Chapter 16 Respiration Functions of the respiratory system Respiration The term respiration includes 3 separate functions: Ventilation: Breathing. Gas exchange: Occurs between air and blood in the lungs. Occurs between blood and tissues. 0 2 utilization: Cellular respiration. Fig not in book Steps in Respiration 1
Fig. 16.1 Type I cell Type II cell Fig. 16.4 Organization of the respiratory system. Low -resistance pathway for airflow Defends against yucky stuff Warms and moistens air When you have kids it enables you to yell at them. ϖ No gas exchange The conducting zone Fig. 16.5 2
Respiratory Zone Region of gas exchange between air and blood. Includes respiratory bronchioles. Must contain alveoli. Gas exchange occurs by diffusion. Fig. 16.4 Figure not in book Fig. 16.8 3
Figure not in book Ventilation and Lung Mechanics Step 1: Getting air into and out of lungs Remember: F = ΔP/R F = flow ΔP = pressure difference (mmhg) R = resistance to flow. Ventilation and Lung Mechanics Step 1: Getting air into and out of lungs Fig not in book 4
Fig not in book Really, Really Important Point! During inspiration and expiration volume of lungs is made to change. By Boyle s law, these changes cause changes in alveolar pressure which drives air into or out of lungs. Volume of lungs depends on: Transpulmonary pressure - difference in pressure between outside and inside of lungs. Elasticity (stretchability) of lungs. 5
Surface Tension Fig. 16.11 Law of Laplace: Pressure in alveoli is directly proportional to surface tension and inversely proportional to radius of alveoli. Creating the Intrapleural Pressure Pull of lungs inward and chestwall outward on intrapleural fluid causes a negative pressure within this space. Fig. 16.15 6
Fig not in book Fig not in book Lung Compliance C L = magnitude of change in lung volume (ΔV L ) produced by a given change in transpulmonary pressure. C L = ΔV L /Δ (P alv - P ip ) Greater the lung compliance the it is to expand the lungs at any given transpulmonary pressure. 7
Fig not in book Determinants of Lung Compliance Stretchability Surface tension at air-water interfaces within alveoli. Assets of surfactant. Phospholipid produced by alveolar type II cells. Lowers surface tension. Reduces attractive forces of hydrogen bonding by becoming interspersed between H 2 0 molecules. As alveoli radius decreases, surfactant s ability to lower surface tension increases. Surfactant Fig. 16.12 8
Fig. 16.14 See also table 16.2 Pulmonary Function Tests Assessed by spirometry. Subject breathes into a closed system in which air is trapped within a bell floating in H 2 0. The bell moves up when the subject exhales and down when the subject inhales. Schematic of a spirometer (left) and the spirometer you will be using in lab (above). 9
Tidal volume: Amount of air expired with each breath. Vital capacity: The maximum amount of air that can be forcefully exhaled after maximum inhalation. Spirogram Fig. 16.16 Table 16.3 Terms Used to Describe Lung Volumes and Capacities Term Lung Volumes Tidal volume Inspiratory reserve volume Expiratory reserve volume Residual volume Lung Capacities Total lung capacity Vital capacity Inspiratory capacity Functional residual capacity Definition The four nonoverlapping components of the total lung capacity The volume of gas inspired or expired in an unforced respiratory cycle The maximum volume of gas that can be inspired during forced breathing in addition to tidal volume The maximum volume of gas that can be expired during forced breathing in addition to tidal volume The volume of gas remaining in the lungs after a maximum expiration Measurements that are the sum of two or more lung volumes The total amount of gas in the lungs after a maximum inspiration The maximum amount of gas that can be expired after a maximum inspiration The maximum amount of gas that can be inspired after a normal tidal expiration The amount of gas remaining in the lungs after a normal tidal expiration Figure not in book 10
