome is more common in patients with Ebstein’s anomaly (anomalous attachment and downward displacement of the tricuspid valve leaflets), mitral valve prolapse, hypertrophic cardiomyopathy, and dilated cardiomyopathy. Most tachyarrhythmias result from AV re-entry tachycardia and lead to a symptomatic narrow-complex tachycardia. A real concern is when WPW exists and a patient develop atrial fibrillation or flutter. In such cases, abnormal conduction down the AV bypass tract with retrograde conduction back up the AV node could result in a rapid, wide-complex and irregular tachycardia that can be life threatening.

AV dissociation

• ✓ Independent atrial and ventricular rates


• ✓ Ventricular rate ≥ atrial rate


• ✓ Regular P-P and R-R interval measurements with changes in position of P waves in relation to the QRS complex (i.e. P waves “march out” at their own pace)

Abnormal QRS Voltage or Axis

Low voltage, limb leads

• ✓ QRS amplitude <5 mm in all limb leads


• ✓ Associated conditions: chronic obstructive pulmonary disease, obesity, myxedema, pericardial/pleural effusion, restrictive/infiltrative cardiomyopathies

Low voltage, precordial leads

• ✓ QRS amplitude <10 mm in all precordial leads


• ✓ Associated conditions: chronic obstructive pulmonary disease, obesity, myxedema, pericardial/pleural effusion, restrictive/infiltrative cardiomyopathy

Left axis deviation

• ✓ Mean ventricular (QRS) axis: -30° to -90°


• ✓ Associated conditions: left anterior fascicular block, left bundle branch block, inferior myocardial infarction, left ventricular hypertrophy, chronic obstructive pulmonary disease, ostium primum atrial septal defect, hyperkalemia

Rightward axis

• ✓ Mean ventricular (QRS) axis: +90° to +110°

Right axis deviation

• ✓ Mean ventricular (QRS) axis: +110° to +180°


• ✓ Associated conditions: left posterior fascicular block, right ventricular hypertrophy, lateral myocardial infarction, vertically positioned heart, chronic obstructive pulmonary disease, pulmonary embolism, dextrocardia, lead reversal, and ostium secundum atrial septal defect

Right superior axis

• ✓ Mean ventricular (QRS) axis: +180° to +270° (or -90° to -180°)


• ✓ Also referred to as northwest axis, extreme axis deviation, or “no man’s land”


• ✓ Associated conditions: ventricular tachycardia

Indeterminate axis

• ✓ Biphasic QRS complex in leads I, aVL, and II

Electrical alternans

• ✓ Beat-to-beat variability in amplitude or direction of P, QRS, and/or T waves


• ✓ Associated conditions: pericardial effusion (only ~33% with QRS alternans have a pericardial effusion and only ~12% with pericardial effusions have electrical alternans), hypertension, coronary artery disease, severe heart failure, supraventricular/ventricular tachycardia, deep respirations

Ventricular Hypertrophy

Left ventricular hypertrophy (LVH)

• ✓ Cornell criteria: [R wave (avL)] + [S wave (V3)] >28 mm (men) or >20 mm (women)


• ✓ Sokolow-Lyon criteria: [S wave in V1] + [R wave in V5 or V6] >35 mm if >40 years old, >40 mm if 30-40 years old, and >60 mm if 16-30 years old


• ✓ Sokolow-Lyon ‘stand-alone’ criteria: R wave in aVL >12 mm


• ✓ Minimal voltage criteria: meets ≥1 voltage criteria, but could be a normal variant


• ✓ Moderate voltage criteria: meets ≥2 voltage criteria, but could be a normal variant


• ✓ Note: Many criteria for LVH exist; most are quite specific but lack overall sensitivity. In general, sensitivity and specificity of various criteria vary based upon the population studied and method used to define moderate to severe LVH. Of the criteria listed, the Sokolow-Lyon ‘stand-alone’ criteria is probably the most specific (~92%), while the Cornell criteria is the most sensitive (~31%).

