Pulmonary Function Tests
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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). -
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. -
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. -
Respiratory Therapy Pocket Reference
Pulmonary Physiology Volume Control Pressure Control Pressure Support Respiratory Therapy “AC” Assist Control; AC-VC, ~CMV (controlled mandatory Measure of static lung compliance. If in AC-VC, perform a.k.a. a.k.a. AC-PC; Assist Control Pressure Control; ~CMV-PC a.k.a PS (~BiPAP). Spontaneous: Pressure-present inspiratory pause (when there is no flow, there is no effect ventilation = all modes with RR and fixed Ti) PPlateau of Resistance; Pplat@Palv); or set Pause Time ~0.5s; RR, Pinsp, PEEP, FiO2, Flow Trigger, rise time, I:E (set Pocket Reference RR, Vt, PEEP, FiO2, Flow Trigger, Flow pattern, I:E (either Settings Pinsp, PEEP, FiO2, Flow Trigger, Rise time Target: < 30, Optimal: ~ 25 Settings directly or by inspiratory time Ti) Settings directly or via peak flow, Ti settings) Decreasing Ramp (potentially more physiologic) PIP: Total inspiratory work by vent; Reflects resistance & - Decreasing Ramp (potentially more physiologic) Card design by Respiratory care providers from: Square wave/constant vs Decreasing Ramp (potentially Flow Determined by: 1) PS level, 2) R, Rise Time ( rise time ® PPeak inspiratory compliance; Normal ~20 cmH20 (@8cc/kg and adult ETT); - Peak Flow determined by 1) Pinsp level, 2) R, 3)Ti (shorter Flow more physiologic) ¯ peak flow and 3.) pt effort Resp failure 30-40 (low VT use); Concern if >40. Flow = more flow), 4) pressure rise time (¯ Rise Time ® Peak v 0.9 Flow), 5) pt effort ( effort ® peak flow) Pplat-PEEP: tidal stress (lung injury & mortality risk). Target Determined by set RR, Vt, & Flow Pattern (i.e. for any set I:E Determined by patient effort & flow termination (“Esens” – PDriving peak flow, Square (¯ Ti) & Ramp ( Ti); Normal Ti: 1-1.5s; see below “Breath Termination”) < 15 cmH2O. -
Respiratory Physiology
Physiology Unit 4 RESPIRATORY PHYSIOLOGY Respiraon • External respiraon – ven3laon – gas exchange • Internal respiraon – cellular respiraon – gas exchange • Respiratory Cycle – Inspiraon • Moving atmospheric air into the lungs – Expiraon • Moving air out of the lungs Lungs vs. Balloons • A lung is similar to a balloon in that it resists stretch, tending to collapse almost totally unless held inflated by a pressure difference between its inside and outside • Lungs and the chest have elas3c proper3es Lung Compliance • Compliance – Elas3city – Tendency to recoil – Tendency of an elas3c structure to oppose stretching or distor3on * Resists distension • Surface tension * Resists distension - Surfactant • Reduces surface tension • Increases compliance (makes them easier to stretch) Airway Resistance F = ΔP/R • Same variables that affect resistance in blood vessels – Tube length, tube radius, fric3on – Tube radius most important factor • Airway resistance is so small that small pressure differences produce large volumes of air flow – Average atmosphere-to-alveoli pressure difference is 1 mmHg, but 500 mL of air is moved (%dal volume) – Low pressure and low resistance • Pulmonary 1/10th of systemic vascular resistance Ven3laon • Exchange of air between atmosphere and alveoli • Atmospheric air pressure is 760 mmHg at sea level • Air moves by bulk flow – F = ΔP/R – F = (Palv – Patm)/R Boyle’s Law • Boyle’s law = (P/V) • Pressure of a given quan3ty of gas is inversely propor3onal to volume • An increase in the volume of the container (lungs) decreases the pressure of the gas (air) Ven3laon Mechanics • Lung volume depends on: 1. Transpulmonary pressure (Ptp) • Inside to outside of the lung • Ptp = Palv – Pip • The force that keeps the lungs inflated • Transmural pressure – Across the wall 2. -
