1. The document discusses mechanical ventilation in restrictive pulmonary diseases. It outlines causes of restrictive diseases including lung parenchyma disorders, pleural disorders, and extra-pulmonary disorders.
2. Lung parenchyma disorders discussed in detail include interstitial lung diseases like sarcoidosis and hypersensitivity pneumonitis, occupational lung diseases, and atelectatic disorders like ARDS.
3. The key characteristics of restrictive diseases are decreased vital capacity, total lung capacity, and gas exchange. Ventilator settings for restrictive diseases aim to use low tidal volumes and pressures to prevent further lung injury.
Community Acquired Pneumonia and other types of pneumonia
for medical students
Detailed information on pneumonia including the following
Definition
Classification
Aetiology
Pathogenesis
Pathological states
Investigations
Treatment & follow up
Complications
Medication
Hospital acquired pneumonia and it’s treatment and management and prevention
Other types of pneumonia
And pneumonia in immune compromised patients
PNEUMONIA,
DEFINITION
Pneumonia is an infection of the pulmonary parenchyma.
To the pathologist, pneumonia is an infection of the alveoli ,distal airways, and interstitium of the lung that is manifested by increased weight of the lungs, replacement of normal lung’s sponginess by consolidation ,and alveoli filled with white blood cells ,red blood cells and fibrin .To the clinician, pneumonia is a constellation of symptoms and signs in combination with at least one opacity on CXR.
Epidemiology
Between 5 and 10 million cases of infectious pneumonia occur annually in the United States and result in more than 1 million hospitalizations.
Pneumonia is a leading cause of death worldwide, the sixth leading cause of death in the United States, and the most common lethal infectious disease.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
3. Objectives
To able to know pathophysiology of restrictive pulmonary diseases
To able to know clinical presentation of restrictive pulmonary diseases
To able to list some diagnostic modalities of restrictive pulmonary
diseases
To be able to manage restrictive pulmonary diseases
To be able to manage ventilator settings in restrictive pulmonary
diseases
4. Restrictive pulmonary diseases
• Restrictive pulmonary diseases Result from Decreased Lung Expansion or reduced
lung compliance that requires greater pressure to inflate the lungs due to
pathologies in :
lung parenchyma
Pleura
chest wall
neuromuscular function
• They represent acute or chronic patterns of lung dysfunctions.
• They are Classified as
Pulmonary
pleural
Extra - pulmonary
6. Restrictive pulmonary diseases……..
• Restrictive pulmonary diseases are characterized by :
Decrease in vital capacity (VC) - total volume of air that can be displaced in or out
from the lungs by maximal inspiratory or expiratory effort = TV + IRV Or Tv + ERV.
Decrease Total lung capacity (TLC) - is the measured total amount of air that the
lung can hold= ERV + TV + IRV.
Decrease functional residual capacity (FRC) - the volume remaining in the lungs
after a normal, passive exhalation.
Decrease residual volume (RV) - is the volume of air remaining in the lungs after
maximum forceful expiration.
• The greater the decrease in lung volume, greater the severity of disease.
• Their ABG values
Decreased PaO2
Normal or increased PaCO2
7. 1. Lung parenchyma disorders…….
• Interstitial lung disease can be two types :
A - Diffuse Interstitial Lung Disease :
Pathogenesis is an immune reaction that brings lung tissue infiltration and
Persistent alveolitis leads to obliteration of alveolar capillaries, reorganization of
lung parenchyma resulting in irreversible fibrosis and large air-filled sacs (cysts)
with dilated terminal and respiratory bronchioles.
B - Fibrotic Interstitial Lung Disease :
Pathogenesis fibroblastic proliferation and deposition of large amount of collagen
caused by increased mesenchymal cells and fibroblasts in interstitium then
alveolar walls become thickened with increased amounts of fibrous tissue
At the end-stage of disease it results destraction and loss of alveolar walls
8. 1. Lung parenchyma disorders…….
Clinical manifestations of both are progressive dyspnea with exercise with
desaturation, rapid-shallow breathing ,irritating nonproductive cough and
clubbing of nail beds (40%-80%).
Bibasilar end-expiratory crackles,cyanosis (late finding),anorexia, weight
loss,inability to increase cardiac output with exercise.
Diagnosis is chest x-ray ,PFT (decreased VC, TLC, diffusing capacity) ,open lung
biopsy,transbronchial biopsy,Gallium-67 scan and bronchoalveolar lavage.
Treatment is smoking cessation,avoid environmental exposure to cause,anti-
inflammatory agents,immunosuppressive agents and lung transplant.
9. 1. Lung parenchyma disorders……
• B1 - Sarcoidosis
Etiology - Acute or chronic systemic disease of unknown cause.
Immunologic activation of alveolar macrophage to unknown trigger.
