Advanced Modes of Ventilation: Concerns for the OR
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Airway Pressures and Volutrauma
Airway Pressures and Volutrauma Airway Pressures and Volutrauma: Is Measuring Tracheal Pressure Worth the Hassle? Monitoring airway pressures during mechanical ventilation is a standard of care.1 Sequential recording of airway pressures not only provides information regarding changes in pulmonary impedance but also allows safety parameters to be set. Safety parameters include high- and low-pressure alarms during positive pressure breaths and disconnect alarms. These standards are, of course, based on our experience with volume control ventilation in adults. During pressure control ventilation, monitoring airway pressures remains important, but volume monitoring and alarms are also required. Airway pressures and work of breathing are also important components of derived variables, including airway resistance, static compliance, dynamic compliance, and intrinsic positive end-expiratory pressure (auto-PEEP), measured at the bedside.2 The requisite pressures for these variables include peak inspiratory pressure, inspiratory plateau pressure, expiratory plateau pressure, and change in airway pressure within a breath. Plateau pressures should be measured at periods of zero flow during both volume control and pressure control ventilation. Change in airway pressure should be measured relative to change in volume delivery to the lung (pressure-volume loop) to elucidate work of breathing. See the related study on Page 1179. Evidence that mechanical ventilation can cause and exacerbate acute lung injury has been steadily mounting.3-5 While most of this evidence has originated from laboratory animal studies, recent clinical reports appear to support this concept.6,7 Traditionally, ventilator-induced lung injury brings to mind the clinical picture of tension pneumothorax. Barotrauma (from the root word baro, which means pressure) is typically associated with excessive airway pressures. -
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. -
Increasing the Inspiratory Time and I:E Ratio During Mechanical Ventilation
Müller-Redetzky et al. Critical Care (2015) 19:23 DOI 10.1186/s13054-015-0759-2 RESEARCH Open Access Increasing the inspiratory time and I:E ratio during mechanical ventilation aggravates ventilator-induced lung injury in mice Holger C Müller-Redetzky1*, Matthias Felten1, Katharina Hellwig1, Sandra-Maria Wienhold1, Jan Naujoks1, Bastian Opitz1, Olivia Kershaw2, Achim D Gruber2, Norbert Suttorp1 and Martin Witzenrath1 Abstract Introduction: Lung-protective ventilation reduced acute respiratory distress syndrome (ARDS) mortality. To minimize ventilator-induced lung injury (VILI), tidal volume is limited, high plateau pressures are avoided, and positive end-expiratory pressure (PEEP) is applied. However, the impact of specific ventilatory patterns on VILI is not well defined. Increasing inspiratory time and thereby the inspiratory/expiratory ratio (I:E ratio) may improve oxygenation, but may also be harmful as the absolute stress and strain over time increase. We thus hypothesized that increasing inspiratory time and I:E ratio aggravates VILI. Methods: VILI was induced in mice by high tidal-volume ventilation (HVT 34 ml/kg). Low tidal-volume ventilation (LVT 9 ml/kg) was used in control groups. PEEP was set to 2 cm H2O, FiO2 was 0.5 in all groups. HVT and LVT mice were ventilated with either I:E of 1:2 (LVT 1:2, HVT 1:2) or 1:1 (LVT 1:1, HVT 1:1) for 4 hours or until an alternative end point, defined as mean arterial blood pressure below 40 mm Hg. Dynamic hyperinflation due to the increased I:E ratio was excluded in a separate group of animals. Survival, lung compliance, oxygenation, pulmonary permeability, markers of pulmonary and systemic inflammation (leukocyte differentiation in lung and blood, analyses of pulmonary interleukin-6, interleukin-1β, keratinocyte-derived chemokine, monocyte chemoattractant protein-1), and histopathologic pulmonary changes were analyzed. -
