535410521-o2-and-Co2-Transport.pptx2.physiology

Physiology

1. Transport of Oxygen and Carbon Dioxide in Blood and Tissue Fluids Mohammed Zoghaibi , PhD [email protected] 0506338400 Chapter 41, pages 527-537

2. Introduction HB= transports 30 to 100x as much as O 2  as could be transported in the form of dissolved O 2  in the water of the blood. O2 + glucose= co2 in respiration of cells CO 2 , like O 2 , combines with chemical substances in the blood that increase CO 2  transport 15- to 20-fold.

3. Structure of hb It is a buffer protein It has neg amino acids to hook protons aka h + = naughty monkeys Binds reversibly to oxygen Stabilises proton concen in blood to maintain acid base balance NO can bind to hb just like o2 So when hb binds to o2 it also binds to no So no also goes along with 02 No is a vasodilator so dilates arterioles

4. Co2 Co2 lipid soluble so can go to rbc When pp is high it will get pushed from cell to isf to capillaries to rbc In rbc co2 dec Why? Co2 meets cute enzyme called carbonic anhydrase which binds it to water This makes carbonic acid Anhydrase then breaks down into bicarbonate and protons The hb in rbcs then grabs the protons The bicarb goes out via a protein But we don’t want lots of h in cell and lots of bicarbonate out So the protein is a pen exchanger and gives a cl to rbc aka the chloride shift Remember h20 always follows na and cl because it loves salt So if cl goes In So will water So by time rbc goes from capillarys arterial side to venous side it’s a. It swollen so that’s why there’s more hametocti on venous side So most of co2 actually goes from tissue to lungs as bicarbonate Some of carbon dioxide = dissolved 5% 5% = carbamenohaemoglobin Hb chain of amino acids – binds to amine group and shoves h off to go to lungs When co2 joins hb the protons make hb acidici and if hb aicidc then o2 won’t stat for hb so o2 is release makers sense if co2 being given off then need o2 in those tissues for aerobic respiration this is called bohr effect happens in tissues and systemic capillaries

5. Bohr effect Co2 protons Bind to hb Reducechb affinity to o2 Delivers o2 to tissues

6. Types of Hemoglobin Adult HBA= CARRIES 4 O2 BECAUSE HAS 4 CHAINS – 2A AND 2B and loves 02 Methemoglobin . -When Fe in HB= oxidative state aka Fe3+ , so doesn’t bind O 2 . Causes = oxidation of Fe2+ to Fe3+. congenital bec of deficient methemoglobin reductase made by liver , an enzyme in red blood cells that normally keeps iron in its reduced state. Fetal hemoglobin (HBF ) α2γ2 .- 02 likes baby Gamma more so O2 goes to baby from mum replaced by hemoglobin A within the first year of life. Hemoglobin S = HBS = sickle cell disease. HBS< hba AFFINTIY FOR 02 The α = fine , problem with β HBS In deoxygenated form, = sickle rods- changes RBC shape so can block BVs

7. Transport of Oxygen in the Arterial Blood 98% of the blood in LA has come via pulmonary capillary and has become oxygenated up to a P O 2  of about 104 mm Hg . 2 %of blood from aorta via bronchial circulation, which supplies mainly the deep tissues of the lungs and is not exposed to lung air so has less oxygen Shunt flow = blood is shunted past gas exchange areas with P O 2 of 40 mm Hg. This less oxygen blood mixes with oxygenated blood in LA aka venous admixture of blood So PO2 from aorta= mixed blood so po2= 104mmhg

8. Transport of Oxygen in the Arterial Blood, (continue) Figure shows changes in P O 2  in the pulmonary capillary blood, systemic arterial blood, and systemic capillary blood, demonstrating the effect of venous admixture.

