Anatomy  Physiology Bio 2402 Lecture

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Anatomy Physiology Bio 2402 Lecture

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1. Anatomy & Physiology Bio 2402 Lecture Instructor: Daryl Beatty Day 4 Class 4 The Heart, Part 2

2. Review: Cardiac Cycle Beginning of control system

3. Review of Cardiac Blood Flow Be able to trace flow, from start to finish Questions: How do the valves work Name the parts & vessels Questions: How do the valves work Name the parts & vessels

4. Sequence of blood flow Right atrium ? tricuspid valve ? right ventricle Right ventricle ? pulmonary semilunar valve ? pulmonary arteries ? lungs Lungs ? pulmonary veins ? left atrium Left atrium ? bicuspid valve ? left ventricle Left ventricle ? aortic semilunar valve ? aorta Aorta ? systemic circulation

5. Two systems: Pulmonary Systemic

6. Review of Cardiac Blood Flow Function of chordae tendineae and papillary muscles? What opens and closes the valves? Questions: How do the valves work Name the parts & vessels Questions: How do the valves work Name the parts & vessels

7. New section for today

8. Control system - Autorhythmic Fibers See figure 18.14 on page 694 These fibers have an unstable resting potential due to Na+ & Ca++ leakage in.

9. Control system - Autorhythmic Fibers See figure 18.14 on page 694 These fibers have an unstable resting potential due to Na+ & Ca++ leakage in.

10. Control system - role of instability of RMP Sinoatrial node (SA) – Inherent rate of 100 BPM “Sinus Rhythm” – Heart’s pacemaker Location: Upper RA Fastest cells in system

11. Atrial (Bainbridge) Reflex Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria Causes stimulation of the SA node Stimulates baroreceptors in the atria, causing increased SNS (Sympathetic Nervous System) stimulation

12. Control system - Atrioventricular Node (AV) –

13. Control system - Atrioventricular Node (AV) – Impulse is delayed here 0.1 second (Why?)

14. Control system - Atrioventricular bundle – (Bundle of His)

15. Control system - Atrioventricular bundle – (Bundle of His) The only electrical connection between atria and ventricles Rapidly conducts through Right Bundle branch, (RBB), Left Bundle Branch (LBB) and Purkinje fibers

16. Control system - Right Bundle branch, (RBB), - stimulates septal cells Left Bundle Branch (LBB) – septal cells Purkinje fibers- most important, stimulates most of the ventricular walls, and first stimulates the papillary muscles (why?)

17. Control system - Time required: 220 ms from SA node to complete depolarization. Longer time indicates conduction defect

18. Intrinsic Conduction System Autorhythmic cells: Initiate action potentials Have unstable resting potentials called pacemaker potentials Use calcium influx (rather than sodium) for rising phase of the action potential

19. Pacemaker and Action Potentials of the Heart

20. Sequence of Excitation Sinoatrial (SA) node generates impulses about 75 times/minute Atrioventricular (AV) node delays the impulse approximately 0.1 second Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)

21. Sequence of Excitation AV bundle splits into two pathways in the interventricular septum (bundle branches) Bundle branches carry the impulse toward the apex of the heart Purkinje fibers carry the impulse to the heart apex and ventricular walls

22. Cardiac Intrinsic Conduction

23. Heart Excitation Related to ECG

24. Heart Excitation Related to ECG

25. Heart Excitation Related to ECG

26. Heart Excitation Related to ECG

27. Heart Excitation Related to ECG

28. Extrinsic Innervation Heart is stimulated by the sympathetic cardioacceleratory center Heart is inhibited by the parasympathetic cardioinhibitory center

29. ECG – What it means Electrical activity is recorded by electrocardiogram (ECG) P wave corresponds to depolarization of SA node QRS complex corresponds to ventricular depolarization T wave corresponds to ventricular repolarization Atrial repolarization record is masked by the larger QRS complex SEE IP 9 Intrinsic Conduction System pages 3-6

30. ECG

31. Heart Sounds - valves Heart sounds (lub-dup) are associated with closing of heart valves First sound occurs as AV (Tricuspid and Mitral) valves close and signifies beginning of systole Second sound occurs when SL (Pulmonary & Aortic) valves close at the beginning of ventricular diastole

32. Cardiac Cycle Cardiac cycle refers to all events associated with blood flow through the heart Systole – contraction of heart muscle Diastole – relaxation of heart muscle

