Acute respiratory distress syndrome

2. Ddx
• Cardiogenic pulmonary Edema
• ARDS
• Bilateral pneumonia
• Alveolar haemorrhage
• Acute interstitial lung diseases (e.g., acute interstitial pneumonitis)
• Acute immunologic injury (e.g., hypersensitivity Pneumonitis)
• Toxin injury (e.g., radiation pneumonitis)

3. ACUTE RESPIRATORY
DISTRESS SYNDROME
ARDS

4. What is ARDS?
• As per the Berlin definition:
1. Onset: Acute-Within 1 week of clinical insult or
new or worsening respiratory symptoms
2. Chest Imaging (Xray or CT): Bilateral opacities not fully
explained by effusions, lobar/lung collapse, or Nodules
3. Origin of Edema: Respiratory failure not fully explained by
cardiac failure or fluid overload with objective assessment
(eg: ECHO, BNP, Cardiac Catheterization) to exclude hydrostatic
edema if no risk factor is present.

5. What is ARDS?
4. Hypoxemia
• Mild: PaO2/FiO2 200-300
• Moderate: PaO2/FiO2 100-200
• Severe: PaO2/FiO2 ≤100
** with PEEP or CPAP ≥ 5cm H2O

6. Etiology
• Can be caused by both pulmonary and non pulmonary causes like:
• DIRECT LUNG INJURY INDIRECT LUNG INJURY
Pneumonia Sepsis
Aspiration of gastric contents Pancreatitis
Pulmonary contusion Multiple transfusions
Near-drowning Burns
Toxic inhalation injury Severe trauma
Fat embolism

7. Risk Factors
• There are a variety of risk factors, including
• Alcohol abuse
• Obesity
• Patients who present with Acute Physiology and
Chronic Health Evaluation (APACHE) scores > 16
• Increased use of transfusions
• Septic shock
• Chronic conditions like DM, HTN, Malignancy,
Immunocompromised states, CLD, CKD etc.

8. Pathogenesis

9. Pathogenesis
• 3 phases-Exudative, Proliferative, Fibrotic
• Exudative Phase:
• Diffuse Alveolar Damage/Capillary endothelial damage
• Type 1 Pneumocytes/Endothelial cells
• Loss of tight junctions
• Inflammatory mediators release
• Neutrophilic infiltration
• Leakage of protein rich fluid + Inflammatory cells leading to
• Edema and Hyaline membrane formation – Hallmark of ARDS

11. Pathogenesis
• Exudative Phase
• Alveolar edema mainly involves dependent portions
• Collapse of large segments of lung leading to intrapulmonary
shunting and hypoxemia
• To compensate, work of breathing increases leading to dypnoea
• There is a concurrent injury to pulmonary vasculature as well
• So, even in normal areas of lung, reduced arterial blood flow leads
to increased dead space and hypercapnia

12. Pathogenesis
• Proliferative Phase:
• First signs of resolution are often evident in this phase, with the
initiation of lung repair
• Organization of alveolar exudates, and a shift from neutrophil- to
lymphocyte-predominant pulmonary infiltrates.
• Type II pneumocytes proliferate
• Synthesize new pulmonary surfactant and differentiate into type I
pneumocytes.

13. Pathogenesis
• Fibrotic Phase:
• Not all patient progress to the fibrotic stage. Mechanism not well
understood.
• Alveolar edema and inflammatory exudates of earlier phases
convert to extensive alveolar-duct and interstitial fibrosis.
• Marked disruption of acinar architecture leads to emphysema-like
changes, with large bullae.
• Intimal fibroproliferation in the pulmonary microcirculation causes
progressive vascular occlusion and pulmonary hypertension.
• Consequently there is an increased risk of pneumothorax,
reduction in lung compliance, and increased pulmonary dead
space.