9. PO2s and Pco2s Po2 pCO2 Alveoli 104 40 BLOOD IN PULMONARY Capillaries at arterial end 40 45 Aorta 95 Capillary of tissues at aterial end entering caps 95 40 ISF- in tissues 40 45 IC – in tissues 0-40 average= 23 46 Po2 in venous tissue leaving capillaries 40 45 Therefore, the  initial  pressure difference that causes O 2  to go from alveoli pulmonary capillary is 104 − 40, or 64 mm Hg . P O 2  in peripheral/IC tissues always< than the P O 2  in peripheral capillaries. Capillaries are far from cells. Co2 Dp = 5 45-40 =5 need 5 mmHg dp for co2 to move from pulmonary capillaries into the alveoli. P CO 2  of the pulmonary capillary blood falls to almost exactly equal the alveolar P CO 2  of 40 mm Hg before it has passed more than about one third the distance through the capillaries.

10. Diffusion of Oxygen from the Alveoli to the Pulmonary Capillary Blood

11. Diffusion of Oxygen from the Alveoli to the Pulmonary Capillary Blood- O2 transfer in Emphysema, fibrosis and strenuous exercise. Normal transfer of O2 and CO2 and normal exercise.

12. Diffusion of Oxygen from the Alveoli to the Pulmonary Capillary Blood In the lungs of the normal person at rest, oxygen transport = perfusion-limited. In pathology (e.g., fibrosis), oxygen transfer becomes diffusion limited.

13. Increasing Blood Flow Raises Interstitial Fluid PO 2 . In summary, tissue P O 2  is determined by a balance between (1) the rate of O 2  transport to the tissues in the blood and (2) the rate at which the O 2  is used by the tissues

14. Diffusion of Oxygen from the Alveoli to the Pulmonary Capillary Blood

15. Diffusion of CO 2 from Peripheral Tissue Cells into the Capillaries and from the Pulmonary Capillaries into Alveoli When O 2  is used by the cells, virtually all of it becomes CO 2 , Inc co2 - CO 2  diffuses from the cells from high to low into capillaries Co2 = carried by blood to lungs. In the lungs, it diffuses from the pulmonary capillaries into the alveoli and is expired. CO 2  also diffuses opposite to the diffusion of O 2 . But co2 is 20x faster than 02 because its 20x more soluble so needs less DP to diffuse .

16. Diffusion of CO 2 from Peripheral Tissue Cells into the Capillaries and from the Pulmonary Capillaries into Alveoli (continue) Po2 pCO2 Alveoli 104 40 BLOOD IN PULMONARY Capillaries at arterial end 40 45 Aorta 95 Capillary of tissues at aterial end entering caps 95 40 ISF- in tissues 40 45 IC – in tissues 0-40 average= 23 46 Po2 in venous tissue leaving capillaries 40 45

17. Effect of Rate of Tissue Metabolism and Tissue Blood Flow on Interstitial PCO 2

18. Role of Hemoglobin in Oxygen Transport

19. Reversible Combination of O 2  with Hemoglobin

20. Oxygen-Hemoglobin Dissociation Curve. Shows affinity of O2 for HB so shows percent saturation of hemoglobin . In beginning systemic venous blood coming from tissues aka peripheral so low oxygen so P O 2  = 40 mm Hg, saturation of hemoglobin= 75 % . After resp - blood leaving the lungs entering systemic arteries = P O 2  95 mm Hg, - duh its oxygenated so obv high PO2 At 95mmhg , sat of systemic arterial blood = 97 % .

21. Maximum Amount of Oxygen That Can Combine with the Hemoglobin of the Blood.

22. Amount of Oxygen Released from the Hemoglobin When Systemic Arterial Blood Flows through the Tissues So total O 2  + hb = 97 % sAT AKA 19.4 mL/100 mL of blood.  Upon passing VIA tissue capillaries, 02 dec So vol = 14.4 mL (P O 2  of 40 mm Hg, 75% saturated hemoglobin). Thus, under normal conditions, about 5 mL of O 2  are transported from the lungs to the tissues by each 100 mL of blood flow .

23. Transport of Oxygen Is Markedly Increased during Strenuous Exercise During heavy exercise: Muscle interstitial fluid P O 2  dec 40 mm Hg to 15 mm Hg. 4.4 mL of O 2  remain bound with the hemoglobin in each 100 mL of blood. Thus, 19.4 − 4.4, or 15 mL , is the quantity of O 2  actually delivered to the tissues by each 100 mL of blood flow ( three times normal, 3-fold ). Remember, cardiac output can increase to six to seven times in well-trained marathon runners, that means: 6 or 7 × 3 = 20-fold increase in O 2  transport to the tissues.

