anesthetics Flashcards
(40 cards)
measurement of anesthetic potency
potency=concentration of anesthetic that prevents movement in response to pain
for inhaled anesthetics, minimal alveolar concentration (MAC)- prevents movement in response to pain of 50% of subjects
mechanism of anesthesia
multicomponent common effects by all anesthetics include membrane hyperpolarization, and effects on synaptic function–> inhibitory neurotransmission is increased and excitatory neurotransmission is reduced
likely molecular target: GABAa receptors, GABA- regulated chloride channel, function is enhanced by most but not all anesthetics, anesthetics produce allosteric interactions; not a direct effect on GABA binding
NMDA receptors, Glutamate- regulated cation channel
stages of anesthesia
premedication, induction (needs to be non frightening, usually IV anesthetic is used, emergency inhaled)
parenterally administered anesthetics
generalities: used to facilitate rapid induction of anesthesia and have replaced inhalation as the preferred method of anesthesia induction
all are hydrophobic and a single IV bolus results in high concentration in brain and sp cd within a single circulation time–> rapid induction of anesthesia
subsequently, blood levels drop and the anesthetic redistributes back into the blood from the brain–> in other tissues where its slowly released and metabolized (t.5 of the anesthetic in the body and the duration of action are not the same)
Barbituates and sodium thiopental (10-30 seconds) duration of action= 10 minutes
sodium thiopental
used to induce anesthesia, produces uncosciousness in seconds, duration of action is 10 minutes
has a long half life (12 hours) so hung over after anesthesia has worn off. Dose should be reduced if premedicated with other CNS depressants including opiates, benzodiazepines and alpha 2 agonists
Intra arterial injection can produce sever inflammation and can even be necrotic so this is not done, can be administered to peds rectally
sodium thiopental side effects
CNS- reduces cerebral oxygen utilization and as a consequence reduces cerebral blood flow and intracranial pressure
CV- produces vasodilation (mainly venous side), can produce hypotension, with impaired ability to compensate venodilation, not CI in patients with coronary artery disease bc demand is reduced, no arrythmogenic effects
respiratory depression
propofol
onset and duration of anesthesia are the same as barbituates, maintains and induces anesthesia, is used to maintain and induce anesthesia
antimimetic: advanatge to avoid nauseated following surgery
shorter half life than thiopental: used when you dont want hangover, rapidly metabolized in liver and in lungs to inactive metabolite excreted in urine
SE of propofol
pain upon injection, can be given with lidocaine or administered into larger veins
prodrug for popofol, fospropofol (watersoluble and less paiful on injection)
can produce excitation during induction
CNS: same as barbituates
CV: more severe decrease in BP than thiopental, produces both vasodilation and depression of myocardial contractility, age related, blunts baroreceptors (use with caution in patients with intolerace of decreased BP_
more respiratory dpression than thiopental
propofol has demonstrated abuse liability
etomidate
induces anesthesia in pts at risk for hypotension
high incidence of pain on injection and myclonus (quick jerk)
Pain is dealt with using lidocain and myoclonus is reduced premedication with benzodiazepines or opiates
etomidate SE
CNS: like thiopental
CV: less than thiopental and propofol which is the major advantage of etomidate
produces a small increase in HR with little to no decrease in BP
less respiratory depression than thiopental
Drawbacks: significantly more nausea and vomiting than thiopental
increased post-surgical mortality due to suppression of the adrenocortical stress response, primarily when the anasthetic has been given for a prolonged period of time. therefore only used to induce anesthesia in patients prone to hemodynamic problems
ketamine
produces dissociative anesthesia
Characterized by: progound analgesia, unresponsiveness to commands even though eyes can be open, amnesia (incomplete unless used with benzodiazepines) spontaneous respiration, typically administed iv but can also be used via intramuscular, oral and rectal routes
Advantages: profound analgesia, very little respiratory depression, bronchodialation
ketamine SE
produces nystagmus, salivation lacrimation spontaneuous limb movements and increased muscle tone
increased intracranial pressure
emergence delerium hallucinations, vivd dreams, illusions, not really used, can be used in combo with benzodiazepines to reduce symptoms
increased BP due to indirect sympathomimetic activity
usefulness: reserved for pts with bronchospasm, children undergoing short painful procedures
midazolam
short acting benzodiazepine used for conscious sedation, anxiolysis and amnesia during minor surgical procedures
