Hyperventilation: a Possible Explanation for Long-Lasting Exercise Intolerance in Mild COVID-19 Survivors?

Total Page:16

File Type:pdf, Size:1020Kb

Hyperventilation: a Possible Explanation for Long-Lasting Exercise Intolerance in Mild COVID-19 Survivors? fphys-11-614590 January 18, 2021 Time: 10:37 # 1 PERSPECTIVE published: 18 January 2021 doi: 10.3389/fphys.2020.614590 Hyperventilation: A Possible Explanation for Long-Lasting Exercise Intolerance in Mild COVID-19 Survivors? Justina Motiejunaite1,2*, Pauline Balagny1,3, Florence Arnoult1, Laurence Mangin1,4, Catherine Bancal1, Marie-Pia d’Ortho1,2 and Justine Frija-Masson1,2 1 Service de Physiologie-Explorations Fonctionnelles, FHU APOLLO, Assistance Publique Hôpitaux de Paris, Hôpital Bichat-Claude Bernard, Paris, France, 2 INSERM, UMR 1141 NeuroDiderot, Université de Paris, Paris, France, 3 INSERM, UMS 011, Population-based Epidemiological Cohorts Unit, Villejuif, France, 4 UMR 7057, CNRS, Laboratoire Matière et Système Complexes, Paris, France Since the outbreak of the coronavirus (COVID-19) pandemic, most attention has focused on containing transmission and addressing the surge of critically ill patients in acute care settings. As we enter the second phase of the pandemic, emphasis must evolve to post-acute care of COVID-19 survivors. Persisting cardiorespiratory symptoms have been reported at several months after the onset of the infection. Information Edited by: is lacking on the pathophysiology of exercise intolerance after COVID-19. Previous Adriana Castello Costa Girardi, outbreaks of coronaviruses have been associated with persistent dyspnea, muscle University of São Paulo, Brazil weakness, fatigue and reduced quality of life. The extent of Covid-19 sequelae remains Reviewed by: Marli Maria Knorst, to be evaluated, but persisting cardiorespiratory symptoms in COVID-19 survivors can Federal University of Rio Grande do be described as two distinct entities. The first type of post-Covid symptoms are directly Sul, Brazil Ren-Jay Shei, related to organ injury in the acute phase, or the complications of treatment. The Mallinckrodt (United States), second type of persisting symptoms can affect patients even with mild initial disease United States presentation without evidence of organ damage. The mechanisms are still poorly *Correspondence: qualified to date. There is a lack of correlation between initial symptom severity and Justina Motiejunaite [email protected] residual symptoms at exertion. We report exercise hyperventilation as a major limiting orcid.org/0000-0001-8385-528X factor in COVID-19 survivors. The origin of this hyperventilation may be related to an Specialty section: abnormality of ventilatory control, by either hyperactivity of activator systems (automatic This article was submitted to and cortical ventilatory control, peripheral afferents, and sensory cortex) or failure of Integrative Physiology, inhibitory systems (endorphins) in the aftermath of pulmonary infection. Hyperventilation- a section of the journal Frontiers in Physiology induced hypocapnia can cause a multitude of extremely disabling symptoms such as Received: 06 October 2020 dyspnea, tachycardia, chest pain, fatigue, dizziness and syncope at exertion. Accepted: 24 December 2020 Published: 18 January 2021 Keywords: COVID-19, hyperventilation syndrome, dyspnea, cardiopulmonary exercise testing, SARS-CoV-2, exercise hyperventilation, persisting symptoms Citation: Motiejunaite J, Balagny P, Arnoult F, Mangin L, Bancal C, INTRODUCTION d’Ortho M-P and Frija-Masson J (2021) Hyperventilation: A Possible Explanation for Long-Lasting Exercise The infection with severe respiratory syndrome coronavirus 2 (SARS-CoV-2) was declared a Intolerance in Mild COVID-19 pandemic on March 11, 2020. As of November 2020, the novel coronavirus, hereafter referred Survivors? Front. Physiol. 11:614590. to as COVID-19, has affected more than 60 million people worldwide (Center, 2020; Simpson doi: 10.3389/fphys.2020.614590 and Robinson, 2020). For the majority (81%), infection with COVID-19 manifests as a mild Frontiers in Physiology| www.frontiersin.org 1 January 2021| Volume 11| Article 614590 fphys-11-614590 January 18, 2021 Time: 10:37 # 2 Motiejunaite et al. Hyperventilation and Exercise Intolerance in COVID-19 disease. Fever (88.7%), cough (57.6%), and dyspnea (45.6%) oxygen during hospital stay. At one-month follow-up, 74% of were the most commonly reported symptoms in a recent participants reported shortness of breath. Carfi et al.