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DIAGNOSIS & MANAGMENT OF
Acute Respiratory Distress Syndrome
DR. VITRAG SHAH
FIRST YEAR FNB RESIDENT,
DEPARTMENT OF CCEM,
...
SYMPTOMS…………
• Fever/chills
• Headache, myalgia
• Sore throat
• Cough
• Coryza
• Prostration
• Range of symptoms differs b...
OUTLINE
 What is ARDS
 Berlin vs AECC definition & LIS
 Risk Factors
 Etiology
 Clinical course & Pathophysiology
 D...
WHAT IS ARDS??
 A type of inflammatory lung injury that is neither a
primary disease or a single entity.
 Rather, it is ...
 Physicians think they do a lot for a patient when they
give his disease a name --Immanuel Kant
 First described as clin...
THE BERLIN DEFINITION:-
 The Berlin Definition of ARDS (published in 2012) replace the
American-European Consensus Confer...
SpO2 can be substituted for the PaO2 to calculate the SpO2/FIO2 ratio, which may be
more a feasible method of identifying ...
WHAT’S NOT INCLUDED…..
 The draft definition of severe ARDS included the more
extensive involvement on the frontal chest ...
PCWP:
 The problem is that the wedge pressure is not a measure
of capillary hydrostatic pressure,
 The PCWP is a measure...
vitrag24-www.medicalgeek.com
MURRAY LUNG INJURY SCORE (LIS)
 Radiography
 Oxygenation
 Compliance
 PEEP
 But doesn’t exclude left heart failure
vi...
vitrag24-www.medicalgeek.com
 Risk Factors
 Older age
 Chronic alcohol abuse
 Metabolic acidosis
 Critical illness.
 Trauma patients
 >80% of ca...
CLINICAL DISORDERS ASSOCIATED WITH THE
DEVELOPMENT OF ARDS
 Indirect insult
 Common
 Sepsis
 Severe trauma
 Shock
 ...
CLINICAL COURSE AND
PATHOPHYSIOLOGY
The natural history of ARDS is marked by three phases
1. Exudative (First 7 days)
2. P...
vitrag24-www.medicalgeek.com
Alveolar
Damage
Capillary
Damage
Leakage
Oedema
Fluid
Inflammatory
Cellular
Infiltrates
V/Q
Mismatch
Atelectasis
↓Thoracic...
ARDS– PROBLEMS & CONCERNS
 Strain (stretch) due to over distension of compliant
alveoli leading to volutrauma.
 High ins...
 Earliest clinical signs of ARDS are tachypnea &
progressive hypoxemia usually refractory to oxygen ,
which usually leads...
PROGRESSION OF ARDS:
If the injurious factor is not removed,
the amount of inflammatory mediators
released by the lungs in...
vitrag24-www.medicalgeek.com
DIFFERENTIAL DIAGNOSIS
 Most common
 Cardiogenic pulmonary edema
 Diffuse pneumonia
 Alveolar hemorrhage
 Less freque...
vitrag24-www.medicalgeek.com
1. CHEST X- RAY .
 A homogeneous infiltrate and the absence of
pleural effusions is more characteristic of
ARDS.
 Patchy...
2. Severity of Hypoxemia:
 In the early stages of ARDS, the hypoxemia is often more
pronounced than the CXR abnormality
...
3. BNP
 In patients with hypoxic respiratory failure :
 An BNP level of less than 100 pg/mL in a patient
with bilateral ...
4. Bronchoalveolar Lavage:
The most reliable method for confirming or
excluding the diagnosis of ARDS .
A.) Neutrophils
 ...
B.) Total Protein:
 Because inflammatory exudates are rich in proteinaceous
material, lavage fluid similarly rich in prot...
 Although not specific, BAL can be used as evidence of ARDS
if other causes of lung inflammation (e.g., pneumonia) can be...
MANAGEMENT OF ARDS
 General principles & supportive care
 Role of NIV
 Lung-Protective Ventilation Protocol
• LVV & VIL...
Management of ARDS:-
General Principles:
(1) Early recognition and treatment of the underlying medical
and surgical disord...
MANAGEMENT OF HYPOXEMIA
 Decrease oxygen consumption
 Increase oxygen delivery
 Ventilatory strategies (LPV)
vitrag24-w...
DECREASE OXYGEN CONSUMPTION
 In diseases with severe pulmonary shunting,
increasing the saturation of mixed venous blood
...
INCREASE OXYGEN DELIVERY
 DO 2 = 10 x CO x (1.34 x Hgb x SaO 2 + 0.003 x
PaO 2 )
 where DO 2 is oxygen delivered, CO is ...
ROLE OF NIV
 No trials have compared NIV to invasive mechanical
ventilation, and the only evidence at present is studies ...
vitrag24-www.medicalgeek.com
vitrag24-www.medicalgeek.com
PaO2 55-80 mmhg
vitrag24-www.medicalgeek.com
The slope of this relationship represents the compliance of the respiratory system, and the goal
should be to ventilate pa...
Lung-Protective Ventilation:
 Since the introduction of positive-pressure mechanical
ventilation, large inflation volumes...
 CXR in ARDS show homogeneous pattern
of lung infiltration.
 CT images reveal that the lung infiltration in
ARDS is not ...
Ventilator-Induced Lung Injury
MECHANISM
 The following mechanisms of lung injury have been described:
1) Atelectrauma : ...
Lung-Protective Ventilation:
vitrag24-www.medicalgeek.com
Low-Volume Ventilation(LVV)
LVV protocol is designed to achieve three
goals :
 Maintain a tidal volume of 6 mL/kg using
p...
MEDIAN ORGAN FAILURE
FREE DAYS
6ml/kg.
12ml/kg
.
vitrag24-www.medicalgeek.com
vitrag24-www.medicalgeek.com
Permissive Hypercapnia
 One of the consequences of low volume ventilation is a
reduction in CO2 elimination via the lungs...
 One of the more troublesome side effects of hypercapnia
is brainstem respiratory stimulation with subsequent
hyperventil...
OPEN LUNG VENTILATION
 It is a stratergy that combines low tidal volume ventilation & enough
applied PEEP to maximize alv...
STRATEGY………..?
Aerated
Non aerated
recruitable
Non aerated
Non recruitable
vitrag24-www.medicalgeek.com
vitrag24-www.medicalgeek.com
Titration of PEEP by oxygenation after assessment of lung recruitability. PEEP/FIO2
tables are from the ALVEOLI Trial. Adj...
