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ECG

Last updated: September 21, 2021

Summary

Electrocardiography is an important diagnostic tool in cardiology. External electrodes are used to measure the electrical conduction signals of the heart and record them as characteristic lines on graph paper (an electrocardiogram; ECG). The interpretation of the amplitude and duration of these lines allows for the assessment of normal cardiac physiology as well as the detection of cardiac arrhythmias, conduction system abnormalities, or ischemia. This article provides an overview of the most essential components of the ECG.

Procedure/application

Overview ^[1]^[2]

Definition: An ECG represents a recording of the electrical activity of the heart that is captured via external electrodes and transcribed onto graph paper as ECG leads (for more information on the electrical activity of the heart, see “Conducting system of the heart”).
Electrodes
- Physical conductive pads attached to the patient's chest and limbs
- Detect the direction of the depolarization vectors
Leads : graphical representation of the depolarization vectors of the heart
- Six precordial leads (V1–V6) capture the electrical activity of the heart in a horizontal plane.
- Six limb leads (I, II, III, aVL, aVF, aVR ) capture the electrical activity of the heart in a vertical plane.
  - Input from three of the limb electrodes is combined to form the six limb leads.
  - The fourth electrode is neutral.

Schematic of normal ECG

Electrode placement ^[1]^[2]

Four limb electrodes
- Left arm
- Right arm
- Left leg
- Right leg (neutral electrode)
Six chest electrodes
- V1: fourth intercostal space, right parasternal region
- V2: fourth intercostal space, left parasternal region
- V3: midway between V2 and V4
- V4: fifth intercostal space, left midclavicular line
- V5: fifth intercostal space, left anterior axillary line
- V6: fifth intercostal space, left midaxillary line

Anatomical relationships of leads ^[1]^[2]

Limb leads
- I: left ventricle, lateral wall
- II, III: inferior surface of the heart
- aVL: left ventricle, high part of the lateral wall
- aVR: right heart and basal septum ^[3]
Precordial leads
- V1 and V2: ventricular septum and right ventricle
- V3 and V4: anterior wall of the left ventricle
- V5 and V6: lateral wall of the left ventricle and apex of the heart
- V7–V9: posterior wall of the left ventricle ^[4]
- V1R–V6R: right ventricle

Anatomical relationships of ECG leads
	Limb leads	Precordial leads	Corresponding heart structure
Inferior leads	II III aVF	N/A	Inferior surface of the heart
Lateral leads	I aVL	V5 V6	Left ventricle, lateral wall
Anteroseptal leads	N/A	V1–V4	Anterior wall of both ventricles Ventricular septum

ECG paper ^[1]

ECG paper speed
- In the US, the ECG paper speed is generally 25 mm/s.
- Alternatively, a paper speed of 50 mm/s can be used.
Machine calibration: 1 mV = 1 cm (i.e., 1 mV of electrical activity results in a 1 cm vertical deflection on the grid paper)
Rhythm strip: a prolonged 10-second recording of a lead (usually lead II)
ECG grid paper
- Small squares of 1 mm²
  - Horizontally: 1 mm = 0.04 s (0.02 s for a paper speed of 50 mm/s)
  - Vertically: 1 mm = 0.1 mV
- Large squares of 5 mm²
  - Horizontally: 5 mm = 5 x 0.04 s = 0.2 s (0.1 s for a paper speed of 50 mm/s)
  - Vertically: 5 mm = 5 x 0.1 mV = 0.5 mV

It is easy to misinterpret an ECG if the paper speed and calibration are not taken into account.

Normal ECG findings

Interpretation/findings

ECG components ^[2]^[5]

Overview

Wave: a deflection of the ECG line due to any change in the electrical activity of the heart (e.g., P wave, T wave)
- Positive (upward) deflection: the electrical impulse is moving toward the electrode
- Negative (downward) deflection: the electrical impulse is moving away from the electrode
- Equiphasic (equally upward and downward) deflection: the electrical impulse is moving perpendicular to the electrode
- Some waves form complexes (e.g., QRS complex).
Segment: the line between two different waves, excluding the waves (e.g., ST segment)
Interval: includes a segment and one (or more) waves (e.g., PR interval)

Key components ^[6]

P wave: atrial depolarization originating in the sinoatrial node (SA node)
PR interval: depolarization originating in the SA node and traveling through the atria, the AV node, and the His-Purkinje system
QRS complex: ventricular depolarization
ST segment: the duration between ventricular depolarization and repolarization
T wave: ventricular repolarization
QT interval: total time of ventricular depolarization and repolarization
U wave: occurs after the T wave; exact origin unknown ^[7]

Normal ECG

Approach to ECG interpretation ^[2]

When interpreting an ECG, it is important to keep in mind the patient's clinical picture and, if possible, compare the current ECG with previous ones.
A thorough ECG interpretation algorithm should assess:
1. Heart rhythm (best seen in lead II)
2. Heart rate (any lead)
3. Cardiac axis (leads I and aVF)
4. P-wave morphology and size (best seen in lead II)
5. PR-interval duration (best seen in lead II)
6. QRS-complex morphology and duration (assessed in all leads individually)
7. ST-segment morphology (assessed in all leads individually)
8. T-wave morphology (assessed in all leads individually)
9. QT-interval duration (lead aVL)
10. U-wave morphology (leads V2–V4)

ECG interpretation algorithm

Determination of heart rate and rhythm

Determination of the heart rhythm ^[1]

The heart rhythm is assessed by evaluating the frequency and regularity of the P waves and the QRS complexes, as well as the relationship between the two.
A 10-second rhythm strip is required to assess the heart rhythm.
Any abnormalities of the heart rhythm should prompt further evaluation (see “Cardiac arrhythmias”).

Sinus rhythm

Definition: a physiological heart rhythm and age-appropriate heart rate set by the SA node
Sinus rhythm features
- P wave
  - Positive in leads I, II, and aVF
  - Negative in lead aVR
  - Followed by a QRS complex
- Regular PR interval
- QRS complex: preceded by a P wave
Respiratory sinus arrhythmia: a variation of the heart rate during respiration, which is normal and common in young adults ^[8]

Normal ECG Normal ECG with sinus arrhythmia

Determination of the heart rate ^[1]

The ventricular rate can be calculated by using the frequency of the QRS complexes, which correlate with ventricular systoles.
The atrial rate, which correlates with atrial systole, can be calculated by using the frequency of the P waves (e.g., when assessing supraventricular arrhythmias).
In clinical settings, the heart rate can be measured with an ECG ruler.