(2020) also systematic review (Rodriguez-Morales et al., 2020). However, for assessed persistent symptoms in patients discharged from the a significant minority, and particularly those older than 65 years hospital. At 2 months follow-up, half of the patients reported and with comorbidities, the infection requires management persistent fatigue, whereas dyspnea (43%) and chest pain (22%) in an intensive care unit due to acute respiratory distress were also highly prevalent. These findings are in line with the syndrome (ARDS) (Pascarella et al., 2020). Since the outbreak studies by Wong et al.(2020) and Garrigues et al.(2020), of the pandemic, most attention has focused on containing both of which found nearly half of the patients complaining of transmission and managing the wave of critically ill patients breathlessness at 3 months after hospital discharge. in acute care settings. As we enter the second phase of the The persistence of cardiorespiratory symptoms in survivors of pandemic, emphasis must evolve to post-acute care of COVID- severe COVID-19 can be partly explained by the pathophysiology 19 survivors. For these patients, having defeated the virus is of organ damage during the initial phase of the disease. The just the beginning of an unknown recovery path. There are SARS-CoV-2 virus predominantly affects the respiratory system, increasing reports of persisting and recurrent symptoms at although other organ systems can be compromised as well. The several months after the onset of the infection (Carfi et al., virus uses angiotensin-converting enzyme-2 (ACE2) receptors in 2020; Goërtz et al., 2020), dyspnea at exertion being one of the pneumocytes of the epithelial alveolar lining to infect the host, most common complaints. The extent and severity of the lasting thus causing lung injury (Varga et al., 2020). Diffuse alveolar sequelae remain to be evaluated, but persisting cardiorespiratory damage was showed by several post-mortem studies (Carsana symptoms in COVID-19 survivors can be described as two et al., 2020; Schaller et al., 2020), leading to hypotheses of residual distinct entities. The first type of post-Covid consequences are pulmonary function impairment at long term. These hypotheses directly related to organ damage in the acute phase, either due are supported by the available evidence on previous coronavirus to the viral infection and the ensuing inflammatory response, outbreaks. A recent meta-analysis (Ahmed et al., 2020) of studies or the complications of treatment in the intensive care setting on SARS-CoV and MERS-CoV reported that approximately one (Li et al., 2006; Zhou et al., 2014; Mart and Ware, 2020). The third of hospitalized patients had persisting lung abnormalities persisting cardiorespiratory symptoms related to cardiac and after their acute illness. Prospective studies on SARS-CoV,MERS- lung injury in COVID-19 will be summarized below. The second CoV as well as short-term follow-up studies on the current type of persisting symptoms can affect patients even with mild SARS-CoV-2 epidemic are summarized in Table 1. These studies initial disease presentation without evidence of severe organ demonstrate mostly a mild pulmonary function impairment damage. Sustained fatigue and exercise intolerance are the most and the functional disability appears out of proportion to the frequent complaints in patients not requiring hospitalization degree of lung function impairment. For example, a 2005 study (Goërtz et al., 2020; Tenforde et al., 2020). In these patients, there on SARS-CoV by Hui et al.(2005) found that the exercise is a striking lack of correlation between initial symptom severity capacity 6 months after disease onset was considerably lower and residual symptoms at exertion. The mechanisms behind than that of normal controls in the same age groups. However, post-Covid exercise intolerance are most likely complex and still significant impairment of surface area gas exchange was only poorly qualified to date. In this article, we aimed to review the found in 15% of the patients. Along with Hui’ study, Ong available evidence on persisting exercise intolerance experienced et al.