Ventilatory management in obstructive airway diseasesVitrag Shah
Presentation on ventilatory management in COPD & Asthma
Updated information till 26/5/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36441-ventilatory-management-obstructive-airway-diseases-presentation.html
Non-invasive ventilation (NIV) is the use of breathing support administered through a face mask or nasal mask. Learn more about NIV in this presentation by Dr Somnath Longani, consultant Anaesthesiologist & Intensivist, Midland Healthcare & Research Center, lucknow
https://midlandhealthcare.org/
Ventilatory management in obstructive airway diseasesVitrag Shah
Presentation on ventilatory management in COPD & Asthma
Updated information till 26/5/16
For powerpoint format, contact dr.vitrag@gmail.com
http://www.medicalgeek.com/presentation/36441-ventilatory-management-obstructive-airway-diseases-presentation.html
Non-invasive ventilation (NIV) is the use of breathing support administered through a face mask or nasal mask. Learn more about NIV in this presentation by Dr Somnath Longani, consultant Anaesthesiologist & Intensivist, Midland Healthcare & Research Center, lucknow
https://midlandhealthcare.org/
Presentation of Dr. Dean Hess at 10th Pulmonary Medicine Update Course, Cairo, Egypt. Pulmonary Medicine Update Course is organized by Scribe : www.scribeofegypt.com
MECHANICAL VENTILATION IN NEUROLOGICAL AND NEUROLOGICAL CASES.pptxNeurologyKota
20% of all patients requiring mechanical ventilation suffer from neurological dysfunction.
Major contributor to prolongation of mechanical ventilation in over a third of patients admitted in ICU.
Respiratory conditions in Critically ill Surgical patientMohamed Alasmar
للزملاء المتقدمين لامتحانات اجنبية زي MRCS
و للزملاء اللي منتقلين حديثا للعمل بالمملكة المتحدة او بينوو العمل فيها
تابعونا علي الصفحة الجراح
https://www.facebook.com/algarra7/
الفيديو على اليوتيوب
https://youtu.be/gLuRAzmCchI
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.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
2. Respiratory Failure
• Patients with respiratory insufficiency can be due
to three conditions:
• (1) hypoxemic respiratory failure
• (2) ventilatory, or hypercapnic, respiratory failure
• (3) impaired upper airway.
However, often more than one of these factors
contributes to respiratory failure.
Calculation of the alveol ararterial difference (A-a
gradient) can be useful.
3. Hypoxemic Respiratory Failure
• Recognized by an acute fall in P02 or
oxyhemoglobin saturation (for example, a P02
to less than or equal to 60 mm Hg or PO2
/fraction of inspired oxygen [FiO2] less than or
equal to 200
• Conditions causing acute hypoxemic
respiratory failure include alveolar collapse
and flooding with fluid, pus, or blood.
4. Hypoxemic Respiratory Failure
• Pathophysiology:
• Continued perfusion of these unventilated
lung unit can lead to profound, refractory
hypoxemia
• Hypoxemia does not correct with increased
alveolar ventilation or supplemental oxygen.
• PEEP: PEEP opens up, or "recruits," flooded or
collapsed alveoli.
•
5. Acute Lung Injury & Acute Respiratory
Distress Syndrome
• Definitions
– ALI: PO2 /fraction of inspired oxygen [FiO2]in liter
is less than 300
– ARDS: PO2 /fraction of inspired oxygen [FiO2]in
liter is less than 300 ( more severe ALI)
ALI /ARDS is a noncardiogenic form of pulmonary
edema characterized by acute and persistent lung
inflammation and increased vascular permeability
( Damaged and leaky pipes)
6. Acute Lung Injury & Acute Respiratory Distress
Syndrome
• Pulmonary artery catheters for the management of
medical ICU patients offers no survival benefit.
