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Regulation of Heart Pumping <ul><li>(1)  INTRINSIC  cardiac regulation of pumping in response to changes in volume of bloo...
Frank-Starling Law <ul><li>“ Volume of blood ejected by the ventricle depends on the volume present in the ventricle at th...
Explanation  of FS Law
Concept of  Contractility <ul><li>Inherent cardiac M Ca++ based ability –  INOTROPISM </li></ul><ul><ul><ul><li>Modified b...
Heart Control by  ANS <ul><li>Sympathetic   </li></ul><ul><ul><ul><li>NE via action on Beta-1 receptors </li></ul></ul></u...
Heart Control by  ANS <ul><li>Parasympathetic </li></ul><ul><ul><li>SA node, atria & AV node have supply, ventricles don’t...
Determinants of Performance of Heart as a Pump <ul><li>4 factors:  </li></ul><ul><ul><ul><li>‘ Loading’ conditions of the ...
 
S-A Nodal Action Potential <ul><ul><li>I ca L (long-lasting) </li></ul></ul><ul><ul><li>I ca T (transient) </li></ul></ul>...
Cardiac Impulse <ul><li>Initiated in SA node </li></ul><ul><li>Spreads radially into atrial muscle mostly @ 0.3 m/sec </li...
Cardiac Impulse <ul><li>After AV node  </li></ul><ul><ul><li>Velocity is maximum </li></ul></ul><ul><ul><li>Bundle of HIS ...
 
Normal ECG <ul><li>ECG is produced only when current flows through the heart and this occurs only when the heart is partia...
Normal ECG <ul><li>P wave </li></ul><ul><ul><ul><li>Atria depolarize before contraction </li></ul></ul></ul><ul><ul><ul><l...
Normal ECG <ul><li>PR interval – 0.16 sec </li></ul><ul><ul><ul><li>Time b/w beginning of P wave and beginning of QRS comp...
Dipole <ul><li>The electric dipole consists of two equal and opposite charges,  +q  and  –q , separated by a distance  d <...
<ul><li>A wave of depolarization heading toward the  +ve  electrode is recorded as a  +ve  voltage </li></ul><ul><ul><ul><...
Vectors and Mean Electrical Axis <ul><li>Individual waves of depol. –  electrical vectors </li></ul><ul><li>Summation of e...
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Upload 19 04-11

