Respiratory System Physiology Mimi Jakoi, Phd Jennifer Carbrey, Phd
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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 -
Maximum Expiratory Flow Rates in Induced Bronchoconstriction in Man
Maximum expiratory flow rates in induced bronchoconstriction in man A. Bouhuys, … , B. M. Kim, A. Zapletal J Clin Invest. 1969;48(6):1159-1168. https://doi.org/10.1172/JCI106073. Research Article We evaluated changes of maximum expiratory flow-volume (MEFV) curves and of partial expiratory flow-volume (PEFV) curves caused by bronchoconstrictor drugs and dust, and compared these to the reverse changes induced by a bronchodilator drug in previously bronchoconstricted subjects. Measurements of maximum flow at constant lung inflation (i.e. liters thoracic gas volume) showed larger changes, both after constriction and after dilation, than measurements of peak expiratory flow rate, 1 sec forced expiratory volume and the slope of the effort-independent portion of MEFV curves. Changes of flow rates on PEFV curves (made after inspiration to mid-vital capacity) were usually larger than those of flow rates on MEFV curves (made after inspiration to total lung capacity). The decreased maximum flow rates after constrictor agents are not caused by changes in lung static recoil force and are attributed to narrowing of small airways, i.e., airways which are uncompressed during forced expirations. Changes of maximum expiratory flow rates at constant lung inflation (e.g. 60% of the control total lung capacity) provide an objective and sensitive measurement of changes in airway caliber which remains valid if total lung capacity is altered during treatment. Find the latest version: https://jci.me/106073/pdf Maximum Expiratory Flow Rates in Induced Bronchoconstriction in Man A. Bouiuys, V. R. HuNTr, B. M. Kim, and A. ZAPLETAL From the John B. Pierce Foundation Laboratory and the Yale University School of Medicine, New Haven, Connecticut 06510 A B S T R A C T We evaluated changes of maximum ex- rates are best studied as a function of lung volume. -
The Oxyhaemoglobin Dissociation Curve in Critical Illness
Basic sciences review The Oxyhaemoglobin Dissociation Curve in Critical Illness T. J. MORGAN Intensive Care Facility, Division of Anaesthesiology and Intensive Care, Royal Brisbane Hospital, Brisbane, QUEENSLAND ABSTRACT Objective: To review the status of haemoglobin-oxygen affinity in critical illness and investigate the potential to improve gas exchange, tissue oxygenation and outcome by manipulations of the oxyhaemoglobin dissociation curve. Data sources: Articles and published peer-review abstracts. Summary of review: The P50 of a species is determined by natural selection according to animal size, tissue metabolic requirements and ambient oxygen tension. In right to left shunting mathematical modeling indicates that an increased P50 defends capillary oxygenation, the one exception being sustained hypercapnia. Increasing the P50 should also be protective in tissue ischaemia, and this is supported by modeling and experimental evidence. Most studies of critically ill patients have indicated reduced 2,3-DPG concentrations. This is probably due to acidaemia, and the in vivo P50 is likely to be normal despite low 2,3-DPG levels. It may soon be possible to achieve significant P50 elevations without potentially harmful manipulations of acid-base balance or hazardous drug therapy. Conclusions: Despite encouraging theoretical and experimental data, it is not known whether manipulations of the P50 in critical illness can improve gas exchange and tissue oxygenation or improve outcome. The status of the P50 may warrant more routine quantification and consideration along with the traditional determinants of tissue oxygen availability. (Critical Care and Resuscitation 1999; 1: 93-100) Key words: Critical illness, haemoglobin-oxygen affinity, ischaemia, P50, tissue oxygenation, shunt In intensive care practice, manipulations to improve in the tissues. -
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. -