• Ruling out cardiogenic edema relies on clinical,
laboratory, and echocardiographic evaluation
• More than 60 disorders can precipitate ALl and ARDS
• Sepsis and Pneumonia is the most common cause
of ALI ?ARDS
7. Heart Failure
• Left ventricular dysfunction can result in acute
onset of bilateral pulmonary infiltrates that
are radiographically indistinguishable from ALI
• The hypoxemia associated with cardiogenic
edema may rapidly improve with aggressive
diuresis combined with temporizing measures
such as noninvasive positive pressure
ventilation (NPPV).
9. Hypercarbic Respiratory Failure
• Ventilatory respiratory failure refers to inadequate
alveolar ventilation or increased CO2 Production
• P CO2 = (VCO2 , x k)/VA (where k is constant = 0.863)
• Fever and increased mechanical work of breathing
are important clinical causes of elevated CO2
• Decreased respiratory drive, weakness of respiratory
muscles, and elevated dead-space ventilation
contribute-to reduced Ventilation
10.
11. Respiratory Failure: Restrictive Lung
Disease
• Extrapulmonary
These disorders include chest wall diseases such
as kyphoscoliosis, morbid obesity, large pleural
effusions, and elevated intra-abdominal pressure
from ascites, bowel edema etc.
• Pulmonary
• Ventilatory failure due to fibrotic lung disease
typically is accompanied by severe hypoxemia
and carries a poor prognosis
13. Definition..
• Noninvasive ventilation is the delivery of
ventilatory support without the need for an
invasive artificial airway
• In patients with new-onset respiratory fail-
ure, NPPV often entails the use of a ventilator
that delivers breaths through a tight-fitting mask
placed over the patient's nose and/or mouth.
14. How does NIV work?
• Reduction in inspiratory muscle work and
avoidance of respiratory muscle fatigue
• Tidal volume is increased
• CPAP counterbalances the inspiratory
threshold work related to intrinsic PEEP.
• NIV improves respiratory system compliance
by reversing microatelectasis of the lung.
15. Advantages of NIV
• Noninvasiveness
– Application (compared with endotracheal
intubation)
– Easy to implement b.
– Easy to remove Allows intermittent application
– Improves patient comfort
– Reduces the need for sedation
– Oral patency (preserves speech, swallowing, and
cough, reduces the need for nasoenteric tubes)
16. • Avoid the resistive work imposed by the
endotracheal tube
• Avoids the complications of endotracheal
intubation
– Early (local trauma, aspiration)
– Late (injury to the the hypopharynx, larynx, and
trachea, nosocomial infections)
17. Disadvantages of NIV
• 1.System
– Slower correction of gas exchange abnormalities
– Increased initial time commitment
– Gastric distension (occurs in <2% patients)
• 2.Mask
– Air leakage
– Transient hypoxemia from accidental removal
– Eye irritation
– Facial skin necrosis –most common complication.
3. Lack of airway access and protection
– Suctioning of secretions
– aspiration
18. Location of NIV
• NIV can be administered in the emergency
department, intermediate care unit, or general
respiratory ward
• It all depend on the experience of your team
19. Who can administer NIV?
• By physicians, nurses, or respiratory care therapists,
• Depends on staff experience and availability of
resources for monitoring, and managing
complications
• For the first few hours, one-to-one monitoring by a
skilled and experienced nurse, respiratory therapist,
or physician is mandatory.
• Immediate access to staff skilled in invasive airway
management.
20. Interface
Nasal masks
• less dead space
• less claustrophobia
• allow for expectoration
vomiting and oral intake
• vocalize
facial mask
dyspnoeic patients
are usually mouth
breathers
More dead space
21. Humidification during NIV
No humidification: drying of nasal mucosa;
increased airway resistance; decreased
compliance.
HME lessens the efficacy of NIV
Only pass-over humidifiers should be used
Intensive Care Med. 2002;28
22. Aerosol bronchodilator delivery during NIV
• Optimum nebulizer position: between the leak
port and patient connection
• Optimum ventilator settings: high inspiratory
pressure and low expiratory pressure.
• Optimum RR 20/mt. Rather than 10/mt.
