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Chapter 16.2

Chapter 16.2. Respiratory Physiology. 16-1. Chapter 16.2 Outline Control of Ventilation Hemoglobin CO 2 Transport and Acid-Base Balance Exercise and Altitude Effects. 16-2. Control of Ventilation. 16-50. Brain Stem Respiratory Centers.

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Chapter 16.2

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  1. Chapter 16.2 Respiratory Physiology 16-1

  2. Chapter 16.2 Outline • Control of Ventilation • Hemoglobin • CO2 Transport and Acid-Base Balance • Exercise and Altitude Effects 16-2

  3. Control of Ventilation 16-50

  4. Brain Stem Respiratory Centers • Automatic breathing is generated by a rhythmicity center in medulla oblongata • Consists of inspiratory neurons that drive inspiration and expiratory neurons that inhibit inspiratory neurons • Their activity varies in a reciprocal way and may be due to pacemaker neurons 16-51

  5. Brain Stem Respiratory Centers continued • Inspiratory neurons stimulate spinal motor neurons that innervate respiratory muscles • Expiration is passive and occurs when inspiratories are inhibited 16-52

  6. Pons Respiratory Centers • Activities of medullary rhythmicity center are influenced by centers in pons • Apneustic center promotes inspiration by stimulating inspiratories in medulla • Pneumotaxic center antagonizes apneustic center, inhibiting inspiration 16-53

  7. Chemoreceptors • Automatic breathing is influenced by activity of chemoreceptors that monitor blood PCO2, PO2, and pH • Central chemoreceptors are in medulla • Peripheral chemoreceptors are in large arteries near heart (aortic bodies) and in carotids (carotid bodies) 16-54

  8. CNS Control of Breathing 16-55

  9. Effects of Blood PCO2 and pH on Ventilation • Chemoreceptors modify ventilation to maintain normal CO2, O2, and pH levels • PCO2 is most crucial because of its effects on blood pH • H2O + CO2 H2CO3 H+ + HCO3- • Hyperventilation causes low CO2 (hypocapnia) • Hypoventilation causes high CO2 (hypercapnia) 16-56

  10. Effects of Blood PCO2 and pH on Ventilation continued 16-57

  11. Effects of Blood PCO2 and pH on Ventilation continued • Brain chemoreceptors are responsible for greatest effects on ventilation • H+ can't cross BBB but CO2 can, which is why it is monitored and has greatest effects • Rate and depth of ventilation adjusted to maintain arterial PCO2 of ~40 mm Hg • Peripheral chemoreceptors do not respond to PCO2, only to H+ levels 16-58

  12. Effects of Blood PCO2 and pH on Ventilation continued 16-59

  13. Effects of Blood PO2 on Ventilation • Low blood PO2 (hypoxemia) has little effect on ventilation • Does influence chemoreceptor sensitivity to PCO2 • PO2 has to fall to about half normal before ventilation is significantly affected • Emphysema blunts chemoreceptor response to PCO2 • Oftentimes ventilation is stimulated by hypoxic drive rather than PCO2 16-60

  14. Comparison of PCO2 and PO2 Effects on Ventilation 16-61

  15. Effects of Pulmonary Receptors on Ventilation • Lungs have receptors that influence brain respiratory control centers via sensory fibers in vagus • Unmyelinated C fibers are stimulated by noxious substances such as capsaicin • Causes apnea followed by rapid, shallow breathing • Irritant receptors are rapidly adapting; respond to smoke, smog, and particulates • Causes cough 16-62

  16. Effects of Pulmonary Receptors on Ventilation continued • Hering-Breuer reflex is mediated by stretch receptors activated during inspiration • Inhibits respiratory centers to prevent overinflation of lungs 16-63

  17. Hemoglobin 16-64

  18. Hemoglobin (Hb) and O2 Transport • Loading of Hb with O2 occurs in lungs; unloading in tissues • Affinity of Hb for O2 changes with a number of physiological variables 16-65

  19. Hemoglobin (Hb) and O2 Transport continued • Each Hb has 4 globin polypeptide chains and 4 heme groups that bind O2 • Each heme has a ferrous ion that can bind 1 O2 • So each Hb can carry 4 O2s 16-66

