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Lecture 9 (Cardiovascular IV) PDF

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Summary

This lecture covers Cardiovascular IV, focusing on blood volume, microcirculation, and fluid exchange. It details the learning objectives, capillary function, transcapillary exchange, and bulk flow, including pressure gradients and Starling forces. The lecture also addresses edema formation, mechanisms and clinical examples.

Full Transcript

Cardiovascular IV: Blood Volume Microcirculation & Fluid Exchange ANSC 3080 G. Bedecarrats Learning Objectives  Describe the role of the microcirculation in fluid and macromolecular exchange  Explain the general mechanisms of transcapillary exchange  Explai...

Cardiovascular IV: Blood Volume Microcirculation & Fluid Exchange ANSC 3080 G. Bedecarrats Learning Objectives  Describe the role of the microcirculation in fluid and macromolecular exchange  Explain the general mechanisms of transcapillary exchange  Explain the forces regulating the net movement of fluid across the capillary wall  Describe the basic mechanisms of edema formation Capillaries  Contains only about 5 % of the blood  Site of water-nutrients-wastes-gases exchanges with interstitial fluid and tissues  7-8 m diameter, 0.5 mm in length Red blood cells ~7.5 m in diameter  Single layer of endothelial cells  Dense networks each cell of a tissue within 100 m of a capillary  Receive blood from smallest arterioles Also from metarterioles = connection between arteriole and capillaries network  Density of capillaries vary depending on the metabolic activity of the tissue  Metarterioles possess rings of smooth muscle tissue that can open and close on demand  In skeletal muscle: all open during exercising  Small diameter = very slow flow  Resistance reduced by the extent of the parallel ramifications Transcapillary Exchange  Diffusion: depends on capillary type and substance properties – follows gradient between blood and interstitial fluid Lipid soluble substances exchange freely across cell membrane (O2 and CO2) Most capillaries have pores or clefts that allow transfer of water and lipid-insoluble molecules (Na+, Cl-, glucose, amino acids). Size and number of pores depend on the tissue Some capillaries are fenestrated (intestine, liver, kidneys) – vesicles fuse to form large gaps across endothelial cell membrane allowing water and water soluble macromolecules to pass Bulk Flow = Fluid Exchange  Mass movement of water and dissolved substances  Takes place across the capillary walls  Towards interstitial fluid = filtration  Towards the intravascular fluid (blood) = absorption  Maintains fluid balance between intravascular and interstitial fluid  Dependent on:  Pressure gradients (Hydrostatic and osmotic)  Permeability of vessel (porosity)  Size of diffusion surface  Blood flow Pressure Gradients Hydrostatic pressure  Filtration pressure Pressure from heart arterioles capillaries Pressure in interstitial fluid is close to 0 Pushes fluid out of vessel Colloid osmotic pressure (oncotic)  Due to big proteins that stay in vessel  Counter balances hydrostatic pressure Starling Forces = Opposing forces  Net movement of fluid depends on balance between filtration (hydrostatic) and osmotic (oncotic) pressures  Hydrostatic pressure difference pushing fluid out  Osmotic pressure difference pushing fluid in. Remains constant along capillary length  Along capillary: In the first portion: hydrostatic stronger (more fluid out) Toward the end: hydrostatic  = less fluid out; and if hydrostatic < osmotic = fluid moves in a, b: normal situation c: arteriole dilation d: lower osmotic pressure e: arteriole constrict Where Does the Fluid Go?  Net effect is generally accumulation of fluid into interstitial tissue  Picked up by the lymphatic system Drained to the large veins Called lymphatic drainage  Fluid that remained in the blood collects into venules and goes back to the heart  If lymphatic system cannot keep up  edema formation Physiological Significance  Diffusion = nutrient and gas exchange  Bulk flow = stabilize blood volume using interstitial fluid as a buffer Blood loss =  in pressure =  in hydrostatic = fluid enters back Excess fluid intake =  in pressure =  in hydrostatic = fluid accumulates in interstitial Low protein in plasma =  in osmotic = fluid out High protein in plasma =  in osmotic = fluid in Edema Formation  Abnormal accumulation of interstitial fluid  Four mechanisms responsible:  hydrostatic pressure in blood vessels  arterial pressure (hypertension)  venous pressure (right sided heart failure)  interstitial protein concentration Inflammation of capillaries, become “leaky”  oncotic pressure Loss of proteins (GI disease), liver dz., poor diet  Obstruction of lymphatic vessels Edema: Clinical Example  8-year-old horse with “dependent edema”  Swelling of legs and other “dependent” areas  Right sided heart failure due to tricuspid valve insufficiency  Venous congestion  Increased filtration pressure Plaque of edema

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