DOCSLIB.ORG

Module G: Oxygen Transport • Oxygen Transport Studies • Tissue Hypoxia • Cyanosis • Polycythemia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Module G: Oxygen Transport • Oxygen Transport Studies • Tissue Hypoxia • Cyanosis • Polycythemia Topics to Cover • Oxygen Transport • Oxygen Dissociation Curve Module G: Oxygen Transport • Oxygen Transport Studies • Tissue Hypoxia • Cyanosis • Polycythemia Oxygen Transport Dissolved Oxygen • As oxygen diffuses across the A-C membrane, it • Oxygen is carried from the lungs to the dissolves into the plasma and remains in that tissues in two different fashions: fashion until it reaches the tissue. • Oxygen Dissolved in the blood plasma (PO ) 2 • Expressed as a partial pressure - PO2 • Oxygen Combined with Hemoglobin (SO2) • Normal arterial level = 80-100 mm hg • Normal venous level = 35 – 45 mm hg • The quantity of oxygen dissolves is a function of Henry’s law. •At 37 C 0.003 ml of oxygen will dissolve in 100 ml of blood. (Henry’s Law) • At 100 mm hg PaO2, the amount of dissolved oxygen is 0.3 ml O2/100 ml blood (0.3 vol%). Combined Oxygen • Dissolved oxygen is inadequate for metabolic needs. • Need a substance which will bind to oxygen and carry it, BUT will release it when needed. • Voila! Hemoglobin! • Miracle #2…As we’ll see later, hemoglobin also carries carbon dioxide and is a key buffer of [H+]. 1 Hemoglobin chains • Each RBC contains approximately 280 million molecules of hemoglobin chains • Adult Hemoglobin (Hb A) consists of • 4 Heme Groups – Primarily iron in the Fe+2 (ferrous) state. Heme • 4 Globulin – 4 amino acid chains (2 & 2 ) Units • One heme group binds with one of the amino acid chains and oxygen binds with the iron in the heme group in a reversible way. +2 O2 + Fe FeO2 (Oxyhemoglobin) FERROUS Hemoglobin & the RBC • “Normal” hemoglobin level • 15 g/dl (men) & 13-14 g/dl (women) - Malley •15 +1.5 g/dl (men) & 13.5 + 1.5 g/dl (women) – Egan •15 +2 (men) & 14 + 2 (women) - Easy • Why do women have less? • The hemoglobin molecule resides in the erythrocyte and is responsible for giving the blood its red color. • The affinity of hemoglobin for oxygen • Hundreds of hemoglobin variants. increases with each oxygen molecule • Normal: A, A2, F • Abnormal: S, H attached • “All or Nothing” Oxygen Saturation • Saturation = Sites Filled Total Sites Available • Example: • 80 sites filled = 80% saturation 100 sites available • Oxygen Saturation only talks about how much hemoglobin is saturated, NOT how much hemoglobin is present. 2 Quantity of Oxygen Bound to Combined Oxygen Hemoglobin • Each gram of Hemoglobin combines with • Not all hemoglobin molecules are bound with 1.34 mL of oxygen. oxygen. • Normal saturation •O2 bound to Hb = 1.34 mL O2 x 15 g Hb • Arterial (SaO ) – 97% = 20.1 vol% O 2 2 • Venous (SO2) – 75% • Some “desaturated” hemoglobin exists because of normal physiologic shunts: • Mixing of poorly saturated venous blood with arterial blood • Thebesian, bronchial, and pleural veins • Intrapulmonary shunts (perfused alveoli that are not ventilated) • 20.1 vol% O2 x 0.97 = 19.5 vol% O2 • Hemoglobin not bound with oxygen is called reduced hemoglobin. Oxygen Content Oxygen Dissociation Curve • The total amount of oxygen in 100 mL of blood is the sum of the dissolved oxygen & • The the oxygen bound to hemoglobin. relationship between the • Arterial Content partial •CaO = (Hb x 1.34 x SaO ) + (PaO x .003) 2 2 2 pressure of • Venous Content oxygen and •CO2 = (Hb x 1.34 x SO2) + (PO2 x .003) • Capillary Content the saturation of oxygen is •CćO2 = (Hb x 1.34 x SćO2) + (PćO2 x .003) •SćO2 = Ideal Saturation = 100% not linear. •PćO = Ideal Partial Pressure = PAO 2 2 • 2 lines Steep Portion of Curve Flat Portion of Curve • “Dissociation Portion” of curve. • “Association Portion” of curve. • Between 10 and 60 mm Hg. • Greater than 60 mm Hg. • Large increases in PO2 yield small increases in • Small increases in PO yield large 2 SO2. increases in SO2. • At the pulmonary capillary, blood comes in contact with increased alveolar PO and oxygen • At the tissue capillary, blood comes in 2 diffuses from the alveolus to the capillary. As the contact with reduced tissue PO2 and PO2 rises, oxygen binds with the hemoglobin oxygen diffuses from the capillary to the (increasing SO2). tissue. As the PO2 falls, oxygen bound to • Very little rise in oxygen saturation above 100 mm Hg of PaO . the hemoglobin (SO2) is released. 