DOCSLIB.ORG

Chronic Hypoventilation Syndromes and Sleep-Related Hypoventilation

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Chronic Hypoventilation Syndromes and Sleep-Related Hypoventilation Review Article Chronic hypoventilation syndromes and sleep-related hypoventilation Sebastian Böing1*, Winfried J. Randerath1,2* 1Institute of Pneumology, Clinic for Pneumology and Allergology, Centre of Sleep Medicine and Respiratory Care, Bethanien Hospital, Solingen, Germany; 2University of Cologne, Solingen, Germany *These authors contributed equally to this work. Contributions: (I) Conception and design: All authors; (II) Administrative support: C Miltz; (III) Provision of study materials or patients: None; (IV) Collection and assembly of data: All authors; (V) Data analysis and interpretation: All authors.; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. Correspondence to: Winfried J. Randerath, MD, FCCP, Professor of Medicine. Institute of Pneumology, Clinic for Pneumology and Allergology, Centre of Sleep Medicine and Respiratory Care, Bethanien Hospital, University of Cologne, Aufderhöherstraße 169-175, 42699 Solingen, Germany. Email: [email protected]. Abstract: Chronic hypoventilation affects patients with disorders on any level of the respiratory system. The generation of respiratory impulses can be impaired in congenital disorders, such as central congenital alveolar hypoventilation, in alterations of the brain stem or complex diseases like obesity hypoventilation. The translation of the impulses via spinal cord and nerves to the respiratory muscles can be impaired in neurological diseases. Thoraco-skeletal or muscular diseases may inhibit the execution of the impulses. All hypoventilation disorders are characterized by a reduction of the minute ventilation with an increase of daytime hypercapnia. As sleep reduces minute ventilation substantially in healthy persons and much more pronounced in patients with underlying thoraco-pulmonary diseases, hypoventilation manifests firstly during sleep. Therefore, sleep related hypoventilation may be an early stage of chronic hypoventilation disorders. After treatment of any prevailing underlying disease, symptomatic therapy with non-invasive ventilation (NIV) is required. The adaptation of the treatment should be performed under close medical supervision. Pressure support algorithms have become most frequently used. The most recent devices automatically apply pressure support and vary inspiratory and expiratory pressures and breathing frequency in order to stabilize upper airways, normalize ventilation, achieve best synchronicity between patient and device and aim at optimizing patients’ adherence. Keywords: Chronic hypoventilation syndromes; sleep related hypoventilation; hypercapnic respiratory failure; pathophysiology; obesity hypoventilation syndrome (OHS) Submitted Jan 02, 2015. Accepted for publication Jun 05, 2015. doi: 10.3978/j.issn.2072-1439.2015.06.10 View this article at: http://dx.doi.org/10.3978/j.issn.2072-1439.2015.06.10 Introduction respectively, and destabilize the acid-base balance. However, consecutive increases of the pH value (respiratory alkalosis) Under physiological conditions, alveolar ventilation is closely or decreases (respiratory acidosis) are only measured adapted to metabolism. The minute ventilation is regulated during acute changes of ventilation. In contrast, if hyper- according to the prevailing carbon dioxide production so that or hypoventilation continues for hours, the pH level is the arterial carbon dioxide partial pressure (PaCO ) is adjusted − 2 stabilized by variations of the renal bicarbonate (HCO3 ) to values between 35-45 mmHg. Increases (hyperventilation) excretion (1). Therefore, chronic hypoventilation or decreases (hypoventilation) of the minute ventilation lead syndromes are characterized by: to excess elimination or accumulation of carbon dioxide, • Diminishment of the minute ventilation, i.e., © Journal of Thoracic Disease. All rights reserved. www.jthoracdis.com J Thorac Dis 2015;7(8):1273-1285 1274 Böing and Randerath. Chronic hypoventilation syndromes reductions of the tidal volume or breathing frequency; failure after general anesthesia, severe respiratory illness • Elevation of the PaCO2 >45 mmHg; or respiratory depressants (6). However, in most cases − • pH level in a normal range and an increase of HCO3 hypoventilation begins during childhood and is more (metabolic compensation). pronounced during sleep. The failure of central respiratory Chronic hypoventilation is also called hypercapnic drive may be associated with respiratory rest during sleep. respiratory failure or type II respiratory failure. The CCHS may be accompanied with other phenomena like diminution of minute ventilation can generate from all levels Hirschsprung’s disease, cardiac arrhythmia, and tumors (6,7). of the respiratory system including insufficient respiratory Idiopathic central alveolar hypoventilation is diagnosed drive (brain stem), impaired transmission of the breathing if diseases of lung parenchyma, airways, pulmonary impulses (spinal cord, peripheral nerve), and