Physiological Prinicples of Carbon Monoxide Poisoning Frank R
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Hemoglobin C Trait (AC) Hemoglobin Eletrophoresis and a Mean Corpuscular Volume
Inheritance Pattern for SHOULD WE, THE PARENTS, TAKE A BLOOD TEST? Sickle Cell Disease - SC Before you have your next baby, we suggest that you and Hemoglobin your partner get special blood test. We all have two sets of genes for hemoglobin. One set is passed on to the baby When one parent has sickle cell trait (AS) and the from each parent. The testing should include, at minimum, a C Trait (AC) other has hemoglobin C trait (AC) hemoglobin eletrophoresis and a mean corpuscular volume. A sickle solubility test (sickledex) is not sufficient! & Your Baby Only if both you and your partner are tested can you know their baby exactly what kind of hemoglobin condition your next child A S may have A C could have. Look carefully at the inheritance pattern for the possibilities of having a baby with the SC form of sickle cell disease. A A A counselor can tell you if any of your future children could have a form of sickle cell disease. AA (normal hemoglobin) For more information or Contact your local SCDAA organization or other health A C agency at: AC (hemoglobin C trait) or A S Or contact the SCDAA National Office at the address and AS (sickle cell trait) or telephone number below. Stay connected with Get Connected the first patient powered registry S C SC (a type of sickle cell disease) Register at www.getconnectedscd.com It does not matter what their other babies have, their Sickle Cell Disease next one has the same four possibilities: AA, AC, AS, or SC. -
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. -
Adult, Embryonic and Fetal Hemoglobin Are Expressed in Human Glioblastoma Cells
514 INTERNATIONAL JOURNAL OF ONCOLOGY 44: 514-520, 2014 Adult, embryonic and fetal hemoglobin are expressed in human glioblastoma cells MARWAN EMARA1,2, A. ROBERT TURNER1 and JOAN ALLALUNIS-TURNER1 1Department of Oncology, University of Alberta and Alberta Health Services, Cross Cancer Institute, Edmonton, AB T6G 1Z2, Canada; 2Center for Aging and Associated Diseases, Zewail City of Science and Technology, Cairo, Egypt Received September 7, 2013; Accepted October 7, 2013 DOI: 10.3892/ijo.2013.2186 Abstract. Hemoglobin is a hemoprotein, produced mainly in Introduction erythrocytes circulating in the blood. However, non-erythroid hemoglobins have been previously reported in other cell Globins are hemo-containing proteins, have the ability to types including human and rodent neurons of embryonic bind gaseous ligands [oxygen (O2), nitric oxide (NO) and and adult brain, but not astrocytes and oligodendrocytes. carbon monoxide (CO)] reversibly. They have been described Human glioblastoma multiforme (GBM) is the most aggres- in prokaryotes, fungi, plants and animals with an enormous sive tumor among gliomas. However, despite extensive basic diversity of structure and function (1). To date, hemoglobin, and clinical research studies on GBM cells, little is known myoglobin, neuroglobin (Ngb) and cytoglobin (Cygb) repre- about glial defence mechanisms that allow these cells to sent the vertebrate globin family with distinct function and survive and resist various types of treatment. We have tissue distributions (2). During ontogeny, developing erythro- shown previously that the newest members of vertebrate blasts sequentially express embryonic {[Gower 1 (ζ2ε2), globin family, neuroglobin (Ngb) and cytoglobin (Cygb), are Gower 2 (α2ε2), and Portland 1 (ζ2γ2)] to fetal [Hb F(α2γ2)] expressed in human GBM cells. -
Hemoglobin C Trait What Does This Mean for My Baby, Me and My Family?
