Ecg basics & cardicac physiology


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Ecg basics & cardicac physiology

  2. 2. Heart is a pumping organ
  3. 3. How heart keeps pumping?1.special structure of cardiac muscle syncytial nature both resting membrane potential & action potential are different form skeletal rhythmicity of heart
  4. 4. Action potential of heart muscle
  5. 5. Factors affecting action potential 1 K+ concentration 2 Ca++ concentration 3Na+ concentration 4 temperature
  6. 6. Excitation contraction coupling
  7. 7. Excitation contraction coupling
  8. 8. 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
  9. 9. Cardiac cycle
  10. 10. Atrial systole
  11. 11. IMC
  12. 12. ejection phase
  13. 13. IMR
  14. 14. Heart sounds
  15. 15. 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
  16. 16. Parasympathetic innervation
  17. 17. Effects of autonomic stimulation Chronotropic effect Dromotropic effect Bathmotropic effect Inotropic effect
  18. 18. 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.
  19. 19. 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 elevatedEnergy expenditure is measured by oxygen comsumption
  20. 20. Special conductive system
  21. 21. Rate of discharge SA node 70-80 bpm AVnode 40-60 bpm AV bundle 15-40 bpm
  22. 22. Autorhythmicity of SA node
  23. 23. Autorhythmicity of SA node
  24. 24. Autorhythmicity of SA node
  25. 25. Autorhythmicity of SA node
  26. 26. Autorhythmicity of SA node
  27. 27. Special conductive system Nodal delay .09sec AV node .04 sec penetrating portion Additional .03 sec internodal pathway
  28. 28. Ectopic pacemaker Heart block Stokes Adams syndrome
  29. 29. ECG
  30. 30.  Heart muscle wraps around heart like a double spiral with a fibrous septa between the spiral layers.
  31. 31. Flow of current
  32. 32. leads
  33. 33. 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
  34. 34. Axis of leads
  35. 35. 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
  36. 36. Vector analysis Closer the angle higher is the component +ve vector: reading above the baseline - ve vector: reading below the baseline
  37. 37. Mean vector
  38. 38. Axis deviation1Normal: 20degree to left, 100 degree to right Lt Rt Expiration Inspiration Supine Standing Fat Tall/ lean2Hypertrophy / conduction block
  39. 39. Left Deviation : pathological Hypertension Aortic valve stenosis Regurgitation LBBB
  40. 40. LBBB Left Deviation
  41. 41. Right Deviation Pulmonary stenosis Fallots tetralogy VSD Pulmonary hypertension RBBB
  42. 42. Right Deviation
  43. 43. Vector analysis: axis deviation
  44. 44. 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
  45. 45. Low voltage ECG 1 decreased current production low muscle mass: common in old MI propagation also slowed- prolongation
  46. 46.  2 reduced conduction A. pericardial effusion B. pulmonary emphysema 3 flow in AP axis rotation of axis
  47. 47. 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
  48. 48. Bizzare QRS complex 1 scar tissue 2 Multiple block
  49. 49. Current of injury
  50. 50. 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
  51. 51. Current of injury J pointNo 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 shiftAs 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
  52. 52. Current of injury
  53. 53. Current of injury
  55. 55. Arrhythmias 1 tachycardia>100bpm, normal but shorter wavesCauses:Temperature- 10beats/degree F upto 105degreeSympathetic stimulationtoxicity
  56. 56.  2 bradycardia:<60 bpmAthletes, carotid sinus syndromeDue to increased vagal stimulation
  57. 57. 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%
  58. 58. Sinoatrial block Block in SA node No P wave AV nodal rhythm Normal QRS-T Slow
  59. 59. 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
  60. 60. AV blockA. 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.
  61. 61.  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
  62. 62. Third degree No impulse propagation to AV node Atrioventricular dissociation
  63. 63. Atria 100 bpm ventricle 40 bpm
  64. 64. 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
  65. 65. Arborisation block Purkinje fibre dysfunction due to chronic myocardial damage
  66. 66. Other abnormalities Stokes Adams syndromeBorderline ischemia of conductive tissue Electrical alternans tachycardiaIschaemiaMyocarditisDigitalis toxicity
  67. 67. Premature beats Extrasystole & compensatory pauseo Local areas of ischemiao Small calcified plaques at different points of heart- irritatingo Mechanical stimulation during cardiac catheterisationo Toxic irritation nicotine, caffeine, drugso Pulse deficite & bigeminal pulse
  68. 68.  AV nodal/ bundle premature contraction P wave not distinct, atria & ventricles depolarises at the same time Ventricular premature contraction prolonged QRS due to volume conductionHigh voltage as one voltage depolarises before anotherInverted t wave
  69. 69. 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 heartDecreaesd conduction speed: high K+, ischemia, purkinje blockLow refractory period: repeated stimulant/ epinephrine
  70. 70. Thank you