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2 23-8 Gas Exchange Gas Exchange Depends on:Occurs between blood and alveolar air Across the respiratory membrane Depends on: Partial pressures of the gases Diffusion of molecules between gas and liquid

3 23-8 Gas Exchange The Gas LawsDiffusion occurs in response to concentration gradients Rate of diffusion depends on physical principles, or gas laws For example, Boyle’s law

4 23-8 Gas Exchange Dalton’s Law and Partial PressuresComposition of Air Nitrogen (N2) is about 78.6% Oxygen (O2) is about 20.9% Water vapor (H2O) is about 0.5% Carbon dioxide (CO2) is about 0.04%

5 23-8 Gas Exchange Diffusion between Liquids and Gases Henry’s LawWhen gas under pressure comes in contact with liquid Gas dissolves in liquid until equilibrium is reached At a given temperature Amount of a gas in solution is proportional to partial pressure of that gas The actual amount of a gas in solution (at given partial pressure and temperature) Depends on the solubility of that gas in that particular liquid

6 Figure 23-18 Henry’s Law and the Relationship between Solubility and Pressure6

7 Increasing the pressure drives gas molecules Figure 23-18a Henry’s Law and the Relationship between Solubility and Pressure Example Soda is put into the can under pressure, and the gas (carbon dioxide) is in solution at equilibrium. Increasing the pressure drives gas molecules into solution until an equilibrium is established. 7

8 When the gas pressure decreases, dissolved Figure 23-18b Henry’s Law and the Relationship between Solubility and Pressure Example Opening the can of soda relieves the pressure, and bubbles form as the dissolved gas leaves the solution. When the gas pressure decreases, dissolved gas molecules leave the solution until a new equilibrium is reached. 8

9 23-8 Gas Exchange Diffusion and Respiratory FunctionDirection and rate of diffusion of gases across the respiratory membrane Determine different partial pressures and solubilities

10 23-8 Gas Exchange Five Reasons for Efficiency of Gas ExchangeSubstantial differences in partial pressure across the respiratory membrane Distances involved in gas exchange are short O2 and CO2 are lipid soluble Total surface area is large Blood flow and airflow are coordinated

11 23-8 Gas Exchange Partial Pressures in Alveolar Air and Alveolar Capillaries Blood arriving in pulmonary arteries has: Low PO2 High PCO2 The concentration gradient causes: O2 to enter blood CO2 to leave blood Rapid exchange allows blood and alveolar air to reach equilibrium

12 23-8 Gas Exchange Partial Pressures in the Systemic CircuitOxygenated blood mixes with deoxygenated blood from conducting passageways Lowers the PO2 of blood entering systemic circuit (drops to about 95 mm Hg)

13 23-8 Gas Exchange Partial Pressures in the Systemic CircuitInterstitial Fluid PO2 40 mm Hg PCO2 45 mm Hg Concentration gradient in peripheral capillaries is opposite of lungs CO2 diffuses into blood O2 diffuses out of blood

14 23-9 Gas Transport Gas Pickup and DeliveryBlood plasma cannot transport enough O2 or CO2 to meet physiological needs Red Blood Cells (RBCs) Transport O2 to, and CO2 from, peripheral tissues Remove O2 and CO2 from plasma, allowing gases to diffuse into blood

15 23-9 Gas Transport Oxygen TransportO2 binds to iron ions in hemoglobin (Hb) molecules In a reversible reaction New molecule is called oxyhemoglobin (HbO2) Each RBC has about 280 million Hb molecules Each binds four oxygen molecules

16 23-9 Gas Transport Hemoglobin SaturationThe percentage of heme units in a hemoglobin molecule that contain bound oxygen Environmental Factors Affecting Hemoglobin PO2 of blood Blood pH Temperature Metabolic activity within RBCs

17 23-9 Gas Transport Oxygen–Hemoglobin Saturation CurveA graph relating the saturation of hemoglobin to partial pressure of oxygen Higher PO2 results in greater Hb saturation Curve rather than a straight line because Hb changes shape each time a molecule of O2 is bound Each O2 bound makes next O2 binding easier Allows Hb to bind O2 when O2 levels are low

18 23-9 Gas Transport Oxygen Reserves O2 diffusesFrom peripheral capillaries (high PO2) Into interstitial fluid (low PO2) Amount of O2 released depends on interstitial PO2 Up to 3/4 may be reserved by RBCs