  20. Hemoglobin (Hb) and O2 Transport continued • Most O2 in blood is bound to Hb inside RBCs as oxyhemoglobin • Each RBC has about 280 million molecules of Hb • Hb greatly increases O2 carrying capacity of blood 16-67

  21. Hemoglobin (Hb) and O2 Transport continued • Methemoglobin contains ferric iron (Fe3+) -- the oxidized form • Lacks electron to bind with O2 • Blood normally contains a small amount • Carboxyhemoglobin is heme combined with carbon monoxide • Bond with carbon monoxide is 210 times stronger than bond with oxygen • So heme can't bind O2 16-68

  22. Hemoglobin (Hb) and O2 Transport continued • O2-carrying capacity of blood depends on its Hb levels • In anemia, Hb levels are below normal • In polycythemia, Hb levels are above normal • Hb production controlled by erythropoietin (EPO) • Production stimulated by low PO2 in kidneys • Hb levels in men are higher because androgens promote RBC production 16-69

  23. Hemoglobin (Hb) and O2 Transport continued • High PO2 of lungs favors loading; low PO2 in tissues favors unloading • Ideally, Hb-O2 affinity should allow maximum loading in lungs and unloading in tissues 16-70

  24. Oxyhemoglobin Dissociation Curve • Gives % of Hb sites that have bound O2 at different PO2s • Reflects loading and unloading of O2 • Differences in % saturation in lungs and tissues are shown at right • In steep part of curve, small changes in PO2 cause big changes in % saturation 16-71

  25. Oxyhemoglobin Dissociation Curve continued • Is affected by changes in Hb-O2 affinity caused by pH and temperature • Affinity decreases when pH decreases (Bohr Effect) or temp increases • Occurs in tissues where temp, CO2 and acidity are high • Causes Hb-O2 curve to shift right and more unloading of O2 16-72

  26. 16-73

  27. Effect of 2,3 DPG on O2 Transport • RBCs have no mitochondria; can’t perform aerobic respiration • 2,3-DPG is a byproduct of glycolysis in RBCs • Its production is increased by low O2 levels • Causes Hb to have lower O2 affinity, shifting curve to right 16-74

  28. Effect of 2,3 DPG on O2 Transport • In anemia, total blood Hb levels fall, causing each RBC to produce more DPG • Fetal hemoglobin (HbF) has 2 g-chains in place of b-chains of HbA • HbF can’t bind DPG, causing it to have higher O2 affinity • Facilitates O2 transfer from mom to baby 16-75

  29. Sickle-cell Anemia • Sickle-cell anemia affects 8-11% of African Americans • HbS has valine substituted for glutamic acid at 1 site on b chains • At low PO2, HbS crosslinks to form a “paracrystalline gel” inside RBCs • Makes RBCs less flexible and more fragile 16-76

  30. Thalassemia • Thalassemia affects primarily people of Mediterranean descent • Has decreased synthesis of a or b chains; increased synthesis of g chains 16-77

  31. Myoglobin • Is a red pigment found exclusively in striated muscle • Slow-twitch skeletal and cardiac muscle fibers are rich in myoglobin 16-78

  32. Myoglobin • Has only 1 globin; binds only 1 O2 • Has higher affinity for O2 than Hb; is shifted to extreme left • Releases O2 only at low PO2 • Serves in O2 storage, particularly in heart during systole 16-79

  33. CO2 Transport and Acid-Base Balance 16-80

  34. CO2 Transport • CO2 transported in blood as dissolved CO2(10%), carbaminohemoglobin (20%), and bicarbonate ion, HCO3-, (70%) • In RBCs carbonic anhydrase catalyzes formation of H2CO3 from CO2 + H2O 16-81

  35. Chloride Shift • High CO2 levels in tissues causes the reaction CO2 + H2O  H2CO3 H+ + HCO3-to shift right in RBCs • Results in high H+ and HCO3- levels in RBCs • H+ is buffered by proteins • HCO3- diffuses down concentration and charge gradient into blood causing RBC to become more + • So Cl- moves into RBC (chloride shift) 16-82