Pathogenesis is development of multiple, uniform, noncaseating epithelioid
granulomas.
Affects multiple organs like Lymph nodes, lung tissue (most common),Skin, eyes,
spleen, liver, kidney, bone marrow.
Fibrotic and surrounded by large histiocytes may occur in bronchial airways.
Due to abnormal T-cell function.
10. 1. Lung parenchyma disorders…….
Clinical manifestations are malaise, fatigue,weight loss,fever,dyspnea of
insidious onset,dry, nonproductive cough,erythema nodosum,macules, papules,
hyperpigmentation,subcutaneous nodules,hepatosplenomegaly and
lymphadenopathy.
Diagnosis is leukopenia, anemia,increased eosinophil count,elevated
sedimentation rate,increased Ca++ levels (5%),elevated liver enzymes ,anergy
(70%),elevated angiotensin-converting enzyme in active disease (40%-80%).
Bronchoalveolar lavage,monitors cell content,fluid has increased lymphocytes
and high CD4/CD8 cell ratio and chest x-ray.
Definitive diagnosis is trans bronchial lung biopsy which shows non caseating
granulomas.
11. 1. Lung parenchyma disorders……
Sarcoidosis chest x-ray stages :
Stage 0 - Normal
Stage 1 - Good prognosis - Hilar adenopathy alone
Stage 2 - Hilar adenopathy and bilateral pulmonary infiltrates
Stage 3 - Pulmonary infiltrates without adenopathy
Stage 4 - Advanced fibrosis with evidence of honeycombing, hilar retraction,
bullae, cysts, and emphysema.
Treatment of sarcoidosis is corticosteroids and immunosuppressive agents.
13. 1. Lung parenchyma disorders……..
A1 - Hypersensitivity Pneumonitis or
known as extrinsic allergic alveolitis :
Restrictive and occupational disease
Predominant in nonsmokers (80%-95%)
Pathogenesis is antigen combines with serum antibody in alveolar walls; leads to
type III hypersensitivity reaction then antigen-antibody complexes then elicit
granulomatous inflammation leading to lung tissue injury.
Must have delayed hypersensitivity (type IV) reaction to antigen to develop
pneumonitis.
Clinical manifestations acute Symptoms start 4-6 hr after exposure and resolve
in 18- 24 hr.
General symptoms chills, sweating, shivering ,myalgias,nausea,malaise, lethargy
and Headache.
14. 1. Lung parenchyma disorders……..
Acute respiratory symptoms are dyspnea at rest,dry cough,tachypnea,chest
discomfort.
Physical findings are cyanosis (late) and Crackles in lung bases.
Intermediate symptoms are acute febrile episodes,progressive pulmonary
fibrosis with cough,dyspnea, fatigue,cor pulmonale.
Chronic symptoms are progressive, diffuse pulmonary fibrosis in upper lobes
(hallmark of disease).
15. 1. Lung parenchyma disorders…..
• Diagnosis of Hypersensitivity Pneumonitis
Chest x-ray - acute/subacute - transient, bilateral pulmonary infiltrates - increased
bronchial markings with alveolar nodular infiltrates.
Chronic - Diffuse reticulonodular infiltrates and Fibrosis. Laboratory is increased
WBCs .
Others are Skin testing with causative antigen,red, indurated hemorrhagic
reaction 4-12 hr after injection.
PFTs show decreased lung volumes and diffusing capacity.
• Treatment hypersensitivity pneumonitis
Treatment is identifying offending agent and prevent further exposure.
Oral corticosteroids.
16. 1. Lung parenchyma disorders……
B2 . Occupational Lung Diseases :
Etiology - result from inhalation of toxic gases or foreign particles and
atmospheric pollutants have large effect on occupational respiratory
diseases.
Pneumoconiosis - caused by inhalation of inorganic dust particles and
greater the exposure, the worse the consequences.
Anthracosis - “Coal miner’s lung” or “black lung” .
Silicosis - Silica inhalation.
Asbestosis - Asbestos inhalation
17. 1. Lung parenchyma disorders……..
• Predisposing factors for occupational lung disease :
Preexisting lung disease
Exposure to atmospheric pollutants
Duration of dust exposure
Amount of dust concentration
Particle size of pollutant
• Pathogenesis - Pollutants interfere and paralyze cilia - interference with ciliary
action - impaired clearance effect - Inability to remove the particle.
Alveolar macrophages try to engulf and remove the particle - Macrophages
secrete lysozymes to control foreign particle activity - Enzymes damage alveolar
walls causing deposition of fibrous materials.
18. 1. Lung parenchyma disorders…….
• Clinical manifestations
Symptoms depend on predisposing factor
Pneumoconiosis - produces no signs or symptoms in early stage Usually symptom
free up to 10-20 years with chronic exposure.