19 23-9 Gas Transport Carbon Monoxide CO from burning fuelsBinds strongly to hemoglobin Takes the place of O2 Can result in carbon monoxide poisoning

20 23-9 Gas Transport The Oxygen–Hemoglobin Saturation CurveIs standardized for normal blood (pH 7.4, 37C) When pH drops or temperature rises: More oxygen is released Curve shifts to right When pH rises or temperature drops: Less oxygen is released Curve shifts to left

21 Figure 23-20 An Oxygen-Hemoglobin Saturation Curve(mm Hg) P O 2 % saturation of Hb 10 13.5 Oxyhemoglobin (% saturation) 20 35 30 57 40 75 50 83.5 60 89 70 92.7 80 94.5 90 96.5 100 97.5 (mm Hg) P O 2 21

22 23-9 Gas Transport Hemoglobin and pH CO2 diffuses into RBCBohr effect is the result of pH on hemoglobin-saturation curve Caused by CO2 CO2 diffuses into RBC An enzyme, called carbonic anhydrase, catalyzes reaction with H2O Produces carbonic acid (H2CO3) Dissociates into hydrogen ion (H+) and bicarbonate ion (HCO3) Hydrogen ions diffuse out of RBC, lowering pH

23 Effect of pH. When the pH drops below Figure 23-21a The Effects of pH and Temperature on Hemoglobin Saturation 7.6 7.4 7.2 Oxyhemoglobin (% saturation) P (mm Hg) O 2 Effect of pH. When the pH drops below normal levels, more oxygen is released; the oxygen–hemoglobin saturation curve shifts to the right. When the pH increases, less oxygen is released; the curve shifts to the left. 23

24 23-9 Gas Transport Hemoglobin and TemperatureTemperature increase = hemoglobin releases more oxygen Temperature decrease = hemoglobin holds oxygen more tightly Temperature effects are significant only in active tissues that are generating large amounts of heat For example, active skeletal muscles

25 Effect of temperature. When the temperature rises, more oxygen is Figure 23-21b The Effects of pH and Temperature on Hemoglobin Saturation 10°C 20°C 38°C 43°C Oxyhemoglobin (% saturation) (mm Hg) P O 2 Effect of temperature. When the temperature rises, more oxygen is released; the oxygen–hemoglobin saturation curve shifts to the right. 25

26 23-9 Gas Transport Hemoglobin and BPG 2,3-bisphosphoglycerate (BPG)RBCs generate ATP by glycolysis Forming lactic acid and BPG BPG directly affects O2 binding and release More BPG, more oxygen released

27 23-9 Gas Transport BPG Levels BPG levels rise:When pH increases When stimulated by certain hormones If BPG levels are too low: Hemoglobin will not release oxygen

28 23-9 Gas Transport Fetal Hemoglobin The structure of fetal hemoglobinDiffers from that of adult Hb At the same PO2: Fetal Hb binds more O2 than adult Hb Which allows fetus to take O2 from maternal blood

29 Figure 23-22 A Functional Comparison of Fetal and Adult HemoglobinFetal hemoglobin Adult hemoglobin Oxyhemoglobin (% saturation) P O 2 (mm Hg) 29

30 23-9 Gas Transport Carbon Dioxide Transport (CO2)Is generated as a by-product of aerobic metabolism (cellular respiration) CO2 in the bloodstream can be carried three ways Converted to carbonic acid Bound to hemoglobin within red blood cells Dissolved in plasma

31 23-10 Control of RespirationLocal Regulation of Gas Transport and Alveolar Function Rising PCO2 levels Relax smooth muscle in arterioles and capillaries Increase blood flow Coordination of lung perfusion and alveolar ventilation Shifting blood flow PCO2 levels Control bronchoconstriction and bronchodilation

32 23-10 Control of RespirationThe Respiratory Centers of the Brain When oxygen demand rises: Cardiac output and respiratory rates increase under neural control Have both voluntary and involuntary components

33 23-10 Control of RespirationThe Respiratory Centers of the Brain Voluntary centers in cerebral cortex affect: Respiratory centers of pons and medulla oblongata Motor neurons that control respiratory muscles The Respiratory Centers Three pairs of nuclei in the reticular formation of medulla oblongata and pons Regulate respiratory muscles In response to sensory information via respiratory reflexes

