Pulmonary Physiology
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Ventilation Patterns Influence Airway Secretion Movement Marcia S Volpe, Alexander B Adams MPH RRT FAARC, Marcelo B P Amato MD, and John J Marini MD
Original Contributions Ventilation Patterns Influence Airway Secretion Movement Marcia S Volpe, Alexander B Adams MPH RRT FAARC, Marcelo B P Amato MD, and John J Marini MD BACKGROUND: Retention of airway secretions is a common and serious problem in ventilated patients. Treating or avoiding secretion retention with mucus thinning, patient-positioning, airway suctioning, or chest or airway vibration or percussion may provide short-term benefit. METHODS: In a series of laboratory experiments with a test-lung system we examined the role of ventilator settings and lung-impedance on secretion retention and expulsion. Known quantities of a synthetic dye-stained mucus simulant with clinically relevant properties were injected into a transparent tube the diameter of an adult trachea and exposed to various mechanical-ventilation conditions. Mucus- simulant movement was measured with a photodensitometric technique and examined with image- analysis software. We tested 2 mucus-simulant viscosities and various peak flows, inspiratory/ expiratory flow ratios, intrinsic positive end-expiratory pressures, ventilation waveforms, and impedance values. RESULTS: Ventilator settings that produced flow bias had a major effect on mucus movement. Expiratory flow bias associated with intrinsic positive end-expiratory pressure generated by elevated minute ventilation moved mucus toward the airway opening, whereas in- trinsic positive end-expiratory pressure generated by increased airway resistance moved the mucus toward the lungs. Inter-lung transfer of mucus simulant occurred rapidly across the “carinal divider” between interconnected test lungs set to radically different compliances; the mucus moved out of the low-compliance lung and into the high-compliance lung. CONCLUSIONS: The move- ment of mucus simulant was influenced by the ventilation pattern and lung impedance. -
COVID-19 Pneumonia: Different Respiratory Treatment for Different Phenotypes? L
Intensive Care Medicine EDITORIAL Un-edited accepted proof COVID-19 pneumonia: different respiratory treatment for different phenotypes? L. Gattinoni1, D. Chiumello2, P. Caironi3, M. Busana1, F. Romitti1, L. Brazzi4, L. Camporota5 Affiliations: 1Department of Anesthesiology and Intensive Care, Medical University of GöttinGen 4Department of Anesthesia, Intensive Care and Emergency - 'Città della Salute e della Scienza’ Hospital - Turin 5Department of Adult Critical Care, Guy’s and St Thomas’ NHS Foundation Trust, Health Centre for Human and Applied Physiological Sciences - London Corresponding author: Luciano Gattinoni Department of Anesthesiology and Intensive Care, Medical University of Göttingen, Robert-Koch Straße 40, 37075, Göttingen, Germany Conflict of interests: The authors have no conflict of interest to disclose NOTE: This article is the pre-proof author’s accepted version. The final edited version will appear soon on the website of the journal Intensive Care Medicine with the following DOI number: DOI 10.1007/s00134-020-06033-2 1 Gattinoni L. et al. COVID-19 pneumonia: different respiratory treatment for different phenotypes? (2020) Intensive Care Medicine; DOI: 10.1007/s00134-020-06033-2 Intensive Care Medicine EDITORIAL Un-edited accepted proof The Surviving Sepsis CampaiGn panel (ahead of print, DOI: 10.1007/s00134-020-06022-5) recently recommended that “mechanically ventilated patients with COVID-19 should be managed similarly to other patients with acute respiratory failure in the ICU.” Yet, COVID-19 pneumonia [1], despite falling in most of the circumstances under the Berlin definition of ARDS [2], is a specific disease, whose distinctive features are severe hypoxemia often associated with near normal respiratory system compliance (more than 50% of the 150 patients measured by the authors and further confirmed by several colleagues in Northern Italy). -
Gas Exchange
