ACADEMICS - Some medical articles

Reading an ECG - Part I

The ECG is a recording of the electrical activity of the heart – the cardiac impulse as it passes from the SA node, through the atria (P wave), the AV node (is it  PR interval? ), to the ventricles (QRS complex). (T is the repolarisation or recovery of ventricles). What about atrial repolarisation?

          Any given ECG lead records the ECG from a particular point in a particular plane; it does not record a particular chamber in isolation but it may show some chamber’s activity better because it is along the line of the chamber’s electrical activity or near to it.

          Let us see how the normal ECG looks like in different leads. We need to review 2 things here. First, the direction of the cardiac impulse.  It starts from the SA node (not seen on ECG) and activates the atria in a downward, leftward, posteriorish direction (see in class); after a small delay in the AV node, the ventricles are rapidly activated as the impulse passes along the His bundle, Purkinje system (so? Narrow QRS) – here the LV is ‘bigger’ and its forces dominate the RV forces. Thus the net ventricular impulse also goes downward, leftward and posteriorish. (see in class) Ventricular repolarisation is in the reverse direction of depolarization and so the T wave is in the same direction as the QRS complex.

          Second, let us see how the leads are oriented. (diagram in class) The standard leads are in the frontal or coronal plane – L I as along an outstretched left hand, parallel to the ground, denoted as 0 deg. L II is +60 deg. and in the direction of the heart towards the left leg. L III is another 60 i.e. +120 deg. Next, aVF is straight down at +90 deg; aVL and aVR are like the upper limbs of letter Y – and equidistant – so +210 or – 150 for aVR and – 30 for aVL.  

          The chest leads are round the chest in a transverse or cross sectional plane. V1 is at the right and front (Rt. 4^th space near sternum); V6 is at the right below the axilla; the other chest leads are in between.

The leads can be divided into groups on a spatial basis – V1 to V4 are anterior leads. L2, L3 and aVF are inferior leads. L1 and aVL and V5, V6 look somewhat similar and are the anterolateral leads and reflect the LV forces more because they face that chamber. V3R and V4R (and V1 a little bit) record RV forces when the RV is dominant. (discuss in class) ECG Complexes will record a positive wave in a lead when the net forces are going towards that lead strongly (a negative wave if in a totally opposite direction); if the impulse is perpendicular to a lead, that lead will show minimal or equiphasic deflection.

So, how does the normal ECG transcribe itself in different leads. (diagram in class)

We saw that the atrial depolarization or P wave goes down, left and posteriorish – so it is positive in L2 & aVF, and L1 and V6, maybe V5; negativish in V1 and negative in aVR. (actually all waves are negative in aVR – why?).

The QRS complex also similarly shows a dominant positive R wave in left leads (L1, aVL, V5, V6) and L2, aVF. As expected, the chest leads show a wonderful evolution of the R wave slowly growing in size from V1 to V6 and the S wave slowly diminishing. This is normal R wave progression in chest leads.

The T wave is normally in the same direction as the net QRS complex – so it is upright where R is big and negative where S or QS is big as in aVR and V1.

The intervening segments PR, ST and TP are all isolectric and at the same level.

Now, let us see how to read an ECG –

Know the clinical details; it helps to know what to expect in the ECG.

Check the rhythm and the rate.

See the P wave and then P-R interval

Study the QRS for duration, axis and progression in chest leads, and q waves.

See the ST segment and T wave

Check the QT interval.

See for chamber hypertrophy, ischemia, arrhythmias, etc.

1. It always helps to know the clinical details so that we know what to look for – e.g. in a 60 yr. diabetic / hypertensive with chest pain and sweating, we would be interested in looking for an MI; in a child with rheumatic fever, we may be interested in the PR interval for any AV block.

2. See the rhythm – for regularity and origin of impulse. Count the distance in mm. to see if regular; or mark 3-4 complexes on a paper (see in class) and follow consecutive complexes to see if they are regular.