33. Phases of Cardiac Cycle Ventricular filling – mid-to-late diastole Heart blood pressure is low as blood enters atria and flows into ventricles AV valves are open, then atrial systole occurs

34. Phases of Cardiac Cycle Ventricular systole Atria relax Rising ventricular pressure results in closing of AV valves Isovolumetric contraction phase Ventricular ejection phase opens semilunar valves

35. Phases of Cardiac Cycle Isovolumetric relaxation – early diastole Ventricles relax Backflow of blood in aorta and pulmonary trunk closes semilunar valves Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves SEE IP9 Cardiac Cycle pages 3-19

36. Cardiac Output (CO) and Reserve CO is the amount of blood pumped by each ventricle in one minute CO is the product of heart rate (HR) and stroke volume (SV) HR is the number of heart beats per minute SV is the amount of blood pumped out by a ventricle with each beat Cardiac reserve is the difference between resting and maximal CO

37. Cardiac Output (CO) - Example CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat) CO = 5250 ml/min (5.25 L/min)

38. Stroke Volume SV = end diastolic volume (EDV) minus end systolic volume (ESV) EDV = amount of blood collected in a ventricle during diastole ESV = amount of blood remaining in a ventricle after contraction

39. What affects Stroke Volume? Preload – amount ventricles are stretched by contained blood Contractility – cardiac cell contractile force due to factors other than EDV Afterload – back pressure exerted by blood in the large arteries leaving the heart

40. Frank-Starling Law of the Heart Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume Slow heartbeat and exercise increase venous return to the heart, increasing SV Blood loss and extremely rapid heartbeat decrease SV

41. Preload and Afterload

42. Chemical Regulation of Heart The hormones epinephrine and thyroxine increase heart rate Intra- and extracellular ion concentrations (Ca++, K+, Na+) must be maintained for normal heart function SEE IP9 – Cardiac Output pages 3-9

43. Regulation of Heart Rate: Autonomic Nervous System Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone

44. Heart Contractility and Norepinephrine Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system

45. Extrinsic Factors Influencing Stroke Volume Agents/factors that decrease contractility include: Acidosis Increased extracellular K+ Calcium channel blockers

46. Extrinsic Factors Influencing Stroke Volume Contractility is the increase in contractile strength, independent of stretch and EDV (End Diastolic Volume) Increase in contractility comes from: Increased sympathetic stimuli Certain hormones Ca2+ and some drugs

47. Cardiac Output The big picture All factors: Key: Be able to identify whether a factor influences SV or HR, and which direction

48. Control system - Clinical Applications Arrhythmias Uncoordinated atrial and ventricular contractions

49. Control system - Clinical Applications Ectopic Foci – Depolarization (beat) originates someplace other than SA node. May be triggered by high caffeine or nicotine Most common cause is low oxygen to a region of the heart Premature Ventricular contractions (PVC’s) most serious.

50. Control system - Clinical Applications Ventricular Tachycardia – rapid rate stimulated by ventricular ectopic foci.

51. Control system - Clinical Applications Ventricular Fibrillation – This is the quivering of muscle – uncoordinated No pumping is occurring Use of defibrillator is indicated here

52. Control system - Clinical Applications Congestive Heart Failure Walls thinning, loss of strength May be on either side (r or l) If on left, fluid builds up in lungs (why?) Treatment: Digitalis – (From poisonous Foxglove family of plants) – slows the rate, but increases strength (contractility)

53. Clinical: What is a “Heart attack”? (Page 692 Btm Left) Ishemia results in: anaerobic metabolism - lactic acid formation: Rising acidity hinders ATP & cannot pump out Ca++, then: Gap junctions close - cells electrically isolated, and: If ischemic area is large, pumping action impaired.

54. Clinical Application – CHF Congestive Heart Failure Congestive heart failure (CHF) is caused by: Coronary atherosclerosis Persistent high blood pressure Multiple myocardial infarcts Dilated cardiomyopathy (DCM)

55. Age-Related Changes Affecting the Heart Sclerosis and thickening of valve flaps Decline in cardiac reserve – (max HR) Fibrosis of cardiac muscle – (normal) Atherosclerosis (You are as old as your arteries)

56. Developmental Aspects of the Heart Contraction detectable at 23 days

57. Developmental Aspects of the Heart Contraction detectable at 23 days 4 chambers by day 25

58. Fetal Heart Development Fetal heart structures that bypass pulmonary circulation Foramen ovale connects the two atria Ductus arteriosus connects pulmonary trunk and the aorta

59. Congenital Heart Defects

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