2. Chapter 12: Cardiovascular Physiology

3. Chapter 12: Cardiovascular Physiology CO = HR x SV, as follows. The heart is the pump that moves the blood. Its activity can be expressed as “cardiac output (CO)” in reference to the amount of blood moved per unit of time.

4. Chapter 12: Cardiovascular Physiology (cont.) A small fraction of cardiac muscle cells, called the autorhythmic cells, determine the heart rate (HR). A much larger group, making up 99% of the total cells in the heart, constitutes the contractile cells. Their activity determines the stroke volume (SV).

5. Mean arterial pressure, which drives the blood, is the sum of the diastolic pressure plus one-third of the difference between the systolic and diastolic pressures. Chapter 12: Cardiovascular Physiology (cont.) The autonomic system dynamically adjusts CO and MAP. Blood composition and hemostasis are described.

6. Plasma includes water, ions, proteins, nutrients, hormones, wastes, etc. The hematocrit is a rapid assessment of blood composition. It is the percent of the blood volume that is composed of RBCs (red blood cells). Figure 12-1 Section :A: Overview

7. The heart is the pump that propels the blood through the systemic and pulmonary circuits. Red color indicates blood that is fully oxygenated. Blue color represents blood that is only partially oxygenated. Figure 12-2

8. The distribution of blood in a comfortable, resting person is shown here. Dynamic adjustments in blood delivery allow a person to respond to widely varying circumstances, including emergencies. Figure 12-3

9. Though pressure is higher in the lower “tube,” the flow rates in the pair of tubes is identical because they both have the same pressure difference (90 mm Hg) between points P 1 and P 2. Figure 12-4

11. The major external and internal parts of the heart are shown in this diagram. The black arrows indicate the route taken by the blood as it is pumped along. Figure 12-6 Section :B:

12. Figure 12-7

13. The general route of the blood through the body is shown, including passage through the heart (colored box). Figure 12-8

14. Figure 12-9 Cardiac muscle structure

15. Figure 12-10 Conducting system of the heart

16. The sinoatrial node is the heart’s pacemaker because it initiates each wave of excitation with atrial contraction. The Bundle of His and other parts of the conducting system deliver the excitation to the apex of the heart so that ventricular contraction occurs in an upward sweep. Figure 12-11 Sequence of cardiac excitation

17. Figure 12-13 The action potential of a myocardial pumping cell. The rapid opening of voltage- gated sodium channels is responsible for the rapid depolarization phase.

18. Figure 12-12 The prolonged “plateau” of depolarization is due to the slow but prolonged opening of voltage-gated calcium channels PLUS closure of potassium channels. The action potential of a myocardial pumping cell.

19. Figure 12-12 Opening of potassium channels results in the repolarization phase. The action potential of a myocardial pumping cell.

20. Figure 12-12 The action potential of a myocardial pumping cell. Opening of potassium channels results in the repolarization phase. The prolonged “plateau” of depolarization is due to the slow but prolonged opening of voltage-gated calcium channels PLUS closure of potassium channels. The rapid opening of voltage-gated sodium channels is responsible for the rapid depolarization phase.

21. Figure 12-13 Sodium ions “leaking” in through the F-type [funny] channels PLUS calcium ions moving in through the T [calcium]channels cause a threshold graded depolarization. The rapid opening of voltage-gated calcium channels is responsible for the rapid depolarization phase. Reopening of potassium channels PLUS closing of calcium channels are responsible for the repolarization phase. The action potential of an autorhythmic cardiac cell.

22. The relationship between the electrocardiogram ( ECG ), recorded as the difference between currents at the left and right wrists, and an action potential typical of ventricular myocardial cells. Figure 12-14

23. Figure 12-15a Einthoven’s triangle

24. Figure 12-15b

26. Figure 12-16 Normal Partial block Complete block

27. Calcium ions regulate the contraction of cardiac muscle: the entry of extracellular calcium ions causes the release of calcium from the sarcoplasmic reticulum, the source of about 95% of the calcium in the cytosol. Figure 12-17 Excitation contraction coupling in cardiac muscle

28. The prolonged refractory period of cardiac muscle prevents tetanus, and allows time for ventricles to fill with blood prior to pumping. Figure 12-18 Refractory period of cardiac muscle

29. Figure 12-19a Mechanical events of the cardiac cycle Systole: ventricles contracting and ejection

30. Figure 12-19b Diastole: ventricles relaxed and filling

31. Pressure and volume changes in the left heart during a contraction cycle. Figure 12-20

32. Pressure changes in the right heart during a contraction cycle. Figure 12-21 Pulmonary circulation pressures

33. Heart Sounds Figure 12-22

34. Figure 12-23 The cardiac output: control of heart rate

35. To speed up the heart rate: deliver the sympathetic hormone, epinephrine, and/or release more sympathetic neurotransmitter (norepinephrine), and/or reduce release of parasympathetic neurotransmitter (acetylcholine). Figure 12-24

36. To increase the heart’s stroke volume: fill it more fully with blood. The increased stretch of the ventricle will align its actin and myosin in a more optimal pattern of overlap. Figure 12-25 Frank-Starling mechanism

37. To further increase the stroke volume: fill it more fully with blood AND deliver sympathetic signals (norepinephrine and epinephrine); it will also relax more rapidly, allowing more time to refill. Figure 12-26 Stroke volume and sympathetic nerves

38. Sympathetic signals (norepinephrine and epinephrine) cause a stronger and more rapid contraction and a more rapid relaxation. Figure 12-27 Effects of sympathetic stimulation on ventricular contraction and relaxation