Prevention of Ventilator Associated Complications
Prevention of Ventilator associated complications Authors: Dr Aparna Chandrasekaran* & Dr Ashok Deorari From: Department of Pediatrics , WHO CC AIIMS , New Delhi-110029 & * Neonatologist , Childs Trust Medical Research Foundation and Kanchi Kamakoti Childs Trust Hospital, Chennai -600034. Word count Text: 4890 (excluding tables and references) Figures: 1; Panels: 2 Key words: Ventilator associated complications, bronchopulmonary dysplasia Abbreviations: VAP- Ventilator associated pneumonia , BPD- Bronchopulmonary dysplasia, ELBW- Extremely low birth weight, VLBW- Very low birth weight, ROP- Retinopathy of prematurity, CPAP- Continuous positive airway pressure, I.M.- intramuscular, CI- Confidence intervals, PPROM- Preterm prelabour rupture of membranes, RCT- Randomised control trial, RR- Relative risk, PEEP- Peak end expiratory pressure Background: The last two decades have witnessed a dramatic reduction in neonatal mortality from 4.4 million newborn deaths annually in 1990 to 2.9 million deaths yearly in the year 2012, a reduction by 35%. In India, neonatal mortality has decreased by 42% during the same period. (1) With the increasing survival and therapeutic advances, the new paradigm is now on providing best quality of care and preventing complications related to therapy. Assisted ventilation dates back to 1879, when the Aerophone Pulmonaire, the world’s earliest ventilator was developed. This was essentially a simple tube connected to a rubber bulb. The tube was placed in the infant’s airway and the bulb was alternately compressed and released to produce inspiration and expiration. (2) With better understanding of pulmonary physiology and mechanics , lung protective strategies have evolved in the last two decades, with new resuscitation devices that limit pressure (T-piece resuscitator), non-invasive ventilation, microprocessors that allow synchronised breaths and regulate volume and high frequency oscillators/ jet ventilators. -
The Future of Mechanical Ventilation: Lessons from the Present and the Past Luciano Gattinoni1*, John J
Gattinoni et al. Critical Care (2017) 21:183 DOI 10.1186/s13054-017-1750-x REVIEW Open Access The future of mechanical ventilation: lessons from the present and the past Luciano Gattinoni1*, John J. Marini2, Francesca Collino1, Giorgia Maiolo1, Francesca Rapetti1, Tommaso Tonetti1, Francesco Vasques1 and Michael Quintel1 Abstract The adverse effects of mechanical ventilation in acute respiratory distress syndrome (ARDS) arise from two main causes: unphysiological increases of transpulmonary pressure and unphysiological increases/decreases of pleural pressure during positive or negative pressure ventilation. The transpulmonary pressure-related side effects primarily account for ventilator-induced lung injury (VILI) while the pleural pressure-related side effects primarily account for hemodynamic alterations. The changes of transpulmonary pressure and pleural pressure resulting from a given applied driving pressure depend on the relative elastances of the lung and chest wall. The term ‘volutrauma’ should refer to excessive strain, while ‘barotrauma’ should refer to excessive stress. Strains exceeding 1.5, corresponding to a stress above ~20 cmH2O in humans, are severely damaging in experimental animals. Apart from high tidal volumes and high transpulmonary pressures, the respiratory rate and inspiratory flow may also play roles in the genesis of VILI. We do not know which fraction of mortality is attributable to VILI with ventilation comparable to that reported in recent clinical practice surveys (tidal volume ~7.5 ml/kg, positive end-expiratory pressure (PEEP) ~8 cmH2O, rate ~20 bpm, associated mortality ~35%). Therefore, a more complete and individually personalized understanding of ARDS lung mechanics and its interaction with the ventilator is needed to improve future care. -
Mechanical Ventilation
