Systems Physiology Lecture 13 Hematology, rheology and hemostasis What is blood chemistry? RBC?s hypoxia and erythropoiesis (EPO) Hematocrit and hemoglobin Fluid energy and fluid hemodynamics Platelets (thrombocytes) and hemostasis Anticoagulant therapy What is hematocrit and how is it measured? Centrifuge blood sample Measure components as % by volume Plasma = 55-58% Erythrocytes = 42-45% Buffy Coat =<%, Leukocytes and Platelets Hematocrit = % packed erythrocytes ? 42-45 Formed elements(cells) in the blood Estimating RBC Circulating RBC count Hematocrit (Hct. Crit) Hemoglobin (Hb) Platelets are called thrombocytes Memorize table with Arrows Glucose ? Postprandial state relative to glucose? approx 2 hours after you began eating your most recent meal Blood glucose should be between 100 and 125mg / dL Fasted state ? blood glucose should be between 80-90mg/dL, A fasting state blood glucose will be slightly lower to postprandial state Osmolality of plasma ? 280-300 Reflects the health of organs including the cardiovascular system and the kidneys, physician would look at kidneys or dietary habits Partial pressure of C02, 02 CO2 ? 40 O2 ? 80-100 Arterial versus veinous, how pH will vary Veinous will be more acidic, lower ? 7.2-7.35 Mixed and nonmixed, mixed is in right atrium or right ventrical ? arterial 7.32-7.42 Potassium and Sodium K = 4 Na = 140 Red blood cells Mature state ? no nucleus, anucleated Reason is to conserve space for hemoglobin in the cell Hemoglobin has 37-34 picograms Without water 95% of the mass of the cell is hemoglobin (transports oxygen) The red cell does not have to state in the same morphology, flexible Capillary is smaller ? RBC becomes deformed and squeezes through capillary Structure and function of Hemoglobin A (HBA) Globin and 4 heme groups Globin = 4 polypeptides Heme ? iron-containing group Iron has to be combined to both ferric and ferrous Carries oxygen 98.5% oxygen bound to HbA 1.5% dissolved in plasma Oxygenated HB ? briht red Deoxygenated Hb ? dark red Also carries CO2, H+ and CO Carrying capacity ? how much oxygen for each 100ml of blood Influenced by concentration of hemoglobin Influenced by partial pressure of Oxygen in the blood pO2 Only the dissolved fraction of Oxygen that can exert a partial pressure Erythropoiesis Kidney senses hypoxia *anemia) and increases endogenous erythropoietin production Erythropoetin acts on the E progenitor cells on the bone marrow to produce new RBCs Kidney senses increased tissue oxygenation Kidney decreases erythropoietin production Testing the renal critmeter hypothesis As blood is withdrawn and Hb concentration decrease, circulating levels of EPO increase. This combined with the kidney?s regulation of extracellular volume (circulating plasma volume) makes it the ideal organ to regulate blood hematocrit and all that is affected by it.. Summary and conclusions Production of RBC?s under physiological control EPO one of the regulators EPO produced in renal tissue; acts on marrow Hct plus ECV (including plasma vol) regulated Fluid energy and hemodynamics Total energy of flowing blood The true driving force for flow is a difference, not in pressure, but of total fluid energy between any two points E = P+pgh+1/2pv Where E total energy ergs/cm3, P is pressure in dynes/cm2, rho is density, g is acceleration of gravity, H is height in centimeters, height above some arbitrary datum level, V is velocity of that fluid at that point (arbitrary datum level) Reference points for physiological pressure Left vs. right side of heart regardless of upright vs prone vs supine body position) Volume vs velocity of flow Q=Ei-Eo/R or (Q=Pi-Po/R) Where Q volume of flow (ml/min etc) E or P, energy or pressure, R resistance to flow (mmHg/ml/min) V=Q/A Where V means linear velocity (cm/sec, etc). Q, volume of flow, A area of flow (cm2) Resistance to flow means a more narrow vessel will produce an impediment to flow than a wider vessel, the longer ? greater resistance than shorter Viscosity of fluid affects flow inversely, the more viscous a fluid, the lower the volume of flow Blood flows in lamina ? layers of blood closer to the walls of vessel flow more slowly than the layers closer to the central axis of the vessel Poiseuille?s Equation Q = pi(P1-Po)r^4/ 8nl Relationships among volume flow, velocity, and cross-sectional area Stenosis ? means constriction of aorta itself or some valves that impede blood fluid Summary Fluid, including blood, in closed conduits flows as the result of energy gradients Flow can be expressed as velocity or volume Two impediments to flow are resistance and viscosity What is hemostasis and why is it important? The volume of blood is in a closed space Fixed volume confined to a fixed space Wall of blood vessel is injured, the injury itself sets in motion a variety of stimuli response reaction Intrinsic and Extrinsic Intrinsic ? refers to everything inside the endothelial cells, inside the lumen of the vessel Extrinsic ? refers to anything outside the lumen of the vessel The endothelium is the interface between what happens inside and outside of the luminal vessel The damage causes platelets to adhere to the damaged endothelium, to adhere to each other, to go from inactive to activated state, then releasing chemokines that can begin to respond to the damage and try to maintain hemostasis. Once the vessel is damaged ? 3 important events to maintain blood volume 1. basal constriction ? will markedly reduce blood flow to vessel 2. adhesion and activation of platelets 3. the aggregation of platelets at site of injury and formation of platelet clotting Physiological actions of platelets Blood Vessel Damage ( Exposure of Subendothelium ( vWf Binds to Collagen Fibers ( Platelets Bind to vWf ( Platelet Adhesion, Platelet Aggregation, Activation (release action) Activated platelets and the ?release reaction? Fibrin clot at the site of vascular wound Fibrinogen Fibrin ( loose) Fibrin * mesh) (Fibrin clot Physiological pathways leading to the formation of clots Fig 16.9 Intrinsic Pathway ? everything in Plasma Extrinsic Pathway ? from damaged tissue Note: There are both intrinsic and extrinsic factors that play important roles in the intravascular formation of clots and hemostasis.
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