morphological vessels, chest volume or neuromuscular diseases (NMD), or functional abnormalities of the musculo-skeletal system drug treatment, obesity or congenital hypoventilation of the thorax. Failure of the respiratory regulation on the can be excluded (3,5). Several questions on idiopathic one hand or execution of the impulses on the other hand central alveolar hypoventilation are unresolved. The represent different facets of the pathophysiology which can pathophysiology is unclear although an impairment of be described as “won’t breathe” and “can’t breathe” (2). the hypercapnic and hypoxic chemoresponsiveness and Congenital central alveolar hypoventilation and opioid respiratory drive has been discussed. use represent examples of central disturbances, while Late-onset central hypoventilation with hypothalamic amyotrophic lateral sclerosis (ALS), phrenic nerve palsy, dysfunction is a disorder of the central control of ventilation (3). muscle dystrophies, idiopathic sclerosis are examples of It can be diagnosed if sleep related hypoventilation develops insufficient execution of ventilation. However, the obesity after the first years of life. The patients present with obesity, hypoventilation syndrome (OHS) combines components endocrine abnormalities of hypothalamic origin, severe of both pathomechanisms. Chronic hypoventilation with emotional or behavioral disturbances or a tumor of neural daytime hypercapnia and sleep-related hypoventilation origin (two of these four findings are required). Moreover, (SRH) do not differ substantially. Actually, SRH seems mutations of the PHOX2B-gene and other disorders to represent an early stage of chronic hypoventilation. explaining hypoventilation have to be excluded. Although Nevertheless, this hypothesis has to be confirmed and the disease is associated with hyperphagia, hypoventilation the number of patients with advancing severity has to be persists even if patients lose weight. Diabetes insipidus, evaluated in future research. inappropriate antidiuretic hormone hypersecretion, The most recent edition of the International precocious puberty, hypogonadism, hyperprolactinemia, Classification of Sleep Disorders (3) describes six subtypes hyperthyroidism and decreased growth hormone secretion of hypoventilation disorders in the chapter of sleep related are associated endocrine dysfunctions (3,5). breathing disorders: In contrast to these rare disorders, the OHS and chronic • OHS; hypoventilation due to medical disorders or pharmaceutical • Congenital central alveolar hypoventilation syndrome influences represent the huge majority of chronic and SRH. (CCHS); OHS patients are characterized by obesity (BMI >30 kg/m2) • Late-onset central hypoventilation with hypothalamic and wakefulness hypercapnia. Hypoventilation in OHS dysfunction; cannot primarily be explained by other thoraco-pulmonary, • Idiopathic central alveolar hypoventilation; neuromuscular or idiopathic diseases or pharmaceutical • Sleep related hypoventilation due to a medication or influences (3,5,8,9) (Table 1). substance; Sleep related hypoventilation due to a medical disorder • Sleep related hypoventilation due to a medical disorder. is diagnosed in patients with underlying diseases of the The term CCHS replaces the name “Ondine’s curse”. lung parenchyma or the airways, the pulmonary vessels or CCHS requires evidence of a mutation of the PHOX2B- neurological or musculo-skeletal disorders. In addition, gene leading to a diffuse imbalance of the autonomic system. SRH can be induced by drugs which depress ventilatory Differences in the mutation discriminate congenital from drive or impair muscle function. Long-acting narcotics, de novo development (4). Despite its congenital character, anesthetics, sedatives and muscle relaxants and also alcohol the disease may manifest in adulthood in some cases (3,5). have been discussed (3,5). Chronic opioid intake may be Late-onset phenotypes may present with respiratory associated with central apnoeas, atactic respiration but also © Journal of Thoracic Disease. All rights reserved. www.jthoracdis.com J Thorac Dis 2015;7(8):1273-1285 Journal of Thoracic Disease, Vol 7, No 8 August 2015 1275 Table 1 Characteristics of the obesity hypoventilation syndrome (OHS) Definition criteria Description Chronic hypoventilation Hypercapnia in wakefulness and sleep (PaCO2 ≥45 mmHg or 6 kPa) Obesity Body mass index (BMI) ≥30 kg/m² Absence of other causes of hypercapnia Diseases of the lung parenchyma, airways, pulmonary vessels Neurological, musculo-skeletal or other idiopathic disorders Congenital
Load more

Recommended publications
  • Expiratory Positive Airway Pressure (EPAP) for Obstructive Sleep Apnea