My Baby Has Hemoglobin C Trait What does this mean for my baby, me and my family? Your baby's newborn screening test showed tell them their chance to have a baby with a that he or she has hemoglobin C trait (this is hemoglobin disease. also referred to as being a “hemoglobin C carrier”). Babies who have hemoglobin C trait What does having a baby with hemoglobin are no more likely to get sick than any other C trait mean for me, my partner and for baby. They do not need any special medical future pregnancies? treatment. Hemoglobin C trait will not change Since your baby has hemoglobin C trait, this into a disease later on. means that either you or your partner or both of you have hemoglobin C trait. In almost all What causes hemoglobin C trait? cases, ONLY ONE OF YOU will have Hemoglobin C trait happens when the part of hemoglobin C trait. the red blood cell that carries oxygen throughout the body is changed. This part that Most people do not know that they have is changed is called hemoglobin. Hemoglobin hemoglobin C trait. Now that your baby is is important because it picks up oxygen in the known to have hemoglobin C trait, both you lungs and carries it to the other parts of the and your partner have the option of being body. tested. Testing involves a blood test. People usually have one type of hemoglobin. IF ONLY ONE OF YOU HAS HEMOGLOBIN This is called hemoglobin A. Babies with C TRAIT, in every pregnancy there is a: hemoglobin C trait have a second type of • 1 in 2 (50%) chance to have a baby with hemoglobin called hemoglobin C, as well as only the usual hemoglobin A. -
Pathological Conditions Involving Extracellular Hemoglobin
Pathological Conditions Involving Extracellular Hemoglobin: Molecular Mechanisms, Clinical Significance, and Novel Therapeutic Opportunities for alpha(1)-Microglobulin Gram, Magnus; Allhorn, Maria; Bülow, Leif; Hansson, Stefan; Ley, David; Olsson, Martin L; Schmidtchen, Artur; Åkerström, Bo Published in: Antioxidants & Redox Signaling DOI: 10.1089/ars.2011.4282 2012 Link to publication Citation for published version (APA): Gram, M., Allhorn, M., Bülow, L., Hansson, S., Ley, D., Olsson, M. L., Schmidtchen, A., & Åkerström, B. (2012). Pathological Conditions Involving Extracellular Hemoglobin: Molecular Mechanisms, Clinical Significance, and Novel Therapeutic Opportunities for alpha(1)-Microglobulin. Antioxidants & Redox Signaling, 17(5), 813-846. https://doi.org/10.1089/ars.2011.4282 Total number of authors: 8 General rights Unless other specific re-use rights are stated the following general rights apply: Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. • Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal Read more about Creative commons licenses: https://creativecommons.org/licenses/ Take down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. -
Brownie's THIRD LUNG
BrMARINEownie GROUP’s Owner’s Manual Variable Speed Hand Carry Hookah Diving System ADVENTURE IS ALWAYS ON THE LINE! VSHCDC Systems This manual is also available online 3001 NW 25th Avenue, Pompano Beach, FL 33069 USA Ph +1.954.462.5570 Fx +1.954.462.6115 www.BrowniesMarineGroup.com CONGRATULATIONS ON YOUR PURCHASE OF A BROWNIE’S SYSTEM You now have in your possession the finest, most reliable, surface supplied breathing air system available. The operation is designed with your safety and convenience in mind, and by carefully reading this brief manual you can be assured of many hours of trouble-free enjoyment. READ ALL SAFETY RULES AND OPERATING INSTRUCTIONS CONTAINED IN THIS MANUAL AND FOLLOW THEM WITH EACH USE OF THIS PRODUCT. MANUAL SAFETY NOTICES Important instructions concerning the endangerment of personnel, technical safety or operator safety will be specially emphasized in this manual by placing the information in the following types of safety notices. DANGER DANGER INDICATES AN IMMINENTLY HAZARDOUS SITUATION WHICH, IF NOT AVOIDED, WILL RESULT IN DEATH OR SERIOUS INJURY. THIS IS LIMITED TO THE MOST EXTREME SITUATIONS. WARNING WARNING INDICATES A POTENTIALLY HAZARDOUS SITUATION WHICH, IF NOT AVOIDED, COULD RESULT IN DEATH OR INJURY. CAUTION CAUTION INDICATES A POTENTIALLY HAZARDOUS SITUATION WHICH, IF NOT AVOIDED, MAY RESULT IN MINOR OR MODERATE INJURY. IT MAY ALSO BE USED TO ALERT AGAINST UNSAFE PRACTICES. NOTE NOTE ADVISE OF TECHNICAL REQUIREMENTS THAT REQUIRE PARTICULAR ATTENTION BY THE OPERATOR OR THE MAINTENANCE TECHNICIAN FOR PROPER MAINTENANCE AND UTILIZATION OF THE EQUIPMENT. REGISTER YOUR PRODUCT ONLINE Go to www.BrowniesMarineGroup.com to register your product. -
What Are the Health Effects from Exposure to Carbon Monoxide?
