The document discusses cardiac axis and mean QRS axis, which represents the direction of electrical spread during ventricular depolarization. It is measured in the frontal plane based on the limb leads. The lead with the tallest R wave is closest to the axis. The normal range is -30 to +120 degrees with right and left axis deviations indicating abnormalities. Common causes of axis changes are also listed.

1. Cardiac axis

2. Background
• The spread of the cardiac impulse gives rise to
the main deflections of the ECG.
• The total electrical activity at any one moment
of time can be summated and represented by
a single electrical force.
• This force has magnitude and direction and is
termed the instantaneous vector.

3. • All the vectors occurring in the ventricles
during the production of the QRS can be
averaged.
• The direction of the resulting vector of
electrical spread is called the MEAN QRS AXIS.

4. • It is customary to measure this only in the
frontal plane.
• It is based on the orientation of the limb
leads, I, II , III, aVR, aVL & aVF.
• The limb lead with the tallest R wave will be
the closest to the QRS axis.

5. • Magnitude and direction of potential
• Instant vector – at particular instant during
cardiac cycle
• Mean vector -Ventricle depolarization :
direction of potential –base to apex

6. • Triaxial reference system
• Hexa-axial reference system

7. • Calculating mean axis from Std Lead ECG

8. • MEA of normal
ventricle= -30° to +120°
• RAD
• +120° to +180°
• Rt ventricular
hypertrophy
• Rt bundle branch block
• Posterior /inferior MI

9. • LAD : -30° to -90°
• Left ventricular
hypertrophy
• Obesity
• Left bundle branch block
• Anterolateral MI

10. • Vector cardiography

11. • HIS bundle electrogram
• Using intracardiac electrodes
• A deflection-
activation of AV node
• H spike-
Transmission through
His bundle
• V deflection-
ventricular depolarisation
• Uses
• In heart blocks

12. • PA interval
• First appearance of atrial depolarization to A
wave
• 27msec
• AH interval -92msec
• HV interval – 43msec

13. • Cardiac arrhthymias
• Distruption of normal rhthym
• Sinus rhthym – SA node –pacemaker, P wave
followed by QRS complex, P-R & Q-T interval –
normal.
• Sinus arrhthymia
• Normal sinus rhthym except varied RR interval
• Phases of respiration
• Children
• Endurance athelets

14. • Sinus tachycardia
• Fever
• Hyperthyroidism
Sinus bradycardiac
Endurance athelets
Sick sinus syndrome
Marked bradycardia with dizziness & syncope

15. • Conduction blocks
• SA nodal block
• AV nodal block
• Bundle branch block

16. • SA nodal block
• Elderly pt recovering from coronary artery
occlusion
• AV node becomes pacemaker –AV nodal
rhthym/ junctional rhythm
• Inverted P wave , normal QRS , slow HR

17. • AV nodal block
• First degree
• Second degree
• Complete
• First degree
• Slowing of conduction at AV node

18. • Second degree
• Not all atrial impluses are conducted to
ventricles
• One ventricular contraction after every 2,3 /4
atrial contractions
• Mobitz type I (Wenckebach phenomenon)
• Progressive lengthening of PR interval & finally
failure of one impulse
• Mobitz type II(Periodic block)
• Occasional failure of conduction
• Atrial:ventricular rate= 6:5 or 8:7

19. • Third degree /complete AV nodal block
• No impulse transmission to ventricles
• Ventricles beats at their own rhthym-
idioventricular rhthym
• Ventricular asystole –dizziness & fainting –
Stokes-Adams syndrome
• ECG- complete dissociation between P wave &
QRS complex-atrioventricular dissociation
• In organic heart diseases
• Septal MI

21. • Myocardial Infarction
• ST segment elevation (zone of injury)
• Inverted T wave(surrounding tissue)
• Deep Q wave(dead muscle)

23. • Within mins to hrs ST seg elevation with Tall T
wave
• After 2days T waves-inverted
• After a week deep Q wave
• ST seg and T waves starts become normal

24. Infarction. When myocardial injury persists, MI is
the result.
• During the earliest stage of MI, known as the
hyperacute phase, the T waves become tall
and narrow. This configuration is referred to as
hyperacute or peaked T waves.
• Within a few hours, these hyperacute T waves
invert.
• Next, the ST segments elevate, a pattern that
usually lasts from several hours to several
days.

25. • In addition to the ST segment elevations in the
leads of the ECG facing the injured heart, the
leads facing away from the injured area may
show ST segment depression.
• This finding is known as reciprocal ST segment
changes.
• Reciprocal changes are most likely to be seen at
the onset of infarction, but their presence on the
ECG does not last long.
• Reciprocal ST segment depressions may simply be
a mirror image of the ST segment elevations.

26. • Anterior wall-Lead I, aVL & chest leads
• Inferior wall- II, III, aVF
• Lateral wall – Lead I, aVL, & V6
• Reciprocal changes- L-II, L-III, aVF & V1

28. • Physiological changes in acute MI
• Injury current- affected to unaffected part
• 1.Decline in RMP
• 2.Delayed depolarization
• 3.Rapid repolarization

29. • Decline in RMP
• Ischaemic necrosis- K efflux & Na influx
• Inside of cell- less negative
• Extracellular current flows into the infarct

30. • During depolarization
• Infarcted area- slowly depolarized
• Inside of infarcted cells attains positivity later
(remains negative)
• Extracellular current flows out of infarct

31. • During repolarization
• Infarct cell-Rapid repolarization due to
opening of K channels (K efflux)
• Inside becomes negative

32. • Therefore there is
• Resultant extracellular current flow out of
infarct during depolarization & repolarization
• Flow of current towards recording electrode
over infarcted area causes increased positivity
between S and T wave- ST seg elevation.

34. • Anterior wall- anterior des left co A
• Inferior wall-posterior des rt co A
• posterior wall- Left circumflexleft co A