BTS Guideline for Oxygen Use in Adults in Healthcare and Emergency
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Breathing & Buoyancy Control: Stop, Breathe, Think, And
Breathing & Buoyancy control: Stop, Breathe, Think, and then Act For an introduction to this five part series see: House of Cards 'As a child I was fascinated by the way marine creatures just held their position in the water and the one creature that captivated my curiosity and inspired my direction more than any is the Nautilus. Hanging motionless in any depth of water and the inspiration for the design of the submarine with multiple air chambers within its shell to hold perfect buoyancy it is truly a grand master of the art of buoyancy. Buoyancy really is the ultimate Foundation skill in the repertoire of a diver, whether they are a beginner or an explorer. It is the base on which all other skills are laid. With good buoyancy a problem does not become an emergency it remains a problem to be solved calmly under control. The secret to mastery of buoyancy is control of breathing, which also gives many additional advantages to the skill set of a safe diver. Calming one's breathing can dissipate stress, give a sense of well being and control. Once the breathing is calmed, the heart rate will calm too and any situation can be thought through, processed and solved. Always ‘Stop, Breathe, Think and then Act.' Breath control is used in martial arts as a control of the flow of energy, in prenatal training and in child birth. At a simpler more every day level, just pausing to take several slow deep breaths can resolve physical or psychological stress in many scenarios found in daily life. -
The Stethoscope: Some Preliminary Investigations
695 ORIGINAL ARTICLE The stethoscope: some preliminary investigations P D Welsby, G Parry, D Smith Postgrad Med J: first published as on 5 January 2004. Downloaded from ............................................................................................................................... See end of article for Postgrad Med J 2003;79:695–698 authors’ affiliations ....................... Correspondence to: Dr Philip D Welsby, Western General Hospital, Edinburgh EH4 2XU, UK; [email protected] Submitted 21 April 2003 Textbooks, clinicians, and medical teachers differ as to whether the stethoscope bell or diaphragm should Accepted 30 June 2003 be used for auscultating respiratory sounds at the chest wall. Logic and our results suggest that stethoscope ....................... diaphragms are more appropriate. HISTORICAL ASPECTS note is increased as the amplitude of the sound rises, Hippocrates advised ‘‘immediate auscultation’’ (the applica- resulting in masking of higher frequency components by tion of the ear to the patient’s chest) to hear ‘‘transmitted lower frequencies—‘‘turning up the volume accentuates the sounds from within’’. However, in 1816 a French doctor, base’’ as anyone with teenage children will have noted. Rene´The´ophile Hyacinth Laennec invented the stethoscope,1 Breath sounds are generated by turbulent air flow in the which thereafter became the identity symbol of the physician. trachea and proximal bronchi. Airflow in the small airways Laennec apparently had observed two children sending and alveoli is of lower velocity and laminar in type and is 6 signals to each other by scraping one end of a long piece of therefore silent. What is heard at the chest wall depends on solid wood with a pin, and listening with an ear pressed to the conductive and filtering effect of lung tissue and the the other end.2 Later, in 1816, Laennec was called to a young characteristics of the chest wall. -
Hypoxia Signaling in Cardiovascular Diseases
DOI: 10.5772/intechopen.80456 ProvisionalChapter chapter 3 Hypoxia Signaling in Cardiovascular Diseases NehaNeha Gupta Gupta and Mohammad Zahid AshrafZahid Ashraf Additional information is available at the end of the chapter http://dx.doi.org/10.5772/intechopen.80456 Abstract Cardiovascular diseases such as stroke, coronary artery disease, and thrombosis remain a global health burden. Understanding the mechanism of these diseases paves the way for development of prophylactics/therapeutics. It is well known at cellular levels; the patho- physiology of most of the cardiovascular disease involves a complicated yet coordinated signaling networks triggered in response to either cellular or tissue levels of hypoxic