This document provides an overview of acute respiratory distress syndrome (ARDS). It defines ARDS and describes its three phases: exudative, proliferative, and fibrotic. ARDS is caused by lung injury from medical or surgical disorders and results in hypoxemia. Treatment focuses on treating the underlying cause, mechanical ventilation with low tidal volumes to prevent further lung injury, and maintaining a normal fluid balance to reduce pulmonary edema. While various adjunctive therapies have been investigated, supportive care remains the primary treatment approach.
Interstitial lung diseases (ILDs) are a group of more than 200 different disorders that cause scarring in the lungs. Scar tissue in the lungs can make it harder for you to breathe normally. In ILDs, scarring damages tissues in or around the lungs’ air sacs and airways.
Acute respiratory distress syndrome (ARDS) occurs when fluid builds up in the tiny, elastic air sacs (alveoli) in your lungs. The fluid keeps your lungs from filling with enough air, which means less oxygen reaches your bloodstream. This deprives your organs of the oxygen they need to function.
Interstitial lung diseases (ILDs) are a group of more than 200 different disorders that cause scarring in the lungs. Scar tissue in the lungs can make it harder for you to breathe normally. In ILDs, scarring damages tissues in or around the lungs’ air sacs and airways.
Acute respiratory distress syndrome (ARDS) occurs when fluid builds up in the tiny, elastic air sacs (alveoli) in your lungs. The fluid keeps your lungs from filling with enough air, which means less oxygen reaches your bloodstream. This deprives your organs of the oxygen they need to function.
Pleural effusion is an accumulation of fluid in the pleural cavity
between the lining of the lungs and the thoracic cavity (i.e., the visceral
and parietal pleurae
).
Apparently a lengthy presentation actually very good for junior physicians as it covers all aspects of assessment, diagnosis and treatment of pleural effusion
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
Updates on Acute respiratory distress syndromeHamdi Turkey
These lecture notes were made by Dr. Hamdi Turkey (Pulmonologist at Taiz university)
** Contents:
- Historical view on ARDS
- New definition of ARDS
- Precipitating risk factors
- Pathophysiology of ARDS
- Clinical picture, Diagnosis, Management and Prognosis
Do Not Forget To Visit Our Pages On Facebook on the following Links:
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Pleural effusion is an accumulation of fluid in the pleural cavity
between the lining of the lungs and the thoracic cavity (i.e., the visceral
and parietal pleurae
).
Apparently a lengthy presentation actually very good for junior physicians as it covers all aspects of assessment, diagnosis and treatment of pleural effusion
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
Updates on Acute respiratory distress syndromeHamdi Turkey
These lecture notes were made by Dr. Hamdi Turkey (Pulmonologist at Taiz university)
** Contents:
- Historical view on ARDS
- New definition of ARDS
- Precipitating risk factors
- Pathophysiology of ARDS
- Clinical picture, Diagnosis, Management and Prognosis
Do Not Forget To Visit Our Pages On Facebook on the following Links:
https://www.facebook.com/groups/569435236444761/
AND
https://www.facebook.com/groups/690331650977113/
ACUTE RESPIRATORY DISTRESS SYNDROME AND HOW TO MANAGEmataharitimoer MT
ACUTE RESPIRATORY DISTRESS SYNDROME AND HOW TO MANAGE
Wahju Aniwidyaningsih
Division of Interventional Pulmonology & Respiratory Critical Care
Department of Pulmonology & Respiratory Medicine
Faculty of Medicine University of Indonesia – Persahabatan Hospital
Disampaikan pada acara PIT VI IDI Kota Bogor | 9 Nopember 2013
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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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
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
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
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
2. Introduction
• Acute respiratory distress syndrome (ARDS) is a clinical syndrome of
severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary
infiltrates leading to respiratory failure.
• ARDS is caused by diffuse lung injury from many underlying medical
and surgical disorders.
• The lung injury may be direct, as occurs in toxic inhalation, or indirect, as
occurs in sepsis.
3. • Acute lung injury (ALI) is a less severe disorder but has the potential to
evolve into ARDS.
• The arterial (a) PO2 (in mmHg)/FIO2 (inspiratory O2 fraction) <200
mmHg is characteristic of ARDS, while a PaO2/FIO2 between 200 and
300 identifies patients with ALI who are likely to benefit from aggressive
therapy.
4.
5.
6. The Berlin Definition of ARDS requires that all of the
following criteria be present to diagnose ARDS
Respiratory symptoms must have begun within one week of a known
clinical insult, or the patient must have new or worsening symptoms
during the past week.
Bilateral opacities consistent with pulmonary edema must be present on
a chest radiograph or computed tomographic (CT) scan.