    Subject: Expiratory Positive Airway Pressure (EPAP) for Obstructive Sleep Original Effective Date: Apnea 10/30/13 Policy Number: MCP-145 Revision Date(s): 11/8/2016, 12/10/19 Review Date: 12/16/15, 9/19/17, 7/10/18, 12/10/19, 12 9/20 MCPC Approval Date: 7/10/18, 12/10/19, 12/9/20 Contents DISCLAIMER ............................................................................................................................................................................. 1 Description of Procedure/Service/Pharmaceutical .................................................................................................................. 1 Position Statement ................................................................................................................................................................... 2 Limitations ............................................................................................................................................................................... 3 Summary of Medical Evidence................................................................................................................................................ 3 Coding Information: ................................................................................................................................................................ 7 Resource References ................................................................................................................................................................ 7 REVIEW/REVISION
    [Show full text]
  • The Management of Chronic Insomnia Disorder and Obstructive Sleep
    VA/DoD CLINICAL PRACTICE GUIDELINES The Management of Chronic Module A: Screening for Sleep Disorders Module B: Management of Chronic Insomnia Disorder Insomnia Disorder and 1 11 Adults with a provisional diagnosis of 15 Adult patient 14 Obstructive Sleep Apnea chronic insomnia disorder Refer to trained CBT-I or BBT-I Did the patient 2 provider, either in-person or using complete CBT-I or Sidebar 1: Clinical Features of OSA and Chronic Insomnia Disorder Does the patient, their bed 12 telehealth BBT-I? 3 OSA (see Appendix D in the full CPG for detailed ICSD -3 diagnostic criteria): partner, or their healthcare No Confirm diagnosis and then use SDM and encourage 20 Initiate short-term Yes • Sleepiness provider have complaints Exit algorithm behaviorally-based interventions for chronic insomnia No and/or concerns about the (i.e., CBT-I or BBT-I) (See Sidebar 3) pharmacotherapy • Loud, bothersome snoring patient’s sleep? treatment and/or CIH • Witnessed apneas 16 Yes 13 Was CBT-I or • Nightly gasping/choking 4 Is the patient ablea and willing Yes BBT-I 2 b • Obesity (BMI >30 kg/m ) Perform a clinical assessment, to complete CBT-I or BBT-I? 21 effective? Yes • Treatment resistant hypertension including use of validated screening No No Did insomnia remit after 17 Chronic Insomnia Disorder (see Appendix D in the full CPG for detailed tools (e.g., ISI and STOP 18 Is short-term pharmacotherapy Yes treatment with CIH or short- ICSD-3 diagnostic criteria): questionnaire) (See Sidebar 1) and/or CIH appropriate? (See Refer to sleep term pharmacotherapy with • Difficulty initiating sleep, difficulty maintaining sleep, or early -morning Sidebars 4 and 5) specialist for further no additional medication No assessment awakenings 6 No 5 19 required? • The sleep disturbance causes clinically significant distress or impairment in Are screening, history, Manage the important areas of functioning and/or physical exam No diagnosed sleep Reassess or reconsider behavioral treatments as needed.
    [Show full text]
  • 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]
  • Diagnosis, Management and Pathophysiology of Central Sleep Apnea in Children ⇑ Anya T
    Paediatric Respiratory Reviews 30 (2019) 49–57 Contents lists available at ScienceDirect Paediatric Respiratory Reviews Review Diagnosis, management and pathophysiology of central sleep apnea in children ⇑ Anya T. McLaren a, Saadoun Bin-Hasan b, Indra Narang a,c, a Division of Respiratory Medicine, The Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G1X8, Canada b Department of Pediatrics, Division of Respiratory Medicine, Farwaniya Hospital, Kuwait c Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada Educational aims The reader will be able to: Identify the different types of pediatric central sleep apnea (CSA) Describe the clinical presentation of CSA in children Discuss the pathophysiology of CSA Understand the evaluation of CSA in the pediatric population article info summary Keywords: Central sleep apnea (CSA) is thought to occur in about 1–5% of healthy children. CSA occurs more com- Central sleep apnea monly in children with underlying disease and the presence of CSA may influence the course of their dis- Sleep disordered breathing ease. CSA can be classified based on the presence or absence of hypercapnia as well as the underlying Hypoventilation condition it is associated with. The management of CSA needs to be tailored to the patient and may Children include medication, non-invasive ventilation, and surgical intervention. Screening children at high risk will allow for earlier diagnosis and timely therapeutic interventions for this population. The review will highlight the pathophysiology, prevalence and diagnosis of CSA in children. An algorithm for the manage- ment of CSA in healthy children and children with underlying co-morbidities will be outlined. Ó 2018 Elsevier Ltd.