milieu. Information related to types of hypoxia and signaling mechanism associated to such complications if complied and presented in a comprehensive manner shall prove relevant in proposing common therapeutic targets for wide array of cardiovascular com- plications. The relative functional roles of hypoxia-triggered signaling pathways are also an area of current research. Based upon these facts, this chapter discusses the types of hypoxia and role of hypoxia-mediated signaling pathways in various types of commonly occurring cardiovascular disorders. Keywords: hypoxia, signaling, cardiovascular disorders, thrombosis, therapeutics 1. Introduction Oxygen concentration below the tissue specific physiological levels is termed as ‘Hypoxia’. Depending upon the cause of oxygen scarcity, hypoxia can be classified into Hypoxic hypoxia (occurs due to deficiency in oxygen exchange in lungs or arises due to reduced partial pres- sure of oxygen in air), Anemic hypoxia (arises when the transport of oxygen is affected), stagnant hypoxia (due to delayed blood renewal, or insufficient blood flow) or histotoxic hypoxia (body is not able to use the available oxygen) [1]. -
Monitoring Anesthetic Depth
ANESTHETIC MONITORING Lyon Lee DVM PhD DACVA MONITORING ANESTHETIC DEPTH • The central nervous system is progressively depressed under general anesthesia. • Different stages of anesthesia will accompany different physiological reflexes and responses (see table below, Guedel’s signs and stages). Table 1. Guedel’s (1937) Signs and Stages of Anesthesia based on ‘Ether’ anesthesia in cats. Stages Description 1 Inducement, excitement, pupils constricted, voluntary struggling Obtunded reflexes, pupil diameters start to dilate, still excited, 2 involuntary struggling 3 Planes There are three planes- light, medium, and deep More decreased reflexes, pupils constricted, brisk palpebral reflex, Light corneal reflex, absence of swallowing reflex, lacrimation still present, no involuntary muscle movement. Ideal plane for most invasive procedures, pupils dilated, loss of pain, Medium loss of palpebral reflex, corneal reflexes present. Respiratory depression, severe muscle relaxation, bradycardia, no Deep (early overdose) reflexes (palpebral, corneal), pupils dilated Very deep anesthesia. Respiration ceases, cardiovascular function 4 depresses and death ensues immediately. • Due to arrival of newer inhalation anesthetics and concurrent use of injectable anesthetics and neuromuscular blockers the above classic signs do not fit well in most circumstances. • Modern concept has two stages simply dividing it into ‘awake’ and ‘unconscious’. • One should recognize and familiarize the reflexes with different physiologic signs to avoid any untoward side effects and complications • The system must be continuously monitored, and not neglected in favor of other signs of anesthesia. • Take all the information into account, not just one sign of anesthetic depth. • A major problem faced by all anesthetists is to avoid both ‘too light’ anesthesia with the risk of sudden violent movement and the dangerous ‘too deep’ anesthesia stage. -
Asphyxia Neonatorum
CLINICAL REVIEW Asphyxia Neonatorum Raul C. Banagale, MD, and Steven M. Donn, MD Ann Arbor, Michigan Various biochemical and structural changes affecting the newborn’s well being develop as a result of perinatal asphyxia. Central nervous system ab normalities are frequent complications with high mortality and morbidity. Cardiac compromise may lead to dysrhythmias and cardiogenic shock. Coagulopathy in the form of disseminated intravascular coagulation or mas sive pulmonary hemorrhage are potentially lethal complications. Necrotizing enterocolitis, acute renal failure, and endocrine problems affecting fluid elec trolyte balance are likely to occur. Even the adrenal glands and pancreas are vulnerable to perinatal oxygen deprivation. The best form of management appears to be anticipation, early identification, and prevention of potential obstetrical-neonatal problems. Every effort should be made to carry out ef fective resuscitation measures on the depressed infant at the time of delivery. erinatal asphyxia produces a wide diversity of in molecules brought into the alveoli inadequately com Pjury in the newborn. Severe birth asphyxia, evi pensate for the uptake by the blood, causing decreases denced by Apgar scores of three or less at one minute, in alveolar oxygen pressure (P02), arterial P02 (Pa02) develops not only in the preterm but also in the term and arterial oxygen saturation. Correspondingly, arte and post-term infant. The knowledge encompassing rial carbon dioxide pressure (PaC02) rises because the the causes, detection, diagnosis, and management of insufficient ventilation cannot expel the volume of the clinical entities resulting from perinatal oxygen carbon dioxide that is added to the alveoli by the pul deprivation has been further enriched by investigators monary capillary blood. -
