VENTILATOR STRATEGIES Patrick Cullinan, DO FCCM, FACOI, FACOEP San Antonio, TX
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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. -
Advanced Modes of Ventilation: Concerns for the OR
Scott, Benjamin K., MD Advanced Modes of Ventilation: Concerns for the OR WHAT I AM NOT GOING TO COVER ADVANCED MODES OF “Adaptive” Advanced Modes that focus on synchrony VENTILATION: ✪ Proportional assist CONCERNS FOR THE OR ✪ Adaptive Support ✪ Neurally Adjusted Ventilatory Assist BENJAMIN K. SCOTT, MD DEPARTMENT OF ANESTHESIOLOGY UNIVERSITY OF COLORADO SCHOOL OF MEDICINE Why? ✪ Evidence of benefit is lacking ✪ Generally interchangeable with standard intraop modes DISCLOSURES PATHOPHYSIOLOGY OF THE SICK LUNG 1. ARDS Ashbaugh and Petty: 1967 case series of 12 ICU patients ✪ Tachypnea and hypoxemia NONE ✪ Opacification on CXR ✪ Poor lung compliance ✪ Diversity of primary insult Ashbaugh DG, Bigelow DB, Petty TL et al. Acute Respiratory Distress in Adults. Lancet. 1967 LEARNING OBJECTIVES PATHOPHYSIOLOGY OF THE SICK LUNG ARDS: The Berlin Definition (c. 2011) 1. Review the pathophysiology of the diseased or injured lung 2. Understand recent strategies in mechanical ventilation, ARDS is an acute diffuse, inflammatory lung injury, leading to particularly focusing on “low‐stretch” and “open‐lung” increased pulmonary vascular permeability, increased lung weight, techniques. and loss of aerated lung tissue...[With] hypoxemia and bilateral radiographic opacities, associated with increased venous 3. Discuss strategies for OR management of patients on admixture, increased physiological dead space and decreased “advanced” vent modes lung compliance. 4. Apply these concepts to routine OR vent management The ARDS Definition Task Force*. Acute Respiratory Distress Syndrome: The Berlin Definition. JAMA. 2012;307(23):2526-2533 Scott, Benjamin K., MD Advanced Modes of Ventilation: Concerns for the OR PATHOPHYSIOLOGY OF THE SICK LUNG VENTILATING THE NON-COMPLIANT LUNG ARDS: The Berlin Definition (c. -
Clinical Management of Severe Acute Respiratory Infections When Novel Coronavirus Is Suspected: What to Do and What Not to Do
INTERIM GUIDANCE DOCUMENT Clinical management of severe acute respiratory infections when novel coronavirus is suspected: What to do and what not to do Introduction 2 Section 1. Early recognition and management 3 Section 2. Management of severe respiratory distress, hypoxemia and ARDS 6 Section 3. Management of septic shock 8 Section 4. Prevention of complications 9 References 10 Acknowledgements 12 Introduction The emergence of novel coronavirus in 2012 (see http://www.who.int/csr/disease/coronavirus_infections/en/index. html for the latest updates) has presented challenges for clinical management. Pneumonia has been the most common clinical presentation; five patients developed Acute Respira- tory Distress Syndrome (ARDS). Renal failure, pericarditis and disseminated intravascular coagulation (DIC) have also occurred. Our knowledge of the clinical features of coronavirus infection is limited and no virus-specific preven- tion or treatment (e.g. vaccine or antiviral drugs) is available. Thus, this interim guidance document aims to help clinicians with supportive management of patients who have acute respiratory failure and septic shock as a consequence of severe infection. Because other complications have been seen (renal failure, pericarditis, DIC, as above) clinicians should monitor for the development of these and other complications of severe infection and treat them according to local management guidelines. As all confirmed cases reported to date have occurred in adults, this document focuses on the care of adolescents and adults. Paediatric considerations will be added later. This document will be updated as more information becomes available and after the revised Surviving Sepsis Campaign Guidelines are published later this year (1). This document is for clinicians taking care of critically ill patients with severe acute respiratory infec- tion (SARI). -
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. -
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. -
Near Drowning
Near Drowning McHenry Western Lake County EMS Definition • Near drowning means the person almost died from not being able to breathe under water. Near Drownings • Defined as: Survival of Victim for more than 24* following submission in a fluid medium. • Leading cause of death in children 1-4 years of age. • Second leading cause of death in children 1-14 years of age. • 85 % are caused from falls into pools or natural bodies of water. • Male/Female ratio is 4-1 Near Drowning • Submersion injury occurs when a person is submerged in water, attempts to breathe, and either aspirates water (wet) or has laryngospasm (dry). Response • If a person has been rescued from a near drowning situation, quick first aid and medical attention are extremely important. Statistics • 6,000 to 8,000 people drown each year. Most of them are within a short distance of shore. • A person who is drowning can not shout for help. • Watch for uneven swimming motions that indicate swimmer is getting tired Statistics • Children can drown in only a few inches of water. • Suspect an accident if you see someone fully clothed • If the person is a cold water drowning, you may be able to revive them. Near Drowning Risk Factor by Age 600 500 400 300 Male Female 200 100 0 0-4 yr 5-9 yr 10-14 yr 15-19 Ref: Paul A. Checchia, MD - Loma Linda University Children’s Hospital Near Drowning • “Tragically 90% of all fatal submersion incidents occur within ten yards of safety.” Robinson, Ped Emer Care; 1987 Causes • Leaving small children unattended around bath tubs and pools • Drinking -
