Mechanics of Ventilation
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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. -
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 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 Block Physiology 439 Team Work
Mechanics of pulmonary ventilation Respiratory Block Physiology 439 team work •Black: in male / female slides •Red : important Editing file •Pink: in female slides only •Blue: in male slides only •Green: notes @physiology439 •Gray: extra information •Textbook: Guyton + Linda Objectives : List the muscles of respiration and describe their roles during inspiration 01 and expiration Identify the importance of the following pressure in respiration: atmospheric, 02 intra-alveolar, intrapleural and transpulmonary Explain why intrapleural pressure is always subatmospheric under normal 03 conditions, and the significance of the thin layer of the intrapleural fluid surrounding the lung Define lung compliance and list the determinants of compliance 04 Mechanics of breathing Air movement depends upon : Boyle’s Law: Pulmonary Ventilation : the Volume depends on physical movement of air into PxV=K 1 2 P1xV1=P2xV2 3 movement of diaphragm and out of the lungs and ribs P= pressure , V= volume, K= constant Respiratory muscles Inspiratory muscle Expiratory muscle It is a passive process that depends on During resting Diaphragm and external intercostal the recoil tendency of the lung and need no muscle contraction Accessory muscles e.g It is an active process and need muscles Sternomastoid, anterior serratus, scalene During forced contraction the abdominal muscles and muscles contract in addition to the the internal intercostal muscles muscles of resting inspiration During deep forceful inhalation accessory muscles of inspiration -Expiration during forceful -
Role of the Allergist-Immunologist and Upper Airway Allergy in Sleep-Disordered Breathing
AAAAI Work Group Report Role of the Allergist-Immunologist and Upper Airway Allergy in Sleep-Disordered Breathing Dennis Shusterman, MD, MPHa, Fuad M. Baroody, MDb, Timothy Craig, DOc, Samuel Friedlander, MDd, Talal Nsouli, MDe, and Bernard Silverman, MD, MPHf; on behalf of the American Academy of Allergy, Asthma & Immunology’s Rhinitis, Rhinosinusitis and Ocular Allergy Committee Work Group on Rhinitis and Sleep-disordered Breathing San Francisco, Calif; Chicago, Ill; Hershey, Pa; Solon, Ohio; Washington, DC; and Brooklyn, NY BACKGROUND: Sleep-disordered breathing in general and RESULTS: Survey results were returned by 339 of 4881 active obstructive sleep apnea in particular are commonly encountered members (7%). More than two-third of respondents routinely conditions in allergy practice. Physiologically, nasal (or asked about sleep problems, believed that sleep-disordered nasopharyngeal) obstruction from rhinitis, nasal polyposis, or breathing was a problem for at least a “substantial minority” adenotonsillar hypertrophy are credible contributors to snoring (10%-30%) of their adult patients, and believed that medical and nocturnal respiratory obstructive events. Nevertheless, therapy for upper airway inflammatory conditions could existing practice parameters largely relegate the role of the potentially help ameliorate sleep-related complaints. Literature allergist to adjunctive treatment in cases of continuous positive review supported the connection between high-grade nasal airway pressure intolerance. congestion/adenotonsillar hypertrophy and obstructive sleep OBJECTIVES: To survey active American Academy of Allergy, apnea, and at least in the case of pediatric patients, supported the Asthma & Immunology members regarding their perceptions use of anti-inflammatory medication in the initial management and practices concerning sleep-disordered breathing in adult and of obstructive sleep apnea of mild-to-moderate severity. -
Pulmonary Adaptations the Respiratory System
Dr. Robergs Fall, 2010 Pulmonary Adaptations The Respiratory System Pulmonary Physiology 1 Dr. Robergs Fall, 2010 This is a cast of the airways that conduct air to the lungs. Why is this morphology potentially detrimental to air conductance into and from the lungs? Note; The respiratory zone has the greatest surface area and a dense capillary network. Pulmonary Physiology 2 Dr. Robergs Fall, 2010 Note the density of the alveoli and Note the dense capillary their thin walls. network that surrounds alveoli. Surfactant A phospholipoprotein molecule, secreted by specialized cells of the lung, that lines the surface of alveoli and respiratory bronchioles. Surfactant lowers the surface tension of the alveoli membranes, preventing the collapse of alveoli during exhalation and increasing compliance during inspiration. Respiration The process of gas exchange, which for the human body involves oxygen (O2) and carbon dioxide (CO2). Internal respiration - at the cellular level External respiration - at the lung Pulmonary Physiology 3 Dr. Robergs Fall, 2010 The distribution of surfactant is aided by holes that connect alveoli called Pores of Kohn. Ventilation The movement of air into and from the lung by the process of bulk flow. Ventilation (VE) (L/min) = frequency (br/min) x tidal volume (L) For rest conditions, VE (L/min) = 12 (br/min) x 0.5 (L) = 6 L/min For exercise at VO2max, VE (L/min) = 60 (br/min) x 3.0 (L) = 180 L/min Compliance - the property of being able to increase size or volume with only small changes in pressure. Pulmonary Physiology 4 Dr. Robergs Fall, 2010 Ventilation During Rest Inspiration is controlled by a repetitive discharge of action potentials from the inspiratory center. -
Dynamic Mechanics of the Lung Answer to the Last Class’S Question