Heart rate (HR) estimation methods

Regular QRS rhythm
- HR = 300/number of large (5 mm²) boxes between two successive QRS complexes (e.g., if you count 5 large boxes between one R wave and the next, the HR is approx. 300 ÷ 5 = 60/min)
- HR = 150/R-R interval in cm (e.g., if there are 2 cm in between two consecutive R waves, HR = 150/2 = 75/min)
- HR = 60/R-R interval in seconds (e.g., if there is a 0.5 s interval between two successive R waves, HR = 60/0.5 = 120/min)
Irregular QRS rhythm: HR = 6 x total number of QRS complexes on a standard 10-second ECG rhythm strip (e.g., if you count 10 QRS complexes on a standard 10-second ECG rhythm strip, the HR is approx. 6 x 10 = 60/min)

Normal resting heart rate according to age

Normal resting heart rate according to age ^[9]
Age	Bradycardia	Normal heart rate	Tachycardia
Newborns (0–1 month)	< 70/min	70–190/min	> 190/min
Infants (1–11 months)	< 80/min	80–160/min	> 160/min
Children (1–2 years)	< 80/min	80–130/min	> 130/min
Children (3–4 years)	< 80/min	80–120/min	> 120/min
Children (5–6 years)	< 75/min	75–115/min	> 115/min
Children (7–9 years)	< 70/min	70–110/min	> 110/min
Children (> 10 years) Adults	< 60/min	60–100/min	> 100/min
Adult athletes	< 40/min	40–60/min	> 60/min

Sinus bradycardia

Determination of the cardiac axis

Definition ^[1]

The electrical axis of the heart represents the mean direction of ventricular depolarization in a frontal plane.
The normal cardiac axis in an adult is between -30° and +90°.

Methods for determining the cardiac axis ^[1]

There are several methods to determine the cardiac axis using the QRS complex polarity. The axis is calculated according to the hexaxial reference system (Cabrera circle).

Isoelectric (equiphasic) QRS complex method
1. Determine the lead in which the QRS complexes are isoelectric (equally positive and negative).
2. Assess the two leads perpendicular to this lead on the Cabrera circle.
3. The cardiac axis corresponds to the perpendicular lead with positive QRS complexes.
Leads I and aVF method
1. Determine the QRS complex polarity in leads I and aVF.
  - Positive QRS complex: the area above the isoelectric line and under the curve is larger than the area under the isoelectric line above the curve
  - Negative QRS complex: the area under the isoelectric line and above the curve is larger than the area above the isoelectric line and under the curve
2. The cardiac axis can be approximated by evaluating the combinations of the QRS complex polarities in leads I and aVF. ^[10]
  - Positive in both leads I and aVF: normal axis (0°–90°)
  - Positive in lead I and negative in aVF: left axis deviation (-90°–-30°) or normal axis (-30°–0°)
  - Negative in lead I and positive in aVF: right axis deviation (90°–180°)
  - Negative in both leads I and aVF: extreme right axis deviation (-180°–-90°)
3. Lead II can be used for a more accurate determination of the cardiac axis if the QRS complex is positive in lead I and negative in aVF.
  - Negative QRS complex in lead II: left axis deviation
  - Positive or isoelectric QRS complex in lead II: normal axis

Principles of the Cabrera circle (hexaxial reference system)

Cardiac axis deviation

Deviation of the cardiac axis ^[11]
Axis	QRS polarity		Degrees	Common causes
Axis	Lead I	Lead aVF	Degrees	Common causes
Left axis deviation	+	-	-90°–-30°	Normal variant (the likelihood of this variant increases with age) Left ventricular hypertrophy (LVH) Left bundle branch block (LBBB) Left anterior fascicular block (LAFB) Inferior MI Wolff-Parkinson-White (WPW) syndrome
Normal	+	+	-30°–90°	Normal axis
Right axis deviation	-	+	90°–180°	Normal variant (e.g., in neonates, or in patients with a vertical heart with an axis of 90°) Right ventricular hypertrophy (RVH) Right bundle branch block (RBBB) Left posterior fascicular block (LPFB) Anterolateral MI Right ventricular strain (e.g., pulmonary embolism, COPD, pulmonary hypertension, pulmonary stenosis) WPW
Extreme right axis deviation	-	-	-180°–-90°	Severe RVH Lateral MI

ECG with normal cardiac axis Left axis deviation Left bundle branch block with left axis deviation Right ventricular hypertrophy with extreme right axis deviation

P wave

Physiology ^[6]
- The P wave represents atrial depolarization, which originates in the SA node.
- The P wave has a lower amplitude and a more curved shape compared to QRS complex waves because of the slower depolarization magnitude and a slight delay in left atria (LA) depolarization compared to the right atria (RA)
Morphology ^[6]
- Present in all leads
- Duration: < 0.12 s (in all leads) ^[12]
- Amplitude: < 0.25 mV (in all leads) ^[13]
- Polarity
  - Positive in leads I, II, and aVF
  - Negative in lead aVR
  - Biphasic in lead V1: negative deflection < 1 mm ^[12]

Abnormalities of the P wave ^[6]^[13]
Abnormality	ECG findings	Pathophysiology	Etiology
P pulmonale	Amplitude: ≥ 0.25 mV in leads II, III, and aVF ^[13]	Right atrial enlargement → slower depolarization of the RA → synchronized RA and LA depolarization → ↑ magnitude of the atrial depolarization → ↑ amplitude of the P wave	COPD Lung fibrosis Primary pulmonary hypertension Congenital heart defects (e.g., pulmonary stenosis, tetralogy of Fallot) Tricuspid stenosis Acute pulmonary embolism (transient P pulmonale) Any other cause of RA strain
P mitrale	Duration: ≥ 0.12 sec Polarity Bifid in lead II: peak-to-peak interval of > 0.04 sec Biphasic in lead V1: negative deflection > 1 mm ^[12]	Left atrial enlargement → slower depolarization of the LA → longer duration of atrial depolarization → ↑ duration and bifid aspect of the P wave	Restrictive cardiomyopathy Rheumatic heart disease ^[14] Constrictive pericarditis
Biatrial enlargement	Combination of P mitrale and P pulmonale		Mitral valve disease Aortic valve disease Chronic hypertension Hypertrophic cardiomyopathy Any other cause of LA strain