Gas exchange Gas exchange occurs as a result of respiration, when carbon dioxide is excreted and oxygen taken up, and photosynthesis, when oxygen is excreted and carbon dioxide is taken up. The rate of gas exchange is affected by: • the area available for diffusion • the distance over which diffusion occurs • the concentration gradient across the gas exchange surface • the speed with which molecules diffuse through membranes. Efficient gas exchange systems must: • have a large surface area to volume ratio • be thin • have mechanisms for maintaining steep concentration gradients across themselves • be permeable to gases. Single-celled organisms are aquatic and their cell surface membrane has a sufficiently large surface area to volume ratio to act as an efficient gas exchange surface. In larger organisms, permeable, thin, flat structures have all the properties of efficient gas exchange surfaces but need water to prevent their dehydration and give them mechanical support. Since the solubility of oxygen in water is low, organisms that obtain their oxygen from water can maintain only a low metabolic rate. In small and thin organisms, the distance from gas exchange surface to the inside of the organism is short enough for diffusion of gases to be efficient. Diffusion gradients are maintained because gases are continually used up or produced. In larger organisms, simple diffusion is not an efficient way of transporting gases between cells in the body and the gas exchange surface. In many animals a blood circulatory system carries gases to and from the gas exchange surface. The gas-carrying capacity of the blood is increased by respiratory pigments, such as haemoglobin. -
The Physiology of Cardiopulmonary Resuscitation
Society for Critical Care Anesthesiologists Section Editor: Avery Tung E REVIEW ARTICLE CME The Physiology of Cardiopulmonary Resuscitation Keith G. Lurie, MD, Edward C. Nemergut, MD, Demetris Yannopoulos, MD, and Michael Sweeney, MD * † ‡ § Outcomes after cardiac arrest remain poor more than a half a century after closed chest cardiopulmonary resuscitation (CPR) was first described. This review article is focused on recent insights into the physiology of blood flow to the heart and brain during CPR. Over the past 20 years, a greater understanding of heart–brain–lung interactions has resulted in novel resuscitation methods and technologies that significantly improve outcomes from cardiac arrest. This article highlights the importance of attention to CPR quality, recent approaches to regulate intrathoracic pressure to improve cerebral and systemic perfusion, and ongo- ing research related to the ways to mitigate reperfusion injury during CPR. Taken together, these new approaches in adult and pediatric patients provide an innovative, physiologically based road map to increase survival and quality of life after cardiac arrest. (Anesth Analg 2016;122:767–83) udden cardiac arrest remains a leading cause of pre- during CPR, and new approaches to reduce injury associ- hospital and in-hospital death.1 Efforts to resuscitate ated with reperfusion.3,5–8,10–48 Given the debate surrounding patients after cardiac arrest have preoccupied scien- what is known, what we think we know, and what remains S 1,2 tists and clinicians for decades. However, the majority unknown about resuscitation science, this article also pro- of patients are never successfully resuscitated.1,3–5 Based vides some contrarian and nihilistic points of view. -
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. -
The Oxyhaemoglobin Dissociation Curve in Critical Illness
Basic sciences review The Oxyhaemoglobin Dissociation Curve in Critical Illness T. J. MORGAN Intensive Care Facility, Division of Anaesthesiology and Intensive Care, Royal Brisbane Hospital, Brisbane, QUEENSLAND ABSTRACT Objective: To review the status of haemoglobin-oxygen affinity in critical illness and investigate the potential to improve gas exchange, tissue oxygenation and outcome by manipulations of the oxyhaemoglobin dissociation curve. Data sources: Articles and published peer-review abstracts. Summary of review: The P50 of a species is determined by natural selection according to animal size, tissue metabolic requirements and ambient oxygen tension. In right to left shunting mathematical modeling indicates that an increased P50 defends capillary oxygenation, the one exception being sustained hypercapnia. Increasing the P50 should also be protective in tissue ischaemia, and this is supported by modeling and experimental evidence. Most studies of critically ill patients have indicated reduced 2,3-DPG concentrations. This is probably due to acidaemia, and the in vivo P50 is likely to be normal despite low 2,3-DPG levels. It may soon be possible to achieve significant P50 elevations without potentially harmful manipulations of acid-base balance or hazardous drug therapy. Conclusions: Despite encouraging theoretical and experimental data, it is not known whether manipulations of the P50 in critical illness can improve gas exchange and tissue oxygenation or improve outcome. The status of the P50 may warrant more routine quantification and consideration along with the traditional determinants of tissue oxygen availability. (Critical Care and Resuscitation 1999; 1: 93-100) Key words: Critical illness, haemoglobin-oxygen affinity, ischaemia, P50, tissue oxygenation, shunt In intensive care practice, manipulations to improve in the tissues. -