2 3 Key Points to Remember • The amount of oxygen that is saturated on the hemoglobin (SO2) is dependent on the amount dissolved (PO2). • Between a PaO2 of 60 and 100 mm Hg, the curve is flat. • This means that small changes in PaO2 can occur without a big drop in saturation and oxygen content. • At the tissues, where the PO2 is about 40 mm Hg, the curve is steep. • This means that small changes in PO2 will result in a large amount of oxygen being unloaded. Rules of Thumb of the P Oxyhemoglobin Curve 50 • The degree to which oxygen is attracted to hemoglobin can be assessed by PO2 SO2 evaluating at what PO2 there is a 50% PO2 SO2 SO (P ). 27 50 2 50 •Normal P value is 27 mm Hg 40 70 50 40 75 •As P50 increases/decreases, we say the 50 80 “curve has shifted”. 60 90 •P less than 27: Shift to the left. 60 90 50 •P greater than 27: Shift to the right. 250 100 50 Leftward Shift of the OHDC Rightward Shift of the OHDC • Left Shift. • Right Shift. • Increased oxygen affinity for hemoglobin. • Decreased oxygen affinity for hemoglobin. • This is the expected shift at the lungs (Left- • This is the expected shift at the tissues. Lungs). • For any given PO2, SO2 will be lower. • For any given PO , SO will be higher. 2 2 • Increasing P50. • Decreasing P50. • ELEVATED THINGS CAUSE A RIGHT SHIFT • LOW THINGS CAUSE A LEFT SHIFT (Up-Right) • H+ concentration (pH, alkalosis) • H+ concentration ( pH, acidosis) • Temperature (Hypothermia) • Temperature (Hyperthermia) • Carbon Dioxide (PCO2, Hypocarbia) • Carbon Dioxide (PCO2, Hypercarbia) • 2,3 DPG • 2,3 DPG 4 2,3 DPG • 2,3 DPG is an organic phosphate normally found in the RBC that has a tendency to bind with Hemoglobin and thereby decrease the affinity of Hemoglobin for oxygen. • It promotes a rightward shift and enhances oxygen unloading at the tissues. This shift is + longer in duration than that due to [H ], PCO2 or temperature. • A doubling of DPG will result in a 10 torr increase in P50. 2,3 DPG Bohr Effect • The levels increase with • The effect of CO on the OHDC is known • Cellular hypoxia. 2 • Anemia as the Bohr Effect. • Hypoxemia secondary to COPD • (OH – Bohr) • Congenital Heart Disease • High PCO2 levels and low pH decrease • Ascent to high altitudes affinity of hemoglobin for oxygen (a right- • The levels decrease with ward shift). • Septic Shock • Acidemia • This occurs at the tissues where a high • Stored blood level of PCO2 and acidemia contribute to • No DPG after 2 weeks of storage. the unloading of oxygen. Arterial-Venous Oxygen Oxygen Transport Content Difference • The volume of oxygen leaving the left •C(a-)O2 •CaO–CO ventricle each minute. 2 2 • The venous blood is “mixed venous” blood •CaO2 x CO x 10 = 20 ml O2 x 5 L/min x 10 obtained from the pulmonary artery via a • Make sure to convert CO to L/min! pulmonary artery catheter. • Normal CaO : 20 vol% • Normal value is 1,000 mL O2 / min 2 • Normal CO : 15 vol% • Decreased oxygen delivery occurs when 2 • Normal CaO2 –CO2: 5 vol% there is: • Decreased with: • A decreased blood oxygenation • Increased CO • Decreased hemoglobin concentration • Certain Poisons •Hypothermia • Decreased cardiac output. 