Lecture notes on Respiratory insufficiency and Oxygen therapy by the Department of anaesthesia university of Jos

1. RESPIRATORY
INSUFFICIENCY AND OXYGEN
THERAPY
DR. H. Y. EMBU
PROFESSOR OF ANAESTHESIOLOGY
DEPT. OF ANAESTHESIA
UNIJOS

2. LEARNING OUTCOMES
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At the end of this lecture you should be
able to;
Classify hypoxia
Define and classify respiratory failure
Explain the different methods of
administering oxygen
Enumerate complications of oxygen therapy

3. RESPIRATORY INSUFFICIENCY
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The most common consequence of
respiratory insufficiency is hypoxia
This is a state of reduced O2 for tissue
respiration
It is classified into;
1. Hypoxic hypoxia (Hypoxaemia)
2. Anaemic hypoxia; here there is normal
arterial PO2 but reduced Hb e.g. anaemia

4. RESPIRATORY INSUFFICIENCY
• 3. Stagnant (ischaemic) hypoxia; There is
normal PO2 and Hb but reduced tissue
blood flow
May be due to decreased cardiac output
or interruption of blood flow

5. RESPIRATORY INSUFFICIENCY
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4. Histotoxic (cytotoxic) hypoxia; Normal
arterial PO2, Hb availability and blood flow
but inability of tissues to utilize O2. e.g.
cyanide poisoning, carbonmonoxide
poisoning
Anaerobic metabolism increases lactate
production

6. RESPIRATORY INSUFFICIENCY
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IMPLICATIONS OF HYPOXIA
Membrane pumps cease to function with
impairment of normal intra/extracellular
ion balance
Irreversible cell damage may follow, the
brain and heart being most susceptible
Of the 4 classes of hypoxia, hypoxaemia is
the one that readily responds to oxygen
therapy

7. RESPIRATORY INSUFFICIENCY
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Hypoxaemia is arterial PO2 under 12KPa
(90mmHg)
This may be caused by;
Hypoventilation
Diffusion impairment e.g. pulmonary
fibrosis
V/Q mismatch e.g. right to left shunt

8. RESPIRATORY INSUFFICIENCY
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Reduced FIO2 e.g. due to high altitude or
inadvertent hypoxic gas delivery during
IPPV, resuscitation or anaesthesia
Effects of hypoxaemia include cyanosis,
confusion, drowsiness, excitement,
headache, nausea, unconsciousness,
convulsions and death follows unless
corrected

9. RESPIRATORY INSUFFICIENCY
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Myocardial depression, arrhythmias,
bradycardia, coronary and cerebral
vasodilatation and renal impairment may
occur
Carotid and aortic body stimulation lead to
tachycardia, hypertension and
hyperventilation

10. RESPIRATORY INSUFFICIENCY
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Acute hypoxaemia with 85% Hb saturation
may cause mental impairment, becoming
severe at 75% saturation
Unconsciousness occurs at 65%
saturation
TREATMENT:
Treat cause
Institute oxygen therapy

11. RESPIRATORY FAILURE
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Defined as an arterial PO2 at sea level,
breathing air and at rest below 8KPa
(60mmHg) without intracardiac shunt
This is divided into;
1. TYPE I FAILURE: Hypoxaemia
accompanied by normal or low arterial
PCO2

12. RESPIRATORY FAILURE
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Causes of Type I failure include; chest
infection, asthma, pulmonary oedema,
pulmonary embolism, ARDS, aspiration
pneumonitis etc
2. TYPE II FAILURE (VENTILATORY
FAILURE): hypoxaemia accompanied by
arterial PCO2 exceeding 6.5KPa (49mmHg)

13. RESPIRATORY FAILURE
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Causes of type II failure include;
A. REDUCED CENTRAL DRIVE by;
Drugs e.g. opioids, barbiturates,
inhalational anaesthetics
Hypocapnoea following IPPV
Metabolic disturbances e.g. alkalosis,
hyperglycaemia

14. REDUCED CENTRAL DRIVE…
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Intracranial pathologies e.g. CVA, tumours,
infections, head injury with raised
intracranial pressure
Hypothermia
Alveolar hypoventilation and sleep apnoea

15. IMPAIRED PERIPHERAL MECH. OF
BREATHING by;
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Airway obstruction
Restriction of breathing due to pain,
obesity, severe ascites, tight bandages,
circumferential burns
Neuromuscular junction impairment e.g.
depolarizing and non-depolarizing
neuromuscular blockade, Myasthenia
gravis

16. IMPAIRED PERIPHERAL MECH. OF
BREATHING by;
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Chest diseases e.g. COPD, pneumothorax,
asthma, flail chest
Muscular weakness e.g. electrolyte
disturbances, muscular dystrophy,
myopathy associated with critical illness

17. IMPAIRED PERIPHERAL MECH. OF
BREATHING by;
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Nerve lesions e.g. spinal cord injury,
phrenic nerve injury, motor neurone
disease, poliomyelitis, Guillain-Barre’
syndrome, critical illness polyneuropathy
Increased dead space e.g. embolism

18. RESPIRATORY FAILURE
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TREATMENT
Treat underlined cause
Sitting patient up increases FRC and often
improves oxygenation
Oxygen therapy (use with caution in type II
failure)

19. TREATMENT….
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Aminophyllin may have an inotropic action
on the diaphragm and may reduce
respiratory muscle fatigue esp. in
neonates
Carbonic anhydrase inhibitors may
increase respiratory drive in COPD

20. TREATMENT….
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Respiratory stimulants e.g. doxapram may
be used in trying to avoid IPPV
CPAP
IPPV
ECMO

21. OXYGEN THERAPY
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O2 therapy is medically indicated for both
pulmonary and non-pulmonary disorders
The primary goal of O2 therapy is to
prevent tissue hypoxia
When O2 is administered to correct arterial
hypoxaemia, a tension of 60mmHg is
generally considered minimally acceptable

22. OXYGEN THERAPY
• Lower tensions may be acceptable for
patients with chronic hypoxaemia and CO2
retention while higher O2 tension may be
desirable for patients with hypotension,
anaemia, low cardiac output,
carbonmonoxide and cyanide poisoning

23. METHODS OF ADMINISTRATION OF O2
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Precise control over the inspired O2
concentration is especially desirable in
patients with respiratory diseases
Methods include;
A. FIXED PERFORMANCE DEVICES: i.e.
FIO2 is constant despite changes in
inspiratory flow rate

24. FIXED PERFORMANCE DEVICES e.g..
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Oxygen tent
Anaesthetic breathing systems
High Air Flow O2 Enrichers (HAFOE); the
feed connector to a plastic face mask
incorporates holes designed to allow
entrainment of atmospheric air into the O2
stream by jet mixing e.g. ventimasks to
deliver 24%, 28%, 35%, 40% or 50% O2

32. VARIABLE PERFORMANCE
DEVICES
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The actual FIO2 depends on inspiratory
flow rate
EXAMPLES
Nasal cannulae;
The inspired O2 concentration increases
approximately 3-4% per litre of O2 given
through nasal cannulae in most adults

33. Nasal cannulae…
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Inspired O2 concentration of > 40-50%
cannot be reliably achieved
Flow of > 4-6 L/min for prolonged periods
are poorly tolerated because of drying and
crusting of the nasal mucosa
PLASTIC MASKS e.g. moulded hard
plastic, Edinburgh: soft plastic, MC soft
plastic with foam padded edges

35. Plastic masks….
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They deliver 25-30% O2 at 2L/min O2 flow
and 30-40% at 4L/min
Non-rebreathing masks provide nearly
100% O2 due to the one-way valve
Partially rebreathing masks provide up to
80% O2
Other means of O2 administration include;
IPPV, CPAP, Hyperbaric oxygen

36. HAZARDS OF O2 THERAPY
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O2 therapy can result in both respiratory
and non respiratory toxicity
Important factors include patient
susceptibility, the inspired O2
concentration and the duration of
treatment

37. HAZARDS OF O2 THERAPY
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HYPOVENTILATION: This is primarily seen
in patients with COPD
ABSORPTION ATELECTASIS
High concentration of O2 can cause
pulmonary atelectasis in areas of low V/
Q ratios when the more insoluble N2 is
replaced by O2 in these areas,

38. ABSORPTION ATELECTASIS….
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This is because the alveolar volume
decreases because of greater uptake of O2
This can lead to progressive V/Q
mismatch

39. PULMONARY TOXICITY
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Prolonged high concentration of O2 is known to
damage the lungs
Toxicity is dependent both on the partial
pressure of the inspired gases and the duration
of the exposure
Although 100% O2 for up to 10-20 hours is
generally considered safe (at sea level),
concentrations > 50-60% for longer periods may
lead to toxicity and are undesirable

40. PULMONARY TOXICITY
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O2 toxicity is thought to be due to
intracellular generation of highly reactive
O2 metabolites (free radicals) e.g.
superoxides and activated hydroxyl ions,
singlet O2 and H2O2
These metabolites are cytotoxic because
they readily react with cellular DNA,
sulfhydryl proteins and lipids

41. PULMONARY TOXICITY
• O2 – mediated injury of the lungs leads to
reduced vital capacity, compliance and
diffusing capacity and increased A.V.
shunt and dead space may occur within
24-36 hours

42. PULMONARY TOXICITY
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Changes include endothelial damage and
reduced mucous clearance with infiltration
by inflammatory cells including
neutrophils and macrophages
Surfactant may decrease and capillary
permeability may increase
Eventually fibrosis may occur similar to
ARDS

43. HAZARDS OF O2 THERAPY…..
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RETROLENTAL FIBROPLASIA
(RETINOPATHY OF THE PREMATURE)
HYPERBARIC O2 TOXICITY
At 2 atmospheres of 100% O2,
pulmonary manifestations (mainly
dyspnoea) are often apparent within 8
hours.

44. HYPERBARIC O2 TOXICITY….
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Above 2 atmospheres, neurologic signs
predominate
Behavioural changes, nausea, vertigo
and muscular twitching may precede
frank convulsions
FIRE HAZARDS
Increased risks of fires and explosions

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