CO Lesson 2 CARBON MONOXIDE: LESSON TWO What are the Health Effects from Exposure to Carbon Monoxide? LESSON SUMMARY Carbon monoxide (CO) is an odorless, tasteless, colorless and nonirritating Grade Level: 9 – 12 gas that is impossible to detect by an exposed person. CO is produced by the Subject(s) Addressed: incomplete combustion of carbon-based fuels, including gas, wood, oil and Science, Biology coal. Exposure to CO is the leading cause of fatal poisonings in the United Class Time: 1 Period States and many other countries. When inhaled, CO is readily absorbed from the lungs into the bloodstream, where it binds tightly to hemoglobin in the Inquiry Category: Guided place of oxygen. CORE UNDERSTANDING/OBJECTIVES By the end of this lesson, students will have a basic understanding of the physiological mechanisms underlying CO toxicity. For specific learning and standards addressed, please see pages 30 and 31. MATERIALS INCORPORATION OF TECHNOLOGY Computer and/or projector with video capabilities INDIAN EDUCATION FOR ALL Fires utilizing carbon-based fuels, such as wood, produce carbon monoxide as a dangerous byproduct when the combustion is incomplete. Fire was important for the survival of early Native American tribes. The traditional teepees were well designed with sophisticated airflow patterns, enabling fires to be contained within the shelter while minimizing carbon monoxide exposure. However, fire was used for purposes other than just heat and cooking. According to the historian Henry Lewis, Native Americans used fire to aid in hunting, crop management, insect collection, warfare and many other activities. Today, fire is used to heat rocks used in sweat lodges. -
The Future of Mechanical Ventilation: Lessons from the Present and the Past Luciano Gattinoni1*, John J
Gattinoni et al. Critical Care (2017) 21:183 DOI 10.1186/s13054-017-1750-x REVIEW Open Access The future of mechanical ventilation: lessons from the present and the past Luciano Gattinoni1*, John J. Marini2, Francesca Collino1, Giorgia Maiolo1, Francesca Rapetti1, Tommaso Tonetti1, Francesco Vasques1 and Michael Quintel1 Abstract The adverse effects of mechanical ventilation in acute respiratory distress syndrome (ARDS) arise from two main causes: unphysiological increases of transpulmonary pressure and unphysiological increases/decreases of pleural pressure during positive or negative pressure ventilation. The transpulmonary pressure-related side effects primarily account for ventilator-induced lung injury (VILI) while the pleural pressure-related side effects primarily account for hemodynamic alterations. The changes of transpulmonary pressure and pleural pressure resulting from a given applied driving pressure depend on the relative elastances of the lung and chest wall. The term ‘volutrauma’ should refer to excessive strain, while ‘barotrauma’ should refer to excessive stress. Strains exceeding 1.5, corresponding to a stress above ~20 cmH2O in humans, are severely damaging in experimental animals. Apart from high tidal volumes and high transpulmonary pressures, the respiratory rate and inspiratory flow may also play roles in the genesis of VILI. We do not know which fraction of mortality is attributable to VILI with ventilation comparable to that reported in recent clinical practice surveys (tidal volume ~7.5 ml/kg, positive end-expiratory pressure (PEEP) ~8 cmH2O, rate ~20 bpm, associated mortality ~35%). Therefore, a more complete and individually personalized understanding of ARDS lung mechanics and its interaction with the ventilator is needed to improve future care. -
Pathogenesis of Hemolytic Anemia in Homozygous Hemoglobin C Disease
