ECG

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.

General

• Leads: A 12-lead ECG with six limb leads (I, II, III, aVL, aVF, aVR ) and six precordial leads (V₁–V₆) is standard.
  • Interpretation of the limb leads
    • I → left ventricle, lateral wall
    • II, III, and aVF → left ventricle, inferior wall (inferior ECG leads)
    • aVL → left ventricle, high part of the lateral wall
    • aVR → reciprocal of the left lateral side leads (II, aVL, V₅ and V₆)
  • Interpretation of the precordial leads
    • V₁ and V₂ → both ventricles, anterior wall
    • V₃ and V₄ → anterior wall of the left ventricle and parts of the septum
    • V₅ and V₆ → lateral wall of the left ventricle and apex of the heart
• 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

• Definition: A continuous, ambulatory battery operated ECG worn by patients for 24-48 hours
• Indications
  • Daily or near-daily symptoms of:
    • Syncope
    • Palpitations
  • Patients who are unable to use other ambulatory ECG monitoring devices
  • Assessing effect of new atrial fibrillation rate control medication (e.g., metoprolol)
  • Screening for ventricular ectopy in high-risk patients (e.g., cardiomyopathy, acute coronary syndrome)
• 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]

• 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 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
  • Normal heart rate: 60–100/min
  • Tachycardia: > 100/min (see also tachycardic arrhythmias)
  • Bradycardia: < 50-60/min (see also bradycardic arrhythmias)

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:
       • Determine the atrial and ventricular heart rates.
       • Is there an abnormal number of P waves compared to QRS complexes?
     • 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]

• 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:

• Exact determination of the axis is done with the Cabrera circle

References:^[5][9][10]

References:^[11]

• The time between the beginning of the P wave and the beginning of the Q wave
• The PR interval represents atrioventricular transmission.

References:^[12][13]

• 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)
    • Signs of right bundle branch block (RBBB) are primarily seen in leads V_1,2
      • Prolonged QRS complex
      • rSR' formation (typical M shape/ “rabbit ear” shape)
      • Wide S wave in lead I
      • T wave inversions and ST-segment depression in V₁–-V₃
      • Final negativity (intrinsicoid deflection) in V_1,2 after > 0.03 s
    • Signs of left bundle branch block (LBBB) are primarily seen in leads I, V_5,6
      • Prolonged QRS complex
      • Broad, notched R wave
      • Loss of Q waves
      • Possible rSR' formation in V₅ or ₆
      • Deep S wave in V_1,2
      • Final negativity (intrinsicoid deflection) in V_5,6 after > 0.05

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): S_{V1 or 2} + R_{V5 or 6} ≥ 3.5 mV
    • Right ventricular hypertrophy (RVH): R_{V1 or 2} + S_{V5 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]

Physiological

• The Q wave represents the beginning of ventricular depolarization.
• A narrow (≤ 40 ms) Q wave is physiological in:
  • All limb leads
  • aVR
  • V₅ and V₆

Pathological

• Pathological Q waves are characteristically:
  • Abnormally wide (≥ 40 ms)
  • Abnormally deep (≥ 0.2 mV or > 25% of the R wave amplitude) or, detectable in V₁–V₃
• Etiology
  • Myocardial injury or replacement
    • Myocardial infarction
    • Cardiac infiltrative disease (e.g., sarcoidosis, amyloidosis)
  • Ventricular enlargement
    • Acute pulmonary embolism
    • Hypertrophic cardiomyopathy
  • Altered ventricular conduction
    • Left bundle branch block
    • Wolff-Parkinson-White syndrome

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

Physiological

• The ST segment represents the interval between ventricular depolarization and repolarization
• It is physiologically horizontal on the isoelectric line.

