'I Can't Breathe'
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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. -
Slipping Rib Syndrome
Slipping Rib Syndrome Jackie Dozier, BS Edited by Lisa E McMahon, MD FACS FAAP David M Notrica, MD FACS FAAP Case Presentation AA is a 12 year old female who presented with a 7 month history of right-sided chest/rib pain. She states that the pain was not preceded by trauma and she had never experienced pain like this before. She has been seen in the past by her pediatrician, chiropractor, and sports medicine physician for her pain. In May 2012, she was seen in the ER after having manipulations done on her ribs by a sports medicine physician. Pain at that time was constant throughout the day and kept her from sleeping. However, it was relieved with hydrocodone/acetaminophen in the ER. Case Presentation Over the following months, the pain became progressively worse and then constant. She also developed shortness of breath. She is a swimmer and says she has had difficulty practicing due to the pain and SOB. AA was seen by a pediatric surgeon and scheduled for an interventional pain management service consult for a test injection. Following good temporary relief by local injection, she was scheduled costal cartilage removal to treat her pain. What is Slipping Rib Syndrome? •Slipping Rib Syndrome (SRS) is caused by hypermobility of the anterior ends of the false rib costal cartilages, which leads to slipping of the affected rib under the superior adjacent rib. •SRS an lead to irritation of the intercostal nerve or strain of the muscles surrounding the rib. •SRS is often misdiagnosed and can lead to months or years of unresolved abdominal and/or thoracic pain. -
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. -
Signs and Symptoms of COPD
American Thoracic Society PATIENT EDUCATION | INFORMATION SERIES Signs and Symptoms of COPD Chronic obstructive pulmonary disease (COPD) can cause shortness of breath, tiredness, Short ness of Breath production of mucus, and cough. Many people with COPD develop most if not all, of these signs Avo iding Activities and symptoms. Sho rtness wit of Breath h Man s Why is shortness of breath a symptom of COPD? y Activitie Shortness of breath (or breathlessness) is a common Avoiding symptom of COPD because the obstruction in the A breathing tubes makes it difficult to move air in and ny Activity out of your lungs. This produces a feeling of difficulty breathing (See ATS Patient Information Series fact sheet Shor f B tness o on Breathlessness). Unfortunately, people try to avoid this reath Sitting feeling by becoming less and less active. This plan may or Standing work at first, but in time it leads to a downward spiral of: avoiding activities which leads to getting out of shape or becoming deconditioned, and this can result in even more Is tiredness a symptom of COPD? shortness of breath with activity (see diagram). Tiredness (or fatigue) is a common symptom in COPD. What can I do to treat shortness of breath? Tiredness may discourage you from keeping active, which leads to greater loss of energy, which then leads to more If your shortness of breath is from COPD, you can do several tiredness. When this cycle begins it is sometimes hard to things to control it: break. CLIP AND COPY AND CLIP ■■ Take your medications regularly. -
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]. -
Hypercapnia in Hemodialysis (HD)
ISSN: 2692-532X DOI: 10.33552/AUN.2020.01.000508 Annals of Urology & Nephrology Mini Review Copyright © All rights are reserved by David Tovbin Hypercapnia in Hemodialysis (HD) David Tovbin* Department of Nephrology, Emek Medical Center, Israel *Corresponding author: David Tovbin, Department of Nephrology, Emek Medical Received Date: February 04, 2019 Center, Afula, Israel. Published Date: February 14, 2019 Introduction 2 case reports and in our experience with similar patients, BiPAP Acute intra-dialytic exacerbation of hypercapnia in hemodialysis prevented intra-dialytic exacerbation of hypercapnia and possibly (HD) patient has been initially reported 18 years ago [1]. Subsequent respiratory arrest [1,2]. In recent years, new interest was raised similar case was reported few