(2004) performed cardiopulmonary exercises testing in 46 by COVID-19 survivors. We also report exercise hyperventilation SARS-CoV patients at 3 months after hospital discharge. Half as a major limiting factor that can cause a multitude of extremely of the patients had abnormalities in the pulmonary function disabling symptoms such as dyspnea, tachycardia, chest pain, tests, but the impairment was mild in almost all cases. However, fatigue, dizziness, and syncope at exertion. To our knowledge, 41% of the patients had impairment of exercise capacity not this is the first report of a possible explanation for prolonged due to ventilatory limitation. The discordance of the results of exercise intolerance in long-lasting COVID-19. pulmonary function and exercise testing has been attributed to several factors, such as physical deconditioning, muscle weakness and poor motivation. The recent data in SARS-CoV-2 by Arnold PERSISTING CARIORESPIRATORY et al.(2020) demonstrates that even 74% of survivors complained of persistent breathlessness and excessive fatigue at 3 months after SYMPTOMS IN CORONAVIRUS hospital discharge. Yet abnormal pulmonary
Recommended publications
  • Review of Systems Form
    Child’s name or label Since the last visit, how are your child’s symptoms? Better? Worse? The same? Please describe: Any new health problems, consultations, ER visits, hospital admissions, procedures or surgeries since your last visit? None Evaluations or tests done since the last visit: MRI EEG Blood work Child Study Team evaluation Neuropsychological testing ImPACT test Audiology Nutritionist consultation Questionnaires Physician Consultations:______________________ Other: ____________________ None If your child takes medications, please list the medications and doses here: 1.__________________________________________________ 4.__________________________________________ 2._________________________________________________ 5._________________________________________ 3.__________________________________________________ 6.__________________________________________ PEDS NEURO REVIEW OF SYSTEMS: Please list symptoms your child has since the last visit. Describe “yes” responses. NEUROLOGICAL KNOWN EYE CONDITIONS YES NO ___________________ HYPERACTIVITY YES NO ___________________ EAR, NOSE AND THROAT SEIZURES YES NO ___________________ HEARING LOSS OR DEFICIT YES NO ___________________ FAINTING YES NO ___________________ SLEEP APNEA YES NO ___________________ SNORING YES NO ___________________ CARDIOVASCULAR HEADACHES YES NO ___________________ RAPID OR IRREGULAR HEART BEAT YES NO ___________________ TICS YES NO ___________________ CHEST PAIN OR EXERCISE INTOLERANCE YES NO ___________________ INATTENTION
    [Show full text]
  • NIH Public Access Author Manuscript Auton Neurosci
    NIH Public Access Author Manuscript Auton Neurosci. Author manuscript; available in PMC 2016 March 01. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Auton Neurosci. 2015 March ; 188: 86–89. doi:10.1016/j.autneu.2014.11.008. Exercise in the Postural Orthostatic Tachycardia Syndrome Qi Fu and Benjamin D. Levine Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, The University of Texas Southwestern Medical Center, Dallas, TX, USA Abstract Patients with the Postural Orthostatic Tachycardia Syndrome (POTS) have orthostatic intolerance, as well as exercise intolerance. Peak oxygen uptake (VO2peak) is generally lower in these patients compared with healthy sedentary individuals, suggesting a lower physical fitness level. During acute exercise, POTS patients have an excessive increase in heart rate and reduced stroke volume for each level of absolute workload; however, when expressed at relative workload (%VO2peak), there is no difference in the heart rate response between patients and healthy individuals. The relationship between cardiac output and VO2 is similar between POTS patients and healthy individuals. Short-term (i.e., 3 months) exercise training increases cardiac size and mass, blood volume, and VO2peak in POTS patients. Exercise performance is improved after training. Specifically, stroke volume is greater and heart rate is lower at any given VO2 during exercise after training versus before training. Peak heart rate is the same but peak stroke volume and cardiac output are greater after training. Heart rate recovery from peak exercise is significantly faster after training, indicating an improvement in autonomic circulatory control. These results suggest that patients with POTS have no intrinsic abnormality of heart rate regulation during exercise.
