DOCSLIB.ORG

Effects of Hypercapnia and Hypocapnia on Respiratory Resistance in Normal and Asthmatic Subjects Thorax: First Published As 10.1136/Thx.46.1.28 on 1 January 1991

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Effects of Hypercapnia and Hypocapnia on Respiratory Resistance in Normal and Asthmatic Subjects Thorax: First Published As 10.1136/Thx.46.1.28 on 1 January 1991 28 Thorax 1991;46:28-32 Effects of hypercapnia and hypocapnia on respiratory resistance in normal and asthmatic subjects Thorax: first published as 10.1136/thx.46.1.28 on 1 January 1991. Downloaded from F J J van den Elshout, C L A van Herwaarden, H Th M Folgering Abstract tigate the effect of change in end tidal Pco2 on The effects of hypercapnia and hypocap- airway calibre without the confounding effects nia on respiratory resistance were of heat and water loss from the airway studied in 15 healthy subjects and 30 mucosa. The forced oscillation technique was asthmatic subjects. Respiratory resis- used because the measurements obtained with tance (impedance) was measured with this method are collected during spontaneous the pseudo-random noise forced oscilla- breathing. Forced expiratory manoeuvres, tion technique while the subjects which may influence bronchial tone," were rebreathed from a wet spirometer in a thus avoided. closed respiratory circuit in which end tidal carbon dioxide tension (Pco2) could be controlled. Hypercapnia was induced Methods by partially short circuiting the carbon EQUIPMENT dioxide absorber, and hypocapnia by Oscillatory respiratory resistance (impedance) voluntary hyperventilation. The cir- was measured with the pseudo-random noise culating air was saturated with water forced oscillation technique using the vapour and kept at body temperature apparatus developed by Landser et al and ambient pressure. A rise of end tidal (Oscillaire, Jones, Chicago).'2 '3 A loudspeaker Pco2 of 1 kPa caused a significant fall in generates pressure changes at the mouth in the respiratory resistance in both normal form of a pseudo-random noise signal contain- and asthmatic subjects (15% and 9% res- ing all harmonics of 4-52 Hz superimposed on pectively). A fall of Pco2 of 1 kPa did not spontaneous breathing. Mouth pressure and cause any significant change in flow signals are recorded by two identical impedance in the control group. In the differential transducers (Validyne MP 445). asthmatic patients resistance increased Fourier analysis allows the calculation of http://thorax.bmj.com/ by 13%, reactance fell by 45%, and the impedance at 4-52 Hz from the data, which frequency dependence of resistance rose were collected over eight seconds. The validity 240%. These findings confirm that of the measurements was evaluated by a hypocapnia may contribute to airway coherence function that assessed the amount of obstruction in asthmatic patients, even noise and alinearity in the signals'2 14; only data when water and heat loss are prevented. with a coherence function of 095 or more were retained. The impedance data were subdivided into resistance and reactance and were com- on October 1, 2021 by guest. Protected copyright. Many specific and non-specific broncho- puted over the range 4-52 Hz in steps of 4 Hz. constrictor challenges are used to measure Resistance (Rrs), computed as the ratio of the bronchial reactivity, including allergens, in phase components of pressure and flow, is irritants, cholinergic drugs, mediators, exer- determined by the resistive properties of the cise, and hyperventilation. For exercise and respiratory system (airways, lung tissue, and hyperventilation challenge respiratory heat chest wall). Reactance (Xrs) was computed as loss and increased osmolarity of the airway the ratio of the components of pressure and mucosa are probably the most important fac- flow, which are 90° out of phase. This part of tors contributing to bronchoconstriction,1-3 impedance is determined by the elasticity and though hypocapnia may also contribute.' mass inertia of the airways, lung tissue, and Ventilation is increased in both hypocapnia, thorax and the inertia of the air within the when this is induced experimentally by volun- bronchi."1-'5 The variables measured in this tary hyperventilation, and hypercapnia, which study were (1) total respiratory resistance (Rrs) stimulates ventilation. The increase in ventila- at each frequency tested (4-8-12 .. 