1. SS 1 Filtration Secretion Reabsorption

2. Circulatory System Circulates Nutrients: glucose, amino acids, fatty acids, ketones, etc Wastes: Hormones: bound & free Gases: CO 2 and O 2 Formed Elements: Cells and Cell Fragments –Erythrocytes, Leukocytes, Thrombocytes = Platelets Other roles of the Cardiovascular System Thermoregulation Blood Clotting Reproduction (ex: penile erection) S 2

3. Figure 12.01 Blood volume ~ 5 liters Serum = plasma – clotting factors Formed elements Components…… Blood doping & erythropoietin (hormone that stimulates erythrocyte production in bone marrow) to increase hematocrit Entering and Exiting the blood Discontinuous capillaries in bone marrow, spleen, & liver permit erythrocytes to enter and exit blood. Hct = percentage of blood volume occupied by RBCs Anemia EPO and “The Scoop on Tissie” S 3

4. Fig. 12.02 Arteries..away from heart Veins..return to heart Regional blood flow determined by arteries and arterioles. Resting Cardiac Output = 5L/min for each side! When left heart can’t pump all the blood it receives from pulmonary circuit (due to high aortic pressure and/or damage to left ventricle) blood accumulates in pulmonary circuit. This is congestive heart failure. Symptom: shortness of breath. S 4

5. Figure 12.04 CO = 5L/min for each circuit Up to 35 L/min in strenuous exercise S 5

6. What’s missing? Microcirculation Pulmonary circuit Systemic Circuit CO = 5 liters/min Exchange Vessels Resistance Vessels Capacitance vessels S 6 Recall Portal Systems!Arterial Blood Pressure

7. Pulmonary circuit Systemic Circuit S 7 Pressure gradients makes fluids move. Moving fluids flow, but flow is limited by resistance. Resistance creates pressure. Arterioles establish Mean Arterial Pressure

8. F=Q=ΔP/R Flow = Pressure gradient/Resistance from Ohm’s Law (V=IR) R = 8Lη/πr 4 Q= ΔP πr 4 8Lη Poiseulle’s equation Smooth muscles determine radius Double radius … 16x flow Half radius….1/16 th flow Radius of arterioles regulates Q to organs S 8

9. MAP = CO x TPR Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance MAP = (HR x SV) x TPR S 14

10. Cardiac Output = Heart Rate X Stroke Volume What regulates heart rate? CO = HR x SV 5L/min = 72 beat/min x 70 ml/beat The Cardiac Cycle animation S 1 What regulates Stroke Volume?

11. Figure 12.07 Bicuspid =Mitral Tricuspid Problems with valves: ….Stenosis (narrowing) →Heart Murmurs (turbulent flow past a constriction) note: origin of neonatal heat murmurs (foramen ovale) ….Prolapse (eversion) allows backflow (also generates murmurs) Semilunar Valves Heart sounds produced by valve closings Animation Heart murmurs ≠ heart sounds S 4

12. Figure 12.13 Cardiac Myofiber Plateau phase Cardiac Myofiber action potential Long refractory period prevents summation in cardiac myofibers S 3

13. Figure 12.11 SA node cells do not have stable resting membrane potential, spontaneously produce AP, are Pacemaker cells S 5 S 4

14. Figure 12.14 Pacemaker Cells in Conducting System: SA Node and Bundle of His Ectopic Pacemaker Locations other than SA Node S 5 Cardiac Pacemaker action potential These cells set the rhythm & control Heart Rate.

15. 1QQ # 14: Answer one. 1.A) Which vessels are classified as exchange vessels? B) Why are they called exchange vessels? 2.A) What produces a heart sound? B) What produces a heart murmur? 3.With all other factors held constant, how would blood flow be affected by a doubling of the pressure gradient? 4.A) Explain how a heart can continue to beat even if the SA node is not functioning. B) Would this heart rate be faster or slower than the rate produced by the SA node?

