DOCSLIB.ORG

HYPERCAPNIC HYPERVENTILATION SPEEDS EMERGENCE from INHALED ANESTHESIA by Nishant a Gopalakrishnan a Dissertation Submitted to T

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
HYPERCAPNIC HYPERVENTILATION SPEEDS EMERGENCE from INHALED ANESTHESIA by Nishant a Gopalakrishnan a Dissertation Submitted to T HYPERCAPNIC HYPERVENTILATION SPEEDS EMERGENCE FROM INHALED ANESTHESIA By Nishant A Gopalakrishnan A dissertation submitted to the faculty of The University of Utah in partial fulfillment of the requirements of Doctor of Philosophy Department of Bioengineering The University of Utah December 2006 Copyright © Nishant A Gopalakrishnan 2006 All Rights Reserved THE UNIVERSITY OF UTAH GRADUATE SCHOOL SUPERVISORY COMMITTEE APPROVAL of a dissertation submitted by This dissertation has been read by each member of the following supervisory committee and by majority vote has been found to be satisfactory. __________________ _________________________________________ Chair: __________________ _________________________________________ __________________ _________________________________________ __________________ _________________________________________ __________________ _________________________________________ THE UNIVERSITY OF UTAH GRADUATE SCHOOL FINAL READING APPROVAL To the Graduate Council of the University of Utah: I have read the dissertation of in its final form and have found that (1) its format, citations, and bibliographic style are consistent and acceptable; (2) its illustrative materials including figures, tables, and charts are in place; and (3) the final manuscript is satisfactory to the supervisory committee and is ready for submission to The Graduate School. ________________________ ______________________________________ Date Chair: Supervisory Committee Approved for the Major Department _____________________________________ Chair/Dean Approved for the Graduate Council _____________________________________ David S. Chapman Dean of The Graduate School ABSTRACT Anesthetic clearance from the lungs and the circle breathing system can be maximized using hyperventilation and high fresh gas flow. However, the concomitant clearance of CO2 also lowers arterial partial pressure of CO2 thereby decreasing cerebral blood flow and hence the clearance of anesthetic from the brain. Emergence time from inhaled anesthesia can be significantly reduced by maintaining hypercapnia (feedback controlled infusion of CO2 or rebreathing) during hyperventilation. We anesthetized seven pigs with 2 MACPIG (minimum alveolar concentration) of isoflurane and four each with 2 MACPIG of sevoflurane or 1 MACPIG of desflurane. After two hours of anesthesia, the animals were hyperventilated and the time to movement of multiple limbs was measured under hypocapnic (EtCO2=22 mmHg) and hypercapnic (EtCO2=55 mmHg) conditions. Emergence time from isoflurane and sevoflurane anesthesia was shortened by an average of 65% with rebreathing or with the CO2 controller (p<0.05). The emergence times obtained from rebreathing were not statistically different from those obtained from precisely tuned feedback controller. We evaluated the differences in emergence time in fifty two surgical patients undergoing 1 MAC of isoflurane, sevoflurane or desflurane anesthesia under mild hypocapnia (EtCO2=29 mmHg) and mild hypercapnia (EtCO2=55 mmHg). The minute ventilation in half the patients was doubled during emergence and hypercapnia was maintained by insertion of additional airway dead space to keep the EtCO2 close to 55 mmHg during hyperventilation. A charcoal canister adsorbed volatile anesthetic agent from the rebreathed dead space. Fresh gas flow was raised to 10 L/min during emergence in all the patients. The time between turning off the vaporizer and the time when the patients opened their eyes in response to command was faster