5 Oxygen Extraction Ratio Pulmonary Shunting • Def: The amount of oxygen extracted by the peripheral • PERFUSION WITHOUT VENTILATION. tissues divided by the amount of oxygen delivered to the • Pulmonary shunt is that portion of the cardiac peripheral cells. output that enters the left side of the heart • aka: Oxygen coefficient ratio & Oxygen utilization ratio without coming in contact with an alveolus. •O2ER = (CaO2-CO2)/CaO2 • “True” Shunt – No contact • Normal is 25% • Anatomic shunts (Thebesian, Pleural, Bronchial) •Increased with: •Decreased with: • Cardiac anomalies •Decreased .CO •Increased Cardiac Output • “Shunt-Like” (Relative) Shunt •Increased VO •Skeletal Muscle Relaxation 2 • Some ventilation, but not enough to allow for complete •Exercise •Peripheral Shunting equilibration between alveolar gas and perfusion. •Seizures •Certain Poisons • Shunts are refractory to oxygen therapy. •Shivering •Hypothermia •Hyperthermia •Increased Hemoglobin • Delivery of oxygen therapy will NOT help (at least to the expected degree). •Anemia •Increased PaO2 •Low PaO2 Venous Admixture Alveolar-arterial Gradient • The mixing of oxygenated blood with •PAO2-PaO2 “contaminated” deoxygenated blood • More on this in today’s 1060 class. resulting in a reduction in: •PaO2 •SaO2 Shunt Equation Shunt Equation Example • So just how much blood is shunted? You obtain the following data on you patient. • Q CcO CaO What is the percent shunt present? S 2 2 QT CcO2 CvO2 aCO aO aO • Where CćO2 = (Hb x 1.34) + (PAO2 * .003) pH: 7.25 P 2: 28 torr P 2: 68 torr S 2: 91% • You will need PB: 749 PO2: 38 torr SO2: 72 % Hb: 13 gm% •PBARO – Barometric Pressure FIO2: .90 •PaO2 – Arterial Partial Pressure of Oxygen •Steps: • Calculate CaO •PaCO2 – Arterial Partial Pressure of Carbon Dioxide 2 • Calculate CO •PO2 – Venous Partial Pressure of Oxygen 2 •Calculate PAO • Hb – Hemoglobin concentration 2 • Calculate CćO •PAO – Alveolar Partial Pressure of Oxygen 2 2 • Plug in numbers & solve! •FIO2 – Fractional Concentration of Inspired Oxygen 6 Shunt – Clinical Significance Tissue Hypoxia • Normal Shunt: 3 to 5% • Hypoxemia: Reduced oxygen in blood • Shunts above 15% are associated with (PaO2). significant hypoxemia. • Hypoxia: Reduced oxygen at the tissue. • Four types: • Hypoxic (Hypoxemic) Hypoxia • Anemic Hypoxia • Circulatory Hypoxia • Histotoxic Hypoxia Hypoxic Hypoxia Anemic Hypoxia • Tissues have inadequate oxygen levels • Tissues have inadequate oxygen levels because there is inadequate levels in the secondary to reduced oxygen carrying O blood (reduced Pa 2).
Load more

Recommended publications
  • Mitochondrial Dysfunction After Severe Tbi: a New Translational Target?
    -Edición provisional- MITOCHONDRIAL DYSFUNCTION AFTER SEVERE TBI: A NEW TRANSLATIONAL TARGET? Juan Sahuquillo, MD, PhD1, Marian Vidal-Jorge2, Angela Sánchez-Guerrero2 Department of Neurosurgery1, Neurotraumatology and Neurosurgery Research Unit2 Vall d’Hebron University Hospital Universitat Autònoma de Barcelona, Barcelona, Spain Significant advances in the treatment of TBI have been limited by a lack of knowledge of the biochemical, cellular and molecular changes involved in its pathophysiology. These obstacles have been overcome to a certain degree by new monitoring tools —cerebral microdialysis (MD) and monitoring of partial pressure of oxygen in the brain (PtiO2)— that have allowed clinicians to explore the metabolic disturbances of the injured brain with unprecedented detail. The data gathered by these monitoring tools in the past two decades has provided an opportunity to take a second look at the pathophysiology of TBI, motivating clinical researchers to redefine some of the unchallenged traditional concepts. The hypothesis that mitochondrial dysfunction is at the core of many acute metabolic disorders observed in acute TBI is one of the old concepts that deserves a second look and is the focus of this chapter. New neuromonitoring techniques, including PtiO2 and MD monitoring, are widely used in neurocritical care units, allowing for the quasi-continuous profiling of brain oxygen supply and brain metabolism [1, 2]. Data provided by these tools have cast doubt on the predominant role of ischemia in the pathophysiology of TBI. Many studies have found that the injured brain may experience severe alterations of energetic metabolism in the presence of CBF and oxygen supply well above the ischemic range[3-5].
