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BP4 - BLOOD PRESSURE REGULATION.pptx, physiology
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- 2. • Physiological mechanismsby which BP homeostasis occurs Short term • Baroreceptor R. • Chemoreceptor R. • CNS ischemic • Other Intermediate • RA vasoconstrictor system • Stress relaxation • Capillary fluid shift mechanism Long term • Direct mechanism – Pr. Diuresis and natriuresis • Indirect – Hormonal – RAAS, ADH, ANP
- 3. SHORT TERM REGULATIONOF BP • First line of defence against a/c changes in arterial BP • Neural
- 4. 1. Baroreceptor reflex mechanism •Baroreceptors – Stretch receptors in the wall of heart and blood vessels • Spray type N endings • Increase in pressure – stretch of baroreceptors – transmit signals at higher rate to Brain stem centres – FB signals to bring BP back to normal
- 5. Baroreceptors Carotid sinus andAortic arch R – Monitors high pressure circulation Cardiopulmonary R - Walls of the right and left atria at the entrance of the superior and inferior Venaecavae and the pulmonary veins, as well as in the pulmonary circulation – In low pressure part
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- 7. Baroreceptor reflex pathway Best known mechanismfor arterial pressure control
- 8. Increase in MAP Increased dischargein IX and X Cr. N Stimulation of NTS Two efferent from NTS Sympathetic and Parasympathetic
- 9. IN SYMPATHETIC NS NTSstimulate CVLM & IVLM (Glu) Inhibition of RVLM (GABA) Reduced sympathetic discharge Decreased HR, BP & CO
- 10. IN PARASYMPATHETIC NS NTSstimulate Nu. Ambigus & DMN Increased Vagal activity Vasodilation, venodilation, bradycardia and decreased BP Decreased HR, BP & CO
- 11. II. Chemorecptors • Carotidbody & Aortic body • Activated primarily by Hypoxia, and also by high pCO2 and H+ • Powerful activation occurs when MAP falls below 80 mmHg – Powerful at pressures below normal MAP • Operates at a range of 40 – 100 mm Hg MAP
- 12. Hypoxia, hypercapnia and acidosis Stimulationof CR & transmitted through IX & Xth nerve NTS Excitation of RVLM Elevation of arterial pressure
- 13. III. CNS ischemicresponse • Hypoxia & Hypercapnia – direct stimulation of RVLM – Strong excitation of neurons – Systemic arterial pressure rises to very high levels – CNS ISCHEMIC RESPONSE • MAP may increase as high as 250 mm Hg • Most powerful stimulation to sympathetic vasoconstrictor system but becomes active only when MAP falls below 60 mm Hg • Greatest degree of stimulation – 15 – 20 mm Hg.
- 14. • Emergency pressurecontrol system • Acts very rapidly & powerfully to prevent further decrease in arterial pressure. • LAST DITCH STAND
- 15. CUSHING REACTION /CUSHING REFLEX • Special type of CNS ischemic response • Results due to increased ICP • High ICP – ischemia of RVLM – local hypoxia and hypercapnia – increased discharge from RVLM – Increased MAP – Restores blood flow to medulla • Helps to protect vital organs • Increase in MAP associated with bradycardia in CUSHING REFLEX
- 16. EXCEPTIONS TO GENERALRULE: • In Bezold Jarisch reflex –Tachycardia & Hypotension • In Cushing reflex – Hypertension & Bradycardia
- 17. • Physiological mechanismsby which BP homeostasis occurs Short term • Baroreceptor R. • Chemoreceptor R. • CNS ischemic • Other Intermediate • RA vasoconstrictor system • Stress relaxation • Capillary fluid shift mechanism Long term • Direct mechanism – Pr. Diuresis and natriuresis • Indirect – Hormonal – RAAS, ADH, ANP
- 18. Intermediate mechanisms • Activatedwithin minutes to several hours • Effects lasts for days • Three main mechanism: RA vasoconstrictor system Stress relaxation Capillary fluid shift mechanism
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- 20. Stress relaxation andReverse stress relaxation of vasculature • Increase in blood volume - Increase in BP – more stretch on the blood vessels - relaxation of blood vessel wall – low VR – low cardiac output – restoration of BP to normal. • Reduced blood volume – reduced BP – less stress on vessel wall - vessel wall tone increased - tight blood vessels – BP is brought back to normal.
- 21. Capillary fluid shiftmechanism
- 22. LONG TERM REGULATIONOF BLOOD PRESSURE
- 23. LONG TERM MECHANISMS •Act when nervous mechanism lose their ability to oppose changes in pressure. • Closely connected with homeostasis of body fluid volume • Kidneys play a dominant role. • Includes: DIRECT MECHANISMS - Renal fluid volume pressure control mechanisms – PRESSURE DIURESIS AND PRESSURE NATRIURESIS INDIRECT MECHANISMS – Through hormones
- 24. Decrease in arterial pressure Renalischemia Reduced GFR Water and electrolyte retention Increased ECF volume Increased CO & BP
- 25. Pressure natriuresis • Increasein BP by 30 – 50 mm Hg – 2 -3 fold increase in urinary Na output • Also, • ANP – directly acts on kidney to inhibit Na reabsorption • Increase capillary permeability • Relaxes VSM • Inhibit renin secretion • Counteract pressor response of catecholamines & AT - II
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- 27. 1. RAAS • Powerfulmechanism • Requires 20 minutes to become fully active • Can rapidly return arterial pressure halfway back to normal within a few minutes • AT – II – Powerful vasoconstrictor, especially arterioles • AT – II – Act on kidney to decrease excretion of NaCl & H2O • Act via direct and indirect ways
- 28. Direct effect ofAT – II • Constricts renal arterioles • Causes rapid reabsorption of Na & H2O from tubules – decrease urine output • Act on thirst centres – increase ADH secretion – increased H2O retention
- 29. Indirect effects ofAT – II • AT – II – acts on Adrenal cortex – increase aldosterone – high salt & water reabsorption • Facilitate the secretion of NE from sympathetic nerve endings Direct action of AT – II on kidney is 30 times as potent as the indirect effect through aldosterone
- 31. 2. Role ofADH • Reduced blood volume or reduced arterial pressure – reduced stretch of BR & Cardiopulmonary receptors – increased ADH secretion – increased fluid reabsorption