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Day 6a-P5ECFV CONTROL2 (9) 2.pptx
- 1. CONTROL OF ECF VOLUME DR.HAMISI MKINDI,MD. TO DOWNLOAD CONTACT: hermyc@live.com
- 2. Regulation of ECF Volume has two basic components •Relative distribution between Blood & IF •The absolute volume of ECF
- 3. Extracellular (33%) Intracellular (66%) Interstitial (25%) Plasma (8%) Absolute Relative (14 L) (28 L) (42 L) (10.5 L) (3.5 L)
- 4. The volume of the extracellular fluid (ECF) includes both •blood plasma and the interstitial fluid.
- 5. Transcellular Fluid Plasma Fluid Distribution in the Human Body 42 Liters 28 Liters 14 Liters
- 6. Of the 14 liters in extracellular fluid compartment: •3.5 liters constitute blood plasma volume •And 10.5 liters is interstitial fluid.
- 7. Normally changes in the ECF volume produce proportional changes in blood plasma volume. • In effect the effective circulating volume
- 8. The effective circulating volume is a functional blood volume •Reflects the extent of tissue perfusion, •As sensed by the fullness or pressure in blood vessels.
- 9. The control mechanisms that defend effective circulating volume include •Stretch receptors in carotid sinus and aorta •And volume receptors in cardiac atria and pulmonary vasculature.
- 10. When small amounts of fluid accumulate in blood 20-30% stays within the blood •When ECF increases 30-50% above normal, •Almost all the additional fluid goes into IF
- 11. A loss in plasma volume is likewise shared proportionally between IF and PV
- 12. These will trigger changes in the Starling forces across a capillary •That determine the traffic of fluid between IF and PV
- 13. Capillary hydrostatic pressure main force governs the capillary fluid shift •Is controlled by local myogenic, neurogenic, •Humoral modulation of arterial resistance
- 14. Dilated Resistance Vessels Constricted Resistance Vessels
- 15. Fluid moves into the capillaries when capillary hydrostatic pressure decreases; •Fluid moves out when the pressure increases •Providing mechanism to alter plasma volume •Ultimately the effective circulatory volume.
- 16. Vasoconstriction with reduction in capillary pressure CAPILLARY FLUID SHIFT
- 17. Capillary Fluid Shift provides a mechanism for sharing •Plasma and interstitial volume
- 18. Two separate, but closely inter- related, control systems regulate •The volume and osmolality of the extracellular fluid (ECF).
- 19. ECF osmolality is regulated by monitoring and adjusting total body water content.
- 20. The absolute ECF volume is regulated by monitoring and • Adjusting total body NaCl content.
- 21. As long as ECF osmolarity is kept constant Na+ content determines the volume of ECF
- 22. Na+ with its associated anions is the main osmotic constituent of ECF.
- 23. Na+ with its associated anions produce an osmotic pressure •That holds water within ECF.
- 25. Though ECFV regulation is achieved largely by modulating Na+ content. •However ECF volume regulation requires •Proper functioning osmoregulation
- 26. Two primary systems responsible for osmolarity control include •The Osmoreceptor-ADH system and •The thirst mechanism.
- 27. When ECF Na+ content increases, THIS increase in ECF osmolarity stimulates • THIRST to increase water intake; but also stimulates • ADH secretion minimising renal water loss • Osmolarity is corrected but with increased ECFV.
- 29. The thirst and ADH elements share a common osmoreceptor mechanism
- 31. Sodium balance in effect controls ECFV: •Ultimately controls blood volume
- 32. The mechanism that maintains plasma osmolarity is very sensitive •The need to conserve volume is more powerful •Osmolarity can be sacrificed preserve volume
- 34. SODIUM BALANCE To maintain Na+ balance salt intake must precisely match its rate of excretion.
- 35. In the steady state, Na+ intake equals Na+ loss thru renal/extrarenal paths •Normally extrarenal Na+ output is negligible. •Amount of Na+ ingested equal renal Na+ loss.
