Hypoxia can result from decreased oxygen content in the blood or failure to ventilate the lungs adequately. It presents with low oxygen saturation, lethargy, agitation, tachycardia, and potentially cyanosis. Causes include equipment issues, gas problems, ventilation failure, shunting of blood, poor oxygen delivery, and increased demand. Immediate management involves providing 100% oxygen, securing the airway, suctioning secretions, and addressing any ventilation problems while diagnosing the underlying cause. Ongoing monitoring and supplemental oxygen may be needed postoperatively to ensure adequate oxygenation.

1. HYPOXIA INOR

2. DEFINITION
Decreased arterial oxygen content in blood as
measured by pulse oximetry or arterial blood
gas analysis,
Usually transient as a result of atelectasis
and/or alveolar hypoventilation

3. Presentation
SpO 2 <90%
PaO 2 <60 mmHg
Patient is frequently lethargic and may be uncooperative
or agitated.
Tachycardia and hypertension may be associated with
hypoxia.
Tissue cyanosis may be seen in severe cases

4. Causes
Equipment's malfunction
Hypoxic gas mixture:
Incorrect flow meter settings
Second gas effect (especially on extubation)
Oxygen failure
Anesthetic machine error

5. Failure toventilate
Causes
• Ventilatory depression or narcosis
• Inadequate IPPV
• Disconnection
• Misplaced ETT (oesophagus/endobronchial)
• Obstruction to airway, ETT, filter, mount,circuit, etc.
• Increase Airway resistance (laryngospasm,
bronchospasm, anaphylaxis)
• Decrease FRC (pneumothorax, i intra-abdominal
pressure, morbid obesity)

6. Shunt
Atelectasis
Airway secretions
Decrease Hypoxic pulmonary vasoconstriction
(vasodilators or B 2 agonists)
CCF with pulmonary oedema
Aspiration of gastric contents
Pre-existing pathology (e.g. VSD, ASD + decrease SVR
with reversal of flow)

7. Poor oxygen delivery
• Systemic hypoperfusion (hypovolaemia,
sepsis)
• Embolus gas /air/ thrombus/ cement/ fat/
amniotic fluid)
• Local problems (cold limb, Raynaud’s,
sickle)

8. Increasedoxygendemand
• Sepsis
• Malignant hyperthermia

9. Riskfactors
• Reduced FRC (obesity, intestinal obstruction,
pregnancy) reduces oxygen reserves.
• Failure to preoxygenate exacerbates any airway
difficulties at induction.
• Laryngospasm can result in negative pressure
pulmonary oedema.
• Head and neck surgery (shared access to the airway)
increases the risk of undetected disconnection.

10. Continue…
• History of congenital heart disease or detection
of a heart murmur (left to right communication).
• Chronic lung disease.
• Sickle cell disease.
• Methaemoglobinaemia (interpreted as
deoxyhaemoglobin by pulse oximeters).

11. Diagnosis;pre-requisite
• FiO 2 : use an oxygen analyser at all times.
• Ventilation: cross-check rise and fall of chest with
auscultation over stomach and in both axillae,
• Capnograph trace, measured expired tidal volume,
and airway pressure.
• Measurement error: does patient appear cyanosed?
Beware in anaemia when 5g/dl deoxyhaemoglobin
may not be visible.
• Aspiration/airway secretions: auscultate and
aspirate using tracheal suction catheter ― litmus
paper.

12. Differential diagnosis
• Suspect tension pneumothorax (particularly following
central line insertion) if IPPV and trachea shifted away
from a hyperresonant lung field with diminished breath
sounds. Neck veins may be engorged; Treat
immediately by decompressing the pleural cavity with
an open cannula placed in the 2nd intercostal space in
the mid- clavicular line.
• Suspect hypovolaemia if patient has HR >100bpm, RR
>20bpm,capillary return >2s, cool peripheries,
collapsed veins, a narrow and peaked arterial line
trace, or marked respiratory swing to either CVP or
arterial line trace.

13. Differential diagnosis
• Suspect air or gas embolus if patient had a pre-existing low CVP
and open venousbed. Signs are variable but may include sudden
decrease ETCO 2 ,
• Decrease SpO 2 , loss of palpable pulse, PEA, and subsequent
rise in CVP.
• Suspect fat embolus or cement reaction in the presence of
multiple bony injuries or long bone intramedullary surgery.
• Malignanthyperthermia: especially if accompaniedby increase
ETCO 2 , increase RR, Increase HR.
• Anaphylaxis—cardiovascularcollapse 88%, erythema 45%,
bronchospasm36%, angio-oedema 24%, rash 13%, urticaria 8.5%.

14. Differential diagnosis
• Suspect cardiac failure if patient has HR >100bpm, RR
>20bpm, engorged central veins, capillary return >2s,
cool peripheries,
• pulmonary oedema, or worsening SpO 2 with fluid
challenge.

15. Investigations
SpO 2
Capnography
CXR; ABGs
CVP and
Echocardiography

16. Immediatemanagement
• 100% oxygen; check FiO 2 ; expose patient and check
for central cyanosis; check ventilation bilaterally;
hand ventilate on a simple system giving 3–4 large
breaths
• initially to recruit alveoli; secure airway;
endotracheal suction; initially remove any PEEP;
• Give adrenaline if accompanied by poorly palpable
pulses

17. Immediatemanagement
• ABC —expose the chest, all the breathing circuit, and
all airway connections.
Administer 100% O 2 by manual ventilation—at least 3–
4 large breaths initially will help to recruit collapsed
alveoli
(and gives continuous tactile feedback about the state
of the airway).If no improvement

18. Immediatemanagement
• Confirm FiO 2: if there is any doubt about inspired
oxygen concentration from the anaesthetic machine,
use a separate cylinder supply
• As a last resort use room air via a self-inflating bag =
21% O 2 ).
• Misplaced ETT —cross-check rise and fall of chest
with auscultation over stomach and in both axillae
and the capnograph trace

19. Immediatemanagement
• Ventilation problem : simplify the breathing system
until the problem is removed, i.e. switch to bag rather
than the ventilator,
• Use a Bain circuit instead of the circle system,
• Try a self-infl ating bag, + mask rather than ETT, etc.

20. Immediatemanagement
• Diagnosis of the source of a leak or obstruction: is not
as important initially as oxygenation of the patient.
• Make the patient safe first then use a systematic
approach. The fastest way to isolate the problem is
probably by division. For instance,
• Does breaking the circuit at the ETT connector leave
the problem on the patient side or the anaesthetic
machine side?

21. ManagementATPOSTOP
• Provide supplemental O 2 via nasal cannula or face
mask to maintain adequate oxygenation.
• Insert an artificial airway if airway obstruction is
present.
• Intubation and mechanical ventilation may be required
if the patient does not respond to supplemental O 2 .
• Arterial blood gas analysis is useful to determine PaO
2 and PaCO 2
• Cardiovascular support may be necessary in extreme
cases of arterial hypoxia.