14. Timeline

15. Clinical Feature
• Dyspnea
• Cyanosis
• Diffuse crepitations
• Tachypnea
• Tachycardia
• Use of Acc. Muscles of respiration
• ABG-Hypoxemia, Increased A-a O2 gradient

16. Treatment
• Main focus is on treating the underlying pathology with supportive
management which requires:
• Maintaining the Airway
• Oxygenation
• Supporting hemodynamic function.
• The five P's of supportive therapy include
• Protective lung ventilation,
• Perfusion,
• Positioning,
• Preventing complications
• Protocol weaning

18. Stepwise management principles
• Strategies to avoid invasive ventilation
• Lung protective invasive ventilation
• Rescue strategies for hypoxia:
• Recruitment Manouvers
• Prone positioning
• HFOV/APRV
• ECMO
• Inhaled NO/Prostaglandins

19. Advantages of HFNC
• Hgiher Fio2 delivery (21%-100%)
• Reduction in anatomical dead space
• Reduces work of breathing
• PEEP generation which causes recruitment
• Delivery of warmed and humidified gases

20. Predictors of HFNC failure
• ROX index=
𝑆𝑝𝑜2
𝐹𝑖𝑂2
𝑅𝑒𝑠𝑝𝑖𝑟𝑎𝑡𝑜𝑟𝑦 𝑅𝑎𝑡𝑒
• Essentially if Spo2 is falling OR Higher FiO2 is needed or Patient’s RR is
increasing s/o NIV failure
• HFNC (after 2 hrs)=ROX index <2.85
• HFNC (after 6 hrs or 12 hrs)=ROX index <3.85

22. HFNC Failed … Now What?

23. NIV (BiPAP/CPAP)
• HACOR SCORE
• Bedside predictor of NIV failure
• HACOR Score>5 after 1 hr of NIV = 80% failure of NIV regardless of
disease severity, Diagnosis, Age.

25. Why so many predictors for
NIV are being used?
Can’t we just wait and watch?

26. No

27. Why not?
Late intubation and late use of mechanical ventilation is associated
with increased mortality!

29. Why the need for mechanical ventilation?
• Most patients of ARDS require mechanical ventilation as they
frequently become fatigued from increased work of breathing and
progressive hypoxemia, requiring mechanical ventilation for support.

30. Mechanical Ventilation-A double edged sword
• Can lead to Ventilator -Induced Lung Injury Despite its lifesaving
potential
• Arises from three principal mechanisms (explain):
• Volutrauma
• Atelectrauma
• Biotrauma-High FiO2>65% aggravates Alveolar damage due to oxygen
toxicity

31. Solution?
• LUNG PROTECTIVE VENTILATION aka Low VT ventilation (4 to 8 mL/Kg of
PBW. Usually 6 mL/kg of predicted body weight)
• PBW=50 or 45.5 + 2.3*(ht in inches – 60)
• Plateau pressure ≤30 cm H2O
• FiO2 target <65%
• Provide PEEP(Low vs High->12cm H2O)
• Find the best PEEP by titrate with respect to PaO2, FiO2
• Aim is to prevent alveolar collapse and also prevent over distention
• PEEP<<CPAP
• Permissive Hypercapnia (Increase RR, Bicarb)
• SpO2 target =85 to 90%

32. Step by step ventilator management
PART I: VENTILATOR SETUP AND ADJUSTMENT
1. Calculate predicted body weight (PBW)
2. Select any ventilator mode as per clinical discretion
3. Set ventilator settings to achieve initial VT = 8 ml/kg PBW
4. Reduce VT by 1 ml/kg at intervals ≤ 2 hours until VT = 6ml/kg PBW.
5. Set initial rate to approximate baseline minute ventilation
(not > 35 bpm).
6. Adjust VT and RR to achieve pH, oxygenation and plateau pressure
goals as mentioned.

33. Step by step ventilator management
• OXYGENATION GOAL: PaO2 55-80 mmHg or SpO2 88-95%
• Use a minimum PEEP of 5 cm H2O. Consider use of incremental
FiO2/PEEP combinations such as shown below (not required) to
achieve goal.

34. Step by step ventilator management
PLATEAU PRESSURE GOAL: ≤ 30 cm H2O
Check Pplat (0.5 second inspiratory pause), at least q 4h and after each
change in PEEP or VT.
• If Pplat > 30 cm H2O: decrease VT by 1ml/kg steps (minimum = 4
ml/kg).
• If Pplat < 25 cm H2O and VT< 6 ml/kg, increase VT by 1 ml/kg until
• Pplat > 25 cm H2O or VT = 6 ml/kg.
• If Pplat < 30 and dys-synchrony occurs: may increase VT in 1ml/kg
increments to 7 or 8 ml/kg if Pplat remains < 30 cm H2O.