P pulmonale P mitrale ECG in left ventricular hypertrophy

PR interval

Physiology ^[5]
- PR interval
  - Measured from the start of the P wave to the start of the QRS complex, which may be a Q wave or an R wave
  - Includes the P wave and the PR segment
  - Represents the depolarization originating in the SA node and traveling through the atria, the AV node, and the His-Purkinje system
  - Mainly assessed in lead II ^[15]
- PR segment
  - Reflects the transmission of the electrical impulse through the AV node
  - Considered the reference isoelectric line for the remainder of the ECG components
Morphology
- Duration: 0.12–0.20 s ^[2]
- Amplitude and polarity: P wave followed by an isoelectric line (see “P wave”)
- Precedes each QRS complex

Abnormalities of the PR interval ^[16]
Criteria	ECG findings	Pathophysiology	Etiology
Duration	≤ 0.12 s	Ectopic electrical pathways → faster impulse transmission to the ventricles → shorter PR interval	WPW Preexcitation syndromes
	≥ 0.2 s	Delay of electrical impulse transmission at the AV node → slower transmission to the ventricles → longer PR interval	First-degree AV block
	PR interval progressively lengthens until a QRS complex is dropped	Malfunctioning of infranodal or AV nodal cells → failure of impulse transmission to the ventricles → dropped QRS complex	Second-degree AV block (Mobitz type I/Wenkebach)
Relationship to QRS			Second-degree AV block (Mobitz type I/Wenkebach)
	Constant PR interval More P waves than QRS complexes A constant QRS complex drop (e.g., P/QRS ratio of 3/2 or 4/3)		Second-degree AV block (Mobitz type II)
	Irregular PR interval (complete dissociation of P waves and QRS complexes) Regular PP interval Regular QRS interval	No conduction of electrical impulses from the atria to the ventricles → junctional or ventricular escape rhythm → QRS complexes independent from P waves	Third-degree AV block
Amplitude	PR-segment depression	Atrial injury or inflammation → abnormal atrial repolarization → PR-segment depression ^[17]	Pericarditis Pericardial effusion Atrial ischemia or infarction

First-degree atrioventricular block Second-degree atrioventricular block: Mobitz I/Wenckebach Third-degree atrioventricular block (complete heart block) Acute pericarditis

QRS complex

Overview

Physiology ^[5]

The QRS complex represents ventricular depolarization and corresponds to ventricular systole.
Because of a faster depolarization magnitude of the ventricles , the waves of the QRS complex have a sharp appearance.

QRS complex components ^[5]

Q wave
- The first negative deflection of the QRS complex
- Represents depolarization of the interventricular septum (left-to-right direction) via the bundle of His
- Q waves are a normal finding in leads I, III, aVL, V5, and V6 (see “Pathological Q waves” below).
R wave
- Any positive deflection in the QRS complex
- Represents depolarization of the left ventricular myocardium (right-to-left direction)
S wave
- A negative deflection after an R wave
- Depolarization of the upper lateral ventricular wall via Purkinje fibers (left-to-right direction)
Intrinsicoid deflection ^[18]
- The interval between the onset of the Q wave and the peak of the R wave
- Delayed intrinsicoid deflection (> 0.05 s) is associated with an increased risk of heart failure. ^[19]

Morphology ^[5]

Duration
- QRS complex: < 0.1 s
- Q wave: < 0.04 s
- R wave > S wave
Amplitude
- Q wave: < 0.2 mV
- R wave: progressively increases from lead V1 to V5
- S wave: progressively decreases from lead V1 to V5

“From V1 to V5, there's sunSet and sunRise”: From leads V1 to V5, S wave Sets while R wave Rises.

QRS complex abnormalities

Abnormalities of QRS-complex waves

Overview of QRS-complex wave abnormalities
Abnormality	ECG findings	Pathophysiology	Etiology
Pathological Q waves ^[5]^[20]	Abnormally wide (≥ 40 ms) Abnormally deep (≥ 0.2 mV or > 25% of the R wave amplitude) or detectable in V1–V3	Myocardial ischemia → myocyte necrosis beneath the electrode → electrical “window” resulting from dead tissue → electrode reading of electrical activity of opposite myocardial wall → Q wave ^[21]	Myocardial injury Myocardial infarction Cardiac infiltrative disease (e.g., sarcoidosis, amyloidosis) Ventricular enlargement Hypertrophic cardiomyopathy Hypertensive heart disease Other cardiomyopathies Altered ventricular conduction LBBB WPW Acute pulmonary embolism Congenital heart disease Incorrect placement of the upper limb leads
Dominant R wave ^[13]	Tall R wave in lead V1 Normal in children and young adults	Increase in the depolarization vector toward lead V1 → tall R wave	RVH RBBB Posterior myocardial infarction HCM WPW
Poor R-wave progression ^[22]	Absence of the normal increase in the size of R waves from lead V1 to V6 May be a normal variant	Ventricular depolarization vector reduced or directed posteriorly → deviation of the depolarization vector away from electrodes → insufficient increase in the size of the R wave and deep S waves	Anterior wall myocardial infarction Right heart strain (e.g., in COPD) ^[13] RVH LBBB LAFB WPW Incorrect electrode placement
Persistent S wave	Presence of an S wave in all precordial leads

A new pathological Q wave is most likely an indication of myocardial infarction.

Pathological Q wave ST-elevation myocardial infarction Poor R-wave progression Persistent S wave

Bundle branch blocks

Incomplete bundle branch block: QRS duration of 0.1–0.12 s
Complete bundle branch block: QRS duration ≥ 0.12 s