These opacities must not be fully explained by pleural effusions, lobar collapse,
lung collapse, or pulmonary nodules.
7. The patient’s respiratory failure must not be fully explained by cardiac
failure or fluid overload.
An objective assessment (eg, echocardiography) to exclude hydrostatic
pulmonary edema is required if no risk factors for ARDS are present.
A moderate to severe impairment of oxygenation must be present, as
defined by the ratio of arterial oxygen tension to fraction of inspired
oxygen (PaO 2 /FiO 2 ).
The severity of the hypoxemia defines the severity of the ARDS:
8. • Mild ARDS
• The PaO 2 /FiO 2 is >200 mmHg, but ≤300 mmHg, on ventilator settings that include
positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP)
≥5 cm H 2 O.
• Moderate ARDS
• The PaO 2 /FiO 2 is >100 mmHg, but ≤200 mmHg, on ventilator settings that include
PEEP ≥5 cm H 2 O.
• Severe ARDS
• The PaO 2 /FiO 2 is ≤100 mmHg on ventilators setting that include PEEP ≥5 cm H 2 O.
9. • The annual incidences of ALI and ARDS are estimated to be up to
80/100,000 and 60/100,000, respectively.
• Approximately 10% of all intensive care unit (ICU) admissions suffer
from acute respiratory failure, with ~20% of these patients meeting
criteria for ALI or ARDS.
10. Etiology
While many medical and surgical illnesses have been associated with the
development of ALI and ARDS, most cases (>80%) are caused by a
relatively small number of clinical disorders, namely,
• Severe sepsis syndrome and/or
• Bacterial pneumonia (40–50%),
• Trauma,
• Multiple transfusions,
• Aspiration of gastric contents, and
• Drug overdose.
11. • Among patients with trauma,
• pulmonary contusion,
• multiple bone fractures, and
• chest wall trauma/flail chest are the most frequently reported surgical
conditions in ARDS.
• whereas head trauma, near-drowning, toxic inhalation, and burns are rare
causes.
12. • The risks of developing ARDS are increased in patients suffering from
more than one predisposing medical or surgical condition (e.g., the risk
for ARDS increases from 25% in patients with severe trauma to 56% in
patients with trauma and sepsis).
• Several other clinical variables have been associated with the
development of ARDS.
13. • These include older age, chronic alcohol abuse, metabolic acidosis, and
severity of critical illness.
• Trauma patients with an acute physiology and chronic health evaluation
(APACHE) II score ≥16 have a 2.5-fold increase in the risk of
developing ARDS, and those with a score >20 have an incidence of
ARDS that is more than threefold greater than those with APACHE II
scores 9.
14. Clinical Course and Pathophysiology
The natural history of ARDS is marked by three phases—
• Exudative,
• Proliferative, and
• Fibrotic—each with characteristic clinical and pathologic features.
15. Exudative Phase
• In this phase, alveolar capillary endothelial cells and type I pneumocytes
(alveolar epithelial cells) are injured, leading to the los of the normally
tight alveolar barrier to fluid and macromolecules.
• Edema fluid that is rich in protein accumulates in the interstitial and
alveolar spaces.
• Significant concentrations of cytokines (e.g., interleukin 1, interleukin 8,
and tumor necrosis factor α) and lipid mediators (e.g., leukotriene B4) are
present in the lung in this acute phase.
16. • In response to proinflammatory mediators, leukocytes (especially
neutrophils) traffic into the pulmonary interstitium and alveoli.
• In addition, condensed plasma proteins aggregate in the air spaces with
cellular debris and dysfunctional pulmonary surfactant to form hyaline
membrane whorls.
• Pulmonary vascular injury also occurs early in ARDS, with vascular
obliteration by microthrombi and fibrocellular proliferation (Fig. 268-3).
17. representative computed tomographic scan of the
chest during the exudative phase of ARDS in which
dependent alveolar edema and atelectasis predominate
18. Proliferative Phase
• This phase of ARDS usually lasts from day 7 to day 21. Most patients recover
rapidly and are liberated from mechanical ventilation during this phase.
• Despite this improvement, many still experience dyspnea, tachypnea, and
hypoxemia.
• Some patients develop progressive lung injury and early changes of pulmonary
fibrosis during the proliferative phase.
• Histologically, the first signs of resolution are often evident in this phase with
the initiation of lung repair, organization of alveolar exudates, and a shift from
a neutrophil- to a lymphocyte-predominant pulmonary infiltrate.
19. • As part of the reparative process, there is a proliferation of type II
pneumocytes along alveolar basement membranes.
