Written and checked by licensed physicians—but use at your own risk. Read our disclaimer.

banner image

amboss

Trusted medical answers—in seconds.

Get access to 1,100+ medical articles with instant search
and clinical tools.

Try free for 5 days

ECG

Last updated: September 24, 2020

Summary

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 article 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
    • 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
  • 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

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 thorough, algorithmic approach to ECG interpretation that assesses every aspect of the ECG ensures that no abnormalities are 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).
  • 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 (5 mm) squares 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 the number of QRS complexes on the rhythm strip of a standard ECG by 5.
      • 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.
    • A more exact method to calculate the heart rate (HR)
      • If paper speed is 25 mm/s: HR = 150/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 frequency, regularity, and relationships between the P waves and QRS complexes.
  • Implementation
    1. P wave assessment
      1. Are they visible in any lead?
      2. Determine the atrial rate (i.e., PP interval).
      3. Determine the morphology of the P waves.
    2. Relationship of P waves to QRS complexes
      • A 1:1 relationship of P with QRS is normal. If not present:
      • A P wave before every QRS, and a QRS after every P are normal.
    3. QRS morphology
      • Normal duration: 0.07–0.10 seconds
      • Wide QRS: > 0.12 seconds or 3 small squares
    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 morphology of the P waves
  2. A regular QRS complex follows every P wave.
  3. Normal, 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 complexes in leads I and aVF:
Axis Lead Degrees Common causes
I aVF
Left-axis deviation + - (-30°)–(-90°) Normal variant (especially with age), LVH, LBBB, LAFB, inferior MI
Normal + +

(-30°)–(+90°)

Normal axis
Right-axis deviation - + (+90°)–(+180°) Normal variant, 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 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:[12][13]

Interpretation of the QRS complex

  • The QRS complex represents depolarization of the ventricles and corresponds approximately to ventricular systole.
  • Interpretation of the duration
    • ≤ 100 ms = normal
    • 100–110 ms = incomplete bundle branch block (BBB)
    • ≥ 120 ms = complete bundle branch block (BBB)

The name William Morrow can help you identify LBBB and RBBB by looking at the QRS morphology in V1 and V6. In LBBB the QRS looks like a W in V1 and an M in V6 (WiLLiaM), in RBBB the QRS looks like an M in V1 and a W in V6 (MoRRoW).

  • Interpretation of amplitude
    • Amplitude of the QRS complex in the precordial leads is used to assess for ventricular hypertrophy
    • Various 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

The dominant waves seen in right ventricular hypertrophy can be remembered with the phrase “R1ght 5ignS” (R in V1 and S in V5)

Patients with ventricular 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:[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

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]

T wave

Physiological

Pathological

T-wave inversion

Peaked T wave

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]

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]

