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Heart physiology

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Heart physiology

  1. 1. Heart Physiology Department of Physiology SKZMDC
  2. 4. Cardiac Muscle <ul><li>Cardiac Muscle </li></ul><ul><ul><ul><li>Atrial muscle </li></ul></ul></ul><ul><ul><ul><li>Ventricular muscle </li></ul></ul></ul><ul><ul><ul><li>Specialized excitatory & conductive muscle fibers </li></ul></ul></ul><ul><li>Cardiac Muscle as a Syncytium </li></ul><ul><ul><ul><li>Intercalated disc “communicating” junctions (gap junctions) - totally free diffusion of ions </li></ul></ul></ul><ul><ul><ul><li>Atrial syncytium </li></ul></ul></ul><ul><ul><ul><li>Ventricular syncytium </li></ul></ul></ul>
  3. 5. Cardiac Muscle - Histology
  4. 8. Cardiac Muscle Action Potential <ul><li>Depolarization </li></ul><ul><ul><ul><li>Fast Na + channels </li></ul></ul></ul><ul><li>Plateau </li></ul><ul><ul><ul><li>Slow Ca ++ channels </li></ul></ul></ul><ul><ul><ul><ul><li>Slow to open </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Slow to close </li></ul></ul></ul></ul><ul><ul><ul><li>After depol. cardiac muscle membrane permeability to K + decreases </li></ul></ul></ul><ul><ul><ul><li>Ca ++ thus pumped in – excitation-contraction coupling </li></ul></ul></ul><ul><li>Repolarization </li></ul><ul><ul><ul><li>Slow K + channels </li></ul></ul></ul><ul><li>Refractory Periods </li></ul><ul><ul><ul><li>0.25 - 0.3 sec (Absolute) </li></ul></ul></ul><ul><ul><ul><ul><li>Corresponds to plateau </li></ul></ul></ul></ul><ul><ul><ul><li>0.05 sec (Relative) </li></ul></ul></ul>
  5. 9. AP Comparison
  6. 10. Cardiac Muscle Action Potential
  7. 11. Cardiac Muscle Action Potential
  8. 12. Problem <ul><li>A drug is found to partially inactivate fast sodium channels. </li></ul><ul><li>Q: How would this drug alter the action potential in a ventricular myocyte? </li></ul><ul><li>Q: How would the drug alter conduction velocity within the ventricle? </li></ul>
  9. 13. Cardiac Cycle <ul><li>Cardiac events occurring from beginning of one heartbeat to the beginning of the next beat </li></ul><ul><li>Each cycle – INITIATED by SA node </li></ul><ul><ul><ul><ul><li>Spontaneous generation of AP in SA node </li></ul></ul></ul></ul><ul><ul><ul><ul><li>AP travels through both atria </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Through A-V bundle into the ventricles </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>AV node delay (more than 0.1 second) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Hence atria contract ahead of ventricles </li></ul></ul></ul></ul></ul><ul><li>Diastole and Systole </li></ul><ul><ul><ul><ul><li>Period of relaxation – Diastole </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Heart fills with blood </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Period of contraction – Systole </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Ejection of blood </li></ul></ul></ul></ul></ul>
  10. 14. Cardiac Cycle - Components <ul><li>ECG is the event marker </li></ul><ul><li>1. Atrial Systole </li></ul><ul><ul><ul><ul><li>Follows P wave (electric activation of atria) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Contributes to ventricular filling </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Forms the ‘ a wave ’ in the venous pulse curve </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricular filling by atrial systole – 4 th heart sound (not audible in normal adults) </li></ul></ul></ul></ul><ul><li>2. Isovolumetric contraction of Ventricle </li></ul><ul><ul><ul><ul><li>Occurs after QRS wave (electric activation of ventricles) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricular P raised above atrial P: </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>AV valves close ( 1 st heart sound ) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Split in 1 st heart sound may occur (since mitral valve closes b/f tricuspid) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricular P rises – NO CHANGE IN VOLUME </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Aortic valve is closed </li></ul></ul></ul></ul></ul>
  11. 15. Cardiac Cycle - Components <ul><li>3. Rapid Ventricular Ejection </li></ul><ul><ul><ul><ul><li>Ventricular P reaches its max. </li></ul></ul></ul></ul><ul><ul><ul><ul><li>When it b/c greater than aortic P – aortic valve opens </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Rapid ejection of blood takes place </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricular volume decreases rapidly </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Atrial filling begins </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Onset of “T wave” (ventricular repolarization) – marks end of vent. contraction & ejection </li></ul></ul></ul></ul><ul><li>4. Reduced Ventricular Ejection </li></ul><ul><ul><ul><ul><li>Slower ejection of blood from ventricles </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricle P decreases </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Aortic P decreases (runoff of blood from large arteries into smaller arteries) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Atrial filling continues </li></ul></ul></ul></ul>
  12. 16. Cardiac Cycle - Components <ul><li>5. Isovolumetric Ventricular Relaxation </li></ul><ul><ul><ul><ul><li>Ventricle replorization is complete (end of “T wave”) </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Aortic valve closes (followed by pulmonic valve) </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>2 nd heart sound </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Splitting occurs during inspiration </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>AV valves remain closed mostly during this phase </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricle P drops rapidly </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricle volume remains CONSTANT – all valves are closed </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Incisura </li></ul></ul></ul></ul><ul><ul><ul><ul><li>When ventricle P b/c < atrial P – mitral valve opens </li></ul></ul></ul></ul><ul><li>6. Rapid Ventricular Filling </li></ul><ul><ul><ul><ul><li>Post-mitral valve opening – rapid filling of ventricles occurs </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Aortic P continues to decrease – more run-off of blood </li></ul></ul></ul></ul><ul><ul><ul><ul><li>3 rd heart sound (due to rapid flow from atria to ventricles </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Normally heard in children </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Abnormal in adults </li></ul></ul></ul></ul></ul><ul><li>7. Reduced Ventricular Filling (Diastasis) </li></ul><ul><ul><ul><ul><li>Longest phase of cardiac cycle </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Ventricular filling slows down </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Diastasis time period depends on heart rate! </li></ul></ul></ul></ul>
  13. 19. Cardiac Cycle <ul><li>End-diastolic volume (130 ml) </li></ul><ul><li>End-systolic volume (50 ml) </li></ul><ul><li>Stroke volume (70 to 90 ml - @ rest) </li></ul><ul><li>Ejection fraction </li></ul><ul><ul><ul><ul><li>% of end-diastolic ventricular volume that is ejected with each stroke </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Is about 65% </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Valuable index of ventricular function </li></ul></ul></ul></ul><ul><li>Preload </li></ul><ul><li>Afterload </li></ul>
  14. 20. Cardiac Chamber Pressures
  15. 21. Length (L) –Tension (T) Curve Isolated Cardiac Muscle
  16. 22. Pressure (‘T’) – Volume (‘L’) Curve – Whole Heart <ul><li>PV loops: </li></ul><ul><ul><li>Depict cardiac cycle </li></ul></ul><ul><ul><li>Show effects of Preload, afterload & inotropic state on cardiac pumping ability (SV) </li></ul></ul>
  17. 24. 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>
  18. 25. 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>
  19. 26. Explanation of FS Law
  20. 27. 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>
  21. 28. 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>
  22. 29. 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>
  23. 30. 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>

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