Pathological

ST elevation

• An ST elevation is significant if:
  • ≥ 0.1 mV in limb leads, or
  • ≥ 0.2 mV in precordial leads!
• The hallmark ECG finding of myocardial infarction!
  • If significant ST elevations are present in ≥ 2 anatomically contiguous leads (corresponding to occlusion of a specific artery)
  • The ischemia can be localized by which leads show ST elevation:
    • Lateral MI (left circumflex artery occlusion): I, aVL, V_5-6
    • Anterior MI (left anterior descending (LAD) artery occlusion): V_1-4
    • Inferior MI (terminal branches of right or left coronary artery occlusion): II, III, aVF
• Widespread ST elevations suggest pericarditis
• LBBB may cause ST elevations due to repolarization abnormalities, therefore ST elevation cannot be used to diagnose MI in the presence of a LBBB.
• Small, concave ST elevations may be a normal finding in young, healthy adults due to early repolarization.
• From descending R: The most important cause is a myocardial infarction.
• From (deep) S: perimyocarditis

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, as patients are mostly asymptomatic
  • Syncope
  • Sudden cardiac death
• Diagnosis
  • Brugada pattern on ECG: Pseudo-RBBB with ST elevation in leads V_1-2
  • Rule out underlying heart disease (e.g., stress test and echocardiography)
• Treatment
  • Implantable cardiac defibrillator (ICD) placement
  • Screen all 1^st-degree relatives annually with clinical exam and ECG
• Complications
  • Syncope
  • Sudden cardiac death
  • Increased risk of atrial fibrillation

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

ST depression

• Differential diagnosis
  • Subendocardial myocardial ischemia; (MI) (i.e., NSTEMI)
  • Stress-induced MI (sign of coronary artery disease)
  • Reciprocal change from MI
  • Ventricular hypertrophy
    • Left ventricular hypertrophy: ST depression with pre-terminal T-wave inversion in V_4-6
    • Right ventricular hypertrophy: ST depression with pre-terminal T-wave inversion in V_1-3(4)
  • Digoxin effect
  • Hypokalemia
  • LBBB
• The shape of the ST segment suggests the etiology of the depression.
  • Downsloping ST depression or horizontal ST depression: myocardial ischemia
  • Upsloping ST depression: mild manifestations may be normal, but may also occur in cases of tachycardia; sign of coronary heart disease if significantly manifested
  • Sagging type ST-segment depression: characteristic of digoxin intake

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

Physiological

• The T wave represents the repolarization of the ventricles
• The T wave is physiologically concordant to the QRS complex: positive if the QRS complex is positive or negative if the QRS complex is negative.

Pathological

T-wave inversion

• Small T-wave inversions may be normal in the limb leads
• Differential diagnosis
  • Coronary heart disease
  • Ventricular hypertrophy
  • Perimyocarditis
  • Myocardial infarction (STEMI (in the intermediate stage) or NSTEMI)
  • Ventricular aneurysm
  • Intracranial hemorrhage
  • LBBB
  • Acid/base disturbance
• The shape of the T wave may help to narrow the differential diagnosis.
  • Pre-terminal T-wave inversion: If the T wave is bisected, it points to the left. It may occur in:
    • Perimyocarditis
    • Ventricular hypertrophy
    • Coronary heart disease
  • Terminal T-wave inversion: If the T wave is bisected, it points either to the right or upwards. It may occur in:
    • Intracranial hemorrhage
    • Perimyocarditis
    • A persistent negative T wave following myocardial infarction may suggest an aneurysm.
    • Myocardial infarction (STEMI (in the intermediate stage) or NSTEMI)

Peaked T wave

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

Hyperacute T wave

• Broad, asymmetrically-peaked
• Differential diagnosis
  • Early stages of ST (segment) elevation myocardial infarction (STEMI)
  • Prinzmetal's angina

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]

Physiological

• Measured from the beginning of the Q wave to the end of the T wave
• Represents the entire duration of ventricular depolarization and repolarization
• Varies with heart rate, so correction for the heart rate is necessary (=QTc )
  • QTc normally < 350–440 ms

Pathological

Prolongation of the QT interval

Possible differential diagnoses include:

• Hypocalcemia
• Hypokalemia
• Inflammatory heart diseases (myocarditis, pericarditis)
• Bundle branch block
• High vagal tone
• Rare congenital syndromes (e.g., congenital long QT syndromes such as Romano-Ward syndrome)
• Acquired long QT syndrome
• Hypothyroidism
• Drug side effect (e.g., antiarrhythmic agents, antidepressants, phenothiazines, 1^st-generation antihistamines)

Shortening of the QT interval

Possible differential diagnoses include:

• Hypercalcemia
• Hyperkalemia
• Digoxin effect
• Increased sympathetic tone (e.g., hyperthyroidism or fever)

References:^{[5][30][31][32]}

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]