Factors Determining Maximum Inspiratory Flow and Maximum Expiratory Flow of the Lung
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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. -
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. -
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. -
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. -
Interrelationship Between Lung Volume, Expiratory Flow, and Lung Transfer Factor in Fibrosing Alveolitis
Thorax: first published as 10.1136/thx.36.11.858 on 1 November 1981. Downloaded from thorax 1981 ;36:858-862 Interrelationship between lung volume, expiratory flow, and lung transfer factor in fibrosing alveolitis JN PANDE From the Respiratory Laboratory, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India ABSTRACT Fifty patients with fibrosing alveolitis studied on 104 occasions exhibited significant direct correlations between vital capacity (VC), maximum mid-expiratory flow rate (MMFR), and transfer factor for carbon monoxide (TLCO). Forced expired volume in the first second (FEV,)/VC ratio bore a weak negative correlation with VC. Peak expiratory flow, MMFR, and maximum flow rates at 50 % and 25 % of VC were often reduced in patients with severe grades of pulmonary dys- function. It appears that as the severity of the fibrotic process increases, the lung volumes shrink and the transfer factor for CO decreases. The total lung capacity decreases predominantly on account of reduction in VC. With a decrease in lung volume the MMFR also falls. Decrease in flow rates at low lung volumes is greater as compared to the fall in peak flow. The expiratory flow rates how- ever were normal or even increased when related to absolute lung volume. Some patients exhibit disproportionate expiratory slowing as evidenced by a decrease in MMFR which is out of propor- tion to the reduction in VC. These patients also have a reduced FEV1,/VC ratio. These changes are probably the consequence of associated peripheral airway narrowing. copyright. Increased elastic recoil of the lung limiting maximal 33 women. Their age ranged from 16-68 years (mean inflation is considered to be the main abnormality of ± SE 42-1 ± 1-7 years). -
Ventilatory Management of ALI/ARDS J J Cordingley, B F Keogh
729 REVIEW SERIES Thorax: first published as 10.1136/thorax.57.8.729 on 1 August 2002. Downloaded from The pulmonary physician in critical care c 8: Ventilatory management of ALI/ARDS J J Cordingley, B F Keogh ............................................................................................................................. Thorax 2002;57:729–734 Current data relating to ventilation in ARDS are system (lung + chest wall) in a ventilated patient reviewed. Recent studies suggest that reduced mortality is calculated by dividing the tidal volume (Vt) by end inspiratory plateau pressure (Pplat) minus may be achieved by using a strategy which aims at end expiratory pressure + intrinsic PEEP preventing overdistension of lungs. (PEEPi). As the pathology of ARDS is heterogene- .......................................................................... ous, calculating static compliance does not provide information about regional variations in lung recruitment and varies according to lung he ventilatory management of patients with volume. Much attention has therefore focused on acute lung injury (ALI) and acute respiratory analysis of the pressure-volume (PV) curve. Tdistress syndrome (ARDS) has evolved in The static PV curve of the respiratory system conjunction with advances in understanding of can be obtained by inserting pauses during an the underlying pathophysiology. In particular, inflation-deflation cycle. A number of different evidence that mechanical ventilation has an methods have been described including the use of influence on lung injury and patient outcome has 1 a large syringe (super-syringe), or holding a emerged over the past three decades. The present understanding of optimal ventilatory manage- mechanical ventilator at end inspiration of ment is outlined and other methods of respiratory varying tidal volumes. The principles and meth- support are reviewed. -
Frequency Dependence of Compliance in the Evaluation of Patients with Unexplained Respiratory Symptoms