Bundle branch blocks
Abnormality	ECG findings	Pathophysiology	Etiology
Left bundle branch block (LBBB) ^[11]^[16]	No R wave in lead V1 Deep S waves (forming a characteristic W shape) Wide, notched R waves in leads I, aVL, V5, V6 (forming a characteristic M shape) Loss of Q waves in the lateral leads ^[23]	BBB → transmission of impulse via remaining functional branch or fascicle → slower ventricular depolarization → long QRS complex	Cardiac Coronary artery disease Myocardial infarction Hypertension Myocardial contusion Restrictive cardiomyopathy Dilated cardiomyopathy Hyperkalemia Digoxin toxicity Degenerative disease of the conduction tissue
Right bundle branch block (RBBB) ^[11]	An rsr', rsR', or rSR' complex (forming a characteristic “rabbit ears” or M shape) in leads V1, V2 Tall secondary R wave in lead V1 Wide, slurred S wave in leads I, V5, V6 Associated feature: ST segment depression and T-wave inversion in leads V1, V2, and sometimes V3 Usually a normal axis Normal variant in ∼ 5% of individuals ^[6]		Cardiac Coronary artery disease Myocardial infarction Myocardial contusion Mitral stenosis Pulmonary Pulmonary hypertension Pulmonary embolism COPD Congenital heart defects Atrial septal defect VSD Pulmonary stenosis Tetralogy of Fallot Brugada syndrome (a pseudo-RBBB) Degenerative disease of the conduction tissue
Bifascicular block ^[24]	An RBBB with either of the following: Left anterior fascicular block (common form) Left axis deviation qR pattern in lead aVL Left posterior fascicular block (rare) Right axis deviation rS pattern in leads I and aVL qR pattern in leads III and aVF		Coronary artery disease Valvular heart disease Hypertension Cardiomyopathies Chagas disease

New-onset left bundle branch block with concurrent angina should be treated immediately as acute coronary syndrome (ACS).

“WiLLiaM MoRRoW:” 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).

Left bundle branch block Anterior ST-elevation myocardial infarction and sequential AV pacing Right bundle branch block Respiratory sinus arrhythmia and right bundle branch block

Ventricular hypertrophy

Ventricular hypertrophy
Abnormality	ECG findings	Pathophysiology	Etiology
Left ventricular hypertrophy (LVH) ^[12]	Sokolow-Lyon criteria:R_V5or R_V6+ S_V1or S_V2≥ 3.5 mV ^[25] Left ventricular strain pattern: ST depression with T wave inversion in the left precordial leads in a resting ECG ^[26]	Increased muscle mass (hypertrophy) → taller R waves (in leads V5, V6) and S waves (in leads V1, V2)	Hypertension Aortic stenosis Coarctation of the aorta Mitral regurgitation Hypertrophic cardiomyopathy Myocarditis VSD
Right ventricular hypertrophy (RVH) ^[13]	Any of the following may suggest RVH: ^[25] Right axis deviation Dominant R wave in lead V1 (R wave > 0.6 mV or R/S > 1) Deep S wave in lead V5 (> 1 mV) or V6 (> 0.3 mV) Sokolow-Lyon criteria: R_V1or R₂ + S_V5or S₆ ≥ 1.05 mV	Increased muscle mass (hypertrophy) → taller R waves (in leads V1, V2) and deeper S waves (in leads V5, V6)	Pulmonary hypertension Pulmonary embolism COPD Mitral stenosis Congenital heart defects

“R1ght 5ignS:” R in V1 and S in V5 are the dominant waves seen in right ventricular hypertrophy.

Bigeminy and left ventricular hypertrophy Right ventricular hypertrophy with extreme right axis deviation

ST segment

Overview ^[5]

Physiology: represents the interval between ventricular depolarization and repolarization ^[27]
Morphology
- Horizontal isoelectric line, but may slope upward slightly before the T wave
- Extends from the J point (end of the S wave) to the start of the T wave

Abnormalities of the ST segment

Abnormalities of the ST segment ^[28]
Abnormality	ECG findings		Etiology
ST elevation ^[29]	One of the following: ≥ 0.1 mV in limb leads ≥ 0.2 mV in precordial leads		Normal finding: small, concave ST elevations in young, healthy adults due to early repolarization STEMI: significant ST elevations in ≥ 2 anatomically contiguous leads (see “Localization of the myocardial infarction on ECG”) LBBB Pericarditis: widespread ST elevations Pulmonary embolism Perimyocarditis Brugada pattern Left ventricular aneurysm ^[30]
ST depression ^[31]	≥ 0.05 mV (or 0.5 mm) in leads V2 and V3 ≥ 0.1 mV in all other leads	Downsloping ST depression or horizontal ST depression	Subendocardial myocardial ischemia, i.e., NSTEMI Stress-induced myocardial ischemia Reciprocal change from myocardial infarction
		Upsloping ST depression	Normal during tachycardia May indicate myocardial ischemia if the clinical picture suggests acute coronary syndrome ^[32]
		Sagging type ST-segment depression	Digoxin
		Secondary repolarization abnormalities	Ventricular hypertrophy LBBB
		Nonspecific ST-segment depression	Hypokalemia
J wave ^[33]	Positive deflection at the J point		Brugada syndrome Idiopathic ventricular fibrillation Hypercalcemia Hypothermia

Types of ST-segment elevation Acute anterior ST-elevation myocardial infarction (STEMI) Acute inferior ST-elevation myocardial infarction (STEMI) Types of ST segment depression Digitalis (digoxin) effect Osborn Wave (J waves) in hypothermia

Brugada syndrome ^[34]

Definition: a rare autosomal dominant genetic mutation that leads to abnormal cardiac conduction and sudden death
Etiology: The most common identified mutation affects cardiac voltage-gated sodium channels.
Epidemiology
- Most common in Asian men
- Symptoms mostly manifest in adulthood.
Clinical features
- Often an incidental finding, as most patients are asymptomatic
- Syncope
- Polymorphic ventricular tachycardia
- Ventricular fibrillation
Diagnostics
- ECG findings
  - Brugada pattern: pseudo-RBBB with ST elevation in leads V1–V3
  - J waves in leads V1–V3 ^[33]
- Rule out underlying heart disease (e.g., cardiac stress test and echocardiography).
Treatment
- General measures
  - Avoid certain medications (e.g., certain antiarrhythmics, psychotropics, anesthetic agents). ^[35]
  - Avoid excessive alcohol intake, cocaine, and large meals.
  - Treat fever with antipyretics.
- Implantable cardiac defibrillator (ICD)
- Screen all first-degree relatives annually with clinical examination and ECG.
Complications
- Sudden cardiac death
- Increased risk of atrial fibrillation ^[36]

Brugada syndrome

T wave

Overview ^[5]

Physiology: : The T wave represents ventricular repolarization.
Morphology
- Shape: asymmetrical, with the downward slope steeper than the initial upward slope
- Amplitude: < 10 mm (between 1/8 and 2/3 of the R wave)
- Polarity: physiologically concordant to the QRS complex (positive if the QRS complex is positive or negative if the QRS complex is negative)