Late clinical features - chronic hypoxemia - cor pulmonale and Respiratory
failure.
• Diagnosis of occupational lung disease
Chest x-ray - no changes without symptoms with progression to micronodular
mottling and haziness,nodules,fibroses and calcifications.
PFTs and ABG – showing hypoxemia and hypercapnia.
Treatment - Preventive measures are key to limiting onset and severity and
medical treatments are Corticosteroids - Bronchodilators and O2 therapy.
In critical care patients with pneumoconiosis that are in the ICU for acute
respiratory failure, can be put on non-invasive mechanical ventilation.
19. 1.Lung parenchyma disorders……
• Mechanical ventilation in interstitial lung disease
High positive end-expiratory pressure (PEEP) levels greater than > 10 cm H2O,
APACHE score III-predicted mortality.
Ventilator setting should be low tidal volumes, low PEEP levels, and a rapid
respiratory rate should be the breathing pattern employed, regardless of
whether volume-controlled or pressure-controlled ventilation is used.
Due to the severe impairment of the respiratory mechanics, the fibrotic lung is at
high risk of developing ventilator-induced lung injury if you used high PEEP.
experts recommend keeping the static PL at end-inspiration below 15–20 cmH2O
in homogeneous and below 10–12 cmH2O in hetrogeneous lung parenchyma,
such as in ARDS.
For patients with acute exacerbation of ILD,lung protective ventilation like ARDS
is used.
20. 1. Lung parenchyma disorders…….
C. ATELECTATIC DISORDERS
C1 - Acute (Adult) Respiratory Distress Syndrome (ARDS) :
Etiology –it occurs in association with other pathophysiologic processes
and mortality rate 30%-60%.
Causes of ARDS are - Severe trauma,Sepsis (>40%) ,aspiration of gastric
acid (>30%) ,fat emboli syndrome and Shock.
Pathogenesis of ARDS is widespread pulmonary inflammation leads to non
cardiogenic pulmonary edema associated with “leaky” pulmonary
capillaries.
Atelectasis associated with lack of surfactant resulting in decreases surface
tension in small alveoli and prevents them from collapsing which is
associated with inflammatory deposition of proteins.
21. 1. Lung parenchyma disorders……
Pathogenesis - Injury to alveoli from a wide variety of disorders results changes in
alveolar diameter.
Injury to pulmonary circulation results disruptions in O2 transport and utilization.
severe hypoxemia caused by intrapulmonary shunting of blood - Perfusion of
large numbers of alveoli that are poorly or not ventilated.
Decrease in lung compliance due to loss or inactivation of surfactant with
subsequent increased recoil pressure - proteinaceous fluid fills alveoli that
impairs ventilation.
Decrease in FRC results in very stiff, noncompliant lungs associated with alveolar
edema and exudate exaggerate surface tension forces - alveolar closure leads to
atelectasis and loss of lung volume.
22. 1. Lung parenchyma disorders……….
• Clinical manifestations
Early - Sudden marked respiratory distress - Slight increase in pulse rate -
Dyspnea - Low PaO2 - Shallow, rapid breathing.
Late - Tachycardia - Tachypnea - Hypotension - Marked restlessness -Crackles,
rhonchi on auscultation - Use of accessory muscles - Intercostal and sternal
retractions – Cyanosis.
• Diagnosis of ARDS
Hallmark is hypoxemia refractory to increased levels of supplemental O2.
ABG - Hypoxia - Acidosis – Hypercapnia.
PFTs - Decrease in FVR - Decreased lung volumes - Decreased lung compliance
and VA/Q mismatch with large right-to-left shift.
Chest x-ray - Normal with progression to diffuse bilateral “whiteout”lungs.
24. 1. Lung parenchyma disorders……….
• According to the Kigali modification, ARDS was defined without the need of PEEP,
with the presence of bilateral opacities at chest radiograph or lung ultrasound
and hypoxia was defined with a cutoff of SpO2/FIO2 less than or equal to 315.
25. 1. Lung parenchyma disorders……..
Diagnosis -Open-lung biopsy shows - Atelectasis - Hyaline membranes - Cellular
debris - Interstitial and alveolar edema.
• Treatment of ARDS
Mostly supportive - Enhance tissue oxygenation until inflammation resolves.
Identify underlying cause and address the cause.
Maintain fluid and electrolyte balance.
Block system inflammatory cells.
Volume ventilator using pressure support and mechanical ventilation with
positive end-expiratory pressure (PEEP).
Increases FRV and prevents alveolar collapse at end- expiration and forces edema
out of alveoli.
26. 1. Lung parenchyma disorders……
• Treatment of ARDS
FIO2 reduced as soon as possible for improvement of pso2.
