Anaesthesia Flashcards
What are the three stages of general anaesthesia?
- Induction
- Maintenance
- Emergence
What are the three A’s of general anesthesia?
- AMNESIA - lack of response and recall to noxious stimuli – Unconsciousness
- ANALGESIA - pain relief
- AKINESIS - Immobilisation/paralysis
What are the three types of drugs that make up the ‘triad of anaesthesia?’
- Hypnotic agents
- Analgesics
- Muscle relaxants
What are induction agents and what is there aim? What are the two ways in which an individual can be induced?
Transition from an awake to an anesthetised state.
- IV - induce loss of consciousness in one-arm brain circulation time (10-20 secs; lasting for 4-10 mins)
- Inhalational Induction - usually amnesia maintenance
What are the IV induction agents?
- Propofol
- Etomidate
- Ketamine
- Thiopentone
What are the characteristics of propofol?
- Dose
- Mechanism
- Advantages
- Disadvantages
- CIs
‘Milk’ (MJ overdose!) - most common
- 1.5 – 2.5 mg/kg: titrated against patient response (anaesthesia onset)
- Enhances inhibitory function of the GABA through GABA-A receptors
-
Rapid induction (<30 secs) and emergence (lasts 2-5 mins)
- Anti-emetic properties (↓ incidence of postop N&V (PONV))
- Excellent suppression of pharyngeal reflexes and good brochodilator
-
Rapid induction (<30 secs) and emergence (lasts 2-5 mins)
- Lipid based - pain on injection
- Marked ↓BP (systemic vasodilatation), ↓HR ↓RR (act on respiratory centre),
- Involuntary movements
- Allergies/rashes - contains soya, eggs
- Lipid based - pain on injection
-
Children - “propofol infusion syndrome”
- metabolic acidosis, lipidaemia, cardiac, arrhythmias and increased mortality
-
Children - “propofol infusion syndrome”
What are the characteristics of Thiopentone?
1 Dose
2Type of drug and Mechanism
3 Advantages
4 Disadvantages
5 CIs
‘Pale yellow powder’
- 4-5 mg/kg
- Barbituate - Binds to GABA-A receptor and enhances inhibitory effects of GABA
-
Rapid induction (<30sec) (∴ main use = rapid sequence induction)
- Anticonvulsant properties
- Can imprvoe neurological outcomes ( ↓cerebral blood flow (↓ICP), ↓metabolic rate and ↓oxygen demand - ‘Barbitutate coma’
-
Rapid induction (<30sec) (∴ main use = rapid sequence induction)
- Depresses heart contractile force (↓BP/Q BUT ↑HR) - caution in hypovolaemia
- ↓RR
- Depresses heart contractile force (↓BP/Q BUT ↑HR) - caution in hypovolaemia
- Airway reflexes well preserved (vs propofol) - coughing/laryngospasm
- Rash/bronchospasm (causes histamine release)
- Intrarterial Injection - thrombosis and gangrene
5. Porphyria (overproduction and excretion of porphyrins) - can precipitate prophyria due to hepatic enzyme induction
What are the characteristics of etomidate?
Dose
Mechanism
Advantages
Disadvantages/CIs
- Non-barbituate - 0.3 mg/kg
- Binds to GABA-A receptor and enhances inhibitory effects of GABA
- Haemodynamic stability - minimal ↓BP/Q
- Lowest incidence of hypersensitivity reactions
- Haemodynamic stability - minimal ↓BP/Q
- Pain on injection (lipid emulsion)
- Involuntary movements
- High incidence of post-op N&V
- Adreno-cortical suppression (suppressed for up to 72hrs) - ∴
- Pain on injection (lipid emulsion)
CI in critically ill/septic shock patients (↑ mortality)
What are the characteristics of Ketamine?
Dose
Mechanism
Advantages
Disadvantages/CIs
Dose: 1 - 1.5 mg/kg. Slow onset (90 secs) and lasts 5-10 mins
Mech:
- Anatagonises NMDA (↓effects of glutamate (main excitatory NT) ► dissociative anaesthesia (conscious but insensitive to pain) - anterograde amnesia
- Acts on opioid and muscarinic receptors. Also effects Na/Ca movement across cell membranes ► Profound analgesia
- Inhibits monoamine reuptake ► anti-depressant effects
- Because of above, can be used as sole anaesthetic for SHORT procedure
Advan:
- minimal effect on resp drive, protective airway reflexes = intact ∴ good preshopital
- ↑HR/BP/Q - useful in shocked, unwell patients
- Bronchodilator - role in management of severe asthma
Disadvan:
- Hypersalivation ► airway obstruction (Tx with anti- muscarinic e.g. glycopyrrolate)
- N&V
- Catalepsy - open eyes, slow nystagmus gaze. Intact corneal/light reflexes
- Emergence phenomenon: vivid dreams, hallucinations
- Hypertonus, occassional purposeful movements
What are the inhalation/volatile agents for maintaining (usually) /inducing amnesia?
- Sevoflurane
- Desflurane
- Isoflurane
- Enflurane - rare
What is the definition of minimum alveolar concentration (MAC)?