Anatomical Dead Space Not all of the inspired air reaches the alveoli. As fresh air is inhaled it is mixed with anatomical dead space. Conducting zone and alveoli where 0 2 concentration is lower than normal and C0 2 concentration is higher than normal. Alveolar ventilation: F x (TV- DS) F = frequency (breaths/min.). TV = tidal volume. DS = dead space. Airway resistance and restrictive vs. obstructive disorders Recall: F = (P atm - P alv ) / R Resistance depends on: Airway Radii and Resistance Airway radii affected by Physical factors going down the wrong pipe Asthma caused by chemical factors (see below). Neural factors Epinephrine Chemical factors CIGARETTE SMOKE, pollutants, viruses allergens, bronchoconstrictor chemicals 11
Restrictive disorder: Vital capacity is reduced. FVC is normal. Obstructive disorder: Restrictive and Obstructive Disorders VC is normal. FEV 1 is reduced. Fig. 16.17 Gas Exchange Dalton s Law: Total pressure of a gas mixture is = to the sum of the pressures that each gas in the mixture would exert independently. P ATM = P N2 + P 02 + P Co2 = 760 mm Hg 0 2 humidified. H 2 0 contributes to partial pressure (~ 47 mm Hg) P0 2 (sea level) = 150 mm Hg. Fig. 16.20 12
Significance of Blood P 02 and P C02 Measurements At normal P 02 arterial blood is about 100 mm Hg. P 02 systemic veins = ~ 40 mm Hg. P C02 systemic veins = ~ 46 mm Hg Fig. 16.23 Figure not in book - Applying numbers to previous figure. Gas Exchange Dalton s Law: Total pressure of a gas mixture is = to the sum of the pressures that each gas in the mixture would exert independently. P ATM = P N2 + P 0 + P Co2 = 760 mm Hg 13
Fig. 16.32 Measuring efficacy of lung function. NOTE these numbers Fig. 16.23 Defining Ventilation Minute ventilation - total ventilation per minute Alveolar Ventilation - total volume of fresh air enter the alveoli per minute = efficacy of breath Physiologic dead space - sum of anatomic and alveolar dead space. 14
Restrictive disorder: Restrictive and Obstructive Disorders Vital capacity is reduced. FVC is normal. Obstructive disorder: VC is normal. FEV 1 is reduced. Fig. 16.17 FEV 1 Forced Expiratory Volume/sec. Fraction of total forced vital capacity expired in 1 sec. The FEV1 of a person with obstructive lung disease would be 80% of vital capacity. The FEV1 of a person with restrictive lung disease would 80% of vital capacity. 15
Alveolar Gas Pressure Alveolar P O2 and P CO2 determine the systemic arterial P O2 and P CO2. Alveolar P O2 values determined by P O2 of atmospheric air Rate of alveolar ventilation Rate of total body oxygen consumption Alveolar P CO2 values determined by Rate of alveolar ventilation Rate of total body carbon dioxide production Relevance of Partial Pressures High altitude => in P O2 of inspired air and in alveolar P O2. Decreased alveolar ventilation => in P O2 of inspired air and in alveolar P O2. Increased cellular metabolism => in alveolar P O2. Getting O 2 into and CO 2 out of body: the bottom line(s) In alveoli P O2 and P CO2 on two sides of alveolar-capillary membrane result in net diffusion, CO 2 out and O 2 in. More capillaries involved, more total O 2 /CO 2 exchange. Need for fewer or greater numbers of alveoli in gas exchange (impairment of gas exchange:o 2 ). 16
Getting O 2 into and CO 2 out of body: the bottom line(s) In alveoli Ventilation-perfusion inequality = mismatching of air supply and blood supply on an individual alveoli. Lowers P O2 of systemic arterial blood. Caused by Ventilated blood in alveoli with no blood supply No blood flowing to some alveoli. Compensation by vasoconstriction Getting O 2 into and CO 2 out of body: the bottom line(s) In tissues Low P O2 and high P CO2 in tissues results in net movement of O 2 into tissues and net CO 2 movement out of tissues. We will revisit this momentarily. Breathing Lesson (control of breathing) Medulla oblongata (medullary inspiratory neurons). Pons Pulmonary stretch receptors Peripheral chemoreceptors - Central chemoreceptors 17
Regulation of Breathing Neurons in the medulla oblongata forms the rhythmicity center: Controls automatic breathing. Brain stem respiratory centers: Medulla. Pons. Fig. 16.25 Rhythmicity Center Dorsal respiratory group (DRG). Regulate activity of phrenic nerve. Project to and stimulate spinal interneurons that innervate respiratory muscles. Considered the I neurons. Ventral respiratory group (VRG). Passive process. Controls motor neurons to the internal intercostal muscles. Considered the E neurons. Activity of expiratory neurons inhibit inspiratory neurons. Pons Respiratory Centers: Influence medullary rhythmicity Apneustic center: Promote inspiration by stimulating the inspiratory neurons in the medulla. Provide constant stimulus for inspiration. Pneumotaxic center: Antagonize the apneustic center. Inhibits inspiration. 18
