Download ECG Interpretation

ECG Interpretation
The key to analysis of all ECGs is to have a method for review and apply this to all
ECGs.
This guide is not a thorough review of methods for analysis of ECGs. It is aimed to
assist teaching of ECG interpretation with actual ECGs for analysis and discussion.
REMINDERS.
Wave Denomination:
Q – first downward deflection.
R – Forst upward deflection.
S – downward deflection following an R wave.
R1 – second upward deflection.
S1 – second downward deflection following a R1.
Lead types:
Bipolar leads:
-I, II, III.
-Measures differences in potential between 2 leads as expressed in Einthovens
triangle.
Unipolar leads:
-V1-V6 (Precordial leads).
-Lead compares potential with that of a reference point that averages total
body potential.
-Posterior leads – V7, V8, V9.
-V4R – Measure potential on RHS of heart. Lead is placed in same position at
V4 but on RHS of patient.
Augmented unipolar leads:
- aVR, aVL, aVF.
- Compare potential with central point of Einthovens triangle.
- Augmented to increase size of complexes.
The Normal ECG:
Durations:
- PR interval: 120 -200ms (5 small squares).
Measured from beginning of P wave to beginning of QRS complex.
- QRS duration: <120ms (3 small squares).
- QT interval: 400ms (2 large squares).
Measured from beginning of Q to the end of T wave.
- QTc = QT interval/√RR interval.
Cardiac axis:
- Normal = -30 to +120 degrees.
QRS complex:
- Small Q waves permissible in I, aVL, V6.
- RSR pattern in V1 normal if duration <120ms (partial RBBB).
- R wave < S in V1.
- R in V6 < 25mm.
- R in V6 plus S in V1 <35mm.
T wave may be inverted in: III, aVR, V1.
RBBB:
QRS duration >120ms.
RSR pattern.
Inverted T waves V1-3.
Deep and wide S waves in V6.
LBBB:
QRS duration >120ms.
“M” pattern in V6.
No septal Q waves.
Inverted T waves I, aVL, V5-6.
SYSTEM FOR REVIEW OF ECGs.
1. Rate.
There is a standard rate for ECG machines to run (25mm/sec).
Each large square: 0.2sec = 200ms. (i.e. 5 large squares/sec).
HR calculated by dividing 300 by number of large squares between QRS
complexes (eg 2 large squares – HR = 150/min)
2. Rhythm.
3. Axis.
Quickly calculated by using leads I and aVF. These leads look at right angles of
the heart.
Lead I.
aVF
Note: a positive deflection in aVF is directed downwards.
A normal axis is -30 to +120 degrees.
Left axis deviation (LAD) is -30 to -90 degrees.
Right axis deviation (RAD) is +120 to +180 degrees.
The Electrical Axis
-90
aVR
-150
aVL
-30
I
0
+180
III
+120
II
+60
aVF
+90
Bundle and fascicle blocks:
The R bundle branch has no main divisions. The L bundle has 2 – the anterior
and posterior fascicles.
RBBB:
Incomplete – RSR1 pattern, QRS < 0.12 sec.
Complete – RSR1 pattern, QRS > 0.12 sec.
When the R bundle branch is blocked the cardiac axis is usually normal,
because there is normal depolarisation of the L ventricle with its large muscle
mass.
LBBB:
LBBB – QRS > 0.12 sec.
DETAILS.
L anterior hemiblock:
Axis < -30 degrees.
QRS < 0.12 sec
If the anterior fascicle is blocked the left ventricle depolarises through the
posterior fascicle and so the cardiac axis is deviated to the left. Left axis
deviation is therefore due to the left anterior fascicular block.
Note the QRS duration remains <120ms with a pure anterior fascicular block.
L posterior hemiblock:
Axis > 120 degrees.
QRS < 0.12 sec.
The posterior fascicle rarely is selectively blocked. If it does occur it causes a
R axis deviation.
If there is a RBBB and a Left anterior fascicular block the ECG shows a
RBBB and left axis deviation (LAD). This may be called a bifascicular block.
4. P wave
- P mitrale - Broad and bifid P waves. Seen with Left atrial hypertrophy
(LAH).
- P pulmonale – Peaked P waves (Height >2.5mm). Seen with Right
atrial hypertrophy (RAH) (eg pulmonary hypertension).
5. QRS wave
This is widened if there is a BBB or if depolarisation starts in ventricular muscle.
Increased height of the QRS complex is seen with increased muscle mass.
Pathological Q waves: Greater than 1 small square +/- deeper than 2mm.
6. T waves.
T waves may be normal and yet inverted in III, avR and V1.
Inversion is usually associated with BBB, ischaemia and ventricular hypertrophy.
7. ST segments.
ST segments should be isoelectric.
They may be described as depressed or elevated.
Common Abnormalities
LV hypertrophy:
Large R wave in V6 plus large S wave in V1 (R+S >35mm).
RV hypertrophy:
R axis deviation.
R in V1 + S V6 >11 mm.
Ischaemia:
Q waves – old infarct
STD
TWI
Infarction – STE, NSTEMI
Inferior AMI – II, III, aVF.
R sided chest leads should be done to look for STE in V4R – indicating
RV infarction. This occurs in ~ 30% of patients with an inferior AMI.
Anterior AMI – V2-4
Posterior AMI – ST depression in V1-2. Posterior leads show the STE.
Lateral AMI – I, aVL, V5-6.
Ectopic beats:
Narrow complex (QRS <120ms) – supraventricular in origin.
Wide complex (QRS >120ms) – ventricular in origin.
Rhythm Disturbances
Bradyarrhythmias (HR<60/min):
HR < 60/min.
-
Regular P waves followed by QRS complexes – sinus bradycardia.
-
P waves before some but not all QRS complexes – second degree heart
block.
a) Wenchebach: Progressive PR lengthening followed by a
nonconducted P wave. Repeated cycles.
b) Mobitz Type 2: Occasional nonconducted beats. Eg 2:1 – 2 P waves
per QRS complex. Normal P wave rate.
-
No relationship between P waves and QRS complexes – third degree
heart block.
-
No P waves – sinus arrest.
- QRS narrow (<120ms) – nodal escape rhythm.
- Wide QRS (>120ms) – ventricular escape rhythm.
Tachyarrythmias:
HR > 100/min.
These are grouped into narrow complex (QRS<120ms) or wide complex (QRS >
120ms) tachyarrythmias.
Narrow complex:
- No P waves
- Irregular - Atrial fibrillation
- Regular – Atrial flutter or supraventricular tachycardia (SVT).
-
Normal P waves
- Sinus tachycardia
-
Abnormal P waves
- Irregular – Multifocal atrial tachycardia
- Regular – Atrial tachycardia.
Wide Complex:
- VT
-
-
SVT with conduction abnormality – eg bundle branch block with AF.
Torsade de Pointe
VF
Electrolyte effects on ECGs:
Hyponatremia:
May be associated with low voltage complexes.
Hyperkalemia:
Tall peaked T waves.
Atrial paralysis (no P waves).
Prolongation of QRS complexes.
Ventricular arrhythmias.
Hypokalemia:
Prolongation of PR interval.
Prominent U waves.
Occasional late TWI in precordial leads.
QT interval appears prolonged if T and U waves merge (the real QT is not
prolonged).
Hypercalcemia:
Shortened QT interval.
Widening of T waves.
Bradyarrhythmias, BBB.
Hypocalcemia:
Prolonged QT.
ST prolongation.
TW abnormalities.