54.2 Anaesthesia Flashcards
What are the 2 main classes of general anaesthetic agent? (with examples)
*Intravenous (e.g. propofol)
*Inhalation (e.g. isoflurane and sevoflurane)
What are intravenous anaesthetics used for? Why?
Intravenous - induction of anaesthesia
*more rapid progression to stage 3 (surgical anaesthesia), ↓ time spent in stage 2 (excitement).
*Short ½ life in blood
*eliminated slowly → not for maintenance (Propofol → exception)
What are inhalation anaesthetics used for? Why?
Volatile/ inhalation anaesthetics → maintenance of sedation.
*As arterial blood concentration can be rapidly altered by changing the alveolar PP of the drug = effective control + allows rapid adaptation of stage of anaesthesia.
What is the definition of MAC?
Minimum Alveolar concentration of an inhalation anaesthetic.
*Defined as the pulmonary concentration sufficient to generate loss of motor response to pain in 50% of individuals.
What does a decreased MAC indicate?
↑ potency
Why is MAC useful?
MAC used as is additive → can use multiple anaesthetics to ↑ MAC, while keeping drug doses ↓
What are the proposed theories for the mechanism of action of general anaesthetics?
-Lipid theory
-GABA potentiators
-Inhibition of glutamate mediated NMDA receptors
What are the three main criteria which needs to be met during anaesthesia?
Hypnosis/narcosis (unconsciousness)
Analgesia (Loss of response to painful stimuli)
Relaxation (Loss of reflexes)
What is the effect of anaesthetics on peripheral smooth muscle (vasculature)?
Anaesthetics block voltage gated calcium channels (VSMC don’t depolarise in response to sympathetic tone)
VASODILATION
What is the mechanism of the effect of general anaesthetics on heart contractility?
Decreased inotropy
Reduces intracellular calcium ion concentration and impaired transmembrane calcium flux via L-type calcium channel inhibition
What are the physiological challenges associated with general anaesthesia?
*Cardiovascular depression
*Respiratory depression
*Thermoregulation
What are the effects of general anaesthesia on the CV system?
Decrease in cardiac output and venous pressure (with greater compliance and venodilation) = arterial blood pressure falls = dangerous to the perfusion of downstream tissues
How are the effects on the CV system managed?
*Drugs administered to restore CO, arterial + venous pressures
*IV fluids (colloids + crystalloids) → ↑ ECV + mean circulatory pressure → promote tissue perfusion
*Cardiac inotropes (e.g. adrenaline) → act on GSβ1Rs to ↑ Ca2+ influx + ↑ cardiac contractility (+ ↑ gradient of starling curve)
Can ↑ risk of arrhythmias due to risk of afterdepolarisations.
*Vasoconstrictors (e.g. NA/ ephedrine/ phenylephrine) → act as α1 agonists → ↑ arterial BP.
*Antimuscarinics (e.g. atropine/ glycopyrrolate) → block M2 to prevent heart from being inappropriately driven by unopposed vagus nerve (as SNS abolished). Hence, protection from bradycardia.
What is the effect of general anaesthetics on the respiratory system?
Respiratory depression: insufficient exchange between O2/ CO2 → build up of CO2 → can be fatal.
How can the respiratory effects be managed?
*Intubation + mechanical ventilation → via endotracheal intubation.
*Maintains airway patency + prevents hypoxia/ hypercapnia (stop PCO2 building to dangerously high concentrations (decreased ventilation) )
*NMJ blockers used for muscle paralysis to allow endotracheal intubation.
*Antimuscarinics (e.g. glycopyrrolate) → ↓ secretions
*Respiratory stimulants (e.g. doxapram + almitrine) → to correct postoperative respiratory depression.
*Thought to act on carotid bodies to block BK K+channels → depo → ↑ AP frequency + ↑ ventilation
*Mimicking effects of endogenous hypoxia.