Concordant negative T wave

Abnormalities of the T wave

Abnormalities of the T wave ^[5]^[37]
Abnormality	ECG findings ^[28]		Pathophysiology	Etiology
T-wave inversion ^[38]	Amplitude ≥ -0.1 mV May be a normal finding in: Leads III, aVR, or V1 Children New-onset T-wave inversion (i.e., not present on the patient's previous ECGs)		May be due to any of the following: Ventricular repolarization vector directed away from the electrode of the ECG lead Changes in myocardial cellular electrophysiology (e.g., during ischemia or infarction) Changes in the sequence of ventricular activation (e.g., in bundle branch blocks or cardiac hypertrophy)	Coronary artery disease (myocardial ischemia) Bundle branch blocks Pulmonary embolism Perimyocarditis Ventricular hypertrophy Digoxin Intracranial hemorrhage Persistent juvenile T-wave pattern Wellens syndrome
T-wave flattening	Amplitude between 0.1 mV and -0.1 mV T wave appears flatter than normal.			Hypokalemia Hypoglycemia Myocardial ischemia Hypothyroidism
Peaked T wave	Tall, narrow	Symmetrically peaked		Hyperkalemia Hypermagnesemia
Peaked T wave	Tall, narrow	Asymmetrically peaked		High vagal tone
Hyperacute T wave	Broad, asymmetrically peaked			Early stages of a STEMI Prinzmetal angina
Biphasic T wave	T wave consisting of an upward and downward deflection The initial deflection is variable and can be either up or down.			Initial positive deflection Acute myocardial ischemia Wellens syndrome Initial negative deflection: hypokalemia

If electrical conduction of the heart is abnormal (e.g., bundle branch block), the ST segment and T wave cannot be reliably evaluated because of abnormal repolarization.

ECG of a patient with pulmonary embolism Flat T waves in hypokalemia Abnormalities of the T-wave

QT interval

Overview ^[28]

Represents the entire duration of ventricular depolarization and repolarization
Measured from the beginning of the QRS complex to the end of the T wave
Measured in the lead with the longest QT interval

Corrected QT interval (QTc) ^[28]

General
- Correction for the QT interval is necessary, as it varies with heart rate.
- QTc = QT interval/√R-R interval (seconds)
Duration
- Adult men: QTc = 390–450 ms
- Adult women: QTc = 390–460 ms

Generally, the QT interval should not be more than half of the R-R interval.

Abnormalities of the QT interval

QT interval abnormalities
Condition	ECG findings ^[28]	Pathophysiology	Etiology
Prolonged QT interval ^[39]	> 450 ms in men > 460 ms in women	Usually due to abnormal ventricular repolarization → prolonged QT interval	Congenital long QT syndromes (e.g., Romano-Ward syndrome, Jervell and Lange-Nielsen syndrome) Acquired long QT syndrome Drug side effects (e.g., antiarrhythmic agents, antidepressants, antipsychotics, phenothiazines, 1^st-generation antihistamines, some antibiotics) Electrolyte disturbances (e.g., hypocalcemia, hypokalemia, hypomagnesemia) Cardiac abnormalities (e.g., inflammatory heart diseases, bradycardia, myocardial ischemia) Arsenic poisoning
Shortened QT interval ^[40]	< 390 ms	Abnormal ventricular depolarization or repolarization (depending on the etiology) → shortened QT interval	Hypercalcemia Hyperkalemia Digoxin effect Increased sympathetic tone (e.g., hyperthyroidism, fever) Congenital short QT syndrome

A prolonged QT interval is associated with sudden cardiac death, usually due to acute ventricular arrhythmias. ^[39]

U wave

General ^[5]
- Small deflection after the T wave
- Polarity is the same as the T wave
- Best seen in leads V2 to V4, but not always visible
- Normal finding in athletes
Etiology
- Exact origin is unknown
- Thought to be due to delayed repolarization of the midmyocardial cells (myocardium) and the His-Purkinje system
Causes of prominent U waves ^[5]

Clinical applications of ECG

Ambulatory ECG monitoring ^[41]

Description: ECG devices can be used in the outpatient setting to monitor and record the cardiac rhythm over a prolonged period of time.
Types
- Continuous: Holter monitor ^[42]
  - A continuous, ambulatory, battery-operated ECG recorder worn for 24–48 hours
  - Common metrics
    - Average, minimum, and maximum heart rate
    - Heart-rate variability
    - Episodes and duration of arrhythmias
    - QRS late potentials
    - ST-segment changes
    - Analysis of the P and T waves
  - Limitations
    - The short duration of monitoring results in a low diagnostic yield.
    - Devices are not waterproof.
    - The patient needs to document symptoms separately.
- Intermittent
  - Event recorder
    - A device used in the evaluation of arrhythmias or syncope to record the patient's heart rhythm during symptomatic episodes
    - Devices are triggered to record data either by the patient (when experiencing symptoms) or automatically (when an arrhythmia is detected)
  - Loop recorder
    - A type of event recorder that can be triggered either automatically or manually by the patient
    - Records the patient's heart rhythm up to an hour prior to the arrhythmic event as well as during the event
    - External recorders: worn externally for short periods of time (4–6 weeks)
    - Implantable loop recorders: can be used for up to 36 months (e.g., for patients with more infrequent episodes)
- Pacemakers or implanted cardioverter defibrillators
- Patient-led monitoring (e.g., via a smartwatch)
Indications
- Daily or near-daily symptoms of:
- Assessment of the effects of new rate-control medication (e.g., metoprolol) or pacemaker function
- Screening for ventricular ectopy in high-risk patients (e.g., patients with cardiomyopathy or acute coronary syndrome)

Other clinical applications of ECG

Diagnosis of ACS (see also “ECG changes in STEMI”)
Cardiac arrhythmias
Cardiac tamponade
Pericarditis
Long QT syndrome
Cardiac stress test
Sick sinus syndrome
Pericardial effusion

