Pulmonary: Control of Ventilation
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
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. -
Physiologic Effects of Noninvasive Ventilation
Physiologic Effects of Noninvasive Ventilation Neil R MacIntyre Introduction NIV Can Augment Minute Ventilation NIV Unloads Ventilatory Muscles NIV Resets the Ventilatory Control System Alveolar Recruitment and Gas Exchange Other Physiologic Effects of NIV: Intended and Unintended Maintaining Upper-Airway Patency Reducing Imposed Triggering Loads From Auto-PEEP Cardiac Interactions: Both Beneficial and Harmful Ventilator-Induced Lung Injury Production of Auto-PEEP Patient-Ventilator Interactions Summary Noninvasive ventilation (NIV) has a number of physiologic effects similar to invasive ventilation. The major effects are to augment minute ventilation and reduce muscle loading. These effects, in turn, can have profound effects on the patient’s ventilator control system, both acutely and chron- ically. Because NIV can be supplied with PEEP, the maintenance of alveolar recruitment is also made possible and the triggering load imposed by auto-PEEP can be reduced. NIV (or simply mask CPAP) can maintain upper-airway patency during sleep in patients with obstructive sleep apnea. NIV can have multiple effects on cardiac function. By reducing venous return, it can help in patients with heart failure or fluid overload, but it can compromise cardiac output in others. NIV can also increase right ventricular afterload or function to reduce left ventricular afterload. Potential det- rimental physiologic effects of NIV are ventilator-induced lung injury, auto-PEEP development, and discomfort/muscle overload from poor patient–ventilator interactions. Key words: invasive ventilation; noninvasive ventilation; minute and alveolar ventilation; ventilation distribution; ventilation-perfusion match- ing; control of ventilation; ventilatory muscles; work of breathing; patient–ventilator interactions; ventilator- induced lung injury. [Respir Care 2019;64(6):617–628. -
Control of Respiration Central Control of Ventilation
Control of Respiration Control of Respiration Bioengineering 6000 CV Physiology Central Control of Ventilation • Goal: maintain sufficient ventilation with minimal energy – Ventilation should match perfusion • Process steps: – Ventilation mechanics + aerodynamics • Points of Regulation – Breathing rate and depth, coughing, swallowing, breath holding – Musculature: very precise control • Sensors: – Chemoreceptors: central and peripheral – Stretch receptors in the lungs, bronchi, and bronchioles • Feedback: – Nerves – Central processor: • Pattern generator of breathing depth/amplitude • Rhythm generator for breathing rate Control of Respiration Bioengineering 6000 CV Physiology Peripheral Chemosensors • Carotid and Aortic bodies • Sensitive to PO2, PsCO2, and pH (CO2 sensitivity may originate in pH) • Responses are coupled • Adapt to CO2 levels • All O2 sensing is here! • Carotid body sensors more sensitive than aortic bodies Control of Respiration Bioengineering 6000 CV Physiology O2 Sensor Details • Glomus cells • K-channel with O2 sensor • O2 opens channel and hyperpolarizes cell • Drop in O2 causes reduction in K current and a depolarization • Resulting Ca2+ influx triggers release of dopamine • Dopamine initiates action potentials in sensory nerve Control of Respiration Bioengineering 6000 CV Physiology Central CO2/pH Chemoreceptors • Sensitive to pH in CSF • CSF poorly buffered • H+ passes poorly through BBB but CO2 passes easily • Blood pH transmitted via CO2 to CSF • Adapt to elevated CO2 levels (reduced pH) by transfer of - - HCO3 -
Statistical Mechanics I: Exam Review 1 Solution
