dr Bipul Borthakur

1. RESPIRATORY FAILURE
• Dr BIPUL BORTHAKUR
PROF Orthopaedics, SILCHAR ,ASSAM,INDIA

2. DEFINITION
• The inability of the respiratory system to adequately oxygenate the
blood with or without a concurrent alteration in carbon dioxide
elimination

3. ACUTE AND CHRONIC
• Depending on underlying cause
• Acute
eg: drug overdose, pneumonia, pneumothorax
• Chronic
eg: severe COPD

4. TYPES
Type I
hypoxemic respiratory failure
Type II
hypercapneic respiratory failure

5. Type I - Hypoxemic Failure
•Oxygenation failure
•PaO2 < 60 mmHg OR < 8 kpa
•PaCO2 normal or < 35 mmHg
•pH normal or elevated

6. Type I - Hypoxemic Failure
• ventilation (VA) and perfusion (Q) mismatching is the most common
cause of hypoxemia.
• Either by increasing the dead space or by wasted ventilation

7. Causes of Type I - RespiratoryFailure
COPD
Asthma
Pneumonia
Pulmonary embolism
Pneumothorax
Pulmonary edema
ARDS
Pulmonary fibrosis
 Obesity
 Lymphatic carcinamatosis
 Pnueumoconiosis
 Granulomatous lung disease
 Cyanotic cong heart disease
 Bronchiectasis
 Crush lung injury
 FAT embolism

8. Type II hypercapneic respiratory failure
• Ventilation failure
• PaO2 < 60 mmHg
• PaCO2 > 45 mmHg OR >6.7 kpa
• pH < 7.35

9. CAUSES OF Type II
hypercapneic respiratory failure
 COPD
 Asthma
 Drug overdose/Poisoning
 Myasthenia gravis
 Polyneuropathy
 Poliomyelitis
 Myopathy,Porphyria
 Head/ cervical cord injury
• Primary alveolar
hypoventilation
• Sleep apnoea syndrome
• Pulmonary edema
• ARDS
• Myxedema
• Laryngeal edema
• Tetanus
• Foreign body

10. Type III respiratory failure
(perioperative respiratory failure)
 commonly in the perioperative period, due to lung atelectasis.
 After general anesthesia, decreases in functional residual capacity
lead to collapse of dependent lung units.
 treated by
 frequent changes in position, chest physiotherapy,
upright positioning
 aggressive control of incisional and/or abdominal
pain.
 Noninvasive positive-pressure ventilation

11. Type IV respiratory failure
• due to hypoperfusion of respiratory muscles in patients in shock.
• Normally, respiratory muscles consume <5% of the total CO and O2
delivery.
• Patients in shock often suffer respiratory distress due to
pulmonary edema, lactic acidosis, and anemia.
then, up to 40% of CO may go to respiratory
muscles.

12. • Intubation and mechanical ventilation can allow redistribution of the
CO away from the respiratory muscles and back to vital organs while
the shock is treated

13. Patient Presentation
Neurological
Restlessness
Anxiety
Confusion
Headache
convulsions
Lethargy to coma

14. Patient Presentation
• Neurological
•Hypercapnoea also produce
tremor,myoclonic jerks, asterexis etc.
Increased CNS blood flow causes raised ICT- headache and papilloedema.
Headache on waking up is common in chronic hypercapnia, may be due to
increased CO2 retention in sleep

15. Patient Presentation
•Cardiovascular
•Tachycardia
•Elevated blood pressure early
•Eventual hypotension.
•Cardiac dysrythmias

16. Patient Presentation
Skin
•Hypercarbia – warm,flushed skin with a
bounding pulse, wet.
•Hypoxemia -cold and wet

17. Patient Presentation
Respiratory
Increased rate and depth
(hyperpnea)
Central cyanosis, due to
hypoxemia
Dyspnea - subjective feeling of
difficult breathing

18. Patient Presentation
Renal
Decreased UOP
Erythropoietin release with
hypoxemia
Excretion of H+ and retention of
HCO3
- with respiratory acidosis

19. Patient Presentation
•Gastrointestinal
•Decreased bowel sounds
•Reduced gastric pH with tissue
hypoxia , leads to gastric erosions and
bleeding

20. Immediate determination of upper
airway patency
Examination for central and peripheral
cyanosis
Measurement of the respiratory rate
Observation of the depth and pattern of
respiration
Initial Assessment and Stabilization
of Respiratory Failure

21. •Assess the configuration of the chest wall and
its movement during the respiratory cycle
•Palpation and auscultation over each
hemithorax
•Signs of respiratory distress including flaring
of nostrils, pursed-lip breathing, and use of
accessory muscles of respiration

22. •Above observations allow an initial
assessment of respiratory drive,
pump function, and delivery of gas to
the lungs

23. INVESTIGATIONS
• ARTERIAL BLOOD GAS MEASUREMENT
• PULSE OXIMETRY
NON INVASIVE, BUT NO INFORMATION REGARDING Va ,PCO2

24. PULSE OXIMETRY
• There is a relationship between the amount of oxygen dissolved in the blood
and the amount attached to the hemoglobin.
• Normal Oxyhemoglobin Dissociation Curve
• 97% saturation = 97 PaO2 (normal)
• 90% saturation = 60 PaO2 (danger)
• 80% saturation = 45 PaO2 (severe hypoxia)

25. MANAGEMENT
• Initial therapy be implemented before the specific DIAGNOSIS
• Adequate airway protection, oxygenation, and ventilation should be assured and
stabilize the Patient
• Hypoxemia and hypercarbia can rapidly lead to circulatory failure and death
• THEN, if possible treat the primary condition.