Oxygenation and Oxygen Therapy
Rules on Oxygen Therapy: Physiology: 1. PO2, SaO2, CaO2 are all related but different. 2. PaO2 is a sensitive and non-specific indicator of the lungs’ ability to exchange gases with the atmosphere. 3. FIO2 is the same at all altitudes 4. Normal PaO2 decreases with age 5. The body does not store oxygen Therapy & Diagnosis: 1. Supplemental O2 is an FIO2 > 21% and is a drug. 2. A reduced PaO2 is a non-specific finding. 3. A normal PaO2 and alveolar-arterial PO2 difference (A-a gradient) do NOT rule out pulmonary embolism. 4. High FIO2 doesn’t affect COPD hypoxic drive 5. A given liter flow rate of nasal O2 does not equal any specific FIO2. 6. Face masks cannot deliver 100% oxygen unless there is a tight seal. 7. No need to humidify if flow of 4 LPM or less Indications for Oxygen Therapy: 1. Hypoxemia 2. Increased work of breathing 3. Increased myocardial work 4. Pulmonary hypertension Delivery Devices: 1. Nasal Cannula a. 1 – 6 LPM b. FIO2 0.24 – 0.44 (approx 4% per liter flow) c. FIO2 decreases as Ve increases 2. Simple Mask a. 5 – 8 LPM b. FIO2 0.35 – 0.55 (approx 4% per liter flow) c. Minimum flow 5 LPM to flush CO2 from mask 3. Venturi Mask a. Variable LPM b. FIO2 0.24 – 0.50 c. Flow and corresponding FIO2 varies by manufacturer 4. Partial Rebreather a. 6 – 10 LPM b. FIO2 0.50 – 0.70 c. Flow must be sufficient to keep reservoir bag from deflating upon inspiration 5. -
Introduction to Airway Resistance Measurements
Introduction to airway resistance measurements Dr. David Kaminsky Department of Medicine The University of Vermont VT 05405 Burlington UNITED STATES OF AMERICA [email protected] AIMS Review physiology of airway resistance Survey measures of airway resistance Provide examples of clinical applications Highlight research applications SUMMARY Airway resistance (Raw) is one of the fundamental features of the mechanics of the respiratory system. While the flow-volume loop offers insight into the volume and flow of air, it is limited in terms of specific information regarding lung mechanics. Airway resistance is the ratio of driving pressure divided by flow through the airways. It specifies the pressure required to achieve a flow of air with a velocity of 1L/sec. If the airway is represented by a simple, rigid tube, with laminar flow of air through it, the airway resistance Raw = (8 x L x )/ r4, where L = length of the tube, = viscosity of the gas, and r = radius of the tube. It is important to note that the r4 relationship demonstrates how sensitive resistance is to the size of the tube, varying inversely with the 4th power of the radius. The inner diameter of the airway is itself determined by many factors, including airway smooth muscle contractile state, airway wall thickness (related to inflammation, edema and remodeling), airway wall buckling and formation of mucosal folds, the interdependence, or linkage, of airway and surrounding lung parenchyma, and the intrinsic elastic recoil of the lung parenchyma, which serves as a load on the airway and variably resists bronchoconstriction. Of course, the airways are not rigid tubes, and in fact flow is a complex process involving both laminar and turbulent conditions, so this calculation of Raw is an approximation only. -
17 the Respiratory System
Mechanics of Breathing The Respiratory System 17 Bones and Muscles of the Thorax Surround the Lungs Pleural Sacs Enclose the Lungs Airways Connect Lungs to the External Environment The Airways Warm, Humidify, and Filter Inspired Air Alveoli Are the Site of Gas Exchange Pulmonary Circulation Is High-Flow, Low-Pressure G a s L a w s Air Is a Mixture of Gases Gases Move Down Pressure Gradients Boyle’s Law Describes Pressure-Volume Relationships Ventilation Lung Volumes Change During Ventilation During Ventilation, Air Flows Because of Pressure Gradients Inspiration Occurs When Alveolar Pressure Decreases Expiration Occurs When Alveolar Pressure Increases Intrapleural Pressure Changes During Ventilation Lung Compliance and Elastance May Change in Disease States Surfactant Decreases the Work of Breathing Airway Diameter Determines Airway Resistance Rate and Depth of Breathing Determine the Effi ciency of Breathing Gas Composition in the Alveoli Varies Little During Normal Breathing Ventilation and Alveolar Blood Flow Are Matched Auscultation and Spirometry Assess Pulmonary Function This being of mine, whatever it really is, consists of a little fl esh, a little breath, and the part which governs. — Marcus Aurelius Antoninus ( C . E . 