Chapter 22 the Respiratory System
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Solutes and Solution
Solutes and Solution The first rule of solubility is “likes dissolve likes” Polar or ionic substances are soluble in polar solvents Non-polar substances are soluble in non- polar solvents Solutes and Solution There must be a reason why a substance is soluble in a solvent: either the solution process lowers the overall enthalpy of the system (Hrxn < 0) Or the solution process increases the overall entropy of the system (Srxn > 0) Entropy is a measure of the amount of disorder in a system—entropy must increase for any spontaneous change 1 Solutes and Solution The forces that drive the dissolution of a solute usually involve both enthalpy and entropy terms Hsoln < 0 for most species The creation of a solution takes a more ordered system (solid phase or pure liquid phase) and makes more disordered system (solute molecules are more randomly distributed throughout the solution) Saturation and Equilibrium If we have enough solute available, a solution can become saturated—the point when no more solute may be accepted into the solvent Saturation indicates an equilibrium between the pure solute and solvent and the solution solute + solvent solution KC 2 Saturation and Equilibrium solute + solvent solution KC The magnitude of KC indicates how soluble a solute is in that particular solvent If KC is large, the solute is very soluble If KC is small, the solute is only slightly soluble Saturation and Equilibrium Examples: + - NaCl(s) + H2O(l) Na (aq) + Cl (aq) KC = 37.3 A saturated solution of NaCl has a [Na+] = 6.11 M and [Cl-] = -
Job Hazard Analysis
Identifying and Evaluating Hazards in Research Laboratories Guidelines developed by the Hazards Identification and Evaluation Task Force of the American Chemical Society’s Committee on Chemical Safety Copyright 2013 American Chemical Society Table of Contents FOREWORD ................................................................................................................................................... 3 ACKNOWLEDGEMENTS ................................................................................................................................. 5 Task Force Members ..................................................................................................................................... 6 1. SCOPE AND APPLICATION ..................................................................................................................... 7 2. DEFINITIONS .......................................................................................................................................... 7 3. HAZARDS IDENTIFICATION AND EVALUATION ................................................................................... 10 4. ESTABLISHING ROLES AND RESPONSIBILITIES .................................................................................... 14 5. CHOOSING AND USING A TECHNIQUE FROM THIS GUIDE ................................................................. 17 6. CHANGE CONTROL .............................................................................................................................. 19 7. ASSESSING -
Human Physiology an Integrated Approach
Gas Exchange and Transport Gas Exchange in the Lungs and Tissues 18 Lower Alveolar P Decreases Oxygen Uptake O2 Diff usion Problems Cause Hypoxia Gas Solubility Aff ects Diff usion Gas Transport in the Blood Hemoglobin Binds to Oxygen Oxygen Binding Obeys the Law of Mass Action Hemoglobin Transports Most Oxygen to the Tissues P Determines Oxygen-Hb Binding O2 Oxygen Binding Is Expressed As a Percentage Several Factors Aff ect Oxygen-Hb Binding Carbon Dioxide Is Transported in Three Ways Regulation of Ventilation Neurons in the Medulla Control Breathing Carbon Dioxide, Oxygen, and pH Infl uence Ventilation Protective Refl exes Guard the Lungs Higher Brain Centers Aff ect Patterns of Ventilation The successful ascent of Everest without supplementary oxygen is one of the great sagas of the 20th century. — John B. West, Climbing with O’s , NOVA Online (www.pbs.org) Background Basics Exchange epithelia pH and buff ers Law of mass action Cerebrospinal fl uid Simple diff usion Autonomic and somatic motor neurons Structure of the brain stem Red blood cells and Giant liposomes hemoglobin of pulmonary Blood-brain barrier surfactant (40X) From Chapter 18 of Human Physiology: An Integrated Approach, Sixth Edition. Dee Unglaub Silverthorn. Copyright © 2013 by Pearson Education, Inc. All rights reserved. 