approach to ECG: HEARTS


How do you read an ECG? The standard answer is “rate, rhythm, axis, ST changes,” but what does this mean and how is this useful? We need an approach to ECG that is systematic. Think about HEARTS

HEART RATE/RHYTHM: if you start by categorizing the rhythm based on rate, regularity, and width, you can then use the presence/absence/type of P wave to pinpoint the rhythm



ELECTRICAL CONDUCTION: look at conduction intervals, which can be altered by electrical, structural, metabolic or toxic causes

  • P wave absent: C(MI, SSS, myocarditis) E(hyperkalemia)
  • PR:
    • depression: pericarditis
    • short: accessory (LGL, WPW plus delta)
    • long: AV node block: myo/endocarditis, MI, hyperkalemia, beta blocker
  • QRS wide: “WIDE”
    • WPW
    • Interventricular conduction delay, RBBB, LPFB, LAFB, LBBB
    • Drug: TCA, cocaine
    • Electrolyte: hyperkalemia
  • QT: decrease (hypercalcemia), increase (hypoK/Ca/Mg/thyroid, anti-biotic/arrhythmic/depressant/psychotic/histamine, congenital)



  • normal
  • left axis: (+I, -aVF): “LEFT”
    • LVH
    • Electrode pacing
    • Fascicle: LAFB, LBBB
    • Thrombosis: inferior Q
  • right axis: (-I, +aVF): “RIGHT”
    • RVH
    • Ischemic: lateral Q
    • Gradient pulmonary pressure: pulmonary HTN
    • Hemiblock: LPFB
    • Thrombosis: PE



  • size
    • increased: hypertrophy
    • decreased: adipose/breast tissue, emphysema, pericardial effusion (+/- electrical alternans)
  • progression
    • late: CAD, CMO, aneurysm
    • early (tall R in V1): “R-WAVED”
      • RBBB
      • WPW
      • Acute MI (posterior)
      • Ventricular hypertrophy (RVH), strain
      • Electrode misplaced
      • Dextrocardia, muscular Dystrophy


TENSION (hypertrophy from chronic hypertension)

  • RAE: r/o tricuspid valvulopathy or pulmonary hypertension
  • LAE r/o mitral valvulopathy or LV failure
  • RVH: tall R in V1-2: r/o other causes for early R-wave progression
  • LVH: high voltages, poor R-progression, lateral lead strain


ST AND OTHER CHANGES: consider these last because they can be altered by rate, conduction, and tension changes

  • Q wave: H E (LBBB) A R (cardiomyopathy, aneurysm) T (LVH, HOCM), S (MI)
  • Epsilon wave: ARVD
  • ST elevation: “ELEVATIONS”
    • Electrolyte (hyperkalemia)
    • fixed
      • LBBB (r/o new or old + Sgarbosa)
      • Early repolarization (J point elevation)
      • Ventricular hypertrophy
      • Aneurysm
    • dynamic
      • Thrombosis: STEMI
      • Inflammation: pericarditis
      • Osborn wave (hypothermia)
      • Non-occlusive spasm
      • Sudden cardiac death: Brugada
  • ST depression: “DEPRESSED”
    • chronic
      • Dilated CMO
      • Enlarge LV
    • Electrolyte
      • Potassium loss
    • Cardiovascular
      • Reciprocal ST elevation
      • Embolism
      • Subendocardial, including de Winter T wave (early STEMI)
      • Shock
    • neuro
      • Encephalon bleed
    • toxic
      • Dig tox
  • T wave: elevation (hyperkalemia, early ischemia); depression (LVH, ischemia)
  • T wave inversion: “FLIPED”:
    • chronic
      • Fascicle block (LBBB/RBBB),
      • LVH
    • cardiovascular
      • Ischemia, including Wellens (LAD)
      • Pulmonary Embolism
    • toxic
      • Dig
  • U wave: Electrolyte (hypokalemia, hypercalcemia), Intox (dig, amio)





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