DOCSLIB.ORG

Cheyne–Stokes Respiration During Sleep: Mechanisms and Potential Interventions

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Cheyne–Stokes Respiration During Sleep: Mechanisms and Potential Interventions SympoSium on ReSpiRatoRy medicine Cheyne–Stokes respiration during sleep: mechanisms and potential interventions Cheyne–Stokes respiration is characterized by a typical waxing and waning pattern in breathing amplitude, interspersed with central apnoeas or hypopnoeas. This article reviews current knowledge regarding Cheyne–Stokes respiration with a particular emphasis on the mechanisms and latest methods of intervention. heyne–Stokes respiration is a form of central Mechanisms sleep-disordered breathing in which there are Normal function Ccyclicalfluctuationsinbreathing.Theseleadto The pathophysiological mechanism leading to Cheyne– periodsofcentralapnoeasandhypopnoeas,whichalter- Stokes respiration is very complex, but the instability in nate with periods of hyperpnoea in a gradual waxing respiratorydriveresultsinfluctuationofPaCO2around andwaningfashion.Cheyne–Stokesrespirationisasso- theapnoeicthreshold.HyperventilationandPaCO2below ciatedwithchangingarterialpartialpressuresofoxygen the apnoeic threshold trigger a central apnoea.The cre- (PaO2) and carbon dioxide (PaCO2) (AlDabal and scendo–decrescendo pattern of respiration in Cheyne– BaHammam, 2010). Cheyne–Stokes respiration is Stokesrespirationisacompensationforthechanginglevels believed to mirror an underlying cardiac disease with ofbloodO2andCO2(AlDabalandBaHammam,2010). subsequent negative consequences for the cardiac dis- ease(Oldenburgetal,2014a).Centralsleepapnoeaand Pathological changes Cheyne–Stokesrespirationoccurin30–50%ofpatients Whenrespiratorydisordersdevelop,resultinginchanges withcongestiveheartfailure(Nodaetal,2013).There tolevelsofPaCO2andPaO2,thisisdetectedandstimu- isanincreaseintheprevalenceofCheyne–Stokesrespi- lates feedback regulation, which increases or decreases ration when the severity of heart failure increases and ventilation accordingly. The PaCO2 can be corrected cardiac function decreases (Bitter et al, 2009). At the graduallyandactiveadjustmentstopsafterthisreturnsto same time, the presence of Cheyne–Stokes respiration the normal range, keeping ventilation at a stable level. accelerates the progression of congestive heart failure, However, changes in PaCO2 may not feed back to the whichisassociatedwithincreasedmortalityandmor- CNSinatimelymanner,andactiveventilationregula- bidity and has a significant impact on quality of life tionpersistswhichmayleadtoovercorrectionofPaCO2. (Duningetal,2013). Atthistime,ifPaCO2fallsbelowtheapnoeicthreshold, Severalphysiologicalorpathologicalfactorsinfluence apnoeaappears(Badr,2009). thesusceptibilitytoCheyne–Stokesrespirationincluding ThenormalPaCO2levelduringsleepisabout6.0kPa sex (male), age (>60years old), PaCO2 (5.0kPa) and a (theeucapnicsleepPaCO2level)andtheapnoeicthresh- history of atrial fibrillation (Noda et al, 2013). Some old is usually 0.27–0.80kPa lower. The sleep apnoeic diseasesincreasesusceptibilitytoCheyne–Stokesrespira- thresholdisequaltoormarginallylowerthanthewake- tion, including those causing a dysfunction of central fulnesseucapnicPaCO2level(Eckertetal,2007).The respiratory control centres in the brainstem (strokes, differencebetweentheeucapnicsleepPaCO2leveland traumaticbraininjuriesandbraintumours)(Duninget the apnoeic threshold is critical in the development of al, 2013; Noda et al, 2013), pulmonary hypertension Cheyne–Stokes respiration: the smaller the difference, (Ulrichetal,2008)orend-stagerenalfailure(Perletal, themorelikelytheoccurrenceofCheyne–Stokesrespira- 2006). tion(Randerath,2009). Factorsincludinghypocapnia,arousal,chemoreceptor Dr Yan Wang* is Consultant, Dr Jie Cao* is Consultant, Professor Jing Feng