    [Show full text]
  • Sleep Bruxism and Sleep-Disordered Breathing
    CRITICAL APPRAISAL Sleep Bruxism and Sleep-Disordered Breathing Author STEVEN D BENDER, DDS*, Associate Editor EDWARD J. SWIFT JR., DMD, MS ABSTRACT Sleep bruxism (SB) is a repetitive jaw muscle activity with clenching or grinding of the teeth during sleep. SB is characterized by what is known as rhythmic masticatory muscle activity (RMMA). RMMA is the laboratory polysomnographic finding that differentiates SB from other oromandibular movements seen during sleep. Most often RMMA episodes are associated with sleep arousal. Some patients will report similar complaints related to both SB and sleep disordered breathing (SDB). There are some reports that would suggest that SB is a result of SDB. It has has been postulated that SB is a compensatory mechanism to re establish muscle tone of the upper airway. While these disorders do in fact often present concomitantly, the relationship between the two is yet to be fully elucidated. This Critical Appraisal reviews 3 recent publications with the intent to better define what relationships may exists between SDB and SB. While the current evidence appears to support the notion that these are often concomitant disorders, it also makes clear that evidence to support the hypothesis that SDB is causative for SB is currently lacking. (J Esthet Restor Dent 00:000–000, 2016) Sleep Bruxismin Patients with Sleep-disordered Breathing T.T. SJOHOLM,€ A.A. LOWE, K. MIYAMOTO, A. FLEETHAM, C.F. RYAN Archives of Oral Biology 2000 (45:889–96) ABSTRACT index of more than five per hour of sleep were excluded. Sleep breathing parameters were measured Objective: The primary objective was to determine the using polysomnagraphic (PSG) recordings.
    [Show full text]
  • Sleep-Apnea-Protocol.Pdf
    Evidence-based Practice Center Systematic Review Protocol Project Title: Continuous Positive Airway Pressure Treatment for Obstructive Sleep Apnea in Medicare Eligible Patients I. Background Sleep apnea is a common disorder that affects people of all ages. It is characterized by periods of airflow cessation (apnea) or reduced airflow (hypopnea) during sleep. Sleep apnea may be caused by mechanical obstruction of the airways resulting in disturbed airflow patterns, by a central loss of respiratory drive, or a combination of the two (mixed). Obstructive sleep apnea- hypopnea syndrome, more commonly called obstructive sleep apnea (OSA), is the most common type of sleep apnea.1 Definition and severity of obstructive sleep apnea Sleep apnea is primarily diagnosed with sleep tests that measure sleep time (and often other sleep measures) and respiratory events. OSA is distinguished from central sleep apnea by the presence of respiratory effort during episodes of apnea and hypopnea (in contrast with central sleep apnea where respiratory effort is lacking). The severity of OSA is typically quantified by the sum of the number of apneas and hypopneas per hour of sleep, a quantity that has been termed the apnea-hypopnea index (AHI). AHI is often used as part of both diagnosis (and, thus, study inclusion criteria) and as a surrogate measure for health outcomes (also called an intermediate outcome) in studies. The American Academy of Sleep Medicine (AASM) publishes scoring manuals for AHI and other physiological events to characterize OSA. In the United States, AASM is the predominant accrediting institution for sleep laboratories. AASM first published its scoring manual in 1999 (known as the “Chicago” Criteria).2 They have amended their definitions of breathing events, sleep time, and how these are measured multiple times since their first set of criteria, with major revisions in 2007,3 and in 2012.4 Minor revisions have been made almost annually since (the current version is v2.6,5 released in 2020).