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Upload 19 04-11

  1. 1. Regulation of Heart Pumping <ul><li>(1) INTRINSIC cardiac regulation of pumping in response to changes in volume of blood flowing into the heart ( Frank-Starling Law ) </li></ul><ul><li>(2) Control of heart rate and strength of heart pumping by ANS </li></ul>
  2. 2. Frank-Starling Law <ul><li>“ Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole” </li></ul><ul><li>Underlying principle </li></ul><ul><ul><li>Length-tension relationship in cardiac muscle fibers </li></ul></ul><ul><li>SV & CO correlate directly with EDV </li></ul><ul><li>EDV correlates with VR </li></ul><ul><li>CO = VR (FS Law ensures this) </li></ul><ul><li>Cardiac muscle normally operates only on the ascending limb of the systolic curve </li></ul>
  3. 3. Explanation of FS Law
  4. 4. Concept of Contractility <ul><li>Inherent cardiac M Ca++ based ability – INOTROPISM </li></ul><ul><ul><ul><li>Modified by ANS, catecholamines </li></ul></ul></ul><ul><li>Loading situations of the heart </li></ul><ul><ul><ul><li>Preload </li></ul></ul></ul><ul><ul><ul><ul><li>Stretch-induced enhancement in contraction </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>More overlapping of thick & thin filaments </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>More Ca ++ sensitivity of troponin C </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>More Ca ++ release from SR </li></ul></ul></ul></ul></ul><ul><ul><ul><li>After load </li></ul></ul></ul>
  5. 5. Heart Control by ANS <ul><li>Sympathetic </li></ul><ul><ul><ul><li>NE via action on Beta-1 receptors </li></ul></ul></ul><ul><ul><ul><ul><li>Positive CHRONOTROPIC </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Increased HR (increase Phase-4 depolarization) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Positive IONOTROPIC </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Increased force of contraction (increased inward Ca++ current during plateau + increases the ability of SR Ca++ pump) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Positive DROMOTROPIC </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Increased conduction velocity through AV node (increased inward Ca++ current) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Decreased PR interval </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Positive BATHMOTROPIC </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Increased excitability of myocardium </li></ul></ul></ul></ul></ul>
  6. 6. Heart Control by ANS <ul><li>Parasympathetic </li></ul><ul><ul><li>SA node, atria & AV node have supply, ventricles don’t! </li></ul></ul><ul><ul><li>Ach via muscarinic receptors </li></ul></ul><ul><ul><ul><li>Negative chronotropic </li></ul></ul></ul><ul><ul><ul><ul><ul><li>Decreasing phase-4 depolarizations </li></ul></ul></ul></ul></ul><ul><ul><ul><li>Negative dromotropic </li></ul></ul></ul><ul><ul><ul><li>Negative ionotropic </li></ul></ul></ul><ul><li>Vagal escape </li></ul>
  7. 7. Determinants of Performance of Heart as a Pump <ul><li>4 factors: </li></ul><ul><ul><ul><li>‘ Loading’ conditions of the cardiac muscle </li></ul></ul></ul><ul><ul><ul><li>(1) Preload , or the initial length to which the muscle is stretched prior to contraction </li></ul></ul></ul><ul><ul><ul><li>(2) Afterload , or all the forces against which cardiac muscle must contract to generate pressure and shorten </li></ul></ul></ul><ul><ul><ul><li>‘ Extrinsic’ factors </li></ul></ul></ul><ul><ul><ul><li>(3) Contractility , or inotropic state </li></ul></ul></ul><ul><ul><ul><li>(4) Inotropic effect of increased heart rate (beats/min) </li></ul></ul></ul>
  8. 9. S-A Nodal Action Potential <ul><ul><li>I ca L (long-lasting) </li></ul></ul><ul><ul><li>I ca T (transient) </li></ul></ul><ul><ul><li>Firing potential: </li></ul></ul><ul><ul><li>-40 mv </li></ul></ul><ul><ul><li>Hyperpolarization </li></ul></ul>
  9. 10. Cardiac Impulse <ul><li>Initiated in SA node </li></ul><ul><li>Spreads radially into atrial muscle mostly @ 0.3 m/sec </li></ul><ul><li>Atrial conduction is done via bands of fibres </li></ul><ul><ul><ul><li>Anterior </li></ul></ul></ul><ul><ul><ul><li>Middle </li></ul></ul></ul><ul><ul><ul><li>Posterior </li></ul></ul></ul><ul><li>Arrives at AV node after 0.03 sec </li></ul><ul><li>AV delay of 0.13 sec occurs </li></ul><ul><ul><ul><li>0.09 in bundle </li></ul></ul></ul><ul><ul><ul><li>0.04 in bundle of HIS </li></ul></ul></ul><ul><ul><ul><li>Reason for delay? </li></ul></ul></ul><ul><ul><ul><li>Benefit of delay? </li></ul></ul></ul><ul><li>Total delay at this point is 0.16 sec </li></ul>
  10. 11. Cardiac Impulse <ul><li>After AV node </li></ul><ul><ul><li>Velocity is maximum </li></ul></ul><ul><ul><li>Bundle of HIS – 1 m/sec </li></ul></ul><ul><ul><li>Purkinje system – 4 m/sec </li></ul></ul><ul><li>From the top of septum – via purkinje system – all of ventricle – 0.06 – 0.1 sec </li></ul><ul><li>Total duration: 0.22 sec </li></ul><ul><li>Parts that are last depolarized </li></ul><ul><ul><ul><li>Posterobasal portion of left ventricle </li></ul></ul></ul><ul><ul><ul><li>Pulmonary conus </li></ul></ul></ul><ul><ul><ul><li>Upper most part of septum </li></ul></ul></ul>
  11. 13. Normal ECG <ul><li>ECG is produced only when current flows through the heart and this occurs only when the heart is partially depolarized/polarized </li></ul>
  12. 14. Normal ECG <ul><li>P wave </li></ul><ul><ul><ul><li>Atria depolarize before contraction </li></ul></ul></ul><ul><ul><ul><li>0.08 - 0.10 sec </li></ul></ul></ul><ul><li>QRS complex </li></ul><ul><ul><ul><li>Ventricles depolarize before contraction </li></ul></ul></ul><ul><ul><ul><li>0.06 – 0.10 sec </li></ul></ul></ul><ul><li>T wave </li></ul><ul><ul><ul><li>Ventricles repolarize </li></ul></ul></ul><ul><ul><ul><li>Atrial T wave is obscured by QRS </li></ul></ul></ul><ul><ul><ul><li>Duration normally not taken </li></ul></ul></ul><ul><li>U wave </li></ul><ul><ul><ul><li>Inconstant finding </li></ul></ul></ul><ul><ul><ul><li>Slow repolarization of papillary muscles </li></ul></ul></ul>
  13. 15. Normal ECG <ul><li>PR interval – 0.16 sec </li></ul><ul><ul><ul><li>Time b/w beginning of P wave and beginning of QRS complex </li></ul></ul></ul><ul><ul><ul><ul><li>Interval between the beginning of electrical excitation of the atria and the beginning of excitation of the ventricles </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Prolonged: Vagal stimulation, AV block </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Shortened: Accelerated AV conduction, sympathetic stimulation </li></ul></ul></ul></ul></ul><ul><li>ST interval (QT minus QRS) – 0.32 sec </li></ul><ul><ul><ul><li>Ventricular repolarization </li></ul></ul></ul><ul><li>Q-T interval – 0.2-0.40 sec </li></ul><ul><ul><ul><li>Ventricular depolarization and ventricular repolarization </li></ul></ul></ul><ul><ul><ul><li>Corresponds to AP duration </li></ul></ul></ul><ul><ul><ul><ul><ul><li>Prolonged: ventricular extrasystole </li></ul></ul></ul></ul></ul>
  14. 16. Dipole <ul><li>The electric dipole consists of two equal and opposite charges, +q and –q , separated by a distance d </li></ul><ul><li>Dipole vector : </li></ul><ul><ul><ul><li>Vector whose magnitude is equal to the dipole moment [voltage] and that points from –ve charge to + one </li></ul></ul></ul><ul><li>Direction of dipole is from –ve towards +ve </li></ul>
  15. 17. <ul><li>A wave of depolarization heading toward the +ve electrode is recorded as a +ve voltage </li></ul><ul><ul><ul><li>Represents Atrial & Vent. Depol . </li></ul></ul></ul><ul><li>A wave of repolarization moving away from a +ve electrode produces a +ve voltage difference </li></ul><ul><ul><ul><li>T-wave (Vent. Repol.) </li></ul></ul></ul><ul><li>A wave of repolarization moving toward a +ve electrode produces a –ve voltage deflection </li></ul><ul><ul><ul><li>Atrial Repol. </li></ul></ul></ul>
  16. 18. Vectors and Mean Electrical Axis <ul><li>Individual waves of depol. – electrical vectors </li></ul><ul><li>Summation of electrical vectors at any instance – mean electrical vector </li></ul>

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