1. BLOOD PRESSURE MECHANISM SHORT TERM CONTROL OF BLOOD PRESSURE

2. Introduction There are two basic mechanisms for regulating blood pressure: (1) short-term mechanisms. regulate blood vessel diameter, heart rate and contractility (2) long-term mechanisms. regulate blood volume Blood Pressure = cardiac outputxperipheral resistance Any change in cardiac output, blood volume or peripheral resistance will lead to a change in blood pressure.

3. Short term control of Blood pressure is mediated by the : nervous system Chemicals that control blood pressure by changing peripheral resistance. ( in sec or minutes) Rapidity of response (beginning within seconds and often increasing the pressure to 2X normal (5 to 10 seconds). Sudden inhibition of nervous cardiovascular stimulation can decrease the arterial pressure (one half normal)(10-40 seconds).

4. I. Nervous System Control BP by changing blood distribution in the body and by changing blood vessel diameter. Sympathetic & Parasympathetic activity will affects veins, arteries & heart tocontrol HR and force of contraction The vasomotor center cluster of sympathetic neurons found in the medulla. It sends efferent motor fibers that innervate smooth muscle of blood vessels. Sympathetic activity Sympathetic activity VASOCONSTRICTION VASODILATATION

5. Short-term Regulation of Rising Blood Pressure Rising blood pressure Stretching of arterial walls Stimulation of baroreceptors in carotid sinus, aortic arch, and other large arteries of the neck and thorax Increased impulses to the brain

6. Baroreceptors The best known of nervous mechanisms for arterial pressure control (baroreceptor reflex) Baroreceptors are stretch receptors found in the carotid body, aortic body and the wall of all large arteries of the neck and thorax. Respond progressively at 60-180 mm Hg. Respond more to a rapidly changing pressure than stationary pressure.

7. Baroreceptors

8. Effect of Baroreceptors Baroreceptors entered the medulla (tractussolitarius) Secondary signals inhibit the vasoconstrictor center of medulla and excite the vagal parasympathetic center EFFECT VASODILATATION OF THE VEINS AND ARTERIOLES DECREASED HEART RATE AND STRENGTH OF HEART CONTRACTION Therefore, excitation of baroreceptors by high pressure in the arteries reflexly causes arterial pressure to decrease (as decrease in PR and CO) NOTE : Conversely, low pressure has opposite effects,reflexly causing the pressure rise back to normal.

9. Increased Parasympathetic Activity Effect of increased parasympathetic and decreased sympathetic activity on heart and blood pressure: Increased activity of vagus (parasympathetic) nerve Decreased activity of sympathetic cardiac Nerves Reduction of heart rate Lower cardiac output Lower blood pressure

10. Decreased Sympathetic Activity Effect of decreased sympathetic activity on arteries and blood pressure: Decreased activity of vasomotor fibers (sympathetic nerve fibers) Relaxation of vascular smooth muscle Increased arterial diameter Lower blood pressure

11. Short-term Regulation of Falling Blood Pressure Baroreceptors inhibited Decreased impulses to the brain Decreased parasympathetic activity, increased sympathetic activity Effects Heart increased heart rate and increased contractility Vessels increased vasoconstriction Adrenal gland release of epinephrine and norepinephrine which enhance heart rate Contractility and vasoconstriction Increased blood pressure

12. Sympathetic Activity on Heart and Blood Pressure Effect of Increased Sympathetic Activity on Heart and Blood Pressure: • Increased activity of sympathetic cardiac nerves • Decreased activity of vagus (parasympathetic) nerve • Increased heart rate and contractility • Higher cardiac output • Increased blood pressure

13. Vasomotor Fibers • Effect of Increased Sympathetic Activity on Arteries and Blood Pressure: • Increased activity of vasomotor fibers (sympathetic nerve fibers) • Constriction of vascular smooth muscle • Decreased arterial diameter • Increased blood pressure

14. Sympathetic Activity on Adrenal Gland and Blood Pressure Effect of increased sympathetic activity on adrenal glands and blood pressure: • Increased sympathetic impulses to adrenal glands. • Release of epinephrine and norepinephrineto bloodstream. • Hormones increase heart rate, contractility and vasoconstriction. Effect is slower-acting and more prolonged than nervous system control. • Increased blood pressure.