Den170044 Summary
DE NOVO CLASSIFICATION REQUEST FOR CLEARMATE REGULATORY INFORMATION FDA identifies this generic type of device as: Isocapnic ventilation device. An isocapnic ventilation device is a prescription device used to administer a blend of carbon dioxide and oxygen gases to a patient to induce hyperventilation. This device may be labeled for use with breathing circuits made of reservoir bags (21 CFR 868.5320), oxygen cannulas (21 CFR 868.5340), masks (21 CFR 868.5550), valves (21 CFR 868.5870), resuscitation bags (21 CFR 868.5915), and/or tubing (21 CFR 868.5925). NEW REGULATION NUMBER: 21 CFR 868.5480 CLASSIFICATION: Class II PRODUCT CODE: QFB BACKGROUND DEVICE NAME: ClearMateTM SUBMISSION NUMBER: DEN170044 DATE OF DE NOVO: August 23, 2017 CONTACT: Thornhill Research, Inc. 5369 W. Wallace Ave Scottsdale, AZ 85254 INDICATIONS FOR USE ClearMateTM is intended to be used by emergency department medical professionals as an adjunctive treatment for patients suffering from carbon monoxide poisoning. The use of ClearMateTM enables accelerated elimination of carbon monoxide from the body by allowing isocapnic hyperventilation through simulated partial rebreathing. LIMITATIONS Intended Patient Population is adults aged greater than 16 years old and a minimum of 40 kg (80.8 lbs) ClearMateTM is intended to be used by emergency department medical professionals. This device should always be used as adjunctive therapy; not intended to replace existing protocol for treating carbon monoxide poisoning. When providing treatment to a non-spontaneously breathing patient using the ClearMate™ non-spontaneous breathing patient circuit, CO2 monitoring equipment for the measurement of expiratory carbon dioxide concentration must be used. PLEASE REFER TO THE LABELING FOR A MORE COMPLETE LIST OF WARNINGS AND CAUTIONS. -
The Effect of Hypercapnia on Estimated Hepatic Blood
THE EFFECT OF HYPERCAPNIA ON ESTIMATED HEPATIC BLOOD FLOW, CIRCULATING SPLANCHNIC BLOOD VOLUME, AND HEPATIC SULFOBROMOPHTHALEIN CLEARANCE DURING GENERAL ANESTHESIA IN MAN Robert M. Epstein, … , Emanuel M. Papper, Stanley E. Bradley J Clin Invest. 1961;40(3):592-598. https://doi.org/10.1172/JCI104288. Research Article Find the latest version: https://jci.me/104288/pdf THE EFFECT OF HYPERCAPNIA ON ESTIMATED HEPATIC BLOOD FLOW, CIRCULATING SPLANCHNIC BLOOD VOL- UME, AND HEPATIC SULFOBROMOPHTHALEIN CLEARANCE DURING GENERAL ANES- THESIA IN MAN * By ROBERT M. EPSTEIN,t HENRY 0. WHEELER,4 M. JACK FRUMIN, DAVID V. HABIF, EMANUEL M. PAPPER AND STANLEY E. BRADLEY (From the Departments of Anesthesiology, Medicine and Surgery, Presbyterian Hospital, and Columbia University College of Physicians and Surgeons, New York, N. Y.) (Submitted for publication August 9, 1960; accepted November 21, 1960) Splanchnic circulatory adjustments during gen- sure that might otherwise arise from excessive eral anesthesia in man are difficult to assess in and unpredictable movements of the diaphragm the absence of precise information regarding the are eliminated. Data of value in elucidating the depth of anesthesia and the regulation of gas vascular response to hypercapnia and anesthesia exchange. The vasoconstriction responsible for may therefore be obtained from measurements of the fall in hepatic blood flow that has been reported splanchnic blood volume as well as blood flow by several investigators (1, 2) may be attributable (7). In the study reported in this paper, me- to the anesthetic agents themselves, to changes in chanically controlled light anesthesia (thiopental- venous return following reduction in activity and nitrous oxide) alone appeared to have no effect tone of skeletal muscles (3), to hypoxia or to upon the splanchnic bed, suggesting that extrane- hypercapnia. -
Some Major Points on the Causes of Hypoxia [Pdf]
