Seminar on Anaesthesia for ARDS

1. ARDS-
Etiology, Clinical Features
and Anaesthetic Management
Presented by:-
Dr SANDEEP SINGH JADON
G. R. MEDICAL COLLEGE GWALIOR MP

2. INTRODUCTION
FIG 1 :Anatomy of Respiratory System

3. Introduction cont..
Fig 2 : Showing Alveoli Structure

4. ARDS
It is characterized by a severe inflammatory process causing diffuse alveolar damage that
results in
• Sudden and progressive pulmonary edema
• Increasing bilateral infiltrates on chest x-ray
• Hypoxemia unresponsive to oxygen supplementation regardless of the amount of PEEP
and
• The absence of an elevated left atrial pressure
• Patients often demonstrate reduced lung compliance

5. Berlin definition of mild, moderate and
severe acute respiratory distress syndrome
(ARDS)
CLINICAL
VARIABLE
MILD ARDS MODERATE ARDS SEVERE ARDS
Onset within 1 week of clinical insult known
to result in ARDS
Same same
Hypoxemia Pa02/fio2 ≤300mmHg – 201mmHg
PEEP or CPAP ≥5cm of H20
Pao2/Fio2 ≤200mmHg –
101 mmHg
PEEP ≥5cm H20
PaO2/Fio2 ≤100mm Hg
PEEP≥ 5cm H20
Chest radiograph Bilateral opacity not explained by
effusion, atelectasis or nodule
Same Same
Non cardiac
etiology
Respiratory failure not fully explained
by cardiogenic pulmonary edema .
Exclude hydrostatic edema if no
clinical risk factor explained.
Same Same

6. ARDS cont…
> Acute respiratory distress syndrome (ARDS) is a life threatening form of respiratory
failure that clinically manifests as marked hypoxemia and respiratory distress.
> Progression to respiratory failure leads to invasive mechanical ventilation in the intensive
care unit.
> ARDS accounts for ~ 10% of admissions to intensive care unit (ICU) and 23% of
ventilated patients, with mortality up to 45% in the severe category.
> Moreover survivors require prolonged rehabilitation till full recovery.

7. Etiology of ARDS
o The most common cause of ARDS is sepsis.
Other causes of ARDS
o 30% of cases of ARDS were due to pneumonia
oGastrointestinal disease (25%)
o Polytrauma (12%)

8. Direct pulmonary injury
-Pneumonia
-Gastric aspiration
-Drowning
-Severe thoracic trauma/pulmonary
contusion
-Smoke and toxic gas inhalation
-Fat emboli
-Reperfusion pulmonary edema(after lung
transplantation)
Indirect (extra pulmonary) lung injury
-Severe sepsis
-Multiple transfusion(TRALI)
-Shock
-Pancreatitis
-Drug overdose(opiates, paraldehyde,paraquate)
-Severe non thoracic trauma
-Disseminated intravascular coagulation
Etiology cont..

9. Factors affecting Risk of ARDS
• Chronic alcohol abuse
• Hypoproteinemia
• Advanced age
• Increased severity and extent of injury or illness as measured by injury severity
score(ISS) or APACHE score
• Hypertransfusion of blood products
• Cigarette smoking

10. Pathophysiology

11. Pathology cont..
⮚ARDS is a consequence of an alveolar injury which produces diffuse alveolar damage. The
injury causes the release of pro inflammatory “cytokines.”
⮚Cytokines recruit neutrophils to the lungs, where they become activated and release toxic
mediators (e.g., reactive oxygen species and proteases) that damage the capillary
endothelium and alveolar epithelium.
⮚ Damage to the capillary endothelium and alveolar epithelium allows protein to escape
from the vascular space.

12. Fig : showing mechanism of fluid exchange across the alveoli
Pathology cont…

13. ⮚In normal healthy lungs there is small amount of fluid that leaks into the interstitium. The
lymphatic system removes this fluid and returns it into the circulation keeping the alveoli
dry.
⮚Healthy lungs regulate the movement of fluid to maintain a small amount of interstitial
fluid and dry alveoli.
⮚The oncotic gradient that favors resorption of fluid is lost and pours into the interstitium,
overwhelming the lymphatic system.
⮚Lung injury interrupts this balance causing excess fluid in both the interstitium and alveoli.
⮚Results of the excess fluid include impaired gas exchange , decreased compliance and
increased pulmonary arterial pressure.

