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Dr. Akif A.B
 It is a clinical syndrome of severe dyspnea of rapid
onset, hypoxemia and diffuse pulmonary
infiltrates leading to respiratory failure.
 Non cardiogenic pulmonary edema.
 Diagnosis of ARDS is based on fulfilling 3 criteria:
 Acute onset (within 1 week)
 Bilateral opacities on chest x-ray
 PaO₂/FiO₂ (arterial to inspired oxygen) ratio of ≤300 on
positive end-expiratory pressure (PEEP) or continuous
positive airway pressure (CPAP) ≥5 cm H₂O
 Exudative phase
 Proliferative phase
 Fibrotic phase
 Alveolar capillary endothelial cells and Type 1
Pneumocytes (Alveolar epithelial membrane) gets
damaged.
 Edema fluid rich in protein accumulates in alveolar
and interstitial space (Mainly in dependent areas)
 Cytokines like IL-1, 8 and TNF-α gets activated
 Leucocytes accumulates at alveolar space
 Dysfunctional surfactant cell leads to formation of Hyaline
membrane
 Decreased gas exchange
 Dyspnea
 Hyperventilation
 Respiratory fatigue
 Respiratory Failure
 7-21 days
 With intervention (mechanical ventilation) there
is clearance of alveolar fluid
 Soluble proteins are removed by diffusion
between alveolar epithelial cells
 Insoluble proteins are removed by endocytosis
and transcytosis through epithelial cells and
phagocytosis through macrophages
 Type II cells begin to differentiate into Type I cells
and reepithelialize denuded alveolar epithelium
 Further epithelialization leads to increased
alveolar clearance
 Many patients of ARDS recover in 3-4weeks
 Few patients develop fibrosis of alveoli and interstitial
space
 Thus requiring long term ventialtion or oxygen
therapy.
 Chest X-ray : Diffuse Bilateral infiltrates
 CXR is 100% sensitive.
 Specificity is poor
 because other conditions may cause bilateral
pulmonary infiltrates, including
 cardiogenic pulmonary oedema
 diffuse alveolar haemorrhage.
 Arterial Blood Gas (ABG)
 A PaO₂/FiO₂ (inspired oxygen) ratio of ≤300 on
positive end expiratory pressure (PEEP) or continuous
positive airway pressure (CPAP) ≥5 cm H₂O is part of
the diagnostic criteria for ARDS
 Sputum, Blood, Urine culture : To look for
underlying infection
 Amylase and Lipase : To rule out Acute pancreatitis
 Beta Natriuretric Peptide (BNP)
 BNP levels <100 nanograms/L (<100 picograms/mL)
 Rules out Heart failure and thus Cardiogenic Pulmonary
edema
 2D-Echo
 Helps in ruling out cardiogenic pulmonary edema
 Pulmonary artery Wedge pressure
 <18mmHg
 Bronchioalveolar Lavage or CT scan of thorax
 To look for pulmonary causes of ARDS
 Oxygenation and Ventilation
 Prone positioning
 Intravenous fluids
 Antimicrobials + identification and treatment of
source of infection
 Supportive care
 Oxygen saturation should be maintained between
88% and 95%, which usually requires mechanical
ventilation with titration of inspired oxygen (FiO₂)
 Occasionally patients can be managed with non-
invasive ventilation, but the failure rate is high and
the majority will require endotracheal intubation.
 Ventilator-associated lung injury may be limited by
the use of a low tidal volume.
 normal volume of air displaced between normal
inhalation and exhalation when extra effort is not
applied.
 In a healthy, young human adult,tidal volume is
approximately 500 mL per inspiration or 7 mL/kg of
body mass.
 Positive end-expiratory pressure (PEEP) is the
pressure in the lungs (alveolar pressure)
above atmospheric pressure (the pressure outside of
the body) that exists at the end of expiration.
 The two types of PEEP are:
 Extrinsic PEEP (PEEP applied by a ventilator)
 Intrinsic PEEP (PEEP caused by an incomplete
exhalation).
 Fraction of inspired oxygen (FiO2) is the fraction of oxygen in
the volume of air being measured.