Dynamic mechanics of the lung Answer to the Last class’s question Resistive (Frictional Forces) Opposing Lung Inflation Frictional opposition occurs only when the system is in motion. Frictional opposition to ventilation has the two components: 1. tissue viscous resistance 2. airway resistance. Tissue Viscous Resistance: the impedance of motion (opposition to flow) caused by displacement of tissues during ventilation that includes the lungs, rib cage, diaphragm, and abdominal organs. The frictional resistance is generated by the movement of each organ surface sliding against the other (e.g., the lung lobes sliding against each other and against the chest wall). Tissue resistance accounts for only approximately 20% of the total resistance to lung inflation. In conditions : obesity, pleural fibrosis, and ascites, the tissue viscous resistance increases the total impedance to ventilation. Airway Resistance (flow resistance) - Resistance to ventilation by the movement of gas through the airways. • accounts for approximately 80% of the frictional resistance to ventilation. • -is usually expressed in units of cm H2O/L/sec: R= ∆P/ ∆V • Airway resistance in healthy adults ranges from approximately 0.5 to 2.5 cm H2O/L/sec. • To cause gas to flow into or out of the lungs at 1 L/sec, a healthy person needs to lower his alveolar pressure 0.5 to 2.5 cm H2O below atmospheric pressure. Measurement of Airway Resistance • Airway resistance is the pressure difference between the alveoli and the mouth divided by a flow rate. Mouth pressure is easily measured with a manometer. Alveolar pressure can be deduced from measurements made in a body plethysmograph. -
Respiratory Physiology.Pdf
Respiratory Physiology • Chapter Outline • Functions of Respiratory System • Organization of Respiratory system • Ventilation and Lung mechanics: Boyle’s Law, Surfactant • 5-steps of respiration: Ventilation, external respiration, transport in blood, internal respiration and utilization of O2 and production of CO2 in cells • Lung volumes and capacities • Anatomical Dead Space • Hemoglobin and transport of gases • Oxygen Hemoglobin dissociation curve • Regulation of breathing: chemoreceptors and breathing center • Lung diseases • Main Functions of Respiratory System • Supplies O2 and removes CO2 • Joins kidney to Regulate pH of blood • Produces sounds for speech • Defends against microbes • Traps and dissolves systemic blood clots • Organization of Respiratory system • Has 3 portions: • Upper Airways: external nares nasal cavity nasopharynx oropharynx laryngopharynx larynx • Conducting zone: trachea bronchi bronchioles terminal bronchioles • Respiratory Zone: respiratory bronchioles alveolar ducts alveoli (main portion of gas exchange) • Conducting zone • Provides a low resistance path to alveoli • Bronchioles are the main site of air flow regulation by ANS and hormones. Bronchodilation versus bronchoconstriction. • Macrophages, mucous and cilia lining it defend against microbes and harmful particles • Epithelium secretes a watery fluid for easy movement of mucous. Cystic Fibrosis is genetic disease in which patient fails to secrete watery fluid and mucous narrows down the airways. • In chronic smokers cilia get damaged leading to mucous accumulation and chronic coughing • Respiratory zone • Main site of exchange of gases is Alveoli = air sacs • Each alveolus is surrounded by large # of pulmonary capillaries. Gases need to pass through 1 layer of very flat alveolar cells and 1 layer of endothelium of capillary wall • Type 1 Alveolar cells: very flat form main wall • Type 2 Alveolar cells: are thick cells and secrete detergent like Surfactant that prevents lung alveoli from collapsing. -
Residual Volume and Total Lung Capacity to Assess Reversibility in Obstructive Lung Disease
Residual Volume and Total Lung Capacity to Assess Reversibility in Obstructive Lung Disease Conor T McCartney MD, Melissa N Weis MD, Gregg L Ruppel MEd RRT RPFT FAARC, and Ravi P Nayak MD BACKGROUND: Reversibility of obstructive lung disease is traditionally defined by changes in FEV1 or FVC in response to bronchodilators. These may not fully reflect changes due to a reduction in hyperinflation or air-trapping, which have important clinical implications. To date, only a handful of studies have examined bronchodilators’ effect on lung volumes. The authors sought to better characterize the response of residual volume and total lung capacity to bronchodilators. METHODS: Responsiveness of residual volume and total lung capacity to bronchodilators was assessed with a retrospective analysis of pulmonary function tests of 965 subjects with obstructive lung disease as defined by the lower limit of normal based on National Health and Nutritional Examination Survey III prediction equations. RESULTS: A statistically significant number of subjects demonstrated response to bronchodilators in their residual volume independent of re- sponse defined by FEV1 or FVC, the American Thoracic Society and European Respiratory Society criteria. Reduced residual volume weakly correlated with response to FEV1 and to FVC. No statistically significant correlation was found between total lung capacity and either FEV1 or FVC. CONCLUSIONS: A significant number of subjects classified as being nonresponsive based on spirometry have reversible residual volumes. Subjects whose residual volumes improve in response to bronchodilators represent an important subgroup of those with obstructive lung disease. The identification of this subgroup better characterizes the heterogeneity of obstructive lung disease. The clinical importance of these findings is unclear but warrants further study. -
The Large Lungs of Elite Swimmers: an Increased Alveolar Number?
