UNCONTROLLED WHEN PRINTED
Wide (Broad) QRS Complex
  • Implies ventricular depolarisation is slow (<0.12s maximum); anything higher is considered ‘wide/broad.’
Causes of Wide QRS:
  • Bundle Branch Block – Ventricle unable to be depolarised due to block
  • Hyperkalaemia – Causes slow transmission in cells
  • Drugs – Antiarrhythmics, antidepressants etc.
  • Pacemaker with ventricular stimulation
  • Wolf-Parkinson-White Syndrome

https://litfl.com/hyperkalaemia-ecg-library/

Broad QRS complexes secondary to hyperkalaemia

https://litfl.com/pre-excitation-syndromes-ecg-library/

Atrial fibrillation in a patient with Wolfe-Parkinson-White Syndrome; rapid, irregular, broad complex tachycardia with a LBBB morphology.

QRS Complex Net Direction
  • Classified into net positions (net positive or negative, based on the sum of the positive or negative areas from the baseline.)
  • No specific calculations, assessment is based upon visual inspection, as per below:
https://en.wikipedia.org/wiki/QRS_complex#/media/File:QRS_nomenclature.svg
ComplexNet determination
rs Net Neutral (equal parts above and below the baseline)
Q Negative (purely negative deflection)
qR Net Positive (most area is above the baseline with some below)
QR Net Positive (most area is above the baseline with some below)
QS Negative (purely negative deflection)
rS Net Negative (most area is below the baseline with some above)
rsR' Net Positive (most area is above the baseline with some below)
RS Net Positive (most area is above the baseline with some below)
qRs Net Positive (most area is above the baseline with some below)

 

QRS Amplitude

Large amplitude (height) in QRS complex can be due to ventricular hypertrophy &/or enlargement as a result due to the larger mass, there is larger electrical signals produced

Electrode to heart distance impact QRS amplitude (hence slender has smaller QRS versus obese) or in patients with hyperinflation of thorax (ie. COPD).

Q-Wave Changes

Must be able to differentiate pathological Q-waves as they provide infarction evidence – dictated by amplitude and duration (width); it is abnormal if:

  • Q-wave Duration > 0.03s AND/OR;
  • Q-wave Amplitude > 25% of the R-Wave amplitude AND;
  • Abnormal Q-wave exist in two (2) contiguous leads (ie. aVF & III / V4 & V5)
31
Normal Q-Wave:

Septal q-wave seen in lateral leads (V5-V6, aVL, & Lead I) due to depolarisation of ventricular septum Isolated & large Q-wave is seen Lead III which amplitude variate with ventilations (respiratory Q-wave).

  • Small Q-waves (do not fulfil pathology) may be seen in all limb leads, plus V4-V6.
  • V1-V3 must only display small q-waves only (not Q-waves)
Abnormal (Pathological) Q-Wave:

Common cause in AMI – Q-wave infarction is caused if AMI leaves pathological Q-waves; must be in two (2) contiguous leads to be abnormal. These causes include:

  • AMI
  • Left side pneumothorax
  • Dextrocardia
  • Perimyocarditis
  • Cardiomyopathy
  • Amyloidosis
  • Bundle Branch Block / Fascicular Blocks
  • Wolf-Parkinson-White (WPW) Syndrome
  • Ventricular hypertrophy
  • Pulmonary Embolism
R-Wave Changes
Amplitude of R-Wave

High amplitudes in R-waves can suggest ventricular enlargement or hypertrophy; this is determined by;

  • V5 & V6 R-wave is < 26mm high
  • V5 & V6 R-wave is < 35mm high
  • V1 S-wave is < 35mm high
  • aVL R-wave is < 12mm high
  • Lead I, II, & III R-wave is < 20mm high

If R-wave in V1 is larger than S-wave in V1 then R-wave should be < 5mm high

Peak time of R-Wave

Internal from beginning of QRS complex to R-wave’s apex – This reflects on the time elapsed from depolarisation to spread from the endocardium to epicardium; A prolonged peak time is due to hypertrophy &/or conduction disturbance.