633 Gas Exchange and Transport he book Into Thin Air by Jon Krakauer chronicles an ill- RUNNING PROBLEM fated trek to the top of Mt. Everest. To reach the summit of Mt. Everest, climbers must pass through the “death zone” T High Altitude located at about 8000 meters (over 26,000 ft ). Of the thousands of people who have attempted the summit, only about 2000 have been In 1981 a group of 20 physiologists, physicians, and successful, and more than 185 have died. -
Mechanisms of Pulmonary Gas Exchange Abnormalities During Experimental Group B Streptococcal Infusion
003 I -3998/85/1909-0922$02.00/0 PEDIATRIC RESEARCH Vol. 19, No. 9, I985 Copyright 0 1985 International Pediatric Research Foundation, Inc. Printed in (I.S. A. Mechanisms of Pulmonary Gas Exchange Abnormalities during Experimental Group B Streptococcal Infusion GREGORY K. SORENSEN, GREGORY J. REDDING, AND WILLIAM E. TRUOG ABSTRACT. Group B streptococcal sepsis in newborns obtained from GBS (5, 6). Arterial Poz fell by 9 torr in association produces pulmonary arterial hypertension and hypoxemia. with the increase in pulmonary arterial pressure (4). In contrast, The purpose of this study was to investigate the mecha- the neonatal piglet infused with GBS demonstrated both pul- nisms by which hypoxemia occurs. Ten anesthetized, ven- monary arterial hypertension and profound arterial hypoxemia tilated piglets were infused with 2 x lo9 colony forming (7). These results suggest that the neonatal pulmonary vascula- unitstkg of Group B streptococci over a 30-min period. ture may respond to bacteremia differently from that of adults. Pulmonary arterial pressure rose from 14 ? 2.8 to 38 ? The relationship between Ppa and the matching of alveolar 6.7 torr after 20 min of the bacterial infusion (p< 0.01). ventilation and pulmonary perfusion, a major determinant of During the same period, cardiac output fell from 295 to arterial oxygenation during room air breathing (8), has not been 184 ml/kg/min (p< 0.02). Arterial Po2 declined from 97 studied in newborns. The predictable rise in Ppa with an infusion 2 7 to 56 2 11 torr (p< 0.02) and mixed venous Po2 fell of group B streptococcus offers an opportunity to delineate the from 39.6 2 5 to 28 2 8 torr (p< 0.05). -
Page 1 of 6 This Is Henry's Law. It Says That at Equilibrium the Ratio of Dissolved NH3 to the Partial Pressure of NH3 Gas In
CHMY 361 HANDOUT#6 October 28, 2012 HOMEWORK #4 Key Was due Friday, Oct. 26 1. Using only data from Table A5, what is the boiling point of water deep in a mine that is so far below sea level that the atmospheric pressure is 1.17 atm? 0 ΔH vap = +44.02 kJ/mol H20(l) --> H2O(g) Q= PH2O /XH2O = K, at ⎛ P2 ⎞ ⎛ K 2 ⎞ ΔH vap ⎛ 1 1 ⎞ ln⎜ ⎟ = ln⎜ ⎟ − ⎜ − ⎟ equilibrium, i.e., the Vapor Pressure ⎝ P1 ⎠ ⎝ K1 ⎠ R ⎝ T2 T1 ⎠ for the pure liquid. ⎛1.17 ⎞ 44,020 ⎛ 1 1 ⎞ ln⎜ ⎟ = − ⎜ − ⎟ = 1 8.3145 ⎜ T 373 ⎟ ⎝ ⎠ ⎝ 2 ⎠ ⎡1.17⎤ − 8.3145ln 1 ⎢ 1 ⎥ 1 = ⎣ ⎦ + = .002651 T2 44,020 373 T2 = 377 2. From table A5, calculate the Henry’s Law constant (i.e., equilibrium constant) for dissolving of NH3(g) in water at 298 K and 340 K. It should have units of Matm-1;What would it be in atm per mole fraction, as in Table 5.1 at 298 K? o For NH3(g) ----> NH3(aq) ΔG = -26.5 - (-16.45) = -10.05 kJ/mol ΔG0 − [NH (aq)] K = e RT = 0.0173 = 3 This is Henry’s Law. It says that at equilibrium the ratio of dissolved P NH3 NH3 to the partial pressure of NH3 gas in contact with the liquid is a constant = 0.0173 (Henry’s Law Constant). This also says [NH3(aq)] =0.0173PNH3 or -1 PNH3 = 0.0173 [NH3(aq)] = 57.8 atm/M x [NH3(aq)] The latter form is like Table 5.1 except it has NH3 concentration in M instead of XNH3. -
CARBON MONOXIDE: the SILENT KILLER Information You Should