Positive End-Expiratory Pressure:
The high PEEP approach is a type of open lung ventilation
that does not require pressure...
vitrag24-www.medicalgeek.com
TITRATING PEEP BY ESOPHAGEAL PRESSURE
 Esophageal pressure is an estimate of pleural pressure.
It can be measured with an...
• PEEP by acting as a “stent” to keep small airways open
at the end of expiration and ↓ shear forces.
• Advantages of PEEP...
Pitfalls of PEEP:
 Increased applied PEEP has the potential to cause
pulmonary barotrauma or ventilator-associated lung
i...
LUNG RECRUITMENT
 If there is recruitable lung, then PEEP will have a favorable
effect and will improve gas exchange in t...
RECRUITMENT MANEUVERS (RMS)
Current evidence suggests that that RMs should not be routinely used on all
ARDS patients unle...
RECRUITMENT MANEUVERS
Anesthesiology 2002, 96:795–802.
CPAP : 35-40 cm H20 for 30-40 seconds
vitrag24-www.medicalgeek.com
RECRUITMENT MANEUVERS
Anesthesiology 2002, 96:795–802.
Curr Opin Crit Care 2003; 9:22–27
Crit Care Med 2004; 32: 2371–77
I...
MODE OF VENTILATOR
Randomized, controlled trials demonstrating superiority of volume
assist control over other modes in th...
vitrag24-www.medicalgeek.com
NEUROMUSCULAR BLOCKERS
 Administration of short-term (up to 48 hours)
neuromuscular blockade to patients with ARDS who
ha...
REFRACTORY HYPOXEMIA
 Following modalities are used for Refractory
Hypoxemia apart from N-M Blockers, High PEEP
& other r...
Prone position:
 In several trials, MV in the prone position improves
oxygenation. Other purported benefits include impro...
POSSIBLE MECHANISMS
 Recruitment of dependent lung zones,
 Increased functional residual capacity (FRC)
 Improved diaph...
OTHER MODES OF MV :
 AIRWAY PRESSURE RELEASE VENTILATION
(APRV):
 Another “open lung” approach
 It is a pressure contro...
APRV
Airway Pressure Release Ventilation
From Mosby’s R. C. Equip. 6th ed. 1999.
vitrag24-www.medicalgeek.com
Inverse ratio ventilation (IRV)
 Oxygenation can also be improved by increasing mean airway
pressure with "inverse ratio ...
o There are potential side effects associated with
prolonging the inspiratory time that should be
considered.
o In additio...
 High-frequency ventilation (HFV) –
 High frequency oscillatory ventilation (HFOV) delivers
small tidal volumes (1–2 mL/...
INHALED NITRIC OXIDE
 Inhaled nitric oxide (5–10 ppm) is a selective
pulmonary vasodilator that can improve arterial
oxyg...
EXTRA CORPOREAL MEMBRANE OXYGENATION:-
 Extracorporeal membrane oxygenation (ECMO) is the use of
a modified heart–lung ma...
vitrag24-www.medicalgeek.com
vitrag24-www.medicalgeek.com
NON-VENTILATORY MANAGEMENT
 Fluid management
 Diuretics
 Steroids
 Blood Transfusion cut-off
 Choice of Inotropic age...
Fluids management:
 Patients with ARDS should receive intravenous fluids
only sufficient to achieve an adequate cardiac o...
 Fluid management in ARDS is usually aimed at reducing
extravascular lung water with diuretics. While this approach
has s...
 The golden rule is that hydrostatic pressures should be
kept as low as possible, provided that oxygen delivery to
the ti...
ROLE OF STEROIDS
IN UNRESOLVING ARDS
Because of apparent benefit in small trials, it was thought that
there might be a rol...
1.Steinberg KP, Hudson LD, Goodman RB, et al found
that in the subgroup of patients randomized 7 to 13 days
after the onse...
HEMOGLOBIN
 Transfusion is often recommended to keep the Hb
above 10 g/dL, but this practice has no scientific
basis or d...
INOTROPIC AGENT
 Cardiac output may be augmented by raising filling
pressures if they are low (if pulmonary edema is not
...
OTHER DRUG THERAPY – UNPROVEN BENIFIT
INHALED VASODILATORS : PGE1 (pulmonary vasodilatation
and anti-inflammatory effects ...
Mortality:
 Recent mortality estimates for ARDS range from
26 to 58% with substantial variability.
 The underlying cause...
Functional Recovery in ARDS Survivors
o ARDS pts experience prolonged
respiratory failure and remain dependent on
mechanic...
 Recovery of lung function is strongly associated with the
extent of lung injury in early ARDS
 When caring for ARDS sur...
FUTURE DIRECTIONS:
 With the high mortality rates associated
with ARDS and sepsis, the search
continues to identify targe...
ROLE OF STEM CELLS – PHASE-I CLINICAL
TRAIL GOING ON
 Stem cells constitute a promising therapeutic strategy for patients...
 JAMA, June 20, 2012—Vol 307, No. 23 : Berlin Definition
 Harrison‘s Principles Of Internal Medicine 19th Edition
 The ...
QUESTIONS…….?