40. Figure 12-28 To increase SV, increase: end-diastolic volume, norepinephrine delivery from sympathetic neurons, and epinephrine delivery from the adrenal medulla. To increase HR, increase: norepinephrine delivery from sympathetic neurons, and epinephrine delivery from adrenal medulla (reduce parasympathetic). It is not possible, under normal circumstances, to increase one but not the other of these determinants of cardiac output. Factors determining the cardiac output

42. Section C: The vascular system

43. Figure 12-29 Pressures in the systemic vessels

44. The blood moved in a single heart contraction stretches out the arteries, so that their recoil continues to push on the blood, keeping it moving during diastole. Figure 12-30

45. Figure 12-31a

46. Figure 12-31b

47. To estimate systolic and diastolic pressures, pressure is released from an inflatable cuff on the upper arm while listening as blood flow returns to the lower arm. Figure 12-32

48. Dynamic adjustments in the blood distribution to the organs is accomplished by relaxation and contraction of circular smooth muscle in the arterioles. Figure 12-33 Arterioles

49. Active hyperemia and flow autoregulation differ in their cause but both result in the production of the same local signals that provoke vasodilation. Figure 12-34 Local control of organ blood flow

50. Sympathetic stimulation of alpha-adrenergic receptors cause vasoconstriction to decrease blood flow to that location. Sympathetic stimulation of beta-adrenergic receptors lead to vasodilation to cause an increase in blood flow to that location. Figure 12-35

51. Diversity among signals that influence contraction/relaxation in vascular circular smooth muscle implies a diversity of receptors and transduction mechanisms. Figure 12-36 Major factors affecting arteriolar radius

52. The capillary is the primary point exchange between the blood and the interstitial fluid (ISF). Intercellular clefts assist the exchange. Capillary walls are a single endothelial cell in thickness. Figure 12-37 Capillaries

53. Capillaries lack smooth muscle, but contraction/relaxation of circular smooth muscle in upstream metarterioles and precapillary sphincters determine the volume of blood each capillary receives. Figure 12-38 Microcirculation

54. Six balls in per minute mandates six balls out per minute. Therefore, the velocity of the balls in the smaller tubes is slower. Figure 12-39

55. There are many, many capillaries, each with slow-moving blood in it, resulting in adequate time and surface area for exchange between the capillary blood and the ISF. Figure 12-39

56. At rest, approx. 60% of the total blood volume is in the veins. Sympathetically mediated venoconstriction can substantially increase venous return to the heart. Figure 12-44 Distribution of the total blood volume in different parts of the CVS

57. Venous flow is assisted by the skeletal muscle pump mechanism working in combination with one-way valves. Figure 12-45 Skeletal muscle pump

58. Alterations in “venous return” alter end-diastolic volume (EDV); increased EDV directly increases stroke volume and cardiac output. Figure 12-46 Major factors determining the peripheral venous return

59. Lymphatic fluid, formed by the slight mismatch between filtration and absorption in the capillaries, returns to the blood in the veins. Figure 12-47 The lymphatic system

61. Section C: Regulation of systemic arterial pressures

62. Figure 12-49 Dynamic changes in vasodilation/vasoconstriction due to changes in the resistance of arterioles can alter the mean arterial pressure (represented as  P).

63. Compensatory changes in arteriolar resistance occur to protect the maintenance of mean arterial pressure (represented as  P). Figure 12-50

64. A summary of dynamic changes in MAP and TPR. Figure 12-51

65. Blood loss causes a reduction in MAP, which, if left unchecked, would result in rapid and irreversible damage to the brain and the heart. Figure 12-52

66. Baroreceptor neurons function as sensors in the homeostatic maintenance of MAP by constantly monitoring pressure in the aortic arch and carotid sinuses. Figure 12-53

67. The action potential frequency in baroreceptor neurons is represented here as being directly proportional to MAP. Figure 12-54

68. Baroreceptor neurons deliver MAP information to the medulla oblongata’s cardiovascular control center (CVCC); the CVCC determines autonomic output to the heart. i.e., MAP is above homeostatic set point i.e., reduce cardiac output Figure 12-55

69. The information reported by baroreceptor neurons sets in motion autonomic responses not only to the heart, but also to arterioles and veins. MAP is more readily moved back closer to the “set point” by this combined approach. Figure 12-56

70. Whatever the cause, an abnormal increase in MAP “squeezes” more fluid out of the blood and into the urine, leading to a reduction in blood volume, which then reduces MAP back closer to the “set point” value. Figure 12-57

72. Loss of blood causes immediate reductions in MAP, but compensatory responses in cardiac output and total peripheral resistance act quickly to restore MAP. Figure 12-58

73. At capillaries, reduced MAP increases absorption and reduces filtration to help “protect” blood volume. Figure 12-59 Autotransfusion mechanism

75. Dynamic adjustments in blood-flow distribution during exercise result from changes in cardiac output and from changes in regional vasodilation/vasoconstriction. Figure 12-61 Distribution of the systemic CO

76. Summary of CV changes during mild exercise

77. Using stored knowledge, along with information from the periphery (afferent input), the CNS coordinates changes in cardiac output and blood-flow distribution during exercise. Figure 12-63 Control of the CVS during exercise

79. The benefits of training include increased cardiovascular capacity during subsequent exercise. Figure 12-64 Changes in CO, HR, SV with increasing workload in untrained and trained individuals

81. Heart failure leads to increased fluid retention, leading to increased blood volume and greater stroke volume; however, the failing heart is less able to handle a large EDV. Figure 12-65

83. An example of angiographic visualization and treatment of blocked blood flow in an impaired heart. Coronary artery disease and its treatment

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