used as an induction agent, used as an adjuct during regional anesthesia, anti anxiety effects make it useful preop
slower induction time and longer duration than thiopental and propofol
metabolized by hyrdroxylation to an active metabolite
SE of midazolam
has been associated with respiratory depression and respiratory arrest especially when used IV to produce conscious sedation
should be used in caution in pts with NMJ diseases, parkinsons bipolar
CV: like thiopental
effects reversed with FLUMAZENIL
inhalation anesthetics general consideration
very low therapeutic indicies LD50 2-4
pharmacokinetics are unique and important
all the compounds are easily vaporized liquids or gases at room temp thus they can be administered by inhalation
rather than a concentration gradient across a barrier, the partial pressure of anesthetics determines transmembrane movement
equilibrium is reached when partial pressures are the same in adjacent compartments (not necessarily equivalent to equal concentration bc solubility can differ)
3 partition coefficients to consider in inhaled anesthetics
blood:gas partition coefficient (determines absorption in lung; inhaled anesthetics are taken into body through gas exchange at the alveoli): measure of the anesthetic in an aqueous versus gaseous environment, low blood:gas coefficient–> rapid equilibration in blood bc there is low solubility in blood, since the concentration in brain cannot rise unless the concentration in blood concentration rises rate of induction of anesthesia is inversely related to the blood gas coefficient
Brain:blood (determines distribution to the brain, which is the site of action)
Fat:blood (determines redistribution and recovery from anestheic effect)
factors that affect induction
anesthetic partial pressure (Fi) in the inspired air (affects the max partial pressure of the gas at the alveoli Fa), ultimately affects the partial pressure in the blood, the rate of transfer will increase as the concentration is increased therefore rapid induction can be achieved with higher concentrations the faster Fa/Fi approaches 1 the faster anesthesia will occur
Alveolar ventilation: directly controls Fa/Fi: increased ventilation increases the rate of rise of Fa/Fi. Magnitude of effect of ventilation is dependent on blood gas partitiion coefficient moderately blood soluble anesthetics are affected more than low soluble agents
Pulmonary blood flow (determined by cardiac output)- increased blood flow slows the rate of rise in Fa/Fi–> decreases the rate of induction of anesthesia, effect is most dramatic for moderately soluble anesthetics
factors that affect tissue distribution
Blood: tissue partition coefficient
tissue blood perfusion; organs with highest perfusion include brain, heart liver, kidneys spanchnic beds
brain-high partition coefficient and high perfusion compared to fat with high partition coefficient but low perfusion
factors that affect anesthetic elimination (rate of recovery from anesthesia)
reverse of induction- blood:gas partition coefficient is the most important determinant- low solubility anesthetics are eliminated fastest
duration of exposure: bc of tissue accumulation–longer the exposure the longer it takes to eliminate the anesthetic
ventilation
metabolism- hepatic metabolism can contribute to recovery from some older anesthetic not a desirable property
malignant hyperthermia
serious adverse effect of gaseous anesthetic exposure, rare but potentially fatal
heritable, pockets of individuals
skeletal muscle disorder, triggered by anesthetic
Consists of muscle rigidit hyperthermia, tachycardia, hyoercapnia, hyperkalemia metabolic acidosis
isoflurane
moderate blood:gas PC, moderate rates of induction and recovery, excreted unchanded in expired air
inhaled anesthetic in us and worldwide
can be used to induce and maintain anesthesia, but is mostly used for maintanence
often used with NO to reduce amount needed
isoflurane SE
airway irritant, coughing, decreases tidal volume, increases respiratory rate, all anesthetics depress respiration in the CNS center and increase PaCO2
Myocardial depression, results in decrease in BP, arrythmias, cerebral vessel vasodilation can result in increased intracranial pressure
desflurane
Volatile liquid at room temp, very low solubility in blood:gas partition coefficient) therefore induction and recovery are rapid
excreted unchanged in expired air
used for outpatient surgeries/maintenance not used to induce because of respiratory irritation
skeletal muscle relaxation
SE: relative to isoflurane, Cv same, Resp: worse as an irritant can produce bronchospasm
sevoflurane
Very low blood:gas partition C
5% administered dose is metabolized to fluoride ion in the liver, there is some concern that can cause renal damgage
degraded to compund A by absobants in the anesthesia administration administration apparatus
Uses: very popular in and out patient, can be used to induce and maintain, children and adults, NOT a respiratory irritant
SE: similar to isoflurane not as much as respiratory depression
