The Heart


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  • Questions: How do the valves work Name the parts & vessels
  • Questions: How do the valves work Name the parts & vessels
  • The Heart

    1. 1. Anatomy & Physiology Bio 2402 Lecture Dr shabeel pn dr shabeel pn
    2. 2. Review: <ul><li>Cardiac Cycle </li></ul><ul><li>Beginning of control system </li></ul>
    3. 3. Review of Cardiac Blood Flow <ul><li>Be able to trace flow, from start to finish </li></ul>
    4. 4. Sequence of blood flow <ul><li>Right atrium  tricuspid valve  right ventricle </li></ul><ul><li>Right ventricle  pulmonary semilunar valve  pulmonary arteries  lungs </li></ul><ul><li>Lungs  pulmonary veins  left atrium </li></ul><ul><li>Left atrium  bicuspid valve  left ventricle </li></ul><ul><li>Left ventricle  aortic semilunar valve  aorta </li></ul><ul><li>Aorta  systemic circulation </li></ul>
    5. 5. Two systems: <ul><li>Pulmonary </li></ul><ul><li>Systemic </li></ul>
    6. 6. Review of Cardiac Blood Flow <ul><li>Function of chordae tendineae and papillary muscles? </li></ul><ul><li>What opens and closes the valves? </li></ul>
    7. 7. New section for today
    8. 8. Control system - Autorhythmic Fibers <ul><li>See figure 18.14 on page 694 </li></ul><ul><li>These fibers have an unstable resting potential due to Na+ & Ca++ leakage in. </li></ul>
    9. 9. Control system - Autorhythmic Fibers <ul><li>See figure 18.14 on page 694 </li></ul><ul><li>These fibers have an unstable resting potential due to Na+ & Ca++ leakage in. </li></ul>
    10. 10. Control system - role of instability of RMP <ul><li>Sinoatrial node (SA) – </li></ul><ul><ul><li>Inherent rate of 100 BPM </li></ul></ul><ul><ul><li>“ Sinus Rhythm” – Heart’s pacemaker </li></ul></ul><ul><ul><li>Location: Upper RA </li></ul></ul><ul><ul><li>Fastest cells in system </li></ul></ul>
    11. 11. Atrial (Bainbridge) Reflex <ul><li>Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria </li></ul><ul><ul><li>Causes stimulation of the SA node </li></ul></ul><ul><ul><li>Stimulates baroreceptors in the atria, causing increased SNS (Sympathetic Nervous System) stimulation </li></ul></ul>
    12. 12. Control system - <ul><li>Atrioventricular Node (AV) – </li></ul>
    13. 13. Control system - <ul><li>Atrioventricular Node (AV) – </li></ul><ul><ul><li>Impulse is delayed here 0.1 second (Why?) </li></ul></ul>
    14. 14. Control system - <ul><li>Atrioventricular bundle – (Bundle of His) </li></ul>
    15. 15. Control system - <ul><li>Atrioventricular bundle – (Bundle of His) </li></ul><ul><li>The only electrical connection between atria and ventricles </li></ul><ul><li>Rapidly conducts through Right Bundle branch, (RBB), Left Bundle Branch (LBB) and Purkinje fibers </li></ul>
    16. 16. Control system - <ul><li>Right Bundle branch, (RBB), - stimulates septal cells </li></ul><ul><li>Left Bundle Branch (LBB) – septal cells </li></ul><ul><li>Purkinje fibers- most important, stimulates most of the ventricular walls, and first stimulates the papillary muscles (why?) </li></ul>
    17. 17. Control system - <ul><li>Time required: 220 ms from SA node to complete depolarization. </li></ul><ul><li>Longer time indicates conduction defect </li></ul>
    18. 18. Intrinsic Conduction System <ul><li>Autorhythmic cells: </li></ul><ul><ul><li>Initiate action potentials </li></ul></ul><ul><ul><li>Have unstable resting potentials called pacemaker potentials </li></ul></ul><ul><ul><li>Use calcium influx (rather than sodium) for rising phase of the action potential </li></ul></ul>
    19. 19. Pacemaker and Action Potentials of the Heart
    20. 20. Sequence of Excitation <ul><li>Sinoatrial (SA) node generates impulses about 75 times/minute </li></ul><ul><li>Atrioventricular (AV) node delays the impulse approximately 0.1 second </li></ul><ul><li>Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His) </li></ul>
    21. 21. Sequence of Excitation <ul><li>AV bundle splits into two pathways in the interventricular septum (bundle branches) </li></ul><ul><ul><li>Bundle branches carry the impulse toward the apex of the heart </li></ul></ul><ul><ul><li>Purkinje fibers carry the impulse to the heart apex and ventricular walls </li></ul></ul>
    22. 22. Cardiac Intrinsic Conduction
    23. 23. Heart Excitation Related to ECG SA node generates impulse; atrial excitation begins Impulse delayed at AV node Impulse passes to heart apex; ventricular excitation begins Ventricular excitation complete SA node AV node Purkinje fibers Bundle branches Figure 18.17