52 Hz) Department of tion may obscure the effects of Pco2 on airway and the average value for all frequencies; (2) Pulmonary Diseases, University of resistance, by increasing respiratory heat loss total respiratory reactance (Xrs) at each Nijmegen, Medical or osmolarity changes. frequency tested and the average value for all Centre Dekkerswald, Acute and chronic airways obstruction in frequencies; (3) resonant frequency-that is, PO Box 9001, 6560 GB Groesbeek, The patients with asthma or chronic obstructive the frequency at which the reactance is zero; (4) Netherlands lung diseases is often accompanied by frequency dependence of the resistance, F JJ van den Elshout hyperventilation."'0 It is still uncertain defined in this study as the ratio (Rrs 12 Hz- C L A van Herwaarden H Th M Folgering whether patients with bronchial hyperrespon- Rrs 52 Hz)/Rrs 52 Hz. siveness to histamine are also hyperresponsive The Oscillaire apparatus was connected to a Reprint requests to: Dr van den Elshout to hypocapnia and hypercapnia. wet spirometer (Pulmotest, Godart, De Bitt, Accepted 11 October 1990 The aim of the present study was to inves- Utrecht, Holland) to form a closed respiratory Effects of hypercapnia and hypocapnia on respiratory resistance in normal and asthmatic subjects 29 histamine causing a decrease in the forced expiratory volume in one second (FEVI) of 20% or more was less than 8 mg/ml'6). The characteristics of the subjects are shown in table 1. Thorax: first published as 10.1136/thx.46.1.28 on 1 January 1991. Downloaded from The patients used inhaled medication only (beta agonist or corticosteroids or both) and this was discontinued at least eight hours before testing. Patients who had had a res- piratory infection in the past six weeks were excluded. The study was approved by the local ethical committee and informed consent was obtained from all subjects. PROCEDURE To establish whether connecting the side tube for C02 sampling spirometer to the Oscillaire changed the capnograph measurements, impedance was measured with Figure 1 Oscillatory resistance apparatus connected to a wet spirometer toform a the Oscillaire alone in 15 subjects (seven heal- closed respiratory circuit to which oxygen was supplied and in which carbon dioxide could be absorbed. thy subjects and eight patients) and, a few minutes later, with the Oscillaire connected to the wet spirometer circuit. In a further 10 circuit to which oxygen was added. Carbon subjects (five healthy subjects and five dioxide could be absorbed as desired by par- patients) the humidity of the air in the tially or totally short circuiting the carbon spirometer circuit was measured continuously dioxide absorber. End tidal Pco2 was measured during the whole procedure. continuously with a rapid infrared analyser All subjects and patients were studied in (Jaeger,Wurzburg, Germany), the sampled air three different conditions: (1) normocapnic (all being returned to the closed spirometer circuit. carbon dioxide was absorbed in the closed End tidal Pco2 was controlled by changing the circuit); (2) hypercapnic (with the carbon di- fraction ofinspiratory air, bypassing the carbon oxide absorber partially shortcircuited); (3) dioxide absorber (fig 1). The air in the res- hypocapnic (the subjects breathing quietly piratory circuit was kept in the BTPS condi- immediately after one minute of voluntary tion. The temperature was maintained at 37°C hyperventilation). by a heating