Inhaled nitric oxide
Mode A/C (CMV) Rate 15 –25 /min Volume/pressure control Pressure or volume
Tidal volume < 8 mL/kg IBW and plateau pressure <30 cm H2O Inspiratory time 1
s PEEP 5 cm H2O FiO2 Sufficient to maintain PaO2 > 60 mm Hg.
In ARDS, lung protection is provided using low tidal volumes, low plateau
transpulmonary pressures, but also a positive end-expiratory pressure (PEEP)
level sufficient to maintain oxygenation.
27. 1. Lung parenchyma disorders……
C2 - Severe Acute Respiratory Syndrome (SARS)
Etiology - Coronavirus
Primary mode of transmission through person to person - Respiratory droplets -
Contact with contaminated objects or surfaces touching mouth, nose, eyes.
Virus epidemic associated with milder disease in infants - children and Severe
respiratory forms in adults.
Median incubation period 4-6 days - Patients become ill within 10 days of
exposure.
Overall mortality rate 10% and 50% for age > 60 years
28. 1. Lung parenchyma disorders……
• Clinical manifestations
Fever (>100.4 F) - Myalgias - Headache - Nonproductive cough and Dyspnea.
• Diagnosis
Chest x-ray – can have evidence within 1 week of symptom onset.
Laboratory - Lymphopenia - Normal/low WBC - Elevated liver enzymes -
Prolonged activated PTT.
Respiratory specimens for PCR from nasopharynx,oropharynx or Sputum.
• Treatment
No definitive treatment recommendations
Symptoms of pneumonia - Hospitalization - O2 therapy - Mechanical ventilation
and Isolation.
29. 1. Lung parenchyma disorders…….
• Ventilator Settings for ALI or ARDS Or SARS
Maintaining a low tidal volume
Monitoring plateau pressure
Setting PEEP based on the FiO2 requirement
Initial Vt : adjust Vt in steps of 1 ml/kg PBW every 1-2 hours until Vt = 6 ml/kg.
Measure inspiratory plateau pressure (Pplat; 0.5 second inspiratory pause) every
4 hours and after each change in PEEP or Vt.
If Pplat > 30 cm H2O, decrease Vt to 5 or 4 ml/kg .
If Pplat < 25 cm H2O, and Vt,6ml/kg, increase Vt by 1 ml/kg PBW
Make subsequent adjustments to RR to maintain pH 7.30-7.45, but do not exceed
RR = 35/min and do not increase set rate if PaCO2 <25 mm Hg
I:E ratio : Acceptable range = 1:1 – 1:3
30. 1. Lung parenchyma disorders…….
Adjust FiO2 and PEEP proportionally to maintain PaO2 55-80 mm Hg or SpO2
88%-95%.
If pH remains <7.30 with RR = 35, consider bicarbonate infusion.
If pH <7.15, Vt may be increased (Pplat may exceed 30 cm H2O).
Alkalosis management - If pH > 7.45 and patient not triggering ventilator,
decrease set RR but not below 6 breath /min.
Using prone positioning and high levels of PEEP to maximize alveolar
recruitment.
31. 1.Lung parenchyma disorders……..
C3 - Infant Respiratory Distress Syndrome or
Hyaline membrane disease
It occurs in 60% infants born <30 weeks not treated with
corticosteroids and in 35% for infants receiving antenatal steroids and
in 5% infants <34 weeks.
High risk factors are birth prior to 25 weeks gestation - birth at
advanced gestational age - poorly controlled diabetes in mother -
deliveries after antepartum hemorrhage - cesarean section without
antecedent labor - perinatal asphyxia - second twin - previous infant
with RDS and Rh factor incompatibility.
Causes is lack of surfactant and premature neonate has difficulty
maintaining high pressures needed for adequate oxygenation related
to soft, compliant chest that’s drawn inward with each inspiratory
contraction of diaphragm.
32. 1. Lung parenchyma disorders……
Pathogenesis - the neonate with IRDS must generate high intrathoracic pressures
(25-30 mm Hg) to maintain patent alveoli that Leads to increased alveolar surface
tension and decreased lung compliance.
Increased work of breathing and decreased ventilation - Progressive atelectasis -
Increased pulmonary vascular resistance - Profound hypoxemia – Acidosis.
Secondary cause is immaturity of capillary blood supply - Leads to VA/Q
mismatch, adding to hypoxemia and metabolic acidosis - Right-to-left shunt from
open foramen ovale or patent ductus arteriosus may increase hypoxemia.
Progressive damage to basement membrane and respiratory epithelial cells -
Causes patchy areas of atelectasis - Increased capillary permeability and leakage
of high-protein fluid into alveoli - Related to cellular damage.
