Shared airway

Optimize the access to the mouth and oropharynx

Good communication
Nasal intubation, LMA vs ETT
Use of adrenaline

Airway, Mallampati.
Size of mouth and mouth opening wrt fractures.
AMPLE history for emergencies
Regular history noting endocarditis risk
Medications

PREMEDICATION:
Atropine, glycopyrrolate
Local anaesthetic (amide vs esters)
Preemptive analgesia
LIDOCAINE TOXICITY
Slurred speech
Altered CNS
Muscle twitching
Seizures
INTRAVENOUS INDUCTION AGENTS & SEDATION TECHNIQUES
Objective of anaesthetic:
To provide a still, comfortable patient and optimize the operating conditions for
surgery.

Types of Agents:
 PROPOFOL
o Enhances the effects of GABA by boosting the binding of GABA
to its receptors
o Potent, ultra-short-acting sedation
[onset: 90-100 secs, offset (dose dependant): 5-10 mins]
 No Analgesia
o Rapidly metabolized by liver  dose dependant decrease in arterial
bp & cardiac output
o High rate of discomfort – severe pain with injection
o No antagonists
EVE’S SIGN –
o Long-term tx  propofol infusion syndrome (PRIS)
inability to touch
o Contraindicated in children the tip of nose
o Used with Remifentanil (synthetic opioid) accurately
 assesses
 MIDAZOLAM [BENDZODIAZEPINES] achievement of
o Enhances the effects of GABA [reduces neuronal excitability] depth of sedation
by binding to GABA-A receptors & allowing greater influx of Cl- ions
o Effects; - amnesia -anticonvulsant -anxiolysis -muscle relaxation &
-SEDATION no analgesia
o Can also cause RESPIRATORY DEPRESSION / hypotension
esp if administered rapidly
o Recovery more rapid (5h) and incidence of venous thrombosis is
less than with diazepam
o Effects are reversed with Flumazenil.
o Contraindications:
 Hypersensitivity
 Erythromycin use (potentiates effect)
 Concomitant use of barbiturates, alcohol, narcotics/other cns
depressants, cimetidine, omeprazole, kava or valerian
 Glaucoma
 Depressed vital signs, shock/coma
 Caution when using with opioids  both are respiratory depressants
  Midazolam + opioid (fentanyl/morphine for analgesia) are used
together but there is an increased risk of oxygen desaturation
and cardiorespiratory complications
 KETAMINE
o Acts as an antagonist for the NMDA (N-methyl-D-aspartate) glutamate
receptor; inhibiting glutamate activity
o Dissociative anaesthesia + analgesia
 BUT can cause EMERGENCE DELIRIUM in adults; not typical in
children < 15 or adults >65
 The incidence of this can be reduced by decreasing dose of ketamine +
using benzodiazepine- (a small hypnotic dose of a short acting
benzodiazepine/barbiturate is recommended to terminate severe
emergence reactions) [NB hypnotic dose = dose req to induce
anaesthesia]
 1:1 with propofol also reduces incidence of emergence delirium
 In typical doses for sedation ketamine does not affect pharyngeal-
laryngeal reflexes  patent airway +spontaneous respiration => can be
used for emergency procedures when fasting cannot be done
 Contraindications: when increased BP would pose a risk of
complications
 SEVOFLURANE for gaseous induction
o Blocks NDMA [excitatory] receptors & enhances [inhibitory pathways]
GABA (exact mechanism not completely understood
o Volatile inhalation agent
o Rapid action & recovery
o Low irritant
 TIVA or INHALATION for maintenance
o TIVA = Total Intravenous Anaesthesia – maintains anaesthesia via repeated
boluses or an infusion of intravenous anaesthesia
o Inhalation involves gaseous anaesthetic delivered via mask or endotracheal
tube

Analgesia
 Local anaesthetic
o Weak base that crosses cell membrane to become ionized and bind to Na
channels  LA blocks Na channels  inhibits depolarization and
transmission of the signal along the nerve
o BUPIVACAINE  used intraoperatively in pts under GA => slow onset +
long duration =. Prolonged pain control post-op 1.5-5.5 hrs – max dose
2.5mg/kg – cardiotoxic
 o LIDOCAINE – most widely used – rapid onset + intermediate – long duration
(1-2hrs) – max dose [w/o epi] 4.4mg/kg [w epi] 7mg/kg
 Dental cartridge has 2.2ml = 44mg
 Should not be given to pts allergic to sulpites
 NSAIDs
o NSAIDs block the activity of COX (COX-1 & COX-2) enzymes which
converts arachidonic acid to prostaglandins (PGs)
 Reducing the PG levels
 Decrease in pain perception
 Reduces inflammation & lowers fever
o Can cause GI effects; irritation, ulceration & bleeding esp in older pts and
those taking corticosteroids, worsen asthma and cause lithium toxicity. Assoc
with thrombotic risk & can lead to acute renal failure in pts with cardiac
failure/renal damage
o Contraindications; pts with current/past peptic ulcers, pregnancy
 Paracetamol
o Mechanism of action not fully understood but thought to act on COX-2
enzymes reducing prostaglandin production => modulates the endogenous
cannabinoid system
o Analgesic & antipyretic
o No gastric irritation BUT can cause liver damage
 Opioids
o Activate mu1 receptor in the CNS
o CODINE – methylmorphine – contraindicated in children – widely used for
post-op pain – dose = 30-60mg +/- paracetamol
o Activation of mu2 receptor = resp depression, sedation, constipation, nausea +
vomiting  contraindicated in pts with acute/chronic respiratory disease &
seizures
o TRAMADOL – mild opioid – acting as opioid receptor agonist; inhibiting
sinal monoamine reuptake  causes less sedation & resp depression but
nausea & vomiting still an issue; [serotonin receptors] 5HT3 antagonists to
prevent this may reduce the analgesic efficacy
Anaesthesia is a phase. It is defined as a continuum in which increasing the depth of
anaesthesia results in;
1. Loss of consciousness
2. Recall
3. Somatic and autonomic reflexes
Vs conscious sedation where pt is able to
maintain their own airway and CVS
Phases of anaesthesia =
 Analgesia
 Excitement
  Surgical anaesthesia
 Overdose
Induction phase of anaesthesia = transition from awake  anaesthetized state
Can be IV or inhalation; inhalation excitatory phases can be very unpleasant BUT with IV
induction pts rapidly move though phase 2 and attain surg anaes much quicker
Period of great physiologic state; - hypotension, arrythmias, hypoventilation/apnea, aspiration
of gastric contents, laryngospasm, adverse drug rxn, involuntary movement
Common induction agents ; propofol, thiopentol, midazolam/diazepam, ketamine
Complications of IV induction: hypotension, hypoxemia, apnea
1. Barbituates [pentothal] {thiopentone} one arm bridge circulation 12 s lasting 5-15min

apnea & loss of airway reflexes, severe hypotension, CNS effects (these dx no longer
available) termination effect via redistribution but final metabolism is via liver
2. Propofol – 2,6 diisopropylphenol. Most commonly used agent today – rapid loss of
consciousness with rapid clear-headed recovery

GA vs Sedation