element and water saturation ofair at 90% or more. DATA ANALYSIS http://thorax.bmj.com/ The subjects had their cheeks and submental The data from three adequate measurements muscles supported and they wore a nose clip were averaged for each of the three conditions during the impedance measurements. (hypocapnia, normocapnia, and hypercapnia). The average values ofRrs and Xrs calculated at SUBJECTS intervals of 4 Hz in the range 4-52 Hz were Forty five subjects were studied: 15 healthy plotted against the frequency at which they subjects and 30 patients with a history of were measured.'2 '3 The changes in impedance data from normocapnic (A) to hypercapnic and asthma and bronchial hyperresponsiveness to on October 1, 2021 by guest. Protected copyright. histamine (the provocative concentration of hypocapnic conditions (B) were calculated for each individual as [(A-B)/(A)] x 100%. For statistical analysis Wilcoxon's test for paired Table 1 Characteristics of the subjects (mean (SEM) values unless otherwise observations was used. The differences be- specified) tween the two groups were tested with the Mann-Whitney U test. Normal Asthmatic Age (y) 28-0 (0 98) 31-7 (1-6) Sex (F:M) 5:10 12:18 Results FEV, (% pred") 107-2 (3-4) 85-5 (3-1) PRELIMINARY STUDIES MEF,0 (% pred34) 95-6 (4 5) 52-4 (3 7) Rrs (cm H2O/l/s) There were no significant differences between At 8 Hz 2-44 (0-14) 4-55 (0-33) the results obtained with the Oscillaire alone (I) At 52 Hz 2 94 (0-19) 4-09 (0-17) and those obtained with the Oscillaire connec- of Average frequencies tested 265 (015) 4-01 (0-19) ted with the wet spirometer circuit (II). The Xrs, average (cm H2O/l/s) 0-89 (0-07) 087 (0-17) Resonant frequency (Hz) 7-46 (0 39) 16-4 (1-65) data measured with I and II were compared by Frequency dependence of the resistance* +0 19 (0-02) -0-01 (0-04) means of a two way linear regression analysis Allergy (skin test with 18 allergens: No of subjects) and analysis of variance. The coefficient of Any positive result 0 27 Negative results 15 3 correlation ranged from 0-94 to 0-98, with a Medication (No of subjects) slope of 0 95 to 1 03, an intercept of -0-03 to Inhaled beta agonist 0 26 +0 05 (p < 0-0001). The SE to the regression Inhaled steroid 0 15 PC20 (mg histamine/ml, geometric mean value) >8 0-44 line varied from 0-02 to 0-06 (2-7%).
Load more

Recommended publications
  • Breathing & Buoyancy Control: Stop, Breathe, Think, And
    Breathing & Buoyancy control: Stop, Breathe, Think, and then Act For an introduction to this five part series see: House of Cards 'As a child I was fascinated by the way marine creatures just held their position in the water and the one creature that captivated my curiosity and inspired my direction more than any is the Nautilus. Hanging motionless in any depth of water and the inspiration for the design of the submarine with multiple air chambers within its shell to hold perfect buoyancy it is truly a grand master of the art of buoyancy. Buoyancy really is the ultimate Foundation skill in the repertoire of a diver, whether they are a beginner or an explorer. It is the base on which all other skills are laid. With good buoyancy a problem does not become an emergency it remains a problem to be solved calmly under control. The secret to mastery of buoyancy is control of breathing, which also gives many additional advantages to the skill set of a safe diver. Calming one's breathing can dissipate stress, give a sense of well being and control. Once the breathing is calmed, the heart rate will calm too and any situation can be thought through, processed and solved. Always ‘Stop, Breathe, Think and then Act.' Breath control is used in martial arts as a control of the flow of energy, in prenatal training and in child birth. At a simpler more every day level, just pausing to take several slow deep breaths can resolve physical or psychological stress in many scenarios found in daily life.