vitrag24-www.medicalgeek.com
THANK YOU
THANK YOU
vitrag24-www.medicalgeek.com
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ARDS - Diagnosis and Management

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ARDS - Diagnosis and Management
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ARDS - Diagnosis and Management

  1. 1. DIAGNOSIS & MANAGMENT OF Acute Respiratory Distress Syndrome DR. VITRAG SHAH FIRST YEAR FNB RESIDENT, DEPARTMENT OF CCEM, SGRH, DELHI MODERATOR DR.RAHUL vitrag24-www.medicalgeek.com
  2. 2. SYMPTOMS………… • Fever/chills • Headache, myalgia • Sore throat • Cough • Coryza • Prostration • Range of symptoms differs by age – Vomiting & diarrhea in children/elderly – Fever alone in infants – May be atypical in elderly • Serious complications can occur among high risk groups vitrag24-www.medicalgeek.com
  3. 3. OUTLINE  What is ARDS  Berlin vs AECC definition & LIS  Risk Factors  Etiology  Clinical course & Pathophysiology  Differential diagnosis  Management  General management & nursing care  Role of NIV  Ventilatory management  Management of Refractory hypoxemia  Non-Ventilatory management  Other drugs/therapies  Prognosis  Future/Research & Role of stem cells  References vitrag24-www.medicalgeek.com
  4. 4. WHAT IS ARDS??  A type of inflammatory lung injury that is neither a primary disease or a single entity.  Rather, it is an expression of myriad other diseases that produce diffuse inflammation in the lungs, often accompanied by inflammatory injury in other organs & it is also the leading cause of acute respiratory failure. vitrag24-www.medicalgeek.com
  5. 5.  Physicians think they do a lot for a patient when they give his disease a name --Immanuel Kant  First described as clinical syndrome in 1967 by Ashbaugh & Petty .  Synonyms: Sponge Lung, Shock lung, Non-cardiogenic pulmonary edema, Capillary leak syndrome, Traumatic wet Lung, Adult hyaline membrane disease, ALI & ARDS, and most recently, Only ARDS. vitrag24-www.medicalgeek.com
  6. 6. THE BERLIN DEFINITION:-  The Berlin Definition of ARDS (published in 2012) replace the American-European Consensus Conference’s definition of ARDS (published in 1994).  The European society of intensive care medicine endorsed by The American Thoracic Society and The Society of Critical Care Medicine developed the Berlin definition in 2012.  The major changes to the Berlin Definition are that the term “acute lung injury” has been eliminated, the pulmonary capillary wedge pressure (ie, pulmonary artery occlusion pressure) criteria has been removed, and minimal ventilator settings have been added. vitrag24-www.medicalgeek.com
  7. 7. SpO2 can be substituted for the PaO2 to calculate the SpO2/FIO2 ratio, which may be more a feasible method of identifying severely ill patients in these resource-limited environments. vitrag24-www.medicalgeek.com
  8. 8. WHAT’S NOT INCLUDED…..  The draft definition of severe ARDS included the more extensive involvement on the frontal chest radiograph (3 or 4 quadrants) { from those with the minimal criterion of “bilateral opacities” (2 quadrants) }, respiratory system compliance (40 mL/cm H2O), positive end expiratory pressure (10 cm H2O), and corrected expired volume per minute (10 L/min).  These variables were identified for further study during the evaluation phase & not included in present criteria. vitrag24-www.medicalgeek.com
  9. 9. PCWP:  The problem is that the wedge pressure is not a measure of capillary hydrostatic pressure,  The PCWP is a measure of LAP and LAP cannot be the same as the pulmonary capillary pressure in presence of blood flow .  If the wedge (left-atrial) pressure were equivalent to the pressure in the pulmonary capillaries, there would be no pressure gradient for flow in the pulmonary veins. Thus, the capillary hydrostatic pressure must be higher than the wedge pressure.So PCWP will underestimate the actual capillary hydrostatic pressure.  This difference is small in the normal lung, but in severe ARDS, the capillary hydrostatic pressure can be double the wedge pressure.  Because of this discrepancy, the wedge pressure should be abandoned as a diagnostic criterion for ARDS. vitrag24-www.medicalgeek.com
  10. 10. vitrag24-www.medicalgeek.com
  11. 11. MURRAY LUNG INJURY SCORE (LIS)  Radiography  Oxygenation  Compliance  PEEP  But doesn’t exclude left heart failure vitrag24-www.medicalgeek.com
  12. 12. vitrag24-www.medicalgeek.com
  13. 13.  Risk Factors  Older age  Chronic alcohol abuse  Metabolic acidosis  Critical illness.  Trauma patients  >80% of cases are caused by:  Sepsis  Bacterial pneumonia  Trauma  Multiple transfusions  Gastric acid aspiration  Drug overdose vitrag24-www.medicalgeek.com
  14. 14. CLINICAL DISORDERS ASSOCIATED WITH THE DEVELOPMENT OF ARDS  Indirect insult  Common  Sepsis  Severe trauma  Shock  Less common  Acute pancreatitis  Cardiopulmonary bypass  Transfusion-related TRALI  DIC  Burns  Head injury  Drug overdose Direct insult  Common  Aspiration pneumonia  Pneumonia Less common  Inhalation injury  Pulmonary contusions  Fat emboli  Near drowning  Reperfusion injury vitrag24-www.medicalgeek.com
  15. 15. CLINICAL COURSE AND PATHOPHYSIOLOGY The natural history of ARDS is marked by three phases 1. Exudative (First 7 days) 2. Proliferative (After 7-21 days) 3. Fibrotic (After 3-4 weeks) Each with characteristic clinical and pathologic features vitrag24-www.medicalgeek.com
  16. 16. vitrag24-www.medicalgeek.com
  17. 17. Alveolar Damage Capillary Damage Leakage Oedema Fluid Inflammatory Cellular Infiltrates V/Q Mismatch Atelectasis ↓Thoracic Compliance ↑Dead Space Hypoxic Vasoconstriction Hypoxia vitrag24 - www.medicalgeek.com
  18. 18. ARDS– PROBLEMS & CONCERNS  Strain (stretch) due to over distension of compliant alveoli leading to volutrauma.  High inspiratory pressures (Pplat) leading to barotrauma.  Release of inflammatory mediators from lung (biotrauma)  Shear stress due to complete closure & re-opening of non-compliant alveoli (atelectrauma). vitrag24-www.medicalgeek.com
  19. 19.  Earliest clinical signs of ARDS are tachypnea & progressive hypoxemia usually refractory to oxygen , which usually leads to diffuse pulmonary infiltrates in chest x-ray within 24 hours & leading to respiratory failure requiring mechanical ventilation within 48 hours of illness. vitrag24-www.medicalgeek.com
  20. 20. PROGRESSION OF ARDS: If the injurious factor is not removed, the amount of inflammatory mediators released by the lungs in ARDS may results in  SIRS - Systemic inflammatory response syndrome  MODS - multi organ dysfunction syndrome This adds up to impaired oxygenation which is the central problem of ARDS, which further impairs oxygen delivery. vitrag24-www.medicalgeek.com