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. -
Simulator Measurement of the Work of Breathing for Underwater
SIMULATOP REASUREBEMT OF THE RORK OF BRIiAPHING FOB UNDEEWATER BREATHING APPARATUS Durcan Moir fliln~ E. Sc. Mar ire Science Stockton stat^ Colfege, New Jers~y,1973 A THESIS SUBEITTED IN PARTIAL PULPILLEEBT OF THE PEQUIREHENTS FOR THE DEGREE OF MASTER OF SCIENCE (KfNES IOLOGY) in the Department of Kicesiology a GUNCAN ROIB BILNE 1977 SIBOH FRASER UNIVERSITY December, 1977 All rights reserved, This thesis may nct t>f reproduced in whole or ir part, by photocopy or cthor means, without permission of tho author. NAYE: Duncan noir flllni TITLE OF THESIS: Hespiration Simulator' Htlasur+m~n* , of the Wark of Bre3thi11y far Und2rwater Breathinq A ppara tus EXhnINING COMnITTEE: Chairman: Dr. E. W. R;inister 'DL. J. n. aorrison Senior Sup:.r visor Dr, T, W. ialv.?rt Dr. A. E. Zhaprssry Ext +rnal Examin~r Prof -.ssor SLlncn Praser IJniv~rsity - at A,,,,,.,: .....................Jet, , V7r PART lAL COPYR lGHT L lCENSE I hereby grant to Simon Fraser University the right to lend my thesis, project or extended essay (the title of which is shown below) to users of the Simon Fraser University Library, and to make partial or single copies only for such users or in response to a request from the library of any other university, or other educational institution, on its own behalf or for one of its users. I further agree that permission for multiple copying of this work for scholarly purposes may be granted by me or the Dean of Graduate Studies. It is understood that copying or publication of this work for financial gain shall not be allowed without my written permission. -
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. -
The Pathophysiology of 'Happy' Hypoxemia in COVID-19
Dhont et al. Respiratory Research (2020) 21:198 https://doi.org/10.1186/s12931-020-01462-5 REVIEW Open Access The pathophysiology of ‘happy’ hypoxemia in COVID-19 Sebastiaan Dhont1* , Eric Derom1,2, Eva Van Braeckel1,2, Pieter Depuydt1,3 and Bart N. Lambrecht1,2,4 Abstract The novel coronavirus disease 2019 (COVID-19) pandemic is a global crisis, challenging healthcare systems worldwide. Many patients present with a remarkable disconnect in rest between profound hypoxemia yet without proportional signs of respiratory distress (i.e. happy hypoxemia) and rapid deterioration can occur. This particular clinical presentation in COVID-19 patients contrasts with the experience of physicians usually treating critically ill patients in respiratory failure and ensuring timely referral to the intensive care unit can, therefore, be challenging. A thorough understanding of the pathophysiological determinants of respiratory drive and hypoxemia may promote a more complete comprehension of a patient’sclinical presentation and management. Preserved oxygen saturation despite low partial pressure of oxygen in arterial blood samples occur, due to leftward shift of the oxyhemoglobin dissociation curve induced by hypoxemia-driven hyperventilation as well as possible direct viral interactions with hemoglobin. Ventilation-perfusion mismatch, ranging from shunts to alveolar dead space ventilation, is the central hallmark and offers various therapeutic targets. Keywords: COVID-19, SARS-CoV-2, Respiratory failure, Hypoxemia, Dyspnea, Gas exchange Take home message COVID-19, little is known about its impact on lung This review describes the pathophysiological abnormal- pathophysiology. COVID-19 has a wide spectrum of ities in COVID-19 that might explain the disconnect be- clinical severity, data classifies cases as mild (81%), se- tween the severity of hypoxemia and the relatively mild vere (14%), or critical (5%) [1–3]. -
PALS Testing Case Scenarios
Testing Case Scenario 1 Hypovolemic Shock (Child) Scenario Lead-in Prehospital: You have been dispatched to transport a 5 year old with a 3-day history of fever Vital Signs and diarrhea. She has been increasingly lethargic in the last 2 hours. Heart rate 140/min ED: You are asked to assess and manage a 5 year old with a 3-day history of fever and Blood pressure 86/52 mm Hg diarrhea. She has been increasingly lethargic in the last 2 hours. Efforts for a peripheral Respiratory rate 36/min intravenous access have been unsuccessful. SpO2 97% on room air General inpatient unit: You are called to assess a 5 year old who has been admitted to the Temperature 38.0°C (100.4°F) ward with a 3-day history of fever and diarrhea. She has been increasingly lethargic in the last Weight 21 kg hour and has had severe ongoing diarrhea. Her intravenous access is no longer functioning. Age 5 years ICU: You are called to the bedside of a 5 year old who has been admitted to the intensive care unit with a 3-day history of fever and diarrhea. She has been increasingly lethargic in the last 2 hours and has had severe ongoing diarrhea. Her intravenous access is no longer functioning. Scenario overview and learning objectives Scenario Overview Emphasis in this scenario should be on identification of compensated hypovolemic shock. Priorities include oxygen, immediate establishment of intravenous (IV) access, and administration of fluid bolus of isotonic crystalloid, repeated as needed to treat shock signs.