Mechanical Ventilation Guidelines
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Effect of Spontaneous Breathing on Ventilator- Induced Lung Injury In
Xia et al. Critical Care 2011, 15:R244 http://ccforum.com/content/15/5/R244 RESEARCH Open Access Effect of spontaneous breathing on ventilator- induced lung injury in mechanically ventilated healthy rabbits: a randomized, controlled, experimental study Jingen Xia, Bing Sun, Hangyong He, Heng Zhang, Chunting Wang and Qingyuan Zhan* Abstract Introduction: Ventilator-induced lung injury (VILI), one of the most serious complications of mechanical ventilation (MV), can impact patients’ clinical prognoses. Compared to control ventilation, preserving spontaneous breathing can improve many physiological features in ventilated patients, such as gas distribution, cardiac performance, and ventilation-perfusion matching. However, the effect of spontaneous breathing on VILI is unknown. The goal of this study was to compare the effects of spontaneous breathing and control ventilation on lung injury in mechanically- ventilated healthy rabbits. Methods: Sixteen healthy New Zealand white rabbits were randomly placed into a spontaneous breathing group (SB Group) and a control ventilation group (CV Group). Both groups were ventilated for eight hours using biphasic positive airway pressure (BIPAP) with similar ventilator parameters: inspiration pressure (PI) resulting in a tidal volume (VT) of 10 to 15 ml/kg, inspiratory-to-expiratory ratio of 1:1, positive end-expiration pressure (PEEP) of 2 cmH2O, and FiO2 of 0.5. Inflammatory markers in blood serum, lung homogenates and bronchoalveolar lavage fluid (BALF), total protein levels in BALF, mRNA expressions of selected cytokines in lung tissue, and lung injury histopathology scores were determined. Results: Animals remained hemodynamically stable throughout the entire experiment. After eight hours of MV, compared to the CV Group, the SB Group had lower PaCO2 values and ratios of dead space to tidal volume, and higher lung compliance. -
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. -
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. -
Biomarkers of Acute Lung Injury: Worth Their Salt? Alastair G Proudfoot1,2†, Matthew Hind1,2† and Mark JD Griffiths1,2*†
Proudfoot et al. BMC Medicine 2011, 9:132 http://www.biomedcentral.com/1741-7015/9/132 Clinical Biomarkers OPINION Open Access Biomarkers of acute lung injury: worth their salt? Alastair G Proudfoot1,2†, Matthew Hind1,2† and Mark JD Griffiths1,2*† Abstract The validation of biomarkers has become a key goal of translational biomedical research. The purpose of this article is to discuss the role of biomarkers in the management of acute lung injury (ALI) and related research. Biomarkers should be sensitive and specific indicators of clinically important processes and should change in a relevant timeframe to affect recruitment to trials or clinical management. We do not believe that they necessarily need to reflect pathogenic processes. We critically examined current strategies used to identify biomarkers and which, owing to expedience, have been dominated by reanalysis of blood derived markers from large multicenter Phase 3 studies. Combining new and existing validated biomarkers with physiological and other data may add predictive power and facilitate the development of important aids to research and therapy. Introduction The natural history of acute lung injury Thesyndromeacutelunginjury(ALI)anditsmore Regardless of the wide variety of insults that cause or severe counterpart acute respiratory distress syndrome contribute to the development of ALI, the response of (ARDS) are defined by radiographic and physiological the lung is largely stereotypic. A combination of tissue changes that characterize patients with acute lung fail- injury and inflammation affecting the gas exchange sur- ure (Table 1) [1]. All age groups may be affected, face of the lung, the alveolar-capillary membrane, causes although the syndrome has a higher incidence and mor- high permeability pulmonary edema. -
1. Ventilator Management
1. Ventilator Management Indications for Mechanical Ventilation Apnea Ventilatory insufficiency Increase in PaCo2 and decrease in ph Refractory hypoxemia Complications Associated with Mechanical Ventilation Hypotension Increased intrathoracic pressure decreases venous return to the heart Increased risk of ventilator associated pneumonia (VAP) Keep HOB at > 30 Maintain frequent, good oral care Problems with endotracheal tube Mucous plugging Tube my become dislodged Kinking or biting of tube Cuff rupture Pneumothorax Initial Ventilator Settings—parameters to be clarified Type of ventilation Mode of ventilation Tidal volume or peak inspiratory setting Respiratory rate FiO2 PEEP (Positive End Expiratory Pressure) Types of Ventilation Volume Cycled Ventilation(VCV) A