- 37. SALT INTAKE AND SALT APPETITE
- 38. Salt “appetite” may be defined as the behavioral drive to ingest salt.
- 39. In most circumstances salt appetite is driven by need: •though there is also an element of preference.
- 40. Salt “Appetite” as reflected at table is most likely acquired.
- 41. There is a regulatory component. • A drive to obtain salt when there is Na+ deficiency, • Seen in herbivores, that eat a low-sodium diet, • Also seen in humans with extreme Na+ deficiency.
- 42. Giraffes and Wildebeests at artificial Salt Lick
- 43. Salt appetite is triggered by a negative sodium balance. •However, sodium appetite is innate; does not need prior experience.
- 44. Salt appetite increases after a prolonged period of Na+ deficiency • A reduction in body sodium content is equivalent to a loss of ECFV.
- 45. Like thirst salt appetite is vital for restoring ECF.
- 46. The onset of salt appetite induced in rats by colloid treatment is • curiously delayed relative to the appearance of thirst.
- 47. Within 1–2 h after onset of hypovolemia an increase in thirst becomes evident. •In contrast appetite for sodium does not increase until well after the onset of hypovolemia. • Sodium appetite increases in a delayed fashion
- 48. An increased drive ingest salt does not become evident until hours or days after a more pronounced increase in thirst.
- 49. Salt appetite and thirst probably share same neuronal centres in the brain
- 50. Neurons projecting to the OVLT control water intake, •Those projecting to vBNST control salt intake.
- 51. WATER DEPLETED STATE SALT DEPLETED STATE Ventral Bed Nucleus of Stria Terminalis Organum Vasculosum Terminalis (Subfornical Organ)
- 52. Angiotensin II drives both thirst and salt appetite
- 53. Lesions of forebrain particularly in the SFO and the OVLT block •Sodium depletion-induced salt appetite
- 54. Sodium appetite, however, is not caused by a decrease in •the plasma concentration of sodium (hyponatraemia)
- 55. Sodium appetite can also be induced in the absence of need for sodium •With use of hormones of sodium deficiency: •Mineralocorticoids and ANG II,
- 56. SODIUM BALANCE
- 57. The capacity of the kidneys to alter sodium excretion •In response to changes in sodium intake is enormous.
- 58. Slight expansion of the ECFV signals the kidney to increase its rate of Na+ excretion.
- 60. The amount of sodium excreted is a function of how much sodium is filtered and how much is reabsorbed;
- 62. Regulation of sodium excretion can be effected by regulating •Rate of Glomerular Filtration •Proportion Tubular reabsorption;
- 63. The critical parameter that the body recognizes as an index of • Changes in Na+ content is the effective circulating volume.
- 64. The control mechanisms that defend effective circulating volume include •Stretch receptors in carotid sinus and aorta •And volume receptors in cardiac atria and pulmonary vasculature.
- 65. Low- and high-pressure receptors sense decreases in effective circulating volume • Restores effective circulating volume •Using four parallel effector pathways •RAAS, ANS, ANP, AVP.
- 67. THANKS
Editor's Notes
- The slide shows the distribution of fluid between intracellular and extracellular fluid and the compartments that constitute ECF.
- This figure shows that the balance of forces changes along the length of a typical capillary as capillary hydrostatic pressure decreases. Net fluid filtration out of plasma occurs at the arterial end of capillary beds, and net fluid reabsorption into plasma occurs toward the venous end. Constricting or dilating of the resistance vessels can raise or reduce the capillary pressure changing the balance of forces in favour of filtration or reabsorption producing appropriate capillary fluid shifts
- The figure depicts the entire control process, consisting of baroreceptors (detectors) afferent and efferent neuronal pathways, control centers in the medulla, and the heart and blood vessels as the effector organs. The negative feedback loop is designed so that increased pressure causes vasodilation and bradycardia, whereas decreased pressure causes vasoconstriction and tachycardia. Vasoconstriction and vasodilatation changes the capillary hydrostatic pressure causing capillary fluid shift. Not reflected are the low-pressure sensors in the pulmonary circulation and atria of the heart. The insert right panel shows the efferent pathways involving parasympathetic and sympathetic neurons.