121–180) Background Basics Ciliated and exchange epithelia Pressure, volume, fl ow, and resistance Pulmonary circulation Surface tension Colored x-ray of the lung Autonomic and somatic showing the motor neurons branching Velocity of fl ow airways. 600 Mechanics of Breathing magine covering the playing surface of a racquetball court cavity to control their contact with the outside air. Internalization (about 75 m2 ) with thin plastic wrap, then crumpling up the creates a humid environment for the exchange of gases with the wrap and stuffi ng it into a 3-liter soft drink bottle. -
Respiratory Support
Intensive Care Nursery House Staff Manual Respiratory Support ABBREVIATIONS FIO2 Fractional concentration of O2 in inspired gas PaO2 Partial pressure of arterial oxygen PAO2 Partial pressure of alveolar oxygen PaCO2 Partial pressure of arterial carbon dioxide PACO2 Partial pressure of alveolar carbon dioxide tcPCO2 Transcutaneous PCO2 PBAR Barometric pressure PH2O Partial pressure of water RQ Respiratory quotient (CO2 production/oxygen consumption) SaO2 Arterial blood hemoglobin oxygen saturation SpO2 Arterial oxygen saturation measured by pulse oximetry PIP Peak inspiratory pressure PEEP Positive end-expiratory pressure CPAP Continuous positive airway pressure PAW Mean airway pressure FRC Functional residual capacity Ti Inspiratory time Te Expiratory time IMV Intermittent mandatory ventilation SIMV Synchronized intermittent mandatory ventilation HFV High frequency ventilation OXYGEN (Oxygen is a drug!): A. Most infants require only enough O2 to maintain SpO2 between 87% to 92%, usually achieved with PaO2 of 40 to 60 mmHg, if pH is normal. Patients with pulmonary hypertension may require a much higher PaO2. B. With tracheal suctioning, it may be necessary to raise the inspired O2 temporarily. This should not be ordered routinely but only when the infant needs it. These orders are good for only 24h. OXYGEN DELIVERY and MEASUREMENT: A. Oxygen blenders allow O2 concentration to be adjusted between 21% and 100%. B. Head Hoods permit non-intubated infants to breathe high concentrations of humidified oxygen. Without a silencer they can be very noisy. C. Nasal Cannulae allow non-intubated infants to breathe high O2 concentrations and to be less encumbered than with a head hood. O2 flows of 0.25-0.5 L/min are usually sufficient to meet oxygen needs. -
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’, -
Respiratory Therapy Pocket Reference
Pulmonary Physiology Volume Control Pressure Control Pressure Support Respiratory Therapy “AC” Assist Control; AC-VC, ~CMV (controlled mandatory Measure of static lung compliance. If in AC-VC, perform a.k.a. a.k.a. AC-PC; Assist Control Pressure Control; ~CMV-PC a.k.a PS (~BiPAP). Spontaneous: Pressure-present inspiratory pause (when there is no flow, there is no effect ventilation = all modes with RR and fixed Ti) PPlateau of Resistance; Pplat@Palv); or set Pause Time ~0.5s; RR, Pinsp, PEEP, FiO2, Flow Trigger, rise time, I:E (set Pocket Reference RR, Vt, PEEP, FiO2, Flow Trigger, Flow pattern, I:E (either Settings Pinsp, PEEP, FiO2, Flow Trigger, Rise time Target: < 30, Optimal: ~ 25 Settings directly or by inspiratory time Ti) Settings directly or via peak flow, Ti settings) Decreasing Ramp (potentially more physiologic) PIP: Total inspiratory work by vent; Reflects resistance & - Decreasing Ramp (potentially more physiologic) Card design by Respiratory care providers from: Square wave/constant vs Decreasing Ramp (potentially Flow Determined by: 1) PS level, 2) R, Rise Time ( rise time ® PPeak inspiratory compliance; Normal ~20 cmH20 (@8cc/kg and adult ETT); - Peak Flow determined by 1) Pinsp level, 2) R, 3)Ti (shorter Flow more physiologic) ¯ peak flow and 3.) pt effort Resp failure 30-40 (low VT use); Concern if >40. Flow = more flow), 4) pressure rise time (¯ Rise Time ® Peak v 0.9 Flow), 5) pt effort ( effort ® peak flow) Pplat-PEEP: tidal stress (lung injury & mortality risk). Target Determined by set RR, Vt, & Flow Pattern (i.e. for any set I:E Determined by patient effort & flow termination (“Esens” – PDriving peak flow, Square (¯ Ti) & Ramp ( Ti); Normal Ti: 1-1.5s; see below “Breath Termination”) < 15 cmH2O. -