pre-selected tidal volume is delivered at the pressure required. Tidal volume guaranteed. Peak inspiratory pressure will vary depending on airway resistance and lung compliance. Pressure Control Time-Cycled Ventilation (PCV) Operator selects inspiratory pressure and inspiratory time Breath is terminated when inspiratory time is reached Inspiratory pressure is guaranteed; tidal volume is dependant on airway resistance and lung compliance Pressure Support (PSV) Requires intact respiratory drive Operator selects inspiratory pressure Patient initiates breath, pressure quickly rises to set pressure and is maintained throughout the inspiratory phase Tidal volume determined by lung compliance and inspiratory effort Modes of Ventilation Assist/Control -
Date 10/15/2018 Page 1 of 12 Protocol Version-I
Feasibility and Impact of Volume Targeted Ventilation for preterm infants born < 32 weeks gestational age with need for invasive Positive Pressure Ventilation in the Delivery Room in reducing neonatal pulmonary morbidities Phase I: Feasibility of Measuring Tidal Volume in the Delivery Room Phase II: Feasibility of providing Volume Targeted Ventilation in the Delivery Room Primary Investigator: Ruben Vaidya, MD Co-Investigators: Paul Visintainer, PhD, Rachana Singh, MD Research Coordinator: TBD Address: Division of Newborn Medicine Department of Pediatrics UMMS-Baystate, Springfield, MA 01199 Phone: 413-794-2400 Email: [email protected] Date 10/15/2018 Page 1 of 12 Protocol Version-I SPECIFIC AIMS AND HYPOTHESIS Bronchopulmonary dysplasia (BPD) continues to be one of the most common long-term pulmonary complications associated with preterm birth. Despite significant decreases in preterm mortality, BPD rates in infants born < 28 weeks gestational age have remained unchanged at approximately 40% i ii iii. This probably is due to the multifactorial pathogenesis of BPD, with lung injury to the immature pulmonary tissue secondary to exposures including but not limited to antenatal/postnatal infection, free oxygen radical toxicity, and/or mechanical ventilation all leading to lung inflammation. Delivery room (DR) practices of preterm infant during initial resuscitation can have a significant impact on occurrence and severity BPD. Current delivery room resuscitation for intubated preterm infants focuses on pressure limited ventilation (PLV), however, rapidly changing pulmonary compliance during the early newborn transition phase results in significant variability in the tidal volume provided to the infant, which in turn can lead to volutrauma, barotrauma and/or atelactetotrauma. -
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................................................................................ -
Respiratory Oscillations in Alveolar Oxygen Tension Measured in Arterial
www.nature.com/scientificreports OPEN Respiratory oscillations in alveolar oxygen tension measured in arterial blood Received: 13 February 2017 Federico Formenti 1,2, Nikhil Bommakanti1, Rongsheng Chen1, John N. Cronin 2, Hanne Accepted: 20 June 2017 McPeak1, Delphine Holopherne-Doran3, Goran Hedenstierna 4, Clive E. W. Hahn1, Anders Published: xx xx xxxx Larsson5 & Andrew D. Farmery1 Arterial oxygen partial pressure can increase during inspiration and decrease during expiration in the presence of a variable shunt fraction, such as with cyclical atelectasis, but it is generally presumed to remain constant within a respiratory cycle in the healthy lung. We measured arterial oxygen partial pressure continuously with a fast intra-vascular sensor in the carotid artery of anaesthetized, mechanically ventilated pigs, without lung injury. Here we demonstrate that arterial oxygen partial pressure shows respiratory oscillations in the uninjured pig lung, in the absence of cyclical atelectasis (as determined with dynamic computed tomography), with oscillation amplitudes that exceeded 50 mmHg, depending on the conditions of mechanical ventilation. These arterial oxygen partial pressure respiratory oscillations can be modelled from a single alveolar compartment and a constant oxygen uptake, without the requirement for an increased shunt fraction during expiration. Our results are likely to contribute to the interpretation of arterial oxygen respiratory oscillations observed during mechanical ventilation in the acute respiratory distress syndrome. In the healthy lung, arterial partial pressure of oxygen (PaO2) is thought to remain almost constant within the respiratory cycle during spontaneous breathing, via a physiological PO2 gradient between the alveoli and the pul- 1 monary circulation . Respiratory PaO2 oscillations smaller than 16 mmHg have been detected with slow response 2 −1 time sensors in animals with uninjured lungs when abnormally large tidal volumes (VT) greater than 20 ml kg or even 30 ml kg−1 were delivered during mechanical ventilation3, 4. -