26. Type I respiratory failure
• GOAL: to increase the oxygen saturation to 85 to 90 % by giving
oxygen at increasing FiO2.
• Maintain adequate cardiac output and correct anemia.
• Treat contitions like fever, agitation, overfeeding, vigorous respiratory
activity & sepsis which increase O2 demand

27. Type I respiratory failure
• prolonged exposure to high FiO2(>50%)/prolonged duration of
treatment is avoided, due to pulmonary toxicity.

28. Type I respiratory failure
 Indications of mechanical ventilation are:
1. Inadequate oxygenation despite of high FiO2
2. Increasing PaCO2 associated with altered mental status or
increasing fatigue
3. Failure to control secretions

29. Type II respiratory failure
• Most commonly COPD, there is some degree of c/c resp failure
leading to hypercapnea.
• Acute on c/c: acidemia and increase in bicarbonate in ABG

30. Type II respiratory failure
1. Relief of hypoxia
 By giving supplemental O2.
by nasal prongs at flow of 1 to 3 L/ min
Or by venturi mask with flow set to 24 to 28 %.
Recheck arterial blood gases/O2 saturation to look for improvement.
PaO2 of > 50 mmHg is considered as adequate

31. Type II respiratory failure
• Avoid sedatives, as they decrease ventilatory drive
• To improve acidosis and hypercapnea and oxygenation respiratory
stimulants like doxapram can be tried, by close monitoring of ABG.

32. Type II respiratory failure
• Non invasive positive pressure ventilation.
 Advantage : avoiding intubation
 Aims at improving ventilation and gas exchange and reduces work of
respiratory muscles

33. Mechanical Ventilation in respiratory failure
 Indications
1. Failure to attain PaO2 of 60 mmHg despite of
FiO2 of 0.6
2. Rapidly increasing hypercapnea, producing
uncompensated acidosis
3. Mental confusion either due to
hypoxemia/hypercapnea
4. Tachypnoea(>35/min)
5. Clinical judgement of impending exhuation of
the patient

34. Airway acsess
• Nasotracheal/ orotracheal intubation
dis adv: laryngeal/ tracheal trauma,
used only up to 72 hrs
• Tracheostomy:
complications; hemorrhage, infection erosion of tube to
esophagus, tracheal stenosis, tube blockade and
respiratory infection

35. Ventilator settings
• Tidal volume of approx 10 ml/kg
• RR of 10 to 20/ min
• So minute ventilation is 100 to 150 ml/kg

36. In COPD/asthma
• In COPD tidal volume is kept at a little lower level(7 – 9 ml/kg) to
avoid auto PEEP and to prevent high inflation pressures to already
over inflated lungs to prevent barotrauma.
• I:E ratio is kept at 1:4 or 1:5 to minimise air trapping
• Peak inflation pressures are kept under 30 – 35 cm H2O
• FiO2 is kept at 35%

37. In COPD/asthma
• Regular monitoring of blood gases is needed.
• Adjust inspired O2 and level of PEEP to PaO2 and minute ventilation
against PaCO2

38. Auto PEEP/ intrinsic PEEP
• Develops in COPD due to decreased elastic recoil, decreased
expiratory flow and expiratory time due to tachypnoea- air trapping
and positive alveolar pressure at end of breathing.
• Can impede venous return and decrease cardiac output. Increase
chance of barotrauma

39. In ARDS..
• Tidal volume is kept low to prevent barotruama and pnuemothorax
and maintaining CVP at a lower range;
• PEEP is maintained at a higher range to minimise FiO2 and prevent
alveolar collapse
• I:E ratio is kept >1:1
• This results in better survival than conventional ventilation
strategies.

40. Managenment of patient on ventilator
• Monitor ECG, heart rate, BP, oxygenation, ABG, urine output
• Do not lower PaCO2 suddenly in a patient whom the resting level is
known to be high.
• Better to aim at treating acidosis
• Adeqaute sedation
• Regular suction of airways
• Adequate nutrition : enteral/ parenteral

41. Weaning..
Some times difficult with COPD
Can be tried when underlying condition/ infection
has subsided, SaO2>90% with FiO2 < 0.4 and
PEEP<5,alveolar ventilation is adequate with pH
normal, cardiovascular function is stable, upper
airway function is normal,
 Weaning index; ratio of beathing frequency to tidal
volume(breaths/min/L) <105 in spont ventilation thru tube,
succesful Extubation is likley

42. Weaning modes
• T piece and CPAP Weaning: best tolerated by patients with
mechanical ventilation for brief periods
• SIMV & PSV modes
best for intubated for extended periods &require gradual respiratory-
muscle reconditioning

43. complications
• Barotrauma(1 – 8%)
more common with ARDS
Assc with high peak airway pressures,
High levels of external and auto PEEP,
High tidal volumes
• GI bleeding due to gastric erosions
• Nosocomial pneumonia
• Cardiac arrhythmias, pulmonary embolism etc

44. Prognosis
• Best predictor of mortality in patients with acute on chronic
respiratory failure is degree of acidemia.
• pH< 7.26 is assc with higher mortality.
• Long term mortality of patients who survive an episode of acute
respiratory failure depends on underlying illness.
Eg: COPD, 50% survival at end of 3 years

45. श्रीभगवानुवाच |
अशोच्यानन्वशोचस्त्वं प्रज्ञावादांश्च च भाे |
गता ूनगता ूंश्च च नानुशोचन्न्त पन्डिता: ||
11||
śhrī bhagavān uvācha
aśhochyān-anvaśhochas-tvaṁ prajñā-vādānśh
cha bhāṣhase
gatāsūn-agatāsūnśh-cha nānuśhochanti
paṇḍitāḥ
meaning-
The Supreme Lord said: While you speak words
of wisdom, you are mourning for that which is
not worthy of grief. The wise lament neither
for the living nor for the dead.