 Medical patients experiencing difficulty breathing are provided
with oxygen-enriched air, which means a higher-than-
atmospheric FiO2.
 Natural air includes 21% oxygen, which is equivalent to FiO2 of
0.21.
 Oxygen-enriched air has a higher FiO2 than 0.21; up to 1.00
which means 100% oxygen.
 FiO2 is typically maintained below 0.5 even with mechanical
ventilation, to avoid oxygen toxicity.
 Respiratory acidosis, which is a common complication
of low tidal volume ventilation, is treated by increasing
the respiratory rate.
 Prone positioning can improve oxygenation in patients
with ARDS and has been shown to reduce mortality in
patients with severe ARDS (PaO₂/FiO₂ <150).
 Complications of prone positioning, includes :
 facial oedema, pressure sores, and dislodgement of
catheters and endotracheal tubes,
 prone positioning should only be considered in patients
with severe ARDS (PaO₂/FiO₂ <150).
 The patient's fluid balance should be maintained as
slightly negative or neutral (providing the patient is
not in shock).
 A central line is recommended to measure the central
venous pressure (CVP), with regular assessments of
fluid status.
 The goal is to keep the CVP <4 cm H₂O.
 In patients who have an infectious cause for ARDS
(e.g., pneumonia or sepsis), the prompt initiation of
antimicrobials is important.
 Empirical antibiotics targeted at the suspected
underlying infection should be used as soon as
possible after obtaining appropriate cultures including
blood, sputum, and urine cultures.
 Once culture results are available, the antimicrobial
regimen can be tailored for the identified organism.
 Prevention of deep vein thrombosis
 Blood glucose control
 Prophylaxis against stress-induced gastrointestinal
Bleeding
 Haemodynamic support to maintain a mean arterial
pressure >60 mmHg
 Transfusion of packed red blood cells in patients with
Hb <70 g/L (<7 g/dL).
 Nutrition should be provided enterally where possible.
 Inhaled or intravenous beta-adrenergic agonists to
promote alveolar fluid clearance and resolution of
pulmonary oedema are not recommended.
 Neither early nor late administration of corticosteroids
has been shown to improve mortality in patients with
ARDS, and their routine use is not recommended.
ARDS

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ARDS

  • 2.  It is a clinical syndrome of severe dyspnea of rapid onset, hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure.  Non cardiogenic pulmonary edema.
  • 3.  Diagnosis of ARDS is based on fulfilling 3 criteria:  Acute onset (within 1 week)  Bilateral opacities on chest x-ray  PaO₂/FiO₂ (arterial to inspired oxygen) ratio of ≤300 on positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H₂O
  • 4.
  • 5.
  • 6.  Exudative phase  Proliferative phase  Fibrotic phase
  • 7.
  • 8.  Alveolar capillary endothelial cells and Type 1 Pneumocytes (Alveolar epithelial membrane) gets damaged.  Edema fluid rich in protein accumulates in alveolar and interstitial space (Mainly in dependent areas)  Cytokines like IL-1, 8 and TNF-α gets activated  Leucocytes accumulates at alveolar space
  • 9.  Dysfunctional surfactant cell leads to formation of Hyaline membrane  Decreased gas exchange  Dyspnea  Hyperventilation  Respiratory fatigue  Respiratory Failure
  • 10.
  • 11.
  • 12.  7-21 days  With intervention (mechanical ventilation) there is clearance of alveolar fluid  Soluble proteins are removed by diffusion between alveolar epithelial cells  Insoluble proteins are removed by endocytosis and transcytosis through epithelial cells and phagocytosis through macrophages
  • 13.  Type II cells begin to differentiate into Type I cells and reepithelialize denuded alveolar epithelium  Further epithelialization leads to increased alveolar clearance
  • 14.  Many patients of ARDS recover in 3-4weeks  Few patients develop fibrosis of alveoli and interstitial space  Thus requiring long term ventialtion or oxygen therapy.
  • 15.  Chest X-ray : Diffuse Bilateral infiltrates  CXR is 100% sensitive.  Specificity is poor  because other conditions may cause bilateral pulmonary infiltrates, including  cardiogenic pulmonary oedema  diffuse alveolar haemorrhage.