Some major points on the causes of Hypoxia, the Effects of Hyperventilation and Breath Holding Times Source Kings College London tutorials: http://www.kcl.ac.uk/teares/gktvc/vc/dental/year1/lectures/rbmsmajorpoints/hypoxiaandhyperventilation.htm The causes of hypoxia Cells use oxygen to obtain their energy and may not function adequately if their supply of oxygen is impeded; this is called hypoxia which is a contraction of hypo-oxia or low level of oxygen. Many cells can respire anaerobically but the cells in the brain cannot and they need a constant supply of oxygen. A shortage of oxygen in the brain progressively produces inappropriate behaviour, unconsciousness and death which can occur within a few minutes if the brain is completely deprived of oxygen. There are many ways in which hypoxia can be produced but they can be divided into 4 types, each of which has fairly similar effects, because of the way the body works. This handout will be mainly concerned with the causes of hypoxia and will consider the effects only briefly; a later handout will go further into the effects. Please note that the space devoted to each cause in this handout reflects the number of words needed to explain it, not its importance. Hypoxic hypoxia This unfortunately named form of hypoxia occurs when the arterial partial pressure of oxygen (PaO2) is reduced so that the blood leaves the lungs without its haemoglobin being fully saturated. Hypoxic hypoxia can be produced in many ways: if there is a low partial pressure of oxygen in the inspired air, as at high altitudes, the PAO2 and the PaO2 will fall. -
A Case of Extreme Hypercapnia
119 Emerg Med J: first published as 10.1136/emj.2003.005009 on 20 January 2004. Downloaded from CASE REPORTS A case of extreme hypercapnia: implications for the prehospital and accident and emergency department management of acutely dyspnoeic patients L Urwin, R Murphy, C Robertson, A Pollok ............................................................................................................................... Emerg Med J 2004;21:119–120 64 year old woman was brought by ambulance to the useful non-invasive technique to aid the assessment of accident and emergency department. She had been peripheral oxygen saturation. In situations of poor perfusion, Areferred by her GP because of increasing dyspnoea, movement and abnormal haemoglobin, however, this tech- cyanosis, and lethargy over the previous four days. On arrival nique may not reliably reflect PaO2 values. More importantly, of the ambulance crew at her home she was noted to be and as shown in our case, there is no definite relation tachycardic and tachypnoeic (respiratory rate 36/min) with a between SaO2 values measured by pulse oximetry and PaCO2 GCS of 5 (E 3, M 1, V 1). She was given oxygen at 6 l/min via values although it has been shown that the more oxygenated a Duo mask, and transferred to hospital. The patient arrived at the accident and emergency department 18 minutes later. In transit, there had been a clinical deterioration. The GCS was now 3 and the respiratory rate 4/min. Oxygen saturation, as measured by a pulse oximeter was 99%. The patient was intubated and positive pressure ventilation started. Arterial blood gas measurements taken at the time of intubation were consistent with acute on chronic respiratory failure (fig 1). -
Physician Examination Procedures Manual
Physician Examination Procedures Manual September 2011 TABLE OF CONTENTS Chapter Page 1 OVERVIEW OF PHYSICIAN EXAMINATION .......................................... 1-1 1.1 The Role of the Physician in NHANES .............................................. 1-1 1.2 Medical Policy Regarding the Examination ....................................... 1-2 1.2.1 Presence in MEC during MEC Examinations ..................... 1-2 1.2.2 Response to Medical Emergencies ...................................... 1-3 1.2.3 Maintenance of Emergency Equipment and Supplies ......... 1-3 1.3 Physician Examination ....................................................................... 1-3 1.4 Maintenance of Physician’s Examination Room ................................ 1-4 2 EQUIPMENT AND SUPPLIES ...................................................................... 2-1 2.1 Description of Equipment & Supplies ................................................ 2-1 2.2 Inventory ............................................................................................. 2-1 2.3 Blood Pressure .................................................................................... 2-1 2.3.1 Blood Pressure Equipment .................................................. 2-2 2.3.2 Blood Pressure Supplies ...................................................... 2-3 2.3.3 Description of Blood Pressure Equipment and Supplies .... 2-3 2.3.4 Blood Pressure Supplies – Description ............................... 2-5 2.3 HPV Supplies ..................................................................................... -