  36. Chloride Shift 16-83

  37. Reverse Chloride Shift • In lungs, CO2 + H2O  H2CO3 H+ + HCO3-, moves to left as CO2 is breathed out • Binding of O2 to Hb decreases its affinity for H+ • H+ combines with HCO3- and more CO2 is formed • Cl- diffuses down concentration and charge gradient out of RBC (reverse chloride shift) 16-84

  38. Acid-Base Balance in Blood • Blood pH is maintained within narrow pH range by lungs and kidneys (normal = 7.4) • Most important buffer in blood is bicarbonate • H2O + CO2  H2CO3  H+ + HCO3- • Excess H+ is buffered by HCO3- • Kidney's role is to excrete H+ into urine 16-85

  39. Effect of Bicarbonate on Blood pH 16-86

  40. Acid-Base Balance in Blood continued • 2 major classes of acids in body: • A volatile acid can be converted to a gas • E.g. CO2 in bicarbonate buffer system can be breathed out • H2O + CO2 H2CO3  H+ + HCO3- • All other acids are nonvolatile and cannot leave blood • E.g. lactic acid, fatty acids, ketone bodies 16-87

  41. Acid-Base Balance in Blood continued • Acidosis is when pH < 7.35; alkalosis is pH > 7.45 • Respiratory acidosis caused by hypoventilation • Causes rise in blood CO2 and thus carbonic acid • Respiratory alkalosis caused by hyperventilation • Results in too little CO2 16-88

  42. Acid-Base Balance in Blood continued • Metabolic acidosis results from excess of nonvolatile acids • E.g. excess ketone bodies in diabetes or loss of HCO3- (for buffering) in diarrhea • Metabolic alkalosis caused by too much HCO3- or too little nonvolatile acids (e.g. from vomiting out stomach acid) 16-89

  43. Acid-Base Balance in Blood continued • Normal pH is obtained when ratio of HCO3- to CO2 is 20 : 1 • Henderson-Hasselbalch equation uses CO2 and HCO3- levels to calculate pH: • pH = 6.1 + log = [HCO3-] [0.03PCO2] 16-90

  44. Respiratory Acid-Base Balance • Ventilation usually adjusted to metabolic rate to maintain normal CO2 levels • With hypoventilation not enough CO2 is breathed out in lungs • Acidity builds, causing respiratory acidosis • With hyperventilation too much CO2 is breathed out in lungs • Acidity drops, causing respiratory alkalosis 16-91

  45. Exercise and Altitude Effects 16-92

  46. Ventilation During Exercise • During exercise, arterial PO2, PCO2, and pH remain fairly constant 16-93

  47. Ventilation During Exercise • During exercise, breathing becomes deeper and more rapid, delivering much more air to lungs (hyperpnea) • 2 mechanisms have been proposed to underlie this increase: • With neurogenic mechanism, sensory activity from exercising muscles stimulates ventilation; and/or motor activity from cerebral cortex stimulates CNS respiratory centers • With humoral mechanism, either PCO2 and pH may be different at chemoreceptors than in arteries • Or there may be cyclic variations in their values that cannot be detected by blood samples 16-94

  48. Lactate Threshold • Is maximum rate of oxygen consumption before blood lactic acid levels rise as a result of anaerobic respiration • Occurs when 50-70% maximum O2 uptake has been reached • Endurance-trained athletes have higher lactate threshold, because of higher cardiac output • Have higher rate of oxygen delivery to muscles and greater numbers of mitochondria and aerobic enzymes 16-95

  49. Acclimatization to High Altitude • Involves increased ventilation, increased DPG, and increased Hb levels • Hypoxic ventilatory response initiates hyperventilation which decreases PCO2 which slows ventilation • Chronic hypoxia increases NO production in lungs which dilates capillaries there • NO binds to Hb and is unloaded in tissues where may also increase dilation and blood flow • NO may also stimulate CNS respiratory centers • Altitude increases DPG, causing Hb-O2 curve to shift to right • Hypoxia causes kidneys to secrete EPO which increases RBCs 16-96

  50. Acclimatization to High Altitude 16-97

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