8.333: Statistical Mechanics I Fall 2007 Test 1 Review Problems The first in-class test will take place on Wednesday 9/26/07 from 2:30 to 4:00 pm. There will be a recitation with test review on Friday 9/21/07. The test is ‘closed book,’ but if you wish you may bring a one-sided sheet of formulas. The test will be composed entirely from a subset of the following problems. Thus if you are familiar and comfortable with these problems, there will be no surprises! ******** You may find the following information helpful: Physical Constants 31 27 Electron mass me 9.1 10− kg Proton mass mp 1.7 10− kg ≈ × 19 ≈ × 34 1 Electron Charge e 1.6 10− C Planck’s const./2π ¯h 1.1 10− Js− ≈ × 8 1 ≈ × 8 2 4 Speed of light c 3.0 10 ms− Stefan’s const. σ 5.7 10− W m− K− ≈ × 23 1 ≈ × 23 1 Boltzmann’s const. k 1.4 10− JK− Avogadro’s number N 6.0 10 mol− B ≈ × 0 ≈ × Conversion Factors 5 2 10 4 1atm 1.0 10 Nm− 1A˚ 10− m 1eV 1.1 10 K ≡ × ≡ ≡ × Thermodynamics dE = T dS+dW¯ For a gas: dW¯ = P dV For a wire: dW¯ = Jdx − Mathematical Formulas √π ∞ n αx n! 1 0 dx x e− = αn+1 2 ! = 2 R 2 2 2 ∞ x √ 2 σ k dx exp ikx 2σ2 = 2πσ exp 2 limN ln N! = N ln N N −∞ − − − →∞ − h i h i R n n ikx ( ik) n ikx ( ik) n e− = ∞ − x ln e− = ∞ − x n=0 n! � � n=1 n! � �c P 2 4 P 3 5 cosh(x) = 1 + x + x + sinh(x) = x + x + x + 2! 4! · · · 3! 5! · · · 2πd/2 Surface area of a unit sphere in d dimensions Sd = (d/2 1)! − 1 1. -
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. -
The Effect of Anemia on the Ventilatory Response to Transient and Steady-State Hypoxia
The effect of anemia on the ventilatory response to transient and steady-state hypoxia. T V Santiago, … , N H Edelman, A P Fishman J Clin Invest. 1975;55(2):410-418. https://doi.org/10.1172/JCI107945. Research Article The effects of anemia upon the ventilatory responses to transient and steady-state hypoxia were studied in unanesthetized goats. Responses to transient hypoxia (inhalation of several breaths of nitrogen) were considered to reflect peripheral chemoreceptor and non-chemoreceptor influences of hypoxia upon ventilatory control. In all goats, severe anemia (hemoglobin 3.1-4.8 g/100ml) markedly heightened the responses to transient hypoxia (from a mean of 0.27 to a mean of 0.75 liter/min/percent fall in SaO2). This phenomenon was substantially reversed by alpha-adrenergic blockade (phenoxybenzamine, 5 mg/kg). In contrast, the ventilatory responses to steady-state hypoxia were unaffected by severe anemia. These data suggest that severe anemia enhances the peripheral chemoreceptor-mediated response to hypoxia through a mechanism involving the alpha-adrenergic system. It also appears that a ventilatory depressant effect of hypoxia which is not mediated by the peripheral chemoreceptors is also enhanced by severe anemia, thereby preventing an increase in the steady-state ventilatory response to hypoxia. Finally, experiments involving variation in oxygen affinity of hemoglobin suggested that O2 tension rather than O2 availability in arterial blood is the major determinant of peripheral chemoreceptor activity. Find the latest version: https://jci.me/107945/pdf The Effect of Anemia on the Ventilatory Response to Transient and Steady-State Hypoxia TEODORO V. SANTIAGO, NORMAN H. -
Respiration the Main Function of the Respiratory System Is Gas Exchange
Respiration The main function of the respiratory system is gas exchange. Gas exchange is achieved through a process called respiration, or breathing. The cardiovascular system and the respiratory system work together to accomplish respiration. External Respiration During external respiration, fresh oxygen from outside the body fills the lungs and alveoli, and carbon dioxide is transported from the body tissues to the lungs. For oxygen to reach the body’s tissues and carbon dioxide to leave the body, gas exchange must occur in the alveolar capillary membrane. The alveoli and the capillaries that surround them make up the alveolar (al-VEE-oh-lar) capillary membrane (Figure 9.5 in the textbook). The alveolar capillary membrane is built for gas exchange, as explained by Fick’s Law. Fick’s Law states that the diffusion of oxygen and carbon dioxide between the capillaries and the alveolar sacs is proportional to the surface area (S.A.) of the lungs, the diffusion constant (D) of each gas, and the difference in partial pressure between each capillary and alveolar sac (P1-P2). According to this law, the diffusion of gases is also inversely related to the thickness of the tissues (T) involved. In simpler terms, thin-walled tissues allow for easier gas exchange. Diffusion = Therefore, oxygen easily diffuses across the membrane of the alveolar sacs and into the capillaries. Carbon dioxide passes from the capillaries into the alveolar sacs, where it can be expelled from the body via the lungs (Figure 9.5). How fast does gas exchange occur in the lungs? Faster than you might think. -
Interfaces in Aquatic Ecosystems: Implications for Transport and Impact of I Anthropogenic Compounds Luhbds-«6KE---C)I‘> "Rol°
