Post operative apnoea
Ben Creagh-Brown
SHO, UHL, November 2003
Overview
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Causes and their associated
management
Paediatric considerations
Controversies
Causes of postoperative
hypoventilation / apnoea
Factors affecting airway
 Factors affecting ventilatory drive
 Factors affecting peripheral drive
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Airway
Airway obstruction
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Blood, clots, secretions: Recovery
position / suction
Airway manoeuvres (jaw thrust, chin lift,
head tilt)
Airways (OP / NP)
Intermittent: OSA
External airway compression (thyroid
surgery)
Laryngospasm
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Direct stimulation of cords or epiglottis by
secretions/blood/FB/OP airway, LMA or
following extubation
May be partial or complete
100% O2, aspirate secretions, IPPV to ‘break’
spasm. Caution inflating stomach
If not improving consider deepening,
Suxamethonium +/- reintubation
Rarely post thyroid surgery: recurrent laryngeal
nerve palsy  cord palsy  obstruction
Bronchospasm
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Irritable airways in smokers
Intrinsic asthma
Anaphylaxis
Effect of drug directly on bronchial muscle or
via histamine release (thiopentone, morphine,
mivacurium, atracurium)
Mx: O2 and bronchodilators, aminophylline,
adrenaline.
Reduced ventilatory drive
Causes
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Intracranial pathology (stroke, tumour, bleed)
Hypothermia
Hypocapnia (CSF lags Serum), severe
hypercapnia
All induction and maintenance drugs (except
ketamine) depress resp. drive. TIVA.
Opiates...
Opiates
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Reduced vent. drive is obvious if RR or VT is low.
Can be subtle if moderate hypercapnia is undetected
- causes hypertension and tachycardia, which may
be mistaken for signs of pain and more opiates given
Elderly and children are particularly sensitive
Beware high spinals or SA epidurals
Naloxone as specific antidote. 400mcg in 1ml, dilute
to 10ml and give in 40mcg boluses. T1/2 20-30mins
(infusion 800mcg in 500ml saline over 6 hours or IM)
Benzodiazepines
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Can be reversed with flumazenil
iv increments of 0.1mg to a maximum
adult dose of 1mg.
However, Flumazenil is expensive, may
cause arrhythmias, hypertension and
convulsions.
It’s use is generally not indicated.
Blood glucose
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Severe hypoglycaemia as a central
cause for reduced ventilatory drive.
Peripheral factors
Causes
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Muscle weakness
Pain
Abdominal distension
Obesity
Tight dressings
Pneumo/haemo thorax
Muscle weakness
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Myasthenia gravis or other myopathies
Electrolyte disturbance
Residual neuromuscular blockade or
inadequate reversal - uncoordinated jerky
movements
VT measurement unreliable estimate of
adequacy of reversal as normal VT with only
20% diaphragmatic power, poor coughing
ability
Adequate reversal of NM
blockade
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Subjective
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Objective
• Grip strength
• Adequate cough
• TOF/DBS visualised
• Sustained head lift 5s
• Vital capacity of 10ml/kg
• TOFR from accelerometer
Limiting NM blockade reversal
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XS NM blocker
Too little time from blockade to reversal
Hypokalaemia, Hypermagnesaemia
Acidosis
Gentamicin
Local anaesthetics
Myopathy
NM monitoring
1.
2.
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Variable individual response to muscle relaxants
Narrow therapeutic window. There is no detectable
block until 75 to 85% of receptors are occupied and
paralysis is complete at 90 to 95% receptor occupancy.
TOF: 4 supramaximal, square wave, pulses of 0.2s at
2Hz. 50mA. TOFR >70% best predicts adequate muscle
power.
DBS: 2 short 50Hz bursts of 3 pulses, 750ms apart.
Meant to be easier to visualise.
Limits to PNS
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Testing TOF/DBS on forearm not same
as testing diaphragm
Neostigmine inhibits metabolism of
acetylcholione. 0.05-0.08mg/kg, peak
effect 7 - 11m, duration 40m
Neostigmine up to 5mg total, in higher
doses can worsen NM function.
Delayed elimination of NM
blockers
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Prolonged NM blockade as drugs persist can
occur with all except atracurium and it’s
derivative cis-atracurium
Renal or hepatic impairment
Atypical enzymes...
Cholinesterase
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The enzyme which hydrolyses acetylcholine
and other choline esters at a more rapid rate
than noncholine esters
Specific cholinesterase - highly specific for
acetylcholine and a few closely related esters
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Nonspecific cholinesterase (serum cholinesterase
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= plasma cholinesterase = pseudocholinesterase =
butyrylcholinesterase = S-type cholinesterase)
Normal range = 4000 – 12,000 IU/L
Atypical plasma cholinesterase
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Prolonged NM block after
suxamethonium or mivacurium
Either due to absent or faulty plasma
cholinesterase
Sux apnoea lasts 20mins to 8 hrs. 2
commonest defective genes – 20 mins.
Genetics
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Pseudocholinesterase deficiency is most common in
people of European descent; it is rare in Asians.
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The normal gene encoding for plasma cholinesterase is
E1u (usual)
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There are three abnormal genes: E1a (atypical), E1s
(silent) and E1f (fluoride-resistant) 94% of the
population are heterozygous for the usual gene (hence
normal response to suxamethonium), E1a
homozygotes occur in 0.03% of the population, E1s
homozygotes in 0.001% and E1f homozygotes in
0.0003% of the population.
Aquired low cholinesterase
levels
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Liver disease
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3rd trimester pregnancy
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Malnutrition
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Severe anaemia
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MI
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Carcinomatosis
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Hypothyroidism
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Drugs: amethocaine, ketamine, pancuronium, oral
contraceptives, propranolol, ecothiopate eye drops,
cytotoxics, organophosphate insecticides or weedkillers.
Dangers of hypercapnia
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Hypertension
Tachycardia
CO2 narcosis (>9kPa)
Unconsciousness, coma, respiratory
arrest
Treatment
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If reversible cause – treat
For Sux/Miva apnoea – consider FFP
Consider use of agent to increase ventilation…
If not immediately reversible and inadequate
ventilation (severe hypercapnia / hypoxia /
clinically deteriorating) then maintain artificial
ventilation with minimal anaesthesia to prevent
awareness
Other mechanical causes of
hypoventilation
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Obesity
Diaphragmatic splinting from abdo
distension or tight dressings
Pain from thoracic or upper abdominal
wounds
Intra pleural air/fluid/blood. NB
Pneumothorax from IPPV in COPD /
occasionally healthy young patients
To artificially increase
ventilation
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Controversial
Doxapram
 Produces respiratory stimulation mediated through the
peripheral carotid chemoreceptors. As the dosage level is
increased, the central respiratory centres in the medulla are
stimulated with progressive stimulation of other parts of the
brain and spinal cord.
 The onset of respiratory stimulation following the recommended
single intravenous injection of doxapram hydrochloride usually
occurs in 20 to 40 seconds with peak effect at 1 to 2 minutes.
The duration of effect may vary from 5 to 12 minutes.
 Increased Vt and RR. CI: CAD, Epilepsy
Aminophylline
 2mg/kg slow IV bolus. Can cause seizures, increases cerebral
O2 requirements, arrhythmias
Paediatric considerations
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Particularly sensitive to temperature
Can be extremely opiate sensitive
Prematures are highly susceptible to
apnoea up to 60 weeks gestational age.
Thanks