Studied by 6 people
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what inhaled drug is a noncompetitive NMDA antagonist?
nitrous oxide
What are the pungent inhaled anesthetics? what does that mean?
most pungent: desflurane
pungent: isoflurane
they cause bronchial/airway irritation (can cause coughing and bronchospasm)
What are the non-pungent inhaled anesthetics? what does that mean?
nitrous oxide, sevoflurane, halothane
they do not cause airway irritation (no coughing or bronchospasm)
Which inhaled anesthetic is an incomplete anesthetic?
nitrous oxide
______ ensures that the anesthetic concentration in the CNS is stable and effective for maintaining anesthesia during the procedure
equilibrium (steady state)
explain what the FA/FI ratio is
The driving force for gas uptake is the ratio between inspired concentration
(partial pressure) and alveolar concentration
______ determines how much anesthetic gas will dissolve in the blood
alveolar partial pressure (concentration)
the higher the partial pressure in the alveolus, the higher the partial pressure in the
blood
The faster the uptake of anesthetic agent, the greater the difference between
inspired and alveolar concentrations and the ________
why?
slower the rate of induction
when uptake is fast, a large amount of anesthetic is absorbed into the blood from the alveoli
An increase in ventilation does what to the rate of induction?
increases it
there is better maintenance of alveolar concentration
explain the relationship between solubility and the speed of induction
more soluble= slower induction
less soluble= faster induction
(remember the 2 graphs with the balls)
explain cardiac output, pulmonary blood flow, and speed of onset
decrease in cardiac output → decreased pulmonary blood flow → faster onset
increase in cardiac output → increased pulmonary blood flow → slower onset
The greater the difference in alveolar and venous gas concentrations,
the ____ the time to achieve equilibrium with brain tissue
greater difference= longer time
what tissue group is first to receive anesthetic and the first to approach steady state?
the vessel rich group (brain, heart, liver, kidney, endocrine organs)
What drug causes these toxicities?
body space volume expansion
diffusion hypoxia
vitamin B12 inhibition
nitrous oxide
What drug causes these toxicities?
CO2 production in desiccated CO2 absorbers
malignant hyperthermia
all of them except nitrous oxide (isoflurane, desflurane, sevoflurane, and halothane)
What drug causes these toxicities?
cortisol synthesis inhibition
myoclonus
etomidate (possibly isoflurane too?)
What drug causes these toxicities?
environmental toxicities
nausea and vomiting
all inhaled anesthetics
What drug causes these toxicities?
nephrotoxicity (potentially) by compound A
sevoflurane
What drug causes these toxicities?
sympathetic stimulation → tachycardia and hypertension
desflurane
explain the relationship between solubility and elimination/recovery
lower solubility = faster elimination
____ is a major route of elimination for the inhaled anesthetics
exhalation
explain the relationship between ventilation and elimination
increased ventilation → increased rate of elimination
explain the relationship between exposure time and elimination time
longer exposure → prolonged elimination time
MAC correlates with ____
potency
1 MAC is equal to what?
the alveolar concentration that prevents movement in 50% of patients in response to
a standardized stimulus (eg, pain of surgical incision)
MAC allows for correlation of what? and comparison of what?
MAC provides a direct correlation between the alveolar anesthetic concentration and the concentration at the sites of action in the CNS
MAC permits comparison of the relative anesthetic potencies of the different anesthetics
explain the effect of isoflurane, desflurane, and sevoflurane on the cardiovascular system
decrease BP with little to no effect on cardiac output
note: desflurane actually increases BP bc of its sympathetic stimulation
all 3 increase HR
explain the effect of nitrous oxide on the cardiovascular system
negligible effects
bronchodilation is most pronounced with ____
sevoflurane
what drug(s) increase cerebral blood flow and intracranial pressure and decrease cerebral metabolic rate?
desflurane and isoflurane
what drug(s) decrease cerebral blood flow and intracranial pressure and decrease cerebral metabolic rate?
sevoflurane
what drug(s) increase cerebral blood flow and intracranial pressure and increase cerebral metabolic rate?
nitrous oxide
What inhaled anesthetic does not relax smooth muscle or skeletal muscle?
nitrous oxide (isoflurane, desflurane, and sevoflurane all relax)
have minimal myocardial depressant effects and favorable hemodynamic profiles and may be suitable for patients with impaired myocardial function
Isoflurane, desflurane, and sevoflurane
____ must be used with caution and close monitoring in patients with coronary artery disease
desflurane (because of its transient sympathetic effects)
what are 4 common effects/postoperative phenomena of anesthetics?
nausea and vomiting, HTN and tachycardia, post-anesthesia shivering, and emergence excitement (restlessness, crying, moaning, thrashing, etc.)
explain halothane hepatitis
Halothane forms is metabolized by CYP2E1, forming the reactive intermediate trifluoroactylchloride that binds covalently to liver proteins forming neo-antigens, which induces an immune attack that results in liver cell damage and inflammation
what is context-sensitive half-time?