33. 1. Lung parenchyma disorders……
• Clinical manifestations
Early - Shallow respirations, diminished breath sounds,intercostal,
subcostal, or sternal retractions,flaring of nares,hypotension,
bradycardia,peripheral edema,low body
temperature,oliguria,tachypnea (60-120 breaths/min).
Late - frothy sputum - central cyanosis - expiratory grunting sound -
paradoxical respirations (seesaw movement of chest wall).
• Diagnosis
ABG - Hypoxemia, metabolic acidosis - Hypercapnia and respiratory
acidosis with progression of disease.
Chest x-ray - Diffuse whiteout or ground glass indicative of diffuse
bilateral atelectasis and alveolar edema and generalized lung
hypoinflation.
35. 1. Lung parenchyma disorders…….
Lecithin-sphingomyelin (L/S) ratio greater than 2 : 1 determines ability of fetus
to secrete surfactant.
Presence of phosphatidyl glycerol indicates pulmonary maturity.
L/S ratio improves with administration of glucocorticoids before delivery.
• Treatment of Hyaline membrane disease
Prevention is primary goal - Maintain adequate oxygen levels (50-90 mm Hg) -
Low FIO2 settings related to high levels over time may result in further alveolar
damage, primary persistent pulmonary hypertension, and retrolental fibroplasia -
Mechanical ventilation with PEEP or continuous positive-airway pressure.
Exogenous surfactant administration (bovine, porcine, or synthetic) - Decreases
mortality 50%.
36. 1. Lung parenchyma disorders…..
High-frequency ventilation - Provides more uniform lung inflation - Improves lung
mechanics - Improves gas exchange.
Antibiotics (infection after culture done or prophylactically until blood cultures
return).
Supportive therapy - Adequate intravenous nutrition - Fluid and electrolyte
balance - Minimal handling - Neutral thermal environment.
Babies with hyaline membrane disease and hypoxemia can be given assisted
ventilation in the form of continuous positive airway pressure (CPAP) or
intermittent positive pressure ventilation (IPPV).
The newborn can be initiated on CPAP (nasal or endotracheal) at 5-6 cm water
with FiO2 of 0.5.
Endotracheal CPAP was preferred in babies.
Despite using CPAP of 10-12 cm water (nasal), or 8-10 cm water (endotracheal)
with FiO2 of 0.8, if the newborn had hypoxemia or hypercarbia, it is an indication
to institute IPPV.
37. 2. Pleural space disorders……
A.Pneumothorax
Primary pneumothorax - occur spontaneously and no underlying disease is
identified - Cigarette smoking is risk factor.
Secondary pneumothorax – occur as result of complications from preexisting
pulmonary disease like Asthma, emphysema, cystic fibrosis, infectious disease
(pneumonia, TB).
Tension pneumothorax - Traumatic origin - Results from penetrating or
nonpenetrating injury.
Pathogenesis of primary - Rupture of small subpleural blebs in apices - Air enter
pleural space, lung collapses, and rib cage springs out.
Pathogenesis of Secondary – As result of complications from an underlying lung
problem - May be due to rupture of cyst of bleb.
38. 2. Pleural space disorders……..
Pathogenesis of Tension - Results form buildup of air under pressure in pleural space -
Air enters pleural space but cannot escape during expiration - Lung on ipsilateral (same)
side collapses and forces mediastinum toward contralateral side - Decreases venous
return and cardiac output.
Open sucking chest wall wound - Air enters during inspiration but cannot escape during
expiration - Leads to shift of mediastinum.
Iatrogenic pneumothorax occurs from a complication of a diagnostic or therapeutic
intervention such as transthoracic-needle aspiration, placement of a central venous
catheter, thoracentesis, lung, and or pleural biopsy, or barotrauma.
• Clinical manifestations
Small pneumothoraces (<20%) are usually not detectable on physical exam - Tachycardia
- Decreased or absent breath sounds on affected side - Hyperresonance - Sudden chest
pain on affected side (90%) - Dyspnea (80%.
Tension and large spontaneous pneumothorax are emergency situations - Severe
tachycardia - Hypotension - Tracheal shift to contralateral side - Neck vein distention -
Hyperresonance - Subcutaneous emphysema.
39. 2. Pleural space disorders…….
• Diagnosis of pneumothorax
ABG - Decreased PaO2, acute respiratory alkalosis.
Chest x-ray - Expiratory films show better demarcation of pleural line than
inspiratory - Decompression of hemidiaphragm on side of pneumothorax - Pleural
line with absence of vessel markings peripheral to this line.
• Treatment of pneumothorax
Management depends on severity of problem and cause of air leak.
Lung collapse <15% - The patient may or may not be hospitalized - Treat
symptomatically and monitor closely.
Lung collapse >15%-25% - Chest tube placement with H2O seal and suction.
Limiting plateau airway pressures and reducing tidal volumes and fio2 less than
60% help minimize the risk of baro trauma.