  21. 21. vitrag24-www.medicalgeek.com
  22. 22. DIFFERENTIAL DIAGNOSIS  Most common  Cardiogenic pulmonary edema  Diffuse pneumonia  Alveolar hemorrhage  Less frequent  Acute interstitial lung diseases(e.g., acute interstitial pneumonitis)  Acute immunologic injury (e.g., hypersensitivity pneumonitis)  Toxin injury (e.g., radiation pneumonitis)  Neurogenic pulmonary edema vitrag24-www.medicalgeek.com
  23. 23. vitrag24-www.medicalgeek.com
  24. 24. 1. CHEST X- RAY .  A homogeneous infiltrate and the absence of pleural effusions is more characteristic of ARDS.  Patchy infiltrates from the hilum, prominent pleural effusions, cardiomegaly & cephalization is more characteristic of cardiogenic pulmonary edema.  However, , pleural effusions can appear in ARDS, and the view is that CXR are not reliable for distinguishing ARDS from cardiogenic pulmonary edema ARDS vs Cardiogenic Pulmonary Edema vitrag24-www.medicalgeek.com
  25. 25. 2. Severity of Hypoxemia:  In the early stages of ARDS, the hypoxemia is often more pronounced than the CXR abnormality  In the early stages of cardiogenic pulmonary edema, the CXR abnormalities are often more pronounced than the hypoxemia.  However, there are exceptions, and severe hypoxemia can occur in cardiogenic pulmonary edema from a low cardiac output vitrag24-www.medicalgeek.com
  26. 26. 3. BNP  In patients with hypoxic respiratory failure :  An BNP level of less than 100 pg/mL in a patient with bilateral infiltrates and hypoxemia favors the diagnosis of ARDS/acute lung injury (ALI) rather than cardiogenic pulmonary edema. vitrag24-www.medicalgeek.com
  27. 27. 4. Bronchoalveolar Lavage: The most reliable method for confirming or excluding the diagnosis of ARDS . A.) Neutrophils  In normal subjects, neutrophils make up less than 5% of the cells recovered in lung lavage fluid, whereas in patients with ARDS, as many as 80% of the recovered cells are neutrophils.  A low neutrophil count in lung lavage fluid can be used to exclude the diagnosis of ARDS, while a high neutrophil count is considered evidence of ARDS . vitrag24-www.medicalgeek.com
  28. 28. B.) Total Protein:  Because inflammatory exudates are rich in proteinaceous material, lavage fluid similarly rich in protein→ evidence of lung inflammation.  When the protein concentration in lung lavage fluid is expressed as a fraction of the total protein concentration, the following criteria can be applied  Protein (lavage/serum) <0.5 = Hydrostatic edema  Protein (lavage/serum) >0.7 = Lung inflammation  Lung inflammation is expected to produce a protein concentration that is greater than 70% of the protein concentration in serum. vitrag24-www.medicalgeek.com
  29. 29.  Although not specific, BAL can be used as evidence of ARDS if other causes of lung inflammation (e.g., pneumonia) can be excluded on clinical grounds.  BAL has not gained widespread acceptance as a diagnostic tool for ARDS, because most ICU physicians use the diagnostic criteria to evaluate possible ARDS. vitrag24-www.medicalgeek.com
  30. 30. MANAGEMENT OF ARDS  General principles & supportive care  Role of NIV  Lung-Protective Ventilation Protocol • LVV & VILI • Permissive hypercapnia • PEEP & Open lung ventilation • Lung Recruitment - Recruitment maneuvers • Mode of ventilator • Approach to patient-ventilator dyssynchrony • Role of Neuromuscular blockers  Management of Refractory Hypoxemia • Prone Position • Other Modes of ventilation • IRV • Inhaled Nitric Oxide • ECMO  Non Ventilatory Management  Fluid management  Diuretics  Steroids  Blood Transfusion cut-off  Choice of Inotropic agent  Other drugs/Therapies  Prognosis  Future/Research & Role of stem cell vitrag24-www.medicalgeek.com
  31. 31. Management of ARDS:- General Principles: (1) Early recognition and treatment of the underlying medical and surgical disorders (e.g., sepsis, aspiration, trauma); (2) Minimizing procedures and their complications; (3) Prophylaxis against venous thromboembolism, gastrointestinal bleeding, and central venous catheter infections; (4) Prompt recognition of nosocomial infections; and provision of adequate nutrition, Glucose control. (5) Use of sedatives and neuromuscular blockade (6) Hemodynamic management (7) Ventilatory strategies to decrease tidal volume (Vt) while maintaining adequate oxygenation vitrag24-www.medicalgeek.com
  32. 32. MANAGEMENT OF HYPOXEMIA  Decrease oxygen consumption  Increase oxygen delivery  Ventilatory strategies (LPV) vitrag24-www.medicalgeek.com
  33. 33. DECREASE OXYGEN CONSUMPTION  In diseases with severe pulmonary shunting, increasing the saturation of mixed venous blood (SvO2 ) may increase the SaO2 . Therapies that decrease oxygen consumption may improve SvO2 (and SaO2 subsequently) by decreasing the amount of oxygen extracted from the blood.  Common causes of increased oxygen consumption include fever, anxiety and pain, and use of respiratory muscles; therefore, arterial saturation may improve after treatment with anti-pyretics, sedatives, analgesics, or paralytics vitrag24-www.medicalgeek.com
  34. 34. INCREASE OXYGEN DELIVERY  DO 2 = 10 x CO x (1.34 x Hgb x SaO 2 + 0.003 x PaO 2 )  where DO 2 is oxygen delivered, CO is cardiac output, Hgb is hemoglobin concentration, SaO 2 is the arterial oxygen saturation, and PaO 2 is the partial pressure of oxygen in arterial blood. As a result, in addition to low SaO 2 , DO 2 may be decreased by a low Hgb and a low CO. In turn, a low DO 2 may decrease SvO 2 . vitrag24-www.medicalgeek.com
  35. 35. ROLE OF NIV  No trials have compared NIV to invasive mechanical ventilation, and the only evidence at present is studies such as that by “Ferrer et al” in which NIPPV is compared with supplemental oxygen by face mask alone. In this particular trial, NIPPV was associated with decreased need for intubation compared with oxygen by face mask in the overall study population, but among patients with ARDS, there were no differences in outcomes.  Their use should only be considered in patients with mild disease (PaO2/FIO2 > 200 and no other organ dysfunction) and immunocompromised patients who are hemodynamically stable, able to tolerate wearing a face mask, and able to maintain a patent airway. vitrag24-www.medicalgeek.com
  36. 36. vitrag24-www.medicalgeek.com
  37. 37. vitrag24-www.medicalgeek.com
  38. 38. PaO2 55-80 mmhg vitrag24-www.medicalgeek.com
