This document provides an overview of respiratory failure and ARDS. It defines the two types of respiratory failure - type 1 hypoxemic respiratory failure and type 2 hypercapnic respiratory failure. It discusses the causes, symptoms, approach and management for each type. It also defines and discusses the diagnosis, causes, pathogenesis and management of ARDS according to the Berlin criteria. The management of ARDS focuses on lung protective ventilation strategies like low tidal volumes, appropriate PEEP and permissive hypercapnia.

1. Respiratory Failure and ARDS
Presenter – Dr Sanika Shukla (jr2)

2. Content-Respiratory Failure
• Definition
• Values of a Normal ABG
• Types of Respiratory Failure
• Type 1 Respiratory Failure
Alveolar-arterial gradient
Symptoms of hypoxemia
Causes of hypoxemia
Approach to a patient with type 1 RF
Management of a patient with type 1 RF
• Type 2 Respiratory Failure
Symptoms of hypercarbia
Approach to a patient with type 2 respiratory failure
Management of a patient with type 2 respiratory failure
• Clinical case scenarios

3. Definition of Respiratory Failure
• Respiratory failure results from the failure of respiratory systems I one
or both of its gas exchange functions- oxygenation and carbon dioxide
elimination.
• There are of two types Type 1 hypoxic respiratory failure
• Type 2 hypercapnic respiratory failure
• Type 3 Respiratory Failure-per operative Respiratory failure
• Type 4 Respiratory Failure- Shock with hypotension

4. ARTERIAL BLOOD GAS NORMAL VALUES
ANALYTE NORMAL VALUE UNITS
pH 7.35-7.45
pCO2 35-45 mm of Hg
pO2 72-104 Mm of Hg
HCO3- 22-30 mEq/L
SpO2 95-100 %
Anion Gap 12+/- 4 mEq/L

5. NORMAL VALUES
VARIABLES NORMAL VALUE
LACTATE LESS THAN 2mmol/L
SODIUM 136-145 mmol/L
POTASSIUM 3.5-4.5 mmol/L
CALCIUM 1.15-1.25 mmol/L

6. Respiratory Failure
• TYPE 1 Respiratory Failure
• PaO2 <60 mm Hg
• PaCO2 normal or low
• With or without widening of the
alveolar-arterial oxygen gradient.
• Hypoxemia due to inadequate gas
exchange
• REQUIRES OXYGEN THERAPY
• Type 2 respiratory Failure
• PaCO2 >45 mmHg
• Associated with hypoxia (PaO2 <60
mm of Hg)
• Respiratory acidosis
• Alveolar hypoventilation due to
pulmonary and extra pulmonary
casues.
• REQUIRES VENTILATORY SUPPORT

7. Type 1 Hypoxemic
Respiratory Failure

8. Alveolar- arterial O2 gradient

9. What is oxygen therapy and why it’s needed?
• Giving oxygen at 21% atmospheric pressure or more than
atmospheric pressure is used to treat or prevent hypoxia and
Hypoxemia.
• Hypoxia refers to reduced oxygen levels at tissues
• Hypoxemia refers to reduced oxygen tension in blood. When PaO2
<60mmHg ( Spo2 <90%)

10. Symptoms and Signs of type 1 Respiratory
Failure
• Restlessness, anxiety
• Irritability, impaired intellectual functioning and consciousness
• Cyanosis
• Tachycardia
• Hypotension

11. Causes of Acute Type 1 Hypoxemic Respiratory
Failure
Hypo
Ventilation
V/Q
mismatch
Shunt
Low Inspired
Oxygen

12. Approach to a patient with Hypoxemic
Respiratory Failure

14. 1.Low Inspired Oxygen
• Decreased FiO2 and eventually
decreased PaO2
• Normal A-a gradient present
• Caused generally at high attitudes

15. 2.Hypoventilation
• Occurs when
ventilation decsreases
less than 4-6 L/ min
• Decrease in PaO2 and
Increased PaCO 2
• A-a gradient normal
• Causes- CNS
depression and
neuromuscular
diseases

16. 3.Ventilation Perfusion Mismatch

17. V/Q Mismatch( Decreased )
Airway Diseases
• COPD
• ASTHMA
• BRONCHOSPASM
Alveolar Filling
• ATELECTASIS( collapsed alveoli)
• Alveolar filling- pus (pneumonia)
• Fluid ARDS/ cardiogenic RF
• Blood – Diffuse alveolar
hemorrage

18. V/Q Mismatch( increased)
 Due to dead space
ventilation.
 Increased A-a
gradient
 Causes
thromboembolism
and pulmonary
embolism

19. 4.Shunts
• The deoxygenated blood
bypasses the ventilated
alveoli and mixes with
oxygenated blood-
Hypoxemia.
• Persistent Hypoxemia
despite 100% O2 inhalation.
• Hypercapnia occur when
shunt is excessive >60%

