• Clinical science

ECG

Abstract

Electrocardiography (ECG) is an important diagnostic tool in cardiology. ECG uses external electrodes to measure the electrical conduction signals of the heart and record them as characteristic lines. These lines allow the axis, rate, and rhythm, as well as the amplitudes of specific parts of the heart (e.g., the P wave, PR interval, QRS complex, ST segment) to be examined–all important interpretive criteria. This learning card provides an overview of the most essential components of the ECG.

Procedure/application

General

  • Leads: A 12-lead ECG with six limb leads (I, II, III, aVL, aVF, aVR ) and six precordial leads (V1–V6) is standard.
  • Paper speed
    • For ECGs, a paper speed of 25 mm/s is usually used in the United States: 1 mm = 0.04 s
    • Alternatively, in other countries a paper speed of 50 mm/s is used: 1 mm = 0.02 s
    • Unfortunately, the grids on the graph paper are sometimes faded or not used at all!
  • Amplitude: 1 mm (vertical) = 0.1 mV

If you don't pay attention to the paper speed, it is easy to misinterpret the heart rate or duration of the cardiac cycle!

Holter monitor

  • Definition: : A continuous, ambulatory battery operated ECG worn by patients for 24-48 hours
  • Indications
  • Common metrics
    • Average, minimum, and maximum heart rate
    • Number of premature beats
    • Episodes of arrhythmia
    • Longest RR interval and any pauses > 3 seconds
    • ST segment changes
    • Patient-reported symptoms
    • Representative (e.g., hourly) ECG tracing samples

References:[1][2][3][4]

Interpretation/findings

  • When interpreting an ECG, it is important to keep the individual patient in mind and, if possible, to compare it with previous ECGs.
  • A personalized algorithmic approach to ECG interpretation that assesses every aspect of the ECG ensures pathologies are not overlooked.

Determination of heart rate and rhythm

Determination of the heart rate

  • The heart rate (i.e., the pulse felt on physical exam) can be calculated by assessing the QRS complexes on ECG (correlating with ventricular systole).
  • The atrial rate is sometimes calculated (e.g., in assessing some supraventricular arrhythmias). Calculated by applying the same methods to the P waves (correlating with atrial systole) that are used when assessing QRS complexes
  • Implementation
    • If the QRS rhythm is regular; (see determination of the heart rhythm below), then the heart rate can be estimated by dividing 300 by the number of “large” (e.g., 5 mm) boxes between successive QRS complexes, or by counting the number of QRS complexes in 6 seconds and multiplying by 10.
      • Careful! This method is only a rough estimate.
      • Only applies if paper speed is 25 mm/s
    • Alternatively, the heart rate may be estimated by multiplying 5 with the number of QRS complexes on the rhythm strip of a standard ECG.
      • Careful! This method of measuring the heart rate is not very precise and only for initial orientation.
      • Only applies to a paper speed of 25 mm/s. Multiply with 10 for a paper speed of 50 mm/s!
    • A more exact method to calculate the heart rate (HR)
      • If paper speed is 25 mm/s: HR = 150/RR interval in cm
      • If paper speed is 50 mm/s: HR = 300/RR interval in cm
      • The heart rate is often measured with an ECG ruler in clinical settings.
  • Interpretation

Determination of the heart rhythm

  • The heart rhythm is assessed by evaluating the appearance and relationship of the various waves (e.g., P, QRS, and T) on ECG.
  • Implementation
    1. P wave assessment
      1. ls it visible in any lead?
      2. Determine the atrial heart rate (i.e., PP interval).
      3. Determine the morphology of the P waves.
        • Sinus P waves are upright in I, II, aVF, and V4-V6.
        • Negative P wave in I, II, or aVF suggests ectopic rhythm.
        • Positive P wave in V1 suggests ectopy from the left atrium.
    2. Relationship of P to QRS
      1. A 1:1 relationship of P with QRS is normal. If not present:
      2. A P wave before every QRS, and a QRS after every P are normal.
        • If no QRS after a P → ectopic atrial beat or AV block
        • If QRS without preceding P → ectopic junctional or ventricular beat
    3. QRS morphology
      • Normal duration: 0.07–0.10 seconds
      • Wide QRS: > 0.12 seconds or 3 “small” blocks
      • If normal in all leads → supraventricular rhythm
        1. If wide (> 0.12 sec, or 3 “small” blocks) → aberrant conduction, pre-excitation, ventricular origin, or ventricular pacing
    4. Some arrhythmias have characteristic features which can help in diagnosis (see cardiac arrhythmias).
    5. Associate any findings with your patient (e.g., history of heart disease, drug ingestion, etc.)
  • Criteria for a sinus rhythm
    1. Normal configuration of the P waves
    2. A regular QRS complex follows every P wave.
    3. Constant PP and RR intervals

See also cardiac arrhythmias.

