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Tags: ECG

ECG DDx

Narrow complex regular tachycardia

1. Sinus Tachycardia
   • One P-wave for every QRS
   • Upright P-waves in limb leads (I, II, III, aVF), & inverted P-wave in aVR
   • Maximum sinus node rate is ~ (220 bpm – Age)
2. Supraventricular Tachycardia (SVT)
   • No distinct P-waves. May be hidden or may follow the QRS complex (“retrograde atrial activity”)
   • Different types (AVRT AVNRT, junctional, etc.) but generally same treatment and management approach for emergency physicians
3. Atrial flutter with 2:1 Conduction
   • 2 atrial beats for every QRS
   • Saw tooth pattern, flipping the ECG upside down and paying attention to all 12 leads will help you identify subtle flutter waves
   • Most missed atrial tachyarrhythmia
   • Always consider when rate is 150 ± 20 bpm
   • Look for atrial activity: “spikey or pokey” T waves or deformed T waves suggestive of buried flutter waves
   • The Bix rule, described by cardiologist Harold Bix, states that if a T-wave is located halfway between two QRS complexes, there is a good chance that P-waves are also buried inside the QRS complexes, think atrial flutter!
   • Consider obtaining a Lewis lead ECG to better assess atrial activity when not clear on standard ECG

Regular Wide Complex Tachycardia

• Monomorphic Ventricular Tachycardia (VT)
  • Most common form of sustained VT
  • HR usually > 120-130 bpm
  • Wide QRS complexes (>120 ms), that should not be too wide (< 200 ms) in the absence of concurrent toxicologic or metabolic derangement
  • QRS complexes have same general appearance in monomorphic VT, as opposed to polymorphic VT (PMVT) where there is constant beat to beat variation in QRS morphology
  • Rhythm typically regular or “almost regular”, if obviously irregular consider atrial fibrillation with aberrant conduction & PMVT
  • May self-terminate, termed “sustained” if lasts > 30s
  • The sinus node continues to initiate atrial contraction independent of ventricular activity (AV dissociation) and may produce a capture beat or fusion beats. However, P waves may be difficult to detect or distinguish from artifact
• SVT with aberrant conduction (BBB, WPW)
  • No clear P-waves, mimics VT
  • If previous ECGs show known BBB in sinus rhythm identical with that during the tachycardia, suggests SVT with aberrancy
  • Safest to consider WCTs of uncertain origin as VT unless good evidence suggests a supraventricular origin, as the ECG cannot reliably distinguish between them
• Accelerated Idioventricular Rhythm (AIVR)
  • Ventricular rhythm with rate of 100-120 bpm, may mimic VT
  • Transient and suggestive of reperfusion, avoid antiarrhythmics
• Sinus tachycardia with Hyperkalemia
  • Look carefully for P-QRS complexes and peaked T waves
  • As hyperkalemia worsens, PR-interval prolongation and loss of P-waves may occur (sino-ventricular rhythm), mimicking VT
  • Really wide QRS complexes (> 200 ms) may be present, always consider hyperkalemia when the QRS complexes appear wider than typical VT
• Sinus tachycardia with Na+ channel blocker toxicity
  • Look carefully for P-QRS complexes, right axis deviation, and a terminal R wave in aVR
  • Severe toxicity may result in really wide QRS complexes (> 200 ms), always consider hyperkalemia & Na+channel blocker toxicity when the QRS seems too wide

Right axis deviation

• Ventricular ectopy
• Acute pulmonary hypertension (e.g., PE)
• Chronic pulmonary hypertension (g., COPD)
• Right ventricular hypertrophy
• hyperK
• Sodium channel blocker toxicity
• left posterior fascicular block
• Old lateral MI (from Q-waves in lead I)
• WPW (Type A)
• Lead misplacement / dextrocardia
• Normal variant in young kids & thin adults with horizontally positioned hearts

Wide QRS complex

• Ventricular beats/ectopy
• Paced beats
• Bundle branch blocks (LBBB, RBBB, etc.)
• Pre-excitation (e.g., WPW)
• Metabolic (e.g., hyperkalemia or severe acidosis)
• Sodium channel blocker toxicity (e.g., TCA, cocaine toxicity, etc.)
• Non-specific intraventricular conduction delay (e.g., LVH, cardiomyopathy)

Tall R wave in V1

• Ventricular beats/ectopy
• Incomplete/Complete RBBB
• Na+ channelopathies (e.g., TCAs, hyperkalaemia, Brugada syndrome, etc.)
• Posterior MI
• Pre-excitation (e.g., Type A WPW)
• Right ventricular hypertrophy (e.g., COPD, Pulmonary HTN, muscular dystrophy, etc.)
• Acute RV strain (PE)
• hypertrophic cardiomyopathy
• Dextrocardia, situs inversus
• Misplaced precordial lead