sensitivityenhancementandtheprolongingofcirculat- is Chief Physician and Professor Bao-Yuan Chen is Chief Physician in the ingtimemayleadtoinstabilityoftherespiratorycontrol Department of Respiratory Diseases, Tianjin Medical University General Hospital, system(Figure 1). Ltd Tianjin, 300052, China Hypocapnia Healthcare Correspondence to: Professor J Feng ([email protected]) In normal conditions, a certain concentration of CO 2 MA *Dr Y Wang and Dr J Cao are joint first authors, canstimulatechemoreceptorsandisnecessaryformain- 2015 and contributed equally to this work tenance of normal breathing. When PaCO2 decreases © 390 BritishJournalofHospitalMedicine,July2015,Vol76,No7 HMED_2015_76_7_390_396.indd 390 25/06/2015 16:24 SympoSium on ReSpiRatoRy medicine excessively,theCO2-dependentstimulationofrespirato- patientswithheartfailure.Intheearlystagesofconges- ry drive will be reduced or even eliminated, leading to tiveheartfailure,thechemoreflexactsasacompensatory Cheyne–Stokes respiration. In patients with Cheyne– mechanism.Later,however,ithelpstosustainthesympa- Stokesrespiration,thePaCO2levelisclosetotheeucap- theticactivation,withdetrimentaleffectsoncardiovascu- nicsleepPaCO2level.Therefore,therespiratorycontrol larfunctionandprognosis(Passinoetal,2010). system in these patients is not stable and a slightly Peripheral chemoreceptors include the carotid body increaseinventilationmaycausePaCO2tobelessthan andtheaorticbody.Centralchemoreceptorsarelocated thethreshold.Inpatientswithchronicheartfailure,left onthesurfaceofthemedullaoblongata.Theyregulate ventricular volume and perfusion pressure increases, respirationthroughchangesinPaO2andhydrogenion which worsens pulmonary congestion and pulmonary (H+) concentration. In patients with congestive heart oedema, elevates pulmonary capillary wedge pressure, failure,carotidbodychemoreceptoractivityisenhanced enhancesJ-receptorandCfibresensorstimulationand and is associated with oscillatory breathing (Cheyne– ultimatelyleadstoexcitationofrespiratorydrive(AlDabal Stokes respiration) patterns, increased sympathetic and BaHammam, 2010). The increased sympathetic nerve activity and increased arrhythmia incidence. activityinpatientswithchronicheartfailureasacom- YuminoandBradley(2008)showedthatthecentraland pensationforcardiacpumpfailure,togetherwithhypox- peripheral chemoreceptor excitability in patients who aemia resulting from obstructive apnoea often as a have heart failure and Cheyne–Stokes respiration, comorbidityofheartfailure,canalsoleadtohyperventi- whetherduringwakingorsleeping,ishigherthanthose lationandhypocapnia. without any sleep-disordered breathing or only with obstructive sleep apnoea. Chemoreceptor sensitivity Arousal enhancementmeansthatthesepatientsmaysufferdras- Arousalfromsleepisanimportantprotectiveresponsein ticreactionstotinybloodPaCO2changes,leadingto ordertorestoregasexchange,butitcanleadtorespiratory apnoeaorhypoventilation. controlinstability.Alowarousalthresholdmaybemore Somehormonesanddrugsaffectchemoreceptorsensi- likely to lead to a repetitive Cheyne–Stokes respiration tivity. Adrenaline or noradrenaline can excite carotid cycleastheindividualoscillatesbetweenwakefulnessand bodychemoreceptorsbecausetheycauselocalvasocon- sleep. Some respiratory events, hypoxaemia, periodic leg strictionandreducethebloodflowtothecarotidbody, movementsinsleep,spontaneousawakening,pain,gastro- leadingtohypoxiaandthenischaemia.Circulatingcon- oesophageal reflux disease and insomnia can all lead to centrations of catecholamine increase in patients with arousals.Sleepstateconversionandlowerarousalthreshold congestiveheartfailureandtheperipheralchemoreceptor maybesufficienttopromoteCheyne–Stokesrespiration. sensitivitywillincreaseaswell(Bracketal,2012).Ina A CO2 level which has reached the threshold during sleep can lead to hypercapnia compared to a relatively Figure 1. The main mechanisms