years later [2]. Common features of to HD dialysate bicarbonate concentration. After standardizing to both patients were morbid obesity, a previously stable HD sessions and an acute respiratory infection at time of hypercapnia [1,2]. HD pre-dialysis serum bicarbonate level was recommended as >22 patients with decreased ventilation reserve, due to morbid obesity inflammation malnutrition complex and comorbidities midweek mEq/L [11]. As higher dialysate bicarbonate concentration became with or without obstructive sleep apnea (OSA) and/or obesity more prevalent, a large observation cohort study demonstrated hypoventilation syndrome (OHS) as well as chronic obstructive that high dialysate bicarbonate concentration was associated pulmonary disease (COPD), are at increased risk. COPD is common with worse outcome especially in the more acidotic patients among HD patients but frequently under-diagnosed [3]. Most [12]. However, still not enough attention is paid to HD dialysate COPD patients do well during HD with only mild- moderate pCO2 bicarbonate in the increasing number of patients with impaired increases and slightly decreased pH as compared to non-COPD ventilation, and to their risk of intra-dialytic exacerbation of chronic HD patients [2,4]. -
Basic Life Support Health Care Provider
ELLIS & ASSOCIATES Health Care Provider Basic Life Support MEETS CURRENT CPR & ECC GUIDELINES Ellis & Associates / Safety & Health HEALTH CARE PROVIDER BASIC LIFE SUPPORT - I Ellis & Associates, Inc. P.O. Box 2160, Windermere, FL 34786-2160 www.jellis.com Copyright © 2016 by Ellis & Associates, LLC All rights reserved. No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the publisher, except in the case of brief quotations embodied in critical reviews and certain other noncommercial uses permitted by copyright law. For permission requests, write to the publisher, addressed “Attention: Permissions Coordinator,” at the address below. Ellis & Associates P.O. Box 2160, Windermere, FL 34786-2160 Ordering Information: Quantity sales. Special discounts are available on quantity purchases by corporations, associations, trade bookstores and wholesalers. For details, contact the publisher at the address above. Disclaimer: The procedures and protocols presented in this manual and the course are based on the most current recommendations of responsible medical sources, including the International Liaison Committee on Resuscitation (ILCOR) 2015 Guidelines for CPR & ECC. Ellis & Associates, however, make no guarantee as to, and assume no responsibility for, the correctness, sufficiency, or completeness of such recommendations or information. Additional procedures may be required under particular circumstances. Ellis & Associates disclaims all liability for damages of any kind arising from the use of, reference to, reliance on, or performance based on such information. Library of Congress Cataloging-in-Publication Data Not Available at Time of Printing ISBN 978-0-9961108-0-8 Unless otherwise indicated on the Credits Page, all photographs and illustrations are copyright protected by Ellis & Associates. -
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. -
Appendix A: Codes Used to Define Principal Diagnosis of COVID-19, Sepsis, Or Respiratory Disease
Appendix A: Codes used to define principal diagnosis of COVID-19, sepsis, or respiratory disease ICD-10 code Description N J21.9 'Acute bronchiolitis, unspecified' 1 J80 'Acute respiratory distress syndrome' 2 J96.01 'Acute respiratory failure with hypoxia' 15 J06.9 'Acute upper respiratory infection, unspecified' 7 U07.1 'COVID-19' 1998 J44.1 'Chronic obstructive pulmonary disease with (acute) exacerbation' 1 R05 'Cough' 1 O99.52 'Diseases of the respiratory system complicating childbirth' 3 O99.512 'Diseases of the respiratory system complicating pregnancy, second trimester' 1 J45.41 'Moderate persistent asthma with (acute) exacerbation' 2 B97.29 'Other coronavirus as the cause of diseases classified elsewhere' 33 J98.8 'Other specified respiratory disorders' 16 A41.89 'Other specified sepsis' 1547 J12.89 'Other viral pneumonia' 222 J12.81 'Pneumonia due to SARS-associated coronavirus' 2 J18.9 'Pneumonia, unspecified organism' 8 R09.2 'Respiratory arrest' 1 J96.91 'Respiratory failure, unspecified with hypoxia' 1 A41.9 'Sepsis, unspecified organism' 155 R06.02 'Shortness of breath' 1 J22 'Unspecified acute lower respiratory infection' 4 J12.9 'Viral pneumonia, unspecified' 6 Appendix B: Average marginal effect by month, main analysis and sensitivity analyses Appendix C: Unadjusted mortality rate over time, by age group Appendix D: Results restricted to COVID-19, sepsis, or respiratory disease Any chronic Adjusted mortality Standardized Average marginal Age, median Male, Mortality, Month N condition, (95% Poisson limits) mortality ratio -