NPPV can be used to deliver continuous PEEP or CPAP to prevents atelectasis,
maintains functional residual capacity and increases cardiac output.
40. 2. Pleural space disorders……..
Chemical pleurodesis - promotes adhesion of visceral pleura to parietal pleura to
prevent further ruptures.
Thoracotomy - Patients with further development of spontaneous pneumothorax
and blebs - Surgery permits stapling or laser pleurodesis of ruptured blebs.
Thorax drainage should be performed except in asymptomatic patients with
occult pneumothorax and Patients who are mechanically ventilated should be
treated immediately with a tube thoracostomy to prevent the development of
tension pneumothorax.
If mechanical ventilation is needed, the ventilator setting should support fistula
closure and limit inflationary pressure (peak, plateau and end-expiratory) and
volume.
Intubation should be performed during spontaneous breathing if possible
because positive-pressure ventilation may enlarge an incomplete rupture and
may worsen symptoms.
41. 2. Pleural space disorders……..
• Pleural Effusion
Pathologic collection of fluid or pus in pleural cavity as result of another disease
process.
Normally - 5-15 ml of serous fluid is contained in pleural space.
There is constant movement of pleural fluid from parietal pleural capillaries to
pleural space - Reabsorbed into parietal lymphatics.
• Five major types
1- Transudates
2 - Exudates
3 - Empyema due to infection in the pleural space
4 - Chylothorax or lymphatic
5 - Hemothorax
42. 2. Pleural space disorders…….
• Clinical manifestations
Vary depending on cause and size of effusion - May be asymptomatic with <300
ml of fluid in pleural cavity - Dyspnea - Decreased chest wall movement - Pleuritic
pain (sharp, worsens with inspiration) - Dry cough.
Absence of breath sounds - Dullness to percussion - Decreased tactile fremitus
over affected area - Contralateral tracheal shift (massive effusion).
• Diagnosis of pleural effusion
Chest x-ray - Pleural-based densities - Infiltrates - Hilar adenopathy - Loculation
of fluid in the pleural Space.
Thoracentesis - Analyze fluid and reduce amount of fluid - pH, LDH, glucose -
Presence of pathologic bacteria.
CT or ultrasonographic tests - Assist in complicated effusions - Distinguish mass
from large effusion.
43. 2. Pleural space disorders……..
Treatment - Directed at underlying cause and relief of symptoms.
Thoracotomy for uncontrolled bleeding greater than 200 ml per hour .
The presence of pleural effusion is associated with a longer duration of
mechanical ventilation and ICU stay.
Drainage of large ≥500 ml pleural effusion in mechanically ventilated patients
improves oxygenation and end-expiratory lung volume.
Oxygenation improvement correlated with an increase in lung volume and a
decrease in trans pulmonary pressure.
Respiratory system compliance, end-expiratory lung volume, and PaO2/FIO2 ratio
all improved.
44. 3. Extra – pulmonary disorders……
A. Neuro muscular diseases
In NMD due to progressive inspiratory muscle weakness and increasing elastic
load induced by reduced lung and thorax compliance, these patients suffer from a
progressive decline in vital capacity (VC) and increase in work of breathing.
A rapid–shallow breathing pattern may be associated with increased work of
breathing and an inability to take deep breaths, leading to chronic micro -
atelectasis and decreased lung and chest wall compliance.
Bulbar muscle weakness (facial, oropharyngeal and laryngeal muscles) can affect
the ability to speak, swallow and clear airway secretions, with the possibility of an
increased likelihood of aspiration.
Significant reduction in VC and restrictive ventilatory pattern is usually seen in
NMD patients.
45. 3. Extra – pulmonary disorders……
A1. Poliomyelitis
Viral disease in which poliovirus attacks motor nerve cells of spinal cord and
brainstem.
New cases rare because of mass vaccination and usually occur in unvaccinated
immigrants - 95% infections asymptomatic.
• Clinical feature
Fever - Headache - Vomiting - Diarrhea - Constipation - Sore throat - Chronic
respiratory insufficiency - Function generally recovers.
46. 3. Extra – pulmonary disorders…….
A2. Amyotrophic Lateral Sclerosis
Clinical feature - males > females.
Degenerative disease of nervous system.
Involves upper and lower motor neurons.
Progressive muscle weakness and wasting.
Muscles innervated from spinal and cranial nerves affected - Eventually profound
weakness of respiratory muscles and death.
There is no cure for ATLS and most patients die after 3 to 5 years of symptom
onset.
47. 3. Extra – pulmonary disorders…….
A3 . Duchenne muscular Dystrophies
Hereditary (X-linked recessive)
• Symptoms
• Progressive muscular weakness - Initially in lower extremities, and wasting.