  39. 39. The slope of this relationship represents the compliance of the respiratory system, and the goal should be to ventilate patients on the steepest portion of the relationship where smaller pressure changes are necessary to achieve the desired tidal volume. Lowering the tidal volume helps avoid the upper, flat portion of this relationship (A), where large changes in pressure are necessary to achieve small volume changes. Application of positive end-expiratory pressure helps avoid the lower, flat portion of this relationship (B) by preventing repetitive opening and closing of the alveoli. vitrag24-www.medicalgeek.com
  40. 40. Lung-Protective Ventilation:  Since the introduction of positive-pressure mechanical ventilation, large inflation volumes(TV) were used to ↓ tendency for atelectasis during MV.  The standard tidal volumes were 10 to 15 mL/kg, which are twice the size of tidal volumes used during quiet breathing (6 to 7 mL/kg).  In patients with ARDS, these large inflation volumes are delivered into lungs that have a marked ↓in functional volume. → VOLUTRAUMA. vitrag24-www.medicalgeek.com
  41. 41.  CXR in ARDS show homogeneous pattern of lung infiltration.  CT images reveal that the lung infiltration in ARDS is not spread evenly throughout the lungs, but rather is confined to dependent lung regions  The remaining area of uninvolved lung is the functional portion of the lungs in ARDS.( baby lungs)  The large inflation volumes delivered by mechanical ventilation cause overdistention and rupture of BABY LUNG→ Ventilator- induced lung injury. vitrag24-www.medicalgeek.com
  42. 42. Ventilator-Induced Lung Injury MECHANISM  The following mechanisms of lung injury have been described: 1) Atelectrauma : collapse of alveoli and surfactant depletion. Ventilation with high FiO2 aggravates alveolar collapse due to absorption atelectasis 2) Oxygen toxicity : While this is well known, it is not clear what concentration of oxygen is toxic over what period of time. It is generally assumed that FiO2 <0.6 is not toxic, however an attempt must be made to maintain the FiO2 as low as possible. 3)Volutrauma : Ventilation at high volumes and pressures can lead to alveolar overdistension, causing increased permeability pulmonary edema in the uninjured lung and enhanced edema in the injured lung. 4)Cyclical shear stress injury : Cyclic opening and closing of atelectatic alveoli during mechanical ventilation create tremendous shear stress at their junctions with open alveoli. This results in damage to the capillary endothelium and the alveolar membrane. 5)Biotrauma : Alveolar over-distension along with the repeated collapse and reopening of the alveoli can result in a whole cascade of proinflammatory cytokines which induce both a pulmonary and systemic cytokine response, aggravating lung injury and causing systemic multiorgan dysfunction. 6)Barotrauma : Pneumothorax, pneumomediastinum, interstitital emphysema. vitrag24-www.medicalgeek.com
  43. 43. Lung-Protective Ventilation: vitrag24-www.medicalgeek.com
  44. 44. Low-Volume Ventilation(LVV) LVV protocol is designed to achieve three goals :  Maintain a tidal volume of 6 mL/kg using predicted body weight,  Keep the end-inspiratory plateau pressure below 30 cm H2O, and  Avoid severe respiratory acidosis. vitrag24-www.medicalgeek.com
  45. 45. MEDIAN ORGAN FAILURE FREE DAYS 6ml/kg. 12ml/kg . vitrag24-www.medicalgeek.com
  46. 46. vitrag24-www.medicalgeek.com
  47. 47. Permissive Hypercapnia  One of the consequences of low volume ventilation is a reduction in CO2 elimination via the lungs leading to hypercapnia and respiratory acidosis. Allowing hypercapnia to persist in favor of maintaining lung-protective low-volume ventilation is known as permissive hypercapnia.  The degree of hypercapnia can be minimized by using the highest respiratory rate that does not induce auto-PEEP and shortening the ventilator tubing to decrease dead space. In addition, changing from a heat and moisture exchanger to a heated humidifier appears to decrease hypercapnia by decreasing dead space ventilation vitrag24-www.medicalgeek.com
  48. 48.  One of the more troublesome side effects of hypercapnia is brainstem respiratory stimulation with subsequent hyperventilation, which often requires neuromuscular blockade to prevent ventilator asynchrony.  Data from clinical trials of permissive hypercapnia show that arterial PCO2 levels of 60 to 70 mm Hg and arterial pH levels of 7.2 to 7.25 are safe for most patients . vitrag24-www.medicalgeek.com
  49. 49. OPEN LUNG VENTILATION  It is a stratergy that combines low tidal volume ventilation & enough applied PEEP to maximize alveolar recruitment. The LTVV aims to mitigate alveolar overdistention, while the applied PEEP seeks to minimize cyclic atelectasis. Togather , these effects are expected to decrese the risk of ventilator associated lung injury.  LTVV is applied as described and applied PEEP is set at least 2 cm above the lower inflection point of the pressure volume curve are used. Applied PEEP of 16 cm H 2 O is used if the lower inflection point is uncertain.  Alternative approach : PEEP set at a high level following a recruitment maneuver and then incrementally decreased until both the static lung compliance decreased and the sPO2 decreased by 2% from the previous measurement. The PEEP is then set 2 cm H 2 O above this level.  PEEP adjustment based on the PEEP–FIO2 protocol used in ARMA is likely the most feasible approach until more data are available. vitrag24-www.medicalgeek.com
  50. 50. STRATEGY………..? Aerated Non aerated recruitable Non aerated Non recruitable vitrag24-www.medicalgeek.com
  51. 51. vitrag24-www.medicalgeek.com
  52. 52. Titration of PEEP by oxygenation after assessment of lung recruitability. PEEP/FIO2 tables are from the ALVEOLI Trial. Adjust PEEP and FIO2 using the two tables as guidelines to maintain PaO2 between 55 and 80 mmHg or SpO2 between 88% and 95%. *Consider the using lower PEEP table as a guideline for PEEP titration for patients who have active barotrauma or adverse PEEP-induced cardiovascular changes. (or decrease in PaCO2 at constant minute ventilation and tidal volume) vitrag24-www.medicalgeek.com
  53. 53. Positive End-Expiratory Pressure: The high PEEP approach is a type of open lung ventilation that does not require pressure-volume curves. This is advantageous because pressure-volume curves are difficult to construct and generally require neuromuscular blockade. Significance of PEEP: Applied PEEP opens collapsed alveoli, which decreases alveolar overdistension because the volume of each subsequent tidal breath is shared by more open alveoli. If the alveoli remain open throughout the respiratory cycle, cyclic atelectasis is also reduced. Alveolar overdistension and cyclic atelectasis are the principal causes of ventilator- associated lung injury. vitrag24-www.medicalgeek.com
  54. 54. vitrag24-www.medicalgeek.com