Breathing Better with a COPD Diagnosis
Difficulty Breathing Chronic Bronchitis Smoker’s Cough Chronic Coughing Wheezing Em- Chronic Obstructive Pulmonary Disease physema Shortness of Breath Feeling of Suffocation Excess Mucus Difficulty Breathing Chronic Bronchitis Smoker’s Cough Chronic Coughing Wheezing Emphysema Shor tness of Breath Feeling of Suffocation Excess Mucus Difficulty Breathing Chronic Bronchitis Smoker’s Cough Chronic Coughing Wheezing Emphysema Shortness of Breath Feeling of Suffocation Excess Mucus Difficulty Breathing Chronic Bronchitis Smoker’s Cough Chron- ic Coughing Wheezing Emphysema Shortness of Breath Feeling of Suffocation Excess Mu- cus DifficultyBreathing Breathing Chronic Bronchitis Better Smoker’s Cough Chronic Coughing Wheezing Emphysema Shortness of Breath Feeling of Suffocation Excess Mucus Difficulty Breathing Chronic Bronchitis Smoker’s Cough Chronic Coughing Wheezing Emphysema Shor tness of Breath Feeling of SuffocationWith Excess a COPDMucus Difficulty Diagnosis Breathing Chronic Bronchitis Smoker’s Cough Chronic Coughing Wheezing Emphysema Shortness of Breath Feeling of did you know? When COPD is severe, shortness of breath and other COPDdid you is the know? 4th leading cause of death in the symptomswhen you can get are in the diagnosed way of doing even the most UnitedCOPD States.is the 4th The leading disease cause kills ofmore death than in 120,000 basicwith tasks, copd such as doing light housework, taking a Americansthe United eachStates year—that’s and causes 1 serious, death every long-term 4 walk,There and are even many bathing things and that getting you can dressed. do to make minutes—anddisability. The causesnumber serious, of people long-term with COPDdisability. is COPDliving withdevelops COPD slowly, easier: and can worsen over time, increasing.The number More of people than 12with million COPD people is increasing. -
Rivaroxaban (Xarelto®)
Rivaroxaban (Xarelto®) To reduce your bleeding and clotting risk it is important that you attend follow-up appointments with your provider, and have blood tests done as your provider orders. What is rivaroxaban (Xarelto®)? • Rivaroxaban is also called Xarelto® • Rivaroxaban(Xarelto®) is used to reduce the risk of blood clots and stroke in people with an abnormal heart rhythm known as atrial fibrillation, in people who have had a blood clot, or in people who have undergone orthopedic surgery. o Blood clots can block a blood vessel cutting off blood supply to the area. o Rarely, clots can break into pieces and travel in the blood stream, lodging in the heart (causing a heart attack), the lungs (causing a pulmonary embolus), or in the brain (causing a stroke). • If you were previously on Warfarin/Coumadin® and you are starting Rivaroxaban(Xarelto®), do not continue taking warfarin. Rivaroxaban(Xarelto®) replaces warfarin. Xarelto 10mg tablet Xarelto 15mg tablet Xarelto 20mg tablet How should I take rivaroxaban (Xarelto®)? • Take Rivaroxaban(Xarelto®) exactly as prescribed by your doctor. • Rivaroxaban(Xarelto®) should be taken with food. • Rivaroxaban(Xarelto®) tablets may be crushed and mixed with applesauce to make the tablet easier to swallow. - 1 - • If you missed a dose: o Take it as soon as you remember on the same day. • Do not stop taking rivaroxaban suddenly without telling your doctor. This can put you at risk of having a stroke or a blood clot. • If you take too much rivaroxaban, call your doctor or the anticoagulation service. If you are experiencing any bleeding which you cannot get to stop, go to the nearest emergency room. -
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.