Respiratory muscles become involved
Leads to hypoxia, hypercapnia, frequent respiratory infections.
Occur in later years (20-30s).
48. 3. Extra – pulmonary disorders….
A4. Guillain-Barré Syndrome
Demyelination of peripheral nerves in history of recent viral or bacterial illness
(66% of cases) followed by ascending paralysis.
Infection involving Campylobacter jejuni often precedes diagnosis.
Weakness and paralysis begin symmetrically in LEs and ascend proximally to UEs
and trunk.
Severe cases - Respiratory muscle weakness accompanies limb and trunk
symptoms.
Natural history of disease leads to recovery.
Minor residual motor deficits (15%-20%).
49. 3. Extra – pulmonary disorders…..
A5 .Myasthenia Gravis
Primary abnormality at neuromuscular junction.
Impairment by decreased number of receptors on muscle.
Weakness and fatigue of voluntary muscles.
Those innervated by cranial nerves.
Peripheral and respiratory muscles can be affected.
Symptoms often managed by appropriate therapy.
Respiratory failure can be due to increasing severity of illness or medication.
Individual episodes of respiratory failure are potentially reversible.
50. 3. Extra – pulmonary disorders……
• Indications for Mechanical Ventilation in Patients with Neuromuscular Disease
Progressive ventilatory failure
Acute ventilatory failure
studies show that long-term noninvasive mechanical ventilation (NIV) especially
bilevel pressure ventilators improves symptoms, gas exchange, quality of life like
for speech, sleep, swallowing, comfort, appearance and security.
Tracheostomy ventilation may be preferred by patients unable to protect their
airways and who wish to maximise survival or when the patient is ventilator
dependent for most of the day.
Oxygenation is not usually an issue
Use CMV (A/C), VCV, Tidal volume should be 4–6 for ARDS patients and 6–
8 ml/kg PBW in patients without ARDS.low PEEP for ARDS patients and titrate fio2
based on pso2.
51. 3 .Extra – pulmonary disorders……
A1 - Chest wall deformities
Hypercapnic ventilatory failure may occur in most chest wall deformities.
Thier physiological effect is, particularly a restrictive ventilatory defect and
decreased compliance of the chest wall.
mechanical abnormalities prevent the lung from normal degree of lung inflation
and deflation.
Noninvasive positive pressure ventilation using full face mask or a mouthpiece
with either pressure- or volume-preset ventilation is likely to be effective.
A peak inspiratory pressure of 20–25 cmH2O is often required with pressure-
preset ventilation and an inspiratory time of 0.8–1 s with an expiratory time of
∼2 s.
Positive end expiratory pressure is not essential, apart from in some bilevel
pressure-support systems useful at a level of 2–4 cmH2O .
52. 3 .Extra – pulmonary disorders……
A1 .Kyphoscoliosis
Pathogenesis - bone deformity of chest wall resulting from kyphosis and
scoliosis.
Higher deformity in vertebral column, greater compromise of respiratory status -
Lung volumes compressed - Atelectasis, VA/Q mismatch, hypoxemia.
Clinical manifestations - Dyspnea on exertion - Rapid, shallow breathing - Chest
wall deformity - Ribs protruding backward, flaring on convex side, crowded on
concave side – Hypoxia , CO2 retention (late).
Diagnosis - PFTs - Hypercapnia, hypoxia - Decreased lung volumes and capacities
- Increased pulmonary arterial pressures.
Chest x-ray - Accentuated bony curves.
53. 3. Extra – pulmonary disorders….
• Treatment Kyphoscoliosis
• Depends on severity and age of patient
Curvatures <20 degrees - Monitor on regular basis - Postural exercise program -
External braces for moderate scoliosis.
Curvatures >40 degrees - Electrical stimulation of paraspinal muscles - Spinal
fusion - Spinal instrumentation (Harrington rod) placement for surgical
stabilization.
Curvatures >60 degrees - Correlate with poor pulmonary function in later life.
54. 3. Extra – pulmonary disorders…..
A2. Ankylosing Spondylitis
Chronic inflammation at site of ligamentous Insertion into spine or sacroiliac
joints - Respiratory system affected by limited chest expansion and formation of
pulmonary fibrosis in upper lobes.
More common in males (10:1) - Common in 2nd or 3rd decade of life - Cause is
unknown - 90% have positive HLA-B27 antigen - Transient acute arthritis of
peripheral joints (50%).
Pathogenesis - Progressive, inflammatory disease - Immobility of vertebral joints
and fixation of ribs - Inflammation affects articular processes, costovertebral
joints, sacroiliac joints - Fibrotic response leads to joint calcification, ligament
ossification, and skeletal immobility.