The Effects of Bronchodilators on Pulmonary Ventilation and Diffusion in Asthma and Emphysema
Thorax: first published as 10.1136/thx.14.2.146 on 1 June 1959. Downloaded from Thorax (1959), 14, 146. THE EFFECTS OF BRONCHODILATORS ON PULMONARY VENTILATION AND DIFFUSION IN ASTHMA AND EMPHYSEMA BY GERARD LORRIMAN From Brompton Hospital and the Institute of Diseases of the Chest, London (RECEIVED FOR PUBLICATION SEPTEMBER 22, 1958) Impairment of ventilation and of the distribution capacity. The proportionate responsibility of of inspired air in asthma and emphysema has these two factors is, however, unknown. Little has been reported by many authors (Beitzke, 1925; been published on the diffusing capacity in asthma. Kountz and Alexander, 1934; Darling, Cournand, Bates (1952) measured the percentage uptake of and Richards, 1944; Baldwin, Cournand, and carbon monoxide in 13 young asthmatics aged Richards, 1949; Bates and Christie, 1950; Beale, 12-19 years and found an abnormally low figure Fowler, and Comroe, 1952), and is the result in only one. Ogilvie and others (1957) mention mainly, if not entirely, of obstruction of the one asthmatic patient whose diffusing capacity was airway. Antispasmodics can relieve the obstruction normal. in asthma, and have also been recommended in The objects of the present investigation were to emphysema (Baldwin and others, 1949; Christie, examine the effects of two drugs, isoprenalinecopyright. 1952). Corticotrophin and cortisone - like given by inhalation and prednisone orally, on the substances have been used with benefit in acute ventilation and diffusing capacity in patients with and chronic asthma (Bordley, Carey, Harvey, asthma and emphysema, and to attempt to assess Howard, Kattus, Newman, and Winkenwerder, the degree to which airway obstruction can depress 1949; Friedlaender and Friedlaender, 1951; the diffusing capacity in these disorders. -
Development of Ventilatory Response to Transient Hypercapnia and Hypercapnic Hypoxia in Term Infants
0031-3998/04/5502-0302 PEDIATRIC RESEARCH Vol. 55, No. 2, 2004 Copyright © 2004 International Pediatric Research Foundation, Inc. Printed in U.S.A. Development of Ventilatory Response to Transient Hypercapnia and Hypercapnic Hypoxia in Term Infants SIGNE SØVIK AND KRISTIN LOSSIUS Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, NO-0317 Oslo [S.S.], and Section of Neonatology, Department of Pediatrics, Rikshospitalet, NO–0027 Oslo [K.L.], Norway ABSTRACT Whereas peripheral chemoreceptor oxygen sensitivity in- was unchanged for hypoxia. Response magnitude was unchanged creases markedly after birth, previous studies of ventilatory for hypercapnia, but increased for the two hypoxic stimuli. In responses to CO2 in term infants have shown no postnatal conclusion, an interaction between the effects of hypercapnia and development. However, the hypercapnic challenges applied have hypoxia on ventilatory response rate emerged between postnatal usually been long-term, which meant that the effect of central d 2 and wk 8 in term infants. Concomitantly, stimulus-response chemoreceptors dominated. Oscillatory breathing, apneas, and time to hypercapnic stimuli declined markedly. The development sighs cause transient PCO2 changes, probably primarily stimulat- of a prompt response to transient hypercapnia may be important ing peripheral chemoreceptors. We wanted to assess whether the for infant respiratory stability. (Pediatr Res 55: 302–309, 2004) immediate ventilatory responses to step changes in inspired CO2 and O2 in term infants undergo postnatal developmental changes. Twenty-six healthy term infants were studied during natural Abbreviations sleep 2 d and 8 wk postnatally. Ventilatory responses to a FiCO2, fraction of inspired carbon dioxide randomized sequence of 15 s hypercapnia (3% CO2), hypoxia fR, respiratory rate ϩ (15% O2), and hypercapnic hypoxia (3% CO2 15% O2) were PaCO2, partial pressure of arterial carbon dioxide recorded breath-by-breath using a pneumotachometer. -