- The figure shows ingestion of salt causes an increase in osmolarity; initially without changes in volume. This stimulates thirst enhancing water intake, stimulates vasopressin secretion increasing renal water retention. Blood volume and pressure increase. The figure also shows that the excess salt can be excreted by the kidney and cardiovascular adjustments can lower pressure to normal
- The slide shows brain osmoreceptor pathways. The primary brain osmoreceptors lie outside the blood–brain barrier. Different neural projections connect the primary osmoreceptors to brain areas responsible for AVP secretion and thirst.Arginine vasopressin-adh
- This slide shows giraffes and wildebeests at a salt lick. A mineral lick (also known as a salt lick) is a place where animals can go to lick essential mineral nutrients from a deposit of salts and other minerals. Mineral licks can be naturally occurring or artificial created (such as blocks of salt) that are placed to the disposal of livestock or animals to lick.
- The slide depicts a water depleted state (left panel) and a sodium depleted state (Right Panel). Angiotensin II stimulates both thirst and salt appetite. Neurons projecting to the OVLT control water intake, while those projecting to the vBNST control salt appetite. The slide also shows that thirst-driving neurons are suppressed under sodium-depleted conditions. In contrast, the salt appetite-driving neurons are suppressed under dehydrated conditions.
- This slide demonstrates the renal response to an abrupt increase in Na+ intake. When the individual increases dietary Na+ intake from 10 to 150 mmol/day urinary Na+ output also increases, but at first lags behind intake. During this initial period there is a positive Na+ balance when Na+ intake exceeds Na+ output. After about 5 days, urinary Na+ output rises to match dietary intake, after which total Na+ content does not increase further. Body weight increases by 1 kg (shown in upper panel in blue). This corresponds, to the accumulation of 140 mmol of Na+ and and accompanying one liter of free water, which makes a gain of 1 L of isotonic saline. NOTE the red curve shows the time course of dietary Na+ intake, and the green curve shows Na+ excretion the golden area between the two curves at the beginning corresponds to the accumulated total body Na+ of 140 mmol. The graph in the right panel shows that urinary Na+ excretion increases linearly with the rise in ECF volume This slide demonstrates the renal response to an abrupt increase in Na+ intake. When the individual increases dietary Na+ intake from 10 to 150 mmol/day urinary Na+ output also increases, but at first lags behind intake. During this initial period there is a positive Na+ balance when Na+ intake exceeds Na+ output. After about 5 days, urinary Na+ output rises to match dietary intake, after which total Na+ content does not increase further. Body weight increases by 1 kg (shown in upper panel in blue). This corresponds, to the accumulation of 140 mmol of Na+ and and accompanying one liter of free water, which makes a gain of 1 L of isotonic saline. NOTE the red curve shows the time course of dietary Na+ intake, and the green curve shows Na+ excretion the golden area between the two curves at the beginning corresponds to the accumulated total body Na+ of 140 mmol. The graph in the right panel shows that urinary Na+ excretion increases linearly with the rise in ECF volume
- The figure shows an overview of segmental sodium handling along the nephron. It indicates the amount of sodium filtered at the glomerulus, the percentage of filtered sodium that is reabsorbed in the various segments of the tubule. The fractional excretion is the percent of filtered Na+ excreted in final urine. This illustrates that the amount of sodium excreted is a function of filtration and tubular reabsorption.
- This figure shows the negative feedback responses to low effective circulating volume (ECV). Decrease in the effective circulating volume is counteracted by activation of the renin-angiotensin-aldosterone axis, stimulation of the sympathetic nervous system via the baroreceptor reflex. Decreased ANP secretion. The slide shows the elements of the control system involved: the controlled variable, the sensors and effectors of the system.