    [Show full text]
  • Job Hazard Analysis
    Identifying and Evaluating Hazards in Research Laboratories Guidelines developed by the Hazards Identification and Evaluation Task Force of the American Chemical Society’s Committee on Chemical Safety Copyright 2013 American Chemical Society Table of Contents FOREWORD ................................................................................................................................................... 3 ACKNOWLEDGEMENTS ................................................................................................................................. 5 Task Force Members ..................................................................................................................................... 6 1. SCOPE AND APPLICATION ..................................................................................................................... 7 2. DEFINITIONS .......................................................................................................................................... 7 3. HAZARDS IDENTIFICATION AND EVALUATION ................................................................................... 10 4. ESTABLISHING ROLES AND RESPONSIBILITIES .................................................................................... 14 5. CHOOSING AND USING A TECHNIQUE FROM THIS GUIDE ................................................................. 17 6. CHANGE CONTROL .............................................................................................................................. 19 7. ASSESSING
    [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]
  • Pathophysiology of Acid Base Balance: the Theory Practice Relationship
    Intensive and Critical Care Nursing (2008) 24, 28—40 ORIGINAL ARTICLE Pathophysiology of acid base balance: The theory practice relationship Sharon L. Edwards ∗ Buckinghamshire Chilterns University College, Chalfont Campus, Newland Park, Gorelands Lane, Chalfont St. Giles, Buckinghamshire HP8 4AD, United Kingdom Accepted 13 May 2007 KEYWORDS Summary There are many disorders/diseases that lead to changes in acid base Acid base balance; balance. These conditions are not rare or uncommon in clinical practice, but every- Arterial blood gases; day occurrences on the ward or in critical care. Conditions such as asthma, chronic Acidosis; obstructive pulmonary disease (bronchitis or emphasaemia), diabetic ketoacidosis, Alkalosis renal disease or failure, any type of shock (sepsis, anaphylaxsis, neurogenic, cardio- genic, hypovolaemia), stress or anxiety which can lead to hyperventilation, and some drugs (sedatives, opoids) leading to reduced ventilation. In addition, some symptoms of disease can cause vomiting and diarrhoea, which effects acid base balance. It is imperative that critical care nurses are aware of changes that occur in relation to altered physiology, leading to an understanding of the changes in patients’ condition that are observed, and why the administration of some immediate therapies such as oxygen is imperative. © 2007 Elsevier Ltd. All rights reserved. Introduction the essential concepts of acid base physiology is necessary so that quick and correct diagnosis can The implications for practice with regards to be determined and appropriate treatment imple- acid base physiology are separated into respi- mented. ratory acidosis and alkalosis, metabolic acidosis The homeostatic imbalances of acid base are and alkalosis, observed in patients with differing examined as the body attempts to maintain pH bal- aetiologies.
    [Show full text]
  • CHEM 301 Assignment #3
    CHEM 301 Assignment #3 Provide solutions to the following questions in a neat and well organized manner. Clearly state assumptions and reference sources for any constants used. Due date: November 18th 1. Methane and carbon dioxide are produced under anaerobic conditions by the fermentation of organic matter, approximated by the following equation 2 {CH2O} CH4 + CO2 As gas bubbles are evolved at the sediment interface at 5 m depth and remain in contact with water at the sediment surface long enough so that equilibrium is attained. The total pressure at this depth is 148 kPa. If the pH is 8.20, calculate the total carbonate concentration in the interstitial water at 25oC. How would you expect your answer to change if these gas bubbles were present at 500 m depth? Strategy: The total pressure inside the gas bubble must be equal to the total pressure on the outside of the gas bubble (or else it would either explode or collapse). Furthermore, the total pressure inside that gas bubble is equal to the sum of the partial pressures of CH4 and CO2. We can then use the partial pressure of CO2 inside the gas bubble and the corresponding Henry’s law constant to calculate the concentration of aqueous CO2 at equilibrium. Given the pH of the solution and the expressions for Ka1 and Ka2, we can determine the concentration of HCO3- and 2- CO3 . (see textbook pgs 241-242; Chap 11, Q9) Solution: The total carbonate concentration is given by; 2- - 2- [CO3 ]T = [CO2(aq)] + [HCO3 ] + [CO3 ] From the pH speciation diagram (Fig.