Chapter 16 I. the Respiratory System Respiratory System Respiration Gas Exchange in Lungs Alveoli
10/24/11 I. The Respiratory System Chapter 16 Respiratory Physiology Lecture PowerPoint Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Respiratory System Respiration • Includes: • Divided into: – Ventilation (breathing) – Gas exchange between blood and lungs and – Respiratory zone: site of gas exchange between blood and tissues – Oxygen utilization by tissues to make ATP – Conduction zone: gets air to the respiratory • Ventilation and gas exchange in lungs = zone external respiration • Oxygen utilization and gas exchange in tissues = internal respiration Gas Exchange in Lungs Alveoli • Occurs via diffusion • Air sacs in the lungs where gas exchange occurs • O2 concentration is higher in the lungs than in the blood, so O2 diffuses into blood. • 300 million of them – Provide large surface area (760 square feet) to increase diffusion rate • CO2 concentration in the blood is higher than in the lungs, so CO2 diffuses out of blood. 1 10/24/11 Alveoli Alveoli Capillary within alveolar wall Bronchiole and alveoli Alveolar Cells Conducting Zone • Air travels down the nasal cavity Pharynx • Type I: 95−97% total surface area where Larynx gas exchange occurs Trachea Right and left primary bronchi • Type II: secrete pulmonary surfactant and Secondary bronchi reabsorb sodium and water, preventing Tertiary bronchi (more branching) Terminal bronchioles fluid buildup Respiratory zone (respiratory bronchioles Terminal alveolar sacs Respiratory Structures Trachea and Respiratory Bronchi 2 10/24/11 Functions of Conducting Zone Functions of Conducting Zone • Transports air to the lungs • Warms, humidifies, filters, and cleans the air – Mucus traps small particles, and cilia move it away from the lungs. • Voice production in the larynx as air passes over the vocal folds Thoracic Cavity Thoracic Cavity Cross Section • Contains the heart, trachea, esophagus, and thymus within the central mediastinum • The lungs fill the rest of the cavity. -
Aerosol Kinetics and Bronchodilator Efficacy During Continuous Positive Airway Pressure Delivered by Face Mask
Thorax 1997;52:171±175 171 Thorax: first published as 10.1136/thx.52.2.171 on 1 February 1997. Downloaded from Aerosol kinetics and bronchodilator eYcacy during continuous positive airway pressure delivered by face mask Scott N Parkes, Andrew D Bersten Abstract hastened recovery and prevented the need for Background ± Rates of fresh gas ¯ow intubation and mechanical ventilation.1 In a (FGF) commonly used when continuous group of patients with dynamic hyperin¯ation positive airway pressure (CPAP) is de- and intrinsic positive end expiratory pressure livered by face mask theoretically reduce (PEEP) Petrof and co-workers2 found that the the delivery and availability of therapeutic application of CPAP to intubated patients sig- aerosols. As it may be hazardous for ni®cantly reduced respiratory work. It seems patients with acute respiratory failure to likely that non-invasive CPAP will produce a interrupt mask CPAP, the eVects of CPAP similar bene®t in patients with acute severe on aerosol kinetics and bronchodilator asthma or acute exacerbations of chronic air- eYcacy were investigated. ¯ow obstruction. However, therapeutic aero- Method ± The eVect of CPAP at 10 cm H2O sols are central to the management of these at a FGF rate of 50 l/min on the delivery patients, and the concurrent administration of of technetium labelled aerosol generated CPAP may interfere with drug delivery to the from a readily available jet nebuliser was distal airway. measured using a bench model of spon- Mask CPAP is optimally applied through a taneous respiration. In a separate clinical continuous fresh gas ¯ow (FGF) circuit as this study the bronchodilator responses to in- imposes less additional work than a demand cremental doses of nebulised salbutamol valve system34 and compensates more eY- were measured in nine stable asthmatic ciently for potential gas leaks around the mask. -
