Hyperventilation and the Body
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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. -
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. -
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]. -
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. -
Relationship Between PCO 2 and Unfavorable Outcome in Infants With
nature publishing group Articles Clinical Investigation Relationship between PCO2 and unfavorable outcome in infants with moderate-to-severe hypoxic ischemic encephalopathy Krithika Lingappan1, Jeffrey R. Kaiser2, Chandra Srinivasan3, Alistair J. Gunn4; on behalf of the CoolCap Study Group BACKGROUND: Abnormal PCO2 is common in infants with term infants with HIE, both minimum and cumulative expo- hypoxic ischemic encephalopathy (HIE). The objective was to sure to hypocapnia in the first 12 h of the trial were associated determine whether hypocapnia was independently associated with death or adverse neurodevelopmental outcome (13). The with unfavorable outcome (death or severe neurodevelopmen- dose–response relationship between PCO2 and outcome for tal disability at 18 mo) in infants with moderate-to-severe HIE. infants with moderate-to-severe HIE is unknown. METHODS: This was a post hoc analysis of the CoolCap Study The risk of developing hypocapnia or hypercapnia may be in which infants were randomized to head cooling or standard affected by severity of brain injury, intensity and duration of care. Blood gases were measured at prespecified times after newborn resuscitation, timing after the primary injury, and/or randomization. PCO2 and follow-up data were available for 196 response to metabolic acidosis. Thus, in this secondary analy- of 234 infants. Analyses were performed to investigate the rela- sis of the CoolCap Study (14), we sought to confirm the obser- tionship between hypocapnia in the first 72 h after randomiza- vation that -
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. -
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. -
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]. -
Laryngeal Spasm Mimicking Asthma and Vitamin D Deficiency
Case Report Allergy Asthma Immunol Res. 2014 May;6(3):267-269. http://dx.doi.org/10.4168/aair.2014.6.3.267 pISSN 2092-7355 • eISSN 2092-7363 Laryngeal Spasm Mimicking Asthma and Vitamin D Deficiency Monica Masoero,1 Michela Bellocchia,1 Antonio Ciuffreda,1 Fabio LM Ricciardolo,2 Giovanni Rolla,1 Caterina Bucca1* 1Department of Medical Sciences, University of Turin, Italy 2Department of Clinical and Biological Sciences, University of Turin, Italy This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. We present a woman with heterozygous carnitine palmitoyl transferase 2 (CPT-2) deficiency who in the last 6 months suffered from episodic dyspnea and choking. Symptoms could not be attributed to her muscular energy defect, since heterozygous CPT-2 deficiency is usually asymptomatic or causes only mild muscle fatigability. Myopathy is usually triggered by concurrent factors, either genetic (additional muscle enzymes defects) or acquired (metabolic stress). The patient was referred to our respiratory clinic for suspect bronchial asthma. Spirometry showed mild decrease in inspiratory flows. Methacholine challenge was negative. Dyspnea was triggered by hyperventilation-induced hypocapnia, which produced marked decrease in airflow rates, particularly in inspiratory flows, consistent with laryngospasm. Nutritional assessment of the patient showed low serum level of calci- um and vitamin D, attributable to avoidance of milk and dairy products for lactose intolerance and to insufficient sunlight exposure. After calcium and vitamin D supplementation episodic laryngospasm disappeared and hypocapnic hyperventilation test induced very mild change in airflow rates. -
Essential Expectations-Avoiding Hypocapnia and Hyperoxemia in Neonatal Encephalopathy
Journal of Pediatrics and Neonatal Care Essential Expectations-Avoiding Hypocapnia and Hyperoxemia in Neonatal Encephalopathy Mini Review Mini Review Therapeutic hypothermia (TH) is the accepted treatment modality for newborns with moderate to severe neonatal Volume 6 Issue 5 - 2017 encephalopathy likely originating from a hypoxic-ischemic event. Numerous randomized, controlled trials and meta-analyses have shown that TH reduces that the risk of death or major Baystate Children’s Hospital, USA neurodevelopmental disability by 25-35% among treated infants *Corresponding author: Jeffrey Shenberger, Baystate [1,2]. Lung injury, with or without effective respiratory control, Children’s Hospital, Division of Newborn Medicine 759 is present in as many as 80% of infants with moderate-to-severe neonatal encephalopathy who meet the inclusion criteria for TH [3]. 