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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. -
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. -
BTS Guideline for Oxygen Use in Adults in Healthcare and Emergency
BTS guideline BTS guideline for oxygen use in adults in healthcare Thorax: first published as 10.1136/thoraxjnl-2016-209729 on 15 May 2017. Downloaded from and emergency settings BRO’Driscoll,1,2 L S Howard,3 J Earis,4 V Mak,5 on behalf of the British Thoracic Society Emergency Oxygen Guideline Group ▸ Additional material is EXECUTIVE SUMMARY OF THE GUIDELINE appropriate oxygen therapy can be started in the published online only. To view Philosophy of the guideline event of unexpected clinical deterioration with please visit the journal online ▸ (http://dx.doi.org/10.1136/ Oxygen is a treatment for hypoxaemia, not hypoxaemia and also to ensure that the oxim- thoraxjnl-2016-209729). breathlessness. Oxygen has not been proven to etry section of the early warning score (EWS) 1 have any consistent effect on the sensation of can be scored appropriately. Respiratory Medicine, Salford ▸ Royal Foundation NHS Trust, breathlessness in non-hypoxaemic patients. The target saturation should be written (or Salford, UK ▸ The essence of this guideline can be summarised ringed) on the drug chart or entered in an elec- 2Manchester Academic Health simply as a requirement for oxygen to be prescribed tronic prescribing system (guidance on figure 1 Sciences Centre (MAHSC), according to a target saturation range and for those (chart 1)). Manchester, UK 3Hammersmith Hospital, who administer oxygen therapy to monitor the Imperial College Healthcare patient and keep within the target saturation range. 3 Oxygen administration NHS Trust, London, UK ▸ The guideline recommends aiming to achieve ▸ Oxygen should be administered by staff who are 4 University of Liverpool, normal or near-normal oxygen saturation for all trained in oxygen administration. -
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. -
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). -
Oxygen Toxicity in Neonatal Rats: the Effect of Endotoxin Treatment on Survival During and Post-02 Exposure
0031-3998/87/2102-0 I 09$02.00/0 PEDIATRIC RESEARCH Vol. 21. No.2, 1987 Copyright© 1987 International Pediatric Research Foundation, Inc. Printed in U.S.A. Oxygen Toxicity in Neonatal Rats: The Effect of Endotoxin Treatment on Survival during and post-02 Exposure LEE FRANK Department ofMedicine, Pulmonary Research Labora10ry, University of Miami School of Medicine, Miami, Florida 33136 ABSTRACT. Neonatal rats were treated with low doses of monary 0 2 toxicity (I, 2). However, there are unique pulmonary bacterial lipopolysaccharide (endotoxin) to test for a pro complications associated with prolonged hyperoxic exposure in tective effect of endotoxin against 02 toxicity and the the neonatal animal which could importantly influence both severe inhibition of normal lung development which occurs short and long-term survival post-02 exposure. These complica during prolonged exposure to hyperoxia. The rationale for tions relate to the known inhibitory action of hyperoxia on lung the prophylactic use of endotoxin included its marked biosynthetic processes (1, 3, 4), and the morphological conse protective effect against pulmonary 0 2 toxicity in adult quences this inhibitory action has on the rapidly growing and rats and its lung growth-promoting effect in experimental differentiating newborn (animal) lung. Several studies have now pulmonary stress models. Neonatal rats (4-5 days old) demonstrated that early postnatal exposure to hyperoxia is as survived a 14-day exposure to >95% 0 2 equally well sociated with marked inhibition of the normal septation process whether treated with saline (39/51 = 76%) or with endo by which the large saccular airspaces characteristic of the new toxin (41/51 = 80%). -
Chronic Lung Disease (Bronchopulmonary Dysplasia)
Intensive Care Nursery House Staff Manual Chronic Lung Disease (Bronchopulmonary Dysplasia) was first described in 1967 as severe chronic lung disease (CLD) in preterm infants with severe Respiratory Distress Syndrome (RDS) who received treatment with 100% O2, high inspiratory ventilator pressures and no PEEP. With antenatal glucocorticoids, surfactant treatment and improved ventilatory techniques, CLD has almost disappeared in larger preterm infants and now affects very preterm infants with or without antecedent RDS. DEFINITION: CLD is defined as a need for increased oxygen: • Infants <32 weeks gestation: oxygen requirement at 36 weeks gestational age (GA) or at discharge (whichever comes first) • Infants ≥32 weeks GA: oxygen requirement at age >28 d or at discharge (whichever comes first) INCIDENCE of CLD is inversely related to birth weight and GA: Birth weight (g) Incidence of CLD* 501-750 34% *UCSF 1998-2002 751-1,000 20% 1,001-1,250 5% 1,251-1,500 3% PATHOLOGY includes areas of atelectasis and emphysema, hyperplasia of airway epithelium and interstitial edema. Late changes include interstitial fibrosis and hypertrophy of airway smooth muscle and pulmonary arteriolar musculature. ETIOLOGICAL FACTORS include: • Lung immaturity with (a) ↑ susceptibility to damage from oxygen, barotrauma and volutrauma, (b) surfactant deficiency and (c) immature antioxidant defenses. • Oxygen toxicity • Barotrauma and volutrauma • Pulmonary edema (excessive fluid administration, patent ductus arteriosus) • Inflammation (multiple associated biochemical -