16. II. Chemoreceptor

17. Chemoreceptor Chemosensitive cells that respond to changes in pCO2 and pO2 and pH levels (Hydrogen ion). pO2 and pH  pCO2 Stimulation of vasomotor center vasoconstriction CO  HR BP (speeding return of blood to the heart and lungs)

18. Chemoreceptor

19. CNS Ischemic Response Severe decrease blood flow to brain Cerebral hypoxia Vasomotor center stimulated – causes powerful vasoconstriction ( INCREASE SYMPATHETIC DISCHARGE – Norepinephrine) Increase blood pressure & blood flow

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22. SHORT TERM REGULATION OF BLOOD PRESSURE

24. Distribution: Almost all segments of the circulation.

25. The innervation is powerful in the kidneys, gut, spleen and skin

27. except the capillaries, precapillary sphincters and most of the metarterioles.

30. Parasympathetic nerve fibers innervate vessels of the blood vessels in

31. Meninges

32. the salivary glands

33. the liver

34. the viscera in pelvis

35. the external genitals

37. Brainstem contains: Pons Medulla In the Medulla are the: Cardiac Acceleratory Centre Cardiac Inhibitory Centre Vasomotor Centre

38. Short-Term Regulation Rapidly Acting Pressure Control Mechanisms, Acting Within Seconds or Minutes. Baroreceptor reflexes (60 – 100 mmHg) Change peripheral resistance, heart rate, and stroke volume in response to changes in blood pressure Chemoreceptor reflexes (40 – 60 mmHg) Sensory receptors sensitive to oxygen lack, carbon dioxide excess, and low pH levels of blood Central Nervous System ischemic response (< 40 mmHg) Results from severe decrease blood flow to the brain

40. Aortic Arch(systemic blood going to body) by vagus nerveAs MAP increases this stretches the receptors and they send a fast train of impulses to the Vasomotor Centre. After the signals enter the tractussolitarius, secondary signals inhibit vasoconstrictor centres and excite the vagal parasympathetic center. This results in a decrease in the frequency of impulses from the Vasomotor Centre and arterioles dilate. Final result is vasodilationand decreases MAP. * CIC activity increases (stimulating the Vagus nerve) - decreases HR and SV. * CAC activity decreases (inhibiting Sympathetic nerves) - decreases CO.

43. Chemoreceptor Reflex

44. CNS Ischemic Response Severe decrease blood flow to brain Cerebral hypoxia Vasomotor center stimulated – causes powerful vasoconstriction ( INCREASE SYMPATHETIC DISCHARGE – Norepinephrine) Increase blood pressure & blood flow

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47. HORMONES INVOLVE IN CALCIUM METABOLISM

50. 40% bound to plasma protein

51. 10% complexed to anion (phosphate, citrate, sulfate)

52. 50%is free ionized(biologically active)

54. Relation of Calcium & Phosphate The calcium and phosphate homeostasis are linked together Calcium complexes with phosphate where more phosphate present then more calcium bind to it and reduce the free ionized calcium fraction in ECF. The less phosphate present the less calcium bind to it and this increase the free, ionized calcium fraction Hence ,decrease phosphate level in blood help plasma Ca level in blood.

55. Parathyroid Hormone (PTH) It is secreted when the blood plasma Ca 2+ is decreased Thus, it prevents hypocalcemia Also acts to decrease concentration of phosphate in the plasma The action is direct in the bone and kidney In the intestine, the action is indirect

56. Action of PTH in bone Increases bone resorption Ca and phosphate are released to the ECF The concentration of Ca in the serum increases

57. Action of PTH in kidney PTH promotes Ca reabsorption and inhibits phosphate reabsorption in the kidney tubules Inhibition of phosphate reabsorption causes it to be excreted in the urine, a condition named phosphaturia Since Ca is reabsorbed, its concentration in the plasma is elevated.