14. Three distinct stages (or phases) of the syndrome including:
⮚ Exudative stage
⮚ Proliferative (or fibroproliferative ) stage
⮚ Fibrotic stage
Acute phase of ARDS
pathology cont….

15. Exudative Stage (0-6 days)
Characterized by-
• Accumulation of excessive fluid in the lungs due to exudation and acute injury.
• Hypoxemia is usually most severe during this phase of acute injury, as is injury to the
endothelium (lining membrane) and epithelium (surface layer of cells).
• Some individuals quickly recover from his first stage; many others progress after about a
week into the second stage.

16. Proliferative stage (7-10 days)
• Connective tissue and other structural elements in the lungs proliferate in response to the
initial injury, including development of fibroblasts.
• The terms “stiff lung “ and “shock lung” frequently used to characterize this stage.
• Abnormally enlarged air spaces and fibrotic tissue (scarring) and increasingly apparent.

17. Fibrotic Stage( >10-14 days)
• Inflammation resolves.
• Oxygenation improves and extubation becomes possible.
• Lung function may continue to improve for as long as 6 to 12 months after onset of
respiratory failure, depending on the precipitating condition and severity of the initial
injury.
• Varying levels of pulmonary fibrotic changes are possible.

18. - The epidemic of coronavirus disease 2019 (COVID-19) caused by Severe Acute Respiratory
Syndrome-Coronavirus-2 (SARS-CoV-2) had rapidly progressed into a pandemic.
.
- Some patients rapidly progress to developing symptoms of severe dyspnea or hypoxemia,
associated with ARDS
.
- Risk factors associated with the development of ARDS and progression from ARDS to death
in COVID-19 pneumonia patients were found to be older age, neutrophilia and coagulation
dysfunction .
.
- Despite some distinct differences between COVID-19-associated ARDS and classical ARDS
as defined by Berlin criteria, general treatment principles, such as lung-protective ventilation
and rehabilitation concepts have been applied in the same way.
ARDS in Covid 19

19. Relationship between SpO2 and PaO2

20. Clinical presentation of ARDS
Early signs and symptoms of ARDS
⮚Restlessness and dyspnoea
⮚Low BP
⮚Confusion , mood swing, disorientation
⮚Cough and fever in pneumonia causing ARDS

21. Late signs and symptoms of ARDS-
⮚ Severe difficulty in breathing i.e laboured, rapid breathing
⮚ Tachycardia and cyanosis
⮚ Thick frothy sputum
⮚ Metabolic acidosis
⮚ Abnormal breath sounds like crackles on auscultation
⮚ On ABG, decreased PaCO2 with respiratory alkalosis and decreased Pao2
Because cardiogenic pulmonary edema must be extinguished from ARDS , we must carefully look
for signs of congestive heart failure or intravascular volume overload, including jugular venous
distention, cardiac murmurs and gallops, hepatomegaly and edema.

22. Approach to clinical diagnosis
⮚Chest radiograph- diffuse, bilateral alveolar infiltrates consistent with pulmonary edema.
⮚Early in the course of the disorder, the infiltrates associated with ARDS may be variable:
mild or dense, interstitial or alveolar, patchy or confluent.
⮚Initially, the infiltrates may have a patchy peripheral distribution, but soon they progress to
diffuse bilateral involvement with ground glass changes or frank alveolar infiltrates.

23. Lung imaging in ARDS
X-ray Image in ARDS CT Image in ARDS

24. Chest Radiograph
⮚Cardiogenic edema: increased heart size, increased width of the vascular pedicle,
vascular redistribution towards upper lobes, the presence of septal lines or a
perihilar (bat’s wing) distribution of the edema.
⮚Lack of these findings, in conjunction with patchy peripheral infiltrates that
extend to the lateral lung margins, suggest ARDS.

25. To exclude cardiogenic pulmonary edema:
⮚Echocardiogram- left ventricular ejection fraction, wall motion and valvular
abnormalities.
⮚Plasma B type natriuretic peptide (BNP)

26. OTHER INVESTIGATIONS
⮚Hematologic -leukopenia or leukocytosis, thrombocytopenia(DIC).
⮚Renal function test- Acute tubular necrosis
⮚Liver function test- hepatocellular injury or cholestasis.
⮚Von Willebrand factor(VWF) may be elevated in patients at risk for ARDS and may be
a marker of endothelial injury
⮚Cytokines-(IL)-1,IL-6 and IL 8 are elevated.

