Cardiac vector and axis

this power point teaches about how to determine the cardiac axis and the vector

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 H is 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

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

21. 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

22. 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.

23. 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.

24. 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

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

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

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

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

29. 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.

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