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Respiratory System

Respiratory System. Lecture 2 Gas Exchange & Regulation. Gas Exchange. occurs between blood & alveolar air across respiratory membrane by diffusion due to concentration gradient differences between O 2 & CO 2 concentrations measured by partial pressures

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Respiratory System

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  1. Respiratory System Lecture 2 Gas Exchange & Regulation

  2. Gas Exchange • occurs between blood & alveolar air • across respiratory membrane • by diffusion due to concentration gradient • differences between O2 & CO2 concentrations • measured by partial pressures • greater difference in partial pressuresgreater rate of diffusion • need to understand partial pressures & diffusion of gases into & out of liquids to understand gas exchange

  3. Dalton’s Law of Partial Pressure • air-mixture of gases & water vapor • consists of N2-78%-most abundant, O2-20.9%water, CO2, Argon • atmospheric pressure is result of collision of all gas molecules • at any time 78.6% of collisions involve N2 & 20.9% involve O2 • each gas contributes to total pressure in proportion to its relative abundance-Dalton’s Law • PressureTotal = Pressure1 + Pressure2 ... Pressuren • pressure contributed by one gas is partial pressure • directly proportional to % of gas in mixture • all partial pressures added = total pressure exerted by gas mixture =760mm Hg • PN2-parital pressure nitrogen = 78.6 X 760 mm Hg-597 mm Hg • PO2 20.9 X 760 = 159 mm Hg

  4. Henry’s Law • at a given temperature, amount of gas in solution is directly proportional to partial pressure (pp) of gas • when gas mixture is in contact with liquid, each gas dissolves in proportion to its partial pressure • actualamount in solution at given pp depends on solubility of that gas in that liquid

  5. Partial Pressures in Alveoli & Alveolar Capillaries • oxygen diffuses from alveolar air (PP is 105mm Hg) into blood in pulmonary capillaries where PO2 is 40 mm Hg • when O2 is diffusing from alveolar air into deoxygenatedblood CO2 is diffusing in opposite direction • PCO2 of deoxygenated blood is 45 mm Hg • PCO2 of alveolar air-40 mm Hg • CO2 diffuses from deoxygenated blood into alveoli • left ventricle pumps oxygenated blood into aorta & through systemic arteries to systemic capillaries • exchange of O2 & CO2 between systemic • capillaries & tissues cells • PO2 of blood in systemic capillaries is 100 mmHg • in tissue cells it is 40mm Hg • as oxygen diffuses out of capillaries into tissues carbon dioxide diffuses in opposite direction • PCO2 of cells is 45 mm Hg • it is 40mm Hg systemic capillary blood

  6. Diffusion at Respiratory Membrane • efficient • large PP differences across membrane • larger PPfaster diffusion • capillary & alveolar membranes are fused distances for diffusion-small • gases are soluble in lipid- pass through surfactant layer easily • surface area ishuge

  7. Gas Transport • Major function of blood • O2 • Co2

  8. Oxygen Transport • dissolved in plasma • normal PO2 of alveoli, 100ml of blood contains 0.3ml of O2 • carried in RBC bound to hemoglobin

  9. Hemoglobin • 4 subunits • 2 & 2ß globular protein chains • each has one heme group • each heme has one iron • each Fe can bind one O2 • every Hb can carry 4 O2s • there are 280 X 106 Hb molecules/RBC • each RBC could carry billion O2 molecules

  10. Oxyhemoglobin • Hb + O2 HbO2- • oxyhemoglobin • reversible • Fe-O2 bond-weak • easily broken without altering either Hb or O2 • HbO2 O2 + Hb • deoxyhemoglobin

  11. Amount of Oxygen Bound to HB • PO2 of plasma • most important factor determining how much O2 binds to Hb • actual amount bound/maximum that could bind = % saturation • all binding sites occupied-100% saturation

  12. Oxyhemoglobin Dissociation Curve • plots % saturation Hb (number of O2 bound) against PO2 • relates saturation of Hb to PP of O2

  13. HbO2 Dissociation Curve • not linear-S-shaped • steep slope-flattens or plateaus • shape due to subunits of Hb • each time Hb binds one O2 shape changes slightly increases ability of Hb to bind another O2 • when PO2 is between 60 -100mmHG,Hb is 90% or more saturated with oxygen • blood picks up nearly full load of O2 from lungs even when PO2 alveolar air is as low as 60mmgHg • increasing PO2 above 80mm Hg adds little to O2 content of blood • PO2 < 50 mm, small drops in PO2 cause large release of O2

  14. Importance of Oxyhemoglobin Dissociation Curve • shape of Hb saturation curve extremely important • over steep initial slopevery small decreases in PO2 results in very large changes in amount of O2 bound or released from Hb • ensures near normal O2 transport even when O2 content of alveolar air decreases (important at high altitudes) • slope of curve allows blood to have high O2 content at fairly low PO2s • PO2 can fall considerably-without greatly reducing oxygen supply

  15. Factors Affecting Affinity of O2 & Hb • various factors increase or decrease affinity (tightness of bond) of Hb to O2 • factors will shift curve to left (higher affinity) or to right (lower affinity) • left-more O2 is bound than released • right-more O2 is released than bound • pH • pCO2 • temperature • BPG