when hypercapnic hyperventilation was maintained using the rebreathing adsorber (p<0.05). The time to tracheal extubation was shortened by 57%. We used a multi compartmental mathematical model to estimate cerebral awakening concentration of anesthetic agent (when patients responded to a command to open eyes) and emergence times from anesthesia. The normalized cerebral awakening concentration to age adjusted MAC for desflurane, sevoflurane and isoflurane were 0.162 ± 0.044, 0.280 ± 0.058 and 0.356 ± 0.105 respectively. The root mean square error of the performance error (calculated as a percent of the predicted value) was between 10% and 24%. The model estimated that there will be at least a 56% reduction in emergence time with hypercapnic hyperventilation. The emergence time after isoflurane, sevoflurane and desflurane anesthesia was shortened significantly by using hypercapnic hyperventilation. The rebreathing device described in the study should be considered following a surgical procedure where a high concentration of the anesthetic agent is maintained right up to the end of the procedure or when surgery ends abruptly without warning. v TABLE OF CONTENTS ABSTRACT. iv LIST OF TABLES . viii LIST OF FIGURES . ix ACNOWLEDGEMENTS. xi 1. INTRODUCTION . 1 1.1. Inhaled Anesthetic Agents. 1 1.2. Anesthesia Delivery System. 2 1.3. MAC and MACawake. 2 1.4. Pharmacology of Inhaled Anesthetics. 4 1.5. Recovery from Anesthesia. 5 1.6. Importance of a Rapid Recovery. 9 1.7. References. 13 2. ANIMAL STUDIES . 15 2.1. Abstract . 15 2.2. Introduction. 16 2.3. Methods. 17 2.4. Results. 27 2.5. Discussion. 38 2.6. Conclusions. 42 2.7. References. 42 3. CLINICAL EVALUATION OF REBREATHING DEVICE . 45 3.1. Abstract . 45 3.2. Introduction. 46 3.3. Methods. 48 3.4. Results. 52 3.5. Discussion. 53 3.6. Conclusions. 64 3.7. References. 65 4. MODEL TO PREDICT EMERGENCE FROM INHALED ANESTHESIA . 68 4.1. Abstract . 68 4.2. Introduction. 69 4.3. Methods. 72 4.4. Results. 86 4.5. Discussion. 87 4.6. Conclusions. 100 4.7. References. 101 5. SUMMARY AND CONCLUSIONS . 104 5.1. Project Overview . 104 5.2. Conclusions . 108 5.3. Limitations of the Study. 109 5.4. Future Work. 110 5.5. References. 111 APPENDIX: EQUATIONS USED IN THE MATHEMATICAL MODEL. 113 vii LIST OF TABLES Table Page 1.1. Tissue/blood partition coefficients. 6 1.2. Average cost of 1 MAC hour of anesthesia. 12 2.1. Average time to spontaneous breathing, EtCO2 during emergence, pre-emergence minute ventilation and emergence minute ventilation. 28 3.1. Patient demographics. 54 3.2. Duration of surgery and total dose of opioids. 55 3.3. EtCO2 at extubation, pre-emergence and emergence BIS and minute ventilation. 56 3.4. Time to open eyes, mouth and extubation. 57 4.1. Volume and blood flow for each compartment. 75 4.2. Partition coefficients used in the model. 76 4.3. Performance measures of the model during each trial. 91 4.4. Estimated emergence times after 0.5, 2 and 8 hours of anesthesia . 92 4.5. Estimated total inhaled and exhaled agent after 0.5,2 and 8 hours of anesthesia. 93 LIST OF FIGURES Figure Page 1.1. Circle breathing circuit. 3 2.1. Block diagram of feedback controller. 19 2.2. Rebreathing device with rebreathing hose, activated charcoal and one-way valves. 21 2.3. Simulated EtCO2 for a various rebreathing hose volumes . 23 2.4. Normalized BIS during emergence from isoflurane and desflurane . 29 2.5. Average time to movement of multiple limbs after isoflurane, sevoflurane and desflurane anesthesia.. 30 2.6. Average time to normalized BIS to rise to 0.95 after isoflurane, sevoflurane and desflurane anesthesia . 31 2.7. Average time to movement of multiple limbs after 1 MAC of desflurane anesthesia. 33 2.8. Typical controller tuning curves for the proportional constant. 34 2.9. Typical controller tuning curves for the integral constant. 