- Minimum alveolar concentration of vapour (%) at steady state
- That prevents the reaction to a standard surgical stimulus (traditionally a set depth/width of skin incision)
- In 50% of subjects
What factors can increase MAC? (i.e. anaesthesia requirements)
Things that increase metabolism
- Infancy (peaks at 6 months)
- High temp
- Pregnancy
- Chronic Alcoholism
- Stimulants (cocaine/amphetamine)
What factors reduce the MAC (i.e. anaesthestic requirement)
Things that REDUCE metabolism…
- Hypoinatraemia
- Hypothermia
- Elderly
- Acute alcohol intoxication
- Pregnancy
- Anemia
- CNS depressant drugs e.g. benzo, opioids
What are the characteristics of Sevoflurane?
- Colour/characteristics
- Uses
- Route and MAC
4 Effects on CV, resp and CNS
SEs
- Clear, colourless, sweet smelling, non- irritant
- Popular for inhalational induction. Maintenance.
- Route: Inhalation, via calibrated vaporiser. MAC: ~2%
- ↓BP (vasodilation), ↓RR, minimal effect on cerebral blood flow
- Malignant Hyperthermia, nephrotoxic (↓ renal blood flow)
What are the characteristics of Isoflurane?
- Colour/characteristics
- Uses
- Route and MAC
4 Effects on CV, resp and CNS
- SEs
- Clear, colourless liquid. Pungent smell
- Maintenance. Pungent smell limits use for induction.
- Routes: Inhalation via calibrated vaporiser. MAC: 1.15%
- Least effect on organ blood flow ↓BP (vasodilation), ↑HR, ↓RR, slight ↑cerebral blood flow/ICP
- Malignant hyperthermia.
What are the characteristics of Desflurane?
- Colour/characteristics
- Uses
- Route and MAC
4 Effects on CV, resp and CNS
- SEs
- Clear colourless liquid. Low lipid solubility (∴ rapid induction and elimination). High volatility.
- Long operations e.g. organ donation. Unsuitable for induction.
- Inhaled via electrically heated vaporiser - dual circuit gas/vapour blender. MAC: 6%
- ↓BP, ↑HR, ↓RR, min effect of cerebral blood flow/ICP
- Malignant hyperthermia. Reduces renal blood flow.
What is the MAC of Enflurane? Why isnt it really used anymore
- MAC: 1.6%
- Potentially causes hepatotoxicity
What is the pathohpysiology of malignant hyperthermia? What triggers it?
Triggers: ALL volatile inhalation agents, Suxamethonium
Pathophysiology:
- Autosomal genetic condition of ryanodine receptor gene
- Triggering agent causes uncontrolled release of cytoplasmic free calcium from skeletal muscle SR
- Causes muscle rigidity ► ↑ metabolism ► body temp
What are the CFs of malignant hyperthermia?
Due to uncontrolled ↑ in intracell Ca ion conc, there is:
- Muscle rigidity
- ↑ metabolism (↑ end tidal CO2 first, ↑ body temp occurs later )
- Rhabdomyolysis - renal failure
(Arrythmias, ↑K+, and DIC may develop)
What are the two types of general analgesias used in anaesthetics?
- Short Acting - rapid acting, high potency (fentanyl = 100x more potent than morphine)
- Long Acting
Name three short acting analgesics. When/why are they used?
- Fentanyl, Remifentanil, Alfentanil
- Intra op analgesia - suppresses response to laryngoscope, reduces surgical pain
Name two long acting analgesics. When/why are they used?
- Morphine, Oxycodone
- Intra-op and post-op analgesia
What other types of analgesics are commonly used?
Most commonly used analgesic
- Paracetamol
Most commonly used oral opioid in adults
- Codeine
Intravenous NSAIDS
- Ketorolac, Parecoxib
What are the two main groups muscle relaxants? How do they exert there action?
-
Depolarising
-
PHASE I: Cause depolarisation by mimicking the effect of Ach to nicotinic receptor. Contraction; fasciculations are seen and repolarisation is inhibited
- Not hydrolysed by acetylcholinesterase, therefore…
- PHASE II:‘Persistent depolarisation’ = desensitisation (end plates lose sensitivity)
-
PHASE I: Cause depolarisation by mimicking the effect of Ach to nicotinic receptor. Contraction; fasciculations are seen and repolarisation is inhibited
-
Non-depolarising
- Competitive antagonist - bind to nicotinic ACh receptors causing gradual muscle paralysis
- Compete with ACh for nicotinic receptor binding, preventing end plate depolarisation and impulse propagation
- Name one depolarising muscle relaxant.
What is:
- It used for
- It’s dose
- The SEs
Suxamethonium
Use: 1. Rapid intubation of the trachea and short periods of neuromuscular blockade. 2. Rapid sequence induction
Dose: 1 - 1.5 mg/kg
SEs:
- Bradycardia
- Muscle pains (due to fasciulations before paralysis)
- Hyperkalaemia
- ↑ICP, IOP and gastric pressure
- Anaphylaxis - skin rash ► bronchospasm
- Malignant hyperthermia
- Suxamethonium apnoea
What is the cause of suxamethonium apnoea?
- Suxamethonium = metabolised by plasma cholinesterase (usually 5-10mins) - some PTs lack /have an altered enzyme ∴ ↓ metabolism
- ∴ PTs may = paralysed for many hrs after administration
- Pts must be anaesthetised/ventilated until after sux eliminated (slow!)
What drug is used to reverse Suxamethonium?
None!
Name the a) short, b) intermediate and c) long acting non-depolarising muscle relaxants
Short: Atracurium, mivacurium (aka nevercurium - hardly used!) (10 letters, earlier in alphabet!)
Intermediate: vecuronium, rocuronium** (10 letters, later in alphabet)
Long: Pancuronium (11 letters!)