Respiratory failure occurs when the respiratory system fails to maintain normal gas exchange, leading to conditions such as hypoxemia and hypercapnia. It can be classified into acute and chronic types, with various causes including COPD exacerbations, pneumonia, and neuromuscular diseases. Management focuses on addressing the underlying cause, correcting blood gas abnormalities, and providing respiratory support, with specific approaches for acute and chronic cases.

1. RESPIRATORY
FAILURE

2. RESPIRATORY FAILURE
Inability of the respiratory system to maintain normal arterial
gas exchange i.e.
Failure to maintain normal arterial oxygen and carbon-di-
oxide tensions
Type I Hypoxemia (Low PaO2,
Normal or low PaCO2)
Type II Hypoxia and Hypercapnia
(Low PaO2 and raised Pa CO2)

3. CAUSES & PATHOPHYSIOLOGY
 Impairment of lung ventilation and/or perfusion due to
diseases of lung, chest wall, pulmonary circulation or
ventilation control.
 Results in low oxygen uptake or impaired CO2 removal
from arterial blood
 Both type I and type II respir failure can be acute or chronic

4. OXYGEN “TRAVEL”
PaO2 (mmHg)
Atmospheric air 150
Trachea Ventilation 120
Alveoli 100
Art. Blood Diffusion 95
Transport
Tissues Delivery 35-40
Venous blood Utilization 35-40

5. OXYGEN
DELIVERY
OXYGEN
DEMAND

6. CAUSES OF ACUTE RESPIRATORY FAILURE
 Ac exacerbation of COPD
 Acute Sever Asthma
 Severe pneumonia & sepsis
 Acute Respiratory Distress Syndrome
 Pneumothorax
 Acute chest infure, flail chest
 Drugs & poisoning: Neuroventilatory failure
 Pulm thromboembolism

7. CAUSES OF CHRONIC RESPIRATORY
FAILURE
 Severe COPD
 Advanced interstitial lung diseases: silicosis, pulmonary fibrosis of
any cause
 Extensive bronchiectasis
 Kyphoscoliosis
 Neuromuscular diseases: Myasthenia gravis, muscular dystrophies
 Obesity and Sleep Apnea Syndrome

8. DIAGNOSIS
 Presence of a disease causing respiratory failure. Investigations for
underlying respiratory/ non-respiratory disease
 Clinical signs of hypoxemia and/ or hypercapnia Oxymetry (O2
saturation measurement, < 90%)
 Assessment of Blood gas tensions i.e partial pressures (PaO2 <90
mmHg;
PaCO2 > 44mmHg)
 Investigations for systemic effects of hypoxia and hypercapnia LFT,
RFT, Cardiac, Hematological etc)

9. CLINICAL FEATURES
Hypoxia: Fatigue, restlessness, cyanosis,
tachypnea, tachcardia, sweating,
Later: cardiac ectopics, arrhythmias,
bradycardia, shock, impaired consciousness,
coma
Hypercapnia: Headache, sweating, mental
confusion, tachycardia, high bounding pulse,
tremors; Later: convulsions, coma, shock

10. HOW TO DETECT HYPOXIA & HYPERCAPNIA?
1. Clinical features
2. Blood gas estimation
Invasive: PO2, PCO2, pH
Noninvasive: SaO2
PtcO2, CO2
End tidal CO2

11. MANAGEMENT
 Management of disease causing respiratory failure
 Management of complications
 Correction of blood gas abnormalities
Oxygen administration
Correction of acid-base anomalies
Assisted respiratory supports

12. OXYGEN THERAPY INDICATIONS
A. Acute: Short term
 Hypoxemia: (PaO2 < 60mmHg)
 Normoxemic hypoxia
(Low QT, Ac. M.I., Anaemia
Hypermetabolism, CO poisoning)
B. Chronic: Long term
 Ch. Respiratory disease
 Hypoxemia – at rest / nocturnal / exertional

13. OXYGEN THERAPY FOR ACUTE HYPOXIA
1. Correct hypoxia as early as possible
2. Higher concentrations required
3. Maintain (near) normal PaO2
4. May require assisted ventilation
5. Gradually scale down O2 concentrations/ weaning

14. COPD: BLOOD GAS ABNORMALITIES
1. Hypoxia: Ventilation: perfusion mismatch
2. Hypercapnia and Acidosis:
Airway obstruction
Alveolar hypoventilation
Respiratory muscle fatigue
Central hypoventilation
 Hypoxic pulmonary vasoconstriction –
Worsening of pulmonary hypertension

15. OXYGEN THERAPY FOR COPD
 Acute exacerbation/ Acute (on chronic) respiratory failure
(Hypercapnic hypoxia): Supplemental oxygen
 Chronic respiratory failure- Long term oxygen therapy
(Domicilliary)

16. OXYGEN FOR AE-COPD
 Worsening of hypoxemia & Hypercapnia
 Small increase in FiO2 - good response
However, this can worsen hypercapnia
CO2 Narcosis
 Release of hypoxic vasoconstriction  Increased dead-space
 Loss of hypoxic respiratory drive
 Haldane effect  ↓ CO2 binding capacity
•Venturi mask preferred to a simple mask
•Avoid oxygen-driven nebulization of drugs

17. MANAGEMENT OF CO2 NARCOSIS
 Titrate FiO2 by the PaO2 to PAO2 ratio
 Appropriate delivery systems
 Management of hypercapnia
Non-invasive respiratory support
Intubation and mechanical ventilation
Respiratory stimulants
Clearing secretions/ antibiotic treatment

18. OXYGEN TOXICITY
SETTINGS
1. ICUs and “Acute” indications
 Mechanical ventilation
 High FiO2 vs. duration
2. Hyperbaric oxygen
3. Domiciliary use

19. OXYGEN RISKS
 Physical – Fire
 Functional – Increased hypoventilation,
Narcosis - High PaCO2
 Cytotoxic damage – proliferative and fibrotic changes in
lungs - ARDS

20. ADULT (OR ACUTE) RESPIRATORY
DISTRESS SYNDROME
Acute respiratory failure, following an acute insult /
catastrophe (systemic or respiratory), in a previously healthy
individual, attributable to diffuse damage to alveolo-capillary
membrane resulting in interstitial and alveolar oedema.

21. CAUSES: PREDISPOSING CONDITIONS
Direct
 Aspiration
 Toxic gases
 Respir burns
 Pancreatitis
 Near drowning
 Lung contusion
 Pneumonia
 Pulm. TB
 Oxygen toxicity
Others
Indirect/Systemic
 Septicemia/Endotoxemia
 Severe trauma/shock
 Surface burns
 Pancreatitis
 Stings/bites/anaphylaxis
 Multiple transfusion
 D.I.C./Drugs
 Obstetric shock
 Fat embolism

22. RISK FACTORS
 Diabetes mellitus
 Burns, wounds, multiple trauma
 Immunosuppressives
 Hepatic failure
 Invasive catheters, devices
 Hyposplenism
 Extremes of age
 Malignancy
 Organ transplant
 Radiation therapy
 Renal failure
 Indwelling urine
catheter
 A.I.D.S.

23. WHEN TO SUSPECT?
 Acute onset of breathlessness
- Respiratory distress
 Presence of a catastrophe
 No known cardiac or pulmonary illness (?)
 No significant relief with therapy for CHF

24. DIAGNOSIS
 Clinical
 Radiological: CXR May be normal in first 24 hrs; Later
fluffy opacities, prominent interstitial lines, consolidations,
pulm edema
 Biochemical for systemic organ function
 Investigations for cause of ARDS
 ECG, ECHO or cardiac cath to rule out the presence of
cardiac edema/ LHF

28. DIFFERENTIAL DIAGNOSIS
 Pulmonary thromboembolism
 Cardiac pulmonary oedema
 Bronchopneumonia
 Fluid overload / Renal failure
 Neurogenic pulmonary oedema
 Acute Interstitial pneumonia

29. COMPLICATIONS
1. Cardiovascular
2. Pulmonary – ARDS
3. Neurological
4. Hepatic failure
5. Renal failure
6. Haematological: Coagulopathy
7. Others: Gastrointestinal, Metabolic

30. MANAGEMENT PRINCIPLES
1. Resuscitation and management of underlying
condition
2. Oxygenation: Respiratory support
3. Fluid & electrolytes
4. Nutrition support
5. Specific organ failure management
6. General care
7. Monitoring

31. RESUSCITATION
Management of shock: Fluids, blood, inotropes
Management of underlying condition:
Drainage/Surgery/Antibiotics/others

32. VENTILATORY MANAGEMENT
Avoid alveolar over distension
Maintain FiO2 < 0.6
Use sufficient PEEP to prevent significant tidal recruitment –
derecruitment
Mode of ventilation is less important
Tolerate hypercapnia, if necessary
Weaning: Spontaneous breathing trials - T-piece, CPAP or PSV.
NIV can be used as a weaning method

33. THANK YOU