  55. 55. TITRATING PEEP BY ESOPHAGEAL PRESSURE  Esophageal pressure is an estimate of pleural pressure. It can be measured with an esophageal balloon catheter and then used to calculate the transpulmonary pressure.  Transpulmonary pressure = airway pressure - pleural pressure  The transpulmonary pressure can then be adjusted by titrating applied PEEP, since airway pressure is related to applied PEEP. Titrating applied PEEP to an end- expiratory transpulmonary pressure between 0 and 10 cm H 2 O may reduce cyclic alveolar collapse, while maintaining an end-inspiratory transpulmonary pressure ≤25 cm H 2 O may reduce alveolar overdistension. vitrag24-www.medicalgeek.com
  56. 56. • PEEP by acting as a “stent” to keep small airways open at the end of expiration and ↓ shear forces. • Advantages of PEEP: • PEEP ↑arterial oxygenation by ↓ intra pulmonary shunting. • Allows reduction in (FiO2) to safer levels hence ↓oxygen toxicity. • PEEP can also open collapsed alveoli and reverse atelectasis - known as lung recruitment, and it increases the available surface area in the lungs for gas exchange vitrag24-www.medicalgeek.com
  57. 57. Pitfalls of PEEP:  Increased applied PEEP has the potential to cause pulmonary barotrauma or ventilator-associated lung injury by increasing the plateau airway pressure and causing alveolar overdistension. It also has the potential to decrease blood pressure by reducing cardiac output. “High applied peep should be administered to the patients with refractory hypoxemia before implimenting other rescue interventions because ARDS patients are a heterogenous group , some of whom may have large areas of recruitable lung that will respond to applied PEEP.” vitrag24-www.medicalgeek.com
  58. 58. LUNG RECRUITMENT  If there is recruitable lung, then PEEP will have a favorable effect and will improve gas exchange in the lungs. However if there is no recruitable lung, PEEP can overdistend the lungs (because the lung volume is lower if areas of atelectasis cannot be aerated) and produce an injury similar to ventilator- induced lung injury.  Areas of atelectasis that contain pockets of aeration are most likely to represent recruitable lung, whereas areas of atelectasis that are airless are unlikely to be recruitable.  The impact of routine recruitment maneuvers on clinical outcomes is unclear, although one meta-analysis found that recruitment maneuvers did not affect mortality, length of hospital stay, or the incidence of barotrauma, despite improving the PaO 2 . vitrag24-www.medicalgeek.com
  59. 59. RECRUITMENT MANEUVERS (RMS) Current evidence suggests that that RMs should not be routinely used on all ARDS patients unless severe hypoxemia persists or as a rescue maneuver to overcome severe hypoxemia, to open the lung when setting PEEP, or following evidence of acute lung derecruitment such as a ventilator circuit disconnect • Vital capacity maneuver (inflation of the lungs up to 40 cm H2O, maintained for 15 - 26 seconds) • Intermittent sighs • Intermittent increase of PEEP • Continuous positive airway pressure (CPAP) of 35-40cm of H20 for 40 seconds. • Increasing the ventilatory pressures to a plateau pressure of 50 cm H2O for 1-2 minutes . • One study found that most of the alveolar recruitment occurred during the first ten seconds of the maneuver . This was followed by a decrease in the blood pressure, which recovered within 30 seconds after the recruitment maneuver. Significant airway overdistention does not occur while single recruitment manuevre and recruited alveoli tend to remain open when lower pressure are instituted. vitrag24-www.medicalgeek.com
  60. 60. RECRUITMENT MANEUVERS Anesthesiology 2002, 96:795–802. CPAP : 35-40 cm H20 for 30-40 seconds vitrag24-www.medicalgeek.com
  61. 61. RECRUITMENT MANEUVERS Anesthesiology 2002, 96:795–802. Curr Opin Crit Care 2003; 9:22–27 Crit Care Med 2004; 32: 2371–77 Intermittent Sigh Intermittent PEEP Progressive PEEP vitrag24-www.medicalgeek.com
  62. 62. MODE OF VENTILATOR Randomized, controlled trials demonstrating superiority of volume assist control over other modes in the management of ARDS are lacking at this time, but it is the mode used in the majority of major clinical trials in patients with ARDS and was the mode used in the ARMA trial, which, as noted above, showed a clear mortality benefit. PCV : Variable flow, so more comfortable if dyssynchrony, prolong i time for oxygenation, control peak pressures vitrag24-www.medicalgeek.com
  63. 63. vitrag24-www.medicalgeek.com
  64. 64. NEUROMUSCULAR BLOCKERS  Administration of short-term (up to 48 hours) neuromuscular blockade to patients with ARDS who have severe gas exchange abnormalities (eg, PaO 2 /FiO 2 ≤120 mmHg) is probably safe and potentially beneficial.  Improvements in patient–ventilator synchrony and elimination of muscle activity and the associated oxygen consumption,  Papazian L, Forel JM, Gacouin A, et al. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med 2010; 363:1107. vitrag24-www.medicalgeek.com
  65. 65. REFRACTORY HYPOXEMIA  Following modalities are used for Refractory Hypoxemia apart from N-M Blockers, High PEEP & other recruitment maneuvers  Prone Position  Other modes of ventilator  IRV  Inhaled Nitric Oxide  ECMO vitrag24-www.medicalgeek.com
  66. 66. Prone position:  In several trials, MV in the prone position improves oxygenation. Other purported benefits include improvements in secretion clearance, increased end-expiratory volume, and decreased mechanical compression of the lungs by the heart.  Switching from the supine to prone position can improve pulmonary gas exchange by diverting blood away from poorly aerated lung regions in the posterior thorax and increasing blood flow in aerated lung regions in the anterior thorax.  The latest PROSEVA (Proning Severe ARDS Patients) trial confirmed these benefits in a formal randomized study. The bulk of data indicates that in severe acute respiratory distress syndrome, carefully performed prone positioning offers an absolute survival advantage of 10–17%, making this intervention highly recommended in this specific population subset.  Can be hazardous, leading to accidental endotracheal extubation, loss of central venous catheters, and orthopedic injury, pressure sores etc. vitrag24-www.medicalgeek.com
  67. 67. POSSIBLE MECHANISMS  Recruitment of dependent lung zones,  Increased functional residual capacity (FRC)  Improved diaphragmatic excursion  Increased cardiac output  Improved ventilation-perfusion matching  Relief of compression of the lung by the heart and Mediastinal structures vitrag24-www.medicalgeek.com