Mechanisms of Pulmonary Gas Exchange Abnormalities During Experimental Group B Streptococcal Infusion
003 I -3998/85/1909-0922$02.00/0 PEDIATRIC RESEARCH Vol. 19, No. 9, I985 Copyright 0 1985 International Pediatric Research Foundation, Inc. Printed in (I.S. A. Mechanisms of Pulmonary Gas Exchange Abnormalities during Experimental Group B Streptococcal Infusion GREGORY K. SORENSEN, GREGORY J. REDDING, AND WILLIAM E. TRUOG ABSTRACT. Group B streptococcal sepsis in newborns obtained from GBS (5, 6). Arterial Poz fell by 9 torr in association produces pulmonary arterial hypertension and hypoxemia. with the increase in pulmonary arterial pressure (4). In contrast, The purpose of this study was to investigate the mecha- the neonatal piglet infused with GBS demonstrated both pul- nisms by which hypoxemia occurs. Ten anesthetized, ven- monary arterial hypertension and profound arterial hypoxemia tilated piglets were infused with 2 x lo9 colony forming (7). These results suggest that the neonatal pulmonary vascula- unitstkg of Group B streptococci over a 30-min period. ture may respond to bacteremia differently from that of adults. Pulmonary arterial pressure rose from 14 ? 2.8 to 38 ? The relationship between Ppa and the matching of alveolar 6.7 torr after 20 min of the bacterial infusion (p< 0.01). ventilation and pulmonary perfusion, a major determinant of During the same period, cardiac output fell from 295 to arterial oxygenation during room air breathing (8), has not been 184 ml/kg/min (p< 0.02). Arterial Po2 declined from 97 studied in newborns. The predictable rise in Ppa with an infusion 2 7 to 56 2 11 torr (p< 0.02) and mixed venous Po2 fell of group B streptococcus offers an opportunity to delineate the from 39.6 2 5 to 28 2 8 torr (p< 0.05). -
Oxygenation and Oxygen Therapy
Rules on Oxygen Therapy: Physiology: 1. PO2, SaO2, CaO2 are all related but different. 2. PaO2 is a sensitive and non-specific indicator of the lungs’ ability to exchange gases with the atmosphere. 3. FIO2 is the same at all altitudes 4. Normal PaO2 decreases with age 5. The body does not store oxygen Therapy & Diagnosis: 1. Supplemental O2 is an FIO2 > 21% and is a drug. 2. A reduced PaO2 is a non-specific finding. 3. A normal PaO2 and alveolar-arterial PO2 difference (A-a gradient) do NOT rule out pulmonary embolism. 4. High FIO2 doesn’t affect COPD hypoxic drive 5. A given liter flow rate of nasal O2 does not equal any specific FIO2. 6. Face masks cannot deliver 100% oxygen unless there is a tight seal. 7. No need to humidify if flow of 4 LPM or less Indications for Oxygen Therapy: 1. Hypoxemia 2. Increased work of breathing 3. Increased myocardial work 4. Pulmonary hypertension Delivery Devices: 1. Nasal Cannula a. 1 – 6 LPM b. FIO2 0.24 – 0.44 (approx 4% per liter flow) c. FIO2 decreases as Ve increases 2. Simple Mask a. 5 – 8 LPM b. FIO2 0.35 – 0.55 (approx 4% per liter flow) c. Minimum flow 5 LPM to flush CO2 from mask 3. Venturi Mask a. Variable LPM b. FIO2 0.24 – 0.50 c. Flow and corresponding FIO2 varies by manufacturer 4. Partial Rebreather a. 6 – 10 LPM b. FIO2 0.50 – 0.70 c. Flow must be sufficient to keep reservoir bag from deflating upon inspiration 5. -
Introduction to Airway Resistance Measurements
Introduction to airway resistance measurements Dr. David Kaminsky Department of Medicine The University of Vermont VT 05405 Burlington UNITED STATES OF AMERICA [email protected] AIMS Review physiology of airway resistance Survey measures of airway resistance Provide examples of clinical applications Highlight research applications SUMMARY Airway resistance (Raw) is one of the fundamental features of the mechanics of the respiratory system. While the flow-volume loop offers insight into the volume and flow of air, it is limited in terms of specific information regarding lung mechanics. Airway resistance is the ratio of driving pressure divided by flow through the airways. It specifies the pressure required to achieve a flow of air with a velocity of 1L/sec. If the airway is represented by a simple, rigid tube, with laminar flow of air through it, the airway resistance Raw = (8 x L x )/ r4, where L = length of the tube, = viscosity of the gas, and r = radius of the tube. It is important to note that the r4 