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ECG Interpretation

6 min read

Assessing a Rhythm Strip in an Unstable/Critical Patient

  1. Is there any electrical activity?
  2. What is the ventricular QRS rate?
  3. Is the QRS rhythm regular or irregular?
  4. Is the QRS complex width normal (‘narrow’) or broad?
  5. Is atrial activity present?
  6. Is atrial activity related to ventricular activity and, if so, how?

Procedure

  • 3-electrode system (gives leads I, II and III)
  • 5-electrode system (gives leads I, II and III and a single unipolar lead depending on the position of the brown lead V1-6)

Basics

Rate, Rhythm, Axis

  • Rate
    • Multiply the number of QRS complexes in the 10 second strip by 6 or do 300 divded by the R-R interval in number of large squares
      • 1 square = 300
      • 2 square = 150
      • 3 square = 100
      • 4 square = 75
      • 5 square = 60
  • Rhythm
    • If in doubt, use a piece of paper to mark out at least 3 consecutive R waves and check the rate is the same further along the rhythm strip
    • Regular rhythm with abnormal P wave preceding each QRS complex ⇒ atrial rhythm
    • Irregular rhythm with P waves ⇒ multifocal atrial rhythm
    • Regular narrow-complex rhythm with no (or retrograde) P waves ⇒ SVT
    • Regular rhythm with visible flutter waves ⇒ atrial flutter
    • Irregular rhythm with no P waves ⇒ atrial fibrillation or atrial flutter with variable AV conduction block
  • Axis
    • Always compare to the TP line
    • LA/RA reversal is defined by features:
      • Lead I becomes inverted
      • Leads II and III switch places
      • Leads aVL and aVR switch places
      • Lead aVF remains unchanged
      • In comparison to dextrocardia, it has normal R-wave progression

P Wave

  • P wave configurations in lead II:
    • P mitrale ⇒ left atrial enlargement
    • P pulmonale ⇒ right atrial enlargement

PR Interval

  • Start of P wave to the start of the QRS complex
  • Normal duration is 120-200 msec (3-5 small squares)
  • First-degree AV block if >200 msec
  • Accessory AV pathway/pre-excitation if <120 msec

Q Waves

  • Pathological if any of:
    • More than 33% of total QRS complex
    • More than 2mm deep
    • More than 40 msec (one small square) width
    • Present in leads V1-3
  • Small Q waves can be normal in leads III and V1 as well as I, aVL and V5-6

QRS Complex

  • Duration
    • Normal duration <120 msec
    • Widened QRS suggests some abnormal ventricular conduction (e.g. bundle branch block, ventricular origin, accessory pathway etc.)
    • A wide QRS complex causes secondary ST segment and T wave changes making it sometimes difficult to interpret
  • Height
    • Low voltage overall may be caused by body habitus, lung hyperinflation (e.g. COPD), hypothermia, hypothyroidism, pericardial effusion, chronic cardiac ischaemia

R Wave Progression

  • QRS complexes are predominantly negative in V1 and become more positive across to V6, being equipotent at V3 or V4

ST Segments

  • Always assess for:
    • Elevation
    • Depression
    • Shape (concave up, concave down, horizontal etc)
      • Concave up shape is less concerning for ischaemia

T Waves

  • Assess for:
    • Orientation
    • Height
  • Normal to have inverted T waves in aVR and V1 and occasionally in V2 and inferior leads

QT Interval

  • Measured from the start of the QTS complex until the end of the T wave
  • Prolonged if:
    • QTc >440 msec in men (440-450 msec considered borderline)
    • QTC >460 msec in women (440-460 msec considerred borderline)
  • A QTc >500 msec is associated with an increased risk of Torsades de Pointes VT

Rule of thumb for QT Intervals

The QT interval should be less than half of the proceeding R-R interval

Other Waves

  • Delta wave (slurred initial upslope on QRS complex) ⇒ ventricular pre-excitation in WPW syndrome
  • J (Osborne wave) notch at junction of QRS and ST segment ⇒ hypothermia, hypercalcaemia, vasospastic angina, SAH
  • U wave (occurs after T wave) ⇒ hypokalaemia, bradycardia