    [Show full text]
  • Full Text HTML
    Neurological Disorders & Epilepsy Journal Special Issue Article “Brain Hypoxia” Letter Seizures Induces Hypoxia and Hypoxia Induces Seizures. A Perverse Relationship that Increases the Risk of SUDEP Jerónimo Auzmendi1,2 and Alberto Lazarowski1* 1Department of Clinical Biochemistry, University of Buenos Aires, Argentina 2National Council for Scientific and Technical Research (CONICET), Argentina ARTICLE INFO LETTER “He uttered a cry and was seen to be rubbing his hands together. His pulse was Received Date: October 11, 2020 Accepted Date: October 25, 2020 immediately examined for but was not palpable” [1]. Published Date: October 28, 2020 Hypoxia is a biological stimulus capable of promoting both rescue and survival KEYWORDS mechanisms, as well as triggering a sequence of irreversible events that lead to death of cell, tissue and even individual. Brain and heart functions depend critically on Seizures adequate energy supply and they are highly susceptible to hypoxic conditions. Hypoxia SUDEP Adequate oxygen supply is needed for the brain and heart to metabolize glucose as its major energy source. But how many type of hypoxia we know, and how much Copyright: © 2020 Alberto severe is the hypoxic condition, when more than one type of hypoxia are Lazarowski, et al., Neurological simultaneously acting? Four types of hypoxia are distinguished in medicine: α- the Disorders & Epilepsy Journal. This is an open access article distributed under hypoxemic hypoxia, due to a decrease in the amount of breathable oxygen or the Creative Commons Attribution cardiopulmonary failure, b- the anemic hypoxia related with decreased amount of License, which permits unrestricted use, functional hemoglobin, c- the stagnant hypoxia, secondary to reduced or unevenly distribution, and reproduction in any medium, provided the original work is distributed flow of blood distribution to the tissues, and mainly result from heart properly cited.
    [Show full text]
  • Effects of Aqueous Extract of Kuding Leaves on Cyanide- Induced Toxicity and Packed Cell Volume (PCV)
    Article Number: 3518D12 A Paper Presented at the WANNPRES 9th Sub-Regional Scientific Meeting, University of Nigeria, Nsukka, Enugu State, Nigeria. 30th May – 2nd June, 2018 Copyright ©2018 Author(s) retain the copyright of this article Conference Proceedings http://www.proceedings.academicjournals.org/ Full Length Research Paper Effects of aqueous extract of kuding leaves on cyanide- induced toxicity and packed cell volume (PCV) Obiajulu Christian Ezeigwe1*, Christopher Onyemeziri Alisa2 and Josephine Ezekwesili-Ofili1 1Department of Applied Biochemistry, Faculty of Biosciences, Nnamdi Azikiwe University, Awka, Anambra State, Nigeria. 2Department of Chemistry, Federal University of Technology, Owerri, Imo State, Nigeria. Cyanide poisoning occurs when a living organism is exposed to a compound that produces cyanide ions (CN−) when dissolved in water. Kuding leaves are Chinese leaves used for weight control. Aqueous extract of kuding leaves was assessed for its effect on cyanide-induced toxicity and packed cell volume (PCV) in Wistar rats. Group A was administered 1% Tween-80 at 5 ml/kg. Group B was not induced but received 400 mg/kg body weight of the extract only, Group C received 3 mg/kg of cyanide without treatment, Group D received 200 mg/kg of the extract, Group E received 300 mg/kg of the extract, and Group F received 400 mg/kg of the extract. PCV was determined using automated haematology analyzer (Mindray-BC-28000). A significant reduction (p>0.05) in weight was observed for the group that received only 400 mg/kg body weight of the extract and the group that received only 3 mg/kg body weight of cyanide for two weeks when compared with the control group.