Interfaces in aquatic ecosystems: Implications for transport and impact of I anthropogenic compounds luhbDS-«6KE---c)I‘> "rol° STER DISTfiStihON OF THIS DOCUMENT iS UNUMITED % In memory of Fetter, victim of human negligence and To my family andfriends Organization Document name LUND UNIVERSITY DOCTORAL DISSERTATION Department of Ecology Date of issue November 19, 1996 Chemical Ecology and Ecotoxicology Ecology Building CODEN: SE- LUNBDS/NBKE-96/1010+136 S-223 62 Lund, Sweden Authors) Sponsoring organization Swedish Environ JOHANNES KNULST mental Research Institute (IVL) Title and subtitle Interfaces in aquatic ecosystems : Implications for transport and impact of anthropogenic compounds Abstract Mechanisms that govern transport, accumulation and toxicity of persistent pollutants at interfaces in aquatic ecosystems were the foci of this thesis . Specific attention was paid to humic substances, their occurrence, composition, and role in exchange processes across interfaces. It was concluded that: The composition of humic substances in aquatic surface microlavers is different from that of the subsurface water and terrestrial humic mat ter. Levels of dissolved organic carbon (DOC)in the aquatic surface micro layer reflect the DOC levels in the subsurface water. While the levels and enrichment of DOC in the microlaver generally show small variations, the levels and enrichment of particulate organic car bon (POC) vary to a great extent. Similarities exist between aquatic surface films, artificial semi-per meable and biological membranes regarding their structure and function ing. Acidification and liming of freshwater ecosystems affect DOC:POC ratio and humic composition of the surface film, thus influencing the parti tioning of pollutants across aquatic interfaces. 21 Properties of lake catchment areas extensively govern DOC:POC ratio both 41 in the surface film and subsurface water. -
Laboratory: Archimedes' Principle
Phy1401: General Physics I Laboratory Page 1 of 4 Laboratory: Archimedes' Principle Introduction: Eureka!! In this lab your goal is to perform some experiments to understand the source of Archimedes’ excitement when he discovered that the buoyant force on an object in a liquid is equal to the weight of the liquid that the object displaces. Archimedes made his discovery without the benefit of Newton's insights. He was arguably the premier scientist of antiquity. Since you have Newton's achievements as part of your intellectual heritage (Phy211) we'll use the concepts of force and equilibrium to measure the buoyant force acting on a (partially or totally) submerged object. Here is the idea behind the experiment. Suppose we hang a small mass from a force sensor, arranged in the configuration shown in the figure below. The bob in the liquid may be partially or totally submerged. H2O Force Sensor mass graduated cylinder According to Archimedes, the upward buoyant force (FB), which the liquid exerts on the object, is equal to the weight of the fluid displaced or: FB = mfluidg = (ρfluidV)g (1). It should be noted, the buoyant force produced by the displacement of fluid in the cylinder will result in a reaction force of equal but opposite magnitude exerted by the bob on the rd liquid (according to Newton’s 3 Law). We will use this action-reaction relation to measure the buoyant “reaction” force with a standard digital scale. While the mass is hanging, the force sensor will measure the tension in the string (FT1), which should be equal to the weight of the suspended mass. -
Floating with Surface Tension from Archimedes to Keller
FLOATING WITH SURFACE TENSION FROM ARCHIMEDES TO KELLER Dominic Vella Mathematical Institute, University of Oxford 1 GFD Newsletter 2006 Faculty of Walsh College JBK @ WHOI Joe was a regular fixture of the Geophysical Fluid Dynamics programme (run at Woods Hole since 1959 – last attended in 2015) usual magic in the Lab. We continue to be endebted to W.H.O.I. Education, who once more provided a perfect atmosphere. Jeanne Fleming, Penny Foster and Janet Fields all contributed importantly to the smooth running of the program. The 2006 GFD Photograph. GFD Photo – 2006 A Sketch of the Summer Ice was the topic under discussion at Walsh Cottage during the 2006 Geophysical Fluid Dynamics Summer Study Program. Professor Grae Worster (University of