  • 16.
  • 17.  Arterial Blood Gas (ABG)  A PaO₂/FiO₂ (inspired oxygen) ratio of ≤300 on positive end expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) ≥5 cm H₂O is part of the diagnostic criteria for ARDS  Sputum, Blood, Urine culture : To look for underlying infection  Amylase and Lipase : To rule out Acute pancreatitis
  • 18.  Beta Natriuretric Peptide (BNP)  BNP levels <100 nanograms/L (<100 picograms/mL)  Rules out Heart failure and thus Cardiogenic Pulmonary edema  2D-Echo  Helps in ruling out cardiogenic pulmonary edema  Pulmonary artery Wedge pressure  <18mmHg  Bronchioalveolar Lavage or CT scan of thorax  To look for pulmonary causes of ARDS
  • 19.  Oxygenation and Ventilation  Prone positioning  Intravenous fluids  Antimicrobials + identification and treatment of source of infection  Supportive care
  • 20.  Oxygen saturation should be maintained between 88% and 95%, which usually requires mechanical ventilation with titration of inspired oxygen (FiO₂)  Occasionally patients can be managed with non- invasive ventilation, but the failure rate is high and the majority will require endotracheal intubation.  Ventilator-associated lung injury may be limited by the use of a low tidal volume.
  • 21.  normal volume of air displaced between normal inhalation and exhalation when extra effort is not applied.  In a healthy, young human adult,tidal volume is approximately 500 mL per inspiration or 7 mL/kg of body mass.
  • 22.  Positive end-expiratory pressure (PEEP) is the pressure in the lungs (alveolar pressure) above atmospheric pressure (the pressure outside of the body) that exists at the end of expiration.  The two types of PEEP are:  Extrinsic PEEP (PEEP applied by a ventilator)  Intrinsic PEEP (PEEP caused by an incomplete exhalation).
  • 23.  Fraction of inspired oxygen (FiO2) is the fraction of oxygen in the volume of air being measured.  Medical patients experiencing difficulty breathing are provided with oxygen-enriched air, which means a higher-than- atmospheric FiO2.  Natural air includes 21% oxygen, which is equivalent to FiO2 of 0.21.  Oxygen-enriched air has a higher FiO2 than 0.21; up to 1.00 which means 100% oxygen.  FiO2 is typically maintained below 0.5 even with mechanical ventilation, to avoid oxygen toxicity.
  • 24.  Respiratory acidosis, which is a common complication of low tidal volume ventilation, is treated by increasing the respiratory rate.
  • 25.  Prone positioning can improve oxygenation in patients with ARDS and has been shown to reduce mortality in patients with severe ARDS (PaO₂/FiO₂ <150).  Complications of prone positioning, includes :  facial oedema, pressure sores, and dislodgement of catheters and endotracheal tubes,  prone positioning should only be considered in patients with severe ARDS (PaO₂/FiO₂ <150).
  • 26.  The patient's fluid balance should be maintained as slightly negative or neutral (providing the patient is not in shock).  A central line is recommended to measure the central venous pressure (CVP), with regular assessments of fluid status.  The goal is to keep the CVP <4 cm H₂O.
  • 27.  In patients who have an infectious cause for ARDS (e.g., pneumonia or sepsis), the prompt initiation of antimicrobials is important.  Empirical antibiotics targeted at the suspected underlying infection should be used as soon as possible after obtaining appropriate cultures including blood, sputum, and urine cultures.  Once culture results are available, the antimicrobial regimen can be tailored for the identified organism.
  • 28.  Prevention of deep vein thrombosis  Blood glucose control  Prophylaxis against stress-induced gastrointestinal Bleeding  Haemodynamic support to maintain a mean arterial pressure >60 mmHg  Transfusion of packed red blood cells in patients with Hb <70 g/L (<7 g/dL).
  • 29.  Nutrition should be provided enterally where possible.  Inhaled or intravenous beta-adrenergic agonists to promote alveolar fluid clearance and resolution of pulmonary oedema are not recommended.  Neither early nor late administration of corticosteroids has been shown to improve mortality in patients with ARDS, and their routine use is not recommended.