and interrelation of Cheyne–Stokes respiration. lowerCO2levelwhichwouldtriggerthisduringarousal, thustriggeringhyperventilation,andultimatelyleadingto Chronic congestive heart failure Cheyne–Stokesrespiration.Ifpatientsimmediatelygointo thesleepstageafterarousals,andthisisfollowedbyhyper- ventilationwhichmaypersistforawhile,thePaCO2will Some respiratory Left ventricular Sympathetic Left rapidly fall below the sleep apnoeic threshold, causing events, volume and activity ↑ ventricular Cheyne–Stokesrespirationagainandleadingtoaseriesof hypoxaemia, perfusion pressure ejection Cheyne–Stokes respiration cycles (Malhotra and Owens, periodic leg ↑, pulmonary fraction 2010).Soarousalsmayplayakeyroleinmaintenanceof movements in congestion, and stroke Functional sleep, spontaneous pulmonary capillary volume ↓ residual hyperventilationinCheyne–Stokesrespiration.Pinnaetal Catecholamine (2012)showedthatfluctuationsinsleep/wakestatearean awakening, pain, wedge pressure ↑ capacity ↓, gastro-oesophageal release ↑ upper airway importantmechanismcontributingtothedevelopmentof reflux disease and instability ↑ oscillatorybreathingpatternsinpatientswithcongestive insomnia Activate J receptors heartfailure.DomenicoPinnaetal(2014)alsofoundthat and C fibre sensors Circulating transitionsbetweenwakefulnessandnon-rapideyemove- Chemoreceptor time ↑ ment sleep paralleled apnoeic events during Cheyne– sensitivity ↑ Stokes respiration in patients with heart failure. They Hyperventilation concludedthattherelationshipsbetweenstatechangesand Arousal Ltd respiratoryeventsareconsistentwiththenotionthatstate Hypocapnia fluctuationspromoteventilatoryinstability. Healthcare Chemoreceptor sensitivity enhancement MA Thepathophysiologicalroleofenhancedchemosensitiv- Respiratory control system instability 2015 © ity to CO2 and/or hypoxia has been emphasized in BritishJournalofHospitalMedicine,July2015,Vol76,No7 391 HMED_2015_76_7_390_396.indd 391 25/06/2015 16:24 SympoSium on ReSpiRatoRy medicine study on rabbits with pacing-induced congestive heart (Farréetal,2004),whichisregardedasa‘gold’standard.
Load more

Recommended publications
  • Approach to Cyanosis in a Neonate.Pdf
    PedsCases Podcast Scripts This podcast can be accessed at www.pedscases.com, Apple Podcasting, Spotify, or your favourite podcasting app. Approach to Cyanosis in a Neonate Developed by Michelle Fric and Dr. Georgeta Apostol for PedsCases.com. June 29, 2020 Introduction Hello, and welcome to this pedscases podcast on an approach to cyanosis in a neonate. My name is Michelle Fric and I am a fourth-year medical student at the University of Alberta. This podcast was made in collaboration with Dr. Georgeta Apostol, a general pediatrician at the Royal Alexandra Hospital Pediatrics Clinic in Edmonton, Alberta. Cyanosis refers to a bluish discoloration of the skin or mucous membranes and is a common finding in newborns. It is a clinical manifestation of the desaturation of arterial or capillary blood and may indicate serious hemodynamic instability. It is important to have an approach to cyanosis, as it can be your only sign of a life-threatening illness. The goal of this podcast is to develop this approach to a cyanotic newborn with a focus on these can’t miss diagnoses. After listening to this podcast, the learner should be able to: 1. Define cyanosis 2. Assess and recognize a cyanotic infant 3. Develop a differential diagnosis 4. Identify immediate investigations and management for a cyanotic infant Background Cyanosis can be further broken down into peripheral and central cyanosis. It is important to distinguish these as it can help you to formulate a differential diagnosis and identify cases that are life-threatening. Peripheral cyanosis affects the distal extremities resulting in blue color of the hands and feet, while the rest of the body remains pinkish and well perfused.