The dragon enters the ice field. Cambridge) was the principal lecturer, and navigated our path through the fluid dynamics of icy processes in GFD. Towards the end of Grae’s lectures, we also held the 2006 GFD Public Lecture. This was given by Schedule of Principal Lectures Greg Dash of the University of Washington, on matters Week 1: of ice physics and a well-known popularization: “Nine Monday, June 19: Introduction to Ice Ices, Cloud Seeding and a Brother’s Farewell; how Kurt Tuesday, June 20: Diffusion-controlled solidification Vonnegut learned the science for Cat’s Cradle (but con- Wednesday, June 21: Interfacial instability in super- veniently left some out).” We again held the talk at Red- cooled fluid field Auditorium, and relaxed in the evening sunshine Thursday, June 22: Interfacial instability in two- at the reception afterwards. As usual, the principal lec- component melts tures were followed by a variety of seminars on topics icy and otherwise. -
Oxygen Transport During Ex Situ Machine Perfusion of Donor Livers Using Red Blood Cells Or Artificial Oxygen Carriers
International Journal of Molecular Sciences Review Oxygen Transport during Ex Situ Machine Perfusion of Donor Livers Using Red Blood Cells or Artificial Oxygen Carriers Silke B. Bodewes 1,2 , Otto B. van Leeuwen 1,3, Adam M. Thorne 1,3, Bianca Lascaris 1,3, Rinse Ubbink 3, Ton Lisman 2 , Diethard Monbaliu 4,5 , Vincent E. De Meijer 1 , Maarten W. N. Nijsten 6 and Robert J. Porte 1,* 1 Section of Hepatobiliary Surgery and Liver Transplantation, Department of Surgery, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands; [email protected] (S.B.B.); [email protected] (O.B.v.L.); [email protected] (A.M.T.); [email protected] (B.L.); [email protected] (V.E.D.M.) 2 Surgical Research Laboratory, Department of Surgery, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands; [email protected] 3 Organ Preservation & Resuscitation Unit, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands; [email protected] 4 Department of Abdominal Transplantation Surgery and Coordination, University Hospitals Leuven, 3000 Leuven, Belgium; [email protected] 5 Transplantation Research Group, Department of Microbiology, Immunology, and Transplantation, Katholieke Universiteit Leuven, 3000 Leuven, Belgium 6 Department of Critical Care, University of Groningen, University Medical Center Groningen, 9713 GZ Groningen, The Netherlands; [email protected] * Correspondence: [email protected]; Tel./Fax: +31-50-3611745 Abstract: Oxygenated ex situ machine perfusion of donor livers is an alternative for static cold preservation that can be performed at temperatures from 0 ◦C to 37 ◦C. -
Hydrostatic Pressure in Small Phospholipid Vesicles
Proc. Natl. Acad. Sci. USA Vol. 76, No. 7, pp. 3318-3319, July 1979 Biophysics Hydrostatic pressure in small phospholipid vesicles (surface tension/phospholipid bilayer) CHARLES TANFORD Whitehead Medical Research Institute and Department of Biochemistry, Duke University Medical Center, Durham, North Carolina 27710 Contributed by Charles Tanford, April 18, 1979 ABSTRACT The internal solvent-filled cavity of a single- condition that phases a and c be at the same pressure requires walled spherical phospholipid vesicle must be at essentially the (Eq. 1) that the interfacial tensions Yab and ybc be related as same pressure as the aqueous medium outside the vesicle. Whether or not the bilayer itself is under elevated pressure = - [2] cannot at present be determined. 'Yab/Ro Yh/Rii, in which R. and Ri are the external and internal radii of the It is a fundamental principle of surface chemistry (law of La- vesicle, respectively. If the surface tensions are not zero, one place) that the hydrostatic pressure on the two sides of a curved of the surface tensions must therefore be negative. Alternatively, surface between two homogeneous fluids is different (see ref. however, the entire system, including the bilayer phase b, can 1, for example). For a spherical surface of radius R, the relation be at the same pressure, with 'Yab and ybc both equal to zero. between the equilibrium pressure Pi on the concave side and Negative surface tensions cannot exist at the interface be- the pressure P2 on the convex side is given by tween two simple homogeneous fluids because the interface disappears when y = 0 and the two fluids become miscible (1).