    [Show full text]
  • CARBON MONOXIDE: the SILENT KILLER Information You Should
    CARBON MONOXIDE: THE SILENT KILLER Information You Should Know Carbon monoxide is a silent killer that can lurk within fossil fuel burning household appliances. Many types of equipment and appliances burn different types of fuel to provide heat, cook, generate electricity, power vehicles and various tools, such as chain saws, weed eaters and leaf blowers. When these units operate properly, they use fresh air for combustion and vent or exhaust carbon dioxide. When fresh air is restricted, through improper ventilation, the units create carbon monoxide, which can saturate the air inside the structure. Carbon Monoxide can be lethal when accidentally inhaled in concentrated doses. Such a situation is referred to as carbon monoxide poisoning. This is a serious condition that is a medical emergency that should be taken care of right away. What Is It? Carbon monoxide, often abbreviated as CO, is a gas produced by burning fossil fuel. What makes it such a silent killer is that it is odorless and colorless. It is extremely difficult to detect until the body has inhaled a detrimental amount of the gas, and if inhaled in high concentrations, it can be fatal. Carbon monoxide causes tissue damage by blocking the body’s ability to absorb enough oxygen. In fact, poisoning from this gas is one of the leading causes of unintentional death from poison. Common Sources of CO Kerosene or fuel-based heaters Fireplaces Gasoline powered equipment and generators Charcoal grills Automobile exhaust Portable generators Tobacco smoke Chimneys, furnaces, and boilers Gas water heaters Wood stoves and gas stoves Properly installed and maintained appliances are safe and efficient.
    [Show full text]
  • Arterial Blood Gases: Acid-Base Balance
    EDUCATIONAL COMMENTARY – ARTERIAL BLOOD GASES: ACID-BASE BALANCE Educational commentary is provided through our affiliation with the American Society for Clinical Pathology (ASCP). To obtain FREE CME/CMLE credits click on Earn CE Credits under Continuing Education on the left side of the screen. **Florida licensees, please note: This exercise will appear in CE Broker under the specialty of Blood Gas Analysis. LEARNING OUTCOMES On completion of this exercise, the participant should be able to • identify the important buffering systems in the human body. • explain the Henderson-Hasselbalch equation and its relationship to the bicarbonate/carbonic acid buffer system. • explain the different acid-base disorders, causes associated with them, and compensatory measures. • evaluate acid-base status using patient pH and pCO2 and bicarbonate levels. Introduction Arterial blood gas values are an important tool for assessing oxygenation and ventilation, evaluating acid- base status, and monitoring the effectiveness of therapy. The human body produces a daily net excess of acid through normal metabolic processes: cellular metabolism produces carbonic, sulfuric, and phosphoric acids. Under normal conditions, the body buffers accumulated hydrogen ions (H+) through a variety of buffering systems, the respiratory center, and kidneys to maintain a plasma pH of between 7.35 and 7.45. This tight maintenance of blood pH is essential: even slight changes in pH can alter the functioning of enzymes, the cellular uptake and use of metabolites, and the uptake and release of oxygen. Although diagnoses are made by physicians, laboratory professionals must be able to interpret arterial blood gas values to judge the validity of the laboratory results they report.
    [Show full text]
  • Den170044 Summary
    DE NOVO CLASSIFICATION REQUEST FOR CLEARMATE REGULATORY INFORMATION FDA identifies this generic type of device as: Isocapnic ventilation device. An isocapnic ventilation device is a prescription device used to administer a blend of carbon dioxide and oxygen gases to a patient to induce hyperventilation. This device may be labeled for use with breathing circuits made of reservoir bags (21 CFR 868.5320), oxygen cannulas (21 CFR 868.5340), masks (21 CFR 868.5550), valves (21 CFR 868.5870), resuscitation bags (21 CFR 868.5915), and/or tubing (21 CFR 868.5925). NEW REGULATION NUMBER: 21 CFR 868.5480 CLASSIFICATION: Class II PRODUCT CODE: QFB BACKGROUND DEVICE NAME: ClearMateTM SUBMISSION NUMBER: DEN170044 DATE OF DE NOVO: August 23, 2017 CONTACT: Thornhill Research, Inc. 5369 W. Wallace Ave Scottsdale, AZ 85254 INDICATIONS FOR USE ClearMateTM is intended to be used by emergency department medical professionals as an adjunctive treatment for patients suffering from carbon monoxide poisoning. The use of ClearMateTM enables accelerated elimination of carbon monoxide from the body by allowing isocapnic hyperventilation through simulated partial rebreathing. LIMITATIONS Intended Patient Population is adults aged greater than 16 years old and a minimum of 40 kg (80.8 lbs) ClearMateTM is intended to be used by emergency department medical professionals. This device should always be used as adjunctive therapy; not intended to replace existing protocol for treating carbon monoxide poisoning. When providing treatment to a non-spontaneously breathing patient using the ClearMate™ non-spontaneous breathing patient circuit, CO2 monitoring equipment for the measurement of expiratory carbon dioxide concentration must be used. PLEASE REFER TO THE LABELING FOR A MORE COMPLETE LIST OF WARNINGS AND CAUTIONS.