    [Show full text]
  • Cyanide Poisoning After Bitter Almond Ingestion
    CASE REPORTS continue therapy with cholestyramine after many years of administration. ABBREVIATIONS USED IN TEXT REFERENCES A-ao2 = alveolar-arterial difference in oxygen CVP=central venous pressure 1. Riely C, Collier E, Jensen P, et al: Arteriohepatic dysplasia: A benign syndrome of intrahepatic cholestasis with multiple organ Flo2=fraction of inspired oxygen involvement. Ann Intern Med 91:520-527, Oct 1979 PCWP=pulmonary capillary wedge pressure 2. Watson DH, Miller V: Arteriohepatic dysplasia. Arch Dis Child 48:459-466, Jun 1973 Qs/Qt=right-to-left intrapulmonary shunt 3. Alagille D, Odievre M, Gautier M, et al: Hepatic ductular SEM =standard error of the mean hypoplasia associated with characteristic facies, vertebral malfor- T/2 = cyanide half-life in blood mations, retarded physical, mental and sexual development and cardiac murmur. J Pediatr 86:63-71, Jan 1975 4. Alagille D, Habib EC, Thomassin N: L'atr6sie des voies bili- aires intrah6patiques avec voies biliaries extrahepatiques permeables chez l'enfant. Journees Paris Pediatr pp 301-318, 1969 poisoning, Graham and colleagues2 noted the 5. Alagille D, Thomassin N: L'atresie des voies biliares intra- h6patiques avec voies biliaires extrahepatiques permeables chez paucity of cases in which cyanide blood levels had l'enfant. Rev Med Chir Mal Foie 45:93-104, 1970 been reported. They further questioned the effi- 6. Greenwood RJ, Rosenthal A, Crocker A, et al: Syndrome of intrahepatic biliary dysgenesis and cardiovascular malformations. cacy and safety of the traditional therapy of Pediatrics 58:243-247, Aug 1976 7. Henriksen M, Langmark F, Sorland S, et al: Hereditary intravenous sodium nitrite and sodium thiosulfate.
    [Show full text]
  • Cyanide-Induced Cytochrome A,A3 Oxidation-Reduction Responses in Rat Brain in Vivo
    Cyanide-induced cytochrome a,a3 oxidation-reduction responses in rat brain in vivo. C A Piantadosi, … , A L Sylvia, F F Jöbsis J Clin Invest. 1983;72(4):1224-1233. https://doi.org/10.1172/JCI111078. Research Article The sensitivity of the brain to cyanide-induced histotoxic hypoxia and the protective effects of known cyanide antagonists, have been assessed in vivo by reflectance spectrophotometry. Cyanide-related changes in cytochrome a,a3 (cytochrome c oxidase) oxidation-reduction (redox) state, tissue hemoglobin saturation, and local blood volume were continuously monitored in cerebral cortex of rats. Noncumulative, dose-dependent inhibition of the in situ mitochondrial respiratory chain was evaluated directly by measuring increases in reduction levels of the terminal oxidase. These transient cytochrome a,a3 reductions were accompanied by increases in regional cerebral hemoglobin saturation and blood volume. Cytochrome redox responses were not altered either in magnitude or kinetics by hyperoxia; however, the cyanide-cytochrome dose-response curve was greatly shifted to the right by pretreatment with sodium nitrite, and the recovery rate of cytochrome a,a3 from cyanide-induced reduction was enhanced fourfold by pretreatment with sodium thiosulfate. Find the latest version: https://jci.me/111078/pdf Cyanide-induced Cytochrome a,a3, Oxidation- Reduction Responses in Rat Brain In Vivo C. A. PIANTADOSI, A. L. SYLVIA, and F. F. JOBSIS, Departments of Medicine and Physiology, Duke University Medical Center, Durham, North Carolina 27710 A B S T R A C T The sensitivity of the brain to cyanide- chrome oxidase in vitro with cyanide concentrations induced histotoxic hypoxia and the protective effects as low as 3 X 10' M (9), 50% decreases in cytochrome of known cyanide antagonists, have been assessed in oxidase activity in rat brain homogenates after lethal vivo by reflectance spectrophotometry.