    24. 24. Heart Excitation Related to ECG SA node generates impulse; atrial excitation begins SA node
    25. 25. Heart Excitation Related to ECG Impulse delayed at AV node AV node
    26. 26. Heart Excitation Related to ECG Impulse passes to heart apex; ventricular excitation begins Bundle branches
    27. 27. Heart Excitation Related to ECG Ventricular excitation complete Purkinje fibers
    28. 28. Extrinsic Innervation <ul><li>Heart is stimulated by the sympathetic cardioacceleratory center </li></ul><ul><li>Heart is inhibited by the parasympathetic cardioinhibitory center </li></ul>
    29. 29. ECG – What it means <ul><li>Electrical activity is recorded by electrocardiogram (ECG) </li></ul><ul><li>P wave corresponds to depolarization of SA node </li></ul><ul><li>QRS complex corresponds to ventricular depolarization </li></ul><ul><li>T wave corresponds to ventricular repolarization </li></ul><ul><li>Atrial repolarization record is masked by the larger QRS complex </li></ul><ul><li>SEE IP 9 Intrinsic Conduction System pages 3-6 </li></ul>
    30. 30. ECG
    31. 31. Heart Sounds - valves <ul><li>Heart sounds (lub-dup) are associated with closing of heart valves </li></ul><ul><ul><li>First sound occurs as AV (Tricuspid and Mitral) valves close and signifies beginning of systole </li></ul></ul><ul><ul><li>Second sound occurs when SL (Pulmonary & Aortic) valves close at the beginning of ventricular diastole </li></ul></ul>
    32. 32. Cardiac Cycle <ul><li>Cardiac cycle refers to all events associated with blood flow through the heart </li></ul><ul><ul><li>Systole – contraction of heart muscle </li></ul></ul><ul><ul><li>Diastole – relaxation of heart muscle </li></ul></ul>
    33. 33. Phases of Cardiac Cycle <ul><li>Ventricular filling – mid-to-late diastole </li></ul><ul><ul><li>Heart blood pressure is low as blood enters atria and flows into ventricles </li></ul></ul><ul><ul><li>AV valves are open, then atrial systole occurs </li></ul></ul>
    34. 34. Phases of Cardiac Cycle <ul><li>Ventricular systole </li></ul><ul><ul><li>Atria relax </li></ul></ul><ul><ul><li>Rising ventricular pressure results in closing of AV valves </li></ul></ul><ul><ul><li>Isovolumetric contraction phase </li></ul></ul><ul><ul><li>Ventricular ejection phase opens semilunar valves </li></ul></ul>
    35. 35. Phases of Cardiac Cycle <ul><li>Isovolumetric relaxation – early diastole </li></ul><ul><ul><li>Ventricles relax </li></ul></ul><ul><ul><li>Backflow of blood in aorta and pulmonary trunk closes semilunar valves </li></ul></ul><ul><li>Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves </li></ul><ul><li>SEE IP9 Cardiac Cycle pages 3-19 </li></ul>
    36. 36. Cardiac Output (CO) and Reserve <ul><li>CO is the amount of blood pumped by each ventricle in one minute </li></ul><ul><li>CO is the product of heart rate (HR) and stroke volume (SV) </li></ul><ul><li>HR is the number of heart beats per minute </li></ul><ul><li>SV is the amount of blood pumped out by a ventricle with each beat </li></ul><ul><li>Cardiac reserve is the difference between resting and maximal CO </li></ul>
    37. 37. Cardiac Output (CO) - Example <ul><li>CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat) </li></ul><ul><li>CO = 5250 ml/min (5.25 L/min) </li></ul>
    38. 38. Stroke Volume <ul><li>SV = end diastolic volume (EDV) minus end systolic volume (ESV) </li></ul><ul><li>EDV = amount of blood collected in a ventricle during diastole </li></ul><ul><li>ESV = amount of blood remaining in a ventricle after contraction </li></ul>
    39. 39. What affects Stroke Volume? <ul><li>Preload – amount ventricles are stretched by contained blood </li></ul><ul><li>Contractility – cardiac cell contractile force due to factors other than EDV </li></ul><ul><li>Afterload – back pressure exerted by blood in the large arteries leaving the heart </li></ul>
    40. 40. Frank-Starling Law of the Heart <ul><li>Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume </li></ul><ul><li>Slow heartbeat and exercise increase venous return to the heart, increasing SV </li></ul><ul><li>Blood loss and extremely rapid heartbeat decrease SV </li></ul>
    41. 41. Preload and Afterload
    42. 42. Chemical Regulation of Heart <ul><li>The hormones epinephrine and thyroxine increase heart rate </li></ul><ul><li>Intra- and extracellular ion concentrations (Ca++, K+, Na+) must be maintained for normal heart function </li></ul><ul><li>SEE IP9 – Cardiac Output pages 3-9 </li></ul>