    [Show full text]
  • Relationship Between PCO 2 and Unfavorable Outcome in Infants With
    nature publishing group Articles Clinical Investigation Relationship between PCO2 and unfavorable outcome in infants with moderate-to-severe hypoxic ischemic encephalopathy Krithika Lingappan1, Jeffrey R. Kaiser2, Chandra Srinivasan3, Alistair J. Gunn4; on behalf of the CoolCap Study Group BACKGROUND: Abnormal PCO2 is common in infants with term infants with HIE, both minimum and cumulative expo- hypoxic ischemic encephalopathy (HIE). The objective was to sure to hypocapnia in the first 12 h of the trial were associated determine whether hypocapnia was independently associated with death or adverse neurodevelopmental outcome (13). The with unfavorable outcome (death or severe neurodevelopmen- dose–response relationship between PCO2 and outcome for tal disability at 18 mo) in infants with moderate-to-severe HIE. infants with moderate-to-severe HIE is unknown. METHODS: This was a post hoc analysis of the CoolCap Study The risk of developing hypocapnia or hypercapnia may be in which infants were randomized to head cooling or standard affected by severity of brain injury, intensity and duration of care. Blood gases were measured at prespecified times after newborn resuscitation, timing after the primary injury, and/or randomization. PCO2 and follow-up data were available for 196 response to metabolic acidosis. Thus, in this secondary analy- of 234 infants. Analyses were performed to investigate the rela- sis of the CoolCap Study (14), we sought to confirm the obser- tionship between hypocapnia in the first 72 h after randomiza- vation that
    [Show full text]
  • BTS Guideline for Oxygen Use in Adults in Healthcare and Emergency
    BTS guideline BTS guideline for oxygen use in adults in healthcare Thorax: first published as 10.1136/thoraxjnl-2016-209729 on 15 May 2017. Downloaded from and emergency settings BRO’Driscoll,1,2 L S Howard,3 J Earis,4 V Mak,5 on behalf of the British Thoracic Society Emergency Oxygen Guideline Group ▸ Additional material is EXECUTIVE SUMMARY OF THE GUIDELINE appropriate oxygen therapy can be started in the published online only. To view Philosophy of the guideline event of unexpected clinical deterioration with please visit the journal online ▸ (http://dx.doi.org/10.1136/ Oxygen is a treatment for hypoxaemia, not hypoxaemia and also to ensure that the oxim- thoraxjnl-2016-209729). breathlessness. Oxygen has not been proven to etry section of the early warning score (EWS) 1 have any consistent effect on the sensation of can be scored appropriately. Respiratory Medicine, Salford ▸ Royal Foundation NHS Trust, breathlessness in non-hypoxaemic patients. The target saturation should be written (or Salford, UK ▸ The essence of this guideline can be summarised ringed) on the drug chart or entered in an elec- 2Manchester Academic Health simply as a requirement for oxygen to be prescribed tronic prescribing system (guidance on figure 1 Sciences Centre (MAHSC), according to a target saturation range and for those (chart 1)). Manchester, UK 3Hammersmith Hospital, who administer oxygen therapy to monitor the Imperial College Healthcare patient and keep within the target saturation range. 3 Oxygen administration NHS Trust, London, UK ▸ The guideline recommends aiming to achieve ▸ Oxygen should be administered by staff who are 4 University of Liverpool, normal or near-normal oxygen saturation for all trained in oxygen administration.