relationship demonstrates how sensitive resistance is to the size of the tube, varying inversely with the 4th power of the radius. The inner diameter of the airway is itself determined by many factors, including airway smooth muscle contractile state, airway wall thickness (related to inflammation, edema and remodeling), airway wall buckling and formation of mucosal folds, the interdependence, or linkage, of airway and surrounding lung parenchyma, and the intrinsic elastic recoil of the lung parenchyma, which serves as a load on the airway and variably resists bronchoconstriction. Of course, the airways are not rigid tubes, and in fact flow is a complex process involving both laminar and turbulent conditions, so this calculation of Raw is an approximation only. -
Hyperoxia-Induced Pulmonary Vascular and Lung Abnormalities in Young Rats and Potential for Recovery
003 1-399818511910-1059$02.00/0 PEDIATRIC RESEARCH Vol. 19, No. 10, 1985 Copyright O 1985 International Pediatric Research Foundation, Inc. Prinfed in U.S.A. Hyperoxia-Induced Pulmonary Vascular and Lung Abnormalities in Young Rats and Potential for Recovery WENDY LEE WILSON, MICHELLE MULLEN, PETER M. OLLEY, AND MARLENE RABINOVITCH Departments of Cardiology and Pathology, Research Institute, The Hospital for Sick Children and Departments of Pediatrics and Pathology, University of Toronto, Toronto, Canada ABSTRACT. We carried out morphometric studies to The newborn infant, especially the premature with hyaline assess the effects of increasing durations of hyperoxic membrane disease, may require prolonged high oxygen therapy. exposure on the developing rat lung and to evaluate the Hyperoxia is damaging to lung tissue presumably because the potential for new growth and for regression of structural relatively inert O2 molecule undergoes univalent reduction to abnormalities on return to room air. From day 10 of life form highly reactive free radicals which are cytotoxic (1). Some Sprague-Dawley rats were either exposed to hyperoxia protection is afforded by the antioxidant enzyme systems of the (0.8F102) for 2-8 wk or were removed after 2 wk and lungs, superoxide dismutase, catalase, and glutathione peroxidase allowed to "recover" in room air for 2-6 wk. Litter mates (2-5) but the induction of these enzymes is often insufficient to maintained in room air served as age matched controls. prevent tissue damage. In the clinical setting it has been difficult Every 2 wk experimental and control rats from each group to separate the role of oxygen toxicity from other variables such were weighed and killed. -
Asthma Initiative Content
WAO Symposium Why Are Small Airways Important In Asthma? “Physiology Of Small Airways Disease” Thomas B Casale, MD Professor Of Medicine Chief, Allergy/Immunology Creighton University Omaha, NE USA Disease Process in Asthma is Located in All Parts of Bronchial Tree Including Small Airways and Alveoli Workgroep Inhalatie Technologie, Jun 1999. Relevant Questions On Small Airway Involvement In Asthma • How can „small airway disease‟ be defined? • What is the link between small airway abnormalities and clinical presentation in asthma ? • When does small airway involvement become relevant in the natural history of the disease? • Is it possible to reverse small airway abnormalities with pharmacological treatment? Contoli et al Allergy 2010; 65: 141–151 Pathophysiologic Changes in the Small Airways of Asthma Patients Transbronchial Biopsies 1 Lumen occlusion 2 Subepithelial fibrosis 3 Increase in smooth muscle mass 4 Inflammatory infiltrate 1 Immunostaining of eosinophils in small airway with major basic protein (in red) 2 Shows large number of eosinophils around the small airway Contoli M, et al. Allergy. 2010;65:141-151. Structural Alterations in Small Airways Associated With Fatal Asthma Small airway of a Small airway of a control subject subject with fatal asthma Mucus plugging Structural alterations in small airways have been implicated as an underlying reason for increased asthma severity and AHR….. Difficult to control asthma. Mauad T, et al. Am J Respir Crit Care Med. 2004;70:857-862. Differences In ECM Composition In Small Airways Between Fatal Asthma And Controls Dolhnikoff et al, JACI 2009; 123:1090-1097 Is There Differential Inflammation in Proximal and More Distal Airways? • Some studies suggest that the cellular infiltrate increases toward the periphery, but others show similar or decreased infiltration – May reflect heterogeneity of asthma as well as the different methods used in the studies . -
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.