“Post” COVID-19 Lungs in the Operating Room
“Post” COVID-19 Lungs in the Operating Room Kalina Nedeff, M.D., Austin Smith, D.O., Catalina Carvajal, D.O., Laszlo Balazs M.D. Introduction Results Discussion • 58 year-old male recently diagnosed with COVID-19 presented with • Patient later developed intermittent atrial fibrillation with rapid ventricular • Coronavirus (COVID-19) is an infectious disease caused by a newly worsening shortness of breath. response intermixed with bradycardia discovered strain that mainly affects the upper respiratory system • Pulse oximetry revealed 86% SpO2 on room air with improvement to 94% • Patient necessitated additional vasopressor support as well as blood • The virus is primarily spread through respiratory droplets SpO2 on 3L of oxygen via nasal cannula. products to maintain hemodynamics • Patients affected with COVID that end up on mechanical ventilation may • Patient was treated with remdesivir, ceftriaxone, azithromycin, steroids, • Copious bloody secretions were suctioned from the tracheostomy develop COVID Pneumonia which progresses to acute respiratory vitamins and anticoagulation. • Family ultimately decided to implement comfort measures distress syndrome (ARDS). • New-onset atrial fibrillation was discovered, with hypotension which • The lungs become inflamed and fill with fluid, making oxygen diffusion in required vasopressor support and declining respiratory status prompting capillaries difficult. endotracheal intubation with mechanical ventilation. • For mechanically ventilated adults with COVID-19 and ARDS, lung • Patient continued -
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. -
Tidal Volume Settings in Adult Mechanical Ventilation
Setting the Tidal Volume In Adults Receiving Mechanical Ventilation: Lessons Learned From Recent Investigations Todd Bocklage, MPA, RRT Assistant Manager – Respiratory Care Services & Pulmonary Function Lab University of Missouri Health Care University Hospital & Women’s and Children’s Hospital Columbia, Missouri Robert A. Balk, MD J. Bailey Carter, MD Professor of Medicine Director – Division of Pulmonary and Critical Care Medicine Rush Medical College and Rush University Medical Center Chicago, IL Corresponding Author: Robert A. Balk, MD Division of Pulmonary and Critical Care Medicine Rush University Medical Center 1725 W. Harrison, Suite 054 Chicago, IL 60612 T 312-942-2552 F 312-942-8187 Email [email protected] Disclosure: Both authors are members of the National Board of Respiratory Care. Neither author has other real or potential conflicts of interest or other disclosures to declare. Introduction Selecting the optimum tidal volume for adult patients on ventilatory support is critical to achieving the best clinical outcomes. Over the years, guidelines about tidal volumes have varied including times when sigh breaths were set to prevent the development of atelectasis. The purpose of this article is to describe the transition that examination committees have made over the last several years in which lung protection has become the primary goal when making decisions about mechanical ventilation. Ventilator Induced Lung Injury Since the introduction of mechanical ventilatory support over 60 years ago, there has been an increasing body of -
Modes of Mechanical Ventilation
Modes of Mechanical Ventilation And Protocol Overview • Lungs use ventilation (tidal volume and respiratory rate) to transfer CO2 from the blood to the alveoli and out of the body. Oxygenation (PEEP and FiO2) occurs when the oxygen transfers from the air in the lungs to the blood stream Overview • Mechanical ventilation provides positive pressure ventilation, while normal breathing is negative pressure Volume Control • Set respiratory rate, volume, FiO2, PEEP, and pause time. • “Square waveform” – Higher PIP (Peak Inspiratory Pressure is the highest level of pressure applied to the lungs – Low mean pressure (better venous return and cardiac output) Pressure Regulated Volume Control • Set respiratory rate, volume, FiO2, and PEEP • “Ramp waveform” – Least peak pressures – High mean airway pressure (helps lung inflation and oxygenation) Pressure Support/CPAP • Set pressure support above PEEP, PEEP, and FiO2 • Patient triggers breath with no dialed in volume nor respiratory rate • Volumes should be 85-90% of ideal volume • PIP=PS+PEEP • Mode before extubation. PS usually weaned down to 10 or 8 and PEEP to 5 Pressure Control • Set respiratory rate, pressure above PEEP, PEEP, and FiO2 • Patient’s volume will be determined on when the breath is shut off when set pressure is reached (PEEP + PC= PIP) Synchronized Intermittent Mandatory Ventilation • Used with PRVC, VC, or PC • Set settings of mode and PS Bi Vent • Set P High, PEEP, T High, T PEEP, PS above P High, PS above PEEP, and FiO2 • Uses high MAP to oxygenate – Mean Airway Pressure correlates