35 2.10. Response of the controller for a step change in ventilation and set point. 36 2.11. Inspired agent concentration for the rebreathing device with and without valves. 37 3.1. Rebreathing device . 50 3.2. Normalized BIS during emergence from isoflurane, sevoflurane and desflurane anesthesia. 58 3.3. Average time to tracheal extubation after isoflurane, sevoflurane and desflurane anesthesia . 59 3.4. Average time to normalized BIS to rise to 0.95 after isoflurane, sevoflurane and desflurane anesthesia. 60 4.1. Schematic of the compartments in the model. 73 4.2. Predicted and measured emergence times from 1 MAC of desflurane . 88 4.3. Predicted and measured emergence times from 1 MAC of sevoflurane. 89 4.4. Predicted and measured emergence times from 1 MAC of isoflurane. 90 4.5. Estimated emergence times from 1 MAC of desflurane for different combinations of EtCO2 and minute ventilation. 94 4.6. Estimated emergence times from 1 MAC of sevoflurane for different combinations of EtCO2 and minute ventilation. 95 4.7. Estimated emergence times from 1 MAC of isoflurane for different combinations of EtCO2 and minute ventilation. 96 x ACKNOWLEDGMENTS First and foremost, I would like to thank Dr Westenskow for his generous support and for providing me with an opportunity to work with him on this project. I will always look back on my five years in the Anesthesia Bioengineering Laboratory with great fondness. I appreciate the time and guidance provided by the members of my supervisory committee: Dwayne Westenskow, Joseph Orr, Douglas Christensen, Kenneth Horch and Derek Sakata. I am also indebted to Robert G. Loeb at the University of Arizona, who reviewed this dissertation and provided many useful comments. I would like to thank Dr Sakata for his guidance and assistance with the clinical studies and Scott Mc James for his assistance with the animal studies. I would also like to thank Joseph Orr for his able guidance throughout the project. I am grateful to Anecare Laboratories for their support and interest in this project, to the Society of Technology in Anesthesia and the Anesthesiology Department at the University of Utah for the financial support they have provided.
Load more

Recommended publications
  • Maintenance of Airway Pressure During Filter Exchange Due to Auto-Triggering
    Maintenance of Airway Pressure During Filter Exchange Due to Auto-Triggering Joakim Engstro¨m MSc CCRN, Henrik Reinius MD, Camilla Fro¨jd PhD CCRN, Hans Jonsson MSc CCRN, Go¨ran Hedenstierna MD PhD, and Anders Larsson MD PhD BACKGROUND: Daily routine ventilator-filter exchange interrupts the integrity of the ventilator circuit. We hypothesized that this might reduce positive airway pressure in mechanically ventilated ICU patients, inducing alveolar collapse and causing impaired oxygenation and compliance of the respiratory system. METHODS: We studied 40 consecutive ICU subjects (P /F ratio < 300 mm aO2 IO2 Hg), mechanically ventilated with pressure-regulated volume control or pressure support and > PEEP 5cmH2O. Before the filter exchange, (baseline) tidal volume, breathing frequency, end-inspiratory plateau pressure, and PEEP were recorded. Compliance of the respiratory system was calculated; F , blood pressure, and pulse rate were registered; and P ,P , pH, and base IO2 aO2 aCO2 excess were measured. Measurements were repeated 15 and 60 min after the filter exchange. In addition, a bench test was performed with a precision test lung with similar compliance and ؎ resistance as in the clinical study. RESULTS: The exchange of the filter took 3.5 ؎ 1.2 s (mean SD). There was no significant change in P (89 ؎ 16 mm Hg at baseline vs 86 ؎ 16 mm Hg at 15 aO2 or in compliance of the respiratory system (41 ؎ 11 (24. ؍ min and 88 ؎ 18 mm Hg at 60 min, P ؍ ؎ ؎ mL/cm H2O at baseline vs 40 12 mL/cm H2O at 15 min and 40 12 mL/cm H2O at 60 min, P .32).