Chest Auscultation: Presence/Absence and Equality of Normal/Abnormal and Adventitious Breath Sounds and Heart Sounds A
Northwest Community EMS System Continuing Education: January 2012 RESPIRATORY ASSESSMENT Independent Study Materials Connie J. Mattera, M.S., R.N., EMT-P COGNITIVE OBJECTIVES Upon completion of the class, independent study materials and post-test question bank, each participant will independently do the following with a degree of accuracy that meets or exceeds the standards established for their scope of practice: 1. Integrate complex knowledge of pulmonary anatomy, physiology, & pathophysiology to sequence the steps of an organized physical exam using four maneuvers of assessment (inspection, palpation, percussion, and auscultation) and appropriate technique for patients of all ages. (National EMS Education Standards) 2. Integrate assessment findings in pts who present w/ respiratory distress to form an accurate field impression. This includes developing a list of differential diagnoses using higher order thinking and critical reasoning. (National EMS Education Standards) 3. Describe the signs and symptoms of compromised ventilations/inadequate gas exchange. 4. Recognize the three immediate life-threatening thoracic injuries that must be detected and resuscitated during the “B” portion of the primary assessment. 5. Explain the difference between pulse oximetry and capnography monitoring and the type of information that can be obtained from each of them. 6. Compare and contrast those patients who need supplemental oxygen and those that would be harmed by hyperoxia, giving an explanation of the risks associated with each. 7. Select the correct oxygen delivery device and liter flow to support ventilations and oxygenation in a patient with ventilatory distress, impaired gas exchange or ineffective breathing patterns including those patients who benefit from CPAP. 8. Explain the components to obtain when assessing a patient history using SAMPLE and OPQRST. -
The Role of Hypercapnia in Acute Respiratory Failure Luis Morales-Quinteros1* , Marta Camprubí-Rimblas2,4, Josep Bringué2,9, Lieuwe D
Morales-Quinteros et al. Intensive Care Medicine Experimental 2019, 7(Suppl 1):39 Intensive Care Medicine https://doi.org/10.1186/s40635-019-0239-0 Experimental REVIEW Open Access The role of hypercapnia in acute respiratory failure Luis Morales-Quinteros1* , Marta Camprubí-Rimblas2,4, Josep Bringué2,9, Lieuwe D. Bos5,6,7, Marcus J. Schultz5,7,8 and Antonio Artigas1,2,3,4,9 From The 3rd International Symposium on Acute Pulmonary Injury Translational Research, under the auspices of the: ‘IN- SPIRES®' Amsterdam, the Netherlands. 4-5 December 2018 * Correspondence: luchomq2077@ gmail.com Abstract 1Intensive Care Unit, Hospital Universitario Sagrado Corazón, The biological effects and physiological consequences of hypercapnia are increasingly Carrer de Viladomat, 288, 08029 understood. The literature on hypercapnia is confusing, and at times contradictory. Barcelona, Spain On the one hand, it may have protective effects through attenuation of pulmonary Full list of author information is available at the end of the article inflammation and oxidative stress. On the other hand, it may also have deleterious effects through inhibition of alveolar wound repair, reabsorption of alveolar fluid, and alveolar cell proliferation. Besides, hypercapnia has meaningful effects on lung physiology such as airway resistance, lung oxygenation, diaphragm function, and pulmonary vascular tree. In acute respiratory distress syndrome, lung-protective ventilation strategies using low tidal volume and low airway pressure are strongly advocated as these have strong potential to improve outcome. These strategies may come at a price of hypercapnia and hypercapnic acidosis. One approach is to accept it (permissive hypercapnia); another approach is to treat it through extracorporeal means.