The Chemoreflex Control of Breathing and Its Measurement
933 Continuing Medical Education The chemoreflex control of breathing James Duffin PhD and measurement The chemoreflex control of breathing is described in terms of a Le contrrle chimiorEflexe de la respiration est dEcrit comme un graphical model. The central chemoreflex, the ventilatory modEle graphique. Le centre chimiordflexe, #1 rEponse respira- response to carbon dioxide mediated by the central chemorecep- toire au C02 mEdiEe par les chEmorEcepteurs centrmLr sont tors, is modelled as a straight-line relation between the dEcrits comme une relation directe entre la rEponse respira- ventilatory response and the arterial level of carbon dioxide. toire et les niveaux de C02 artdriels. Le chimior~flexe ptariph~- The peripheral chemoreflex, the ventilatory response to carbon rique, la r~ponse ventilatoire au C02 et I'hypoxie mddi~s par les dioxide and hypoxia mediated by the peripheral chemorecep- chEmorEcepteurs p~riph~riques sont subdivis~es en deux rela- tors, is broken into two relations. First, a straight.line relation tions. PremiErement, une relation directe entre la rdponse between the ventilatory response and the arterial level of carbon ventilatoire et le niveau artEriel de COz dont la pente (sensiti- dioxide whose slope (sensitivity) increases as the oxygen level vitE) augmente a vec les variations du niveau d' oxygEne d' hyper- varies from hyperoxic to hypoxic. Second, a rectangular oxique c} hypoxique. Deuxidmement, une relation hyperbolique hyperbolic relation between the ventilatory response and the rectangulaire entre la rdponse respiratoire et le niveau artEriel arterial level of oxygen with ventilation increasing with increas- d' oxygOne avecla ventilation augmentant avec I' augmentation ing hypoxia. The three ventilatory response relations (one de l'hypoxie. -
Respiratory Gas Exchange in the Lungs
RESPIRATORY GAS EXCHANGE Alveolar PO2 = 105 mmHg; Pulmonary artery PO2 = 40 mmHg PO2 gradient across respiratory membrane 65 mmHg (105 mmHg – 40 mmHg) Results in pulmonary vein PO2 ~100 mmHg Partial Pressures of Respiratory Gases • According to Dalton’s law, in a gas mixture, the pressure exerted by each individual gas is independent of the pressures of other gases in the mixture. • The partial pressure of a particular gas is equal to its fractional concentration times the total pressure of all the gases in the mixture. • Atmospheric air : Oxygen constitutes 20.93% of dry atmospheric air. At a standard barometric pressure of 760 mm Hg, PO2 = 0.2093 × 760 mm Hg = 159 mm Hg Similarly , PCO2= 0.3 mm Hg PN2= 600 mm Hg Inspired Air: PIO2= FIO2 (PB-PH2O)= 0.2093 (760-47)= 149 mm Hg PICO2= 0.3 mm Hg PIN2= 564 mm Hg Alveolar air at standard barometric pressure • 2.5 to 3 L of gas is already in the lungs at the FRC and the approximately 350 mL per breath enters the alveoli with every breath. • About 250 mL of oxygen continuously diffuses from the alveoli into the pulmonary capillary blood per minute at rest and 200 mL of carbon dioxide diffuses from the mixed venous blood in the pulmonary capillaries into the alveoli per minute. • The PO2 and PCO2 of mixed venous blood are about 40 mm Hg and 45 to 46 mm Hg, respectively • The PO2 and PCO2 in the alveolar air are determined by the alveolar ventilation, the pulmonary capillary perfusion, the oxygen consumption, and the carbon dioxide production.