1. ECG BASICS
&
PHYSIOLOGY
OF
HEART
SUBHANJAN DAS

2. Heart is a pumping organ

4. How heart keeps pumping?
1.special structure of cardiac muscle
 syncytial nature
 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
 2 Ca++ concentration
 3Na+ concentration
 4 temperature

7. Excitation contraction coupling

8. Excitation contraction coupling

9. Duration of contraction
 Atria 0.2sec
 Ventricle 0.3 sec
 Normally contraction time is 40% of cardiac
cycle. When heart rate increases 3 times it is
65% of cardiac cycle.
 Relaxation 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
 2 autonomic innervation
 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
 Dromotropic effect
 Bathmotropic effect
 Inotropic effect

20. Effects of autonomic stimulation
 Sympathetic stimulation: HR can go upto 250
bpm in young individual.
 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.

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

22. Special conductive system

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

24. Autorhythmicity of SA node

25. Autorhythmicity of SA node

26. Autorhythmicity of SA node

27. Autorhythmicity of SA node

28. Autorhythmicity of SA node

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

30. Ectopic pacemaker
 Heart block
 Stokes Adams syndrome

31. ECG

38.  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.
 + pole connected to chest, -ve to all 3 limbs
 Infrequently 7th & 8th chest leads & esophageal
leads used.
 aVR- Rt +ve
 aVF- Lt leg +ve
 aVL- Lt arm +ve
 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:
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
 +ve vector: reading above the baseline
 - ve vector: reading below the baseline

52. Mean vector

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

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

55. LBBB Left Deviation

56. Right Deviation
 Pulmonary stenosis
 Fallots tetralogy
 VSD
 Pulmonary hypertension
 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
 Abnormally large: summation of all 3 leads
>4mv
 Cause :hypertrophy

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

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

63. Prolonged QRS complex
 Normal : 0.06- 0.08 sec
 Hpertrophy or dilatation of ventricles:
conduction prolonged .09- .12sec
 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
 2 Multiple block

65. Current of injury

66. Current of injury
 Injured area: depolarised- emits –Ve charge.
 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.
 Axis deviation also present

67. Current of injury
 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
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

69. Current of injury

70. T WAVE ABNORMALITY

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

72.  2 bradycardia:
<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
 No P wave
 AV nodal rhythm
 Normal QRS-T
 Slow

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

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

77.  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.
2:1/3:2/3:1 rhythms are present sometimes

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

80. Atria 100 bpm ventricle 40 bpm

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

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

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

84. Premature beats
 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
P wave not distinct, atria & ventricles depolarises
at the same time
 Ventricular premature contraction
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
 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:
Long pathway – dilated heart
Decreaesd conduction speed: high K+, ischemia,
purkinje block
Low refractory period: repeated stimulant/ epinephrine

95. Thank you