1 / 50

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.

lacey-allison
Télécharger la présentation

Chapter 16.2

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related