    [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]
  • Central Hypoventilation with PHOX2B Expansion Mutation Presenting in Adulthood S Barratt, a H Kendrick, F Buchanan, a T Whittle
    919 CASE REPORT Thorax: first published as 10.1136/thx.2006.068908 on 1 October 2007. Downloaded from Central hypoventilation with PHOX2B expansion mutation presenting in adulthood S Barratt, A H Kendrick, F Buchanan, A T Whittle ................................................................................................................................... Thorax 2007;62:919–920. doi: 10.1136/thx.2006.068908 suggested cardiac enlargement and an ECG showed right heart Congenital central hypoventilation syndrome most commonly strain. Oxygen saturation by pulse oximetry (SpO2) on air was presents in neonates with sleep related hypoventilation; late 80% and arterial blood gas analysis on 24% fractional inspired onset cases have occurred up to the age of 10 years. It is oxygen showed hypercapnic respiratory failure (pH 7.21, associated with mutations in the PHOX2B gene, encoding a oxygen tension 8.6 kPa, carbon dioxide tension 10.3 kPa). He transcription factor involved in autonomic nervous system was polycythaemic with haematocrit 64%. He was treated with development. The case history is described of an adult who antibiotics, diuretics, controlled oxygen therapy and face mask presented with chronic respiratory failure due to PHOX2B non-invasive positive pressure ventilation (NIV). mutation-associated central hypoventilation and an impaired From day 2 his daytime oxygenation was satisfactory on low response to hypercapnia. flow oxygen without ventilatory support; he remained on nocturnal NIV. Two attempts to record overnight oximetry without ventilatory support failed: his SpO2 fell below 50% due ongenital central hypoventilation syndrome (CCHS, to apnoea within 30 min of sleep onset and the nursing staff ‘‘Ondine’s Curse’’) classically presents in neonates with recommenced NIV on each occasion. Overnight oximetry on air Csleep-dependent hypoventilation.
    [Show full text]
  • Apnea of Prematurity
    www.jpnim.com Open Access eISSN: 2281-0692 Journal of Pediatric and Neonatal Individualized Medicine 2013;2(2):e020213 doi: 10.7363/020213 Advance publication: 2013 Aug 20 Review Apnea of prematurity Piermichele Paolillo, Simonetta Picone Neonatology Department, Neonatal Pathology, Neonatal Intensive Care Unit, Policlinico Casilino Hospital, Rome, Italy Proceedings Proceedings of the 9th International Workshop on Neonatology · Cagliari (Italy) · October 23rd-26th, 2013 · Learned lessons, changing practice and cutting-edge research Abstract Apnea of prematurity (AOP) is one of the most frequent pathologies in the Neonatal Intensive Care Unit, with an incidence inversely related to gestational age. Its etiology is often multi factorial and diagnosis of idiopathic forms requires exclusion of other underlying diseases. Despite being a self- limiting condition which regresses with the maturation of the newborn, possible long-term effects of recurring apneas and the degree of desaturation and bradycardia who may lead to abnormal neurological outcome are not yet clarified. Therefore AOP needs careful evaluation of its etiology and adequate therapy that can be both pharmacological and non-pharmacological. Keywords Apnea of prematurity, idiopathic and secondary apnea, caffeine. Corresponding author Piermichele Paolillo, Neonatology Department, Neonatal Pathology, Neonatal Intensive Care Unit, Ospedale Policlinico Casilino, Rome, Italy; email: [email protected]. How to cite Paolillo P, Picone S. Apnea of Prematurity. J Pediatr Neonat Individual Med. 2013;2(2):e020213. doi: 10.7363/020213. Definition and pathophysiology Apnea of prematurity (AOP) is defined as the cessation of breathing for over 15-20 seconds and is accompanied by oxygen desaturation (SpO2 less than or equal to 80% for ≥ 4 seconds) and/or bradycardia (HR < 2/3 of the basic HR for ≥ 4 seconds) in neonates with a gestational age less then 37 weeks [1, 2].
    [Show full text]
  • Central-Sleep-Apnea-Facilitator-Guide
    Vidya Krishnan and Sutapa Mukherjee for the Sleep Education for Pulmonary Fellows and Practitioners, SRN ATS Committee, 2015 Facilitators Guide I.A. In a patient of this age and presentation the broad category of sleep disorders include: 1) 1) Sleep disordered breathing conditions: OSA, CSA, hypoventilation 2) 2) Insomnia (patients with HF rarely sleep 7-8 hours but usually <4/night and have developed horrible sleep hygiene 3) 3) Parasomnias like REM behavioral disorder (if treated with beta blockers) 4) 4) RLS like symptoms from renal insufficiency/failure, iron deficiency I.B. What are known risk factors for Central Sleep Apnea? 1) age - >65 years old 2) sex – men>women – higher apneic threshold in men 3) heart failure 4) stroke – especially in first 3 months after stroke 5) opioid use 6) renal failure II. A. What is a central sleep apnea? Cessation of airflow for at least 10 seconds, without respiratory effort during the event. II. B. How does your assessment for central sleep apnea risk alter with the given information? - oxycodone can increase risk of central sleep apnea - new onset atrial fibrillation and increased left atrial size can increase the risk of CSA in SHF patient - oropharyngeal exam does not support increased risk of OSA II. C. What are the syndromic presentations of central sleep apnea? What type of central sleep apnea might you expect to see on a sleep study in this patient at this time? 1. Primary central sleep apnea 2. Secondary central sleep apnea a. Cheyne Stokes Respiration b. Secondary to a medical condition – CNS diseases, neuromuscular disease, severe abnormalities in pulmonary mechanics (such as kyphoscoliosis) c.