Fundamentals of MMeecchhaanniiccaall VVeennttiillaattiioonn A short course on the theory and application of mechanical ventilators Robert L. Chatburn, BS, RRT-NPS, FAARC Director Respiratory Care Department University Hospitals of Cleveland Associate Professor Department of Pediatrics Case Western Reserve University Cleveland, Ohio Mandu Press Ltd. Cleveland Heights, Ohio Published by: Mandu Press Ltd. PO Box 18284 Cleveland Heights, OH 44118-0284 All rights reserved. This book, or any parts thereof, may not be used or reproduced by any means, electronic or mechanical, including photocopying, recording or by any information storage and retrieval system, without written permission from the publisher, except for the inclusion of brief quotations in a review. First Edition Copyright 2003 by Robert L. Chatburn Library of Congress Control Number: 2003103281 ISBN, printed edition: 0-9729438-2-X ISBN, PDF edition: 0-9729438-3-8 First printing: 2003 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the author and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, express or implied, with respect to the contents of the publication. Table of Contents 1. INTRODUCTION TO VENTILATION..............................1 Self Assessment Questions.......................................................... 4 Definitions................................................................................ -
Biotrauma During Ultra-Low Tidal Volume
Amado‑Rodríguez et al. Ann. Intensive Care (2021) 11:132 https://doi.org/10.1186/s13613‑021‑00919‑0 RESEARCH Open Access Biotrauma during ultra‑low tidal volume ventilation and venoarterial extracorporeal membrane oxygenation in cardiogenic shock: a randomized crossover clinical trial Laura Amado‑Rodríguez1,2,3* , Cecilia Del Busto1,2, Inés López‑Alonso2,3, Diego Parra1,2, Juan Mayordomo‑Colunga2,3,4, Miguel Arias‑Guillén3,5, Rodrigo Albillos‑Almaraz1,2, Paula Martín‑Vicente2,3,6, Cecilia López‑Martínez2,3, Covadonga Huidobro2,3, Luigi Camporota7, Arthur S. Slutsky8 and Guillermo M. Albaiceta1,2,3,6 Abstract Background: Cardiogenic pulmonary oedema (CPE) may contribute to ventilator‑associated lung injury (VALI) in patients with cardiogenic shock. The appropriate ventilatory strategy remains unclear. We aimed to evaluate the impact of ultra‑low tidal volume ventilation with tidal volume of 3 ml/kg predicted body weight (PBW) in patients with CPE and veno–arterial extracorporeal membrane oxygenation (V–A ECMO) on lung infammation compared to conventional ventilation. Methods: A single‑centre randomized crossover trial was performed in the Cardiac Intensive Care Unit (ICU) at a ter‑ tiary university hospital. Seventeen adults requiring V–A ECMO and mechanical ventilation due to cardiogenic shock were included from February 2017 to December 2018. Patients were ventilated for two consecutive periods of 24 h with tidal volumes of 6 and 3 ml/kg of PBW, respectively, applied in random order. Primary outcome was the change in proinfammatory mediators in bronchoalveolar lavage fuid (BALF) between both ventilatory strategies. Results: Ventilation with 3 ml/kg PBW yielded lower driving pressures and end‑expiratory lung volumes. -
Pressure Control Ventilation .Pdf
Crit Care Clin 23 (2007) 183–199 Pressure Control Ventilation Dane Nichols, MD*, Sai Haranath, MBBS Division of Pulmonary & Critical Care Medicine, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Mailcode UHN-67, Portland, OR 97239, USA As mechanical ventilators become increasingly sophisticated, clinicians are faced with a variety of ventilatory modes that use volume, pressure, and time in combination to achieve the overall goal of assisted ventilation. Although much has been written about the advantages and disadvantages of these increasingly complex modalities, currently there is no convincing evi- dence of the superiority of one mode of ventilation over another. It is also important to bear in mind that individual patient characteristics must be considered when adopting a particular mode of ventilatory support. As em- phasized in the 1993 American College of Chest Physicians Consensus Con- ference on Mechanical