    [Show full text]
  • Cell Injury PATHWAYS of INJURY
    GENERAL PATHOLOGY Cell Injury PATHWAYS OF INJURY HYPOXIC INJURY Interference with Energy Production Direct Damage to membranes DR. M. TARIQ JAVED Professor Department of Pathology, Faculty of Veterinary Science, University of Agriculture, Faisalabad, Pakistan. Web: https://sites.goocities.ws/mtjaved 1 2 Hypoxic Injury 1. INTERFERENCE WITH ENERGY PRODUCTION hypoxia decreased O2 at the cell anoxia complete lack of O2 Hypoxic Injury Hypoxemia decreased O2 in the blood ischemia reduced blood supply to the tissue leads to hypoxia 3 4 1 Hypoxaemia Ischaemia Too little oxygen in the blood Occlusion of the blood vessels Too little oxygen in the air Failure of the heart to pump Failure to properly ventilate the lungs enough blood Failure of the lungs to properly oxygenate the blood Failure of the heart to pump enough blood through the lungs Tremendously increased dead space (i.e., pulmonary thromboembolus) 5 6 Haemoglobin problems Failure of the Cells to Utilize (anaemic hypoxia) Oxygen (cytochromes) Inadequate circulating red cell mass (histotoxic hypoxia) (anaemia) Inability of haemoglobin to carry the • Cyanide poisoning oxygen (carbon monoxide poisoning) • Rotenone poisoning High affinity haemoglobin that will not • Dinitrophenol poisoning give up their oxygen to the tissues (methemoglobinemia) 7 8 2 Cell Deprived of oxygen Interrupts oxidative metabolism Depletion of Energy Sources (Glucose) Decreased Energy in the cell Na/K pump failure 9 10 11 3 13 14 Biochemical “point of no return”: Inability to restore mitochondrial function phospholipase activation mitochondrial permeability increases Plasma membrane defects-contributing factors phospholipase activation degradation of membrane phospholipids lipid degradation products membrane detergent effect Ca2+ proteases cytoskeletal degradation membrane detachment 16 15 4 3 R’s of success: Respect for self, Respect for others Responsibility for all your actions 17 18 19 5.
    [Show full text]
  • Acute Hydrogen Sulfide Poisoning in a Dairy Farmer
    Clinical Toxicology (2007) 45, 420–423 Copyright © Informa Healthcare ISSN: 1556-3650 print / 1556-9519 online DOI: 10.1080/15563650601118010 CASELCLT REPORT Acute hydrogen sulfide poisoning in a dairy farmer GREGGAcute hydrogen sulfide poisoning GERASIMON, M.D.1, STEVEN BENNETT, M.D., FCCP2, JEFFREY MUSSER, DO3, and JOHN RINARD, DO4 1Major, Medical Corps, U.S. Army, Internal Medicine, Womack Army Medical Center, Fort Bragg, North Carolina, USA 2Major, Medical Corps, U.S. Army, Pulmonary and Critical Care Medicine, Madigan Army Medical Center, Tacoma, Washington, USA 3Major, Medical Corps, U.S. Army, Critical Care Medicine, Madigan Army Medical Center, Tacoma, Washington, USA 4Captain, Medical Corps, U.S. Army, Internal Medicine, Madigan Army Medical Center, Tacoma, Washington, USA Introduction. Hydrogen sulfide is a lipid-soluble gas produced in occupational settings and from decaying organic matter. We present a 36- year-old man who developed acute respiratory arrest from hydrogen sulfide poisoning while performing work as a dairy farmer. Case report. The subject entered a poorly ventilated tank containing degrading eggs and, within seconds, collapsed. Coworkers were able to extract him within minutes but he was apneic. He was intubated by emergency medical services and subsequently managed with supportive care in the intensive care unit. Upon admission, a powerful rotten egg scent was noted and a hydrogen sulfide poisoning was suspected. Serum analysis for the presence of thiosulfate confirmed the diagnosis. Nitrite therapy was not administered as the subject arrived outside of the therapeutic window of effectiveness and showed evidence of excellent oxygenation. His examinations following arrival were consistent with an anoxic brain injury which slowly improved several months after the incident with intensive neuro-rehabilitation.