58. Action of PTH on intestine PTH has no direct effect on the intestine It indirectly increases Ca and phosphate absorption to the small intestine by activating vitamin D Vitamin D will promote Ca uptake by the intestine

60. Other effect of 1,25 dihydroxycholecalciferol : The formation of :- 1. a calcium stimulated ATPase in the brush border of the epithelial cells 2. an alkaline phosphatase in the epithelial cells

61. Effect on Intestine Vitamin D also promote phosphate absorption Usually phosphate absorb easily, phosphate flux through the gastrointestinal epithelium is enhance by vitamin D It is a direct effect of 1,25-dihydroxycholecalciferol Action on calcium absorption : the calcium in-turn acting as a transport mediator for the phosphate

62. Effect on renal (kidney) Vitamin D also decrease renal calcium and phosphate excretion. Also increases calcium and phosphate absorption by the epithelial cells of the renal tubules, thereby tending to decrease excretion of this substances in the urine

63. Effect on bone and it relation to parathyroid hormone activity Vitamin D play important role in both bone absorption and deposition. Extreme quantities of vitamin D causes absorption of bone. Absences of vitamin D, the effect of PTH in causing bone absorption is greatly reduce or even prevented. Vitamin D in small quantities promote bone calcification which is vit D increase calcium and phosphate absorption from intestine

64. Effect on bone and it relation to parathyroid hormone activity Vitamin D play important role in both bone absorption and deposition. Extreme quantities of vitamin D causes absorption of bone. Absences of vitamin D, the effect of PTH in causing bone absorption is greatly reduce or even prevented. Vitamin D in small quantities promote bone calcification which is vit D increase calcium and phosphate absorption from intestine

65. calcitonin

66. biosynthesis Calcitonin is formed by the proteolytic cleavage of a larger prepropeptide, which is the product of the CALC1 gene (CALCA). The CALC1 gene belongs to a superfamily of related protein hormone precursors including islet amyloid precursor protein, calcitonin gene-related peptide, and the precursor of adrenomedullin.

67. physiology The hormone participates in calcium (Ca2+) and phosphorus metabolism. In many ways, calcitonin counteracts parathyroid hormone(PTH). -To be specific, calcitonin affects blood Ca2+ levels in four ways: -Inhibits Ca2+ absorption by the intestines -Inhibits osteoclast activity in bones -Inhibits phosphate reabsorption by the kidney tubules Increases absolute Ca2+ and Mg2+ reabsorption by the kidney tubules, calcitonin is a renal Ca-conserving hormone. Secretion of calcitonin is stimulated by: -an increase in serum [Ca2+] --gastrin and pentagastrin.

68. actions this actions, in a broad sense, are: Bone mineral metabolism: - Protect against Ca2+ loss from skeleton during periods of Ca2+ stress such as pregnancy and lactation Serum calcium level regulation - Prevent postprandial hypercalcemia resulting from absorption of Ca2+ from foods during a meal -Vitamin D regulationA satiety hormone: - Inhibit food intake in rats and monkeys- May have CNS action involving the regulation of feeding and appetite

69. receptor The calcitonin receptor, found primarily on osteoclasts, is a G protein-coupled receptor, which is coupled by Gs to adenylylcyclase and thereby to the generation of cAMP in target cells. It also affect the ovaries in women and the testes in men.

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71. ELECTROCARDIOGRAM Normal ECG and Leads

72. What is ECG? Transthoracic interpretation of the electrical activity of the heart over time captured and externally recorded by skin electrodes. The sum of the electrical activity generated by the heart.

73. How do ECG works? It works by detecting and amplifying the tiny electrical changes on the skin that are caused when the heart muscle "depolarises" during each heart beat. ECG is measured by placing skin electrodes on the body surface at different locations. This electrodes are connected in different configuration to a amplifier and a recorder.

74. Normal ECG Character? The ECG comprise of several waves: P wave QRS complex T wave

76. What is P wave? Caused by the electrical potentials generated when the atria depolarise before the contractions begins. This is depolarization wave.

78. What is QRS complex? It is caused by potentials generated when the ventricles depolarized before contraction. This is depolarization wave.

80. What is T wave? It is caused by potential generated as the ventricles recover from the state of depolarization. It is known as repolarization wave.

83. What is ECG Leads? They are electrical cable attaching the electrodes to the ECG recorder. They also may refer to the tracing of the voltage difference between two of the electrodes and is what is actually produced by the ECG recorder.

84. How many leads are there? There are 12 leads: 3 limbs lead (I, II, III) 3 Augmented leads (aVR, aVL, aVF) 6 Precordial Leads (V1 – V6)

85. Limbs lead

86. Precordial Leads

87. Augmented Leads

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