Ventilation, ‘‘although the quantitative response of a given physiologic variable may be predictable, the qualitative response is highly variable and patient specific’’ [1]. Partly because of the inherent difficulties in working with pressure venti- lation, the Acute Respiratory Distress Syndrome (ARDS) Network chose to use a volume mode of support for their landmark low tidal volumetrial [2]. The preference for volume ventilation at ARDS Network centers was later demonstrated in a retrospective study of clinicians’ early approach to me- chanical ventilation in acute lung injury/ARDS. Pressure control was used in only 10% of the patient population before study entry. There was a mod- est tendency to use pressure control ventilation (PCV) in patients with more severe oxygenation defects (PaO2/FiO2, or P/F !200) and a greater toler- ance for higher airway pressures when using this mode. -
Ventilator-Associated Lung Injury During Assisted Mechanical Ventilation
409 Ventilator-Associated Lung Injury during Assisted Mechanical Ventilation Felipe Saddy, MD, MSc1,2,3 Yuda Sutherasan, MD4,5 Patricia R. M. Rocco, MD, PhD1 Paolo Pelosi, MD4 1 Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute Address for correspondence Paolo Pelosi, MD, Department of Surgical of Biophysics, Federal University of Rio de Janeiro, Ilha do Fundão, Rio Sciences and Integrated Diagnostics, University of Genoa, IRCCS San de Janeiro, Brazil Martino – IST, Genoa, Italy (e-mail: [email protected]). 2 ICU Hospital Pró Cardíaco, Rio de Janeiro, Brazil 3 Ventilatory Care Unit Hospital Copa D’Or, Rio de Janeiro, Brazil 4 Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, IRCCS San Martino – IST, Genoa, Italy 5 Division of Pulmonary and Critical Care Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand Semin Respir Crit Care Med 2014;35:409–417. Abstract Assisted mechanical ventilation (MV) may be a favorable alternative to controlled MV at the early phase of acute respiratory distress syndrome (ARDS), since it requires less sedation, no paralysis and is associated with less hemodynamic deterioration, better distal organ perfusion, and lung protection, thus reducing the risk of ventilator- associated lung injury (VALI). In the present review, we discuss VALI in relation to assisted MV strategies, such as volume assist–control ventilation, pressure assist– control ventilation, pressure support ventilation (PSV), airway pressure release ventila- -
A A-A DO2, 152–156 Abgs. See Arterial Blood Gases Accelerating
Index A A-a DO2, 152–156 ABGs. See Arterial blood gases Accelerating waveform, 123 ACMV. See Volume assist-control mode Acute hypoxemic respiratory failure (AHRF), 424–426 Acute respiratory distress syndrome (ARDS) case study, 523–524 characterization criteria, 248–249 historical aspects, 5–6 pathophysiology diffuse alveolar damage (DAD), 251 Starling equation, 250 primary and secondary, 249 ventilatory strategies airway pressures, 253–254 flow waveforms, 254–255 inspiratory time, 259 inverse ratio ventilation, 259 overdistension, 256–258 PEEP, 255–256 permissive hypercapnia, 261–263 prone ventilation, 263–266 recruitment maneuvers, 260–261 respiratory rate, 254 tidal volumes, 253 ventilation modes, 252–253 Acute respiratory failure (ARF). See Noninvasive ventilation (NIV) Adaptive support ventilation (ASV), 109–110 Adjunctive therapies, 479–504 Adenosine triphosphate (ATP), 171 Adsorptive altelectasis, 326–327 Aerosolized antibiotics, 370–371 527 528 Index Aerosol therapy, 486 Airway humidification. See Humidification, airway Airway occlusion pressure, 399 Airway pressure release ventilation (APRV), 97–98 Airway pressures. See Pressure-time scalar Airway resistance (Raw) calculation, 37, 38 Poiseuille’s law, 35 pulmonary elastance (Pel), 35–36 Alarms apnea, 147 high expired minute volume, 143–144 low airway pressure limit, 146 low expired minute volume activating conditions, 142, 143 airway alarm activation, 141, 142 low oxygen concentration (FIO2), 146 oxygen concentration, 146 power failure, 147 two-minute button, 148 upper airway pressure limit, 144–146 upper oxygen concentration (FIO2), 147 Alveolar dead-space, 40 Alveolar ventilation, 42–43 Anatomical dead-space, 40 Antibiotics aerosolized, 370–371 cycling, 374–375 resistance ESBL, 366 MRSA, 368 multi-drug resistance (MDR), 367 principles, 365 selection, 368–370 topical, 362–363 Apnea alarm, 147 APRV. -