CARBON MONOXIDE: THE SILENT KILLER Information You Should Know Carbon monoxide is a silent killer that can lurk within fossil fuel burning household appliances. Many types of equipment and appliances burn different types of fuel to provide heat, cook, generate electricity, power vehicles and various tools, such as chain saws, weed eaters and leaf blowers. When these units operate properly, they use fresh air for combustion and vent or exhaust carbon dioxide. When fresh air is restricted, through improper ventilation, the units create carbon monoxide, which can saturate the air inside the structure. Carbon Monoxide can be lethal when accidentally inhaled in concentrated doses. Such a situation is referred to as carbon monoxide poisoning. This is a serious condition that is a medical emergency that should be taken care of right away. What Is It? Carbon monoxide, often abbreviated as CO, is a gas produced by burning fossil fuel. What makes it such a silent killer is that it is odorless and colorless. It is extremely difficult to detect until the body has inhaled a detrimental amount of the gas, and if inhaled in high concentrations, it can be fatal. Carbon monoxide causes tissue damage by blocking the body’s ability to absorb enough oxygen. In fact, poisoning from this gas is one of the leading causes of unintentional death from poison. Common Sources of CO Kerosene or fuel-based heaters Fireplaces Gasoline powered equipment and generators Charcoal grills Automobile exhaust Portable generators Tobacco smoke Chimneys, furnaces, and boilers Gas water heaters Wood stoves and gas stoves Properly installed and maintained appliances are safe and efficient. -
Oxygenation and Oxygen Therapy
Rules on Oxygen Therapy: Physiology: 1. PO2, SaO2, CaO2 are all related but different. 2. PaO2 is a sensitive and non-specific indicator of the lungs’ ability to exchange gases with the atmosphere. 3. FIO2 is the same at all altitudes 4. Normal PaO2 decreases with age 5. The body does not store oxygen Therapy & Diagnosis: 1. Supplemental O2 is an FIO2 > 21% and is a drug. 2. A reduced PaO2 is a non-specific finding. 3. A normal PaO2 and alveolar-arterial PO2 difference (A-a gradient) do NOT rule out pulmonary embolism. 4. High FIO2 doesn’t affect COPD hypoxic drive 5. A given liter flow rate of nasal O2 does not equal any specific FIO2. 6. Face masks cannot deliver 100% oxygen unless there is a tight seal. 7. No need to humidify if flow of 4 LPM or less Indications for Oxygen Therapy: 1. Hypoxemia 2. Increased work of breathing 3. Increased myocardial work 4. Pulmonary hypertension Delivery Devices: 1. Nasal Cannula a. 1 – 6 LPM b. FIO2 0.24 – 0.44 (approx 4% per liter flow) c. FIO2 decreases as Ve increases 2. Simple Mask a. 5 – 8 LPM b. FIO2 0.35 – 0.55 (approx 4% per liter flow) c. Minimum flow 5 LPM to flush CO2 from mask 3. Venturi Mask a. Variable LPM b. FIO2 0.24 – 0.50 c. Flow and corresponding FIO2 varies by manufacturer 4. Partial Rebreather a. 6 – 10 LPM b. FIO2 0.50 – 0.70 c. Flow must be sufficient to keep reservoir bag from deflating upon inspiration 5. -
Respiratory Physiology - Part B Experimental Determination of Anatomical Dead Space Value (Human 9 - Version Sept
Comp. Vert. Physiology- BI 244 Respiratory Physiology - Part B Experimental Determination of Anatomical Dead Space Value (Human 9 - Version Sept. 10, 2013) [This version has been modified to also serve as a tutorial in how to run HUMAN's artificial organs] Part of the respiratory physiology computer simulation work for this week allows you to obtain a hand-on feeling for the effects of anatomical dead space on alveolar ventilation. The functional importance of dead space can explored via employing HUMAN's artificial respirator to vary the respiration rate and tidal volume. DEAD SPACE DETERMINATION Introduction The lack of unidirectional respiratory medium flow in non-avian air ventilators creates the existence of an anatomical dead space. The anatomical dead space of an air ventilator is a fixed volume not normally under physiological control. However, the relative importance of dead space is adjustable by appropriate respiratory maneuvers. For example, recall the use by panting animals of