55. 3 .Extra – pulmonary disorders……
• Clinical manifestations
Low to mid-back pain and stiffness increased with prolonged rest - Pain and
stiffness decrease with exercise.
Restrictive lung dysfunction - Rib cage movement reduction - Chest wall muscular
atrophy.
Breathing by excursion of diaphragm with rib cage immobilization.
• Diagnosis
PFTs - Decreased VC, TLC, compliance of respiratory system (chest wall).
Chest x-ray - Changes are seen in sacroiliac joints - Destruction of cartilage -
Erosion of bone - Calcification - Bony bridging of joint margins.
Laboratory - Elevated sedimentation rate (85%) - Decreased RBC - Increased WBC
- HLA-B27 antigen (90%).
56. 3 .Extra – pulmonary disorders……
• Treatment
Development of exercise program
Breathing and mobility exercises
Medications – NSAIDs
A3 .Flail Chest
Two or more ribs fractured at two or more distant sites.
Results in unstable, free-floating chest wall segment
Moves paradoxically inward on inspiration
Sternal fractures can cause flail segment
57. 3.Extra – pulmonary disorders…….
Pathogenesis - fracture leads to impairment of negative intrapleural pressure
generation - Causes decreased lung expansion on inspiration - Lung parenchymal
injury - Pulmonary contusion - Decreased lung compliance - Respiratory failure -
Interstitial and alveolar hemorrhage - VA/Q abnormalities.
• Clinical manifestations
Paradoxical motion of chest wall - SOB, cyanosis - Pain on inspiration –
Hypotension - Causes entire chest to move as unit rather than paradoxically.
Pneumothorax, hemothorax, subcutaneous emphysema are common.
• Diagnosis - ABG - Hypoxemia, low arterial PO2.
• Treatment - Managed with mechanical ventilation and Pain management
58. 3.Extra – pulmonary disorders……
Full ventilatory support initially with Sedation, or paralysis may be necessary
initially.
Use Tidal volume 8-10 ml/kg with satisfactory lung compliance and 4-8 ml/kg
with pulmonary contusion and ARDS.
Titrate FiO2 to maintain SpO2 92-95%.
59. 3.Extra – pulmonary disorders…..
A4. Disorders of Obesity
Obesity - is - Excessive body fat - BMI >30 kg/m2 based on body weight and
height.
BMI >30 kg/m2 have increased mortality than with BMI between 20 and 25
kg/m2.
Pathogenesis - Several hormones act on brain receptor to regulate appetite and
metabolism.
Leptin binds to brain receptors, causes releases of neuropeptides - Increase
metabolic rate.
• Effect of obesity on respiratory system
May be associated with hypoventilation and airway obstruction.
Increased abdominal size which forces thoracic contents upward into chest cavity.
61. 3. Extra – pulmonary disorders……..
• Treatment
O2 (morbid obesity)
Weight loss program
Aerobic exercise
Obesity induces functional changes in the respiratory system, resulting in a
reduction of the end-expiratory lung volume, increased incidence of airway
closure and formation of atelectasis, and alterations in lung and chest wall
mechanics.
Non‐invasive ventilation (NIV) may be applied to avoid intubation in obese
patients with acute respiratory failure, without delaying intubation if needed.
In hypercapnic obese patients, higher positive end‐expiratory pressure (PEEP)
might be used for longer periods to reduce the hypercapnia level below 50
mmHg.
Tidal volume should be 4–6 for ARDS patients and 6–8 ml/kg PBW in patients
without ARDS.low PEEP for ARDS patients and titrate fio2 based on pso2.
62. 3.Extra – pulmonary disorders…….
A5. Chest wall burn
• Mechanical Ventilation of Patient with Burn and Inhalation Injury
Post-burn skin contractures of the anterior and lateral abdomen and chest may
result in respiratory compromise due to limitation of rib excursion.
Volume and pressure controlled ventilation most preferred mode in burn injury
patients.
But in inhalational injury ARDS patients lung protective ventilation is most
effective strategy i.e low tidal volume and low PEEP ventilation.
For inhalational injury consider bronchodilators,diuretics,secretion
clearance,prone postioning and Inhaled nitric oxide.
Titrate FiO2 for SpO2 ≧ 92.
63. References
Annals of the American Thoracic Society ,Volume 11, Issue Effects of Pleural Effusion Drainage on
Oxygenation, Respiratory Mechanics, and Hemodynamics in Mechanically Ventilated Patients.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1645517/ mechanical ventilation in hyaline membrane
disease.
Ochiai, R. Mechanical ventilation of acute respiratory distress syndrome. j intensive care 3, 25 (2015).
https://doi.org/10.1186/s40560-015-0091-6.
Ball, L., Pelosi, P. How I ventilate an obese patient. Crit Care 23, 176 (2019).
https://doi.org/10.1186/s13054-019-2466-x