General Anesthetics Flashcards
how might anesthetics interfere with CNS function
altering communication between neurons. Inhibiting excitatory synaptic transmission or enhancing inhibitory transmission
pre-synaptic effects of anesthetics
volatile anesthetics have been shown to decrease glutamate release and increase/decrease GABA release
post-synaptic effects of anesthetics
- inhibit NMDA receptors (glutamate)
- increase frequency or length of time the Cl- channel remains open (GABA)
- increase affinity of receptor for glycine (glycine)
meyer-overton rule
potency of anesthetic gases directly related to their solubility in olive oil
unitary theory of anesthesia
since variety of structurally unrelated drugs obey the rule, they must bind at same hydrophobic site. anesthetics likely bind to hydrophobic pockets on proteins
physical characteristics of inhaled anesthetics
inorganic gas (N2O), volatile liquids (the fluranes)
desflurane vaporizer
desflurane boils at room temperature. dual gas blender. anesthesiologist controls vapor output into circuit by adjusting resistor. vapor is blended with fresh gas flow
inhaled anesthetics uptake and distribution
absorbed from alveoli into pulmonary capillary blood. distributed to site of action (brain) and to reservoirs. variably metabolized, eliminated principally via lungs. partial pressure gradients propel anesthetic to the brain
2nd gas effect
ability of high volume uptake of one gas to accelerate the rate of increase in Pa of a second gas.
Guedel’s 4 stages of CNS depression
- analgesia -> analgesia + amnesia
- excitement/delirium (increased HR, RR, BP)
- surgical anesthesia
- medullary depression; without support of respiration and circulation, death ensues
which inhaled drugs increase heart rate?
isoflurane and desflurane (likely due to pungency stimulating airway receptors and eliciting reflex tachycardia)
CNS effects of volatile agents
dose dependent depression of EEG, sensory evoked potentials, motor evoked potentials, cerebral metabolic rate. Increase in cerebral blood flod, increase in ICP which parallels cerebral blood flow
Cardiovascular effects of volatile agents
decrease in vascular resistance and arterial blood pressure. more blood flow to brain, muscle, and skin, less to liver, kidneys, and gut
respiratory effects of volatile agents
decrease in tidal volume, ventilatory response to hypoxia and hypercarbia. increase in respiratory rate. relaxation of airway smooth muscles
neuromuscular function of volatile agents
directly relax skeletal muscle. potentiate the effects of neuromuscular blockers. trigger malignant hyperthermia in susceptible patients
barbituates
produce hypnosis/sedation only! produce hypnosis by enhancing actions of inhibitory neurotransmitters. Bind to GABAa to enhance Cl- conductance. Inhibit actions of glutamate by blocking NMDA receptors.
what do barbituates and propofol produce?
dose dependent decreases in blood pressure due to vasodilation. dose dependent respiratory depression. barbituates are negative inotropes
propofol
hypnosis through GABAa Cl current enhancing. Inhibits NMDA glutamate receptors. Depresses spinal cord neurons via action at GABAa and glycine receptors. stored in soybean oil/glycerol/egg (watch allergies). anti-emetic at low doses.
propofol infusion syndrome
observed in critically ill patients receiving high dose infusions for more than 48 hours. associated with administration of catecholamines and glucocorticoids in these patients. metabolic acidosis, myocardial failure, rhabdo, hyperkalemia, renal failure.
etomidate
only d-isomer that has anesthetic activity. associated with pain on induction due to propylene glycol solvent. subcortical disinhibition leads to involuntary myoclonic movements. high incidence of N/V post op. single dose inhibits cortisol synth. minimal cardiorespiratory depression! GABAa receptor agonist. NO ANALGESIC ACTIVITY!
ketamine
dose related unconsciousness, amnesia, and analgesia. patients appear to be in cataleptic state. nystagmus, lacrimation, salivation. eyes remain open. CNS site of action may be thalamoneocortical projection system. depresses neuronal function and stimulates limbic system. NMDA receptor antagonist.
ketamine cardiovascular effects
directly stimulates sympathetic nervous system. Increases systemic and pulmonary vascular resistance. Increases heart rate. increases cardiac work and O2 consumption (dont use in ppl with coronary artery disease). increases cerebral blood flow and intracranial pressure
ketamine respiratory effects
bronchodilator. used as induction agent in patients with reactive airway disease, hypovolemia, heart things.
unique uses of ketamine
useful sedative for pediatric patients. combined with propofol for IV procedural sedation. used as adjuvant to general anesthesia to decrease opioid use. Post op use to decrease opioid use. can be used in chronic pain management.