    [Show full text]
  • Hyperventilation Syndrome
    Hyperventilation Syndrome INTRODUCTION ● hyperventilation in the presence of the following should immediately confirm an alternative Hyperventilation syndrome is defined as “a rate of diagnosis: ventilation exceeding metabolic needs and higher than that required to maintain a normal level of plasma CO2”. – cyanosis Physiological hyperventilation can occur in a number of – reduced level of consciousness situations, including life-threatening conditions such as: – reduction in SpO2. ● pulmonary embolism ● diabetic ketoacidosis MANAGEMENT 1,2 ● asthma If ABCD need correction then treat as per medical ● hypovolaemia. guidelines as it is unlikely to be due to hyperventilation syndrome but is more likely to be physiological As a rule, hyperventilation due to emotional stress is hyperventilation secondary to an underlying rare in children, and physical causes are much more pathological process. likely to be responsible for hyperventilation. Maintain a calm approach at all times. Specific presenting features can include: Reassure the patient and try to remove the source of ● acute anxiety the patient’s anxiety, this is particularly important in ● tetany due to calcium imbalance children. ● numbness and tingling of the mouth and lips Coach the patient’s respirations whilst maintaining a calm environment. ● carpopedal spasm ● aching of the muscles of the chest ADDITIONAL INFORMATION ● feeling of light headedness or dizziness. The cause of hyperventilation cannot always be determined with sufficient accuracy (especially in the HISTORY early stages) in the pre hospital environment. Refer to dyspnoea guide Always presume hyperventilation is secondary to hypoxia or other underlying respiratory disorder until proven otherwise. 1,2 ASSESSMENT The resulting hypocapnia will result in respiratory Assess ABCD’s: alkalosis bringing about a decreased level of serum ionised calcium.
    [Show full text]
  • Asphyxia Neonatorum
    CLINICAL REVIEW Asphyxia Neonatorum Raul C. Banagale, MD, and Steven M. Donn, MD Ann Arbor, Michigan Various biochemical and structural changes affecting the newborn’s well­ being develop as a result of perinatal asphyxia. Central nervous system ab­ normalities are frequent complications with high mortality and morbidity. Cardiac compromise may lead to dysrhythmias and cardiogenic shock. Coagulopathy in the form of disseminated intravascular coagulation or mas­ sive pulmonary hemorrhage are potentially lethal complications. Necrotizing enterocolitis, acute renal failure, and endocrine problems affecting fluid elec­ trolyte balance are likely to occur. Even the adrenal glands and pancreas are vulnerable to perinatal oxygen deprivation. The best form of management appears to be anticipation, early identification, and prevention of potential obstetrical-neonatal problems. Every effort should be made to carry out ef­ fective resuscitation measures on the depressed infant at the time of delivery. erinatal asphyxia produces a wide diversity of in­ molecules brought into the alveoli inadequately com­ Pjury in the newborn. Severe birth asphyxia, evi­ pensate for the uptake by the blood, causing decreases denced by Apgar scores of three or less at one minute, in alveolar oxygen pressure (P02), arterial P02 (Pa02) develops not only in the preterm but also in the term and arterial oxygen saturation. Correspondingly, arte­ and post-term infant. The knowledge encompassing rial carbon dioxide pressure (PaC02) rises because the the causes, detection, diagnosis, and management of insufficient ventilation cannot expel the volume of the clinical entities resulting from perinatal oxygen carbon dioxide that is added to the alveoli by the pul­ deprivation has been further enriched by investigators monary capillary blood.
