Control of MAP 1. Short-term (seconds) - baroreceptors CV 6 •Control of MAP •Microcirculation •Problem solving •Mid term tests • Neural control via SNS, PNS 2. Intermediate (minutes) • Hormonal, esp SNS→Epi from adrenal medulla and ADH regulation of blood volume 3. Long-term (hours, days) • Blood volume regulation by kidney (ADH) Control of MAP Sensors 1. Carotid sinus baroreceptor 2. Aortic arch baroreceptor 3. Atrial stretch Baroreceptors # Action potentials from receptor 50 80 MAP 150 1 Baroreceptors Baroreceptors accommodate to chronic high MAP ↑MAP → ↑AP from receptors → ↓SNS, ↑PNS ↓MAP → ↓ AP from receptors → ↑SNS, ↓PNS # Action potentials from receptor With chronically high MAP (2 days), receptors adapt Processing in higher brain centers In short term, baroreceptors can respond to changes in MAP The end effect is to try to maintain MAP near normal 50 80 MAP 150 Increase in MAP leads to increase receptor activity Atrial Stretch receptors • If more blood returns to atria, walls are stretched • Leads to increase heart rate • Arial Stretch receptors also regulate ADH/vasopressin release from pituitary – Bainbridge Reflex • Helps to clear blood from venous side ↑ Vol in atria → ↑ stretch → ↓ADH → vasodilation & increase water loss from kidney (decrease blood volume) HR volume 2 Summary of neural reflexes Baroreceptors and atrial stretch have opposing effects on HR but similar effect on vasodilation They are sensitive to changes in different compartments: Baroreceptors → arterial side Atrial Stretch → venous side • Long-Term MAP regulation – Kidney – Relationship between blood volume & MAP ↑MAP ↑ blood volume ↑water and Na+ loss from kidney ↑ Venous return ↓ blood volume ↑ Cardiac output ↓ venous return ↑ MAP ↓ cardiac output ↑water and Na+ loss from kidney ↓ MAP ↓ blood volume Microcirculation capillaries & lymph Capillaries • Most cells within 100 μm of a capillary – Short diffusion distance • Each capillary a few mm long, 5 μm diameter (hair 100 μm) 3 Transport between capillary and interstitial fluid 98% of exchange by diffusion → concentration gradients & permeability • Lipid-soluble pass through endothelial cell • Non-soluble through water-filled channels Plasma – Intracellular cleft & vesicle channels • Not very permeable to protein RBC – Some endo- and exocytosis for proteins Capillary endothelium Transcapillary gradient • Between plasma and interstitial fluid CO2 least brain leakiness CO2 liver No intracellular clefts huge intracellular clefts Only carrier mediated-transport Very permeable (even proteins) Blood-brain barrier CO2 most cell RBC O2 glucose O2 glut glucose 4 Transport between capillary and interstitial fluid • Bulk flow determined by: 1. Pressure – capillary vs interstitial 2. Osmosis – plasma vs interstitial Bulk Fluid Flow remaining 2% of exchange Capillary Pressure (PC) Extracellular Fluid filtration Plasma absorption Total Vol =10L Net Filtration Pressure(NFP) = (PC-PIF) – (πP- πIF) Interstitial fluid can supply or receive fluid from plasma • PC at arteriole end of capillary > PC at venule end • All others remain constant venule end Arterial end (PC = 35) (πP =28) Osmotic Force Interstitial Fluid Protein (πIF) Interstitial Fluid Pressure (PIF) Interstitial Fluid Total Vol = 5L Osmotic Force Plasma Protein (πP) (πP =28) No fluid movement Pressure (mm Hg) 10 Filtration Fluid out (PC = 15) Δπ 0 (PIF=0) (πIF =3) NFP = (35-0) – (28 - 3) = 10 mm Hg Filtration (fluid out) (πIF =3) (PIF=0) NFP = (15-0) – (28 - 3) = -10 mmHg Absorption (fluid in) Absorption Fluid in -10 Arteriole end ΔP Venule end 5 