Myocardial Ischaemia and Infarction

What to do if you are unsure about ischaemic changes in an ECG (provided the patient is stable)

  • Repeat the ECG in 20 minutes
  • Call for help
  • ECG changes in ischaemia in order:
    1. Hyperacute T waves
    2. ST-segment elevation/depression
    3. Q waves (although not always)
    4. T wave inversion
  • Posterior STEMI features on a standard ECG:
    • Reciprocal changes in anterior leads (V1-3) such as:
      • ST elevation in V1-3
      • Tall, braod (30msec) R waves (uspide down Q waves)
      • Upright T waves
      • Dominant R waves in V2
    • Only 0.5mm of ST elevation in V7, 8 or 9 is required for a diagnosis of posterior STEMI

Posterior OMI

  • ST depression maximal in leads V1-4 without progression to V5-6 is highly concerning for a posterior OMI and can be considered to be posterior MI even in the absence of ST elevation in V7-9
    • This is because of poor conduction through the aerated lung

  • Inferior MI involving the right ventricle ECG features:
    • ST elevation in lead III > lead II
    • ST elevation in V1 > V2
    • ST elevation in V1
    • Consider RV infarct in all cases of inferior MI
    • Proceed with a right sided ECG or use V4RT
    • Be careful of GTN as it can cause hypotension
  • De Winter T waves
    • ECG features
      • Tall, prominent, symmetrical T waves in precordial leads
      • Upsloping ST segment depression >1mm at the J point in the precordial leads (no ST elevation int he precordial leads)
      • Reciprocal ST segmeent elevation in aVR
    • Typical STEMI morphology may precede or follow the De Winter pattern
    • Treat as a STEMi equivalent
  • Wellen’s snydrome
    • ECG features: deeply inverted or biphasic T waves in V2-3
    • Highly specific for critical stenosis of the proximal LAD and often do poorly with medical therapy
    • However do not mix with the right ventricular strain pattern:
  • ST and T wave changes in LBBB/paced rhythms
  • Left main coronary artery occlusion
    • ECG features (although note that these findings aren’t necessarily specific)
      • Widespread ST depression in mostly leads I, II and V4-6
      • ST elevation in aVR ≥1mm
      • ST elevation in aVR ≥ V1
  • Other ECG patterns:
    • ST depression in 2 or more precordial leads may indicate transmural posterior injury
    • Hyperacute T-wave changes may be observed in the early phase of STEMI
    • New RBBB and LAFB is highly associated with proximal LAD occlusion

Conduction Disease

Sinus Node Dysfunction

Sinus Arrhythmia

https://www.youtube.com/watch?v=H6yTQm2h8dc

  • Note that all the P waves as the same morphology indicating that they likely originate from the same area/place

SA Nodal Exit Block

  • Depolorisation of the SA node itself does not produce any discernable ECG features
  • Difficult to diagnose SA nodal exit block on ECG, generally some kind of EP study is needed

Sinus Pause

Sinus Arrest

  • Sinus arrest = long sinus pause
    • Will result in asystole if no escape rhythm present

Sick Sinus Syndrome

  • Sick sinus syndrome = sinus node dysfunction + secondary symptoms (e.g. lightheadedness, syncope, heart failure symptoms)
  • Tachycardia-bradycardia syndrome = sick sinus syndrome + atrial tachyarrhythmia (e.g. atrial flutter or atrial fibrillation)

Tachyarrhythmias

Hypertrophy

  • Broadly speaking, the changes in hypertrophy are:
    • Chamber can take longer to depolarise ⇒ ECG wave increases in duration
    • Chamber can generate more current and larger voltage ⇒ ECG wave increases in amplitude
    • A larger percentage of the total electrical current can move through the expanded temperature resulting in a shift of the axis

Other Cardiac Conditions

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