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector RESPIRATORY MEDICINE (2000) 94, 221±227 doi:10.1053/rmed.1999.0719, available online at http://www.idealibrary.com on Frequency dependence of compliance in the evaluation of patients with unexplained respiratory symptoms R. E. DE LA HOZ,K.I.BERGER,T.T.KLUGH,G.FRIEDMAN-JIMEÂ NEZ AND R. M. GOLDRING New York University School of Medicine, Departments of Medicine and Environmental Medicine; Bellevue Hospital Center, Chest Service, New York, NY, U.S.A. Frequency dependence of compliance (FDC) re¯ects non-homogeneous ventilatory distribution and, in the presence of a normal measured airway resistance, suggests peripheral airways dysfunction. This study evaluated peripheral airway function and bronchial reactivity in irritant exposed or non-exposed individuals with normal routine pulmonary function tests (PFTs) who had persistent unexplained lower respiratory symptoms. Twenty-two patients were identi®ed with persistent respiratory symptoms and with normal chest X-ray and PFTs. Twenty were non-smokers; two had stopped smoking more than 10 years before evaluation. Twelve patients had been exposed to irritants in their workplaces or at home. Non-speci®c bronchial hyper-reactivity (nsBHR) and FDC, pre- and post-bronchodilator, were measured in all patients. Studies were repeated in 6/12 irritant-exposed subjects after exposure removal and inhaled corticosteroid treatment. Whereas 12/22 patients had nsBHR, all 22 subjects demonstrated FDC [dynamic lung compliance/static lung 71 compliance Cdyn,1 /Cst,1 at respiratory frequency 60 min (f60), mean 46%, range 27±67%]. -
“Children Are Not Small Adults!” Derek S
4 The Open Inflammation Journal, 2011, 4, (Suppl 1-M2) 4-15 Open Access “Children are not Small Adults!” Derek S. Wheeler*1,2, Hector R. Wong1,2 and Basilia Zingarelli1,2 1Division of Critical Care Medicine, Cincinnati Children’s Hospital Medical Center, The Kindervelt Laboratory for Critical Care Medicine Research, Cincinnati Children’s Research Foundation, USA 2Department of Pediatrics, University of Cincinnati College of Medicine, USA Abstract: The recognition, diagnosis, and management of sepsis remain among the greatest challenges in pediatric critical care medicine. Sepsis remains among the leading causes of death in both developed and underdeveloped countries and has an incidence that is predicted to increase each year. Unfortunately, promising therapies derived from preclinical models have universally failed to significantly reduce the substantial mortality and morbidity associated with sepsis. There are several key developmental differences in the host response to infection and therapy that clearly delineate pediatric sepsis as a separate, albeit related, entity from adult sepsis. Thus, there remains a critical need for well-designed epidemiologic and mechanistic studies of pediatric sepsis in order to gain a better understanding of these unique developmental differences so that we may provide the appropriate treatment. Herein, we will review the important differences in the pediatric host response to sepsis, highlighting key differences at the whole-organism level, organ system level, and cellular and molecular level. Keywords: Pediatrics, sepsis, shock, severe sepsis, septic shock, SIRS, systemic inflammatory response syndrome, critical care. THE PEDIATRIC HOST RESPONSE TO SEPSIS Sepsis is exceedingly more common in children less than 1 year of age, with rates 10-fold higher during infancy Key Differences at the Whole-organism Level compared to childhood and adolescence [2]. -
Measurement of Functional Residual Capacity of the Lung by Partial CO2 Rebreathing Method During Acute Lung Injury in Animals
Measurement of Functional Residual Capacity of the Lung by Partial CO2 Rebreathing Method During Acute Lung Injury in Animals Lara M Brewer MSc, Dinesh G Haryadi PhD, and Joseph A Orr PhD BACKGROUND: Several techniques for measuring the functional residual capacity (FRC) of the lungs in mechanically ventilated patients have been proposed, each of which is based on either nitrogen wash-out or dilution of tracer gases. These methods are expensive, difficult, time-consum- ing, impractical, or require an intolerably large change in the fraction of inspired oxygen. We propose a CO2 wash-in method that allows automatic and continual FRC measurement in mechan- ically ventilated patients. METHODS: We measured FRC with a CO2 