Category: ECGs

July 19 MOTM – Chest pain

Clinical Picture:

56 year old accountant presented to the Emergency Department at 2pm having developed central chest pain at 1pm after his lunch break at work. He was given aspirin and GTN by the paramedics which resolved his chest pain.

He has borderline type 2 diabetes, but takes no regular medications.

His father and some of his uncles have heart problems.

On examination his observations are within normal limits. He looks well (although the ambulance report notes him to have been sweaty at the scene). His cardiovascular, respiratory and abdominal examinations are unremarkable.

Investigations:

Initial troponin: 6

6h troponin: 8

ECG:

Outcome:

Patient remained chest pain free in A&E and was discharged with advice to present to his GP for a referral to the rapid access chest pain clinic.

Unfortunately the patient sustained a cardiac arrest 2 days later. Despite re-establishing cardiac output he passed away 6 days later on ICU.

What was the mistake?

Initial ECG showed Wellens Syndrome (biphasic T waves in V1-4). This is suggestive of critical stenosis of the left anterior descending artery (LAD). These patients are at very high risk of anterior MI and should be admitted for an inpatient angiogram.

To learn more about Wellens syndrome click here

ECG interpretation

First the basics:

Lead Placement:

Red – right arm

Yellow – left arm

Green – left leg

Black – right leg

Remember limb leads by: Ride Your Green Bike

 

Physical lead representation:

 

ECG cardiac representation:

 

  1. Checks
  • Check for any patient identifiers
  • Any previous ECGs for comparison
  • Often the presence of chest pain is documented on the ECG – this should be noted.
  • Check the calibration

A – standard (10mm/mV or 2 large squares)

B – half (5mm/mV or 1 large square)

C – double (20mm/mV or 4 large squares)

All should be 0.2secs (5 small squares) width

 

  1. Rate

Divide 300 by the number of large squares between 2 QRS complexes

or

Multiply the number of QRS complexes by 6 (ECG is 10 seconds long).

Useful for irregular rhythms.

This ECG has 10 QRS complexes

10 x 6 = 60

Therefore rate is 60 bpm

 

  1. Rhythm

Is it regular, irregular or irregularly irregular?

Is there is a P wave before every QRS complex?

If p waves are present, is the PR duration constant?

Commonly encountered rhythms:

Sinus rhythm:

  • P wave occurs before every QRS complex
  • PR duration 3-5 small square (0.12-0.2secs)
  • PR duration is constant

Normal sinus rhythm: HR 60 – 100bpm

Sinus tachycardia: HR >100bpm

Sinus bradycardia: HR < 60bpm (not considered clinically significant until <50bpm)

Supraventricular tachycardias:

Atrial Fibrillation:

  • RR duration is irregular
  • P waves are absent

Atrial Flutter:

  • Rate classically 75bpm or 150bpm (3:1 or 2:1 block respectively)
  • Saw tooth appearance

Paroxysmal SVT or AV nodal re-entry tachycardia:

  • Regular tachycardia (usually 140-280bpm)
  • Narrow QRS complexes (unless pre-existed bundle branch block)
  • P waves often not visible as buried in QRS complex, but if seen often are inverted in inferior leads
  • QRS alternans (alternating height of QRS complexes)

Ventricular tachycardias:

Ventricular tachycardia:

  • Wide QRS complexes
  • Usually monomorphic (QRS complexes are a similar shape)

Ventricular fibrillation:

  • Chaotic ECG with no identifiable P waves, QRS complexes or T waves#
  1. Axis

Normal axis is -30° to +90°

Axis is the overall direction of travel of electricity within the heart. In a healthy heart the electrical impulse starts in the SA node travels to the AV node, down the Bundle of His and through the Purkinje fibers, therefore normal axis is in this general direction (towards lead II).

Axis can be ascertained in a variety of ways:

  1. Look at the ECG print out! (unlikely to be present in an exam, so make sure you practice the other methods)

  1. Rule of thumbs: https://youtu.be/gy0gkh1foR4
  • Take you own thumbs and use them as a representation of lead I and lead II
  • QRS complex positive = thumb up
  • QRS complex negative = thumb down
  • If both lead I and lead II are positive:
    • 2 thumbs up = normal axis
  • If lead I is positive and lead II is negative:
    • thumbs are leaving each other = left axis deviation
  • If lead I is negative and lead II is positive:
    • thumbs are reaching towards at each other = right axis deviation
  1. Calculating axis:
  • Identify the most isoelectric limb lead (the lead in which the R wave and S wave are of equivalent heights). This identifies the angle perpendicular to the axis, therefore the axis will be 90° from this.
  • Using the diagram above (which you should commit to memory) move 90° clockwise and anticlockwise from your isoelectric lead and identify the closest lead.
  • The lead with the positive QRS complex is the axis.
    • For example:

aVL is the most isoelectric lead

aVL is at -30°

90° anticlockwise = -120° (aVR – negative QRS complex)

90° clockwise = +60° (lead II – positive QRS complex)

Axis = 60° (accurate to within 15°)

Causes of left axis deviation (LAD):

  • Left bundle branch block (LBBB)
  • Left anterior hemiblock
  • Pacemaker
  • Inferior MI
  • Left ventricular hypertrophy
  • Wolff-Parkinson-White

Causes of right axis deviation (RAD):

  • Normal in children and tall, thin adults
  • Right ventricular hypertrophy
  • Lateral MI
  • PE
  • Chronic lung disease
  • Left posterior hemiblock
  • Dextrocardia
  • Wolff-Parkinson-White

Extreme axis deviation:

  • Ventricular arrhythmias
  • Hyperkalaemia
  • Severe right ventricular hypertrophy
  1. P waves

Calculate PR duration – should be between 3 and 5 small squares

If the PR duration is prolonged or not constant with the QRS duration, then this is likely to represent a heart block.