    [Show full text]
  • Congenital Central Hypoventilation Syndrome
    orphananesthesia Anesthesia recommendations for patients suffering from Congenital Central Hypoventilation Syndrome Disease name: Congenital Central Hypoventilation Syndrome ICD 10: G47.3 Synonyms: Undine Syndrome, Ondine’s Curse Central hypoventilation syndrome (CHS) is a rare disorder, which can be both congenital and acquired. Congenital central hypoventilation syndrome (CCHS) is caused by chromosomal mutations in the PHOX2B gene on chromosome 4p12. The non-congenital or acquired form of CHS may be due to brain stem tumour, infarct, or edema. As the acquired form of this disease is quite rare the main focus of this article will be the congenital form of central hypoventilation syndrome. Medicine in progress Perhaps new knowledge Every patient is unique Perhaps the diagnostic is wrong Find more information on the disease, its centres of reference and patient organisations on Orphanet: www.orpha.net 1 Disease summary The main characteristic of CCHS disease is small tidal volumes and monotonous respiratory rates while awake and asleep, with more profound alveolar hypoventilation during sleep. Due to hypoventilation these patients develop hypercapnia and hypoxemia but lack the normal ventilatory responses to overcome these conditions while asleep. However, while awake they do have the ability to consciously alter the rate and depth of breathing. While sleeping, these children will have shallow respirations interspersed with periods of apnoea most commonly during non-REM sleep. CCHS is a lifelong condition and will require some form of ventilatory support throughout life either positive pressure ventilation via tracheostomy or nasal mask. Other forms of long-term management include negative pressure ventilation and diaphragmatic pacing. CCHS usually manifests itself in the new born period with episodes of cyanosis and apnea and most infants will require mechanical ventilation immediately after birth.
    [Show full text]
  • Congenital Central Hypoventilation Syndrome a Neurocristopathy with Disordered Respiratory Control and Autonomic Regulation
    Congenital Central Hypoventilation Syndrome A Neurocristopathy with Disordered Respiratory Control and Autonomic Regulation Casey M. Rand, BSa, Michael S. Carroll, PhDa,b, Debra E. Weese-Mayer, MDa,b,* KEYWORDS PHOX2B Autonomic Respiratory CCHS Hirschsprung Neuroblastoma KEY POINTS Congenital central hypoventilation syndrome (CCHS) is a rare neurocristopathy with disordered respiratory control and autonomic nervous system regulation. CCHS is caused by mutations in the PHOX2B gene, and the PHOX2B genotype/mutation antici- pates the CCHS phenotype, including the severity of hypoventilation, risk of sinus pauses, and risk of associated disorders including Hirschsprung disease and neural crest tumors. It is important to maintain a high index of suspicion in cases of unexplained alveolar hypoventilation, delayed recovery of spontaneous breathing after sedation or anesthesia, or in the event of severe respiratory infection, and unexplained seizures or neurocognitive delay. This will improve identifica- tion and diagnosis of milder CCHS cases and later onset/presentation cases, allowing for success- ful intervention. Early intervention and conservative management are key to long-term outcome and neurocognitive development. Research is underway to better understand the underlying mechanisms and identify targets for treatment advances and drug interventions. INTRODUCTION with autonomic nervous system dysregulation (ANSD), and a result of maldevelopment of neural Congenital central hypoventilation syndrome crest-derived cells (neurocristopathy). The first re- (CCHS) is a rare disorder of respiratory control ported description of CCHS was in 1970 by This work was supported in part by the Chicago Community Trust Foundation PHOX2B Patent Fund and Res- piratory & Autonomic Disorders of Infancy, Childhood, & Adulthood–Foundation for Research & Education (RADICA-FRE). a Center for Autonomic Medicine in Pediatrics (CAMP), Department of Pediatrics, Ann & Robert H.