Right ventricular hypertrophy (RVH)

• ✓ Mean QRS axis ≥+110° (i.e. right axis deviation)


• ✓ V1: R/S ratio >1, qR complex, R wave >7 mm


• ✓ V5 or V6: R/S ratio <1


• ✓ Secondary ST-T segment changes (ST depression or T wave inversion) in right precordial leads (V1-V2)


• ✓ Note: Posterior or inferoposterolateral myocardial infarction can mimic RVH. Factors favoring RVH include concomitant right axis deviation and T wave inversion in V1-V2, while the presence of inferior Q waves favor posterior infarction.

Combined ventricular hypertrophy

• ✓ Exists when criteria for isolated left and right ventricular hypertrophy are met


• ✓ Suspect when criteria for LVH is present with a QRS axis >90° or criteria for right atrial enlargement exists


• ✓ R/S ratio ~1 in both V3 and V4 (Katz-Wachtel phenomenon)

Right bundle branch block (RBBB), complete

• 
  
  
  
  • ✓ Prolonged QRS duration ≥120 ms in adults, >100 ms in children ages 4-16 years of age, and >90 ms in children <8 years of age
  
  
  • ✓ rsR’, rsr’, or rSR’ complexes in V1 or V2, with the secondary R wave (r’ or R’) usually wider than the initial R wave (r); some have a wide and often notched R wave pattern in V1 and/or V2
  
  
  • ✓ S wave duration greater than R wave duration, or S wave duration >40 ms in I and V6 in adults
  
  
  • ✓ Normal R wave peak time in V5 and V6, but >50 ms in V1
  
  
  
  

*The first 3 criteria should be present to make the diagnosis. When a pure dominant R wave with or without a notch is present in V1, the last criteria should be satisfied.

• ✓ Note: RBBB results in secondary ST-T segment changes (ST depression or T wave inversion) unrelated to ischemia in V1-V2. This can be seen in normal adults without structural heart disease; however, in the setting of known coronary artery disease, RBBB carries a 2-fold increase in mortality.

Right bundle branch block (RBBB), incomplete

• ✓ QRS duration: 110-119 ms in adults, 90-100 ms in children 4-16 years of age, and 86-90 ms in children <8 years of age


• ✓ Other criteria are the same as for complete RBBB: (1) rsR’, rsr’, or rSR’ complexes in V1 or V2, with the secondary R wave (r’ or R’) usually wider than the initial R wave (r); few patients may have a wide and often notched R wave pattern in V1 and/or V2; (2) S wave with duration greater than R wave, or S wave duration >40 ms in I and V6 in adults; (3) Normal R peak time in V5 and V6, but >50 ms in V1


• ✓ Note: Incomplete RBBB pattern may occur in the absence of heart disease, particularly when V1 is recorded higher than or to the right of normal position and r’ is <20 ms.

Left anterior fascicular block (LAFB)

• ✓ Mean ventricular (QRS) axis between -45° and -90° in adults with a mean QRS duration <120 ms


• ✓ Typically qR complexes in I and aVL, along with rS complexes in II, aVF, and III


• ✓ qR pattern in aVL with >45 ms delay from beginning of QRS complex to peak of R wave


• ✓ Absence of other causes of left axis deviation (e.g. inferior myocardial infarction, left ventricular hypertrophy)


• ✓ Note: The entire left bundle conduction system of the heart is made up of a left anterior and posterior fascicle. The left anterior fascicle supplies fibers to the anterior and lateral walls of the left ventricle.


• ✓ Note: The above criteria do not apply to patients with congenital heart disease in whom left axis deviation is present in infancy.

Left posterior fascicular block (LPFB)

• ✓ Mean ventricular (QRS) axis between +110° and +180° in adults with a mean QRS duration <120 ms


• ✓ Typically rS complexes in I and aVL, along with qR complexes in II, aVF, and III


• ✓ Absence of other causes of right axis deviation (e.g. lateral myocardial infarction, dextrocardia, right ventricular hypertrophy)


• ✓ Note: The entire left bundle conduction system of the heart is made up of an left anterior and posterior fascicle. The left posterior fascicle supplies fibers to the posterior and inferior wall of the left ventricle. It is shorter and thicker than the left anterior fascicle and receives dual blood supply from both the left and right coronary arteries. Multivessel coronary artery disease is the most common cause of left posterior fascicular block.