    [Show full text]
  • Hyperventilation Syndrome
    Hyperventilation Syndrome INTRODUCTION ● hyperventilation in the presence of the following should immediately confirm an alternative Hyperventilation syndrome is defined as “a rate of diagnosis: ventilation exceeding metabolic needs and higher than that required to maintain a normal level of plasma CO2”. – cyanosis Physiological hyperventilation can occur in a number of – reduced level of consciousness situations, including life-threatening conditions such as: – reduction in SpO2. ● pulmonary embolism ● diabetic ketoacidosis MANAGEMENT 1,2 ● asthma If ABCD need correction then treat as per medical ● hypovolaemia. guidelines as it is unlikely to be due to hyperventilation syndrome but is more likely to be physiological As a rule, hyperventilation due to emotional stress is hyperventilation secondary to an underlying rare in children, and physical causes are much more pathological process. likely to be responsible for hyperventilation. Maintain a calm approach at all times. Specific presenting features can include: Reassure the patient and try to remove the source of ● acute anxiety the patient’s anxiety, this is particularly important in ● tetany due to calcium imbalance children. ● numbness and tingling of the mouth and lips Coach the patient’s respirations whilst maintaining a calm environment. ● carpopedal spasm ● aching of the muscles of the chest ADDITIONAL INFORMATION ● feeling of light headedness or dizziness. The cause of hyperventilation cannot always be determined with sufficient accuracy (especially in the HISTORY early stages) in the pre hospital environment. Refer to dyspnoea guide Always presume hyperventilation is secondary to hypoxia or other underlying respiratory disorder until proven otherwise. 1,2 ASSESSMENT The resulting hypocapnia will result in respiratory Assess ABCD’s: alkalosis bringing about a decreased level of serum ionised calcium.
    [Show full text]
  • 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.
    [Show full text]
  • Prolonged Post-Hyperventilation Apnea in Two Young Adults With
    Munemoto et al. BioPsychoSocial Medicine 2013, 7:9 http://www.bpsmedicine.com/content/7/1/9 CASE REPORT Open Access Prolonged post-hyperventilation apnea in two young adults with hyperventilation syndrome Takao Munemoto1,4*, Akinori Masuda2, Nobuatsu Nagai3, Muneki Tanaka4 and Soejima Yuji5 Abstract Background: The prognosis of hyperventilation syndrome (HVS) is generally good. However, it is important to proceed with care when treating HVS because cases of death following hyperventilation have been reported. This paper was done to demonstrate the clinical risk of post-hyperventilation apnea (PHA) in patients with HVS. Case presentation: We treated two patients with HVS who suffered from PHA. The first, a 21-year-old woman, had a maximum duration of PHA of about 3.5 minutes and an oxygen saturation (SpO2) level of 60%. The second patient, a 22-year-old woman, had a maximum duration of PHA of about 3 minutes and an SpO2 level of 66%. Both patients had loss of consciousness and cyanosis. Because there is no widely accepted regimen for treating patients with prolonged PHA related to HVS, we administered artificial ventilation to both patients using a bag mask and both recovered without any after effects. Conclusion: These cases show that some patients with HVS develop prolonged PHA or severe hypoxia, which has been shown to lead to death in some cases. Proper treatment must be given to patients with HVS who develop PHA to protect against this possibility. If prolonged PHA or severe hypoxemia arises, respiratory assistance using a bag mask must be done immediately. Keywords: Post-hyperventilation apnea, PHA, Hyperventilation syndrome, HVS, Hypocapnia, Hypoxemia Background incidence of death, severe hypoxia, or myocardial infarc- Hyperventilation syndrome (HVS) is characterized by tion in association with the paper-bag method [2].
    [Show full text]
  • VENTILATION THIS IS Evita® V600 Evita® V800
    THIS IS VENTILATION Evita® V800 Evita® V600 D-18935-2010 D-2669-2019 2 | Our mission: Improving outcomes in Intensive Care of patients who are artificially ventilated for 41% at least 14 days, will survive the next year.1 As your specialist in acute care, we focus on reducing mortality rates in the ICU. Supporting patient outcome and increasing staff satisfaction in the ICU via connected technologies and services that help achieve therapeutic goals faster and safer is what drives us. AVOIDING ICU-ACQUIRED WEAKNESS AVOIDING COGNITIVE IMPAIRMENT • Start the weaning process as early as • Provide a comfortable and supportive environment possible to help reduce ventilation time. that helps your patient feel calm and at ease. • Encourage spontaneous breathing, which • Turn the ICU into a healing environment and helps train of respiratory muscles and start enable the patient to feel more comfortable in early mobilisation activities. a family-friendly integrated surrounding. • Improve sedation management and optimise patient interaction. PREVENTION OF VALI / ARDS • Protect the lung with personalised ventilation strategies. • Support spontaneous breathing at any time to provide a seamless transition from controlled ventilation to patient contribution. • Improve clinical results with decision supporting insights from multiple sources. 1) Damuth et al. Lancet Respir Med 2015 D-2795-2019 | 3 1) Damuth et al. Lancet Respir Med 2015 D-3460-2018 4 | All ventilation strategies combined in one device Evita® V600 HIGH-END VENTILATION Evita devices have supported you for over 25 years with high quality standards, the ability to configure and upgrade your machine, and advanced training and service concepts. Experience the next level of ventilator operation.