34 23-10 Control of RespirationRespiratory Centers of the Medulla Oblongata Set the pace of respiration Can be divided into two groups Dorsal respiratory group (DRG) Ventral respiratory group (VRG)

35 23-10 Control of RespirationDorsal Respiratory Group (DRG) Inspiratory center Functions in quiet and forced breathing Ventral Respiratory Group (VRG) Inspiratory and expiratory center Functions only in forced breathing

36 23-10 Control of RespirationQuiet Breathing Brief activity in the DRG Stimulates inspiratory muscles DRG neurons become inactive Allowing passive exhalation

37 Figure 23-25a Basic Regulatory Patterns of RespirationQuiet Breathing INHALATION (2 seconds) Diaphragm and external intercostal muscles contract and inhalation occurs. Dorsal respiratory group active Dorsal respiratory group inhibited Diaphragm and external intercostal muscles relax and passive exhalation occurs. EXHALATION (3 seconds) 37

38 23-10 Control of RespirationForced Breathing Increased activity in DRG Stimulates VRG Which activates accessory inspiratory muscles After inhalation Expiratory center neurons stimulate active exhalation

39 Figure 23-25b Basic Regulatory Patterns of RespirationForced Breathing INHALATION Muscles of inhalation contract, and opposing muscles relax Inhalation occurs, DRG and inspiratory center of VRG are active. Expiratory center of VRG is inhibited. DRG and inspiratory center of VRG are inhibited. Expiratory is active. Muscles of inhalation relax and muscles of exhalation contract. Exhalation occurs. EXHALATION 39

40 23-10 Control of RespirationThe Apneustic and Pneumotaxic Centers of the Pons Paired nuclei that adjust output of respiratory rhythmicity centers Regulating respiratory rate and depth of respiration Apneustic Center Provides continuous stimulation to its DRG center Pneumotaxic Centers Inhibit the apneustic centers Promote passive or active exhalation

41 23-10 Control of RespirationRespiratory Centers and Reflex Controls Interactions between VRG and DRG Establish basic pace and depth of respiration The pneumotaxic center Modifies the pace

42 Figure 23-26 Control of RespirationRespiratory Centers and Reflex Controls The locations and relationships between the major respiratory centers in the pons and medulla oblongata and other factors important to the reflex control of respiration. Pathways for conscious control over respiratory muscles are not shown. Cerebrum HIGHER CENTERS Cerebral cortex Limbic system Hypothalamus CSF CHEMORECEPTORS Pons Pneumotaxic center Apneustic center KEY  Stimulation Medulla oblongata  Inhibition 42

43 Figure 23-26 Control of RespirationRespiratory Centers and Reflex Controls Medulla oblongata N IX and N X Chemoreceptors and baroreceptors of carotid and aortic sinuses Respiratory Rhythmicity Centers N X Dorsal respiratory group (DRG) Stretch receptors of lungs Spinal cord Ventral respiratory group (VRG) Diaphragm Motor neurons controlling diaphragm Motor neurons controlling other respiratory muscles KEY  Stimulation Phrenic nerve  Inhibition 43

44 23-10 Control of RespirationRespiratory Reflexes Chemoreceptors are sensitive to PCO2, PO2, or pH of blood or cerebrospinal fluid Baroreceptors in aortic or carotid sinuses are sensitive to changes in blood pressure Stretch receptors respond to changes in lung volume Irritating physical or chemical stimuli in nasal cavity, larynx, or bronchial tree Other sensations including pain, changes in body temperature, abnormal visceral sensations

45 23-10 Control of RespirationThe Chemoreceptor Reflexes Respiratory centers are strongly influenced by chemoreceptor input from: Glossopharyngeal nerve (N IX) Vagus nerve (N X) Central chemoreceptors that monitor cerebrospinal fluid

46 23-10 Control of RespirationThe Chemoreceptor Reflexes The glossopharyngeal nerve From carotid bodies Stimulated by changes in blood pH or PO2 The vagus nerve From aortic bodies

47 23-10 Control of RespirationThe Chemoreceptor Reflexes Central chemoreceptors that monitor cerebrospinal fluid Are on ventrolateral surface of medulla oblongata Respond to PCO2 and pH of CSF