1st degree heart block:

  • PR duration >5 small squares, but constant

2nd degree heart block:

Mobitz type 1/Wenkebach:

  • Progressive prolongation of the PR interval eventually resulting in a missing QRS complex

Mobitz type 2:

  • P waves occurring at a regular rate
  • Intermittently P waves are not conducted into a QRS complex
    • This can occur in a fixed relationship (ie. 3:1 or 2:1 block) or with no pattern

3rd degree/complete heart block:

  • No association between P waves and QRS complexes
  • Often associated with bradycardia
  • At risk of ventricular standstill

P wave morphology – best assessed in lead II or V1

  • Bifid P waves – left atrial enlargement (mitral disease)
  • Tall P waves (>2.5mm in lead II) – right atrial enlargement (pulmonary hypertension
  1. QRS

Duration 70-100ms (>100ms is abnormal, but >120ms is required to diagnose bundle branch block)

Causes of broad QRS complexes:

  • Bundle branch block
  • Hyperkalaemia
  • Sodium-channel blockade
  • Wolff-Parkinson-White
  • Pacemaker
  • Hypothermia

Left bundle branch block (LBBB)

  • QRS duration >120ms
  • Dominant S wave in V1
  • Broad R wave in V6
  • Left axis deviation

Right bundle branch block (RBBB)

  • Broad QRS >120ms
  • M-shaped QRS complex in V1
  • Wide slurred S wave in V6

Bundle branch blocks can be remembered through the mnemonic ‘William Marrow’

  • LBBB – has a W-shape in V1 and a M-shape in V6 (WiLLiaM)
  • RBBB – has a M-shape in V1 and a W-shape in V6 (MaRRoW)

Are Q waves present?

  • Q waves are considered pathological if they are present in at least 2 contiguous leads and are > 1 small square wide and/or >25% height of R wave. Q waves in V1-V3 are almost always pathological.

R wave progression

  • R waves should progressively increase in height from V1 to V6
  • If R wave height <3mm in V3, then they are considered to have poor R wave progression. This is a suggestion of:
    • prior anteroseptal MI
    • left ventricular hypertrophy
    • dilated cardiomyopathy
    • Inaccurate lead placement (lead I and V6 should look similar)

Left ventricular hypertrophy:

S wave in V1 + R wave in V5 or V6 > 35mm

Right ventricular hypertrophy:

Ratio between R wave and S wave in V1 >1

  1. ST segments

Is elevation or depression present?

ST segment elevation MI (STEMI) is diagnosed when:

  • There is ST elevation in at least 2 contiguous leads of:
    • >2mm in chest leads
    • >1mm in limb leads
  • Horizontal ST depression in V1-V3 (posterior MI)
  • New LBBB
  • ECG meets Sgarbossa criteria in patients with LBBB or ventricular pacing (knowledge of this is not required at undergraduate level)

Left main coronary artery (LMCA) incomplete occlusion is clinically important, but ECG findings can be subtle, they include:

  • Widespread ST depression
  • ST elevation in aVR >1mm
  • ST elevation in aVR >V1

Other causes of ST elevation include:

  • Pericarditis (saddle-shaped ST elevation)
  • Benign early repolarization
  • Brugada syndrome
  • Raised intracranial pressure

ST depression is generally is sign of coronary insufficiency or reciprocal changes during a STEMI.

 

  1. T waves

T waves represent ventricular repolarization

T wave inversion is normal in aVR and V1 and can be a normal variant in lead III.

Also normal in children in V1-V3

Assess morphology:

  • T wave inversion
    • Infarction
    • Ischaemia
    • Bundle branch block
    • PE
    • HOCM
  • Biphasic T waves
    • Post-MI
    • Hypokalamia
    • Wellens syndrome ***can link to MOTM***
  • Peaked T waves
    • Hyperkalaemia
  • Flattened T waves
    • Ischaemia
    • Hypokalemia and other electrolyte disturbance
  1. U waves

U waves occur immediately after the T wave

They are best seen in V2 and V3

Occur in the same direction as the T wave

Prominent U waves occur with:

  • Bradycardia
  • Hypothermia
  • Severe hypokalaemia
  • Digoxin

  1. QT duration

Measured from the beginning of the QRS complex to the end of the T wave.

The QT interval shortens as the heart rate increases, therefore it should be corrected for heart rate.

This can be done via a number of formulas, the most well known being Bazett’s:

QTc = QT / √RR

However, these formulae are not very accurate at extremes of HR and therefore a QTc normogram is recommended.

In the absence of a normogram, QT can be crudely estimated as normal if the T wave finished before the midpoint of the RR interval.

Prolonged QTc puts the patient at risk of VT.

Causes of prolonged QTc:

  • Congenital long QT syndromes
  • Drugs ie. antipsychotics, TCAs, antihistamines, antiarrhythmics
  • Hypothermia
  • Hypokalaemia and other electrolyte disturbances