Eur Respir J 1993, 6, 237-247 The large lungs of elite swimmers: an increased alveolar number? J. Armour*, P.M. Donnelly**, P.T.P. Bye* The large lungs of elite swimmers: an increased alveolar number? J. Armour, P.M. * Institute of Respiratory Medicine, Donnelly, P.T.P. Bye. Royal Prince Alfred Hospital, ABSTRACT: In order to obtain further insight into the mechanisms relating Camperdown, NSW, Australia. to the large lung volumes of swimmers, tests of mechanical lung function, in ** University of Sydney, Sydney, NSW, cluding lung distensibility (K) and elastic recoil, pulmonary diffusion capacity, Australia. and respiratory mouth pressures, together with anthropometric data (height, Correspondence: P.M. Donnelly weight, body surface area, chest width, depth and surface area), were com Institute of Respiratory Medicine pared in eight elite male swimmers, eight elite male long distance athletes and Royal Prince Alfred Hospital eight control subjects. The differences in training profiles of each group were Camperdown NSW 2050 also examined. Australia There was no significant difference in height between the subjects, but the swimmers were younger than both the runners and controls, and both the Keywords: Alveolar distensibility swimmers and controls were heavier than the runners. Of all the training chest enlargement diffusion coefficient variables, only the mean total distance in kilometres covered per week was sig growth hormone nificantly greater in the runners. Whether based on: (a) adolescent predicted lung growth values; or (b) adult male predicted values, swimmers had significantly increased respiratory mouth pressures total lung capacity ((a) 145±22%, (mean±so) (b) 128±15%); vital capacity ((a) swimmers' lungs 146±24%, (b) 124±15%); and inspiratory capacity ((a) 155±33%, (b) 138±29%), but this was not found in the other two groups. -
The Respiratory System - 3 Pressure Changes and Resistance
The Respiratory System - 3 Pressure changes and resistance Jennifer Carbrey Ph.D. Department of Cell Biology image by OCAL, http://www.clker.com/clipart-26501.html, public domain Respiratory System 1. Anatomy and mechanics 2. Lung volumes and compliance 3. Pressure changes and resistance 4. Pulmonary function tests and alveolar ventilation 5. Oxygen transport 6. CO2 transport and V/Q mismatch 7. Regulation of breathing 8. Exercise and hypoxia Respiratory System pleural sac: inner layer covers lungs outer layer is attached to chest wall fluid in between image by OCAL (modified), http://www.clker.com/clipart-12109.html, public domain Pressure & Lung Volumes PA Lungs P Intrapleural fluid ip Chest wall Patm = 0 mm Hg = 760 mm Hg Pressure & Lung Volumes PA Pip = -3 PA – Pip determines lung size and PA - Patm determines air flow Pressure & Lung Volumes end of expiration during expiration PA= +1 PA=0 Pip = -4 Pip = -3 during inspiration end of inspiration PA – Pip determines lung size and PA=0 PA= -1 PA - Patm determines air flow F = (PA- Patm) /R Pip = -5 Pip = -6 P1V1=P2V2 – Boyles Law Resistance & Air Flow F = (PA- Patm) /R Factors that influence resistance: 1. Airway diameter – the smaller the diameter the more resistance in that tube in lung, more tubes as you go further into lung - so combined resistance gets lower as enter lung 2. Lung volume – if have a greater lung volume then airways are not as compressed – can be a compensation to lung disease with increased resistance 3. Muscle tone – parasympathetic stimulation causes bronchiolar smooth muscle to contract; sympathetic stimulation causes relaxation 4.