16. Figure 12.22 Intrinsic Rate = 100 beat/min S 15 2 effects of Parasymp: hyperpolarization & slower depolarization

17. Figure 12.23 Effect of “Beta blockers” NEEPIACh mAChR Effect of atropine Beta-adrenergic receptors S 6

18. Fibrous connective tissue between atria and ventricles prevents the conduction of action potential. Only route is via AV node, bundle of His, bundle branches, Purkinje fibers, and to ventriclular myofibers. What prevents the AP from being conducted from ventricles back to atria? S 7

19. 1 st Heart Sound = Closure of Atrioventricular (AV) valves at beginning of Ventricular Systole 2nd Heart Sound = Closure of Semilunar valves at beginning of Ventricular Diastole S 8 “Sis-toe-lee” “die-ass-toe-lee”

20. Figure 12.20 Systolic Diastolic Ejection Fraction = SV/EDV Atrial Fibrillation Ventricular Fibrillation & Defibrillation Stroke Volume Animation S 9

21. Events are same for Cardiac Cycle for Right Side of Heart; only difference is lower systolic pressures in right atrium and right ventricle. S 10

22. CO = HR x SV 5L/min = 72 beat/min x 70 ml/beat 35 L/min = ? beat/min x ? ml/beat S 1 So far, we’ve dealt with the factors that control Cardiac Output by changing heart rate. + sympathetic - parasympathetic 2 1 3

23. Figure 12.20 Stroke Volume Animation S 2

24. Frank-Starling Law of the Heart FS LoH = SV is proportional to EDV Ventricular Function Curve Does not depend on hormones or nerves Assures that the heart adjusts its output based on VENOUS RETURN Ways to enhance Venous Return: 1) muscle contractions 2) “respiratory pump” 3) venoconstriction S 3 ↑VR→ ↑EDV → ↑SV

25. Fig. 09.21 Low EDV High EDV Length-tension “curve” for Cardiac muscle Overinflation of ventricles leads to less effective pumping S 4

26. Overinflation of ventricles results in reduction in stroke volume S 5 Treatments? …..diuretics

27. Contractility NE from Symp postganglionics & EPI from Adrenal medulla Note: cardiac myofibers NOT innervated by parasympathetic division Increase Ejection Fraction S 6

28. 3 Effects of Sympathetic Stimulation 1: Increase rate of contraction 2: Increase peak tension 3: Decrease twitch duration S 7 Why should the contraction be shorter?

29. Afterload is analogous to trying to pump more air into a tire that is already fully inflated (heart contracting to overcome diastolic pressure.) High blood pressure increases the workload of the heart….. Cardiac hypertrophy….increase chance of irregular conduction of AP through heart S 9 Hypertrophic cardiomyopathy

30. Summary: Control of Stroke Volume End diastolic volume (preload) Contractility (strength of ventricular contraction due to adrenergic stimulation) Pressure in arteries that must be overcome = Afterload FS LoH S 8

31. CO = HR x SV 5L/min = 72 beat/min x 70 ml/beat 35 L/min = ? beat/min x ? ml/beat S 11 Factors that control Cardiac Output by changing heart rate and stroke volume. + sympathetic - parasympathetic EDV (FSLoH) contractility Afterload (MAP)

32. Fig. 12.28 Even persons with heart transplants can adjust CO in the absence of innervation of heart. Summary of Factors that Regulate Cardiac Output S 12

33. S 13 Heart is pump that generates pressure gradient. Blood flows through vessels, which have resistance. Arterioles have greatest resistance and create “backpressure” in the arteries and aorta. Mean Arterial Pressure = diastolic +1/3(systolic – diastolic) = 70 + 1/3(120-70) = 70 + 17 = 87 mm Hg

34. CO = HR x SV 5L/min = 72 beat/min x 70 ml/beat 35 L/min = ? beat/min x ? ml/beat S 11 Factors that control Cardiac Output by changing heart rate and stroke volume. + sympathetic - parasympathetic EDV (FSLoH) contractility Afterload (MAP)

35. Properties of Blood Vessels Arteries Arterioles Capillaries Venules Veins Elastic, low compliance, large diameter, low resistance vessels Variable Resistance vessels Exchange Capacitance vessels, high compliance, low pressure, valves for unidirectional flow All vessels and heart chambers lined with ENDOTHELIAL cells (simple squamous) Wall = simple squamous endothelium No smooth muscle; cannot change diameter S 1

36. Fig. 12.29 AortaBrachial or Femoral artery Pusatile flow Damage to artery vs vein S 2

37. Fig. 12.39b Analogy: river width and flow S 3

38. Fig. 12.30 Elastic recoil of stretched arterial walls during ventricular systole maintains arterial pressure during diastole as blood drains into arterioles. Point of Confusion: Smooth muscles in arterial walls DO NOT rhythmically contract, do not pump! Atherosclerosis S 4 Stretching elastic connective tissue Recoil of elastic connective tissue