partial rebreathing tech- nique, first in a mechanical lung analog, and then in mechanically ventilated animals, before, during, and subsequent to an acute lung injury induced with oleic acid. We compared FRC mea- surements from partial CO2 rebreathing to measurements from a nitrogen wash-out reference method. Using an approved animal protocol, general anesthesia was induced and maintained with propofol in 6 swine (38.8–50.8 kg). A partial CO2 rebreathing monitor was placed in the breathing circuit between the endotracheal tube and the Y-piece. The partial CO2 rebreathing signal obtained from the monitor was used to calculate FRC. FRC was also measured with a nitrogen wash-out measurement technique. In the animal studies we collected data from healthy lungs, and then subsequent to a lung injury that simulated the conditions of acute lung injury/acute respiratory distress syndrome. The injury was created by intravenously infusing 0.09 mL/kg of oleic acid over a 15-min period. -
Ventilator Waveform Analysis
VENTILATOR WAVEFORM ANALYSIS By Dr. M. V. Nagarjuna 1 Seminar Overview 1. Basic Terminology ( Types of variables,,, Breaths, modes of ventilation) 2. Ideal ventilator waveforms (()Scalars) 3. Diagnosing altered physiological states 4. Ventilator Patient Asynchrony and its management. 5. Loops (Pressure volume and Flow volume) 2 Basics phase variables………….. A. Trigger ……. BC What causes the breath to begin? B. Limit …… A What regulates gas flow during the breath? C. Cycle ……. What causes the breath to end? VARIABLES 1. TRIGGER VARIABLE : Initiates the breath Flow (Assist breath) Pressure (Assist Breath) Time (Control Breath) Newer variables (Volume, Shape signal, neural) Flow trigge r better th an Pressure tri gger . With the newer ventilators, difference in work of triggering is of minimal clinical significance. British Journal of Anaesthesia, 2003 4 2. TARGET VARIABLE : Controls the gas delivery during the breath Flow ( Volume Control modes) Pressure ( Pressure Control modes) 3. CYCLE VARIABLE : Cycled from inspiration into expiiiration Volume ( Volume control) Time (Pressure control) Flow (pressure Support) Pressure (Sft(Safety cycling varibl)iable) 5 Modes of Ventilation Mode of ventilation Breath types available Volume Assist Control Volume Control, Volume Assist Pressure Assist Control Pressure Control, Pressure Assist Volume SIMV Volume Control, Volume Assist, Pressure Support Pressure SIMV Pressure Control, Pressure Assist, Pressure Support Pressure Support Pressure support 6 SCALARS 7 FLOW vs TIME 8 Flow versus time Never forget to look at the expiratory limb of the flow waveform The expiratory flow is determined by the elastic recoil of the respiratory system and resistance of intubated airways 9 Types of Inspiratory flow waveforms a. Square wave flow b. -
PFT Interpretation
PFT Interpretation Presented by: Shazhad Manawar, MD Medical Director Respiratory Care & Pulmonary Rehab McLaren Bay Region Introduction History or symptoms suggestive of lung disease. Risk factors for lung disease are present. Pulmonary Function Tests Spirometry Spirometry before and after bronchodilator Lung volumes Diffusing capacity for carbon monoxide Maximal respiratory pressures Flow volume loops Spirometry Volume of air exhaled at specific time points during forceful and complete exhalation. Total exhaled volume, know as the FVC (forced vital capacity). Volume exhaled in the first second, know as the forced expiratory volume in one second (FEV1) Spirometry - continued Ratio (FEV1/FVC) are the most important variables Minimal risk Key diagnostic test Asthma Chronic Obstructive Pulmonary Disease (COPD) Chronic cough Spirometry - continued Monitor a broad spectrum of respiratory diseases. Asthma COPD Interstitial Lung Disease Neuromuscular diseases affecting respiratory muscles Spirometry - continued Slow vital capacity (SVC) Useful measurement when FVC is reduced and airway obstruction is present Post-bronchodilator Determine the degree of reversibility Administration of albuterol Technique is important Increase in the FEV1 of more than 12% or greater than 0.2 L suggests acute bronchodilator responsiveness. Subjective improvements Post-bronchodilator - continued Thus, the lack of an acute bronchodilator response on spirometry should not preclude a one to eight week therapeutic trial of bronchodilators