  68. 68. OTHER MODES OF MV :  AIRWAY PRESSURE RELEASE VENTILATION (APRV):  Another “open lung” approach  It is a pressure control mode with spoteneous breaths; CPAP released periodicaly.  Two CPAP levels Higher CPAP is baseline pressure  Intermittent, brief release of Paw from higher CPAP level to lower CPAP level  Decrease in Paw augments TV  Spontaneous breathing at both upper & lower CPAP  Available on few ventilators  Like BiPAP/BiLevel but time at the lower pressure (“release time”) is usually short  0.6-1sec vitrag24-www.medicalgeek.com
  69. 69. APRV Airway Pressure Release Ventilation From Mosby’s R. C. Equip. 6th ed. 1999. vitrag24-www.medicalgeek.com
  70. 70. Inverse ratio ventilation (IRV)  Oxygenation can also be improved by increasing mean airway pressure with "inverse ratio ventilation."  The inspiratory (I) time is lengthened so that it is longer than the expiratory (E) time (I:E ratio as high as 7:1 have been used).  When the inspiratory time is increased, there is an obligatory decrease in the expiratory time. This can lead to air trapping, auto-PEEP, barotrauma, hemodynamic instability, and decreased oxygen delivery.  ↓ FIO2 to 0.60 to avoid possible oxygen toxicity,  But no mortality benefit in ARDS has been demonstrated. vitrag24-www.medicalgeek.com
  71. 71. o There are potential side effects associated with prolonging the inspiratory time that should be considered. o In addition, a prolonged inspiratory time may require significant sedation or neuromuscular blockage, particulary if the inspiratory time surpasses the expiratory time. vitrag24-www.medicalgeek.com
  72. 72.  High-frequency ventilation (HFV) –  High frequency oscillatory ventilation (HFOV) delivers small tidal volumes (1–2 mL/kg) using rapid pressure oscillations (300 cycles/min). The small tidal volumes limit the risk of volutrauma, and the rapid pressure oscillations create a mean airway pressure that prevents small airway collapse and limits the risk of atelectrauma.  HFOV requires a specialized ventilator  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 no survival benefit. vitrag24-www.medicalgeek.com
  73. 73. INHALED NITRIC OXIDE  Inhaled nitric oxide (5–10 ppm) is a selective pulmonary vasodilator that can improve arterial oxygenation in ARDS by increasing flow to areas of high dead space ventilation. iNO flows only into well ventilated areas, so improves shunt.  However, the increase in arterial oxygenation is temporary (1–4 days), and there is no associated survival benefit  Adverse effects of inhaled nitric oxide include methemoglobinemia (usually mild) and renal dysfunction. vitrag24-www.medicalgeek.com
  74. 74. EXTRA CORPOREAL MEMBRANE OXYGENATION:-  Extracorporeal membrane oxygenation (ECMO) is the use of a modified heart–lung machine to provide respiratory, circulatory, or both support at the bedside, usually for at least a number of days or even weeks.  Extracorporeal membrane oxygenation (ECMO) uses technology derived from cardiopulmonary bypass (CPB) that allows gas exchange outside the body. In addition, circulatory support can also be provided.  ECMO is a valuable option for the management of severe but reversible causes of respiratory failure or cardiogenic shock refractory to conventional treatment.  Veno-venous ECMO is designed to provide gas exchange, while veno-arterial ECMO provides both gas exchange and haemodynamic support.  Acute respiratory distress syndrome associated with pneumonia (viral or bacterial) is the most common cause of refractory hypoxemia that requires ECMO support. vitrag24-www.medicalgeek.com
  75. 75. vitrag24-www.medicalgeek.com
  76. 76. vitrag24-www.medicalgeek.com
  77. 77. NON-VENTILATORY MANAGEMENT  Fluid management  Diuretics  Steroids  Blood Transfusion cut-off  Choice of Inotropic agent vitrag24-www.medicalgeek.com
  78. 78. Fluids management:  Patients with ARDS should receive intravenous fluids only sufficient to achieve an adequate cardiac output, tissue oxygen delivery, and organ function, as assessed by urine output, acid-base status, and arterial pressure.  Once the patient is beyond the early, resuscitative phase of their illness, efforts should be made to decrease the amount of volume administered and maintain an even balance between the volume of fluid administered to and eliminated from the patient, referred to as “euvolemia”. The benefits of this approach were demonstrated in the Fluid and Catheter Treatment Trial (FACTT) .There were no differences in 60-day mortality between the two groups, but the conservative approach was associated with improved gas exchange and shorter duration of mechanical ventilation without increasing the incidence of acute kidney injury or other non- pulmonary organ failures.  Goal: MAP ≥ 65mmHg, avoid hypoperfusion vitrag24-www.medicalgeek.com
  79. 79.  Fluid management in ARDS is usually aimed at reducing extravascular lung water with diuretics. While this approach has shown modest benefits in clinical measures like lung compliance, gas exchange, and length of time on the ventilator, but little survival benefit.  The first problem with the use of diuretic therapy in ARDS is the nature of the lung infiltration. While diuretics can remove the watery edema fluid that forms as a consequence of heart failure, the lung infiltration in ARDS is an inflammatory process, and diuretics don't reduce inflammation.  Diuretic therapy can be tailored to achieve the lowest cardiac filling pressures that do not compromise cardiac output and systemic oxygen transport. ROLE OF DIURETICS vitrag24-www.medicalgeek.com
  80. 80.  The golden rule is that hydrostatic pressures should be kept as low as possible, provided that oxygen delivery to the tissues is not compromised .  As techniques to monitor the regional circulation become available, titration of fluid requirements will become more precise.  There is no place for systematic fluid restriction and diuretics to eliminate edema, as the function of other tissues may deteriorate with inadequate perfusion. vitrag24-www.medicalgeek.com
  81. 81. ROLE OF STEROIDS IN UNRESOLVING ARDS Because of apparent benefit in small trials, it was thought that there might be a role for high-dose corticosteroid therapy in patients with late (fibroproliferative phase) ARDS. However, an ARDS Study Network trial of methylprednisolone for patients with ARDS persisting for at least 7 days demonstrated no benefit in terms of 60-day mortality.Patients treated later in the course of ARDS, 14 days after onset, had worsened mortality with corticosteroid therapy. The benefit of steroids in ARDS may be explained by the ability of steroids to promote collagen breakdown and inhibit fibrosis One of the successful regimens involved methylprednisolone in a dose of 1-2 mg/kg/day. vitrag24-www.medicalgeek.com