48 23-10 Control of RespirationChemoreceptor Stimulation Leads to increased depth and rate of respiration Is subject to adaptation Decreased sensitivity due to chronic stimulation

49 23-10 Control of RespirationHypercapnia An increase in arterial PCO2 Stimulates chemoreceptors in the medulla oblongata To restore homeostasis

50 23-10 Control of RespirationHypercapnia and Hypocapnia Hypoventilation is a common cause of hypercapnia Abnormally low respiration rate Allows CO2 buildup in blood Excessive ventilation, hyperventilation, results in abnormally low PCO2 (hypocapnia) Stimulates chemoreceptors to decrease respiratory rate

51 Figure 23-27a The Chemoreceptor Response to Changes in PCO2Stimulation of arterial chemoreceptors Stimulation of respiratory muscles Increased arterial PCO2 Increased PCO2 , decreased pH in CSF Stimulation of CSF chemoreceptors at medulla oblongata HOMEOSTASIS DISTURBED Increased respiratory rate with increased elimination of CO2 at alveoli Increased arterial PCO2 (hypocapnia) HOMEOSTASIS RESTORED HOMEOSTASIS Start Normal arterial PCO2 Normal arterial PCO2 51

52 Figure 23-27b The Chemoreceptor Response to Changes in PCO2HOMEOSTASIS HOMEOSTASIS RESTORED Start Normal arterial PCO2 Normal arterial PCO2 HOMEOSTASIS DISTURBED Decreased respiratory rate with decreased elimination of CO2 at alveoli Decreased arterial PCO2 (hypocapnia) Decreased arterial PCO2 Decreased PCO2 , increased pH in CSF Reduced stimulation of CSF chemoreceptors Inhibition of arterial chemoreceptors Inhibition of respiratory muscles 52

53 23-10 Control of RespirationThe Baroreceptor Reflexes Carotid and aortic baroreceptor stimulation Affects blood pressure and respiratory centers When blood pressure falls: Respiration increases When blood pressure increases: Respiration decreases

54 23-10 Control of RespirationProtective Reflexes Triggered by receptors in epithelium of respiratory tract when lungs are exposed to: Toxic vapors Chemical irritants Mechanical stimulation Cause sneezing, coughing, and laryngeal spasm

55 23-10 Control of RespirationApnea A period of suspended respiration Normally followed by explosive exhalation to clear airways Sneezing and coughing Laryngeal Spasm Temporarily closes airway To prevent foreign substances from entering

56 23-10 Control of RespirationVoluntary Control of Respiration Strong emotions can stimulate respiratory centers in hypothalamus Emotional stress can activate sympathetic or parasympathetic division of ANS Causing bronchodilation or bronchoconstriction Anticipation of strenuous exercise can increase respiratory rate and cardiac output by sympathetic stimulation

57 23-10 Control of RespirationChanges in the Respiratory System at Birth Before birth Pulmonary vessels are collapsed Lungs contain no air During delivery Placental connection is lost Blood PO2 falls PCO2 rises

58 23-10 Control of RespirationChanges in the Respiratory System at Birth At birth Newborn overcomes force of surface tension to inflate bronchial tree and alveoli and take first breath Large drop in pressure at first breath Pulls blood into pulmonary circulation Closing foramen ovale and ductus arteriosus Redirecting fetal blood circulation patterns Subsequent breaths fully inflate alveoli

59 23-11 Effects of Aging on the Respiratory SystemThree Effects of Aging on the Respiratory System Elastic tissues deteriorate Altering lung compliance and lowering vital capacity Arthritic changes Restrict chest movements Limit respiratory minute volume Emphysema Affects individuals over age 50 Depending on exposure to respiratory irritants (e.g., cigarette smoke)

60 Figure 23-28 Decline in Respiratory Performance with Age and SmokingNever smoked Regular smoker Stopped at age 45 Respiratory performance (% of value at age 25) Disability Stopped at age 65 Death Age (years) 60

61 23-12 Respiratory System IntegrationRespiratory Activity Maintaining homeostatic O2 and CO2 levels in peripheral tissues requires coordination between several systems Particularly the respiratory and cardiovascular systems

62 23-12 Respiratory System IntegrationCoordination of Respiratory and Cardiovascular Systems Improves efficiency of gas exchange by controlling lung perfusion Increases respiratory drive through chemoreceptor stimulation Raises cardiac output and blood flow through baroreceptor stimulation