    [Show full text]
  • The Basics of Ventilator Management Overview How We Breath
    3/23/2019 The Basics of Ventilator Management What are we really trying to do here Peter Lutz, MD Pulmonary and Critical Care Medicine Pulmonary Associates, Mobile, Al Overview • Approach to the physiology of the lung and physiological goals of mechanical Ventilation • Different Modes of Mechanical Ventilation and when they are indicated • Ventilator complications • Ventilator Weaning • Some basic trouble shooting How we breath http://people.eku.edu/ritchisong/301notes6.htm 1 3/23/2019 How a Mechanical Ventilator works • The First Ventilator- the Iron Lung – Worked by creating negative atmospheric pressure around the lung, simulating the negative pressure of inspiration How a Mechanical Ventilator works • The Modern Ventilator – The invention of the demand oxygen valve for WWII pilots if the basis for the modern ventilator https://encrypted-tbn0.gstatic.com/images?q=tbn:ANd9GcRI5v-veZULMbt92bfDmUUW32SrC6ywX1vSzY1xr40aHMdsCVyg6g How a Mechanical Ventilator works • The Modern Ventilator – How it works Inspiratory Limb Flow Sensor Ventilator Pressure Sensor Expiratory Limb 2 3/23/2019 So what are the goals of Mechanical Ventilation • What are we trying to control – Oxygenation • Amount of oxygen we are getting into the blood – Ventilation • The movement of air into and out of the lungs, mainly effects the pH and level of CO 2 in the blood stream Lab Oxygenation Ventilation Pulse Ox Saturation >88-90% Arterial Blood Gas(ABG) Po 2(75-100 mmHg) pCO 2(40mmHg) pH(~7.4) Oxygenation How do we effect Oxygenation • Fraction of Inspired Oxygen (FIO 2) – Percentage of the gas mixture given to the patient that is Oxygen • Room air is 21% • On the vent ranges from 30-100% • So if the patient’s blood oxygen levels are low, we can just increase the amount of oxygen we give them 3 3/23/2019 How do we effect Oxygenation • Positive End Expiratory Pressure (PEEP) – positive pressure that will remains in the airways at the end of the respiratory cycle (end of exhalation) that is greater than the atmospheric pressure in mechanically ventilated patients.
    [Show full text]
  • Effects of Anaesthesia Techniques and Drugs on Pulmonary Function
    Review Article Effects of anaesthesia techniques and drugs on pulmonary function Address for correspondence: Vijay Saraswat Dr. Vijay Saraswat, Department of Anaesthesiology, Apollo Hospitals, Nashik, Maharashtra, India Apollo Hospitals, Nashik, Maharashtra, India. E‑mail: drvsaraswat@gmail. ABSTRACT com The primary task of the lungs is to maintain oxygenation of the blood and eliminate carbon dioxide through the network of capillaries alongside alveoli. This is maintained by utilising ventilatory reserve capacity and by changes in lung mechanics. Induction of anaesthesia impairs pulmonary functions by the loss of consciousness, depression of reflexes, changes in rib cage and haemodynamics. All drugs used during anaesthesia, including inhalational agents, affect pulmonary functions directly by acting on respiratory system or indirectly through their actions on other systems. Volatile anaesthetic agents have more pronounced effects on pulmonary functions compared to intravenous induction agents, leading to hypercarbia and hypoxia. The posture of the patient also leads to major changes in pulmonary functions. Anticholinergics and neuromuscular blocking agents have little effect. Analgesics and Access this article online sedatives in combination with volatile anaesthetics and induction agents may exacerbate Website: www.ijaweb.org their effects. Since multiple agents are used during anaesthesia, ultimate effect may be DOI: 10.4103/0019‑5049.165850 different from when used in isolation. Literature search was done using MeSH key words ‘anesthesia’,
    [Show full text]