    [Show full text]
  • Prolonged Post-Hyperventilation Apnea in Two Young Adults With
    Munemoto et al. BioPsychoSocial Medicine 2013, 7:9 http://www.bpsmedicine.com/content/7/1/9 CASE REPORT Open Access Prolonged post-hyperventilation apnea in two young adults with hyperventilation syndrome Takao Munemoto1,4*, Akinori Masuda2, Nobuatsu Nagai3, Muneki Tanaka4 and Soejima Yuji5 Abstract Background: The prognosis of hyperventilation syndrome (HVS) is generally good. However, it is important to proceed with care when treating HVS because cases of death following hyperventilation have been reported. This paper was done to demonstrate the clinical risk of post-hyperventilation apnea (PHA) in patients with HVS. Case presentation: We treated two patients with HVS who suffered from PHA. The first, a 21-year-old woman, had a maximum duration of PHA of about 3.5 minutes and an oxygen saturation (SpO2) level of 60%. The second patient, a 22-year-old woman, had a maximum duration of PHA of about 3 minutes and an SpO2 level of 66%. Both patients had loss of consciousness and cyanosis. Because there is no widely accepted regimen for treating patients with prolonged PHA related to HVS, we administered artificial ventilation to both patients using a bag mask and both recovered without any after effects. Conclusion: These cases show that some patients with HVS develop prolonged PHA or severe hypoxia, which has been shown to lead to death in some cases. Proper treatment must be given to patients with HVS who develop PHA to protect against this possibility. If prolonged PHA or severe hypoxemia arises, respiratory assistance using a bag mask must be done immediately. Keywords: Post-hyperventilation apnea, PHA, Hyperventilation syndrome, HVS, Hypocapnia, Hypoxemia Background incidence of death, severe hypoxia, or myocardial infarc- Hyperventilation syndrome (HVS) is characterized by tion in association with the paper-bag method [2].
    [Show full text]
  • Pulmonary Hypertension and Exercise Intolerance in Patients with Heart Failure Javed Butler, MD, Don B
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Journal of the American College of Cardiology Vol. 34, No. 6, 1999 © 1999 by the American College of Cardiology ISSN 0735-1097/99/$20.00 Published by Elsevier Science Inc. PII S0735-1097(99)00408-8 Pulmonary Hypertension and Exercise Intolerance in Patients With Heart Failure Javed Butler, MD, Don B. Chomsky, MD, John R. Wilson, MD, FACC Nashville, Tennessee OBJECTIVES This study was undertaken to investigate the relationship between pulmonary hypertension and exercise performance in patients with heart failure. BACKGROUND The exercise capacity of patients with heart failure is frequently reduced. Pulmonary hypertension may contribute to this exercise intolerance by impairing blood flow through the pulmonary circulation. METHOD Three hundred twenty patients with heart failure underwent upright treadmill exercise testing with hemodynamic monitoring. The incidence of pulmonary hypertension and the relation- ship between pulmonary vascular resistance (PVR) and exercise cardiac output and minute oxygen consumption (VO2) were examined. RESULTS Pulmonary vascular resistance was normal (Ͻ1.5 Wood Units; Group 1) in 28% of the patients, mildly elevated (1.5 to 2.49 Wood Units; Group 2) in 36%, moderately elevated (2.5 to 3.49 Wood Units; Group 3) in 17% and severely elevated (Ͼ3.5 Wood Units; Group 4) in 19%. Increasing PVR was associated with significantly lower peak exercise VO2 (Group 1: 13.9 Ϯ 3.7; 2:13.7 Ϯ 3.4; 3: 11.8 Ϯ 2.4; 4: 11.5 Ϯ 2.6 L/min, p Ͻ 0.01 Groups 3 and 4 vs.
    [Show full text]
  • Impact of Atrial Fibrillation on Exercise Capacity And
    ORIGINAL RESEARCH Impact of Atrial Fibrillation on Exercise Capacity and Mortality in Heart Failure With Preserved Ejection Fraction: Insights From Cardiopulmonary Stress Testing Mohamed B. Elshazly, MD; Todd Senn, MD; Yuping Wu, PhD; Bruce Lindsay, MD; Walid Saliba, MD; Oussama Wazni, MD; Leslie Cho, MD Background-—Atrial fibrillation (AF) has been objectively associated with exercise intolerance in patients with heart failure with reduced ejection fraction; however, its impact in patients with heart failure with preserved ejection fraction has not been fully scrutinized. Methods and Results-—We identified 1744 patients with heart failure and ejection fraction ≥50% referred for cardiopulmonary stress testing at the Cleveland Clinic (Cleveland, OH), 239 of whom had AF. We used inverse probability of treatment weighting to balance clinical characteristics between patients with and without AF. A weighted linear regression model, adjusted for unbalanced variables (age, sex, diagnosis, hypertension, and b-blocker use), was used to compare metabolic stress parameters and 8-year total mortality (social security index) between both groups. Weighted mean ejection fraction was 58Æ5.9% in the entire population. After adjusting for unbalanced weighted variables, patients with AF versus those without AF had lower mean peak oxygen consumption (18.5Æ6.2 versus 20.3Æ7.1 mL/kg per minute), oxygen pulse (12.4Æ4.3 versus 12.9Æ4.7 mL/beat), and circulatory power (2877Æ1402 versus 3351Æ1788 mm HgÁmL/kg per minute) (P<0.001 for all comparisons) but similar submaximal exercise capacity (oxygen consumption at anaerobic threshold, 12.0Æ5.1 versus 12.4Æ6.0mL/kg per minute; P =0.3). Both groups had similar peak heart rate, whereas mean peak systolic blood pressure was lower in the AF group (150Æ35 versus 160Æ51 mm Hg; P<0.001).