Pathogenesis of Hemolytic Anemia in Homozygous Hemoglobin C Disease Samuel Charache, … , Richard J. Ugoretz, J. Richard Spurrell J Clin Invest. 1967;46(11):1795-1811. https://doi.org/10.1172/JCI105670. Research Article Hemoglobin C is less soluble than hemoglobin A in red cells, in hemolysates, and in dilute phosphate buffer. Its relative insolubility may be explained by electrostatic interactions between positively charged β6-lysyl groups and negatively charged groups on adjacent molecules. Red cells from patients with homozygous hemoglobin C (CC) disease exhibit aberrant physical properties which suggest that the cells are more rigid than normal erythrocytes. They pass through membrane filters less readily than normal red cells do, and their viscosity is higher than that of normal cells. Differences from normal cells are exaggerated if mean corpuscular hemoglobin concentration (MCHC) is increased, by suspension in hypertonic salt solution. Increased rigidity of CC cells, by accelerating their fragmentation, may be responsible for formation of microspherocytes. These small dense cells are exceptionally rigid, and probably are even more susceptible to fragmentation and sequestration. Rigidity of CC cells can be attributed to a “precrystalline” state of intracellular hemoglobin, in which crystallization does not occur, although the MCHC exceeds the solubility of hemoglobin in hemolysates. Find the latest version: https://jci.me/105670/pdf The Journal of Clinical Investigation Vol. 46, No. 11, 1967 Pathogenesis of Hemolytic Anemia in Homozygous Hemoglobin C Disease * SAMUEL CHARACHE, C. LOCKARD CONLEY, DAVID F. WAUGH, RICHARD J. UGORETZ,4 AND J. RICHARD SPURRELL WITH THE TECHNICAL ASSISTANCE OF ESTHER GAYLE (From the Department of Medicine, The Johns Hopkins University and Hospital, Baltimore, Maryland, and the Department of Biology, Massachusetts Institute of Technology, Boston, Massachusetts) Abstract. -
PHYSIOLOGY of RESPIRATION Respiration Includes 2 Processes: 1) External Respiration – Is the Uptake of O 2 and Excretion Of
PHYSIOLOGY OF RESPIRATION Respiration includes 2 processes: 1) External respiration – is the uptake of O 2 and excretion of CO 2 in the lungs 2) Internal respiration – means the O 2 and CO 2 exchange between the cells and capillary blood The quality of these respiration processes depends on: a) pulmonary ventilation – it means the inflow and outflow of air between the atmosphere and the lung alveoli b) diffusion of oxygen and CO 2 between the alveoli and the blood c) perfusion – of lungs with blood d) transport of O 2 and CO 2 in the blood e) regulation of respiration Nonrespiratory functions: - in voice production - protective reflexes (apnoea, laryngospasm) - defensive reflexes (cough, sneeze) - in thermoregulation STRUCTURE OF THE RESPIRATORY TRACT Upper airways - nose,nasopharynynx - borderline - larynx Lower airways - trachea, bronchi, bronchioles. The airways divide 23 times to 23 generations between the trachea and: Alveoli - 300 milion - total surface area 70 m 2 lined pneumocytes - type I -flat cells - type II - producers of the surfactant - lymphocytes, plasma cells, alveolar macrophages, mast cells.... Innervation : Smooth muscles innervated by autonomic nervous system: - parasympathetic - muscarinic - bronchoconstriction - sympathetic - beta 2 - receptors – bronchodilation - mainly to adrenalin - noncholinergic nonadrenergic innervation - VIP MECHANICS OF VENTILATION Inspiration - an active process - contraction of the inspiratory muscles: - Diaphragm - accounts for 60-75% of the tidal volume - External intercostal muscles - Auxiliary -accessory-inspiratory muscles: Scalene and sternocleidomasoid m.m. Expiration - quiet breathing - passive process - given by elasticity of the chest and lungs - forced expirium - active process – expiratory muscles: - Internal intercostal m.m. - Muscles of the anterior abdominal wall Innervation: Motoneurons: Diaphragm – n.n. -
Observations on the Minor Basic Hemoglobin Component in the Blood of Normal Individuals and Patients with Thalassemia
