1. ECG BASICS & PHYSIOLOGY OF HEART

2. Heart is a pumping organ

4. How heart keeps pumping? 1.special structure of cardiac muscle syncytial nature syncytial nature both resting membrane potential & action potential are different form skeletal muscle both resting membrane potential & action potential are different form skeletal muscle 2.auto rhythmicity of heart

5. Action potential of heart muscle

6. Factors affecting action potential 1 K+ concentration 1 K+ concentration 2 Ca++ concentration 2 Ca++ concentration 3Na+ concentration 3Na+ concentration 4 temperature 4 temperature

7. Excitation contraction coupling

9. Duration of contraction Atria 0.2sec Atria 0.2sec Ventricle 0.3 sec Ventricle 0.3 sec Normally contraction time is 40% of cardiac cycle. When heart rate increases 3 times it is 65% of cardiac cycle. Normally contraction time is 40% of cardiac cycle. When heart rate increases 3 times it is 65% of cardiac cycle. Relaxation decreases Relaxation decreases Ventricular filling decreases Ventricular filling decreases

10. Cardiac cycle

11. Atrial systole

12. IMC

13. ejection phase

14. IMR

15. Heart sounds

17. Regulation of pumping 1Frank Starling mechanism 1Frank Starling mechanism 2 autonomic innervation 2 autonomic innervation Within physiological limit heart pumps all the blood that comes to it without allowing excessive pooling of blood in the veins Within physiological limit heart pumps all the blood that comes to it without allowing excessive pooling of blood in the veins

18. Parasympathetic innervation

19. Effects of autonomic stimulation Chronotropic effect Chronotropic effect Dromotropic effect Dromotropic effect Bathmotropic effect Bathmotropic effect Inotropic effect Inotropic effect

20. Effects of autonomic stimulation Sympathetic stimulation: HR can go upto 250 bpm in young individual. Sympathetic stimulation: HR can go upto 250 bpm in young individual. Parasympathetic stimulation: HR can go down to zero. Although vagal escape follows. Parasympathetic stimulation: HR can go down to zero. Although vagal escape follows. Both Sympathetic and parasympathetic system maintain a low level firing at resting condition. Both Sympathetic and parasympathetic system maintain a low level firing at resting condition.

21. Energy considerations Source: oxidative respiration Source: oxidative respiration FA- biggest source FA- biggest source glucose/ lactate also used glucose/ lactate also used Energy efficiency max 20-25%, rest is converted to heat (HF: 5-10% ) Energy efficiency max 20-25%, rest is converted to heat (HF: 5-10% ) Expenditure increases when Expenditure increases when ventricles are dialated ventricles are dialated BP is elevated BP is elevated Energy expenditure is measured by oxygen comsumption

22. Special conductive system

23. Rate of discharge SA node 70-80 bpm SA node 70-80 bpm AVnode 40-60 bpm AVnode 40-60 bpm AV bundle 15-40 bpm AV bundle 15-40 bpm

24. Autorhythmicity of SA node

29. Special conductive system Nodal delay Nodal delay.09sec AV node.09sec AV node.04 sec penetrating portion.04 sec penetrating portion Additional.03 sec internodal pathway Additional.03 sec internodal pathway

30. Ectopic pacemaker Heart block Heart block Stokes Adams syndrome Stokes Adams syndrome

31. ECG

38. Heart muscle wraps around heart like a double spiral with a fibrous septa between the spiral layers. Heart muscle wraps around heart like a double spiral with a fibrous septa between the spiral layers.

39. Flow of current

40. leads

42. Other leads Chest leads 6 in no. Chest leads 6 in no. + pole connected to chest, -ve to all 3 limbs + pole connected to chest, -ve to all 3 limbs Infrequently 7 th & 8 th chest leads & esophageal leads used. Infrequently 7 th & 8 th chest leads & esophageal leads used. aVR- Rt +ve aVR- Rt +ve aVF- Lt leg +ve aVF- Lt leg +ve aVL- Lt arm +ve aVL- Lt arm +ve Recording of V1 V2 upside down as it is more closer to base rather than apex Recording of V1 V2 upside down as it is more closer to base rather than apex

43. Axis of leads

44. Vector Instantaneous mean vector: Instantaneous mean vector: At any given instance the total amount of current flowing in the heart is represented in magnitude and direction by the vector. Current flows from DEPOLARISED to POLARISED area i.e. NEGATIVE to POSITIVE

45. Vector analysis Closer the angle higher is the component Closer the angle higher is the component +ve vector: reading above the baseline +ve vector: reading above the baseline - ve vector: reading below the baseline - ve vector: reading below the baseline

52. Mean vector

53. Axis deviation 1Normal: 20degree to left, 100 degree to right 20degree to left, 100 degree to right Lt Rt Lt Rt Expiration Inspiration Expiration Inspiration Supine Standing Supine Standing Fat Tall/ lean Fat Tall/ lean 2Hypertrophy / conduction block

54. Left Deviation : pathological Hypertension Hypertension Aortic valve stenosis Aortic valve stenosis Regurgitation Regurgitation LBBB LBBB

55. LBBB Left Deviation

56. Right Deviation Pulmonary stenosis Pulmonary stenosis Fallots tetralogy Fallots tetralogy VSD VSD Pulmonary hypertension Pulmonary hypertension RBBB RBBB

57. Right Deviation

58. Vector analysis: axis deviation

59. High voltage ECG Normally peak of R to bottom of S: 0.5 to 2 mv Normally peak of R to bottom of S: 0.5 to 2 mv Abnormally large: summation of all 3 leads >4mv Abnormally large: summation of all 3 leads >4mv Cause :hypertrophy Cause :hypertrophy