their dead space to reduce a potentially harmful respiratory alkalosis while hyperventilating. In general, for any given level of lung ventilation, the fraction of the tidal volume attributed to dead space will affect the resulting level of alveolar ventilation, and therefore the efficiency (in terms of gas exchange) of that ventilation. [You should, of course, refresh your knowledge of total lung ventilation, tidal volume alveolar ventilation.] Your objective here is to observe the effects of a constant "unknown" dead space on resulting alveolar ventilation by respiring the model at a variety of tidal volume-frequency combinations. You are then asked to calculate the functional dead space based on the data you collect. -
17 the Respiratory System
Mechanics of Breathing The Respiratory System 17 Bones and Muscles of the Thorax Surround the Lungs Pleural Sacs Enclose the Lungs Airways Connect Lungs to the External Environment The Airways Warm, Humidify, and Filter Inspired Air Alveoli Are the Site of Gas Exchange Pulmonary Circulation Is High-Flow, Low-Pressure G a s L a w s Air Is a Mixture of Gases Gases Move Down Pressure Gradients Boyle’s Law Describes Pressure-Volume Relationships Ventilation Lung Volumes Change During Ventilation During Ventilation, Air Flows Because of Pressure Gradients Inspiration Occurs When Alveolar Pressure Decreases Expiration Occurs When Alveolar Pressure Increases Intrapleural Pressure Changes During Ventilation Lung Compliance and Elastance May Change in Disease States Surfactant Decreases the Work of Breathing Airway Diameter Determines Airway Resistance Rate and Depth of Breathing Determine the Effi ciency of Breathing Gas Composition in the Alveoli Varies Little During Normal Breathing Ventilation and Alveolar Blood Flow Are Matched Auscultation and Spirometry Assess Pulmonary Function This being of mine, whatever it really is, consists of a little fl esh, a little breath, and the part which governs. — Marcus Aurelius Antoninus ( C . E . 121–180) Background Basics Ciliated and exchange epithelia Pressure, volume, fl ow, and resistance Pulmonary circulation Surface tension Colored x-ray of the lung Autonomic and somatic showing the motor neurons branching Velocity of fl ow airways. 600 Mechanics of Breathing magine covering the playing surface of a racquetball court cavity to control their contact with the outside air. Internalization (about 75 m2 ) with thin plastic wrap, then crumpling up the creates a humid environment for the exchange of gases with the wrap and stuffi ng it into a 3-liter soft drink bottle. -
Risk Assessment of Recirculation Systems in Salmonid Hatcheries
Norwegian Scientific Committee for Food Safety (VKM) Doc.no 09/808-Final Risk Assessment of Recirculation Systems in Salmonid Hatcheries Opinion of the Panel on Animal Health and Welfare of the Norwegian Scientific Committee for Food Safety Date: 10.01.12 Doc. no.: 09-808-Final ISBN: 978-82-8259-048-8 VKM Report 2012: 01 1 Norwegian Scientific Committee for Food Safety (VKM) Doc.no 09/808-Final Risk Assessment of Recirculation Systems in Salmonid Hatcheries Brit Hjeltnes (chair of ad hoc group) Grete Bæverfjord Ulf Erikson Stein Mortensen Trond Rosten Peter Østergård 2 Norwegian Scientific Committee for Food Safety (VKM) Doc.no 09/808-Final Contributors Persons working for VKM, either as appointed members of the Committee or as ad hoc experts, do this by virtue of their scientific expertise, not as representatives for their employers. The Civil Services Act instructions on legal competence apply for all work prepared by VKM. Acknowledgements The Norwegian Scientific Committee for Food Safety (Vitenskapskomiteen for mattrygghet, VKM) has appointed an ad hoc group consisting of both VKM members and external experts to answer the request from the Norwegian Food Safety Authority. The members of the ad hoc group are acknowledged for their valuable work on this opinion. The members of the ad hoc group are: VKM members Brit Hjeltnes (Chair), Panel on Animal Health and Welfare Ulf Erikson, Panel on Animal Health and Welfare Stein Mortensen, Panel on Animal Health and Welfare External experts Grete Bæverfjord, Nofima Marin, Sunndalsøra Trond Rosten, SINTEF Fisheries and Aquaculture Peter Østergård, Sp/F Aquamed, Faroe Islands Other contributors to the assessment are Frode Mathisen, Anders Fjellheim and Brit Tørud. -