References

  1. Podrid PJ. Ambulatory ECG Monitoring. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/ambulatory-ecg-monitoring. Last updated: January 22, 2016. Accessed: February 22, 2017.
  2. Muruganathan A, Geetha T. Medicine Update 2013. Association of Physicians of India ; 2013
  3. EKG Basics #2 - The Precordial Chest Leads. http://jan.ucc.nau.edu/~daa/heartlung/lectures/ekg2.html. Updated: December 1, 2002. Accessed: April 18, 2018.
  4. Meek S, Morris F. ABC of clinical electrocardiography - Introduction - Leads, rate, rhythm, and cardiac axis. BMJ. 2002; 324 (7334): p.415-8.
  5. Prutkin JM. ECG Tutorial: Basic Principles of ECG Analysis. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/ecg-tutorial-basic-principles-of-ecg-analysis. Last updated: October 29, 2015. Accessed: February 22, 2017.
  6. Sauer WH. Normal Sinus Rhythm and Sinus Arrhythmia. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/normal-sinus-rhythm-and-sinus-arrhythmia. Last updated: November 15, 2016. Accessed: February 22, 2017.
  7. QRS Complex Morphology. https://lifeinthefastlane.com/ecg-library/basics/qrs-complex-morphology/. Updated: April 17, 2017. Accessed: April 18, 2018.
  8. QRS Complex. https://www.healio.com/cardiology/learn-the-heart/ecg-review/ecg-interpretation-tutorial/qrs-complex. . Accessed: April 18, 2018.
  9. Left Axis Deviation. http://lifeinthefastlane.com/ecg-library/basics/left-axis-deviation/. Updated: February 22, 2017. Accessed: February 22, 2017.
  10. Right Axis Deviation. http://lifeinthefastlane.com/ecg-library/basics/right-axis-deviation/. Updated: February 22, 2017. Accessed: February 22, 2017.
  11. Gertsch M. The ECG - A Two-Step Approach to Diagnosis. Springer Science & Business Media ; 2003
  12. Christensen B. Normal Electrocardiography (ECG) Intervals. In: Christensen B, Normal Electrocardiography (ECG) Intervals. New York, NY: WebMD. http://emedicine.medscape.com/article/2172196. Updated: December 11, 2014. Accessed: February 22, 2017.
  13. Prutkin JM. ECG Tutorial: Atrioventricular Block. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/ecg-tutorial-atrioventricular-block. Last updated: March 5, 2018. Accessed: April 20, 2018.
  14. Goldberger AL. Pathogenesis and diagnosis of Q waves on the electrocardiogram. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/pathogenesis-and-diagnosis-of-q-waves-on-the-electrocardiogram. Last updated: May 12, 2015. Accessed: February 22, 2017.
  15. Q Wave. https://lifeinthefastlane.com/ecg-library/basics/q-wave/. Updated: April 17, 2017. Accessed: April 20, 2018.
  16. Prutkin JM. ECG Tutorial: Intraventricular Block. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/ecg-tutorial-intraventricular-block. Last updated: August 2, 2016. Accessed: April 18, 2018.
  17. Prutkin JM. ECG Tutorial: Chamber Enlargement and Hypertrophy. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/ecg-tutorial-chamber-enlargement-and-hypertrophy. Last updated: May 6, 2016. Accessed: April 20, 2018.
  18. Kashou AH, Kashou HE. Rhythm, ST Segment. StatPearls. 2017 .
  19. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  20. Le T, Bhushan V. First Aid for the USMLE Step 1 2015. McGraw-Hill Education ; 2014
  21. Wylie JV, Garlitski AC. Brugada Syndrome: Epidemiology and Pathogenesis. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/brugada-syndrome-epidemiology-and-pathogenesis. Last updated: June 23, 2016. Accessed: February 22, 2017.
  22. Wylie JV, Garlitski AC. Brugada Syndrome: Clinical Presentation, Diagnosis, and Evaluation. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/brugada-syndrome-clinical-presentation-diagnosis-and-evaluation. Last updated: January 5, 2017. Accessed: February 22, 2017.
  23. Wylie JV, Garlitski AC. Brugada Syndrome: Prognosis, Management, and Approach to Screening. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/brugada-syndrome-prognosis-management-and-approach-to-screening. Last updated: June 23, 2016. Accessed: February 22, 2017.
  24. Prutkin JM. ECG Tutorial: Myocardial Ischemia and Infarction. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/ecg-tutorial-myocardial-ischemia-and-infarction. Last updated: March 8, 2016. Accessed: February 22, 2017.
  25. Prutkin JM. ECG Tutorial: ST and T Wave Changes. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/ecg-tutorial-st-and-t-wave-changes. Last updated: August 18, 2016. Accessed: April 20, 2018.
  26. Pollehn T, Brady WJ, Perron AD, Morris F. The electrocardiographic differential diagnosis of ST segment depression. EMJ. 2002; 19 (2): p.129-135. doi: 10.1136/emj.19.2.129 . | Open in Read by QxMD
  27. T Wave. http://lifeinthefastlane.com/ecg-library/basics/t-wave/. Updated: February 22, 2017. Accessed: February 22, 2017.
  28. Said SA, Bloo R, de Nooijer R, Slootweg A. Cardiac and non-cardiac causes of T-wave inversion in the precordial leads in adult subjects: A Dutch case series and review of the literature. World J Cardiol. 2015; 7 (2): p.86. doi: 10.4330/wjc.v7.i2.86 . | Open in Read by QxMD
  29. Suki WN, Massry SG. Therapy of Renal Diseases and Related Disorders. Springer Science & Business Media ; 2012
  30. QT Interval. https://lifeinthefastlane.com/ecg-library/basics/qt_interval/. Updated: November 21, 2017. Accessed: April 23, 2018.
  31. van Noord C, Eijgelsheim M, Stricker BH. Drug- and non-drug-associated QT interval prolongation. Br J Clin Pharmacol. 2010; 70 (1): p.16-23. doi: 10.1111/j.1365-2125.2010.03660.x . | Open in Read by QxMD
  32. Nachimuthu S, Assar MD, Schussler JM. Drug-induced QT interval prolongation: mechanisms and clinical management. Ther Adv Drug Saf. 2012; 3 (5): p.241-253. doi: 10.1177/2042098612454283 . | Open in Read by QxMD
  33. Herold G. Internal Medicine. Herold G ; 2014