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. -
How Am I Supposed to Breathe with No Air? Nikki Lewis, CVT, VTS (ECC) 2016 ISVMA Conference Proceedings
How am I supposed to breathe with no air? Nikki Lewis, CVT, VTS (ECC) 2016 ISVMA Conference Proceedings When the respiratory center begins to fail, functions such as oxygenation and elimination of carbon dioxide are compromised. This results in hypercapnia and hypoxemia. The major components of gas exchange are the lungs and the respiratory muscles which provide a force or pump to the lungs. If either one of these primary functions are compromised it can result in respiratory failure. Assessment of oxygenation and ventilation To accurately define respiratory failure, you must evaluate arterial blood gasses. A partial pressure of oxygen (PaO2) that’s less than 60mmHg and a partial pressure of carbon dioxide (PaCO2) of greater than 50mmHg define respiratory failure. The term partial pressure refers to the total pressure exerted by a single molecule of this gas. There are several molecules all combined in a cell; however, the partial pressure is the single gas’ pressure. Pulse oximetry is another method of quantifying oxygenation, although not as precise as arterial blood gasses. This is an indirect measurement of PaO2. A pulse oximetry measurement of 91-100% typically reflects a PaO2 of 80-100mmHg, which is a normal value. If the pulse oximetry falls below 91% this results in a rapid drop of the PaO2. Several factors can make the pulse oximetry reading false. These include pigmented tissues, motion and methemoglobinemia. Lastly, the measurement of end-tidal CO2 (ETCO2) will evaluate proper gas exchange. This is done by intubating the patient and using capnography. Capnography measures the expired CO2. Normal ETCO2 range is 35-45mmHg. -
Carbon Monoxide Poisoning: Neurologic Aspects by K K Jain MD (Dr
Carbon monoxide poisoning: neurologic aspects By K K Jain MD (Dr. Jain is a consultant in neurology and has no relevant financial relationships to disclose.) Originally released June 6, 1997; last updated April 5, 2016; expires April 5, 2019 Introduction This article includes discussion of carbon monoxide poisoning: neurologic aspects and CO poisoning. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations. Overview Carbon monoxide can produce several nonspecific symptoms and can mimic several diseases. Most of the signs and symptoms are due to hypoxia, which affects mainly the brain. The most significant neurologic and psychiatric manifestations of carbon monoxide poisoning are seen as subacute or late sequelae, often following a period of complete recovery from an acute episode. There is a possible interaction between nitric oxide, a ubiquitous molecule in the human body, and carbon monoxide. Carbon monoxide exposure initiates processes including oxidative stress that triggers activation of N-methyl-D-aspartate neuronal nitric oxide synthase, and these events are necessary for the progression of carbon monoxide–mediated neuropathology. The most important diagnostic test for carbon monoxide poisoning is the direct spectroscopic measurement of carboxyhemoglobin level in the blood. Brain imaging findings frequently correlate with clinical manifestations. Hyperbaric oxygen plays an important role in the management of carbon monoxide poisoning. Key points • Carbon monoxide poisoning can produce several nonspecific symptoms and can mimic several diseases. • Most of the effects are due to hypoxia. • Neurologic sequelae are significant and may be delayed in onset. • Hyperbaric oxygen plays an important role in management of carbon monoxide poisoning. -
Power Equation for Predicting the Risk of Central Nervous System Oxygen Toxicity at Rest
fphys-11-01007 August 17, 2020 Time: 14:44 # 1 ORIGINAL RESEARCH published: 17 August 2020 doi: 10.3389/fphys.2020.01007 Power Equation for Predicting the Risk of Central Nervous System Oxygen Toxicity at Rest Ben Aviner1, Ran Arieli1,2* and Alexandra Yalov3 1 The Israel Naval Medical Institute, Israel Defense Forces Medical Corps, Haifa, Israel, 2 Eliachar Research Laboratory, Western Galilee Medical Center, Nahariya, Israel, 3 HP – Indigo Division, Nes Ziona, Israel Patients undergoing hyperbaric oxygen therapy and divers engaged in underwater activity are at risk of central nervous system oxygen toxicity. An algorithm for predicting CNS oxygen toxicity in active underwater diving has been published previously, but not for humans at rest. Using a procedure similar to that employed for the derivation of our active diving algorithm, we collected data for exposures at rest, in which subjects breathed hyperbaric oxygen while immersed in thermoneutral water at 33◦C(n = 219) Edited by: or in dry conditions (n = 507). The maximal likelihood method was employed to solve for Costantino Balestra, Haute École Bruxelles-Brabant the parameters of the power equation. For immersion, the CNS oxygen toxicity index 2 10:93 (HE2B), Belgium is KI = t × PO2 , where the calculated risk from the Standard Normal distribution 0:5 2 12:99 Reviewed by: is ZI = [ln(KI ) – 8.99)]/0.81. For dry exposures this is KD = t × PO2 , with risk Enrico M. Camporesi, 0:5 ZD = [ln(KD ) – 11.34)]/0.65. We propose a method for interpolating the parameters at USF Health, United States Thijs Wingelaar, metabolic rates between 1 and 4.4 MET.