Most common ECG abnormalities

Most common ECG abnormalities
Condition		Most relevant ECG findings	Most important clinical features
Myocardial infarction
STEMI		In early stages of ischemia Hyperacute T wave (peaked T wave) (without ST elevations) ST-segment elevations in Anteroseptal: V₁–V₂ Anteroapical: V₃–V₄ Anterolateral: V₅–V₆ Lateral: I, aVL Inferior: II, III, aVF Posterior: V₇–V₉ Intermediate stage Absence of R wave T-wave inversion Pathological Q wave	Acute retrosternal chest pain Typically dull, squeezing Commonly radiates to left chest, arm, shoulder, neck, jaw, and/or epigastrium Precipitated by exertion or stress Dyspnea (especially with exertion) Nausea, vomiting Diaphoresis, anxiety Dizziness, lightheadedness, syncope New heart murmur on auscultation (e.g., new S₄)
Supraventricular tachycardia
Atrioventricular nodal reentrant tachycardia		Regular rhythm Typically, narrow QRS complexes Invisible P wave (it falls in or is "buried" in the QRS complex) Heart rate typically 150–220/minute ECG may be normal between episodes of tachycardia.	Symptom onset and resolution are typically abrupt Palpitations Dyspnea Dizziness or presyncope Diaphoresis
Atrioventricular reciprocating tachycardia		Regular rhythm Heart rate 150–250/minute Orthodromic AVRT Narrow QRS complex P wave typically follows QRS complex. Antidromic AVRT Wide QRS complex Shortened PR interval
Multifocal atrial tachycardia		Heart rate 100–200/min Irregularly irregular rhythm P waves: ≥ 3 varying morphologies
Paroxysmal atrial tachycardia		Rhythm can be regular or irregular Heart rate > 100 bpm P wave with an unusual morphology (highly variable) before each normal QRS
Wolff-Parkinson-White syndrome		Regular rhythm While in sinus rhythm, a preexcitation pattern may be present. Short PR interval ECG delta wave Widened QRS
Ventricular tachycardia
Torsades de pointes		Regular rhythm Heart rate typically ≥100/min At least 3 consecutive wide QRS complexes (monomorphic VT or polymorphic VT) Signs of AV dissociation Dissociated P waves Fusion complexes Capture beats	Often asymptomatic Palpitations, syncope Chest pain/pressure Dyspnea, orthopnea Dizziness Hypotension Cardiac arrest
Tachyarrhythmia
Atrial fibrillation		Irregularly irregular RR intervals Commonly tachycardia (atrial rate > ventricular rate) Indiscernible P waves Typically narrow QRS complex (< 0.12 sec)	Mostly asymptomatic Less commonly, symptoms of arrhythmias (e.g., palpitations, dizziness, syncope)	Tachycardia with an irregularly irregular pulse Thromboembolic events (e.g., stroke/TIA)
Atrial flutter		Heart rate: typically 75–150/minute (atrial rate ≥ ventricular rate) The rhythm may be: Regularly irregular if atrial flutter occurs with a variable AV block occurring in a fixed pattern (2:1 or 4:1) Irregularly irregular with a variable block Regular, narrow QRS complexes Sawtooth appearance of P waves: identical flutter waves (F waves) that occur in sequence at a rate of ∼ 300/minute		Tachycardia with a regular pulse
Ventricular fibrillation		Commonly preceded by ventricular tachycardia (heart rate: > 300 bpm) Arrhythmic, fibrillatory baseline Indiscernible QRS complexes Absent P waves	Chest pain Palpitation Shortness of breath Dizziness Ultimately: loss of consciousness, death
AV block
First degree		Rate of SA node = heart rate PR interval > 200 ms No interruption in atrial to ventricular conduction	Mostly asymptomatic, especially with first-degree and Mobitz type I blocks Fatigue Dizziness Syncope Palpitations in the case of irregular rhythms (e.g., Mobitz I) In third-degree: stokes-Adams attacks
Second degree	Mobitz type I (Wenckebach)	Mostly regular rhythm separated by short pauses, which may lead to bradycardia (regularly irregular rhythm) Rate of SA node > heart rate Progressive lengthening of the PR interval until a beat is dropped (a normal P wave is not followed by a QRS complex)
Second degree	Mobitz type II	Single or intermittent nonconducted P waves without QRS complexes The PR interval remains constant. The conduction of atrial impulses to the ventricles typically follows a regular pattern.
Third degree		Complete block with no conduction between the atria and ventricles P waves and QRS complexes have their own regular rhythm but bear no relationship to each other (AV dissociation). Sudden onset 3° AV block can result in ventricular asystole.
Bundle branch block
Left bundle branch block (LBBB)		No R wave in lead V₁ Deep S waves (forming a characteristic W shape) Wide, notched R waves in leads I, aVL, V5, V6 (forming a characteristic M shape)	LBBB itself is asymptomatic. Signs of the underlying condition (e.g., chest pain in MI)
Right bundle branch block (RBBB)		An rsr', rsR', or rSR' complex (forming a characteristic “rabbit ears” or M shape) in leads V₁, V₂ Tall secondary R wave in lead V₁ Wide, slurred S wave in leads I, V₅, V₆	RBBB itself is asymptomatic. Signs of the underlying condition (e.g., cough in COPD)
Hereditary channelopathies
Brugada syndrome		Pseudo-RBBB with ST elevation in leads V1–V3	Mostly asymptomatic Syncope Palpitation Dizziness
Congenital long QT syndrome		Long QT interval corrected for heart rate (QTc) interval Males: > 440 ms Females: > 460 ms	Mostly asymptomatic Palpitations Dizziness Syncope Cardiac arrest Deafness in Jervell and Lange-Nielsen syndrome (not seen in Romano-Ward syndrome)
Unspecific changes
Acute pericarditis		Diffuse (saddle-shaped) ST-segment elevation Diffuse PR-segment depressions T-wave inversions	Pleuritic chest pain Low-grade intermittent fever, tachypnea, dyspnea, nonproductive cough Pericardial friction rub
Cardiac tamponade		Tachycardia Low voltage QRS Electrical alternans	Beck triad (hypotension, muffled heart sounds, and distended neck veins) Pulsus paradoxus Pallor, cold sweats Obstructive shock, cardiac arrest
Hypertrophic cardiomyopathy		Signs of LVH Nonspecific ST- and T-wave changes Septal Q waves in inferior and lateral leads	Frequently asymptomatic Exertional dyspnea Chest pain Dizziness, lightheadedness, syncope Palpitations Sudden cardiac death (particularly during or after intense physical activity)
Restrictive cardiomyopathy		Low voltage ECG (especially in amyloidosis) LBBB and other conduction disorders	Most common: dyspnea Jugular venous distention Peripheral edema, ascites Hepatomegaly
Pulmonary embolism		S_IQ_IIIT_III-pattern New RBBB	Dyspnea and tachypnea Sudden pleuritic chest pain Cough and hemoptysis Possibly decreased breath sounds
Electrolyte imbalances	Hypokalemia	Flattened T waves ST depression Presence of U waves	Palpitations, irregular pulse, syncope Muscle cramps, muscle weakness Decreased deep tendon reflexes Nausea, vomiting, constipation Polyuria
	Hyperkalemia	QRS complex widening Peaked T waves Widening and flattening of P wave	Muscle weakness, paralysis, paresthesia Decreased deep tendon reflexes Nausea, vomiting, diarrhea
	Hypocalcemia	Prolonged QT interval	Tetany, spasms, and cramps (positive Chvostek sign, Trousseau sign) Paresthesias Seizure
	Hypercalcemia	Shortened QT interval	Nephrolithiasis, nephrocalcinosis Bone pain, arthralgias, myalgias, fractures Nausea and vomiting, constipation, anorexia Peptic ulcer disease Pancreatitis
	Hypomagnesemia	Prolonged PR and QT intervals	Anorexia, nausea, vomiting Muscle weakness, muscle cramps/spasms Tremor Ataxia, nystagmus Seizures
Atrial/ventricular enlargement
Right atrial enlargement		P pulmonale	Signs of the underlying condition (e.g., cough in COPD)
Left atrial enlargement		P mitrale	Signs of the underlying condition (e.g., jugular venous distension in restrictive cardiomyopathy)
Left ventricular hypertrophy		Sokolow-Lyon criteria: RV₅ or RV₆ + SV₁ or SV₂≥ 3.5 mV	Signs of the underlying condition (e.g., syncope in aortic stenosis)
Right ventricular hypertrophy		Right axis deviation Dominant R wave in lead V₁ (R wave > 0.6 mV or R/S > 1) Sokolow-Lyon criteria: RV₁ or R_s + SV₅ or S₆ ≥ 1.05 mV	Signs of the underlying condition (e.g., cough in COPD)