Is it regular as in normal sinus rhythm, or in a brady (sinus brady or CHB) or in a tachy (SVT, VT, sinus tachy, atr. flutter usually, etc.)

(Sinus rhythm means there is one P for every QRS and vice versa. )

There may be occasional  irregularity due to an ectopic beat (atrial or ventricular) or an occasional dropped beat (due to AV block or sinus node arrest, etc.)

Or the rhythm may be totally irregular, as seen most commonly in AF.

3. Calculate the rate. Remember in an arrhythmia, we are more interested clinically in the ventricular rate. The ECG paper moves at a speed of 25 mm/sec, so each small square or mm. is 0.04 sec. Thus, count the no. of mm. between 2 successive QRS complexes (peak or any easily identifiable point) and divide 1500 by that – e.g. if the distance between two R peaks is 25mm, the heart rate is 1500/25 = 60.

In arrhythmias, you may have to calculate the P (atrial) and QRS (ventr.) rates separately. Bradycardia is <60 or less; tachycardia is 100 or more.

When the rhythm is irregular as in AF, count the no. of complexes in 6 secs. (150 mm. or 6 big squares) and multiply by 10.

4. Study the P wave – normally it is a small round hump shaped wave, less than 3 mm. tall and less than 3 mm. wide. From this, we can know atrial hypertrophy. In LA enlargement, the P wave is broad and bifid especially in L II; in V1, the P is bifid with a larger negative component. RAH causes a tall peaked P wave. (explanation in class)

5. Calculate the PR interval. Normally it is 3-5mm. (0.12 to 0.2 sec.) – as measured from the start of P to the start of QRS. If it is less, it is preexcitation as in WPW syndrome; if it is more, it is I deg. AV block.

Sometimes the PR is varying – it may slowly increase with each successive drop and then a QRS drops out – as in Wenckebach block (class expln.)  The PR interval totally varies in CHB.

6. Study the QRS complex – its duration, axis, morphology, R progression in chest leads and any abnormal Q waves indicative of MI. The normal duration of QRS is less than 3 mm. If it is wide it indicates the ventricular impulse is not going on the highway – the His Bundle and lt. & rt. Branches, His Purkinje system. i.e. there is a bundle branch block or the impulse is originating in the ventricular muscle (a ventricular ectopic).

Since the ventr. activation is downward and leftward, the axis on the frontal plane is between 0 and +90deg. An easy method to know the axis quadrant is to see LI and aVF – i.e. 0 and 90. If both show net positive QRS complexes the axis is normal. If LI is positive and aVF negative, QRS axis is left axis deviation as in LAHB, LVH, etc. If reverse, it is right axis deviation as in RVH, RBBB etc. (class explanation).

R wave progression refers to the normal increase in R height as we go from V1 to V6. This is lost (there is a diminutive R or a QS complex) in leads V1 to V3 or V4 or even beyond. This is seen in COPD and old anterior MI.

Small q waves are normally seen in left leads – these are septal waves (explanation in class).  Larger abnormal Q waves are seen in MI – this Q is 1mm wide or more & >1/4 of  R wave. Depending  on the site of  MI abnormal Q waves are seen  in the  following leads

Inferior MI  -  LII,  LIII, aVF,

Anteroseptal-V2, V3, V4

Extensive anterior MI –V1-V6, LI aVL

Anterolateral - LI, aVL, V5, V6,

Posterior MI  also occurs. how to diagnose posterior MI in E.C.G(in class)

7. See the ST segment - ST elevation  is seen classically in MI (STEMI) - in leads depending on the site of MI as above.

Pericarditis  is the  other condition  where ST elevation  is seen in all leads except VI and aVR where ST depression  is  seen.

ST depression is seen in non ST elevation MI (NSTEMI) and some cases of unstable angina.

T wave is a rounded wave - abnormalities include inversion which has many causes (chief of which is ischemia) and peaking  in hyperkalemia.

contd.

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