20. Causes of Shunt
Intracardiac
•Right to left shunt
•Tetralogy of Falot
•Eisenmenger’s syndrome
Pulmonary
•A/V malformation
•Pneumonia
•Pulmonary Edema
•Atelectasis
•Pulmonary Haemorrhage
•Pulmonary contusion

22. Management principles of patients
with Hypoxemic respiratory failure
• Rapid restoration of an adequate arterial saturation which
often requires intubation and mechanical ventilation.
• Use of adequate amounts of PEEP to reduce FiO2 to less
than 60%
• Low TV ventilation with permissive hypercapnia in
patients with ARDS.
• General supportive care in the ICU while the patients
pulmonary process resolves.

23. Type 2 Hypercapnic
Respiratory Failure

24. Symptoms of type 2 respiratory failure
• Headache
• Drowsiness and confusion
• Warm extremities, flushing, sweating
• Tremors

26. Acute, Acute on Chronic, Chronic Type 2
Respiratory Failure
• Acute type 2 Respiratory Failure- Type 2 Acute
Respiratory Failure with low pH, high PaCO2 and
normal bicarbonate levels
• Acute on Chronic type 2 Respiratory Failure – low pH,
high PaCO2 and High bicarbonate levels
• Chronic Respiratory Failure- normal pH, raised PaCO2
and HCO3-

27. Principles of managing patients of Hypercapnia
• Rapidly institute adequate ventilation: In carefully selected patients,
non invasive ventilation can be tried prior to intubation and
mechanical ventilation.
• Sedatives and narcotics can be hazardous and can worsen
ventilation and oxygenation in patients with hypercapnia, particularly
those with neuromuscular weakness and severe obstructive lung
disease.
• Cautious use of supplemental oxygen is necessary as oxygen can
worsen hypercapnia by a number of mechanism: worsening of V/Q
matching, the Haldane effect and suppression of central Hypoxemic
drive.

28. ACUTE RESPIRATORY
DISTRESS SYNDROME

29. Content- ARDS
• Definition of ARDS
• Causes of ARDS
• Pathogenesis of ARDS
• Diagnosis of ARDS (Berlin’s Criteria)
• Management of ARDS
General Management protocol
Ventilatory management (Principles of Ventilation)
Lung protective Ventilation
Goals of Ventilation in ARDS
ARDSnet Protocol
Non ventilatory management
Refractory Hypoxemia
Management of Refractory Hypoxemia in ARDS
• Weaning

30. Clinical scenario
• A 25 year old female patient presented with fever with chills and
vomitting. The following day, she noted increased difficulty in
breathing. Extensive bilateral infiltrates were seen on the chest X Ray
and she needs supplemental oxygen to maintain oxygen saturation at
more than 90%. Echocardiography showed normal cardiac function.
• She was getting progressively fatigued and increasingly drowsy and
was intubated.

31. Definition of ARDS
• 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 can be caused by diffuse lung injury may be direct or indirect as
occurs in sepsis.

32. CAUSES OF ARDS

33. Pathogenesis of ARDS
• It is a syndrome that involves injury and increased epithelial-
endothelial permeability of the alveoli. It can occur as a result of
direct chemical, systemic inflammation including sepsis, trauma or
numerous other causes common in critically ill patients.

37. Diagnosis of ARDS (BERLIN’S CRITERIA)
• The Berlin Definition of ARDS was published in 2012 replacing the
American European Consensus Conference’s definition of ARDS
published in 1994.
• The major changes of the Berlin Definition are that the term Acute
Lung Injury has been eliminated , the pulmonary capillary wedge
pressure ( pulmonary artery occlusion pressure) criteria has been
removed and minimal ventilator settings have been added.

38. 1. ONSET
•Acute – Within 1 week of a
clinical insult or new or
worsening respiratory
symptoms.

39. 2.Imaging
CXR
CXR May show fine
granular infiltrates or
ground glass appearance
, and evenly distributed in
all lung fields with no
evidence of pleural
effusion.

40. CT scan
Bilateral
Consolidations
with crazy
pavement
pulmonary Edema
and atelectasis

41. Lung USG
POCUS -Point of
care USG
B lines are seen in cases of
pulmonary edema and ARDS

42. 3. Severity of ARDS( oxygenation)
PaO2/FiO2 ratio Inference
200-300 mm of Hg Mild ARDS
100-200 mm of Hg Moderate ARDS
<100 mm of Hg Severe ARDS

44. PaO2/FiO2 ratio ( P:F RATIO)
Gives
understanding
that the patients
OXYGENATION
with respect to
OXYGEN delivered
is more important
than simply the
PO2 value.
Patient 1 on
Room Air
Patient 2 on
mechanical
ventilation at
FiO2 50%
PaO2 60 90
FiO2 21% 50%
P:F Ratio 285 180

45. 4. Confirmation of a non cardiogenic cause
• Hydrostatic edema is not the primary cause of respiratory failure. If
no ARDS risk factor is present, then some objective evaluation is
required (ECHO TO CHECK THE LVEF).

