ECG Interpretation

ECG Interpretation*

·        Reference: ECG Made Easy, J R Hampton, Churchill Livingston, 1997. Well worth a read

·        5 mm (one large square) = 0.2 secs Þ 300 squares per minute

Leads

·        Depolarisation:

o   R > S: depolarisation spreading toward lead

o   R < S: depolarisation spreading away from lead

·        R = S: depolarisation at right angles to lead

Axis

·        To check axis, look at I, II and III.  Normal is between VL and VF

·        Alternative: cardiac axis is at right angles to lead in which R & S are the same size

·        Right Deviation: ? hypertrophy of RV or tall and thin.

·        Left deviation: ?hypertrophy of LV

QRS Complex in V Leads

·        Shape is determined by:

o  Septum is depolarised first, and the wave spreads from L to R in the septum:

§  V1 initially up as depolarisation in the septum (L ® R) is towards the lead

§  V6 initially down as depolarisation in the septum is away from lead

o  Muscle mass:  LV dominates so V1 is down and V6 is up.

Bundle Branch Block

·        Delay in depolarisation of part of the muscle ® widened QRS. If QRS > 3 small squares (0.12 secs) Þ slowed conduction Þ bundle block or ventricular ectopic beat.

·        Right Bundle Branch Block (Can be benign. ?Atrial septal defect): Left depolarises first, then right. May just be delay to the terminal end of QRS (especially in V5)

·        Left Bundle Branch Block. Always pathological. RV depolarises, then wave spreads to LV. T wave inversion in anterior and lateral leads is common (I, VL, V4 – V6). Wide QRS

o  Left bundle divides into the anterior and posterior fascicles. Failure of the anterior fascicle ® left axis deviation (depolarisation is through the posterior fascicle)

o  If LBBB: ?aortic stenosis, ischaemic disease

·        To determine side of block: W in V1 and M in V6 is Left (WiLLiam). M in V1 and W in V6 is Right (MaRRow). LBBB prevents any further interpretation of the ECG

Reporting an ECG

·        Check rate: bradycardia or tachycardia?

·        Check rhythm:

o   See also Arrhythmias,

o   Regular or irregular

o   Sinus rhythm = one P wave per QRS complex Þ depolarisation begins in SA node.

o   Sinus arrhythmia:

§  Bradycardia: athletes, fainting attacks, hypothermia, myxoedema, drugs

§  Tachycardia: exercise, fear, pain, shock, thyrotoxicosis

o   Supraventricular arrhythmia:

§  = Sinus, atrial or junctional/nodal arrhythmia

§  QRS is normal width (unless also bundle block) 

§  Escape beats are atrial, nodal or ventricular pacemakers that fire if the SA node fails, as they have a slower intrinsic rate. Escape beats come late.

·        Atrial escape: abnormal P wave after SA node fails.  Normal QRS

·        Nodal escape: no P wave (either none or buried in Normal QRS)

·        [Ventricular escape – not supraventricular: usually in complete heart block. Fast P waves. Slow wide QRS. Shape of QRS may vary.]

§  Extrasystole/ectopic beats come early – some part of the heart has depolarised prematurely

o   Distinguish Ventricular Tachycardia and supraventricular tachycardia with bundle branch block:

§  Both have wide QRS

§  But Supraventricular Tachycardia has P waves (check all leads). Compare QRS with normal QRS – if similar then bundle block.

o   Wolff-Parkinson-White Syndrome (a type of ventricular pre-excitation): Accessory conducting bundle, usually to LV ® short PR and QRS has abnormal slurred upstroke (delta wave)

o   Treatments:

§  Atrial Fibrillation: Digoxin

§  Junctional Tachycardia: Carotid sinus pressure then adenosine

§  Atrial Flutter: Carotid sinus pressure, adenosine, flecainide, DC conversation

§  Ventricular Tachycardia: lignocaine, DC conversion

·        Check Cardiac Axis

·        Check P wave: shape:

o   Normal is < 2 * 2 small squares

o   Right atrial hypertrophy (eg tricuspid stenosis) ® peaked P

o   Left atrial hypertrophy (eg mitral stenosis) ® broad, twin-peaked P, especially in II, III, aVF

o   Potassium: ¯K ® ­P, ­K ® ¯P

·        Check conduction intervals - PR interval:

o   From beginning of P wave to beginning of QRS = time for AP to spread from SA node to ventricular muscle.

o   Normal is 0.12 – 0.2 sec. (3 – 5 small squares)

·        Description of QRS Complex.  Width of QRS complex = time for AP to spread through ventricles:

o   Normal is <= 0.12 sec. (3 small squares)

o   ­Height Þ ­muscle mass

o   Right Ventricular Hypertrophy:

§  V1: R becomes higher (> 25 mm)

§  V6: S becomes deeper

§  Also look for:

·        Right axis deviation

·        Peaked P (right atrial hypertrophy)

·        Inverted T in V1 – V3

§  This picture is similar to a PE (which also has a Q wave in III)

o   Left Ventricular Hypertrophy:

§  V1: deep S wave

§  V6: Tall R wave (> 25 mm)

§  Inverted T wave in II, VL, V5 and V6

§  Left axis shift

o   Q waves:

§  Negative wave at start of QRS 

§  If > one small square wide and > 2 mm deep Þ patch of non-active muscle in the wall and the lead is „looking inside‟ the heart, not at the wall Þ old MI. Usually permanent

§  Anterior/septal infarct Þ Q wave in V2, V3 and V4 (Left anterior descending artery)

§  Anterior-lateral infarct Þ Q waves in I, II, VL. V3 – V6 (Left circumflex)

§  Lateral infarct Þ Q wave in I, V5, V6

§  Inferior infarct Þ Q wave in II, III and VF (Þ right coronary artery)

§  Inferior-lateral Þ Q wave in II, III, aVF, V5, V6

o  Bundle Branch Block

·        Description of ST segments:

o  If raised Þ acute injury – recent MI or pericarditis.  Anterior Þ V5, V6.  Inferior Þ III and VF

o  Depression Þ ischaemia not infarction

·        T wave:

o  Normally inverted in aVR and V1 (also V2 in young people and V3 in blacks)

o  If not full thickness infarct Þ T wave inversion but no Q wave (no „window‟ into heart) Þ non-Q wave infarction

o  If abnormal QRS Þ abnormal T of no significance (repolarisation also skewed)

o  Digoxin ® T wave inversion and sloping depression of the ST segment

o  Electrolyte imbalances:

§  ¯K ® T wave flattening

§  ­K ® tall, wide peaked T waves

·        QT interval

o  ¯Ca ® ­QT interval

o  ­Ca ® ¯QT interval

·        Progression following MI:

o  Elevation of ST

o  Q waves appear

o  T becomes inverted – may be permanent

ECG Abnormalities Due to Electrolyte Disturbances