Left bundle branch block (LBBB), complete

• ✓ Mean QRS duration ≥120 ms in adults, >100 ms in children 4-16 years of age, and >90 ms in children <4 years of age


• ✓ Late QRS complex forces should be negative (i.e. terminal S wave) in V1


• ✓ Broad notched or slurred R wave in I, aVL, V5, and V6, with an occasional RS pattern in V5-V6 attributed to displaced transition of QRS complex


• ✓ Absence of q waves in I, V5, and V6, but narrow q waves may be present in aVL in the absence of myocardial pathology


• ✓ Delayed onset of intrinsicoid deflection (>60 ms from beginning of QRS complex to peak of R wave) in V5-V6 but normal in V1-V3 when small initial r waves can be discerned in these leads


• ✓ Note: In the setting of a LBBB, ST and T waves are usually opposite in direction (discordant) to the QRS complex. Positive T waves in leads with upright QRS complexes may be normal (positive concordance). Depressed ST segments and/or negative T waves in leads with negative QRS complexes (negative concordance) are typically abnormal and may even represent myocardial injury. The appearance of a LBBB may change the mean QRS axis in the frontal plane rightward, leftward, or superiorly; this may occur in a rate-dependent manner.

Left bundle branch block (LBBB), incomplete

• ✓ Mean QRS duration between 110-119 ms in adults, between 90-100 ms in children 8-16 years of age, and between 80-90 ms in children <8 years of age


• ✓ Late QRS complex forces should be negative (i.e. terminal S wave) in V1


• ✓ Presence of left ventricular hypertrophy pattern


• ✓ Delayed onset of intrinsicoid deflection (>60 ms from beginning of QRS complex to peak of R wave) in V4, V5, and V6


• ✓ Absent q waves in I, V5, and V6

Intraventricular conduction disturbance, nonspecific type

• ✓ Mean QRS duration ≥120 ms in adults, >100 ms in children 8-16 years of age, and >90 ms in children <8 years of age


• ✓ Specific criteria for right or left bundle branch block not met

Functional (rate-related) aberrancy

• ✓ Mean QRS duration >120 ms in the setting of rapid heart rates, but returns to normal QRS duration at slower heart rates

Anterolateral MI, age recent or probably acute

• ✓ Pathological Q waves (must be ≥30 ms wide and ≥0.1 mV deep in amplitude or QS complex) in anterolateral leads (V2-V6, I, aVL)


• ✓ Evidence of acute or evolving myocardial injury (i.e. ST-elevation in two contiguous leads ≥2 mm in men or ≥1.5 mm in women in V2-V3 and/or ≥1 mm in V4-V6, I, and aVL)


• ✓ Note: Only use this diagnosis when both (1) pathological Q waves and (2) ST-elevation are present. If only ST-elevation is present (without pathological Q waves), ST and/or T wave abnormalities suggesting myocardial injury should be used instead.

Anterolateral MI, age indeterminate or probably old

• ✓ Pathological Q waves (must be ≥30 ms wide and ≥0.1 mV deep in amplitude or QS complex) in anterolateral leads (V2-V6, I, aVL)


• ✓ No evidence of acute or evolving myocardial injury (i.e. no ST-elevation)

Anterior or anteroseptal MI, age recent or probably acute

• ✓ Pathological Q waves (must be ≥30 ms wide and ≥0.1 mV deep in amplitude or QS complex) in anterior (V2-V4) or anteroseptal (V1-V4) leads; Q wave width may only be 20 ms wide in V2-V3


• ✓ Evidence of acute or evolving myocardial injury (i.e. ST-elevation in two contiguous leads ≥2 mm in men or ≥1.5 mm in women in V2-V3 and/or ≥1 mm in other anterior or anteroseptal leads)


• ✓ Note: Only use this diagnosis when both (1) pathological Q waves and (2) ST-elevation are present. If only ST-elevation is present (without pathological Q waves), ST and/or T wave abnormalities suggesting myocardial injury should be used instead.