27. ⮚ Invasive Hemodynamic Monitoring- pulmonary artery wedge pressure(PCWP)
⮚ Bonchoalveolar Lavage- to rule in or rule out acute processes that may have
specific therapies.
Eg: acute eosinophilic pneumonia, diffuse alveolar hemorrhage.

28. MANAGEMENT
Respiratory Supportive
High flow oxygen
Evaluation for
inspiratory failure
Respiratory failure
Ventilatory support
Non invasive
ventilation
HFNC/CPAP/BIPAP
• Antibiotics for pneumonia and sepsis
• Intravascular volume resuscitation
• Inotropes, BT, Nutrition, Analgesia
Sedation
Stable
Monitor and continue on
going treatment
Mechanical ventilation /lung
protective strategy, low VT, high
PEEP
Failure of MV HFOV/ECMO

29. NON INVASIVE VENTILATION IN ARDS

30. 1) Mechanical ventilation
• Lung-protective mechanical ventilation is the cornerstone of ARDS therapy.
• The predominant goal is avoidance of ventilator-induced lung injury, that worsens inflammation
and is associated with worse outcomes in patients who are mechanically ventilated.
• Existing guidelines suggest consideration of higher levels of positive end-expiratory pressure in
patients with moderate-to-severe ARDS.
• Higher PEEP minimizes cyclical alveolar collapse and subsequent shearing injury to the lungs.
• However, excess positive end-expiratory pressure may also impair hemodynamics and lead to lung
overdistention.

31. Strategy for mechanical ventilation for ARDS
(Low Tidal Volume Ventilation)
Parameter Strategy
Low tidal volume 4-6ml/kg of predicted body weight
Plateau pressure <28cm H2O
Mean airway pressure <18-20cm H20
Driving pressure <15cm H2O
Positive End Expiratory Pressure(PEEP) Moderate ARDS<10cm H2O
Severe ARDS,10-15cm H2O
Fio2 <60%
Sedation with or without neuromuscular blockade Adequate
ET tube Cuffed
Suctioning Inline suctioning preferred to open suctioning to avoid
disconnection
Nutrition Enteral nutrition within 24 hour
Position Prone ideally 12-16 hours per day,only if feasible in severe ARDS
Fluids Restrictive fluid strategy,2/3rd of total maintenance fluid
Weaning Daily assessment for weaning

32. ⮚ Increasing the funtional residual capacity
⮚ Re-inflating atelectatic lung areas and recruitment of collapsed alveoli
⮚ Optimizing the ventilation/perfusion ratio
⮚ Reducing the right-to-left shunt
⮚ Avoiding end-expiratory alveolar collapse
Advantages of PEEP

33. ⮚ Inverse ratio ventilation is positive pressure ventilation with an inspiratory-expiratory
ratio of greater than 1.
⮚ It has been used in management of severe ARDS to improve oxygenation when PEEP
has been optimized.
⮚ Normally I:E usually range from 1:2 to 1:5 or higher where as in inverse ratio
ventilation it may be 1:1 or 2:1 higher
⮚ Increasing the inspiratory time increases mean airway pressure without increasing the
inspiratory plateau pressure, which may improve oxygenation.
Role of Inverse ratio ventilation in ARDS

34. 2. Prone positioning
It leads to:-
⮚Reduction of ventral to dorsal transpulmonary pressure difference
⮚Decrease in ventilation-perfusion mismatch
⮚Decrease in lung compression
⮚In supine position, the weight of the heart and posterior abdominal viscera compress the dorsal
lungs thereby increasing the dorsal pleural pressure.
⮚Prone positioning reduces the difference between the dorsal and ventral pleural pressures by
decreasing compression by the heart and abdominal viscera thus making ventilation more uniform.
⮚It also leads to decrease in over-distension of the ventral alveoli and the previously collapsed dorsal
alveoli are now recruited to participate in ventilation.

