Ards respiratory failure

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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

6. www.images.google.co.in 6

7. http://radiology.rsna.org/content/2
13/2/545/F5.large.jpg 7

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
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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
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17. Prognosis
• Mortality 41-65%
• >80 % deaths due to nonpulmonary
complications
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18. • Functional recovery
Recover maximum lung function in 6
months
18

19. Respiratory failure
19

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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).

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• 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

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• 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
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24. Type II Hypercarbic
Respiratory failure causes
• COPD
• Asthma
• Drug overdose
• Poisoning
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25. • Myasthenia Gravis
• Polyneuropathy
• Poliomyelitis
• Sleep apnea syndrome
• Pulmonary edema
• ARDS
• Tetanus
• Foreign body
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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
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• 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
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• 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
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• Gastric dilatation, paralytic ileus
• Head ache on waking up common in
chronic hypercapnia due to progressive
increase in CO2retention during sleep.

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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

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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.

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• 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
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