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ARDS, Respiratory Failure
Dr. Manu Mohan K
Dept. of Pulmonary Medicine
ARDS
• Severe dyspnea of rapid onset
• Hypoxemia
• Diffuse pulmonary infiltrates
• Respiratory failure
2
Etiology
3
Harrison’s Principles of Internal
Medicine 17th
ed.
Clinical features
• Diagnostic criteria for ALI and ARDS
• Oxygenation
ALI – PaO2/FiO2 < 300mm of Hg
ARDS - PaO2/FiO2 < 200mm of Hg
• Onset
Acute
• Chest radiograph
Bilateral alveolar or interstitial infiltrates
4
Harrison’s Principles of Internal
Medicine 17th
ed.
• Absence of left atrial hypertension
PCWP < 18 mm of Hg or no clinical
evidence of increased left atrial
pressure
Harrison’s Principles of Internal
Medicine 17th
ed. 5
www.images.google.co.in 6
http://radiology.rsna.org/content/2
13/2/545/F5.large.jpg 7
Clinical course and
pathophysiology
• Exudative
• Proliferative
• Fibrotic
Harrison’s Principles of Internal
Medicine 17th
ed. 8
Exudative phase
• First 7 days
• Alveolar and interstitial edema
• Hyaline membrane whorls
• Atelectasis
• Decreased lung compliance
Harrison’s Principles of Internal
Medicine 17th
ed. 9
Proliferative Phase
• 7 to 21 days
• Early pulmonary fibrosis
• Proliferation of Type 2 pneumocytes
Harrison’s Principles of Internal
Medicine 17th
ed. 10
Fibrotic stage
• 3 to 4 weeks
• Extensive alveolar duct and interstitial
fibrosis
• Emphysema and bullae
• Pulmonary hypertension
Harrison’s Principles of Internal
Medicine 17th
ed. 11
Treatment
• General
• Mechanical ventilation
Ventilator induced lung injury
Prevention of alveolar collapse
PEEP
Inverse ratio ventilation
Prone position ventilation
Harrison’s Principles of Internal
Medicine 17th
ed. 12
• Other strategies of mechanical ventilation
High frequency ventilation
Extracorporeal membrane oxygenation
Partial liquid ventilation
13
General support during
ventilation
• Fluid management
Maintaining low left atrial filling pressure
• Glucocorticoids
• Other therapies
Surfactant replacement
Nitric oxide inhalation
14
Complications of Mechanical
ventilation
• Pulmonary complications
• Barotrauma
• Nosocomial pneumonia
• Oxygen toxicity
• Tracheal stenosis
• Deconditioning of respiratory muscles
Harrison’s Principles of Internal
Medicine 17th
ed. 15
• Hypotension
• GI - Stress ulcer and mild cholestasis
16
Prognosis
• Mortality 41-65%
• >80 % deaths due to nonpulmonary
complications
17
• Functional recovery
Recover maximum lung function in 6
months
18
Respiratory failure
19
20
Respiratory failure
• When lungs cannot fulfill their primary
function of maintaining adequate gas
exchange at rest, or during exercise
• This results in an inability to maintain
normal blood gases, so that the Po2 (less
than 60) is low with or without Hypercarbia
(more than 50).
21
• Two types of respiratory failure
• Type I and Type II
• Type I - Hypoxemia without Hypercarbia
• Type II- Hypoxemia with Hypercarbia
• It can be acute or chronic
22
• Type I respiratory failure causes
• Chronic bronchitis and emphysema
• Pneumonia
• Pulmonary edema
• Pulmonary fibrosis
• Asthma
• Pneumothorax
• Pulmonary embolism
• Bronchiectasis
• Obesity
• ARDS
• Cyanotic heart disease
23
Type II Hypercarbic
Respiratory failure causes
• COPD
• Asthma
• Drug overdose
• Poisoning
24
• Myasthenia Gravis
• Polyneuropathy
• Poliomyelitis
• Sleep apnea syndrome
• Pulmonary edema
• ARDS
• Tetanus
• Foreign body
25
Mechanism
• Oxygenation failure and ventilatory failure
• Type I respiratory failure
Ventilation perfusion mismatch is marked
Control of ventilation is intact
So excess CO2 is exerted by normal
areas of lung
26
27
• Type II
Ventilatory failure marked
PaCO2 rises due to alveolar
hypoventilation, PaO2 falls.