39. Arteries and Arterial Pressure Mean Arterial Pressure Arteriole Arterioles have two main functions: 1) regulate flow to tissues and organs and 2) responsible for Total Peripheral Resistance which influences Blood Pressure. MAP = CO x TPR Poiseulle’s Equation S 5

40. Fig. 12.50 S 6 Heart Arteries Arterioles Kidneys Gut Sk. Muscle Skin CNS Totol Peripheral Resistance Mean Arterial Pressure Cardiac Output

41. Alpha receptors more common except in skeletal muscle arterioles which have more B2 receptors Receptors for other ligands S 7

42. Fig. 12.36 Metabolic autoregulation, flow autoregulation, myogenic autoregulation No parasympathetic innervation of arterioles! Importance of sympathetic “tone.” Metabolic vasodilators S 8

43. Figure 12.02 Capillaries = 5% of Blood Volume Veins = 60% of Blood Volume Arteries = 10% of Blood Volume Arterioles = Resistance vessels S 4

44. Figure 12.38 Capillaries: Continuous, discontinuous, and fenestrated capillaries: Ex: brain liver endocrine glands Generate vasodilators and vasoconstrictors Arterioles: 1) Extrinsic control by hormones and nerves 2) Intrinsic (local) control by …..a) metabolic autoregulation, …..b) flow autoregulation, and …..c) myogenic autoregulation. S 5

45. 1QQ # 15 Answer one. 1.Describe metabolic autoregulation and list four substances that are classified as metabolic vasodilators. 2.What is the main difference between flow autoregulation and metabolic autoregulation? 3.Explain why the pressure in a major artery doesn’t fall to 0 during ventricular diastole.

46. Capillary exchange by: Diffusion, vesicle transport, bulk flow, mediated transport S 6

47. Fig. 12.40 Diffusion is the most important mode of exchange of nutrients S 7

48. Figure 12.41 Crystalloids Colloids Bulk Flow S 8 = colloids (impermeable proteins)

49. Cell Membrane: selectively permeable Capillaries: highly permeable except to proteins S 9

50. Figure 12.42 Main difference in the Pulmonary circuit? Net filtration = 4L/day Bulk Flow through aqueous channels and intracellular clefts Regulated by arterioles Starling Forces S 10

51. Fig. 12.43 PcPc PcPc PcPc S 11

52. Who Cares? Aunt Esther Cancer of the liver; Failure of hepatocytes to produce plasma colloids S 12

53. Figure 12.41 Crystalloids Colloids Bulk Flow S 13

54. Figure 12.47 Liver & Bone Marrow & Spleen Fate of 4 L/d excess filtrate S 1 Mode of propulsion?

55. Figure 12.44 Veins are Capacitance vessels (high compliance) with valves for unidirectional flow Arteries are low compliance, so any increase in volume increases pressure. S 2

56. Fig. 12.53 MAP = CO x TPR Negative feedback control: stimulus, receptors, afferent pathway(s), integrator, efferent pathway(s), effector(s) response(s) S 3 + other baroreceptors

57. Fig. 12.54 S 4 What happens to the set point for MAP during exercise?

58. MAP = CO x TPR Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance MAP = (HR x SV) x TPR S 2

59. Test 3 Hemorrhage Diagram On one page, create a well-organized diagram for the following. Beginning with a loss of about 1 liter of blood from a vein, diagram the early events associated with hemorrhage and the negative feedback responses to hemorrhage in a well-organized diagram. Write legibly! Completeness, accuracy, and detail, together with the proper sequence earn maximal points. The following abbreviations can be used: ACE, AI, AII, Aldo (aldosterone), JGA, mAChR, Hct, Q, SV, EF (ejection fraction), RBC, HR, EDV, ACh, ANH, ADH, CO, TPR, EPO, VR, MAP, EPI, NE, SAN (SA Node), aAdR, bAdR, Symp (sympathetic), Parasymp (parasympathetic), PV (plasma volume), r (radius), Pc, fAP (frequency of action potentials.) Any other abbreviations must be defined. "If in doubt, write it out!" Use single headed arrows (→) to indicate sequential relationships and doubled-stemmed arrows to indicate increases or decreases. S 6