    [Show full text]
  • Hypoxia , Asphyxia , and Cyanosis
    ﺼﺩﻕﺼﺩﻕ ﺍﺍﷲﷲ ﺍﻟﻌﺍﻟﻌﻅﻅﻴﻡﻴﻡ ﺍﺍﻻﻻﺴﺴﺭﺍﺀﺭﺍﺀ ﺍﻴﺔﺍﻴﺔ 5588 HHypypoxoxiaia ,, AAsspphhyxyxiaia ,, anandd CCyanosiyanosiss HypHypoxiaoxia Def: •• Hypoxiaxia means O2 deficiency at tissue level resulting from disturbance in respiratory processes. •Hypoxemia → ↓ O2 content and PO2 in arterial blood. •• Remember:ber: •• Respiration is the process of transport of atmospheric oxygen to tissues and carbon dioxide from tissues to atmosphere. •• It is divided into 3 divisions;s; I- External Respiration •Pulmonary ventilation •Gas exchange II- Intermediate respiration: •Transport of gases by blood III - Internal Respiration Oxidation of food with release of energy HypHypoxiaoxia Types: It can be divided into: 1) Disturbance in external respiration → Hypoxic hypoxia 2) Disturbance in respiratory function of the blood → •Anaemic hypoxia •Stagnant hypoxia 3) Disturbance in internal respiration → Histotoxic hypoxia. Types and Causes of Hypoxia Hypoxic hypoxia Anaemic hypoxia Stagnant hypoxia histotoxic hypoxia Def., Hypoxia results from Hypoxia results from Hypoxia results from Hypoxia is due to defective oxygenation of deficiency of Hb in reduced tissue defect in internal arterial blood. amount or functions. perfusion respiration 1) ed PO2 in the 1)All types of anaemia 1)General: 1) Cyanide poisoning: Causes ↓ atmospheric air as in high 2)CO poisoning i. Shock. Cyanide blocks more altitude or breathing O2 3) MetHb ii.Congestive heart than 40 enzyme poor mixtures e.g. in 4) Sulph Hb failure. systems mainly mines. iii. Polythycemia. cytochrome oxidase 2) Ventilation defect: 2) Local: system. i. Obstructive disease e.g. ­Obstruction of blood 2) Alcoholic obstruction of the airway . vessels either from poisoning: ii. Restrictive disease e.g. inside by thrombus and Alcohol blocks pulmonary fibrosis . emboli or from outside.
    [Show full text]
  • Hypoxia and Cyanosis Respiratory Block
    Hypoxia and cyanosis Respiratory Block Physiology 439 team work •Black: in male / female slides •Red : important Editing file •Pink: in female slides only •Blue: in male slides only •Green: notes @Physiology_439 •Gray: extra information •Textbook: Guyton + Linda Objectives : Define hypoxia and list its various physiological 01 and pathological causes. Outlines the treatment of hypoxia. 02 Define cyanosis and its clinical presentation 03 Define hypo and hyper-ventilation in terms of 04 arterial PCO2 and PO2. Define hypercapnea and list its causes and 05 manifestations. Helpful video Hypoxia Hypoxia sign not symptom Hypoxia is defined as deficiency of oxygen in the tissue cells. Types of hypoxia Hypoxic or arterial Histotoxic hypoxia Anemic hypoxia Stagnant hypoxia hypoxia (hypoxemia) In males slides only But Causes of hypoxia Explained by girls’ Dr. 1-Inadequate Deficiency of O2 in the oxygenation of the Hypoventilation atmosphere air blood in the lungs (neuromuscular disorders) because of extrinsic (in high attitude) reasons: Diminished respiratory 2-Pulmonary Hypoventilation by increased diseases: airway resistance or decreased Abnormal alveolar membrane diffusion Causes of pulmonary pulmonary compliance. (ventilation/perfusion ratio) thickness in the respiratory membrane due to disease : pneumonia *accumulation of pus*,fibrosis ,pulmonary Edema 3- Inadequate Diminished cellular capacity for tissue capability Poisoning of cellular oxidation enzymes or using oxygen because of vitamin of using O2 toxicity deficiency Causes : 4-Inadequate
    [Show full text]
  • American Osteopathic College of Occupational and Preventive
    American Osteopathic College of Occupational and Preventive Medicine OMED 2013, Mandalay Bay Convention Center, Las Vegas Tuesday, October 1, 2013, Aerospace Medicine Day Office Hypoxia • COL Brian W. Smalley DO, MSPH, CPE Or this… Or even this… Hypoxia • Stateof oxygen deficiency in the blood cells and tissues sufficient to cause impairment of function • 4 Types – Hypoxic – Hypemic – Stagnant – Histotoxic E-1 American Osteopathic College of Occupational and Preventive Medicine OMED 2013, Mandalay Bay Convention Center, Las Vegas Tuesday, October 1, 2013, Aerospace Medicine Day Hypoxic Hypoxia TYPES OF HYPOXIA Reduced pO2 in the lungs HYPOXIC (high altitude) (ALTITUDE) HISTOTOXIC (POISONING) O2 O2 HYPEMIC O2 (BLOOD) O2 Red blood cells STAGNANT (POOLING) Body tissue ALVEOLAR PO2 Oxyhemoglobin AIR Dissociation Curve Po2 = 152 mm Hg Pco2 = 0.3 mm Hg PH2O = 47 mmHg Po2 = Pco2 = 103 mm 40 mm Hg ALVEOLI Hg increased temp, Pco2, or decreased pHshift curve to the right Po2 = 40 mm Hg Po2 = 100 mm Hg Pco2 = 46 mm Hg Pco2 = 40 mm Hg ARTERIES VEINS LUNG CAPILLARIES RIGHT LEFT HEART HEART ALVEOLARAIR AT SEA LEVEL ALVEOLARAIR AT 10,000 FT GAS mmHg GAS mmHg N2 563 N2 376 O2 103 O2 61 CO2 40 CO2 35 H2O 47 H2O 47 TOTAL 760 TOTAL 522 O2Hb SAT = 87% O2Hb SAT = 98% E-2 American Osteopathic College of Occupational and Preventive Medicine OMED 2013, Mandalay Bay Convention Center, Las Vegas Tuesday, October 1, 2013, Aerospace Medicine Day ALVEOLAR AIR AT 34,000 FT ALVEOLARAIR AT 25,000 FT GAS mmHg GAS mmHg N2 179 N2 90 O2 30 O2 26 CO2 27 CO2 24 H2O 47 H2O
    [Show full text]
  • Toxicological Profile for Cyanide
    CYANIDE 25 3. HEALTH EFFECTS 3.1 INTRODUCTION The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and other interested individuals and groups with an overall perspective on the toxicology of cyanide. It contains descriptions and evaluations of toxicological studies and epidemiological investigations and provides conclusions, where possible, on the relevance of toxicity and toxicokinetic data to public health. A glossary and list of acronyms, abbreviations, and symbols can be found at the end of this profile. 3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE To help public health professionals and others address the needs of persons living or working near hazardous waste sites, the information in this section is organized first by route of exposure (inhalation, oral, and dermal) and then by health effect (death, systemic, immunological, neurological, reproductive, developmental, genotoxic, and carcinogenic effects). These data are discussed in terms of three exposure periods: acute (14 days or less), intermediate (15–364 days), and chronic (365 days or more). Levels of significant exposure for each route and duration are presented in tables and illustrated in figures. The points in the figures showing no-observed-adverse-effect levels (NOAELs) or lowest- observed-adverse-effect levels (LOAELs) reflect the actual doses (levels of exposure) used in the studies. LOAELs have been classified into "less serious" or "serious" effects. "Serious" effects are those that evoke failure in a biological system and can lead to morbidity or mortality (e.g., acute respiratory distress or death). "Less serious" effects are those that are not expected to cause significant dysfunction or death, or those whose significance to the organism is not entirely clear.
    [Show full text]
  • Exogenous Hydrogen Sulfide Gas Does Not Induce Hypothermia In
    www.nature.com/scientificreports OPEN Exogenous hydrogen sulfde gas does not induce hypothermia in normoxic mice Received: 20 April 2016 Sebastiaan D. Hemelrijk1, Marcel C. Dirkes1,2, Marit H. N. van Velzen3, Rick Bezemer2,4, Accepted: 7 February 2018 Thomas M. van Gulik1 & Michal Heger 1 Published: xx xx xxxx Hydrogen sulfde (H2S, 80 ppm) gas in an atmosphere of 17.5% oxygen reportedly induces suspended animation in mice; a state analogous to hibernation that entails hypothermia and hypometabolism. However, exogenous H2S in combination with 17.5% oxygen is able to induce hypoxia, which in itself is a trigger of hypometabolism/hypothermia. Using non-invasive thermographic imaging, we demonstrated that mice exposed to hypoxia (5% oxygen) reduce their body temperature to ambient temperature. In contrast, animals exposed to 80 ppm H2S under normoxic conditions did not exhibit a reduction in body temperature compared to normoxic controls. In conclusion, mice induce hypothermia in response to hypoxia but not H2S gas, which contradicts the reported fndings and putative contentions. Hibernation is a hypometabolic state characterized by a regulated decrease in core body temperature (Tb) (i.e., hypothermia) towards ambient temperature (Ta) and consequent reduction in oxygen (O2) consumption and 1 carbon dioxide (CO2) production. It is engaged by several mammalian species to protect the organism from (environmental) stressors such as extreme cold, hypoxia2,3, and starvation4,5 and ultimately death. Te regulated decrease in Tb, which is termed anapyrexia, encompasses the downmodulation of the ‘internal thermostat’ outside of the thermoneutral zone6–10. Te thermoneutral zone constitutes a temperature range in which heat production (from basal metabolism) is in equilibrium with heat loss to the environment.
    [Show full text]