References

Meek S, Morris F. ABC of clinical electrocardiography - Introduction - Leads, rate, rhythm, and cardiac axis. BMJ. 2002; 324 (7334): p.415-8.
Hampton JR. The ECG Made Easy. Churchill Livingstone Elsevier ; 2013
George A, Arumugham PS, Figueredo VM. aVR - the forgotten lead. Exp Clin Cardiol. 2010; 15 (2): p.e36-e44.
van Gorselen EO, Verheugt FW, Meursing BT, Oude Ophuis AJ. Posterior myocardial infarction: the dark side of the moon.. Neth Heart J. 2007; 15 (1): p.16-21.
Meek S. ABC of clinical electrocardiography: Introduction. II---Basic terminology. BMJ. 2002; 324 (7335): p.470-473. doi: 10.1136/bmj.324.7335.470 . | Open in Read by QxMD
Feather A, Randall D, Waterhouse M. Kumar and Clark's Clinical Medicine. Elsevier ; 2020
Nagayoshi Y, Yufu T, Yumoto S. Inverted U-wave and myocardial ischemia. QJM: An International Journal of Medicine. 2018; 111 (7): p.493. doi: 10.1093/qjmed/hcy025 . | Open in Read by QxMD
Ben-Tal A, Shamailov SS, Paton JFR. Evaluating the physiological significance of respiratory sinus arrhythmia: looking beyond ventilation-perfusion efficiency. J Physiol. 2012; 590 (8): p.1989-2008. doi: 10.1113/jphysiol.2011.222422 . | Open in Read by QxMD
Pulse. https://medlineplus.gov/ency/article/003399.htm. Updated: July 2, 2019. Accessed: October 3, 2020.
Kashou AH, Basit H, Chhabra L. Electrical Right and Left Axis Deviation. StatPearls. 2020 .
Surawicz B, Childers R, Deal BJ, Gettes LS. AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram. Circulation. 2009; 119 (10). doi: 10.1161/circulationaha.108.191095 . | Open in Read by QxMD
Edhouse J. ABC of clinical electrocardiography: Conditions affecting the left side of the heart. BMJ. 2002; 324 (7348): p.1264-1267.
Harrigan RA. ABC of clinical electrocardiography: Conditions affecting the right side of the heart. BMJ. 2002; 324 (7347): p.1201-1204. doi: 10.1136/bmj.324.7347.1201 . | Open in Read by QxMD
Sethi T, Singh AP, Singla V, Singh Y. Biatrial enlargement: an unusual cause of massive cardiomegaly. Case Reports. 2013; 2013 (jan31 1): p.bcr-2012-008320-bcr-2012-008320. doi: 10.1136/bcr-2012-008320 . | Open in Read by QxMD
Ram JL, Conn PM. Conn's Handbook of Models for Human Aging. Academic Press ; 2018
Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. J Am Coll Cardiol. 2019; 74 (7): p.e51-e156. doi: 10.1016/j.jacc.2018.10.044 . | Open in Read by QxMD
Kudo Y, Yamasaki F, Doi Y, Sugiura T. Clinical correlates of PR-segment depression in asymptomatic patients with pericardial effusion. J Am Coll Cardiol. 2002; 39 (12): p.2000-2004. doi: 10.1016/s0735-1097(02)01889-2 . | Open in Read by QxMD
O'Neal WT, Qureshi WT, Nazarian S, et al. Electrocardiographic Time to Intrinsicoid Deflection and Heart Failure: The Multi-Ethnic Study of Atherosclerosis.. Clin Cardiol. 2016; 39 (9): p.531-6. doi: 10.1002/clc.22561 . | Open in Read by QxMD
Darouian N, Narayanan K, Aro AL, et al. Delayed intrinsicoid deflection of the QRS complex is associated with sudden cardiac arrest. Heart Rhythm. 2016; 13 (4): p.927-932. doi: 10.1016/j.hrthm.2015.12.022 . | Open in Read by QxMD
MacAlpin RN. Significance of Abnormal Q Waves in the Electrocardiograms of Adults Less than 40 Years Old. Ann Noninvasive Electrocardiol. 2006; 11 (3): p.203-210. doi: 10.1111/j.1542-474x.2006.00105.x . | Open in Read by QxMD
Morris F. ABC of clinical electrocardiography: Acute myocardial infarction - Part I. BMJ. 2002; 324 (7341): p.831-834. doi: 10.1136/bmj.324.7341.831 . | Open in Read by QxMD
MacKenzie R. Poor R-wave progression. J Insur Med. 2005; 37 (1): p.58-62.
Breithardt G, Breithardt OA. Left bundle branch block, an old-new entity.. Journal of cardiovascular translational research. 2012; 5 (2): p.107-16. doi: 10.1007/s12265-011-9344-5 . | Open in Read by QxMD
Elizari MV, Acunzo RS, Ferreiro M. Hemiblocks Revisited. Circulation. 2007; 115 (9): p.1154-1163. doi: 10.1161/circulationaha.106.637389 . | Open in Read by QxMD
Hancock EW, Deal BJ, Mirvis DM, Okin P, Kligfield P, Gettes LS. AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram. Circulation. 2009; 119 (10). doi: 10.1161/circulationaha.108.191097 . | Open in Read by QxMD
Salles G, Cardoso C, Nogueira AR, Bloch K, Muxfeldt E. Importance of the Electrocardiographic Strain Pattern in Patients With Resistant Hypertension. Hypertension. 2006; 48 (3): p.437-442. doi: 10.1161/01.hyp.0000236550.90214.1c . | Open in Read by QxMD
Kashou AH, Kashou HE. Rhythm, ST Segment. StatPearls. 2017 .
