Lecture 29: Inhalation and IV anaesthetics Flashcards
What is the triad of goals for an anaethetist?
Hypnosis = IV or Volatile agent
Immobility = Muscle relaxant
Autonomic Areflexia = Opioids
Modern approach is to find a balance of all of these, ether back in the day could achieve all three but not balanced.
How do volatile agents work?
Inhalation:
P(i) P(A)P(a)P(br)
Exhalation
The agents are not metabolised by the body, they are inhaled, do their job and are exhaled.
How do volatile anaesthetics act?
A ‘Unifying’ explanation based on a non-specific effect such as expansion of lipid bilayer and disruption of receptor and ion channel function
BUT not all lipophilic volatile agents produce anaesthetisa
What is the increasingly likely theory of how volatile anaesthetic agents work?
Increasingly likely it is through GABA modulation in the brain and glycine modulation in the spinal cord
What is MAC?
1 Mac =minimum alveolar concentration (%) producing immobility on standard surgical stimulus in 50% of patients.
I.e more potent agents have lower MAC
MAC is a means of describing dose and potency referenced to a standard clinical effect
Describe the dose response curve for MAC 6% desoflurane and what happens when other drugs are given?
The dose response curve is steep for desoflurane. i.e 6% for 50% probs of no movement. 8% des = 95% no chance.
If fentanyl is given with desoflurane it left shifts the curve.
BUT we dont give desoflurane to stop movement. we give to put to sleep
What increases MAC?
- Young age
- Hyperthermia
- Hyperthyroid
- Drugs i.e meth
- Heavy alcohol
What decreases MAC?
- Old age
- Hypothermia
- Hypothyroid
- Drugs i.e opioids, depressants
- Pregnancy
- Low oxygen, high CO2
How is dosing titrated?
Can supply Fi at 6% but this is all thats inhaled so need to work out a % what means 6% will be the alveolar concentration (Desoflurane)
What can be controlled to achieve F(a) desired?
Fi and minute volume i.e RR. Titrated against end tidal gas.
Whats the difficulty with achieving a desired F(a)?
Constantly takes drugs away there need to increase RR and Fi % value to achieve F(a)
What are the pharmacodynamics of inhaled volatile agents on the CNS?
- Hypnosis, immobility, amnesia
- Decrease CMRO2
- Dose dependent increase CBF and ICP (Care with use in neurosurgery)
What are the pharmacodynamics of inhaled volatile agents on the CVS?
- Peripheral vasodilation, lower BP
- HR unchanged
- Modern agents do not affect SV greatly
What are the pharmacodynamics of the inhaled volatile agents on the RS?
Respiratory depressant
- Impair ventilatory response to hypoxia
- Impair ventilatory response to CO2
(I.e intubation needed to manage RR)
Bronchodilation
What are modern inhalation anaesthetics?
Methyl ethyl ethers
What is the benefit of methyl ethyl ethers?
Increasing fluoride substitution = Decrease solubility, increase stability, decrease flammability, decrease dehalogination
Summarise the modern anaesthetic agents:
Isoflurane - Relative cardiovascular stability
Sevoflurane - Good for gas inductions (can react with CO2 absorber, nephrotoxic byproduct) NOT PUNGENT
Desflurane - Rapid onset and offset. Good for longcases. Greenhouse gas though PUNGENT
What are the types of IV anaesthetic agents?
- Barbiturates (Thiopentone)
- Phenols (Propofol)
- Imidazoles (Etomidate)
- Phencyclidine derivatives (Ketamine)
- Benzodiazepines (Midazolam)
Describe the mechanism of action for IV anaesthetics:
Thiopentone, Propofol, Etomidate, Midazolam all work by enhancing GABA, prolong Cl- current hyperpolarisation
Ketamine: Bind to PCP receptor antagonise glutamate supress excitation
- Also has analgesic effects
What is the pharmacokinetics of IV anaesthetics:
- Highly lipid soluble and cross BBB
- Drug from IV bolus taken up by VRG organs, then leave these organs as less perfused tissues take up drug and concentration in blood falls
- Offset after single IV dose is therefore due primarily to redistribution (NOT METABOLISM)
- > Pt will wake even though total drug in body not changed much
- Actual metabolism is slower
Write some notes on Thiopentone:
- Very rapid onset (10s)
- Rapid offset by redistribution
- Slow clearance (will accumulate in multi-dosing or infusing)
- Metabolised in liver, induces liver enzymes
- Some decrease in PVR and BP (Enhanced in shock)
- Resp depression and loss of airway reflexes
Write some notes on propofol:
- mod rapid onset (20sec)
- Rapid offset by redistribution
- Fast clearance (10x that of thio)
- > Cleaner offset (No hangover)
- > Minor accumulatioon in infusion
- > Can be used as infusion for maintenance
- Metabolised in liver
- Significant decrease in PVR and BP (Enhanced in shock)
- Resp. depression and loss of airway reflexes
Compare and contrast propofol and thiopentone:
- Propofol has replaced thiopentane as standard IV anaesthetic
- > Emphasis on high turnover/day stay (propro wears off faster, less hangover)
- > Can be used in infusion for maintenance (Good for neurosurgery; Dec. CBF and ICP
- > Less enzyme induction
So why bother with anything else? - Both of these agents can cause CV instability
Write some notes on etomidate:
- Remarkable CV stability
- Less resp. depression
- Rapid clearance and good recovery profile
BUT
- Adrenocortical inhibition
- Myoclonus and epileptogenic
Write some notes on ketamine:
- Analgesic
- CV stimulant (Good in shocked patient)
- Preserves airway reflexes and resp. drive
- Increases CMRO2, CBF and ICP (Not good for neurosurgery)
- Dissociative state, emergence slower and complicated by dysphoria
Write some notes on total IV anaesthesia:
- Avoids inhalation route
- Avoids complications of vapour
- > Malignant hyperthermia (Rare)
- > Post-op nausea and vomiting
- > Intracranial hypertension
BUT expensive and no agent monitoring