Clinical features
• Clinical evidence of hypoxemia
• Central cyanosis best assessed by
examining the oral mucous membrane.
• Not useful in anemia
28
29
• CNS effects- irritability impaired
intellectual function and clouding of
consciousness
• Progress to convulsion, coma and death
• Persistent hypoxemia can lead to
secondary polycythemia
Clinical evidence of
hypercapnia
• CNS effects- irritability, confusion,
somnolence and coma, tremor, myoclonic
jerks, asterixis, even seizures, headache,
papilledema.
• Warm flushed skin with bounding pulse.
• Tachycardia and sweating
30
31
• Gastric dilatation, paralytic ileus
• Head ache on waking up common in
chronic hypercapnia due to progressive
increase in CO2retention during sleep.
32
DIAGNOSIS
• ABG
• It is important to measure arterial pH and
assess degree on compensation.
• In acute respiratory failure 10mm of Hg
increase in CO2 increases HCO3 by
1meq/L pH increase by 0.08 units. In
Chronic 10mm Hg increase in CO2
increase pH by 0.03 and HCO3 by
3.5meq/L
33
Management
• Type I
• Treatment of primary cause
• Correction of arterial hypoxemia highest
priority
• The goal should be to increase saturation
of oxygen to at least 85-90% without risk
of oxygen toxicity.
34
• High Fi02 for short period can be used.
The use of PEEP, change in position,
sedation and paralysis may help in
lowering Fi02
• Fever, agitation, overfeeding, vigorous
respiratory activity and sepsis increases
the oxygen demand.
General indication of ventilation
• Inadequate oxygenation despite an
increasing Fi02
• Increased PaCO2 associated with
decreased mental status or increasing
fatigue.
• Failure to control secretions
35
Methods
• Non invasive mechanical ventilation
• Mechanical ventilation
36
Mechanical ventilation
• Indications
• PaO2 less than 60 mm Hg despite FiO2 >
0.6 with hypercapnia
• Rapid increase in CO2 causing
uncompensated
• Respiratory acidosis
• Tachypnea > 35 breaths per minute
• Clinical judgment on impending
exhaustion of the patient
37
Complications
• Barotrauma
• GIT bleeding
• Nosocomial Pneumonia
38
• LTOT - long term oxygen therapy
39
40

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Ards respiratory failure (2)

  • 1. 1 ARDS, Respiratory Failure Dr. Manu Mohan K Dept. of Pulmonary Medicine
  • 2. ARDS • Severe dyspnea of rapid onset • Hypoxemia • Diffuse pulmonary infiltrates • Respiratory failure 2
  • 3. Etiology 3 Harrison’s Principles of Internal Medicine 17th ed.
  • 4. Clinical features • Diagnostic criteria for ALI and ARDS • Oxygenation ALI – PaO2/FiO2 < 300mm of Hg ARDS - PaO2/FiO2 < 200mm of Hg • Onset Acute • Chest radiograph Bilateral alveolar or interstitial infiltrates 4 Harrison’s Principles of Internal Medicine 17th ed.
  • 5. • Absence of left atrial hypertension PCWP < 18 mm of Hg or no clinical evidence of increased left atrial pressure Harrison’s Principles of Internal Medicine 17th ed. 5
  • 8. Clinical course and pathophysiology • Exudative • Proliferative • Fibrotic Harrison’s Principles of Internal Medicine 17th ed. 8
  • 9. Exudative phase • First 7 days • Alveolar and interstitial edema • Hyaline membrane whorls • Atelectasis • Decreased lung compliance Harrison’s Principles of Internal Medicine 17th ed. 9
  • 10. Proliferative Phase • 7 to 21 days • Early pulmonary fibrosis • Proliferation of Type 2 pneumocytes Harrison’s Principles of Internal Medicine 17th ed. 10
  • 11. Fibrotic stage • 3 to 4 weeks • Extensive alveolar duct and interstitial fibrosis • Emphysema and bullae • Pulmonary hypertension Harrison’s Principles of Internal Medicine 17th ed. 11
  • 12. Treatment • General • Mechanical ventilation Ventilator induced lung injury Prevention of alveolar collapse PEEP Inverse ratio ventilation Prone position ventilation Harrison’s Principles of Internal Medicine 17th ed. 12
  • 13. • Other strategies of mechanical ventilation High frequency ventilation Extracorporeal membrane oxygenation Partial liquid ventilation 13
  • 14. General support during ventilation • Fluid management Maintaining low left atrial filling pressure • Glucocorticoids • Other therapies Surfactant replacement Nitric oxide inhalation 14
  • 15. Complications of Mechanical ventilation • Pulmonary complications • Barotrauma • Nosocomial pneumonia • Oxygen toxicity • Tracheal stenosis • Deconditioning of respiratory muscles Harrison’s Principles of Internal Medicine 17th ed. 15
  • 16. • Hypotension • GI - Stress ulcer and mild cholestasis 16
  • 17. Prognosis • Mortality 41-65% • >80 % deaths due to nonpulmonary complications 17
  • 18. • Functional recovery Recover maximum lung function in 6 months 18
  • 20. 20 Respiratory failure • When lungs cannot fulfill their primary function of maintaining adequate gas exchange at rest, or during exercise • This results in an inability to maintain normal blood gases, so that the Po2 (less than 60) is low with or without Hypercarbia (more than 50).