• These specialized epithelial cells synthesize new pulmonary surfactant
and differentiate into type I pneumocytes.
• The presence of alveolar type III procollagen peptide, a marker of
pulmonary fibrosis, is associated with a protracted clinical course and
increased mortality from ARDS.
20. Fibrotic Phase
• While many patients with ARDS recover lung function 3–4 weeks after the
initial pulmonary injury, some will enter a fibrotic phase that may require long-
term support on mechanical ventilators and/or supplemental oxygen.
• Histologically, the alveolar edema and inflammatory exudates of earlier phases
are now converted to extensive alveolar duct and interstitial fibrosis.
• Acinar architecture is markedly disrupted, leading to emphysema-like changes
with large bullae.
• Intimal fibroproliferation in the pulmonary microcirculation leads to
progressive vascular occlusion and pulmonary hypertension.
21. • The physiologic consequences include an increased risk of
• Pneumothorax,
• Reductions in lung compliance, and
• Increased pulmonary dead space.
• Patients in this late phase experience a substantial burden of excess
morbidity.
• Lung biopsy evidence for pulmonary fibrosis in any phase of ARDS is
associated with increased mortality.
22. Excluding cardiogenic pulmonary edema
• An absence of cardiac exam abnormalities (eg, an S3 or S4 gallop, new or
changed murmur),
• Elevated right-sided filling pressures (eg, elevated jugular venous pressure),
and
• Certain radiographic abnormalities (eg,
• pulmonary venous congestion,
• Kerley B lines,
• cardiomegaly, and
• pleural effusions), helps distinguish ARDS from cardiogenic pulmonary
edema.
23. Brain natriuretic peptide (BNP)
• A plasma BNP level below 100 pg/mL favors ARDS, but higher levels
neither confirm heart failure nor exclude ARDS .
• This derives from an observational study of patients with ARDS (n =
33) or cardiogenic pulmonary edema (n = 21).
• The study found that a plasma BNP level less than 100 pg/mL identified
ARDS with a sensitivity, specificity, positive predictive value, and negative
predictive value of 27, 95, 90, and 44 percent, respectively.
24. Echocardiography
• Many clinicians use transthoracic echocardiography as the first-line
diagnostic test if cardiogenic pulmonary edema cannot be excluded by
clinical evaluation and measurement of the BNP level.
• While severe aortic or mitral valve dysfunction,
• Severe diastolic dysfunction, or a
• Severely reduced left ventricular ejection fraction favors cardiogenic
pulmonary edema.
25. • The latter is insufficient to confirm primary cardiogenic pulmonary
edema because some precipitants of ARDS (eg, septic shock) can cause
an acute, severe cardiomyopathy that develops concomitantly with
ARDS.
• In addition, cardiogenic pulmonary edema cannot be excluded on the
basis of an echocardiogram, since diastolic dysfunction and volume
overload may exist even if the left heart function appears normal.
26. Right heart catheterization
• There is ample evidence that there is generally no value to routine right
heart catheterization for either the diagnosis or management of ARDS.
• However, pulmonary artery catheterization may be considered if primary
cardiogenic pulmonary edema cannot be excluded on the basis of the
clinical evaluation, plasma BNP measurement, and echocardiogram.
28. General Principles
Recent reductions in ARDS/ALI mortality are largely the result of
general advances in the care of critically ill patients.
Thus, caring for these patients requires close attention to
I. The recognition and treatment of the underlying medical and surgical
disorders (e.g., sepsis, aspiration, trauma);
II. Minimizing procedures and their complications;
III. Prophylaxis against venous thromboembolism, gastrointestinal bleeding,
aspiration, excessive sedation, and central venous catheter infections;
IV. Prompt recognition of nosocomial infections; and
V. Provision of adequate nutrition.
29. Management of Mechanical Ventilation
• Patients meeting clinical criteria for ARDS frequently fatigue from
increased work of breathing and progressive hypoxemia, requiring
mechanical ventilation for support.
30. Ventilator-Induced Lung Injury
• Despite its life-saving potential, mechanical ventilation can aggravate lung
injury.
• Experimental models have demonstrated that ventilator-induced lung
injury appears to require two processes: repeated alveolar over
distention and recurrent alveolar collapse.
• Clearly evident by chest CT , ARDS is a heterogeneous disorder,
principally involving dependent portions of the lung with relative sparing
of other regions.
31. • Because of their differing compliance, attempts to fully inflate the
consolidated lung may lead to overdistention and injury to the more "normal"
areas of the lung.
• Ventilator-induced injury can be demonstrated in experimental models of ALI,
with high tidal volume (VT) ventilation resulting in additional, synergistic
alveolar damage.
