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Chapter 16 Respiration Respiration • Functions of the respiratory system – – – – – – – – Breathing. • Gas exchange: – Occurs between air and blood in the lungs. – Occurs between blood and tissues. • 02 utilization: – Cellular respiration. Fig. 16.1 Fig not in book Type I cell Steps in Respiration Type II cell Fig. 16.4 Organization of the respiratory system. • The term respiration includes 3 separate functions: • Ventilation: • 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 1 Respiratory Zone • Region of gas exchange between air and blood. • Includes respiratory bronchioles. • Must contain alveoli. • Gas exchange occurs by diffusion. Figure not in book Fig. 16.4 Figure not in book Fig. 16.8 Ventilation and Lung Mechanics Step 1: Getting air into and out of lungs 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. Fig not in book 2 Really, Really Important Point! Fig not in book • 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. Fig. 16.11 Volume of lungs depends on: • Transpulmonary pressure - difference in pressure between outside and inside of lungs. • Elasticity (stretchability) of lungs. Surface Tension • 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 3 Fig not in book Fig not in book Lung Compliance Fig not in book • CL = magnitude of change in lung volume (ΔVL) produced by a given change in transpulmonary pressure. • CL = ΔVL/Δ (Palv - Pip) • Greater the lung compliance the _______ it is to expand the lungs at any given transpulmonary pressure. 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 H20 molecules. • As alveoli radius decreases, surfactant’s ability to lower surface tension increases. Surfactant Fig. 16.12 4 Pulmonary Function Tests • Assessed by spirometry. • Subject breathes into a closed system in which air is trapped within a bell floating in H20. • The bell moves up when the subject exhales and down when the subject inhales. Fig. 16.14 See also table 16.2 • Tidal volume: Amount of air expired with each breath. • Vital capacity: The maximum amount of air that can be forcefully exhaled after maximum inhalation. Schematic of a spirometer (left) and the spirometer you will be using in lab (above). Spirogram Fig. 16.16 Table 16.3 Terms Used to Describe Lung Volumes and Capacities Term Definition Lung Volumes 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 Tidal volume Inspiratory reserve volume Expiratory reserve volume Residual volume Lung Capacities Total lung capacity Vital capacity Inspiratory capacity Functional residual capacity Figure not in book 5 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 02 concentration is lower than normal and C02 concentration is higher than normal. • Alveolar ventilation: F x (TV- DS) – F = frequency (breaths/min.). – TV = tidal volume. – DS = dead space. 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 Airway resistance and restrictive vs. obstructive disorders • Recall: • F = (Patm - Palv) / R • Resistance depends on: – – – Restrictive and Obstructive Disorders • Restrictive disorder: – Vital capacity is reduced. – FVC is normal. • Obstructive disorder: – VC is normal. – FEV1 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. • PATM = PN2 + P02 + PCo2 = 760 mm Hg – 02 humidified. • H20 contributes to partial pressure (~ 47 mm Hg) – P02 (sea level) = 150 mm Hg. Fig. 16.20 6 Significance of Blood P02 and PC02 Measurements • At normal P02 arterial blood is about 100 mm Hg. • P02 systemic veins = ~ 40 mm Hg. • PC02 systemic veins = ~ 46 mm Hg Figure not in book - Applying numbers to previous figure. Fig. 16.23 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. • PATM = PN2 + P0 + PCo2 = 760 mm Hg Fig. 16.32 Measuring efficacy of lung function. Defining Ventilation • Minute ventilation - total ventilation per minute NOTE these numbers • 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. Fig. 16.23 7 Restrictive and Obstructive Disorders • Restrictive disorder: – Vital capacity is reduced. – FVC is normal. • Obstructive disorder: – VC is normal. – FEV1 is reduced. Fig. 16.17 FEV1 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. Relevance of Partial Pressures • High altitude => _______ in PO2 of inspired air and _________ in alveolar PO2. • Decreased alveolar ventilation => ______ in PO2 of inspired air and ________ in alveolar PO2. • Increased cellular metabolism => ________ in alveolar PO2. Alveolar Gas Pressure • Alveolar PO2 and PCO2 determine the systemic arterial PO2 and PCO2. • Alveolar PO2 values determined by – PO2 of atmospheric air – Rate of alveolar ventilation – Rate of total body oxygen consumption • Alveolar PCO2 values determined by – Rate of alveolar ventilation – Rate of total body carbon dioxide production Getting O2 into and CO2 out of body: the bottom line(s) • In alveoli – PO2 and PCO2 on two sides of alveolar-capillary membrane result in net diffusion, CO2 out and O2 in. – More capillaries involved, more total O2/CO2 exchange. – Need for fewer or greater numbers of alveoli in gas exchange (impairment of gas exchange:O2). 8 Getting O2 into and CO2 out of body: the bottom line(s) • In alveoli – Ventilation-perfusion inequality = mismatching of air supply and blood supply on an individual alveoli. – Lowers PO2 of systemic arterial blood. – Caused by Getting O2 into and CO2 out of body: the bottom line(s) • In tissues – Low PO2 and high PCO2 in tissues results in net movement of O2 into tissues and net CO2 movement out of tissues. • We will revisit this momentarily. • Ventilated blood in alveoli with no blood supply • No blood flowing to some alveoli. – Compensation by vasoconstriction Breathing Lesson (control of breathing) • Medulla oblongata (medullary inspiratory neurons). • Pons • Pulmonary stretch receptors • Peripheral chemoreceptors • Central chemoreceptors 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. 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. • Activity of expiratory neurons inhibit inspiratory neurons. 9 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 Fig. 16.28 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. H2C03 • H20 + C02 H+ + HC03• Rate and depth of ventilation adjusted to maintain arterial PC02 of 40 mm Hg. Chemoreceptors • 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. Fig. 16.27 Can say that chemoreceptor sensitivity to PCO2 is augmented by low PO2. Fig. 16.29 Fig. 16.31 10 Moving Oxygen in Blood • Amount of oxygen dissolved in blood directly proportional to PO2 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 P02 delivery to kidneys. • Loading/unloading depends: – P02 of environment. – Affinity between hemoglobin and 02. • Oxyhemoglobin vs. Deoxyhemoglobin. Fig. 16.34 • So what does pH do to O2 affinity of hemoglobin? • Temperature? • 2,3 DPG = Fig. 16.35 More on 2,3DPG 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” 11 Muscle Myoglobin Inherited defects in hemoglobin • Sickle-cell anemia – Valine substitued for glutamic acid at position #6. – Low PO2 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. • 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 02 storage function in cardiac muscles. Fig. 16.37 Carbon dioxide in blood • Dissolved CO2: 1/10 • Carbaminohemoglobin: 1/5 • Bicarbonate: 7/10 Fig. 16.38 Figure not in book Figure not in book 12 Fig not in book Fig. 16.39 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 Compensating acidosis or alkalosis. • Metabolic acidosis or alkalosis - • Respiratory acidosis or alkalosis - 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 PCO2 and H+ concentration. • Metabolic alkalosis - rise in blood pH produced by loss of nonvolatile acids or by excessive accumulation of bicarbonate base. Chemoreceptors • 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. Fig. 16.27 13 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. Fig. not in book • Hypoxic ventilatory response to high altitude (low PO2) – produces hyperventilation – Increase in tidal volume. – Lowers arterial PCO2 – Produces respiratory alkalosis which eventually “blunts” hyperventilatory response. Other respiratory changes due to high altitudes • Increased production of 2,3-DPG. • Increased production of RBCs and hemoglobin. • “Barrel-chest” Figure not in book 14 Figure not in book Figure not in book 15