009-3; Email: Although these encephalopathic newborns often require oxygen Chestnut Street Springfield, MA 01199, USA, Tel: 413-794- supplementation or ventilatory support to provide adequate Received: March 08, 2017 | Published: April 04, 2017 gas exchange, their rapidly changing pulmonary mechanics and respiratory drive makes achieving and maintaining eucapnia and normoxemia clinically challenging. Accumulating evidence from clinical trials illustrates the importance of controlling the Although hypocapnia in neonatal encephalopathy may be partial pressures of carbon dioxide (PCO2) and oxygen (PO2) in a surrogate marker for brain injury severity, PCO2 represents order to maximize neurodevelopmental outcomes and ameliorate secondary brain injury resulting from over ventilation and recovery. As many infants undergoing TH are intubated for apnea, oxygenation. frequenta readily bloodmodifiable gas monitoring factor capable and/or of transcutaneousmaximizing neurologic or end- tidal CO monitoring are essential. -
Hypocapnia in the Pathomechanism of Panic Disorder
375 SPECIAL ARTICLE The role of hyperventilation - hypocapnia in the pathomechanism of panic disorder O papel da hiperventilação - a hipocapnia no patomecanismo do distúrbio de pânico Andras Sikter,1 Ede Frecska,2 Ivan Mario Braun,3 Xenia Gonda,2 Zoltan Rihmer2 Abstract Objective: The authors present a profile of panic disorder based on and generalized from the effects of acute and chronic hyperventilation that are characteristic of the respiratory panic disorder subtype. The review presented attempts to integrate three premises: hyperventilation is a physiological response to hypercapnia; hyperventilation can induce panic attacks; chronic hyperventilation is a protective mechanism against panic attacks. Method: A selective review of the literature was made using the Medline database. Reports of the interrelationships among panic disorder, hyperventilation, acidosis, and alkalosis, as well as catecholamine release and sensitivity, were selected. The findings were structured into an integrated model. Discussion: The panic attacks experienced by individuals with panic disorder develop on the basis of metabolic acidosis, which is a compensatory response to chronic hyperventilation. The attacks are triggered by a sudden increase in (pCO2) when the latent (metabolic) acidosis manifests as hypercapnic acidosis. The acidotic condition induces catecholamine release. Sympathicotonia cannot arise during the hypercapnic phase, since low pH decreases catecholamine sensitivity. Catecholamines can provoke panic when hyperventilation causes the hypercapnia to switch to hypocapnic alkalosis (overcompensation) and catecholamine sensitivity begins to increase. Conclusion: Therapeutic approaches should address long-term regulation of the respiratory pattern and elimination of metabolic acidosis. Descriptors: Acidosis; Catecholamines; Hyperventilation; Hypocapnia; Panic disorder Resumo Objetivo: Os autores apresentam um modelo de transtorno do pânico que se baseia nos efeitos da hiperventilação aguda e crônica, característicos do subtipo respiratório de transtorno do pânico. -
ARC SAC SCIENTIFIC REVIEW Voluntary Hyperventilation Preceding Underwater Swimming
ARC SAC SCIENTIFIC REVIEW Voluntary Hyperventilation Preceding Underwater Swimming Questions to be addressed: Does the evidence available on voluntary hyperventilation preceding underwater swimming support the conclusion that over breathing can lead to a sudden loss of consciousness with or without exercise, and therefore must be prohibited at aquatic facilities? Introduction/Overview: Grimaldi J. (1993) notes that over breathing or hyperventilation is breathing at rate and depth higher than necessary to meet the metabolic needs of the body. Despite the incontrovertible neurophysiology findings that hyperventilation prior to underwater swimming can lead to a sudden loss of consciousness and death due to decreased carbon dioxide level, and has been identified as a contributing factor to drowning. This dangerous practice is still used in varying degrees by swimmers at aquatic facilities. Review Process and Literature Search Performed A National Library of Medicine, MEDLINE, PubMed and PsychInfo database search was conducted for the period of 1905 to 2007. Medline searched using the terms (1) the MeSH headings Search headings included combinations of the terms: exercise and hypercapnia; voluntary overbreathing; hyperventilation and hypercapnia; hyperventilation and breath holding; hyperventilation and decreased cerebral function; hyperventilation and underwater swimming; hyperventilation and loss of consciousness; hyperventilation preceding breath holding and unconsciousness; physiology of breath hold diving; physiology of underwater swimming, cardio- respiratory functions and breath hold diving; hyperventilation, breath holding, exercise, and unconsciousness; hypoxia and loss of consciousness; peripheral vasoconstriction reduced cardiac output and bradycardia; bradycardia and breath holding; oxygen apnea This search yielded 1,789 citations. Journal references were obtained and articles consistent with the research questions were reviewed.