    [Show full text]
  • Statewide Heart Failure Service, Heart Failure Daily Diary
    Available online at www.sciencedirect.com Journal of Science and Medicine in Sport 13 (2010) 288–294 Position statement Exercise & Sports Science Australia Position Statement on exercise training and chronic heart failure Steve E. Selig a,b,∗, Itamar Levinger a,b, Andrew D. Williams c, Neil Smart d, David J. Holland e, Andrew Maiorana f,g, Daniel J. Green h,i, David L. Hare b,j a Institute for Sport, Exercise and Active Living, School of Sport and Exercise Science, Victoria University, Melbourne, Australia b Department of Cardiology, Austin Health, Melbourne, Australia c School of Human Life Sciences, University of Tasmania, Tasmania, Australia d Faculty of Health Science and Medicine, Bond University, QLD, Australia e School of Medicine, University of Queensland, Brisbane, Australia f Cardiac Transplant Unit, Royal Perth Hospital, Australia g School of Physiotherapy, Curtin University of Technology, Australia h School of Sport Science, Exercise and Health, University of Western Australia, Australia i Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, United Kingdom j School of Medicine, University of Melbourne, Australia Received 18 September 2009; received in revised form 18 January 2010; accepted 19 January 2010 Abstract Chronic heart failure (CHF) is a complex syndrome characterised by progressive decline in left ventricular function, low exercise tolerance and raised mortality and morbidity. Regular exercise participation has been shown to be a safe and effective treatment modality in the majority of CHF patients, partially reversing some of the maladaptations evident in myocardial and skeletal muscle function, and resulting in improvements in physical fitness and quality of life, and perhaps reduced mortality.
    [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]
  • Review of Systems Health History Sheet Patient: ______DOB: ______Age: ______Gender: M / F
    603 28 1/4 Road Grand Junction, CO 81506 (970) 263-2600 Review of Systems Health History Sheet Patient: _________________ DOB: ____________ Age: ______ Gender: M / F Please mark any symptoms you are experiencing that are related to your complaint today: Allergic/ Immunologic Ears/Nose/Mouth/Throat Genitourinary Men Only Frequent Sneezing Bleeding Gums Pain with Urinating Pain/Lump in Testicle Hives Difficulty Hearing Blood in Urine Penile Itching, Itching Dizziness Difficulty Urinating Burning or Discharge Runny Nose Dry Mouth Incomplete Emptying Problems Stopping or Sinus Pressure Ear Pain Urinary Frequency Starting Urine Stream Cardiovascular Frequent Infections Loss of Urinary Control Waking to Urinate at Chest Pressure/Pain Frequent Nosebleeds Hematologic / Lymphatic Night Chest Pain on Exertion Hoarseness Easy Bruising / Bleeding Sexual Problems / Irregular Heart Beats Mouth Breathing Swollen Glands Concerns Lightheaded Mouth Ulcers Integumentary (Skin) History of Sexually Swelling (Edema) Nose/Sinus Problems Changes in Moles Transmitted Diseases Shortness of Breath Ringing in Ears Dry Skin Women Only When Lying Down Endocrine Eczema Bleeding Between Shortness of Breath Increased Thirst / Growth / Lesions Periods When Walking Urination Itching Heavy Periods Constitutional Heat/Cold Intolerance Jaundice (Yellow Extreme Menstrual Pain Exercise Intolerance Gastrointestinal Skin or Eyes) Vaginal Itching, Fatigue Abdominal Pain Rash Burning or Discharge Fever Black / Tarry Stool Respiratory Waking to Urinate at Weight Gain (___lbs) Blood
    [Show full text]
  • Central Neurogenic Hyperventilation Related to Post-Hypoxic Thalamic Lesion in a Child