Anterior or anteroseptal MI, age indeterminate or probably old

• ✓ Pathological Q waves (must be ≥30 ms wide and ≥0.1 mV deep in amplitude or QS complex) in anterior (V2-V4) or anteroseptal (V1-V4) leads; Q wave width may only be 20 ms wide in V2-V3


• ✓ No evidence of acute or evolving myocardial injury (i.e. no ST-elevation)

Lateral MI, age recent or probably acute

• ✓ Pathological Q waves (must be ≥30 ms wide and ≥0.1 mV deep in amplitude or QS complex) in lateral leads (I, aVL, V5-V6)


• ✓ Evidence of acute or evolving myocardial injury (i.e. ST-elevation ≥1 mm in two contiguous lateral leads)


• ✓ Note: Only use this diagnosis when both (1) pathological Q waves and (2) ST-elevation are present. If only ST-elevation is present (without pathological Q waves), ST and/or T wave abnormalities suggesting myocardial injury should be used instead.

Lateral MI, age indeterminate or probably old

• ✓ Pathological Q waves (must be ≥30 ms wide and ≥0.1 mV deep in amplitude or QS complex) in lateral leads (I, aVL, V5-V6)


• ✓ No evidence of acute or evolving myocardial injury (i.e. no ST-elevation)

Inferior MI, age recent or probably acute

• ✓ Pathological Q waves (must be ≥30 ms wide and ≥0.1 mV deep in amplitude or QS complex) in at least two inferior leads (II, III, aVF)


• ✓ Evidence of acute or evolving myocardial injury (i.e. ST-elevation ≥1 mm in two contiguous inferior leads)


• ✓ Note: Only use this diagnosis when both (1) pathological Q waves and (2) ST-elevation are present. If only ST-elevation is present (without pathological Q waves), ST and/or T wave abnormalities suggesting myocardial injury should be used instead.

Inferior MI, age indeterminate or probably old

• ✓ Pathological Q waves (must be ≥30 ms wide and ≥0.1 mV deep in amplitude or QS complex) in at least two inferior (II, III, or aVF) leads


• ✓ No evidence of acute or evolving myocardial injury (i.e. no ST-elevation)

Posterior MI, age recent or probably acute

• ✓ Initial R wave >40 ms in width and with R/S ratio >1 in V1-V2, with a concordant positive T wave in the absence of a conduction defect


• ✓ Evidence of acute posterior injury as suggested by ST-segment depression >1-2 mm in V1-V2


• ✓ Note: Since none of the leads in a standard 12-lead ECG overlie the posterior region of the heart, there will be no ST-elevation to suggest acute, isolated, posterior injury. Instead, the precordial leads V1-V2 serve as a mirror image, with tall R waves in these leads being equivalent to posterior Q Waves and ST-depression in these leads being equivalent to posterior injury.

Posterior MI, age indeterminate or probably old

• ✓ Initial R wave >40 ms in width and with R/S ratio >1 in V1-V2, with a concordant positive T wave in the absence of a conduction defect


• ✓ No evidence of acute posterior injury as suggested by ST-segment depression >1-2 mm in V1-V2


• ✓ Exclude other causes of tall R waves in V1-V2 (e.g. right ventricular hypertrophy with associated marked right axis deviation)

Normal variant, early repolarization

• ✓ Elevated take-off of ST-segment at J point (junction between QRS complex and start of ST segment)


• ✓ Concave appearance of ST segment followed by an upright T wave


• ✓ Distinct notch or slur on downstroke of R wave


• ✓ Most commonly seen in V2-V5; sometimes in inferior limb leads (II, III, aVF)


• ✓ No reciprocal ST-segment depression exists


• ✓ Note: A mild degree of ST-elevation exists often in normal healthy adults in the precordial leads.