35. PRONE POSITION CONT…

36. • Placing a patient in a prone position is a multistep process which requires 3-5
personnel while paying close attention to the endotracheal tube, central lines and other
invasive devices in place.
Prone positioning is contraindicated in-
> Patients with facial/neck trauma or spinal instability
> Recent sternotomy
> Large ventral surface burn,
> Elevated intracranial pressure, massive hemoptysis
> Patients at high risk of requiring cardiopulmonary resuscitation (CPR) or
defibrillation.

37. 3. Pharmacological intervention
Corticosteroids
⮚ Different agents and regimens have been studied previously but overall results have been
inconclusive in terms of mortality benefit.
⮚ Recent randomized study shows dexamethasone in patients with ARDS administered within
30 hours of onset of moderate to severe ARDS led to improved 60-day mortality and
increased ventilatory free days at 28 days of randomization when compared to placebo.
⮚ For patients with moderate to severe ARDS (PaO2/FiO2 <200), methylprednisolone should
be considered at dose of 1mg/Kg/day for early (up to 7 days since onset) and at a dose of
2mg/Kg/day for late (after 7 days since onset).
⮚ Methylprednisolone should be weaned slowly over 6–14 days and not stopped rapidly.

38. ⮚ Methylprednisolone is suggested as the agent of choice due its greater penetration
into lung tissue and longer bioavailability compared to prednisolone, however there
are no RCTs comparing different corticosteroid agents in patients with ARDS.
⮚ The most common adverse event in the corticosteroid group was hyperglycemia in
ICU.
⮚ In conclusion, early administration of corticosteroids within 14 days of onset of
moderate to severe ARDS can reduce the duration of mechanical ventilation and
overall mortality and should be considered in such patients provided no
contraindications.

39. Neuromuscular blockade
• The administration of NMBA to mechanically ventilated patients with ARDS reduces the work of
breathing and patient–ventilator asynchrony, especially in awake tachypneic patient with
spontaneous breathing.
• Early administration of a 48-h infusion of NMBA in patients with moderate-to-severe ARDS
(PaO2/FiO2 < 150 mmHg with PEEP ≥ 5) resulted in lower mortality than a strategy of deep
sedation without routine NMBA use.
• In recent trial, which randomized patients with moderate-to-severe ARDS to a 48h continuous
infusion of NMBA with concomitant deep sedation (intervention group) or to a usual-care approach
without routine neuromuscular blockade and with lighter sedation targets (control group), there was
no significant difference in mortality at 90 days.

40. ⮚ Given the current conflicting evidence it is reasonable to conclude that NMBs should
not be routinely used in all severe ARDS patients and are likely beneficial only in
selective patients i.e,
⮚ with severe ARDS with refractory hypoxemia
⮚ patient-ventilator dyssynchrony
⮚ high risk of barotrauma.

41. 4. Fluid management
• Even mild fluid overload may worsen pulmonary edema and thereby exacerbate
hypoxemia in patients with ARDS due to an increase in pulmonary microvascular
permeability.
• An appropriate fluid management strategy should be selected in patients with ARDS
depending on the presence of other organ dysfunction or hemodynamic shock .
• Distinction between primary ARDS (due to aspiration, pneumonia or inhalational injury
which usually can be treated with fluid restriction), from secondary ARDS due to remote
infection or inflammation that requires initial fluid and potential vasoactive therapy is
central in directing initial treatments to stabilize the patient.

42. 5. ECMO ( Extra Corporeal Membrane Oxygenation)
• ECMO is an extracorporeal life support modality used to temporarily support patients with
respiratory and/or cardiac failure that are refractory to conventional treatment.
• The venovenous ECMO (VV-ECMO) configuration is the choice in patients with
respiratory failure with preserved cardiac function and the venoarterial ECMO (VA-
ECMO) configuration is the choice in patients with cardiac failure with or without
respiratory failure.
• Use of such extracorporeal gas exchange support allows for the use of low ventilatory
pressures to the injured lung , hence minimizing ventilator induced lung injury.

43. -Absolute contraindication for ECMO include:
> terminal illness with life expectancy < 6 months
> uncontrolled metastatic cancer,
> acute intracranial hemorrhage or infarction and
> any contradiction to systemic anticoagulation.
- The most common complications of VV-ECMO were bleeding (29.3%), neurological
complications (7.1%) .
- In conclusion, the use of ECMO should be considered in a selected number of patients
with severe ARDS or pH < 7.2 due to uncompensated hypercapnia.

44. Thank you