References:[5][6][7][8]

Determination of the axis

  • The axis represents the spread of intraventricular electrical activity projected along the frontal plane (determined from limb leads I, II, III, aVR, aVL, aVF).
  • The key here is to evaluate the QRS complex, and specifically whether it is positive or negative.
    • Positive: : if the area above the isoelectric line (i.e., the amplitude) is larger than the area beneath
    • Negative: : if the area below the isoelectric line is larger than the area above
  • The main QRS vector (position of the electrical axis of the heart) is close to the lead with the highest positive QRS amplitude.
  • The normal axis of the heart is between -30° and +90°.
  • A rapid approximation of the axis may be made by assessing the QRS in leads I and aVF:
Axis Leads Degrees Common causes
I aVF
Left-axis deviation + - (-30°)–(-90°) LVH, LBBB, LAFB, inferior MI
Normal + +

(-30°)–(+90°)

Normal axis
Right-axis deviation - + (+90°)–(+180°) RVH, LPFB, lateral MI, RV strain (e.g., PE), chronic lung disease (e.g., COPD)
Extreme right-axis deviation - - (-90°)–(-180°) Severe RVH, lateral MI

References:[5][9][10]

Interpretation of the P wave

P wave Interpretation Pathophysiology Possible etiology
  • Elevation of P ≥ 0.25 mV

P pulmonale

Effect of right atrial enlargement

  • Biphasic P wave
  • Prolongation of P > 0.10 s

P mitrale

Effect of left atrial enlargement

  • Biphasic morphology: elevation (≥ 0.25 mV) and prolongation (> 0.10 s)

P biatrial (combination of P mitrale and P pulmonale)

Effect of biatrial enlargement

References:[11]

Interpretation of the QRS complex

WiLLiaM MoRRoW

  • Interpretation of amplitude
    • Amplitude of the QRS complex in the precordial leads is used to assess for ventricular hypertrophy
    • Various unique grading criteria exist for electrocardiographic determination of ventricular hypertrophy. The Sokolow-Lyon criteria are utilized below:
      • Left ventricular hypertrophy (LVH): SV1 or 2 + RV5 or 6 ≥ 3.5 mV
      • Right ventricular hypertrophy (RVH): RV1 or 2 + SV5 or 6 ≥ 1.05 mV

R1ght 5ignS (R in V1 and S in V5) → Sign of right ventricular hypertrophy!

Remember that patients with myocardial hypertrophy may not exhibit these signs on their ECG: These may become apparent later in the course of the disease or they may even be absent in some cases (e.g., severe obesity). However, ECG changes associated with clinical signs confirm the diagnosis of hypertrophy!

References:[12][13]

Interpretation of the PR interval

  • The time between the beginning of the P wave and the beginning of the Q wave
  • The PR interval represents atrioventricular transmission.
PR interval Interpretation
PR interval ≤ 0.2 s Normal
PR interval > 0.2 s First-degree atrioventricular block
PR intervals become progressively longer (but PP intervals remain constant) until a dropped QRS complex occurs after a regular atrial depolarization. Second-degree AV block, Mobitz type I (Wenckebach)
Constant PR intervals (which are usually normal but may be prolonged) followed by one or more non-conducted P waves. Second-degree AV block, Mobitz type II
P waves and QRS complexes occur independently of each other, but in regular intervals → complete dissociation of P waves and QRS complexes. Third-degree AV block

References:[14][15]

Interpretation of the Q wave

Physiological

Pathological

A new pathological Q wave represents myocardial infarction until proven otherwise!
References:[16][17]

ST segment

Physiological

Pathological

ST elevation

Brugada pattern

Associated with Brugada syndrome: rare autosomal dominant condition that affects sodium channels and disturbs repolarization

  • Epidemiology: : most common in Asian males
  • Clinical features
    • Often an incidental finding; during a routine check, as patients are mostly asymptomatic
    • Syncope
    • Sudden cardiac death
  • Diagnosis
  • Treatment
    • Implantable cardiac defibrillator (ICD) placement
    • Screen all 1st-degree relatives annually with clinical exam and ECG
  • Complications

ST elevation from a descending R is likely caused by a myocardial infarction!

ST depression

References:[18][19][20][21][22][23][24][25][26]

Progression of ST elevation myocardial infarction (STEMI) on ECG

The stages of myocardial ischemia are associated with characteristic (but variable) ECG findings:

  1. Hyperacute T waves: very early and transient; usually have disappeared by the time ECG is performed
  2. ST elevation at the J point: point at which the QRS complex completes and returns to the isoelectric line (i.e., the intersection of the S wave and the ST segment)
  3. Progressive ST segment elevation, with added convexity
  4. ST merges with T wave; , forming a QRS-T segment; (i.e., tombstone): usually with associated reciprocal ST depressions (see ST depression)
  5. ST segment returns to isoelectric line, Q wave develops; , and R wave loses amplitude
  6. T-wave inversion
  7. Progressive Q wave deepening and R wave shrinkage
  8. T wave may or may not return to upright position

References:[23]

T wave

Physiological

Pathological

T-wave inversion

Peaked T wave

  • Tall, narrow, symmetrically-peaked
  • Differential diagnosis
    • Hyperkalemia
    • Hypermagnesemia
    • High vagal tone

Hyperacute T wave

Normally, if electric conduction in the heart is pathological (bundle branch block), repolarization is also disturbed → reliable evaluation of the ST segment or T wave is not possible!

New occurrence of a left bundle branch block associated with angina chest pain is defined as a STEMI!

References:[27][28][29]

QT interval

Physiological

Pathological

Prolongation of the QT interval

Possible differential diagnoses include:

Shortening of the QT interval

Possible differential diagnoses include:

References:[5][30][31][32]