24. Hemoglobin “Buffers” Tissue Po 2 If we want 5ml O 2  /100ml blood flow We need to dec P O 2  to 40 mm Hg. How? By HB not releasing o2 so it gives tissue o2 a limit

25. Hemoglobin “Buffers” in exercise In exercise, We need More o2 needs to go to tissues for aerobic repsiratio nto make atp How? So hb needs to release ltos of o2 at a pressure between 15mmhg and 40mmhg Inc blood flow However, this delivery of extra O 2 can be achieved with little further decrease in tissue P O 2  because of (1) the steep slope of the dissociation curve and (2) the increase in tissue blood flow caused by the decreased P O 2 ; that is, a very small fall in P O 2  causes large amounts of extra O 2  to be released from the hemoglobin. Thus, the hemoglobin in the blood automatically delivers O 2  to the tissues at a pressure that is held rather tightly between about 15 and 40 mm Hg.

26. Effect of Rate of Tissue Metabolism and Tissue Blood Flow on Interstitial PCO 2 (continue) If MR = x10inc = inc ISF PCO2 kullu blood flow Dec mr = x.25 = isf pco2 = interstitial fluid P CO 2  to fall to about 41 mm Hg, approaching that of the arterial blood, 40 mm Hg.

27. When Atmospheric Oxygen Concentration Changes Markedly, the Buffer Effect of Hemoglobin Still Maintains Almost Constant Tissue PO 2 The normal P O 2  in the alveoli =104 mm Hg, High altitude= P O 2  dec Low alittue with compressed air, such as deep in the sea, P O 2  inc 10x max “ Even so, the tissue P O 2  changes little” Look at the oxygen-hemoglobin dis­sociation curve: - When the alveolar P O 2  is 60 mm Hg, the arterial hemoglobin is still 89% saturated with O 2 . The tissues still remove about 5 mL of O 2  from each 100 mL of blood, to remove this O 2 , the P O 2 of the venous blood falls to 35 mm Hg (only 5 mm Hg below the normal value of 40 mm Hg). Thus, the tissue P O 2 hardly changes, despite the marked fall in the alveolar P O 2 from 104 to 60 mm Hg.

28. When Atmospheric Oxygen Concentration Changes Markedly, the Buffer Effect of Hemoglobin Still Maintains Almost Constant Tissue PO 2 (continue): Conversely, when the alveolar P O 2  rises as high as 500 mm Hg, the maximum O 2 saturation of hemoglobin can never rise above 100%. Only a small amount of additional O 2  dissolves in the fluid of the blood. Then, when the blood passes through the tissue capillaries and loses several mL of O 2  to the tissues, this reduces the P O 2  of the capillary blood to a value only a few mL greater than the normal 40 mm Hg. Consequently, the level of alveolar oxygen may vary greatly—from 60 to more than 500 mmHg P O2 —and still the P O2 in the peripheral tissues does not vary more than a few millimeters from normal, demonstrating the effectiveness of the tissue “oxygen buffer” function of the blood hemoglobin system.

29. Factors That Shift the Oxygen-Hemoglobin Dissociation Curve—Their Importance for Oxygen Transport When the blood becomes slightly acidic (from 7.4 to 7.2) , the O 2 -hemoglobin dissociation curve shifts to the right. Conversely, an increase in pH from the normal 7.4 to 7.6 shifts the curve a similar amount to the left. Other factors are known to shift the curve, all of which shift the curve to the  right , are (1) increased CO 2  concentration, (2) increased blood temperature, and (3) increased 2,3-biphosphoglycerate (BPG).

30. Factors That Shift the Oxygen-Hemoglobin Dissociation Curve—Their Importance for Oxygen Transport he causes of shift to right can be remembered using the  mnemonic , " CADET , face Right!" for  C O 2 ,  A cid, 2,3- D PG, [Note 1]   E xercise and  T emperature. [2 R ight shift: causes  R elease of O2 from Hb. So dec sat level of O2 blood So o2 goes to tissue

31. Oxygen-Hemoglobin Dissociation Curve P50- - When HB = got 50% O2 – only 2 groups are bound to o2 and other 2 are free So if inc p50 = means 02 has inc If p50 dec, o2 affinity dec Hb-oxygen dissociation curve shifts: effect, location   L eft shift: causes  L oading of O2 in  L ungs.