35. Step by step ventilator management
pH GOAL: 7.30-7.45
Acidosis Management: (pH < 7.30)
• If pH 7.15-7.30: Increase RR until pH > 7.30 or PaCO2 < 25 (Max. set
RR = 35).
• If pH < 7.15: Increase RR to 35.
• If pH remains < 7.15, VT may be increased in 1 ml/kg steps until pH >
7.15 (Pplat target of 30 may be exceeded).
• May give NaHCO3
• Alkalosis Management: (pH > 7.45) Decrease vent rate if possible.

36. When to wean?

37. Weaning
Conduct a SPONTANEOUS BREATHING TRIAL daily when:
1. FiO2 ≤ 0.40 and PEEP ≤ 8 OR FiO2 < 0.50 and PEEP < 5.
2. PEEP and FiO2 ≤ values of previous day.
3. Patient has acceptable spontaneous breathing efforts. (May
decrease vent rate by 50% for 5 minutes to detect effort.)
4. Systolic BP ≥ 90 mmHg without vasopressor support.
5. No neuromuscular blocking agents or blockade.

38. Weaning proper
If all above criteria are met and subject has been in the study for at
least 12 hours, initiate a trial of UP TO 120 minutes of spontaneous
breathing with FiO2 < 0.5 and PEEP < 5:
1. Place on T-piece, trach collar, or CPAP ≤ 5 cm H2O with PS < 5
2. Assess for tolerance as below for up to two hours.
a. SpO2 ≥ 90: and/or PaO2 ≥ 60 mmHg
b. Spontaneous VT ≥ 4 ml/kg PBW
c. RR ≤ 35/min
d. pH ≥ 7.3
e. No respiratory distress (distress= 2 or more of the following)

39. Weaning proper
Feature of respiratory distress:
a) HR > 120% of baseline
b) Marked accessory muscle use
c) Abdominal paradox
d) Diaphoresis
e) Marked dyspnea
3. If tolerated for at least 30 minutes, consider extubation.
4. If not tolerated resume pre-weaning settings.
5.?? NIV

40. Other approaches

41. Other approaches
• Prone Positioning: Reduces ventral to dorsal trans pulmonary
pressure difference. Improves recruitment of dependent lung zones
And also improves VP mismatch.
• Should be done for > 12 hrs a day
• Inverse ratio ventilation- I:E ratio (Upto 7:1) and lower peak
pressures
• High frequency Oscillatory Ventilation: Low Tidal Volumes (1-2
ml/Kg) are given at higher RR. These reduce distention and prevent
VALI.
• Airway Pressure Release Ventilation: Long Duration-High Pressure
followed by Short Duration and Lower Pressure.

42. Other approaches
• ECMO
• Recruitment maneuvers that transiently increase PEEP to high levels
to “recruit” atelectatic lung can increase oxygenation.

43. Fluid Management-2 Approaches
• 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.
• Non pulmonary cause of ARDS on the other hand usually benefit from
a fluid liberal approach.

44. Other pharmacotherapies
1. NEUROMUSCULAR BLOCKADE
• In severe ARDS, sedation alone can be inadequate for the patient-
ventilator synchrony required for lung-protective ventilation.
• Early administration of neuromuscular blockade if needed to facilitate
mechanical ventilation in severe ARDS improves survival and reduces
ICU stay.
2. Inhaled pulmonary vasodialators (NO, inhaled prostacyclins-
epoprostenol)
• Increase oxygenation
• No mortality benefit
• Not a part of guidlines

45. Other pharmacotherapies
3. Antibiotics
? Benefit
-Beta 2 agonists
-Sivelestat: Neutrophil elastase inhibitor
-Simvastatin

46. Glucocorticoids
• Anti inflammatory action
• Recent evidence has shown improved mortality, better outcomes in
patients with moderate and severe ARDS
• Usual doses:
• Moderate ARDS-0.5 to 1 mg/kg for 5 to 10 days
• Severe ARDS-1 to 2 mg/kg for 5 to 10 days
• Yet to be formally incorporated in guidelines

47. Prognostic Markers
1. Severity as per Berlin definition
2. Delta P = P Plateau - PEEP

48. Thank You

49. Fluid Management guidelines