    [Show full text]
  • Sleep Apnea Sleep Apnea
    Health and Safety Guidelines 1 Sleep Apnea Sleep Apnea Normally while sleeping, air is moved at a regular rhythm through the throat and in and out the lungs. When someone has sleep apnea, air movement becomes decreased or stops altogether. Sleep apnea can affect long term health. Types of sleep apnea: 1. Obstructive sleep apnea (narrowing or closure of the throat during sleep) which is seen most commonly, and, 2. Central sleep apnea (the brain is causing a change in breathing control and rhythm) Obstructive sleep apnea (OSA) About 25% of all adults are at risk for sleep apnea of some degree. Men are more commonly affected than women. Other risk factors include: 1. Middle and older age 2. Being overweight 3. Having a small mouth and throat Down syndrome Because of soft tissue and skeletal alterations that lead to upper airway obstruction, people with Down syndrome have an increased risk of obstructive sleep apnea. Statistics show that obstructive sleep apnea occurs in at least 30 to 75% of people with Down syndrome, including those who are not obese. In over half of person’s with Down syndrome whose parents reported no sleep problems, sleep studies showed abnormal results. Sleep apnea causing lowered oxygen levels often contributes to mental impairment. How does obstructive sleep apnea occur? The throat is surrounded by muscles that are active controlling the airway during talking, swallowing and breathing. During sleep, these muscles are much less active. They can fall back into the throat, causing narrowing. In most people this doesn’t affect breathing. However in some the narrowing can cause snoring.
    [Show full text]
  • Noninvasive Positive Pressure Ventilation in the Home
    Technology Assessment Program Noninvasive Positive Pressure Ventilation in the Home Final Technology Assessment Project ID: PULT0717 2/4/2020 Technology Assessment Program Project ID: PULT0717 Noninvasive Positive Pressure Ventilation in the Home (with addendum) Prepared for: Agency for Healthcare Research and Quality U.S. Department of Health and Human Services 5600 Fishers Lane Rockville, MD 20857 www.ahrq.gov Contract No: HHSA290201500013I_HHSA29032004T Prepared by: Mayo Clinic Evidence-based Practice Center Rochester, MN Investigators: Michael Wilson, M.D. Zhen Wang, Ph.D. Claudia C. Dobler, M.D., Ph.D Allison S. Morrow, B.A. Bradley Beuschel, B.S.P.H. Mouaz Alsawas, M.D., M.Sc. Raed Benkhadra, M.D. Mohamed Seisa, M.D. Aniket Mittal, M.D. Manuel Sanchez, M.D. Lubna Daraz, Ph.D Steven Holets, R.R.T. M. Hassan Murad, M.D., M.P.H. Key Messages Purpose of review To evaluate home noninvasive positive pressure ventilation (NIPPV) in adults with chronic respiratory failure in terms of initiation, continuation, effectiveness, adverse events, equipment parameters and required respiratory services. Devices evaluated were home mechanical ventilators (HMV), bi-level positive airway pressure (BPAP) devices, and continuous positive airway pressure (CPAP) devices. Key messages • In patients with COPD, home NIPPV as delivered by a BPAP device (compared to no device) was associated with lower mortality, intubations, hospital admissions, but no change in quality of life (low to moderate SOE). NIPPV as delivered by a HMV device (compared individually with BPAP, CPAP, or no device) was associated with fewer hospital admissions (low SOE). In patients with thoracic restrictive diseases, HMV (compared to no device) was associated with lower mortality (low SOE).
    [Show full text]
  • Daytime Sleepiness
    Med Lav 2017; 108, 4: 260-266 DOI: 10.23749/mdl.v108i4.6497 Daytime sleepiness: more than just Obstructive Sleep Apnea (OSA) Luigi Ferini-Strambi, Marco Sforza, Mattia Poletti, Federica Giarrusso, Andrea Galbiati IRCCS San Raffaele Scientific Institute, Department of Clinical Neurosciences and Università Vita-Salute San Raffaele, Milan, Italy KEY WORDS: Daytime sleepiness; Obstructive Sleep Apnea (OSA); hypersomnia PAROLE CHIAVE: Sonnolenza diurna; Apnee Ostruttive del Sonno (OSA); ipersonnia SUMMARY Excessive Daytime Sleepiness (EDS) is a common condition with a significant impact on quality of life and general health. A mild form of sleepiness can be associated with reduced reactivity and modest distractibility symptoms, but more severe symptomatic forms are characterized by an overwhelming and uncontrollable need to sleep, causing sud- den sleep attacks, amnesia and automatic behaviors. The prevalence in the general population is between 10 and 25%. Furthermore, EDS has been considered a core symptom of obstructive sleep apnea (OSA), as well as being the main symptom of primary hypersomnias such as narcolepsy types 1 and 2, and idiopathic hypersomnia. Moreover, it can be considered secondary to other sleep disorders (Restless Legs Syndrome, Chronic insomnia, Periodic Limb Movements), psychiatric conditions (Depression, Bipolar Disorder) or a consequence of the intake/abuse of drugs and/or substances. An accurate medical history cannot be sufficient for the differential diagnosis, therefore instrumental recordings by means of polysomnography and the Multiple Sleep Latency Test (MSLT) are mandatory for a correct diagnosis and treatment of the underlying cause of EDS. RIASSUNTO «Sonnolenza diurna: più di una semplice Apnea Ostruttiva nel Sonno (OSA)». L’eccessiva sonnolenza diurna (Excessive Daytime Sleepiness, EDS) è una condizione molto comune con un impatto significativo sulla qualità di vita e sulla salute in generale.