The time required for the concentration of drug to decrease by 50% after
stopping a continuous infusion in the context of the duration of the infusion
basically, its the half-time of the drug in relation to the duration of the drug infusion
____ helps predict how long it will take the patient to recover after the infusion is stopped
context-sensitive half-time
(longer infusion = longer context-sensitive half-time)
What IV anesthetics MOA is GABA-A receptors positive allosteric modulator?
propofol, etomidate, midazolam
What IV anesthetics MOA is a noncompetitive NMDA receptor antagonist
ketamine
what drug’s therapeutic use is total intravenous anesthesia, a sedative hypnotic in the ICU, and monitored anesthesia care sedation?
propofol
What 2 drugs are used as sedative-hypnotic in the ICU?
propofol and ketamine
What drug’s disadvantages are:
an infusion syndrome (rare)
egg phosphate in soybean oil vehicle (potential allergens and microbial risk)
propofol
What drug’s disadvantages are:
involuntary myoclonic movements
transient acute adrenal suppression (inhibits 11-beta-hydroxylase → decrease cortisol synthesis)
etomidate
What drug’s disadvantages are:
Sympathetic stimulation increases HR, BP, CO and myocardial O 2 demand (may be harmful in CAD or HTN)
Hallucinations, delirium upon withdrawal, dissociative experiences, nightmares, nausea/vomiting
ketamine
What is propofol infusion syndrome? this definition is specific, but understand it in general
a rare complication: metabolic acidosis, hypotension, hepatomegaly, hyperlipidemia, rhabdomyolysis, CV collapse
What is the fundamental concept that ensures that the anesthetic concentration in the CNS is stable and effective for maintaining anesthesia during the procedure?
When the partial pressure of the anesthetic gas in the inspired air, alveoli, arterial blood, and CNS are in equilibrium (steady state, FA /FI =1), the desired clinical effect will be produced
What four factors influence the uptake of anesthesia?
Inspired concentration of anesthetic gas
Solubility of gas in blood (defined by the blood:gas partition coefficient)
Cardiac output
Alveolar-venous partial pressure difference
Why does faster the uptake of anesthetic agent lead to a slower speed of induction?
When uptake is fast, a large amount of anesthetic is absorbed into the blood from the alveoli → creates a significant difference between the inspired concentration and the alveolar concentration (FA <FI ) as the alveoli are depleted of anesthetic faster than they can be replenished by inhalation → it takes longer to reach equilibrium(FA /FI =1)
Why is the speed of induction slower with the more soluble anesthetic gases?
The more soluble the anesthetic is in blood (the higher the partition coefficient) → the greater the capacity for uptake into the blood → the slower rate of rise in partial pressure → the longer it takes to reach equilibrium
How does an increase in cardiac output lead to a slower speed of induction?
↑ cardiac output → ↑ pulmonary blood flow → the partial pressure of the gas in blood rises more slowly → slower rise in FA /FI towards equilibrium → slower speed of onset
This effect is more pronounced with soluble agents, which achieve equilibrium slower
How does a large alveolar to venous partial pressure difference influence the speed of induction?
Anesthetic gas is taken up from arterial blood into nonneural tissues → venous circulation returns to pulmonary circulation with little or no dissolved anesthetic gas → generates a partial pressure difference between alveolar gas and pulmonary blood.
The greater the difference in gas concentrations, the longer the time to achieve equilibrium with brain tissue
What is the acronym MAC stand for?
Minimum alveolar concentration
How is MAC used in dosing inhaled anesthetics?
Dosing of inhaled anesthetics is guided by MAC and MAC values are additive
Which inhaled anesthetics are potent volatile agents in common use?
Isoflurane, desflurane, sevoflurane
Why is nitrous oxide referred to as a weak anesthetic?
Nitrous oxide has low potency. Even 100% nitrous oxide does not achieve 1 MAC. Therefore, it is combined with a potent volatile anesthetic
Why may isoflurane, desflurane, and sevoflurane be suitable for patients with impaired myocardial function?
Isoflurane, desflurane, and sevoflurane cause vasodilation, which lowers systemic vascular resistance and blood pressure with minimal change in cardiac output (preserves cardiac output) – of course, with close monitoring to ensure patient safety and optimal outcomes
What is the concern with the use of desflurane in patients with coronary artery disease?
Although desflurane causes vasodilation with minimal effect on the force of contraction (inotropy), its transient sympathomimetic properties cause tachycardia and hypertension, especially at high dose. These cardiac effect may induce cardiac ischemia and heart attack
Which inhaled anesthetics are associated with malignant hyperthermia in patients with a genetic disorder in skeletal muscle calcium regulation?
The halogenated anesthetics: isoflurane, desflurane, sevoflurane, and halothane
Not nitrous oxide