    [Show full text]
  • Respiratory System
    Respiratory System Symptoms Respiratory muscle weakness People with myotonic dystrophy commonly have signicant breathing problems that can lead to respiratory failure or require mechanical ventilation in severe cases. These issues may result from muscle weakness (diaphragm, abdominal, and intercostals muscles) and myotonia of respiratory muscles, which lead to poor breathing force and results in low blood oxygen/elevated carbon dioxide levels. Aspiration Breathing of foreign material, including food and drink, saliva, nasal secretions, and stomach uids, into the lungs (aspiration) can result from abnormal swallowing. Without adequate diaphragm, abdomen and chest wall coughing strength to remove the foreign material, the inhaled acidic material can cause chemical injury and inammation in the lungs and bronchial tubes. The injured lungs are then susceptible to infections that can lead to respiratory distress. Sleep apnea Insucient airow due to sleep apnea (periods of absent airow due to narrow airways and interrupted breathing) can result in dangerously low levels of oxygen and high levels of carbon dioxide in the blood. In mild cases, apnea can cause disrupted sleep, excessive fatigue, and morning headaches. In severe cases, apnea can cause high blood pressure, cardiac arrhythmias, and heart attack. The respiratory issues seen with myotonic dystrophy vary depending on the form of the disease. Patterns of Respiratory System Problems Congenital DM1 Prenatal t 'BJMVSFPGDFSFCSBMSFTQJSBUPSZDPOUSPM XIJDINBZSFTVMUJOGFUBMEJTUSFTT t 1VMNPOBSZJNNBUVSJUZ
    [Show full text]
  • End Tidal CO2 and Pulse Oximetry
    CapnographyCapnography McHenryMcHenry WesternWestern LakeLake CountyCounty EMSEMS WhatWhat isis Capnography?Capnography? Capnography is an objective measurement of exhaled CO2 levels. Capnography measures ventilation. It can be used to: Assist in confirmation of intubation. Continually monitor the ET tube placement during transport. Assess ventilation status. Assist in assessment of perfusion. Assess the effectiveness of CPR. Predict critical patient outcomes. CAPNOGRAPHYCAPNOGRAPHY TermTerm capnographycapnography comescomes fromfrom thethe GreekGreek workwork KAPNOS,KAPNOS, meaningmeaning smoke.smoke. AnesthesiaAnesthesia context:context: inspiredinspired andand expiredexpired gasesgases sampledsampled atat thethe YY connector,connector, maskmask oror nasalnasal cannula.cannula. GivesGives insightinsight intointo alterationsalterations inin ventilation,ventilation, cardiaccardiac output,output, distributiondistribution ofof pulmonarypulmonary bloodblood flowflow andand metabolicmetabolic activity.activity. PulmonaryPulmonary PhysiologyPhysiology OxygenationOxygenation vsvs VentilationVentilation MetabolicMetabolic RespirationRespiration TheThe EMSEMS version!version! OxygenationOxygenation –– HowHow wewe getget oxygenoxygen toto thethe tissuestissues VentilationVentilation (the(the movementmovement ofof air)air) –– HowHow wewe getget ridrid ofof carboncarbon dioxide.dioxide. CellularCellular RespirationRespiration Glucose (sugar) + Oxygen → Carbon dioxide + Water + Energy (as ATP ) AlveolarAlveolar RespirationRespiration
    [Show full text]
  • Breathing Problems in Post-Polio
    Breathing Problems in Post-Polio Articles from Post-Polio Health (www.post-polio.org) and Ventilator-Assisted Living (www.ventusers.org) Post-Polio Breathing and Sleep Problems Revisited Post-Polio Health , Vol. 20, No. 2, 2002 The basics of breathing and sleep problems polio survivors may be experiencing Aging and Respiratory Function Post-Polio Health , Vol. 18, No. 1, 2004 The “why” behind the breathing and sleep problems What Is Hypoventilation? Ventilator-Assisted Living , Vol. 17, No. 1, 2003 Concise explanation of underventilation (hypoventilation) Additional Thoughts From Peter C. Gay, MD Post-Polio Health , Vol. 17, No. 2, 2001 Signs and symptoms, oxygen use warning and definition of “abdominal paradox” Hypoventilation? Obstructive Sleep Apnea? Different Tests, Different Treatment Ventilator-Assisted Living, Vol. 19, No. 3, 2005 Explains the tests used for underventilation vs sleep apnea Breathing and Sleep Problems in Polio Survivors International Ventilator Users Network , 2010 More details including clarification of the apneas Tests for Breathing Problems If You Have a Neuromuscular Condition International Ventilator Users Network , 2010 The appropriate tests you should ask your doctor about. Recommended medical reference materials Post-Polio Health International Including International Ventilator Users Network 4207 Lindell Blvd, #110 Saint Louis, MO 63108-2930 USA 314-534-0475 314-534-5070 fax [email protected] [email protected] Post-Polio Breathing and Sleep Problems Revisited Judith R. Fischer, MSLS, Editor, Ventilator-Assisted Living, and Joan L. Headley, MS, Editor, Post-Polio Health “Post-Polio Breathing and Sleep Problems” was published in the fall of 1995 (Polio Network News, Vol. 11, No. 4). As a result of the continual flow of phone calls and emails from polio survivors and family members about this life and death topic, Judith Fischer, editor of Ventilator-Assisted Living (our other quarterly newsletter), and I decided to revisit and revise the original article.