    [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]
  • Respiratory Insufficiency in Patients with ALS at Or Near the End of Life
    Amyotrophic lateral sclerosis (ALS) is a devastating motor neuron disease causing progressive paralysis and eventual death, usually from respiratory failure. Treatment for ALS is focused primarily on optimal symptom manage- ment because there is no known cure. Respiratory symptoms that occur are related to the disease process and can be very distressing for patients and their loved ones. Recommendations on the management of respira- tory insufficiency are provided to help guide clinicians caring for patients with ALS. Hospice and Palliative Care Feature The Management of Andrea L. Torres, APN, CNP Respiratory Insufficiency in Patients With ALS at or Near the End of Life 186 Home Healthcare Nurse www.homehealthcarenurseonline.com Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Introduction 2007). By the time most patients are definitively Amyotrophic lateral sclerosis (ALS) is a devastat- diagnosed, they are often already in an advanced ing motor neuron disease characterized by pro- stage of the disease (Wood-Allum & Shaw, 2010). gressive muscle weakness eventually leading to Life expectancy is typically 3-5 years from the paralysis and death. The onset typically occurs onset of symptoms (Elman et al., 2007). in late middle age, with men slightly more af- fected than women (Wood-Allum & Shaw, 2010). Palliative Care Approaches for ALS Patients The majority of cases of ALS have no known Due to the progressive nature of ALS, early pal- cause; about 10% of ALS cases are linked to a fa- liative care is an essential component in the milial trait (Ferguson & Elman, 2007). Treatment treatment plan, and should begin as soon as the is primarily focused on optimal symptom man- diagnosis of ALS is confirmed (Elman et al., 2007).
    [Show full text]
  • Obstructive Sleep Apnea Causing Chest Pain and Cardiac Arrhythmias
    Journal of Cardiology & Cardiovascular Therapy ISSN 2474-7580 Case Report J Cardiol & Cardiovasc Ther Volume 1 Issue 3 - September 2016 Copyright © All rights are reserved by Irtaqa Ali Hasnain DOI: 10.19080/JOCCT.2016.01.555565 Obstructive Sleep Apnea Causing Chest Pain and Cardiac Arrhythmias Irtaqa Ali Hasnain1 and Mujtaba Ali Hasnain2 1Department of Emergency Medicine, Bahria Town Hospital, Lahore, Pakistan 2Department of Medicine, Saint Barnabas Medical Center, USA Submission: September 16, 2016; Published: September 28, 2016 *Corresponding author: Irtaqa Ali Hasnain, Bahria Town Hospital, 670 Gul Mohar Block, Sector C, Bahria Town, Lahore, Pakistan Introduction Discussion Chest pain is one of the most common complaints for patients Although most patients with obstructive sleep apnea (OSA) presenting to the hospital. It can be a manifestation of coronary present with typical features like snoring, day-time sleepiness, artery disease, acid peptic disease, pleuritis, or musculoskeletal fatigue, and restlessness but they can present with chest pain problems. Patients with obstructive sleep apnea may present or cardiac arrhythmias only. The prevalence of obstructive sleep with chest pain and heart block but lack typical features such as day-time sleepiness, poor concentration, fatigue, and apnea in the general population is 20 percent if defined as an restlessness. Obstructive sleep apnea can cause these problems apnea hypopnea index is the number of apneas and hypopneas apnea hypopnea index greater than five events per hour (the due to episodes of transient nocturnal hypoxia. per hour of sleep). The most important risk factors for obstructive sleep apnea are obesity, craniofacial abnormalities, and upper Patient report airway abnormalities.
    [Show full text]