  • V1 & V2 Right Ventricle < 0.035s
  • V5 & V6 Left Ventricle < 0.045s
32
R-Wave Progression

Should be natural QRS complex progression of amplitude (height) from V1 to V6 – Due to the contraction direction to left and downward, V1 & V2 should be negative.

  • V1 to V2 should be negative due to contraction direction
  • V3 to V4 should be positive then taper off in V5
  • V5 to V6 should tamper off

33

Abnormal Tall R-Waves

For V1 & V2 – Ensure R-wave is not bigger than S-wave (<5mm)

  • Dextrocardia
  • Incorrect lead attachment
  • Posterior AMI
  • RBBB
  • Right Ventricular Hypertrophy
  • Ventricular Tachycardia
  • Wolf-Parkinson-White (WPW) Syndrome
  • Cardiomyopathy
34
T-Wave Analysis

Mostly positive in most leads, with amplitude decreasing with increased age. The ST segment transition to T-wave should be smooth. It can be asymmetrical, as it has a slight upslope (1st half) and downslope (2nd half).

T-Wave changes are easily misinterpreted (mostly inverted T-waves), so take caution.

  • Women have more asymmetrical T-wave and distinct ST-T transition with lower amplitude
  • T-Wave's must be concordant (same direction as net previous QRS complex) to be considered normal.
    • A concordant positive T-wave follows a positive QRS complex
    • A discordant T-wave is positive after a negative QRS; this is considered abnormal
  • Negative T-waves are also termed 'inverted T-waves'
  • The positive area of the QRS complex is greater than the two negative areas combined. The QRS complex is therefore net positive, and therefore concordant with the positive T-wave deflection.

21-Concordance

  • The negative area of the QRS complex is greater than the two positive areas combined. The QRS complex is therefore net negative, and therefore discordant with the positive T-wave deflection.

21-Discordance

Normal T-wave
  • Upright in all leads except aVR and V1
  • Amplitude < 5mm in limb leads, < 10mm in precordial leads (10mm in men, 8mm in women)
Abnormal T-waves
  • Peaked T waves
    • Hyperkalaemia
  • Hyperacute T waves
    • Early stages of STEMI; often precede the ST elevation and Q waves.
  • Inverted T waves
    • Normal finding in children
    • Persistent juvenile T wave pattern
    • Myocardial ischaemia and infarction
    • Bundle branch block
    • Ventricular hypertrophy (‘strain’ patterns)
    • Pulmonary embolism
    • Hypertrophic cardiomyopathy
    • Raised intracranial pressure
  • Biphasic T waves
    • Myocardial ischaemia
    • Hypokalaemia
  • ‘Camel Hump’ T waves
  • Flattened T waves
Tall, narrow, symmetrically peaked T-waves are characteristically seen in hyperkalaemia.
https://litfl.com/t-wave-ecg-library/
Broad, asymmetrically peaked or ‘hyperacute’ T-waves are seen in the early stages of (STEMI)
https://litfl.com/qt-interval-ecg-library/
Inverted T-waves in the right precordial leads (V1-3) are a normal finding in children, representing the dominance of right ventricular forces.
https://litfl.com/t-wave-ecg-library/
Inverted T-waves in the right precordial leads (V1-3) are a normal finding in children, representing the dominance of right ventricular forces.
https://litfl.com/t-wave-ecg-library/
Myocardial Ischaemia and Infarction: T-wave inversions due to myocardial ischaemia or infarction occur in contiguous leads based on the anatomical location of the area of ischaemia/infarction:
  • Inferior = II, III, aVF
  • Lateral = I, aVL, V5-6
  • Anterior = V2-6
Inferior T wave inversion with Q waves, prior to myocardial infarction
https://litfl.com/t-wave-ecg-library/
Left ventricular hypertrophy (LVH) produces T-wave inversion in the lateral leads I, aVL, V5-6, with a similar morphology to that seen in LBBB.
https://litfl.com/t-wave-ecg-library/
Right ventricular hypertrophy produces T-wave inversion in the right precordial leads V1-3 and also the inferior leads (II, III, aVF).
https://litfl.com/t-wave-ecg-library/
Acute right heart strain (e.g. secondary to massive pulmonary embolism) produces a similar pattern to RVH T-wave inversions in the right precordial (V1-3) and inferior (II, III, aVF) leads.
https://litfl.com/t-wave-ecg-library/
Events causing a sudden rise in intracranial pressure (e.g. subarachnoid haemorrhage) produce widespread deep T-wave inversions.
https://litfl.com/t-wave-ecg-library/
Biphasic T waves due to ischaemia – T waves go up, then down
https://litfl.com/t-wave-ecg-library/
Biphasic T waves due to hypokalaemia – T waves go down, then up
https://litfl.com/t-wave-ecg-library/
Children & Adolescent T-Waves:

Usually show inverted T-waves due to different electrical vector (inversion may be present in all leads); should normalise during puberty.

  • Some late adolescent can display inversions in V1-V4 (Persisting Juvenile T-wave)
  • If all T-wave remain inverted in adulthood it is called ‘Idiopathic global T-wave inversion’

Progression in T-waves should follow R-wave progression rule.

Positive T-wave:

< 6mm in limb leads / 8-10mm in V2-V3 – Outside these ranges are abnormal caused by hyperkalaemia; deafferented with hyperacute T-waves seen in ACS (broad-based, high & symmetric).

Negative/Inverted T-wave:

V1 concordant is normal (as V1 QRS is negative); can occur in L3, V2 & aVL – Two inversions in two contiguous leads is a medical concern.

  • Inversion with ST deviation are possible ischemia (usually invert after ischaemic event)
  • Post-AMI the T-wave can be symmetric with varying depth (>10mm or <1mm)
  • T-wave inversion can be chronic after AMI
  • Secondary T-wave inversions can occur from many conditions – They are symmetrical
Flat T-waves:

Low amplitude common in post-ischemia; common in V1-V3 if stent is in LAD or L2, L3, & aVF (RAD/Cx)

Biphasic (Diphasic) T-waves:

Has a positive & negative deflection – Biphasic has no significance and classified as per positive or inverted.

ST Segment Changes

The ST Segment is a reflection on the plateau phase (Phase 2) as membrane potential remains relatively unchanged (most ventricles are in this phase) therefore, there isn’t electrical potential differences in myocardium resulting in the flat & isoelectric ST segment

  • The transition from ST segment to T-wave is smooth & non-abrupt
  • Changes in ST segment usually results in T-wave changes
  • ST Segment extend from J-point to T-wave onset
  • ST height change (in mm) is between J-point & PR segment

ST Segment Deviation Measurement

Ischemia is always confined to a specific area where cell’s membrane potential change as result of the ischemia – therefore electrical potential changes in the myocardium displacing the ST segment up or down.

The magnitude of ST segment elevation or depression is measured from the isoelectric baseline to the J-point.

  • J-point > 4mm above the PR segment baseline = ST Elevation
  • J-point > 3mm below the PR segment baseline = ST Depression

https://litfl.com/j-point-ecg-library/

ST-T Changes

Primary ST-T Change:

Caused by abnormal repolarisation

  • Ischemia
  • Electrolyte Disorders
  • Tachycardia
  • Increased Sympathetic Tone
  • Drugs

Secondary ST-T Change:

Abnormal depolarisation causing abnormal repolarisation

  • Bundle branch blocks
  • Pre-excitation
  • Ventricular hypertrophy
  • Premature ventricular complex
  • Pacemakers stimulated beats
ST Segment Elevation

Ischemia causes straight or convex ST elevation -  Straight ST segments can be upsloping, horizontal or downslope (rare). Non-ischemic ST elevation is usually concaved – Common in any population. Most males under 70yo has ST elevation in V2 & V3 – Therefore take caution

Causes of ST Segment Elevation

  • Acute myocardial infarction
  • Coronary vasospasm (Printzmetal’s angina)
  • Pericarditis
  • Benign early repolarization
  • Left bundle branch block
  • Left ventricular hypertrophy
  • Ventricular aneurysm
  • Brugada syndrome
  • Ventricular paced rhythm
  • Raised intracranial pressure
  • Takotsubo Cardiomyopathy