    [Show full text]
  • Chest Pain and the Hyperventilation Syndrome - Some Aetiological Considerations
    Postgrad Med J: first published as 10.1136/pgmj.61.721.957 on 1 November 1985. Downloaded from Postgraduate Medical Journal (1985) 61, 957-961 Mechanism of disease: Update Chest pain and the hyperventilation syndrome - some aetiological considerations Leisa J. Freeman and P.G.F. Nixon Cardiac Department, Charing Cross Hospital (Fulham), Fulham Palace Road, Hammersmith, London W6 8RF, UK. Chest pain is reported in 50-100% ofpatients with the coronary arteriograms. Hyperventilation and hyperventilation syndrome (Lewis, 1953; Yu et al., ischaemic heart disease clearly were not mutually 1959). The association was first recognized by Da exclusive. This is a vital point. It is time for clinicians to Costa (1871) '. .. the affected soldier, got out of accept that dynamic factors associated with hyperven- breath, could not keep up with his comrades, was tilation are commonplace in the clinical syndromes of annoyed by dizzyness and palpitation and with pain in angina pectoris and coronary insufficiency. The his chest ... chest pain was an almost constant production of chest pain in these cases may be better symptom . .. and often it was the first sign of the understood if the direct consequences ofhyperventila- disorder noticed by the patient'. The association of tion on circulatory and myocardial dynamics are hyperventilation and chest pain with extreme effort considered. and disorders of the heart and circulation was ackn- The mechanical work of hyperventilation increases owledged in the names subsequently ascribed to it, the cardiac output by a small amount (up to 1.3 1/min) such as vasomotor ataxia (Colbeck, 1903); soldier's irrespective of the effect of the blood carbon dioxide heart (Mackenzie, 1916 and effort syndrome (Lewis, level and can be accounted for by the increased oxygen copyright.
    [Show full text]
  • Anesthesia Delivery System Consideration for Use As a Ventilator
    March 23, 2020 Mindray A-Series Anesthesia Delivery System Consideration for use as a Ventilator Dear Valued Customer: In response to the COVID-19 pandemic, the US Food and Drug Administration (FDA) has provided guidance1 that allows for the use of anesthesia delivery systems for continuous ventilation. This is due to the increased demand for mechanical ventilation that is estimated to exceed the available ventilators in Intensive Care Units (ICUs) in the US. While Mindray does not promote anesthesia delivery systems for continuous ventilation, this information is provided in direct response to the current public health crisis. It is advised that the user becomes completely familiar with the information provided and considers all risks and benefits prior to using the anesthesia system for continuous ventilation. When considering the use of an anesthesia delivery system for continuous ventilation, the following functional differences should first be noted: 1） The indications for use are different (please reference the appropriate product Operator’s Manual at https://www.mindraynorthamerica.com/technical-documents/). Specifically, an anesthesia system is used, primarily, in Operating Rooms (ORs) where the case may last for a relatively short period or for several hours, under worst-case conditions. A continuous stand-alone ventilator is used, primarily, in the ICU and may operate continuously for several days. 2） Anesthesia systems are used, primarily, for mandatory ventilation on sedated and muscle- relaxed patients. Continuous stand-alone ventilators are used for spontaneous breathing support. 3） Manual mode on the anesthesia system is used for manually ventilating a patient or letting a patient breathe spontaneously, and is only available on the anesthesia systems (when the APL valve is set to “SP”, the PEEP will be zero (0) and the patient can respire spontaneously).