Observations on the Minor Basic Hemoglobin Component in the Blood of Normal Individuals and Patients with Thalassemia H. G. Kunkel, … , U. Müller-Eberhard, J. Wolf J Clin Invest. 1957;36(11):1615-1625. https://doi.org/10.1172/JCI103561. Research Article Find the latest version: https://jci.me/103561/pdf OBSERVATIONS ON THE MINOR BASIC HEMOGLOBIN COMPONENT IN THE BLOOD OF NORMAL INDIVIDUALS AND PATIENTS WITH THALASSEMIA BY H. G. KUNKEL, R. CEPPELLINI, U. MULLER-EBERHARD, AND J. WOLF (From the Rockefeller Institute for Medical Research, and Institute for the Study of Human Variation, and the Departmet of Pediatrics, Colunma Uniewsity, N. Y.) (Submitted for publication March 6, 1957; accepted April 11, 1957) In a previous report (1) a second hemoglobin was collected from a number of New York hospitals. was described which was found at a concentration The specimens from patients with thalassemia were ob- of tained from Italian and Greek individuals in the hema- approximately 3 per cent in the blood of normal tology clinic at the Babies Hospital, Columbia-Presby- adult individuals. It was found to resemble he- terian Medical Center, New York. Five individuals with moglobin E in electrophoretic properties, but iden- thalassemia in two families were obtained from index tity with this abnormal hemoglobin was not estab- cases at Bellevue Hospital. The great majority of lished. This same component probably had been thalassemia trait cases were parents of children with observed severe Cooley's anemia. In all instances the diagnosis of by previous investigators employing the thalassemia was based on the hematological picture. classical Tiselius procedure in occasional speci- Several individuals who were suspected of having thalas- mens of blood from normal persons (2, 3) and semia were excluded from the study because of un- thalassemia patients (4), but had not been defined certain hematological findings. -
Respiration (Physiology) 1 Respiration (Physiology)
Respiration (physiology) 1 Respiration (physiology) In physiology, respiration (often mistaken with breathing) is defined as the transport of oxygen from the outside air to the cells within tissues, and the transport of carbon dioxide in the opposite direction. This is in contrast to the biochemical definition of respiration, which refers to cellular respiration: the metabolic process by which an organism obtains energy by reacting oxygen with glucose to give water, carbon dioxide and ATP (energy). Although physiologic respiration is necessary to sustain cellular respiration and thus life in animals, the processes are distinct: cellular respiration takes place in individual cells of the animal, while physiologic respiration concerns the bulk flow and transport of metabolites between the organism and the external environment. In unicellular organisms, simple diffusion is sufficient for gas exchange: every cell is constantly bathed in the external environment, with only a short distance for gases to flow across. In contrast, complex multicellular animals such as humans have a much greater distance between the environment and their innermost cells, thus, a respiratory system is needed for effective gas exchange. The respiratory system works in concert with a circulatory system to carry gases to and from the tissues. In air-breathing vertebrates such as humans, respiration of oxygen includes four stages: • Ventilation, moving of the ambient air into and out of the alveoli of the lungs. • Pulmonary gas exchange, exchange of gases between the alveoli and the pulmonary capillaries. • Gas transport, movement of gases within the pulmonary capillaries through the circulation to the peripheral capillaries in the organs, and then a movement of gases back to the lungs along the same circulatory route.