The main factor influencing Pc is volume in capillary ↑ volume ↑ Pc Arterial side: vasoconstriction ↓ flow into capillary ∴ ↓ volume, ↓ Pc vasodilation ↑flow into capillary ∴ ↑volume, ↑ Pc Venous side: venoconstriction ↓ flow out of capillary ∴ ↑ volume, ↑ Pc venodilation ↑flow out of capillary ∴ ↓volume, ↓ Pc • Ratio Reabsorption / Filtration = 0.85 • Remaining 15% of fluid is picked up by lymphatic system Pc • When, excess interstitial fluid accumulates – edema Factors affecting fluid movement from capillary 1. Vasodilation of arterioles → ↑ blood vol in capillary → ↑ Pc → ↑ filtration 2. Vasoconstriction of arterioles → ↓ blood vol in capillary → ↓ Pc → ↓ filtration 3. ↓ plasma volume → ↑ πp → ↑ reabsorp 1. Arteriole vasodilation More fluid out Pressure (mm Hg) 10 Δπ 0 -10 Filtration Fluid out Arteriole end ΔP Absorption Fluid in Venule end 6 2. Arteriole vasoconstriction 3. ↓plasma volume less fluid out less fluid out Δπ Pressure (mm Hg) Filtration Fluid out Arteriole end Absorption Fluid in Δπ Pressure (mm Hg) Absorption Fluid in Filtration Fluid out ΔP Arteriole end Venule end ΔP Venule end 1. Lymphatic system • • gathers excess fluid and protein delivers it back to the CV system 2. Important determinant of PIF & πIF 3. Slow ~2 L / day (compare to CO=5 L/min) πc Pc PIF Protein & fluid πIF lymph 7 • Pc too high, or [protein]plasma too low, drives fluid into interstitial space • If lymph drainage blocked, then protein accumulates in interstitial space, • Elephantiasis – Caused by a small parasitic nematode (Filaria) – Endemic to tropical regions of Asia, Africa, and South America – Infection by transfer of larvae from mosquitoes – Larvae enter into lymphatic vessels and block them – ↑ πIF, draws fluid into IF space πc Pc If lymph drainage disrupted, ↑ πIF →↑ PIF PIF Protein & fluid πIF lymph Aortic pressure Bainbridge reflex CV Summary & Problem Solving 1. 2. 3. 4. 5. 6. Pressure ∝ (volume, compliance) CO=HR(EDV-ESV) Q=(P1-P2)/Resist R∝(η,L,1/r4) MAP=CO x TPR CO = VR NFP = (PC-PIF) – (πP- πIF) viscosity MAP = HR x (EDV-ESV) x TPR VR Venous pressure SNS radius PNS Blood volume Muscle pumps Respiration pump Hormones i.e. Epi autoregulation Metabolic / local Hormones i.e. AngII, ADH, ANP 8 Problem Solving: 1. What is the initial challenge? 2. What receptors respond and what sequence? 3. What reflexes occur? 4. What is the final outcome? Question: What is the physiological response to intravenous infusion of 3L iso-osmotic saline? 1. ↑ BV on venous side, ↑ VR 2. Recruit atrial stretch receptors 2. Why does a decrease in total peripheral resistance increase cardiac output? (direct not reflexes) ↑ HR ↓ ADH → ↑ water loss from kidney - - - vasodilation → ↑ Pc → ↑ filtration → ↓πc → ↑ filtration 3. ↑ VR → ↑ SV (frank-starling) →↑ CO → ↑ MAP 4. Recruit baroreceptors ↓ SNS, ↑ PNS - - - CO VR (l/min) RAP → vasodilation & ↓ TPR CO=VR=HR(EDV-ESV), no change in Psf → ↓ venous tone → ↓ VR Decreased TPR, lead to increase VR. Increase VR, lead to increase EDV Increase EDV lead to increase SV (frank-starling) Increase SV lead to increase CO → ↓ HR → ↓CO → ↓ contractility → ↓CO 5. Overall, ↓ BV and ↓CO, ↓TPR would restore system towards normal Since CO=VR, CO increases 9 3. Why does damage to the right ventricle lead to fluid accumulation in the tissue? ↓ right ventricle function, ↑Central Venous Pressure, leads to ↓VR Leads to increase blood volume in veins Leads to ↑Pvein, leads to↑Pcapillary Since NFP=(Pc-PIF) – (πP- πIF) ↑Pc will lead to ↑ΔP, increase hydrostatic pressure driving fluid out of capillary 10
© Copyright 2024 Paperzz