Normal variant, juvenile T waves

• ✓ Inverted, asymmetric T waves that are typically not deep in V1-V3 only, found in healthy young adults


• ✓ Upright T waves in I, II, and V5-V6

Nonspecific ST and/or T wave abnormalities

• ✓ Mild, <1 mm of ST-segment depression or elevation, and/or


• ✓ Slightly inverted (<2 mm) or flattened T wave

ST and/or T wave abnormalities suggesting myocardial ischemia

• ✓ >1 mm of horizontal or down-sloping ST-segment depression, and/or


• ✓ T-wave inversion ≥2 mm

ST and/or T wave abnormalities suggesting myocardial injury

• ✓ >1 mm ST segment elevation in at least 2 contiguous leads, or


• ✓ >1 mm horizontal or down-sloping ST segment depression in leads V1-V2 (suggesting posterior injury)


• ✓ Note: The repolarization abnormalities in the setting of acute myocardial infarction are usually predictable. Hyperacute T waves (present for minutes) are followed by the development of ST segment elevation. As the infarction evolves, ST segments will decrease and T waves will often invert. Pathological Q waves develop hours to days following the infarction.


• ✓ Use this code in the setting of ST-segment elevation only when pathological Q waves do not exist. When both (1) Q waves and (2) ST-elevation are present together, code the relevant acute Q wave infarction. Likewise, if you code for an acute Q wave infarction, there is no need to secondarily code ST and/or T wave abnormalities suggesting myocardial injury, as this diagnosis is already implied by the primary diagnosis.

ST and/or T wave abnormalities suggesting electrolyte disturbances

• ✓ Peaked T waves due to hyperkalemia


• ✓ ST-T segment depression and/or flattened T waves due to hypokalemia

ST and/or T wave abnormalities secondary to hypertrophy

• ✓ ST-T segment displacement opposite in direction (discordant) to QRS


• ✓ Note: Left ventricular hypertrophy results in down-sloping ST-segment depression and T wave inversion in I, V5, and V6, as well as subtle ST-segment elevation (<1 mm) in V1-V2. Right ventricular hypertrophy results in ST-T segment depression and T-wave inversion in V1-V3.

Prolonged QT interval

• ✓ In general, corrected QT interval (QTc): men >450 ms, women >460 ms


• ✓ Prolonged QT interval will NOT be used if the heart rate is >100 beats/min


• ✓ QTc cutoffs for QRS duration <120 ms: men ≥470 ms, women ≥480 ms; “QT Alert” if ≥500 ms


• ✓ QTc cutoffs for QRS duration ≥120 ms: QTc ≥500 ms; “QT Alert” if ≥550 ms


• ✓ Note: Avoid coding prolonged QT with atrial fibrillation, atrial flutter, or atrial tachycardia (unless ventricular paced)


• ✓ QTc = actual QT interval divided by the square root of the RR interval duration measured in seconds (Bazett’s formula)


• ✓ Note: QT interval should ideally be measured in the lead with the longest QT interval, as long as that lead has an easily visible T wave with distinct termination

Prominent U waves

• ✓ U wave amplitude >1.5 mm


• ✓ Associated conditions: hypokalemia, hypothermia, left ventricular hypertrophy, drugs (e.g. digitalis, quinidine, amiodarone)

Brugada syndrome

• ✓ Pseudo-right bundle branch block and ST-segment elevation in V1-V3


• ✓ Type 1: elevated ST segment descending with upward convexity (coved type) to an inverted T wave


• ✓ Type 2: elevated ST segment descending initially towards the baseline (but remaining ≥1 mm above baseline) and rising again to an upright or biphasic T wave (saddle-back type)


• ✓ Type 3: similar configuration to type 2, but ST-segment elevation ≥1 mm in type 2 and <1 mm in type 3


• ✓ Note: Brugada syndrome has been identified as a cause of sudden cardiac death in structurally normal hearts. Mutations in the SCN5A gene, resulting in a loss-of-function of cardiac sodium channels, have been found in up to one-fourth of families with Brugada syndrome

Digitalis effect

• ✓ Sagging concave upward ST-T segment depression


• ✓ Prolonged PR interval, shortened QT interval, and prominent U wave


• ✓ T wave may be flattened, inverted, or biphasic

Digitalis toxicity

• ✓ Most commonly results in atrial tachycardia, atrial fibrillation with complete heart block and an accelerated junctional rhythm, second- or third-degree atrioventricular block, or bi-directional ventricular tachycardia


• ✓ Note: Digitalis toxicity may be exacerbated by hypokalemia, hypomagnesemia, or hypercalcemia. Cardioversion of atrial fibrillation in the setting of digitalis toxicity can result in prolonged asystole or ventricular fibrillation, and therefore, is contraindicated.