• These findings led to the hypothesis that ventilating patients suffering from
ALI or ARDS with lower VTs would protect against ventilator-induced lung
injury and improve clinical outcomes.
32. • A large-scale, randomized controlled trial sponsored by the National Institutes
of Health and conducted by the ARDS Network compared low VT (6 mL/kg
predicted body weight) ventilation to conventional VT (12 mL/kg predicted
body weight) ventilation.
• Mortality was significantly lower in the low VT patients (31%) compared to
the conventional VT patients (40%).
• This improvement in survival represents the most substantial benefit in ARDS
mortality demonstrated for any therapeutic intervention in ARDS to date.
33. Prevention of Alveolar Collapse
• In ARDS, the presence of alveolar and interstitial fluid and the loss of
surfactant can lead to a marked reduction of lung compliance.
• Without an increase in end-expiratory pressure, significant alveolar
collapse can occur at end-expiration, impairing oxygenation.
• In most clinical settings, positive end-expiratory pressure (PEEP) is
empirically set to minimize FIO2 and maximize PaO2.
34. • On most modern mechanical ventilators, it is possible to construct a static
pressure–volume curve for the respiratory system.
• The lower inflection point on the curve represents alveolar opening (or
"recruitment").
• The pressure at this point, usually 12–15 mmHg in ARDS, is a theoretical
"optimal PEEP" for alveolar recruitment.
• Titration of the PEEP to the lower inflection point on the static pressure–
volume curve has been hypothesized to keep the lung open, improving
oxygenation and protecting against lung injury.
35. • Three large randomized trials have investigated the utility of PEEP-
based strategies to keep the lung open.
• In all three trials, improvement in lung function was evident but there
were no significant differences in overall mortality.
• Until more data become available on the clinical utility of high PEEP, it
is advisable to set PEEP to minimize FIO2 and optimize PaO2.
36. • Measurement of esophageal pressures to estimate transpulmonary
pressure may help identify an optimal PEEP in some patients.
• Oxygenation can also be improved by increasing mean airway pressure
with "inverse ratio ventilation."
• In this technique, the inspiratory (I) time is lengthened so that it is longer
than the expiratory (E) time (I:E > 1:1).
37. • With diminished time to exhale, dynamic hyperinflation leads to
increased end-expiratory pressure, similar to ventilator-prescribed PEEP.
• This mode of ventilation has the advantage of improving oxygenation
with lower peak pressures than conventional ventilation.
• Although inverse ratio ventilation can improve oxygenation and help
reduce FIO2 to 0.60 to avoid possible oxygen toxicity, no mortality
benefit in ARDS has been demonstrated.
38. • Recruitment maneuvers that transiently increase PEEP to "recruit" atelectatic lung
can also increase oxygenation, but a mortality benefit has not been established.
• In several randomized trials, mechanical ventilation in the prone position improved
arterial oxygenation, but its effect on survival and other important clinical outcomes
remains uncertain.
• Moreover, unless the critical-care team is experienced in "proning," repositioning
critically ill patients can be hazardous, leading to accidental endotracheal extubation,
loss of central venous catheters, and orthopedic injury.
• Until validation of its efficacy, prone-position ventilation should be reserved for only
the most critically ill ARDS patients.
39. Other Strategies in Mechanical Ventilation
• Several additional mechanical ventilation strategies that utilize specialized
equipment have been tested in ARDS patients, most with mixed or
disappointing results in adults.
• These include high-frequency ventilation (HFV) [i.e., ventilating at extremely
high respiratory rates (5–20 cycles per second) and low VTs (1–2 mL/kg)].
• Partial liquid ventilation (PLV) with perfluorocarbon, an inert, high-density
liquid that easily solubilizes oxygen and carbon dioxide, has revealed promising
preliminary data on pulmonary function in patients with ARDS but also
without survival benefit.
40. • Lung-replacement therapy with extracorporeal membrane oxygenation
(ECMO), which provides a clear survival benefit in neonatal respiratory
distress syndrome, may also have utility in select adult patients with
ARDS.
• Data in support of the efficacy of "adjunctive" ventilator therapies (e.g.,
high PEEP, inverse ratio ventilation, recruitment maneuvers, prone
positioning, HFV, ECMO, and PLV) remain incomplete, so these
modalities are not routinely used.
41. Fluid Management
• Increased pulmonary vascular permeability leading to interstitial and alveolar
edema rich in protein is a central feature of ARDS.
• In addition, impaired vascular integrity augments the normal increase in
extravascular lung water that occurs with increasing left atrial pressure.