  • 21. 21 • Two types of respiratory failure • Type I and Type II • Type I - Hypoxemia without Hypercarbia • Type II- Hypoxemia with Hypercarbia • It can be acute or chronic
  • 22. 22 • Type I respiratory failure causes • Chronic bronchitis and emphysema • Pneumonia • Pulmonary edema • Pulmonary fibrosis • Asthma • Pneumothorax • Pulmonary embolism • Bronchiectasis
  • 23. • Obesity • ARDS • Cyanotic heart disease 23
  • 24. Type II Hypercarbic Respiratory failure causes • COPD • Asthma • Drug overdose • Poisoning 24
  • 25. • Myasthenia Gravis • Polyneuropathy • Poliomyelitis • Sleep apnea syndrome • Pulmonary edema • ARDS • Tetanus • Foreign body 25
  • 26. Mechanism • Oxygenation failure and ventilatory failure • Type I respiratory failure Ventilation perfusion mismatch is marked Control of ventilation is intact So excess CO2 is exerted by normal areas of lung 26
  • 27. 27 • Type II Ventilatory failure marked PaCO2 rises due to alveolar hypoventilation, PaO2 falls.
  • 28. Clinical features • Clinical evidence of hypoxemia • Central cyanosis best assessed by examining the oral mucous membrane. • Not useful in anemia 28
  • 29. 29 • CNS effects- irritability impaired intellectual function and clouding of consciousness • Progress to convulsion, coma and death • Persistent hypoxemia can lead to secondary polycythemia
  • 30. Clinical evidence of hypercapnia • CNS effects- irritability, confusion, somnolence and coma, tremor, myoclonic jerks, asterixis, even seizures, headache, papilledema. • Warm flushed skin with bounding pulse. • Tachycardia and sweating 30
  • 31. 31 • Gastric dilatation, paralytic ileus • Head ache on waking up common in chronic hypercapnia due to progressive increase in CO2retention during sleep.
  • 32. 32 DIAGNOSIS • ABG • It is important to measure arterial pH and assess degree on compensation. • In acute respiratory failure 10mm of Hg increase in CO2 increases HCO3 by 1meq/L pH increase by 0.08 units. In Chronic 10mm Hg increase in CO2 increase pH by 0.03 and HCO3 by 3.5meq/L
  • 33. 33 Management • Type I • Treatment of primary cause • Correction of arterial hypoxemia highest priority • The goal should be to increase saturation of oxygen to at least 85-90% without risk of oxygen toxicity.
  • 34. 34 • High Fi02 for short period can be used. The use of PEEP, change in position, sedation and paralysis may help in lowering Fi02 • Fever, agitation, overfeeding, vigorous respiratory activity and sepsis increases the oxygen demand.
  • 35. General indication of ventilation • Inadequate oxygenation despite an increasing Fi02 • Increased PaCO2 associated with decreased mental status or increasing fatigue. • Failure to control secretions 35
  • 36. Methods • Non invasive mechanical ventilation • Mechanical ventilation 36
  • 37. Mechanical ventilation • Indications • PaO2 less than 60 mm Hg despite FiO2 > 0.6 with hypercapnia • Rapid increase in CO2 causing uncompensated • Respiratory acidosis • Tachypnea > 35 breaths per minute • Clinical judgment on impending exhaustion of the patient 37
  • 38. Complications • Barotrauma • GIT bleeding • Nosocomial Pneumonia 38
  • 39. • LTOT - long term oxygen therapy 39
  • 40. 40