• 25% of salbutamol dose may be delivered
Crit Care Med. 2002 Nov;30
23. Uses of NIV
1. COPD. Acute exacerbation/domiciliary.
2. Cardiogenic pulmonary edema.
3. Bronchial asthma
4. Post extubation RF
5. Hasten weaning.
24. COPD EXACERBATION: NIV
• Success rates of 80-85%
• Increases pH, reduces PaCO2, reduces the
severity of breathlessness in first 4 h of
treatment
• Decreases the length of hospital stay
• Mortality, intubation rate—is reduced
GOLD 2003
28. Cardiogenic Pulmonary edema….
• Sufficiently high level evidence to favor the use
of CPAP
• There is insufficient evidence to recommend the
use of BiPAP, probably the exception being
patients with hypercapnic CPE.
29. Methodology
• Initial ventilator settings: CPAP (EPAP) 2 cm H2O
& PSV (IPAP) 5 cm H20.
• Mask is held gently on patient’s face.
• Increase the pressures until adequate Vt
(7ml/kg), RR<25/mt, and patient comfortable.
• Titrate FiO2 to achieve SpO2>90%.
• Keep peak pressure <25-30 cm
• Head of the bed elevated
30. Monitoring
Response
Physiological a) Continuous oximetry
b) Exhaled tidal volume
c) ABG should be obtained with 1 hour and,
as necessary, at 2 to 6 hour intervals.
Objective a) Respiratory rate
b) blood pressure
c) pulse rate
Subjective
a) dyspnea
b) comfort
c) mental alertness
32. The Bottom Line
• First 30 min. of NPPV is labor intensive.
• Bedside presence of a respiratory therapist or
nurse
• familiar with this mode is essential.
• Providing reassurance and adequate
explanation
• Be ready to intubate and start on invasive
ventilation.
33. First 30 min. of NPPV is labor intensive.
Bedside presence of a
respiratory therapist or nurse
familiar with this mode is essential.
Providing reassurance and adequate explanation
Be ready to intubate and start on invasive
ventilation.
34. Criteria to discontinue NIV
• Inability to tolerate the mask because of discomfort
or pain
• Inability to improve gas exchange or dyspnea
• Need for endotracheal intubation to manage
secretions or protect airway
• Hemodynamic instability
• ECG – ischemia/arrhythmia
• Failure to improve mental status in those with CO2
narcosis.
Editor's Notes
Hypoxemic Respiratory Failure Acute hypoxemic respiratory failure is recognized by an acute fall in P02 or oxyhemoglobin saturation (for example, a P02to less than or equal to 60 mrn Hg or POy'fraction of inspired oxygen [Pio.] less than or equal to 200 [Po.fess than 200 on 100% oxygen or less than 100 on 50% oxygen]). In pure hypoxemic respiratory failure, the Pco, is typically normal or reduced. Conditions causing acute hypoxemic respiratory fail- ure include alveolar collapse and flooding with fluid, pus, or blood. Continued perfusi9n of these unventilated lung units
Continued perfusion of these unventilated lung unitcan lead to profound, refractory hypoxemia that does not adequately correct with increased alveolar ventilation or supplemental oxygen. Rather, hypoxemia is reversed by application of positive end-expiratory pressure (PEEP) to the lung, which opens up, or "recruits," flooded or collapsed alveoli.