• Maintaining a normal or low left atrial filling pressure minimizes pulmonary
edema and prevents further decrements in arterial oxygenation and lung
compliance, improves pulmonary mechanics, shortens ICU stay and the
duration of mechanical ventilation, and is associated with a lower mortality in
both medical and surgical ICU patients.
42. • Thus, aggressive attempts to reduce left atrial filling pressures with fluid
restriction and diuretics should be an important aspect of ARDS
management, limited only by hypotension and hypoperfusion of critical
organs such as the kidneys.
43. Glucocorticoids
• Inflammatory mediators and leukocytes are abundant in the lungs of
patients with ARDS.
• Many attempts have been made to treat both early and late ARDS with
glucocorticoids to reduce this potentially deleterious pulmonary
inflammation.
• Few studies have shown any benefit. Current evidence does not support
the use of high-dose glucocorticoids in the care of ARDS patients.
44. Other Therapies
• Clinical trials of surfactant replacement and multiple other medical
therapies have proved disappointing.
• Inhaled nitric oxide (NO) can transiently improve oxygenation but does
not improve survival or decrease time on mechanical ventilation.
• Therefore, the use of NO is not currently recommended in ARDS.
45. Recommendations
• Many clinical trials have been undertaken to improve the outcome of
patients with ARDS; most have been unsuccessful in modifying the
natural history.
• The large number and uncertain clinical efficacy of ARDS therapies can
make it difficult for clinicians to select a rational treatment plan, and
these patients' critical illnesses can tempt physicians to try unproven and
potentially harmful therapies.
46.
47. Prognosis
• Mortality
• Recent mortality estimates for ARDS range from 26 to 44%.
• There is substantial variability, but a trend toward improved ARDS outcomes
appears evident.
• Of interest, mortality in ARDS is largely attributable to non pulmonary causes,
with sepsis and non pulmonary organ failure accounting for >80% of deaths.
• Thus, improvement in survival is likely secondary to advances in the care of
septic/infected patients and those with multiple organ failure (Chap. 267).
48. • Several risk factors for mortality to help estimate prognosis have been
identified. Similar to the risk factors for developing ARDS, the major risk
factors for ARDS mortality are also non pulmonary.
• Advanced age is an important risk factor. Patients >75 years of age have a
substantially increased mortality (~60%) compared to those <45 (~20%).
• Also, patients >60 years of age with ARDS and sepsis have a threefold higher
mortality compared to those <60.
• Preexisting organ dysfunction from chronic medical illness is an important
additional risk factor for increased mortality.
49. • In particular, chronic liver disease, cirrhosis, chronic alcohol abuse, chronic
immunosuppression, sepsis, chronic renal disease, any non pulmonary organ
failure, and increased APACHE III scores have also been linked to increased
ARDS mortality.
• Several factors related to the presenting clinical disorders also increase the risk
for ARDS mortality.
• Patients with ARDS from direct lung injury (including pneumonia, pulmonary
contusion, and aspiration; have nearly twice the mortality of those with
indirect causes of lung injury, while surgical and trauma patients with ARDS,
especially those without direct lung injury, have a better survival rate than
other ARDS patients.
50. • Surprisingly, there is little value in predicting ARDS mortality from the
PaO2/FIO2 ratio and any of the following measures of the severity of
lung injury: the level of PEEP used in mechanical ventilation, the
respiratory compliance, the extent of alveolar infiltrates on chest
radiography, and the lung injury score (a composite of all these
variables).
• However, recent data indicate that an early (within 24 hours of
presentation) elevation in dead space and the oxygenation index may
predict increased mortality from ARDS.
51. Functional Recovery in ARDS Survivors
• While it is common for patients with ARDS to experience prolonged respiratory
failure and remain dependent on mechanical ventilation for survival, it is a testament
to the resolving powers of the lung that the majority of patients recover nearly
normal lung function.
• Patients usually recover their maximum lung function within 6 months.
• One year after endotracheal Extubation, more than one-third of ARDS survivors
have normal spirometry values and diffusion capacity.
• Most of the remaining patients have only mild abnormalities in their pulmonary
function. Unlike the risk for mortality, recovery of lung function is strongly
associated with the extent of lung injury in early ARDS.
52. • Low static respiratory compliance, high levels of required PEEP, longer
durations of mechanical ventilation, and high lung injury scores are all
associated with worse recovery of pulmonary function.
• When caring for ARDS survivors, it is important to be aware of the
potential for a substantial burden of emotional and respiratory
symptoms.
• There are significant rates of depression and posttraumatic stress
disorder in ARDS survivors.
Editor's Notes
Several additional diagnostic tests may also be helpful, including measurement of plasma brain natriuretic peptide levels, echocardiography, and right heart catheterization: