Respiratory failure

Respiratory failure by Dr. Bipul Borthakur

1. BASICS OF RESPIRATORY
FAILURE
DR. BIPUL BORTHAKUR (PROFESSOR)
DEPT OF ORTHOPAEDICS, SMCH

2. DEFINITION
The inability of the respiratory system to adequately
oxygenate the blood withor withouta 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
hypercapneicrespiratory
failure

5. Type I -Hypoxemic Failure
Oxygenation failure
PaO
2< 60 mmHg OR < 8
kpa
PaCO
2normal or < 35
mmHg
pH normal or elevated

6. Type I -Hypoxemic Failure
ventilation (V
A) and perfusion (Q) mismatching is the
most commoncause 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
Granulomatouslung
disease
Cyanotic cong heart
disease
Bronchiectasis
Crush lung injury
FAT embolism

8. Type II
hypercapneicrespiratory failure
Ventilation failure
PaO
2< 60 mmHg
PaCO
2> 45 mmHg OR >6.7 kpa
pH < 7.35

9. CAUSES OF Type II
hypercapneicrespiratory 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
(perioperativerespiratory failure)
commonly in the perioperativeperiod, 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 incisionaland/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 O
2delivery.
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
HCO
3
-
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 venturimask 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 exhuationof
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. Managenmentof 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 beathingfrequency to tidal
volume(breaths/min/L) <105 in spontventilation thru tube,
succesfulExtubationis 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. THANK YOU
“tasmādasaktaḥ satataṃ kāryaṃ karma samācara
asakto hyācarankarma paramāpnoti pūruṣaḥ”
“go on efficiently doing your duty at all times without
attachment.
doing work without attachment man attains the supreme.”