    43. 43. Regulation of Heart Rate: Autonomic Nervous System <ul><li>Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise </li></ul><ul><li>Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS </li></ul><ul><li>PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone </li></ul>
    44. 44. Heart Contractility and Norepinephrine <ul><li>Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system </li></ul>GTP GDP Inactive protein kinase A Active protein kinase A ATP cAMP GTP SR Ca 2+ channel Ca 2+ Ca 2+ binds to Troponin Enhanced actin-myosin interaction Extracellular fluid Cytoplasm Adenylate cyclase Ca 2+ channel Ca 2+  1 -Adrenergic receptor Norepinephrine Ca 2+ uptake pump Sarcoplasmic reticulum (SR) Cardiac muscle force and velocity 1 3 2 Figure 18.22
    45. 45. Extrinsic Factors Influencing Stroke Volume <ul><li>Agents/factors that decrease contractility include: </li></ul><ul><ul><li>Acidosis </li></ul></ul><ul><ul><li>Increased extracellular K + </li></ul></ul><ul><ul><li>Calcium channel blockers </li></ul></ul>
    46. 46. Extrinsic Factors Influencing Stroke Volume <ul><li>Contractility is the increase in contractile strength, independent of stretch and EDV (End Diastolic Volume) </li></ul><ul><li>Increase in contractility comes from: </li></ul><ul><ul><li>Increased sympathetic stimuli </li></ul></ul><ul><ul><li>Certain hormones </li></ul></ul><ul><ul><li>Ca 2+ and some drugs </li></ul></ul>
    47. 47. Cardiac Output <ul><li>The big picture </li></ul><ul><li>All factors: </li></ul><ul><li>Key: Be able to identify whether a factor influences SV or HR, and which direction </li></ul>
    48. 48. Control system - Clinical Applications <ul><li>Arrhythmias </li></ul><ul><ul><li>Uncoordinated atrial and ventricular contractions </li></ul></ul>
    49. 49. Control system - Clinical Applications <ul><li>Ectopic Foci – Depolarization (beat) originates someplace other than SA node. </li></ul><ul><ul><li>May be triggered by high caffeine or nicotine </li></ul></ul><ul><ul><li>Most common cause is low oxygen to a region of the heart </li></ul></ul><ul><ul><li>Premature Ventricular contractions (PVC’s) most serious. </li></ul></ul>
    50. 50. Control system - Clinical Applications <ul><li>Ventricular Tachycardia – rapid rate stimulated by ventricular ectopic foci. </li></ul>
    51. 51. Control system - Clinical Applications <ul><li>Ventricular Fibrillation – </li></ul><ul><ul><li>This is the quivering of muscle – uncoordinated </li></ul></ul><ul><ul><li>No pumping is occurring </li></ul></ul><ul><ul><li>Use of defibrillator is indicated here </li></ul></ul>
    52. 52. Control system - Clinical Applications <ul><li>Congestive Heart Failure </li></ul><ul><ul><li>Walls thinning, loss of strength </li></ul></ul><ul><ul><li>May be on either side (r or l) </li></ul></ul><ul><ul><li>If on left, fluid builds up in lungs (why?) </li></ul></ul><ul><ul><li>Treatment: </li></ul></ul><ul><ul><li>Digitalis – (From poisonous Foxglove family of plants) – slows the rate, but increases strength (contractility) </li></ul></ul>
    53. 53. Clinical: What is a “Heart attack”? <ul><li>(Page 692 Btm Left) </li></ul><ul><li>Ishemia results in: </li></ul><ul><li>anaerobic metabolism - lactic acid formation: </li></ul><ul><li>Rising acidity hinders ATP & cannot pump out Ca++, then: </li></ul><ul><li>Gap junctions close - cells electrically isolated, and: </li></ul><ul><li>If ischemic area is large, pumping action impaired. </li></ul>
    54. 54. Clinical Application – CHF Congestive Heart Failure <ul><li>Congestive heart failure (CHF) is caused by: </li></ul><ul><ul><li>Coronary atherosclerosis </li></ul></ul><ul><ul><li>Persistent high blood pressure </li></ul></ul><ul><ul><li>Multiple myocardial infarcts </li></ul></ul><ul><ul><li>Dilated cardiomyopathy (DCM) </li></ul></ul>
    55. 55. Age-Related Changes Affecting the Heart <ul><li>Sclerosis and thickening of valve flaps </li></ul><ul><li>Decline in cardiac reserve – (max HR) </li></ul><ul><li>Fibrosis of cardiac muscle – (normal) </li></ul><ul><li>Atherosclerosis (You are as old as your arteries) </li></ul>
    56. 56. Developmental Aspects of the Heart <ul><li>Contraction detectable at 23 days </li></ul>
    57. 57. Developmental Aspects of the Heart <ul><li>Contraction detectable at 23 days </li></ul><ul><li>4 chambers by day 25 </li></ul>
    58. 58. Fetal Heart Development <ul><li>Fetal heart structures that bypass pulmonary circulation </li></ul><ul><ul><li>Foramen ovale connects the two atria </li></ul></ul><ul><ul><li>Ductus arteriosus connects pulmonary trunk and the aorta </li></ul></ul>
    59. 59. Congenital Heart Defects