  82. 82. 1.Steinberg KP, Hudson LD, Goodman RB, et al found that in the subgroup of patients randomized 7 to 13 days after the onset of ARDS, methylprednisolone caused a non-statistically significant reduction in 60-day mortality (27 versus 36 percent) and 180-day mortality (27 versus 39 percent). In contrast, among patients randomized more than 14 days after the onset of ARDS, methylprednisolone increased 60-day mortality (35 versus 8 percent) and 180- day mortality (44 versus 12 percent). Methylprednisolone increased ventilator-free days, shock-free days, oxygenation, lung compliance, and blood pressure, but also increased neuromuscular weakness. 2. In a double-blind trial, patients with early ARDS (defined as ≤72 hours), Meduri GU, Golden E, Freire AX, et al found that glucocorticoid therapy reduced the duration of mechanical ventilation, length of ICU stay, and ICU mortality (21 versus 43 percent). vitrag24-www.medicalgeek.com
  83. 83. HEMOGLOBIN  Transfusion is often recommended to keep the Hb above 10 g/dL, but this practice has no scientific basis or documented benefit, even in ventilator- dependent patients.  Considering that blood transfusions can cause ARDS, it is wise to avoid transfusing blood products in patients with ARDS AND threshold should be 7 g/dL.  If there is no evidence of tissue dysoxia or impending dysoxia (e.g., an oxygen extraction ratio >50%), there is no need to correct anemia with blood transfusions. vitrag24-www.medicalgeek.com
  84. 84. INOTROPIC AGENT  Cardiac output may be augmented by raising filling pressures if they are low (if pulmonary edema is not exacerbated) or by using inotropic agents. However, raising oxygen delivery to supernormal levels is not clinically useful and may be harmful in some circumstances.  If volume infusion is not indicated, dobutamine is preferred over vasodilators for augmenting the cardiac output because vasodilators will increase intrapulmonary shunt and will add to the gas exchange abnormality in ARDS. Dopamine should be avoided in ARDS because it constricts pulmonary veins, and this will cause an exaggerated rise in the pulmonary capillary hydrostatic pressure. vitrag24-www.medicalgeek.com
  85. 85. OTHER DRUG THERAPY – UNPROVEN BENIFIT INHALED VASODILATORS : PGE1 (pulmonary vasodilatation and anti-inflammatory effects on neutrophils/macrophages) , Aerosolized PGI2 (selective pulmonary vasodilatation of ventilated lung areas), NO GM-CSF Almitrine (selective pulmonary vasoconstrictor of nonventilated lung areas) Surfactant (prevents alveolar collapse and protects against intrapulmonary injury and infection) Antioxidants - dietary oil supplementation – Omega-3 fatty acid, N-acetylcysteine (protect the lung from free oxygen radical production) Anti-inflammatory drugs (Lisofylline, Ibuprofen, ketoconazole, Statin) No recommendation can be made for their use - Rescue modality in the patient with refractory hypoxia? vitrag24-www.medicalgeek.com
  86. 86. Mortality:  Recent mortality estimates for ARDS range from 26 to 58% with substantial variability.  The underlying cause of the ARDS is the most common cause of death among patients who die early. In contrast, nosocomial pneumonia and sepsis are the most common causes of death among patients who die later in their clinical course . Patients uncommonly die from respiratory failure.  Thus, improvement in survival is likely secondary to advances in the care of septic/infected patients and those with multiple organ failure. vitrag24-www.medicalgeek.com
  87. 87. Functional Recovery in ARDS Survivors o ARDS pts experience prolonged respiratory failure and remain dependent on mechanical ventilation for survival. o Patients usually recover their max lung function within 6 mnths. o One year after endotracheal extubation, over a 1/3 of ARDS survivors have normal spirometry values and diffusion capacity. o Most of the remaining patients have only mild abnormalities in their pulmonary function. vitrag24-www.medicalgeek.com
  88. 88.  Recovery of lung function is strongly associated with the extent of lung injury in early ARDS  When caring for ARDS survivors it is important to be aware of the burden of emotional and respiratory symptoms.  There are significant rates of depression and posttraumatic stress disorder in ARDS survivors vitrag24-www.medicalgeek.com
  89. 89. FUTURE DIRECTIONS:  With the high mortality rates associated with ARDS and sepsis, the search continues to identify targets.  Effective anti-sepsis interventions may reduce the incidence of ARDS and improve outcomes from it.  1) Antibodies against macrophage migration inhibitory factor (MIF),  2) Antibodies against high-mobility group B-1 protein (HMGB1),  3.) Stem cell therapy (MSC) vitrag24-www.medicalgeek.com
  90. 90. ROLE OF STEM CELLS – PHASE-I CLINICAL TRAIL GOING ON  Stem cells constitute a promising therapeutic strategy for patients suffering from ALI/ARDS.  MSCs appear closest to clinical translation, given the evidence that they may favourably modulate the immune response to reduce lung injury, while maintaining host immune-competence and also facilitating lung regeneration and repair.  However, gaps remain in our knowledge regarding the mechanisms of action of MSCs, the optimal MSC administration and dosage regimens, and the safety of MSCs in critically ill patients. It is anticipated that these remaining knowledge deficits will be addressed in ongoing and future studies.  Other stem cells, such as ESCs and iPCs, are at an earlier stage in the translational process, but offer the hope of directly replacing injured lung tissue.  Ultimately, lung-derived stem cells may offer the greatest hope for lung diseases, given their role in replacing and repairing the native damaged lung tissues. vitrag24-www.medicalgeek.com
  91. 91.  JAMA, June 20, 2012—Vol 307, No. 23 : Berlin Definition  Harrison‘s Principles Of Internal Medicine 19th Edition  The ICU Book, 3rd Edition - Paul L. Marino  UpToDate : www.uptodate.com  eMedicine : www.medscape.com  Mechanical ventilation 3rd Edition - David W Chang  Susen Pilbeam Text Book Of Mechanical Ventiltor  Human Mesenchymal Stem Cells For Acute Respiratory Distress Syndrome (START)Clinicaltrial : http://clinicaltrials.gov/show/NCT01775774  M, Luks Andrew. 2013. "Ventilatory strategies and supportive care in acute respiratory distress syndrome." Influenza and other respiratory viruses 7 Suppl 3: 8-17. doi:10.1111/irv.12178.  Carl F. Haas, MLS, RRT “Mechanical Ventilation with Lung Protective Strategies: What Works?” Crit Care Clin 27 (2011) 469–486 vitrag24-www.medicalgeek.com
  92. 92. QUESTIONS…….? vitrag24-www.medicalgeek.com
  93. 93. THANK YOU THANK YOU vitrag24-www.medicalgeek.com

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