Ventilator-Induced Lung Injury and Implications for Clinical Management
Ventilator-Induced Lung Injury and Implications for Clinical Management C. EDIBAM Department of Critical Care Medicine, Flinders Medical Centre, Adelaide, SOUTH AUSTRALIA ABSTRACT Objective: To review recent studies in pathogenesis and management of ventilator-induced lung injury. Data sources: Articles and published reviews on ventilator-induced lung injury, barotrauma and acute lung injury. Summary of review: This review summarises the important differences between clinically apparent ‘barotrauma’ and the more subtle changes in lung structure and function associated with ventilation. Of great importance is the understanding that as the underlying lung injury worsens, the degree of injury from mechanical ventilation increases. An inflammatory process results from mechanical stimuli and this may contribute to distant organ dysfunction. A great deal of knowledge has been obtained from the use of animal models, however, one must be cautious about extrapolating these findings directly to the clinical setting without the use of adequately designed clinical trials. Tidal volume reduction and higher levels of PEEP and recruitment manoeuvres should be employed given the available evidence. The use of high frequency techniques, surfactant therapy despite their past track record, may prove to be exciting ‘re-discoveries’. Conclusions: Ventilator- induced lung injury is an iatrogenic disturbance that increases morbidity and mortality associated with acute respiratory distress syndrome. Tidal volume reduction and increased levels of PEEP reduce the plasma levels of inflammatory mediators and the mortality associated with ARDS. (Critical Care and Resuscitation 2000; 2: 269-277) Key words: Ventilator-induced lung injury, adult respiratory distress syndrome, PEEP Barotrauma during mechanical ventilation has long morphologic and physiological changes seen in animal been defined as the clinical appearance of extra- lungs, termed ventilator-induced lung injury (VILI) are pulmonary air (e.g. -
Acute Respiratory Distress Syndrome (ARDS) / Acute Lung Injury
Intensive Care Unit, Prince of Wales Hospital, Chinese University of Hong Kong ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) ACUTE LUNG INJURY (ALI) Definitions Acute lung injury is defined as a syndrome of acute lung inflammation with increased vascular permeability, characterized by the following: 1. Bilateral diffuse pulmonary infiltrates on chest radiograph 2. 200 mmHg <PaO2 / FiO2 < 300 mmHg, irrespective of the level of PEEP 3. No clinical evidence of elevated left atrial pressure or pulmonary capillary wedge pressure <18 mmHg Acute respiratory distress syndrome is defined as a syndrome of acute lung inflammation with increased vascular permeability, characterized by the following: 1. Bilateral diffuse pulmonary infiltrate on chest radiograph 2. PaO2 / FiO2 < 200 mmHg, irrespective of the level of PEEP 3. No clinical evidence of elevated left atrial pressure or pulmonary capillary wedge pressure <18 mmHg ARDS and ALI represent the same disease spectrum but differ in severity Causes of ARDS/ALI: Direct Pulmonary injury Pneumonia Aspiration of gastric contents Pulmonary contusion Fat emboli Near-drowning Inhalation of toxic gases Reperfusion pulmonary oedema following dissolution of pulmonary emboli Extrapulmonary injury Sepsis Severe trauma Massive transfusion of blood Cardiopulmonary bypass Drug overdose Acute pancreatitis Pathophysiology • Inflammation of alveoli with diffuse alveolar injury • Release of pro-inflammatory cytokines • Recruitment of neutrophils to lung to release reactive oxygen species and protease • Loss of barrier