Respiratory System
Respiratory System 1 Respiratory System 2 Respiratory System 3 Respiratory System 4 Respiratory System 5 Respiratory System 6 Respiratory System 7 Respiratory System 8 Respiratory System 9 Respiratory System 10 Respiratory System 11 Respiratory System • Pulmonary Ventilation 12 Respiratory System 13 Respiratory System 14 Respiratory System • Measuring of Lung Function œ Compliance œ the ease at which the lungs and thoracic wall can be expanded œ if reduced it is more difficult to inflate the lungs œ causes: • Damaged lung tissue • Fluid within lung tissue • Decrease in pulmonary surfactant • Anything that impedes lung expansion or contraction œ Respiratory Volumes and Capacities will be covered in Lab œ 15 Respiratory System • Exchange of Oxygen and Carbon Dioxide œ Charles‘ Law œ the volume of a gas is directly proportional to the absolute temperature, assuming the pressure remains constant As gases enter the lung they warm and expand, increasing lung volume œ Dalton‘s Law œ each gas of a mixture of gases exerts its own pressure as if all the other gases were not present œ Henry‘s Law œ the quantity of a gas that will dissolve in a liquid is proportional to the partial pressure of the gas and its solubility coefficient, when the temperature remains constant 16 Respiratory System • External and Internal Respiration 17 Respiratory System • Transport of Oxygen and Carbon Dioxide by the Blood œ Oxygen Transport • 1.5% dissolved in plasma • 98.5% carried with Hbinside of RBC‘s as oxyhemoglobin œ Hbœ made up of protein portion called the globinportion -
Epidemiology and Pulmonary Physiology of Severe Asthma
Epidemiology and Pulmonary Physiology of Severe Asthma a b Jacqueline O’Toole, DO , Lucas Mikulic, MD , c, David A. Kaminsky, MD * KEYWORDS Demographics Phenotype Health care utilization Pulmonary function Lung elastic recoil Ventilation heterogeneity Gas trapping Airway hyperresponsiveness KEY POINTS The definition of severe asthma is still a work in progress. The severity of asthma is predictive of higher health care utilization. Cluster analysis is useful in characterizing severe asthma phenotypes. Airway hyperresponsiveness in severe asthma is a result of abnormal airflow, lung recoil, ventilation, and gas trapping. Patients with severe asthma may have a reduced perception of dyspnea. INTRODUCTION Severe asthma is a characterized by a complex set of clinical, demographic, and physiologic features. In this article, we review both the epidemiology and pulmonary physiology associated with severe asthma. DEMOGRAPHICS OF SEVERE ASTHMA Asthma has long been recognized as a worldwide noncommunicable disease of importance. Within the population of individuals with asthma, there is a subgroup of individuals at high risk for complications, exacerbations, and a poor quality of life. The authors have nothing to disclose. a Department of Medicine, University of Vermont Medical Center, 111 Colchester Avenue, Bur- lington, VT 05401, USA; b Division of Pulmonary and Critical Care Medicine, University of Ver- mont Medical Center, Given D208, 89 Beaumont Avenue, Burlington, VT 05405, USA; c Division of Pulmonary and Critical Care Medicine, University of Vermont College of Medicine, Given D213, 89 Beaumont Avenue, Burlington, VT 05405, USA * Corresponding author. E-mail address: [email protected] Immunol Allergy Clin N Am 36 (2016) 425–438 http://dx.doi.org/10.1016/j.iac.2016.03.001 immunology.theclinics.com 0889-8561/16/$ – see front matter Ó 2016 Elsevier Inc.