Fig. 16.28 Adequacy of ventilation Hypoventilation increase in ratio of carbon dioxide production to alveolar ventilation. hypercapnia Hyperventilation decrease in ratio of carbon dioxide production to alveolar ventilation. hypocapnia Chemoreceptor Control Chemoreceptor input modifies the rate and depth of breathing. Oxygen content of blood decreases more slowly because of the large reservoir of oxygen attached to hemoglobin. Chemoreceptors are more sensitive to changes in P C02. H 2 0 + C0 2 H H + + HC0-2 C0 3 3 Rate and depth of ventilation adjusted to maintain arterial P C02 of 40 mm Hg. 19
2 groups of chemoreceptors that monitor changes in blood P C02, P 02, and ph. Central: Medulla. Peripheral: Carotid and aortic bodies. Control breathing indirectly via sensory nerve fibers to the medulla. Chemoreceptors Fig. 16.27 Fig. 16.29 Can say that chemoreceptor sensitivity to P CO2 is augmented by low P O2. Fig. 16.31 20
Moving Oxygen in Blood Amount of oxygen dissolved in blood directly proportional to P O2 of blood. But oxygen NOT very soluble in water (blood). Hemoglobin to the rescue!!!! Hemoglobin Structure Fig. 16.33 Hemoglobin Hemoglobin production controlled by erythropoietin. Production stimulated by P 02 delivery to kidneys. Loading/unloading depends: P 02 of environment. Affinity between hemoglobin and 0 2. Oxyhemoglobin vs. Deoxyhemoglobin. 21
Fig. 16.34 So what does ph do to O2 affinity of hemoglobin? Temperature? 2,3 DPG = Fig. 16.35 More on 2,3- DPG I want my OXYGEN! Anemia and Increased production of 2,3-DPG with low hemoglobin concentration. Causes increased unloading of oxygen in tissues. Fetal hemoglobin and Gamma chains in lieu of beta chains. Do not bind 2,3-DPG Becomes oxygen pig 22
Inherited defects in hemoglobin Sickle-cell anemia Valine substitued for glutamic acid at position #6. Low P O2 causes cross-linking and formation of paracrystalline gel - sickling of cells. Thalassemia Decreased synthesis of alpha or beta chain of hemoglobin. Get increases in gamma chain synthesis. Muscle Myoglobin Slow-twitch skeletal fibers and cardiac muscle cells are rich in myoglobin. Higher affinity for 0 2 than hemoglobin. Acts as a go-between in the transfer of 0 2 from blood to the mitochondria within muscle cells. May also have an 0 2 storage function in cardiac muscles. Fig. 16.37 Carbon dioxide in blood Dissolved CO 2 : 1/10 Carbaminohemoglobin: 1/5 Bicarbonate: 7/10 23
Fig. 16.38 Figure not in book Figure not in book 24
Fig. 16.39 Fig not in book Adequacy of ventilation Hypoventilation increase in ratio of carbon dioxide production to alveolar ventilation. hypercapnia Hyperventilation decrease in ratio of carbon dioxide production to alveolar ventilation. hypocapnia 25
Respiratory acidosis vs. respiratory alkalosis Respiratory acidosis - increased arterial H + concentration due to CO 2 retention. Metabolic acidosis - increased production of nonvolatile acids or loss of blood bicarbonate, resulting in a fall of blood ph. Respiratory alkalosis - lowering of arterial P CO2 and H + concentration. Metabolic alkalosis - rise in blood ph produced by loss of nonvolatile acids or by excessive accumulation of bicarbonate base. Compensating acidosis or alkalosis. Metabolic acidosis or alkalosis - Respiratory acidosis or alkalosis - 2 groups of chemoreceptors that monitor changes in blood P C02, P 02, and ph. Central: Medulla. Peripheral: Carotid and aortic bodies. Control breathing indirectly via sensory nerve fibers to the medulla. Chemoreceptors Fig. 16.27 26
Fig. not in book Fig. not in book Response to exercise Neurogenic Sensory nerve activity from exercising limbs stimulate respiratory muscles. Input from cerebral cortex stimulates brain stem respiratory centers. Humoral Changes in blood concentrations of gases and signaling molecules. 27
Fig. not in book Hypoxic ventilatory response to high altitude (low P O2 ) produces hyperventilation Increase in tidal volume. Lowers arterial P CO2 Produces respiratory alkalosis which eventually blunts hyperventilatory response. Figure not in book Other respiratory changes due to high altitudes Increased production of 2,3-DPG. Increased production of RBCs and hemoglobin. Barrel-chest 28
Figure not in book Figure not in book 29