Antiarrhythmic drug effect

• ✓ Prolonged QT interval, prominent U waves, and/or non-specific ST-T wave abnormalities

Antiarrhythmic drug toxicity

• ✓ Prolonged QT interval, ventricular arrhythmias (e.g. Torsades de pointes), AV block, and/or sinus arrest

Hyperkalemia

• ✓ Tall, peaked, narrow T waves


• ✓ Shortened QT interval and ST-T segment depression


• ✓ QRS widening and/or bundle branch block


• ✓ Bradycardia and sinus arrest


• ✓ Ventricular tachycardia and fibrillation

Hypokalemia

• ✓ Prominent U waves


• ✓ Prolonged QT interval (occasionally)


• ✓ ST-T segment depression and flattened T waves


• ✓ Various degrees of AV block


• ✓ Ventricular tachycardia and fibrillation

Hypercalcemia

• ✓ Shortened QT interval


• ✓ May prolong PR interval

Hypocalcemia

• ✓ Prolonged QT interval

Atrial septal defect, secundum

• ✓ Incomplete right bundle branch block (typical RSR’ or rSR’ complex in V1 with a QRS duration <120 ms)


• ✓ Right axis deviation (mean QRS axis >110°)


• ✓ Note: Ostium secundum atrial septal defects make up ~70% of all atrial septal defects.

Atrial septal defect, primum

• ✓ Incomplete right bundle branch block (typical RSR’ or rSR’ complex in V1 with a QRS duration <120 ms)


• ✓ Left axis deviation (mean QRS axis >-30°)


• ✓ Note: Ostium primum atrial septal defects make up ~15% of all atrial septal defects. They are associated with cleft anterior mitral valve, mitral regurgitation, and Down’s syndrome.

Dextrocardia, mirror image

• ✓ P wave, QRS complex, and T wave are inverted (upside down) in I and aVL


• ✓ Reverse R wave progression (R wave amplitude greatest in V1 and gets progressively smaller as you move towards V6)


• ✓ Note: Lead reversal can give the appearance of dextrocardia in the limb leads. However, reverse R wave progression should not exist in the setting of limb lead reversal.

Chronic lung disease

• ✓ Right ventricular hypertrophy, right axis deviation (mean QRS axis >+100°), poor R wave progression, and/or low voltage

Acute cor pulmonale including pulmonary embolus

• ✓ S1Q3T3 (large S wave in I, pathological Q wave in III, and T-wave inversion in III) is associated with right ventricular dilation and strain (present in <15-30% of acute pulmonary embolism)


• ✓ Right axis deviation (mean QRS axis >+100°), right bundle branch block, T wave inversion extending from V1-V4, non-specific ST-T segment abnormalities, and/or right atrial enlargement (P-pulmonale) may also be present

Pericardial effusion

• ✓ Low voltage and/or electrical alternans (not very sensitive or specific)

Acute pericarditis

• ✓ Diffuse ST-segment elevation and PR-segment depression


• ✓ aVR +/- V1: ST-segment depression and PR segment elevation


• ✓ Note: If there is diffuse ST-T segment elevation in both the inferior (II, III, aVF) and lateral (I, avL) limb leads, a more global process (e.g. pericarditis) is typically the etiology. ST-elevation secondary to acute myocardial infarction usually involves more focal elevation in the distribution of a single coronary artery with associated reciprocal ST-T segment depression.