60. Low voltage ECG 1 decreased current production 1 decreased current production low muscle mass: common in old MI propagation also slowed- prolongation low muscle mass: common in old MI propagation also slowed- prolongation

62. 2 reduced conduction 2 reduced conduction A. pericardial effusion A. pericardial effusion B. pulmonary emphysema B. pulmonary emphysema 3 flow in AP axis 3 flow in AP axis rotation of axis rotation of axis

63. Prolonged QRS complex Normal : 0.06- 0.08 sec Normal : 0.06- 0.08 sec Hpertrophy or dilatation of ventricles: conduction prolonged.09-.12sec Hpertrophy or dilatation of ventricles: conduction prolonged.09-.12sec Prolongation in BBB- propagation through muscle: Prolongation in BBB- propagation through muscle: >.09 sec abnormal >.12- almost certain to be pathological block in ventricular conduction system >.14 – complete block

64. Bizzare QRS complex 1 scar tissue 1 scar tissue 2 Multiple block 2 Multiple block

65. Current of injury

66. Injured area: depolarised- emits –Ve charge. Injured area: depolarised- emits –Ve charge. Injury: mechanical/ infection/ ischemia Injury: mechanical/ infection/ ischemia As the area remains continuously depolarised a current flow in the ventricle even before QRS starts. This is Current of injury. As the area remains continuously depolarised a current flow in the ventricle even before QRS starts. This is Current of injury. Axis deviation also present Axis deviation also present

67. Current of injury J point J point No current flows when the ventricles are fully depolarised. So the iso electric point is seen at the end of QRS complex.this is called J point. ST segment shift ST segment shift As the Current of injury is present the TP segment is shifted. But in common practice it is considered TP is in iso electric line. So this phenomenon is usually termed as ST segment shift

68. Current of injury

70. T WAVE ABNORMALITY

71. Arrhythmias 1 tachycardia 1 tachycardia >100bpm, normal but shorter waves Causes: Temperature- 10beats/degree F upto 105degree Sympathetic stimulation toxicity

72. 2 bradycardia: 2 bradycardia: <60 bpm <60 bpm Athletes, carotid sinus syndrome Due to increased vagal stimulation

73. Sinus arrhythmia  Can result from any circulatory reflex that alters the strength of the autonomic signal to SA node  Respiratory type results from spill over of signals from the medullary respiratory centre to vasomotor centre.  Normal 5% variation in inspiration and expiration.  Deep breathing: 10%

74. Sinoatrial block Block in SA node Block in SA node No P wave No P wave AV nodal rhythm AV nodal rhythm Normal QRS-T Normal QRS-T Slow Slow

75. AV Blocks Ischemia of AV node/ bundle Ischemia of AV node/ bundle Compression of bundle: scar/ calcified portion Compression of bundle: scar/ calcified portion Inflammation of AV node/ bundle Inflammation of AV node/ bundle myocarditis/ diptheria/ rheumatic fever myocarditis/ diptheria/ rheumatic fever Extreme vagal stimulation: Extreme vagal stimulation: carotid sinus syndrome carotid sinus syndrome

76. AV block A. Incomplete 1. first degree: prolonged PR interval (>.20 sec). Conduction is delayed but no actual blockage. 1. first degree: prolonged PR interval (>.20 sec). Conduction is delayed but no actual blockage. May prolong upto.35-.45 sec May prolong upto.35-.45 sec The measurement of duration gives estimate of severity. The measurement of duration gives estimate of severity.

77. 2. second degree 2. second degree here also PR prolonged. Some beats strong enough to go through block some are not. So for some P wave QRS complex is present whereas for some it is absent. here also PR prolonged. Some beats strong enough to go through block some are not. So for some P wave QRS complex is present whereas for some it is absent. 2:1/3:2/3:1 rhythms are present sometimes

79. Third degree No impulse propagation to AV node No impulse propagation to AV node Atrioventricular dissociation Atrioventricular dissociation

80. Atria 100 bpm ventricle 40 bpm

81. Bundle branch block A branch of the bundle delays propagation A branch of the bundle delays propagation Normal side contracts first Normal side contracts first Duplication of 1 st heart sound Duplication of 1 st heart sound Prolonged QRS Prolonged QRS More severe when on the left side More severe when on the left side

82. Arborisation block Purkinje fibre dysfunction due to chronic myocardial damage Purkinje fibre dysfunction due to chronic myocardial damage

83. Other abnormalities Stokes Adams syndrome Stokes Adams syndrome Borderline ischemia of conductive tissue Electrical alternans Electrical alternans tachycardia tachycardiaIschaemiaMyocarditis Digitalis toxicity

84. Premature beats Extrasystole & compensatory pause Extrasystole & compensatory pause o Local areas of ischemia o Small calcified plaques at different points of heart- irritating o Mechanical stimulation during cardiac catheterisation o Toxic irritation nicotine, caffeine, drugs o Pulse deficite & bigeminal pulse

85. AV nodal/ bundle premature contraction AV nodal/ bundle premature contraction P wave not distinct, atria & ventricles depolarises at the same time P wave not distinct, atria & ventricles depolarises at the same time Ventricular premature contraction Ventricular premature contraction prolonged QRS due to volume conduction prolonged QRS due to volume conduction High voltage as one voltage depolarises before another Inverted t wave

86. Ventricular fibrillation Contraction of ventricular muscle mass without coordination and at a high rate Contraction of ventricular muscle mass without coordination and at a high rate Some of muscle fibres contract at any given time and others relax so heart is neither in systole nor diastole Some of muscle fibres contract at any given time and others relax so heart is neither in systole nor diastole Caused by reentry, facilitated by: Caused by reentry, facilitated by: Long pathway – dilated heart Decreaesd conduction speed: high K+, ischemia, purkinje block Low refractory period: repeated stimulant/ epinephrine

95. Thank you