General Anesthetics

Question 1

how might anesthetics interfere with CNS function

Answer 1

altering communication between neurons. Inhibiting excitatory synaptic transmission or enhancing inhibitory transmission

Question 2

pre-synaptic effects of anesthetics

Answer 2

volatile anesthetics have been shown to decrease glutamate release and increase/decrease GABA release

Question 3

post-synaptic effects of anesthetics

Answer 3

1. inhibit NMDA receptors (glutamate)
2. increase frequency or length of time the Cl- channel remains open (GABA)
3. increase affinity of receptor for glycine (glycine)

Question 4

meyer-overton rule

Answer 4

potency of anesthetic gases directly related to their solubility in olive oil

Question 5

unitary theory of anesthesia

Answer 5

since variety of structurally unrelated drugs obey the rule, they must bind at same hydrophobic site. anesthetics likely bind to hydrophobic pockets on proteins

Question 6

physical characteristics of inhaled anesthetics

Answer 6

inorganic gas (N2O), volatile liquids (the fluranes)

Question 7

desflurane vaporizer

Answer 7

desflurane boils at room temperature. dual gas blender. anesthesiologist controls vapor output into circuit by adjusting resistor. vapor is blended with fresh gas flow

Question 8

inhaled anesthetics uptake and distribution

Answer 8

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

Question 9

2nd gas effect

Answer 9

ability of high volume uptake of one gas to accelerate the rate of increase in Pa of a second gas.

Question 10

Guedel’s 4 stages of CNS depression

Answer 10

1. analgesia -> analgesia + amnesia
2. excitement/delirium (increased HR, RR, BP)
3. surgical anesthesia
4. medullary depression; without support of respiration and circulation, death ensues

Question 11

which inhaled drugs increase heart rate?

Answer 11

isoflurane and desflurane (likely due to pungency stimulating airway receptors and eliciting reflex tachycardia)

Question 12

CNS effects of volatile agents

Answer 12

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

Question 13

Cardiovascular effects of volatile agents

Answer 13

decrease in vascular resistance and arterial blood pressure. more blood flow to brain, muscle, and skin, less to liver, kidneys, and gut

Question 14

respiratory effects of volatile agents

Answer 14

decrease in tidal volume, ventilatory response to hypoxia and hypercarbia. increase in respiratory rate. relaxation of airway smooth muscles

Question 15

neuromuscular function of volatile agents

Answer 15

directly relax skeletal muscle. potentiate the effects of neuromuscular blockers. trigger malignant hyperthermia in susceptible patients

Question 16

barbituates

Answer 16

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.

Question 17

what do barbituates and propofol produce?

Answer 17

dose dependent decreases in blood pressure due to vasodilation. dose dependent respiratory depression. barbituates are negative inotropes

Question 18

propofol

Answer 18

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.

Question 19

propofol infusion syndrome

Answer 19

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.

Question 20

etomidate

Answer 20

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!

Question 21

ketamine

Answer 21

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.

Question 22

ketamine cardiovascular effects

Answer 22

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

Question 23

ketamine respiratory effects

Answer 23

bronchodilator. used as induction agent in patients with reactive airway disease, hypovolemia, heart things.

Question 24

unique uses of ketamine

Answer 24

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.

Question 25

dexmedetomidine

Answer 25

approved for sedation less than 24 hours in ventilated ICU patients. binds alpha 2A and 2B receptors in locuse caeruleus and spinal cord to produce sedation, sympatholysis, and anlgesia. easy to wake up, similar to natural sleep. used for awake procedures in OR, used post op for bariatric surgery. limited respiratory depression

Question 26

what do neuromuscular blockers do?

Answer 26

interrupt transmission of nerve impulses at the neuromuscular junction thus preventing muscles from contracting. structurally related to ACh. positive charge attracts them to muscarinic and nicotinic ACh receptors.

Question 27

succinylcholine

Answer 27

depolarizing agent. stimulates and opens ion channels of all ACh receptors. muscle groups contract in disorganized fashion. rapid onset and short duration. used to facilitate intubation. terminated by diffusion away from NMJ, rapidly hydrolyzed.

Question 28

succinylcholine side effects

Answer 28

stimulation of all cholinergic autonomic receptors. cardiac dysrhythmias. hyperkalemia can be life threatening with pre-existing neuromuscular disease. increased intracocular pressure, intracranial pressure, intragastric pressure. myalgias, masseter spasm

Question 29

non-depolarizing agents

Answer 29

drug-receptor interaction blocks the receptor from binding ACh, thus preventing physiologic depolarization and muscle contraction. effect terminated by diffusion away from NMJ. neuromuscular blockade can be antagonized by administration of an anti-cholinesterase

Question 30

factors effecting reversal of neuromuscular blockade

Answer 30

depth of blockade, duration of action of non-depolarizer, choice and dose of anti-cholinesterase (edrophonium is fastest onset, neostigmine is more complete antagonism, pyridostigmine has longer duration)

Question 31

monitoring NMB: train of four

Answer 31

reduction in muscle response during elecctrical nerve stimulus reflects type and degree of blockade. non-depolarizing blockade has a TOF ration of less than 1, wait for 1-2 twitches prior to reversal. Depolarizing blockade has TOF ratio of 1

Question 32

two drugs used to reverse NMB

Answer 32

glycopyrrolate, atropine. block muscarinic effects by administering anti-muscarinic. glycopyrrolate preferred