    [Show full text]
  • Severe Respiratory Acidosis Resulting from a Compromised Coaxial Circuit
    ISSN: 2377-4630 Dang et al. Int J Anesthetic Anesthesiol 2018, 5:072 DOI: 10.23937/2377-4630/1410072 Volume 5 | Issue 2 International Journal of Open Access Anesthetics and Anesthesiology CASE REPORT When Equipment Misbehaves: Severe Respiratory Acidosis Result- ing from a Compromised Coaxial Circuit 1* 1 2 1 Check for Anh Q Dang , Marc Rozner , Nicole Luongo and Shital Vachhani updates 1Department of Anesthesiology & Perioperative Medicine, The University of Texas MD Anderson Cancer Center, USA 2Department of Anesthesiology-CRNA Support, The University of Texas MD Anderson Cancer Center, USA *Corresponding author: Anh Q Dang (MD), Department of Anesthesiology & Perioperative Medicine, The University of Texas MD Anderson Cancer Center, 1400 Holcombe Boulevard, Unit 409, Houston, TX 77030, USA, Tel: (713)-792-6911, Fax: (713)-745-2956 ratory and expiratory unidirectional valves, inspiratory Abstract and expiratory corrugated tubing, a Y connector, an The construction of a coaxial circle breathing circuit enclos- overflow valve (also called a pop-off or adjustable pres- es the inspiratory limb within the expiratory limb to preserve heat, humidity, anesthetic gas, and oxygen. However, the sure-limiting valve), and a reservoir bag. Circle breath- construction also makes kinks or breaks in the enclosed ing circuits facilitate the use of low-flow systems, and inspiratory limb difficult to detect. With kinking or discon- their low resistance makes them appropriate for both nection of the central inspiratory limb, the patient may re- pediatric and adult patients. breathe expiratory gases, leading to a significant increase in dead space and concomitant respiratory acidosis. We A coaxial system (King Circuits, Noblesville, IN) is a describe a clinical case in which a disconnection in the in- circle breathing circuit that encloses the inspiratory limb ner inspiratory limb of a King (King Circuits, Noblesville, IN) coaxial breathing circuit resulted in severe respiratory aci- within the expiratory limb.
    [Show full text]
  • Central Neurogenic Hyperventilation Related to Post-Hypoxic Thalamic Lesion in a Child
    Neurology International 2016; volume 8:6428 Central neurogenic normal. An emergency brain magnetic reso- nance imaging (MRI) was performed. Correspondence: Pinar Gençpinar, Department of hyperventilation related Although there was no apparent lesion in the Pediatric Neurology, Tepecik Training and to post-hypoxic thalamic lesion brain stem, bilateral diffuse thalamic, putami- Research Hospital, Izmir, Turkey. in a child nal and globus palllideal lesions were detected Tel.: +90.505.887.9258. on MRI (Figures 1 and 2). Examination E-mail: [email protected] Pinar Gençpinar,1 Kamil Karaali,2 revealed tachypnea (respiratory rate, 42/min), but other findings were normal. Arterial blood Key words: Central neurogenic hyperventilation; enay Haspolat,3 O uz Dursun4 thalamus; tachypnea; children. Ş ğ gases (ABGs) were pH, 7.52; PaCO2, 29 mmHg; 1Department of Pediatric Neurology, and PaO2, 142 mmHg. The chest radiograph, Contributions: PG prepared the manuscript; KK Tepecik Training of Research Hospital, electrocardiogram, and echocardiogram were prepared the figures and edited in this respect; 2 Izmir; Department of Radiology, normal. Laboratory studies disclosed the fol- OD and SH edited this manuscript and made final 3Department of Pediatric Neurology, lowing values: hematocrit, 33.7%, white blood version. 4Department of Pediatric Intensive Care cell count, 10.6×109/L; sodium, 140 mEq/L; Unit, Akdeniz University Hospital, potassium, 3.7 mEq/L; serum urea nitrogen; 6 Conflict of interest: the authors declare no poten- Antalya, Turkey mg/dL; creatinine, 0.21 mg/ dL; and glucose, tial conflict of interest. 110 mg/dL. Liver transaminases levels were normal. Serum lactate level was 1.97 mmol/L Received for publication: 23 January 2016.