  16. Hb & pH • as pH decreases shape of Hb changesreleases O2 more readilyslope of curve changes saturation decreases • more O2 released • curve shifts to right • effect of pH on Hb saturation is Bohr Effect

  17. Bohr Effect • Hb acts as buffer for H+ • when H+ bind to amino acids in Hb • they alter its structure slightly decreasing its oxygen carrying capacity • increased H+ ion concentration causes O2 to unload from Hb • binding of O2 to Hb causes unloading of H+ from Hb • elevated pH (lowered H+) increases affinity of Hb for O2 • shifts O2-Hb dissociation curve to left

  18. Hb & Temperature • higher temperature • curve shifts to right • unloading of O2 from Hb is increased • lower temperatures • curve shifts to left • O2 binds more to Hb

  19. Hb & Carbon Dioxide • increase in CO2 • shifts curve to right • more O2 released • decrease in CO2 • shifts curve to left • more O2 bound

  20. Hb & BPG • BPG-2,3 biphosphoglycerate • produced by RBC during glycolysis • higher levels • unloading of oxygen increased • shifts to right • BPG decreases • curve shifts to left • more oxygen is bound • amount of BPG generated drops as RBCs age • BPG drops too lowO2 irreversibly bound to Hb

  21. CO2 Transport • dissolved in plasma • 7% • transported as HCO3 (bicarbonate ion) • 70% • bound to HB • 23% • attaches to –NH2 groups (amino) of histidine • Carbaminohemoglobin HB-CO2

  22. Transport as HCO3 • converted to carbonic acid • unstable • dissociates to hydrogen & bicarbonate ions • HCO3- diffuses from RBCs into plasma • exchanges one HCO3- for one Cl- • chloride shift • maintains electrical neutrality

  23. AT LUNG

  24. AT TISSUES

  25. Control of Respiration • normally cellular rates of absorption & generation of gases are matched by capillary rates of delivery & removal • rates are identical to rates of O2 absorption & CO2 excretion at lungs • if absorption & excretion become unbalanced • homeostatic mechanisms restore equilibrium • changing blood flow & O2 delivery • locally regulated • changing depth & rate of respiration • respiratory centers in brain

  26. Respiratory Centers in Brain • usually breath without conscious thought-involuntary • depends on repetitive stimuli from brain • automatic, unconscious cycle of breathing controlled by respiratory centers in medulla & pons • medullary rhymicity area • pneumotaxic center • apneustic center

  27. Medullary Rhymicity Center • controls basic rhythm of respiration • has an inspiratory & expiratory area • nerves project to diaphragm by phrenic nerve & to intercostals by intercostal nerves • quiet breathing • neuron activity increases for 2 sec. stimulates inspiratory muscles • rib cage expands as diaphragm contracts • inhalation occurs • output ceases abruptly muscles relaxelastic parts recoil exhalation (lasts 3 seconds) • neurons begins to fire again • cycle repeats

  28. Pneumotaxic & Apneustic Centers • located in pons • regulates shift from inspiration to expiration • regulate respiratory rate & depth of respiration in response to sensory stimuli or input from other brain centers • pneumotaxic center-upper pons • transmits inhibitory impulses to inspiratory area • helps turn off inspiratory area before lungs become too full of air • increased pneumotaxic output quickens respiration by shortening duration of each inhalationbreathing rate increases • decreased outputslows respiratory pace • depth of respiration increases • apneustic center sends stimulating impulses to inspiratory area • activates it producing prolonged inhalation. • result is long, deep inhalations

  29. Regulation of Respiratory Centers • conscious or voluntary control • inhale or exhale at will • input form cerebral motor cortex stimulates motor neurons to stimulate respiratory muscles bypassing medulla centers • limited-impossible to override chemoreceptor reflexes • nerve impulses from hypothalamus & limbic system also stimulate respiratory center • allows emotional stimuli to alter respiration

  30. Respiratory Reflexes • brain centers regulate respiratory rate & depth of respiration • in response to sensory stimuli or input from other brain centers • sensory information comes from • central chemoreceptors • peripheral chemoreceptors • proprioceptors • stretch receptors • information from these alters patterns of respiration • changes are respiratory reflexes

  31. Chemoreceptors • central chemoreceptors • neurons in brainstem that respond to changes in pH of cerebrospinal fluid • stimulation increases depth & rate of respiration • peripheral chemoreceptors • carotid & aortic bodies of large arteries • respond to PCO2, pH & PO2 of blood

  32. Respiratory Reflex-CO2 • Hypercapnia • increase in PCO2 • CO2 crosses blood brain barrier rapidly • rise in arterial PCO2 almost immediately elevates CO2 levels in CSFpH decreases excites central chemoreceptors stimulates respiratory centers increases depth & rate of breathing • rapid breathing moves more air in & out of lungsalveolar CO2 decreases accelerates diffusion of CO2 out of alveolar capillaries homeostasis restored • results in hyperventilation

  33. Chemoreceptor Reflexes-CO2 • hyperventilation hypocapnia • low PCO2 • central & peripheral chemoreceptors are not stimulated • Inspiratory center sets its own pace • CO2 accumulates • homeostasis restored

  34. Stretch Receptors • found in smooth muscles of bronchi & bronchioles & in visceral pleura • lung inflation • signal inspiratory & apneustic areas via vagus nerve • Inhibits both • Hering-Breuer Reflex

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