Rautaharju PM, Surawicz B, Gettes LS. AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram. Circulation. 2009; 119 (10). doi: 10.1161/circulationaha.108.191096 . | Open in Read by QxMD
Gard JJ, Bader W, Enriquez-Sarano M, Frye RL, Michelena HI. Uncommon Cause of ST Elevation. Circulation. 2011; 123 (9). doi: 10.1161/circulationaha.110.002477 . | Open in Read by QxMD
Klein LR, Shroff GR, Beeman W, Smith SW. Electrocardiographic criteria to differentiate acute anterior ST-elevation myocardial infarction from left ventricular aneurysm. Am J Emerg Med. 2015; 33 (6): p.786-790. doi: 10.1016/j.ajem.2015.03.044 . | Open in Read by QxMD
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
Khalid U, Birnbaum Y. Clinical Significance of Upsloping ST Depression on Resting Electrocardiogram. Ann Noninvasive Electrocardiol. 2016; 21 (2): p.202-205. doi: 10.1111/anec.12273 . | Open in Read by QxMD
Antzelevitch C, Yan GX, Ackerman MJ, et al. J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge.. Europace. 2017; 19 (4): p.665-694. doi: 10.1093/europace/euw235 . | Open in Read by QxMD
Hayat S, Malik B, Ali Rudwan A, et al. Brugada syndrome: Clinical features, risk stratification, and management. Heart Views. 2020; 21 (2): p.88-96. doi: 10.4103/heartviews.heartviews_44_20 . | Open in Read by QxMD
Postema PG, Neville J, de Jong JSSG, Romero K, Wilde AAM, Woosley RL. Safe drug use in long QT syndrome and Brugada syndrome: comparison of website statistics. Europace. 2013; 15 (7): p.1042-1049. doi: 10.1093/europace/eut018 . | Open in Read by QxMD
Francis J, Antzelevitch C. Atrial Fibrillation and Brugada Syndrome. J Am Coll Cardiol. 2008; 51 (12): p.1149-1153. doi: 10.1016/j.jacc.2007.10.062 . | Open in Read by QxMD
Sampson M. Ambulatory electrocardiography: indications and devices. British Journal of Cardiac Nursing. 2019; 14 (3): p.114-121. doi: 10.12968/bjca.2019.14.3.114 . | Open in Read by QxMD
Steinberg JS, Varma N, Cygankiewicz I, et al. 2017 ISHNE-HRS expert consensus statement on ambulatory ECG and external cardiac monitoring/telemetry. Heart Rhythm. 2017; 14 (7): p.e55-e96. doi: 10.1016/j.hrthm.2017.03.038 . | Open in Read by QxMD
Channer K, Morris F. ABC of clinical electrocardiography: Myocardial ischaemia. BMJ. 2002; 324 (7344): p.1023-1026. doi: 10.1136/bmj.324.7344.1023 . | Open in Read by QxMD
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
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
Patel C, Yan G-X, Antzelevitch C. Short QT Syndrome: From Bench to Bedside. Circ Arrhythm Electrophysiol. 2010; 3 (4): p.401-408. doi: 10.1161/circep.109.921056 . | Open in Read by QxMD
Herold G. Internal Medicine. Herold G ; 2014

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ECG

Summary

Procedure/application

Overview [1][2]

Electrode placement [1][2]

Anatomical relationships of leads [1][2]

ECG paper [1]

Interpretation/findings

ECG components [2][5]

Overview

Key components [6]

Approach to ECG interpretation [2]

Determination of heart rate and rhythm

Determination of the heart rhythm [1]

Sinus rhythm

Determination of the heart rate [1]

Heart rate (HR) estimation methods

Normal resting heart rate according to age

Determination of the cardiac axis

Definition [1]

Methods for determining the cardiac axis [1]

Cardiac axis deviation

P wave

PR interval

QRS complex

Overview

Physiology [5]

QRS complex components [5]

Morphology [5]

QRS complex abnormalities

Abnormalities of QRS-complex waves

Bundle branch blocks

Ventricular hypertrophy

ST segment

Overview [5]

Abnormalities of the ST segment

Brugada syndrome [34]

T wave

Overview [5]

Abnormalities of the T wave

QT interval

Overview [28]

Corrected QT interval (QTc) [28]

Abnormalities of the QT interval

U wave

Clinical applications of ECG

Ambulatory ECG monitoring [41]

Other clinical applications of ECG

Most common ECG abnormalities

References

Overview ^[1]^[2]

Electrode placement ^[1]^[2]

Anatomical relationships of leads ^[1]^[2]

ECG paper ^[1]

ECG components ^[2]^[5]

Key components ^[6]

Approach to ECG interpretation ^[2]

Determination of the heart rhythm ^[1]

Determination of the heart rate ^[1]

Definition ^[1]

Methods for determining the cardiac axis ^[1]

Physiology ^[5]

QRS complex components ^[5]

Morphology ^[5]

Overview ^[5]

Brugada syndrome ^[34]

Overview ^[5]

Overview ^[28]

Corrected QT interval (QTc) ^[28]

Ambulatory ECG monitoring ^[41]