Absolute Measurements of Cerebral Perfusion and Oxygenation in Rats with Near-Infrared Spectroscopy Bertan Hallacoglu1, Angelo Sassaroli1, Irwin H
Absolute measurements of cerebral perfusion and oxygenation in rats with near-infrared spectroscopy Bertan Hallacoglu1, Angelo Sassaroli1, Irwin H. Rosenberg2, Aron Troen2 and Sergio Fantini1 Tufts University Department of Biomedical Engineering, Medford, MA (1) and USDA Human Nutrition Research Center on Aging, Boston, MA (2) Brain microvascular pathology is a common finding in Alzheimer’s disease and other dementias. However, Figure 2 – Time traces of [Hb], [HbO2], [HbT], StO2 and SaO2 during the hypoxia and hypercapnia protocols 10 and 20 weeks after Figure 3 – Illustration of the differences in animal groups and the extent to which microvascular abnormalities cause or contribute to cognitive impairment is unclear. the start of folate deficient diet (blue and red lines represent the mean values for each dietary group, whereas, dashed lines indicate changes within each group between weeks 10 and 20 in Dietary vascular risk factors, including poor folate status are potentially modifiable predictors of cognitive the range corresponding to ± one standard error from the mean). A first striking result is the consistency of baseline values across cerebral tissue saturation (StO2) and concentration of impairment among older adults. Folate deficiency in rat impairs cognition and causes cerebral animals within a group (control or folate deficient), and the reproducibility of baseline values measured at weeks 10 and 20. hemoglobin ([HbT]), blood concentration of hemoglobin ([HbT]b), microvascular damage, without concomitant neurodegeneration [1]. We hypothesized that folate Absolute brain total hemoglobin concentration ([HbT]) and tissue oxygen saturation (StO2) are significantly reduced by folate and partial blood volume (Vb/Vt) Eq. (1). FD rats have deficiency might result in functional decrements in cerebral oxygen delivery and vascular reactivity. -
Epidemiology and Pulmonary Physiology of Severe Asthma
Epidemiology and Pulmonary Physiology of Severe Asthma a b Jacqueline O’Toole, DO , Lucas Mikulic, MD , c, David A. Kaminsky, MD * KEYWORDS Demographics Phenotype Health care utilization Pulmonary function Lung elastic recoil Ventilation heterogeneity Gas trapping Airway hyperresponsiveness KEY POINTS The definition of severe asthma is still a work in progress. The severity of asthma is predictive of higher health care utilization. Cluster analysis is useful in characterizing severe asthma phenotypes. Airway hyperresponsiveness in severe asthma is a result of abnormal airflow, lung recoil, ventilation, and gas trapping. Patients with severe asthma may have a reduced perception of dyspnea. INTRODUCTION Severe asthma is a characterized by a complex set of clinical, demographic, and physiologic features. In this article, we review both the epidemiology and pulmonary physiology associated with severe asthma. DEMOGRAPHICS OF SEVERE ASTHMA Asthma has long been recognized as a worldwide noncommunicable disease of importance. Within the population of individuals with asthma, there is a subgroup of individuals at high risk for complications, exacerbations, and a poor quality of life. The authors have nothing to disclose. a Department of Medicine, University of Vermont Medical Center, 111 Colchester Avenue, Bur- lington, VT 05401, USA; b Division of Pulmonary and Critical Care Medicine, University of Ver- mont Medical Center, Given D208, 89 Beaumont Avenue, Burlington, VT 05405, USA; c Division of Pulmonary and Critical Care Medicine, University of Vermont College of Medicine, Given D213, 89 Beaumont Avenue, Burlington, VT 05405, USA * Corresponding author. E-mail address: [email protected] Immunol Allergy Clin N Am 36 (2016) 425–438 http://dx.doi.org/10.1016/j.iac.2016.03.001 immunology.theclinics.com 0889-8561/16/$ – see front matter Ó 2016 Elsevier Inc.