    Neurology International 2016; volume 8:6428 Central neurogenic normal. An emergency brain magnetic reso- nance imaging (MRI) was performed. Correspondence: Pinar Gençpinar, Department of hyperventilation related Although there was no apparent lesion in the Pediatric Neurology, Tepecik Training and to post-hypoxic thalamic lesion brain stem, bilateral diffuse thalamic, putami- Research Hospital, Izmir, Turkey. in a child nal and globus palllideal lesions were detected Tel.: +90.505.887.9258. on MRI (Figures 1 and 2). Examination E-mail: [email protected] Pinar Gençpinar,1 Kamil Karaali,2 revealed tachypnea (respiratory rate, 42/min), but other findings were normal. Arterial blood Key words: Central neurogenic hyperventilation; enay Haspolat,3 O uz Dursun4 thalamus; tachypnea; children. Ş ğ gases (ABGs) were pH, 7.52; PaCO2, 29 mmHg; 1Department of Pediatric Neurology, and PaO2, 142 mmHg. The chest radiograph, Contributions: PG prepared the manuscript; KK Tepecik Training of Research Hospital, electrocardiogram, and echocardiogram were prepared the figures and edited in this respect; 2 Izmir; Department of Radiology, normal. Laboratory studies disclosed the fol- OD and SH edited this manuscript and made final 3Department of Pediatric Neurology, lowing values: hematocrit, 33.7%, white blood version. 4Department of Pediatric Intensive Care cell count, 10.6×109/L; sodium, 140 mEq/L; Unit, Akdeniz University Hospital, potassium, 3.7 mEq/L; serum urea nitrogen; 6 Conflict of interest: the authors declare no poten- Antalya, Turkey mg/dL; creatinine, 0.21 mg/ dL; and glucose, tial conflict of interest. 110 mg/dL. Liver transaminases levels were normal. Serum lactate level was 1.97 mmol/L Received for publication: 23 January 2016.
    [Show full text]
  • Pathophysiology of Exercise Intolerance in Chronic Diseases: the Role of Diminished Cardiac Performance in Mitochondrial and Heart Failure Patients
    Open Access Heart failure and cardiomyopathies Open Heart: first published as 10.1136/openhrt-2017-000632 on 28 July 2017. Downloaded from Pathophysiology of exercise intolerance in chronic diseases: the role of diminished cardiac performance in mitochondrial and heart failure patients Jodi McCoy,1 Matthew Bates,1,2 Christopher Eggett,1 Mario Siervo,1 Sophie Cassidy,1 Jane Newman,1 Sarah A Moore,3 Grainne Gorman,3,4 Michael I Trenell,1,5 Lazar Velicki,6 Petar M Seferovic,7 John G F Cleland,8 Guy A MacGowan,9 Doug M Turnbull,3,4 Djordje G Jakovljevic1,10 To cite: McCoy J, Bates M, ABSTRACT KEY QUESTIONS Eggett C, et al. Pathophysiology Objective Exercise intolerance is a clinical hallmark of exercise intolerance in of chronic conditions. The present study determined chronic diseases: the role of What is already known about this subject? pathophysiological mechanisms of exercise intolerance in diminished cardiac performance Exercise intolerance is a clinical hallmark of cardiovascular, neuromuscular, and metabolic disorders. ► in mitochondrial and heart chronic conditions and strong predictor of Methods In a prospective cross-sectional observational failure patients. Open Heart morbidity and mortality. 2017;4:e000632. doi:10.1136/ study 152 patients (heart failure reduced ejection openhrt-2017-000632 fraction, n=32; stroke, n=34; mitochondrial disease, What does this study add? n=28; type two diabetes, n=28; and healthy controls, ► The study highlights that pathophysiological n=30) performed cardiopulmonary exercise testing with mechanisms of exercise intolerance differ among Received 22 March 2017 metabolic and haemodynamic measurements. Peak patients groups. Revised 22 May 2017 exercise O consumption and cardiac power output were Accepted 20 June 2017 2 measures of exercise tolerance and cardiac performance.
    [Show full text]