32. Effect of BPG to Cause Rightward Shift of the Oxygen-Hemoglobin Dissociation Curve The normal BPG in the blood keeps the O 2 -hemoglobin dissociation curve shifted slightly to the right all the time. In hypoxic conditions that last longer than a few hours, the quantity of BPG in the blood increases considerably, thus shifting the O 2 -hemoglobin dissociation curve even farther to the right. This shift causes O 2  to be released to the tissues at as much as 10 mm Hg higher tissue O 2  pressure than would be the case without this increased BPG. Therefore, under some conditions, the BPG mechanism can be important for adaptation to hypoxia, especially to hypoxia caused by poor tissue blood flow.

33. Rightward Shift of the Oxygen-Hemoglobin Dissociation Curve during Exercise The exercising muscles release large quantities of CO 2 ; this and several other acids released by the muscles increase the hydrogen ion concentration in the muscle capillary blood. In addition, the temperature of the muscle often rises 2° to 3°C, which can increase O 2 delivery to the muscle fibers even more. All these factors act together to shift the oxygen-hemoglobin dissociation curve  of the muscle capillary blood  considerably to the right.

34. Effect of Blood Flow on Metabolic Use of Oxygen The total amount of O 2  available each minute for use in any given tissue is determined by (1) the quantity of O 2  that can be transported to the tissue in each 100 mL of blood and (2) the rate of blood flow.

35. Transport of Oxygen in the Dissolved State

36. Transport of Oxygen in the Dissolved State

37. Combination of Hemoglobin with Carbon Monoxide—Displacement of O 2

38. Carbon Dioxide Dissociation Curve The  CO 2 dissociation curve —depicts the dependence of total blood CO 2  in all its forms on P CO 2 . normal concentration of CO 2  in the blood = 50 volumes percent, but only 4 volumes percent of this is exchanged during normal transport of CO 2  from the tissues to the lungs.

39. Carbon Dioxide Dissociation Curve That is, the concentration rises to about 52 volumes percent as the blood passes through the tissues and falls to about 48 volumes percent as it passes through the lungs. In lung capilalries after gas exchange Tissue capillaries Lung capillaries

40. Carbon Dioxide Dissociation Curve Small portions of two CO 2 dissociation curves: when the PO 2  is 100 mm Hg, which is the case in the blood capillaries of the lungs, and (2) when the PO 2  is 40 mm Hg, which is the case in the tissue capillaries. Point A shows that the normal PCO 2  of 45 mm Hg in the tissues causes 52 volumes % of CO 2 to combine with the blood. On entering the lungs, the PCO 2  falls to 40 mm Hg and the PO 2  rises to 100 mm Hg. If the CO 2 dissociation curve did not shift because of the Haldane effect, the CO 2 content of the blood would fall only to 50 volumes %, which would be a loss of only 2 volumes % of CO 2 . However, the increase in PO 2  in the lungs lowers the CO 2 dissociation curve from the top curve to the lower curve of the figure, so that the CO 2 content falls to 48 volumes % (point B). 

41. When Oxygen Binds with Hemoglobin, CO 2 Is Released (the Haldane Effect) to Increase CO 2 Transport How - of O 2 + HB in lungs so HB becomes = a stronger acid . This displaces CO 2  from the blood and into the alveoli in two ways. First , = acidic hemoglobin has less tendency to combine with CO 2  to form carbaminohemoglobin, thus displacing much of the CO 2  that is present in the carbamino form to the blood. Second , the increased acidity of the hemoglobin also causes it to release an excess of hydrogen ions, and these ions bind with bicarbonate ions to form carbonic acid, which then dissociates into water and CO 2 , and the CO 2  is released from the blood into the alveoli and, finally, into the air.

42. When Oxygen Binds with Hemoglobin, CO 2 Is Released (the Haldane Effect) to Increase CO 2 Transport