Mechanical Ventilation
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Maintenance of Airway Pressure During Filter Exchange Due to Auto-Triggering
Maintenance of Airway Pressure During Filter Exchange Due to Auto-Triggering Joakim Engstro¨m MSc CCRN, Henrik Reinius MD, Camilla Fro¨jd PhD CCRN, Hans Jonsson MSc CCRN, Go¨ran Hedenstierna MD PhD, and Anders Larsson MD PhD BACKGROUND: Daily routine ventilator-filter exchange interrupts the integrity of the ventilator circuit. We hypothesized that this might reduce positive airway pressure in mechanically ventilated ICU patients, inducing alveolar collapse and causing impaired oxygenation and compliance of the respiratory system. METHODS: We studied 40 consecutive ICU subjects (P /F ratio < 300 mm aO2 IO2 Hg), mechanically ventilated with pressure-regulated volume control or pressure support and > PEEP 5cmH2O. Before the filter exchange, (baseline) tidal volume, breathing frequency, end-inspiratory plateau pressure, and PEEP were recorded. Compliance of the respiratory system was calculated; F , blood pressure, and pulse rate were registered; and P ,P , pH, and base IO2 aO2 aCO2 excess were measured. Measurements were repeated 15 and 60 min after the filter exchange. In addition, a bench test was performed with a precision test lung with similar compliance and ؎ resistance as in the clinical study. RESULTS: The exchange of the filter took 3.5 ؎ 1.2 s (mean SD). There was no significant change in P (89 ؎ 16 mm Hg at baseline vs 86 ؎ 16 mm Hg at 15 aO2 or in compliance of the respiratory system (41 ؎ 11 (24. ؍ min and 88 ؎ 18 mm Hg at 60 min, P ؍ ؎ ؎ mL/cm H2O at baseline vs 40 12 mL/cm H2O at 15 min and 40 12 mL/cm H2O at 60 min, P .32). -
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. -
Management of Primary Blast Lung Injury: a Comparison of Airway Pressure Release Versus Low Tidal Volume Ventilation Timothy E
Scott et al. Intensive Care Medicine Experimental (2020) 8:26 Intensive Care Medicine https://doi.org/10.1186/s40635-020-00314-2 Experimental RESEARCH Open Access Management of primary blast lung injury: a comparison of airway pressure release versus low tidal volume ventilation Timothy E. Scott1, Anup Das2* , Mainul Haque3, Declan G. Bates2 and Jonathan G. Hardman4,5 * Correspondence: anup.das@ warwick.ac.uk Abstract 2School of Engineering, University of Warwick, Coventry CV4 7AL, UK Background: Primary blast lung injury (PBLI) presents as a syndrome of respiratory Full list of author information is distress and haemoptysis resulting from explosive shock wave exposure and is a available at the end of the article frequent cause of mortality and morbidity in both military conflicts and terrorist attacks. The optimal mode of mechanical ventilation for managing PBLI is not currently known, and clinical trials in humans are impossible due to the sporadic and violent nature of the disease. Methods: A high-fidelity multi-organ computational simulator of PBLI pathophysiology was configured to replicate data from 14 PBLI casualties from the conflict in Afghanistan. Adaptive and responsive ventilatory protocols implementing low tidal volume (LTV) ventilation and airway pressure release ventilation (APRV) were applied to each simulated patient for 24 h, allowing direct quantitative comparison of their effects on gas exchange, ventilatory parameters, haemodynamics, extravascular lung water and indices of ventilator-induced lung injury. Results: The simulated patients responded well to both ventilation strategies. Post 24-h investigation period, the APRV arm had similar PF ratios (137 mmHg vs 157 mmHg), lower sub-injury threshold levels of mechanical power (11.9 J/min vs 20.7 J/min) and lower levels of extravascular lung water (501 ml vs 600 ml) compared to conventional LTV. -
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. -
VENTILATION THIS IS Evita® V600 Evita® V800
THIS IS VENTILATION Evita® V800 Evita® V600 D-18935-2010 D-2669-2019 2 | Our mission: Improving outcomes in Intensive Care of patients who are artificially ventilated for 41% at least 14 days, will survive the next year.1 As your specialist in acute care, we focus on reducing mortality rates in the ICU. Supporting patient outcome and increasing staff satisfaction in the ICU via connected technologies and services that help achieve therapeutic goals faster and safer is what drives us. AVOIDING ICU-ACQUIRED WEAKNESS AVOIDING COGNITIVE IMPAIRMENT • Start the weaning process as early as • Provide a comfortable and supportive environment possible to help reduce ventilation time. that helps your patient feel calm and at ease. • Encourage spontaneous breathing, which • Turn the ICU into a healing environment and helps train of respiratory muscles and start enable the patient to feel more comfortable in early mobilisation activities. a family-friendly integrated surrounding. • Improve sedation management and optimise patient interaction. PREVENTION OF VALI / ARDS • Protect the lung with personalised ventilation strategies. • Support spontaneous breathing at any time to provide a seamless transition from controlled ventilation to patient contribution. • Improve clinical results with decision supporting insights from multiple sources. 1) Damuth et al. Lancet Respir Med 2015 D-2795-2019 | 3 1) Damuth et al. Lancet Respir Med 2015 D-3460-2018 4 | All ventilation strategies combined in one device Evita® V600 HIGH-END VENTILATION Evita devices have supported you for over 25 years with high quality standards, the ability to configure and upgrade your machine, and advanced training and service concepts. Experience the next level of ventilator operation. -
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. -
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. -
Anesthesia Delivery System Consideration for Use As a Ventilator
March 23, 2020 Mindray A-Series Anesthesia Delivery System Consideration for use as a Ventilator Dear Valued Customer: In response to the COVID-19 pandemic, the US Food and Drug Administration (FDA) has provided guidance1 that allows for the use of anesthesia delivery systems for continuous ventilation. This is due to the increased demand for mechanical ventilation that is estimated to exceed the available ventilators in Intensive Care Units (ICUs) in the US. While Mindray does not promote anesthesia delivery systems for continuous ventilation, this information is provided in direct response to the current public health crisis. It is advised that the user becomes completely familiar with the information provided and considers all risks and benefits prior to using the anesthesia system for continuous ventilation. When considering the use of an anesthesia delivery system for continuous ventilation, the following functional differences should first be noted: 1) The indications for use are different (please reference the appropriate product Operator’s Manual at https://www.mindraynorthamerica.com/technical-documents/). Specifically, an anesthesia system is used, primarily, in Operating Rooms (ORs) where the case may last for a relatively short period or for several hours, under worst-case conditions. A continuous stand-alone ventilator is used, primarily, in the ICU and may operate continuously for several days. 2) Anesthesia systems are used, primarily, for mandatory ventilation on sedated and muscle- relaxed patients. Continuous stand-alone ventilators are used for spontaneous breathing support. 3) Manual mode on the anesthesia system is used for manually ventilating a patient or letting a patient breathe spontaneously, and is only available on the anesthesia systems (when the APL valve is set to “SP”, the PEEP will be zero (0) and the patient can respire spontaneously). -
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 -
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. -
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.