Poor R-wave Progression (PRWP) Differential

• Defined as a R-wave < 3 mm by lead V3
• 8 L’s of PRWP
  • LAD (Prior anteroseptal MI)
  • Lead misplacement
  • Left bundle branch block
  • Left ventricular hypertrophy
  • left anterior fascicular block
  • Low voltage
  • Long life (elderly)
  • Lungs (COPD)

ST-depression in anteroseptal leads

• Posterior STEMI
  • • Mirror image of septal STEMI in leads V1-V3
      • Large R waves (instead of Q waves)
      • ST-depression (instead of STE)
      • Upright T waves in V1-V3 (instead of inversions)
• Anteroseptal ischemia
• Right bundle branch block (RBBB)
• Severe Hypokalemia
• Miscellaneous

TWI

• Coronary artery disease (ischemia, reperfusion, Wellens waves)
• Pulmonary causes
  • (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
• Neurological causes (elevated intracranial pressure, intracranial hemorrhage, etc.)
• Post-tachycardia, post-shock, post-pacing (“cardiac memory”)
• ARVD (V1-V3)
• Brugada syndrome (V1-V2)
• Wide QRS complexes (BBB’s, PVC’s, Paced rhythms, WPW)
• High left ventricular voltage, LVH or RVH with strain pattern
• Pericarditis, myocarditis
• Vasospasm (cocaine, amphetamines, etc.)
• hyperK, hypokalemia
• Persistent juvenile T wave pattern, normal finding in pediatric ECGs (V1-V3)
• Mitral valve prolapse
• Normal finding in V1, aVR, and lead III

TWI V1-V2

• Anteroseptal ischemia
• Persistent juvenile T wave pattern
• Pulmonary embolism
• RVH with strain
• (I)RBBB
  • usually with ST depression, rsR’, and lateral s waves
• WPW
• Brugada syndrome
• ARVD
• Lead misplacement (V1/V2) placed too high on the chest
  • lead misplacement#V1-2 too high

long QT interval (greatest concern when QTc > 500ms)

• Electrolytes
  • Hypokalemia
  • Hypomagnesemia
  • Hypocalcemia
• Hypothermia
• ACS / cardiac ischemia
• Elevated ICP
• Medications (i.e., Sodium channel blocker toxicity)
• Congenital

Prolonged QT due to abnormal/prolonged T –waves

• Hypokalemia
• Hypomagnesemia
• Medications (i.e., sodium channel blocking drugs)
• Miscellaneous: Elevated ICP, Cardiac ischemia, Congenital

Prolonged QT due to prolonged ST-segment

• Hypocalcemia
• Hypothermia

Non-specific T wave abnormality
TWI <1mm, or flat

Inverted U wave

• U waves are normally small deflections that occur right after the T wave (typically in the same direction as the T wave and best seen in leads V2-V3)
• Normal U wave amplitude is generally ~10% of its associated T wave amplitude and tends to be inversely related to the heart rate
  • (best seen in bradycardia and difficult to appreciate when heart rate is > 90 bpm)
• U wave inversion, or negative U waves ( ≥0.5 mm depth) are abnormal in leads with upright T waves
• Inverted U waves usually occur in antero-lateral leads and are highly specific for the presence of heart disease
  • Most associated with:
    • Hypertensive heart disease
    • Aortic and mitral valvular disease
    • Ischemic heart disease
      • Unstable angina
      • Variant angina
• During exercise testing, U wave inversion was 93% specific (but only 21% sensitive) as a marker for LAD stenosis
  • Gerson, Circulation 1979
• In the setting of cardiac ischemia…
  • Inverted U waves are a specific sign of myocardial ischemia and may be an early marker for unstable angina and evolving MI
  • Association with LAD (or LMCA?) stenosis and the presence of LV dysfunction
  • May occur during pain or painless state

Electrical alternans vs. Respiratory variation

• Electrical alternans describes beat to beat alteration in height (amplitude), duration (interval length), or direction (up or down) of ECG complexes (usually the QRS complex)
• Respiratory variation can occur with the respiratory cycle as the heart shifts in position with inspiration and expiration, resulting in variation of the amplitude of QRS complexes, however not beat to beat as seen in electrical alternans

Early Repolarization vs. STEMI

• Both can have concave ST segment morphology
• Convex and horizontal ST segment morphology is seen in STEMI and not early repolarization
  • J (junction) point = is present in all ECGs and occurs at the junction of the QRS complex to the ST segment
  • The J point marks the end of the QRS complex and is often situated above the baseline, particularly in healthy young males
• Terminal QRS distortion is defined as the absence of both an S wave and J wave in either lead V2 or V3
  • S wave = any deflection at the end of the R wave that dipped below the level of the PQ junction
  • J wave = any positive deflection (notching or slurring) above the level of the ST segment at the J point
    • Distinct from the J point and classically seen in early repolarization and hypothermia

References