    [Show full text]
  • Mechanical Ventilation
    Fundamentals of MMeecchhaanniiccaall VVeennttiillaattiioonn A short course on the theory and application of mechanical ventilators Robert L. Chatburn, BS, RRT-NPS, FAARC Director Respiratory Care Department University Hospitals of Cleveland Associate Professor Department of Pediatrics Case Western Reserve University Cleveland, Ohio Mandu Press Ltd. Cleveland Heights, Ohio Published by: Mandu Press Ltd. PO Box 18284 Cleveland Heights, OH 44118-0284 All rights reserved. This book, or any parts thereof, may not be used or reproduced by any means, electronic or mechanical, including photocopying, recording or by any information storage and retrieval system, without written permission from the publisher, except for the inclusion of brief quotations in a review. First Edition Copyright 2003 by Robert L. Chatburn Library of Congress Control Number: 2003103281 ISBN, printed edition: 0-9729438-2-X ISBN, PDF edition: 0-9729438-3-8 First printing: 2003 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the author and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, express or implied, with respect to the contents of the publication. Table of Contents 1. INTRODUCTION TO VENTILATION..............................1 Self Assessment Questions.......................................................... 4 Definitions................................................................................
    [Show full text]
  • The Pathophysiology of 'Happy' Hypoxemia in COVID-19
    Dhont et al. Respiratory Research (2020) 21:198 https://doi.org/10.1186/s12931-020-01462-5 REVIEW Open Access The pathophysiology of ‘happy’ hypoxemia in COVID-19 Sebastiaan Dhont1* , Eric Derom1,2, Eva Van Braeckel1,2, Pieter Depuydt1,3 and Bart N. Lambrecht1,2,4 Abstract The novel coronavirus disease 2019 (COVID-19) pandemic is a global crisis, challenging healthcare systems worldwide. Many patients present with a remarkable disconnect in rest between profound hypoxemia yet without proportional signs of respiratory distress (i.e. happy hypoxemia) and rapid deterioration can occur. This particular clinical presentation in COVID-19 patients contrasts with the experience of physicians usually treating critically ill patients in respiratory failure and ensuring timely referral to the intensive care unit can, therefore, be challenging. A thorough understanding of the pathophysiological determinants of respiratory drive and hypoxemia may promote a more complete comprehension of a patient’sclinical presentation and management. Preserved oxygen saturation despite low partial pressure of oxygen in arterial blood samples occur, due to leftward shift of the oxyhemoglobin dissociation curve induced by hypoxemia-driven hyperventilation as well as possible direct viral interactions with hemoglobin. Ventilation-perfusion mismatch, ranging from shunts to alveolar dead space ventilation, is the central hallmark and offers various therapeutic targets. Keywords: COVID-19, SARS-CoV-2, Respiratory failure, Hypoxemia, Dyspnea, Gas exchange Take home message COVID-19, little is known about its impact on lung This review describes the pathophysiological abnormal- pathophysiology. COVID-19 has a wide spectrum of ities in COVID-19 that might explain the disconnect be- clinical severity, data classifies cases as mild (81%), se- tween the severity of hypoxemia and the relatively mild vere (14%), or critical (5%) [1–3].
    [Show full text]
  • Anaesthetic Machine Anatomy
    Anaesthetic Machine Anatomy Year Group: BVSc3 + Document Number: CSL_A00 Equipment list: Anaesthetic Machine Anatomy Equipment for this station: • Anaesthetic machine • Name labels • Function labels Considerations for this station: • Do not attempt to attach cylinders or connect the oxygen pipeline, this machine is for reference only and is NOT a working machine. • The first time you try to complete this task it may be worth refreshing your memory of the anaesthetic machine by reading the section of this booklet marked ‘Answers’. Anyone working in the Clinical Skills Lab must read the ‘CSL_I01 Induction’ and agree to abide by the ‘CSL_I00 House Rules’ & ‘CSL_I02 Lab Area Rules’ Please inform a member of staff if equipment is damaged or about to run out. Clinical Skills: Anaesthetic Machine Anatomy 1 2 3 Using the name labels On the bottom of the name On some of the function provided, name each part of label, place a function label labels there are additional the anaesthetic machine (match the circular tabs). questions. (match/stick the white square Place the correct answers in velcro tab to the yellow the space provided (match square tab). the semi-circular tabs). 4 5 You will need to lift the lid Once you have placed all of to find all of the the labels, use the components! information on the following pages of this booklet to check your answers. Here are some online resources and tutorials that you may find useful: 1. http://mhra.gov.uk/learningcentre/AnaestheticMachines/player.html 2. https://www.youtube.com/watch?v=1LY0eAzrIrE ANSWERS: Anaesthetic Machine Anatomy ANSWERS The following pages contain the answers i.e.
    [Show full text]