Acute Lung Injury and the Acute Respiratory Distress Syndrome Acute lung injury (ALl) is a noncardiogenic form of pul- monary edema characterized by acute and persistent lung inflammation and increased vascular permeability. Diffuse inflammatory injury of the alveolar epithelial cells and cap- illary endothelial cells results in leakage of fluid, protein, and inflammatory cells into the interstitium and alveoli. The pathologic correlate is diffuse alveolar damage, but the diagnosis typically is made clinically rather than histologi- cally (Table 39). ALl causes hypoxemic respiratory failure, defined by a Po2/Fio2 less than or equal to 300. The subset of patients with ALl who have severe hypoxemia (Po2/Fio2 less than or equal to 200) is considered to have the acute respiratory dis- tress syndrome (ARDS). In addition to a decreased Po2/Fio2ratio, the diagnosis of either ALlor ARDS requires the pres- ence of bilateral pulmonary infiltrates on a chest radiograph and the absence of evidence to suggest increased left atrial pressure (for example, left ventricular dysfunction). There is substantial evidence that the routine use of pul- monary artery catheters for the management of medical I CD patients (including those with ARDS) offers no survival ben- efit. Therefore, the exclusion of cardiogenic edema increas- ingly relies on clinical, laboratory, and echocardiographic eval- uation to exclude left ventricular dysfunction rather than measurement of the pulmonary capillary wedge pressure. More than 60 disorders can precipitate ALl and ARDS by either direct insult to the lung or by marked systemic inflam- mation elsewhere in the body that releases mediators that can cause pulmonary capillary leak (and also affect multiple
Acute Lung Injury and the Acute Respiratory Distress Syndrome Acute lung injury (ALl) is a noncardiogenic form of pul- monary edema characterized by acute and persistent lung inflammation and increased vascular permeability. Diffuse inflammatory injury of the alveolar epithelial cells and cap- illary endothelial cells results in leakage of fluid, protein, and inflammatory cells into the interstitium and alveoli. The pathologic correlate is diffuse alveolar damage, but the diagnosis typically is made clinically rather than histologi- cally (Table 39). ALl causes hypoxemic respiratory failure, defined by a Po2/Fio2 less than or equal to 300. The subset of patients with ALl who have severe hypoxemia (Po2/Fio2 less than or equal to 200) is considered to have the acute respiratory dis- tress syndrome (ARDS). In addition to a decreased Po2/Fio2ratio, the diagnosis of either ALlor ARDS requires the pres- ence of bilateral pulmonary infiltrates on a chest radiograph and the absence of evidence to suggest increased left atrial pressure (for example, left ventricular dysfunction). There is substantial evidence that the routine use of pul- monary artery catheters for the management of medical I CD patients (including those with ARDS) offers no survival ben- efit. Therefore, the exclusion of cardiogenic edema increas- ingly relies on clinical, laboratory, and echocardiographic eval- uation to exclude left ventricular dysfunction rather than measurement of the pulmonary capillary wedge pressure. More than 60 disorders can precipitate ALl and ARDS by either direct insult to the lung or by marked systemic inflam- mation elsewhere in the body that releases mediators that can cause pulmonary capillary leak (and also affect multiple
Heart Failure Left ventricular dysfunction can result in acute onset ofbilat- eral pulmonary infiltrates that are radiographicallyindistin- guishable from ALL Differentiating cardiogenic from non- cardiogenic edema has important clinical implications because the hypoxemia associated with cardiogenic edema may rapidly improve with aggressive diuresis combined with temporizing measures such as noninvasive positive pressure ventilation (NPPV).
Restrictive Lung Disease Extrapulmonary The mechanical work of breathing is markedly increased in some disorders, thereby precipitating ventilatory failure even in the" absence of intrinsic lung disease or weakness. Such patients have a restrictive pattern on pulmonary function tests. These disorders include chest wall diseases such as kyphosco- liosis, morbid obesity, large pleural effusions, and elevated intra-abdominal pressure from ascites, bowel edJina, or intraoperative gas insufflation. Kyphoscoliosis cannot be sur- gically corrected in adults, but affected patients are suitable candidates for NPPV, particularly at night when accessory muscle compensation is not as effective. Patients with extra- pulmonary causes of restriction who develop infection or other acute illnesses 'may experience sudden declines in ven- tilatoryfunction resulting in the need for intensive care. Pulmonary Ventilatory failure due to fibrotic lung disease typically is accompanied by severe hypoxemia and carries a poor prog- nosis. Exacerbation of idiopathic pulmonary fibrosis, which is characterized by diffuse alveolar damage superimposed on fibrosis, is increasingly recognized as a cause of death in patients with even mild baseline decrements in pulmonary function tests (see also Diffuse Parenchymal Lung Disease).