Hypertrophic cardiomyopathy

• ✓ Abnormal QRS complex characterized by large amplitude QRS (left ventricular hypertrophy), pathological Q waves (pseudo-infarct pattern in the inferior, anterior, or lateral leads), and/or a tall R wave in V1 simulating right ventricular hypertrophy


• ✓ Left axis deviation (mean QRS axis >-30°) in ~20% of patients


• ✓ Nonspecific ST-T segment abnormalities or ST-T segment changes secondary to ventricular hypertrophy


• ✓ Left atrial abnormalities


• ✓ Note: Apical variant of hypertrophic cardiomyopathy results in deep T wave inversions in V4-V6.

Central nervous system disorder

• ✓ Large upright or deeply inverted T waves (usually in precordial leads, but can be diffuse)


• ✓ Prolonged QT interval and prominent U waves


• ✓ Note: ECG findings in central nervous system disease can mimic those seen in the setting of myocardial infarction (focal ST-T segment elevation and/or pathological Q waves) and pericarditis (diffuse ST-segment elevation). Almost any rhythm abnormality can also be present (e.g. sinus tachycardia, junctional rhythm, bradycardia, ventricular tachycardia).

Hypothermia

• ✓ Rhythm is typically sinus bradycardia or atrial fibrillation


• ✓ Prolongation of PR, QRS, and QT intervals


• ✓ Osborne (J) wave: late upright terminal deflection of the QRS complex that increases in amplitude as temperature declines

Myxedema

• ✓ Low QRS voltage in all leads and/or electrical alternans


• ✓ Sinus bradycardia


• ✓ Frequently associated with pericardial effusion


• ✓ Note: Myxedema is a skin and tissue disorder caused by a prolonged hypothyroid state.

Sick sinus syndrome

• ✓ Marked sinus bradycardia, sinus arrest, or sinoatrial exit block


• ✓ May also be characterized by prolonged sinus node recovery time after premature atrial complexes or associated with tachy-brady syndrome

Atrial or coronary sinus pacing

• ✓ Pacemaker stimulus followed by atrial depolarization


• ✓ If the intrinsic sinoatrial rate falls below the pacemaker rate, then atrial pacemaker spikes will occur at a constant (A-A) interval

Ventricular demand pacemaker (VVI), normally functioning

• ✓ Pacemaker stimulus followed by a QRS complex of different morphology than the intrinsic QRS complex


• ✓ VVI mode: paces in the ventricle, senses in the ventricle, and inhibits itself from firing if it senses an intrinsic QRS complex

Dual-chamber pacemaker (DDD), normally functioning

• ✓ DDD mode: paces and senses in both the atrium and ventricle, and inhibits itself from firing if intrinsic atrial or ventricular activity is recognized

Pacemaker malfunction, not constantly capturing (atrium or ventricle)

• ✓ Pacemaker stimulus without appropriate depolarization (at a time interval when the myocardium is not refractory)


• ✓ May be caused by lead fracture, perforation, or displacement; increased pacing threshold secondary to myocardial scar; medications (e.g. flecainide, amiodarone); or electrolyte abnormalities (e.g. hyperkalemia)

Pacemaker malfunction, not constantly sensing (atrium or ventricle)

• ✓ Failure of pacemaker lead to recognize intrinsic depolarization, resulting in attempted pacing at inappropriate intervals (e.g. immediately following a native QRS complex when the myocardium is refractory)

Paced morphology consistent with biventricular pacing/cardiac resynchronization

• ✓ Dual ventricular pacing spikes, typically occurring within 80 ms of each other, resulting from two separate pacing leads (one in the right ventricle and the other placed epicardially via the coronary sinus)


• ✓ May result in a paced right bundle branch block QRS morphology if the epicardial lead is being activated first (usually standard RV apical pacing results in a paced left bundle branch block QRS morphology)

Bigeminy

• ✓ Every other beat is a premature complex (i.e. repeating pattern of 1 normal beat followed by 1 premature beat)

Trigeminy

• ✓ Every third beats is a premature complex (i.e. repeating pattern of 2 normal beats followed by a premature beat)

Short PR interval

• ✓ PR interval <120 ms