Myocardial Infarction

https://litfl.com/st-segment-ecg-library/

ST Segment Morphology in Other Conditions

https://litfl.com/st-segment-ecg-library/
https://litfl.com/st-segment-ecg-library/
ST Segment Depression (STD)

If ST segment is < 0.5 mm then it is acceptable in all leads; anything more is considered pathological

Primary ST Depressions:

  • Exercise & hyperventilation should be < 1mm depressed (normalising after exercise is done)
  • Digoxin causes curved ST segment (seen in most leads
  • Heart failure can cause STD in left-lateral lead (V5-V6, aVL, & Lead I) – horizontal or downslope
  • SVT can be seen in V4-V6 with horizontal or slight upslope – Resolve within minutes
  • Upslope ST with prominent T-wave in most precordial leads = LAD occlusion

Secondary ST Depressions:

  • Common conditions (listed above) causing abnormal depolarisation (altered QRS) causing abnormal repolarisation (altered ST-T).

https://litfl.com/st-segment-ecg-library/

ST segment morphology in myocardial ischaemia

https://litfl.com/st-segment-ecg-library/

ST segment morphology in posterior MI

https://litfl.com/st-segment-ecg-library/
QT Changes

Represents total time for depolarisation and repolarisation (beginning of QRS to end of T-wave). Prolonged QR duration leads to dangerous ventricular arrhythmias – Inversed to heart rate (ie. High HR = Short QT).

  • Congenital cause of prolonged QT includes genetics, & long-QT syndrome
  • Acquired cause of prolonged QT includes medications, & electrolyte disorders
Bazzett’s Formula:

Explains the inverse relationship of QT & heart rate – This creates the corrected QT duration (QTc) calculated automatically – Cannot be used if bradycardia or tachycardia.

Note: All variables are in seconds (s)

QTc Interval Values
  • Males: < 0.450s
  • Females: < 0.460s
  • Short QTc Syndrome can be < 0.390s – uncommon
Prolong QTc Causes:
  • Antiarrhythmics (-mides, -olol, & Amiodarone)
  • Psychiatric medications
  • Antibiotics
  • Hyperkalaemia
  • Hypocalcaemia
  • Hypomagnesemia
  • Cerebrovascular Bleeding
  • Ischemia
  • Cardiomyopathy
  • Bradycardia
  • Hypothyroidism
  • Hypothermia
Short QTc Causes:
  • Hypocalcaemia
  • Digoxin treatment
  • Malignant Arrythmias
QT Dispersion:

Difference between the shortest & longest QT interval. This is due to the variations of QT interval in different leads,

  • Long QT dispersion is increased risk group due to higher incidence of ventricular arrythmias

References

College of Pre-Hospital Care. (2015). 12-Lead ECG Analysis: Self-Directed Learning Package. Version 3. St John Ambulance Ltd.  

Curtis, K., & Ramsden, C. (2016). Emergency and trauma care for Nurses and Paramedics (2nd ed.). Elsevier Australia.

DeLaune, S. C., Ladner, P. K., McTier, L., Tollefson, J., & Lawrence, J. (2016). Australian and New Zealand fundamentals of nursing (1st ed.). Cengage Learning Australia Pty Limited.

ECG & ECHO Learning. (2020). Clinical ECG Interpretation. https://ecgwaves.com/topic/ecg-normal-p-wave-qrs-complex-st-segment-t-wave-j-point/

Life in the Fast Lane. (2020). ECG Library. https://litfl.com/ecg-library/

St John WA Ltd. (2017). Electrocardiography (ECG). Clinical Resources. https://clinical.stjohnwa.com.au/clinical-skills/assessment/vital-signs/electrocardiography-(ecg)

WikiEM. 2020. The Global Emergency Medicine Wiki. https://www.wikem.org


Page contributors:

60825Thanh Bui, AP60825
Event Medic, Emergency Medical Technician &
Volunteer Development Officer

 

16790

Andrew Moffat, AP16790
Volunteer Training Manager & Volunteer Development Officer

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