46. Distinction between Non Cardiogenic (ARDS)
and Cardiogenic Pulmonary Edema
ARDS
• Tachypnea, dyspnea, crepts
• Aspiration, sepsis
• Alveolar flooding with normal
heart size, systolic, diastolic
function.
• Severe Hypoxemia refractory to O2
therapy
• PCWP is normal <18 mm Hg
Cardiogenic Edema
• Tachypnea, dyspnea, crepts
• Left ventricular dysfunction, valvular
disease, IHD
• Cardiomegaly,vascular redistribution,
pleural effusion, perihilar batwing
distribution of infiltrate.
• Hypoxemia improves on high flow O2
• PCWP is high >18 mmHg

47. Management of ARDS
• GENERAL PRINCIPLE:
1. The recognition and treatment of underlying medical/ surgical
disorders. ( pneumonia, sepsis, aspiration, trauma)
2. Standardised “bundled care” approaches for ICU patients , including
prophylaxis against venous thromboembolism, GI bleeding,
aspiration and central venous catheter care

48. VENTILATORY MANAGEMENT
• In the following conditions ARDS, mechanical ventilation should be
initiated electively .
I. Worsening respiratory fatigue due to increased work of breathing.
II. Persistent Hypoxemia (SpO2 <90%) on non rebreathing face mask
or NIV/HFNC.
III. Worsening hypercarbia.

49. Principles of Ventilation in ARDS
• In ARDS , mechanical ventilation is primarily used to reverse
Hypoxemia and decrease the work of breathing.
• High volumes, high airway pressures and repeated opening and
closing of collapsed alveoli May further damage the lung worsen the
ARDS, and contribute to systemic inflammation. Open the lung and
keep it open.

50. • ARDS mechanical ventilation protocol is based on the concept that
the lung is largely consolidated and can be viewed as a “baby lung”,
with only one third of the alveoli remain open.
• The concept of a “sponge lung” implies the gravitational effect of
lung injury ie the dependant portion of the lung is more Atelectatic
and the appropriate ventilation strategy can open up or recruit these
shut alveoli. Frequent positioning of the patient changes the pattern
of aeration of the lung.

51. Lung Protective Ventilation

52. 1. Tidal Volume
• Ideal tidal volume 6-8 ml/kg acc to ideal body weight( low tidal
volume)
• Low tidal volume to avoid overdistension of the health alveoli( avoid
VOLUTRAUMA)
• This lung protective ,low tidal volume ventilation strategy has become
standard of care for patients with ARDS and subsequent studies have
associated improved outcomes even in patients without ARDS.

53. 2. PEEP( Post expiratory end pressure) and
FiO2
• PEEP of at least 5 cm H2O to prevent the collapse of small airways at the
end of expiration.
• Goal is to maximise alveolar recuitment and prevent cycles of
recuitment/derecruitment of atelectatic portion of lung.
• In severe and diffuse ARDS, start with a higher PEEP of 10-12
• Situations FiO2 >50% is needed to maintain the target SpO2 of 88%-95%,
PEEP levels above 5 cm H2O can be used to improve arterial oxygenation
and reduce the FiO2 to safer levels.

54. Permissive Hypercapnia
• During low tidal volume ventilation, hypercapnia often occurs.
• Because of low tidal volume ventilation, “permissive hypercapnia” is
acceptable to persist as long as there is no evidence of harm-
targeting a pH greater than 7.25.

55. Goals of Ventilation in a case of ARDS
Tidal Volume 6ml/kg
Plateau
Pressure
<30cm H2O
SpO2 88-95%
PaO2 55-80 mmHg
pH 7.3-7.45

58. Non Ventilatory Management
1. Fluid Management
• The lung consolidation in ARDS is an inflammatory exudate and
should not be influenced by fluid balance.
• However preventing positive fluid balance will prevent unwanted
fluid accumulation in the lungs, hence reduces the time of mechanical
ventilation.

59. •2. Neuromuscular Blockage
•Neuromuscular blocking agents have been used
to facilitate synchrony with mechanical
ventilation by removing spontaneous chest wall
and diaphragm motion.

61. THANKYOU
References – The Washington manual of Critical Care
Morgan and Mikhail Clinical Anaesthesiology
The ICU Book Paul Marino
ICU Protocols
Harrisions Principles of Internal Medicine