    [Show full text]
  • Respiratory Rehabilitation Program Why Is Sleep Important? Your Body
    Respiratory Rehabilitation Program Sleep Why is sleep important? Your body needs rest and sleep just like it needs food and air. We spend about 1/3 of our lives sleeping. Sleep is a very organized sequence of events that follows a regular, cyclic pattern each night. What happens during sleep is still a mystery to researchers. We do know that it is important for normal motor, cognitive and emotional function. We all feel the need to sleep. After sleeping well, we feel rested and more alert. It is easy to take sleep for granted. Sleep deprivation is common in our society. Lack of sleep can contribute to daytime sleepiness, lack of energy, reduced alertness, impaired judgement, anxiety, reduced exercise tolerance and deterioration in lung function. What about sleep and lung disease? Many people with lung disease have problems sleeping. Some complaints include: trouble falling asleep waking up often trouble falling back to sleep not feeling rested A lack of sleep is often caused by coughing, shortness of breath, chest pain, inactivity, medications, alcohol and age-related changes. Some people with lung disease may also suffer from sleep disorders called: obstructive sleep apnea nocturnal hypoventilation. Obstructive Sleep Apnea This is often called the ‘snoring disease’. Sleep apnea can be a life- threatening problem because breathing is interrupted or stops during sleep. Each time breathing stops, the blood oxygen goes down and the carbon dioxide level goes up. This causes you to wake up. When this happens often, you sleep poorly. This can lead to what is called chronic sleep deprivation. Chronic sleep deprivation causes a sleepy feeling during the day, morning headaches and high blood pressure.
    [Show full text]
  • Obesity Hypoventilation Syndrome (OHS), Can Be a Serious, but Treatable, Complication of Being Obese
    American Thoracic Society PATIENT EDUCATION | INFORMATION SERIES Obesity Hypoventilation Syndrome Obesity hypoventilation syndrome (OHS), can be a serious, but treatable, complication of being obese. What is Obesity Hypoventilation life threatening or result Syndrome (OHS)? in the need to be in OHS is a breathing disorder seen in some people the hospital for serious who are obese that leads to low oxygen levels complications. If left and too much carbon dioxide in your blood. Low untreated, the lack of oxygen and high carbon dioxide levels may develop oxygen can put a strain because of a condition called hypoventilation. on your heart. When Hypoventilation means you are not moving enough treated, your symptoms air in and out of your lungs. With OHS, you may also may be reduced or relieved entirely. Treatment have problems sleeping because of obstructive sleep could improve your quality of life and decrease your apnea. The three main features of OHS are: chances of further complications ■ obesity due to untreated OHS. ■ daytime hypoventilation Do we know what causes OHS besides ■ sleep disordered breathing (such as obstructive obesity? sleep apnea) The cause (or causes) of OHS are not fully OHS has also been called Pickwickian Syndrome understood. OHS may be a combination of your brain being unable to correctly manage your CLIP AND COPY AND CLIP because a character described by the famous author Charles Dickens in his novel, The Posthumous Papers breathing, excess fat producing hormones that of the Pickwick Club,has similar OHS symptoms. cause you to breathe ineffectively, and the extra weight placed on your chest that makes it much What are the symptoms of OHS? more difficult for you to breathe normally.
    [Show full text]