Unit 06: IV Anesthetics Flashcards
history of anesthetics
- many surgical procedures would not eb possible without use of general anesthetics
- in late 1700 discovered that inhalation of volatile chemicals could affect consciousnes
ex included nitrous oxide and diethyl ether, they were used in parties in early 1800s but not for surgery
- many lipid soluble volatile chemicals can cause general anesthesia but only few can do so wthout causeing irreversible effects
ether
C4H10O
- inhalant introducted in 1846
- demonstrated little respiratroy or cardiovascular depression and relatively non-toxic
- does have pungent odour and expolsive properties
- now used as starter fluid in combustion engines
Chloroform
CHCl3
early general anesthetic
- inhalant introducted in 1847
- non pungent odor and non explosive
- can be hepatotoxic resulting in severe cardiovascular depresion
- was preferred inhalant until almost 1950
Nitrous oxide
- early gneral anesthetic
- only considered for partial anesthesia b pateints remain conscious but is excellent analgesic (painkiller)
- todau used in dental clinics, hospitals and few veterinary clinics to reduce amount of hydrocarbon anesthetic required
cyclepropane
- early general anesthetic
- used to be most populat
- associated with explosions in operating room bc has flammable properties
sodium pentobarbial
- barbiturate that is effective and relatively safe if used with caution (narrow safty margin)
- elimination of drug requries hepatic metabolism- metabolism is too slow in emergency situations
- injectible anesthetic
halogenated hyrocarbon anesthetics
- Halothane used in 1950s, compared to other inhalents was much mroe safe
- has not ben replaced with otehr halogenated hydrocarbon anesthetics: isoflurance, sevoflurane and desflurane
what are steps in anestheesisa
- start with alert patient
- sedative or anxiolytic administered and unconscious state is induced and maintains
*patient is premedicated
- general anesthesia is induced rapidly with injectible drug
- pateitn then transferred to an inhalant for maintenance
- after surgery the patient recovers
*premedications are combo of drugs given prioir to general anesthesia, generally administered via intramuscular or intravenous route
what is the purpose of premedication?
- induce sedation and provide analgesia
- sedation decreases the patients interest in theri surroundings making them less anxious and less likely to be uncooperative while analgesia aids with intraoperation and post operation pain
- premedications may or may not include as anticholineric to reduce respiratory secretions and salivation depending on effects of other drugs being used
what is an induction agent?
- utilized to produce general anesthesia and are administed via IV
- goal is to rapidly render the patient unconscious
- effect does wear off rapidly and longer lasting agents generally not used bc of associated risk
- the patient is then maintained in unconscious state with an inhalable anesthetic
what are the stages or planes of anesthesia during induction?
- Stage of analgesia: intitally analgesia then unconsciousness
- analgesia, amnesia and euphroia
- stage is variable and depends on anestheic agent used
- Stage of excitment: strugglng delirium, irregualt breathing, vomiting, urination, defecation (still unconscious)
- stage or plane of aurgical anesthesia: regular breathing returns, movement cease, decreasing eye movement
* stage where surgery occurs - Stage of medullary depression (if process goes too far): breathing stops, no eye movement, cardia depressions and arrest (death)
**goal is to get patient through the excitement phase (stage II) quickly, even before it is oberved. since inhalent anesthetics induce unconsciousess too slow rapid acting injectible anesthetics are used intiitally - stage II maintained with an inhalent
Mechanism of action of Barbiturates
- bidn to GABA receotrs in CNS, enhcances ability of GABA to open Cl- channels and inhibit action potentials
*simialr to benzodiazepines that potentiate GABAs action but at higher concentrations
- Barbiturates also activate the receptor without GABA present leading to more intense depression and is overall more dangerous
- black various cation channels like glutamate gated channels (ex NMDA) or voltage gated sodium channels which further supresses excitation
- they are metabolized by hepatic enzymes and toher drugs may inhibit these enzymes which would allow bariturate levels to become otxic
what is sodium thiopental
- only barbiturate still used for induction
- has “ultra-short” duration wiht rapid induction and receory rate
- administered thorugh IV injection
- following multiple doses can accumualte in system and result in a longer ercovery
- recovery invovles redistribution from the brain to the muscle and fat which occurs within minutes then metabolism slows down over several hours (groggy feeling)
physiological effects of sodium thiopentl
(inc side effetcs)
- effects on CNS include dose dependent depression in 10-30 seconds and unconsciousness for 1 1/2 -3 min
Respiratory depression (dose dependent) → apnea bouts
Cardiovascular depression → can be fatal if CVS disease present
Enhance pain sensitivity
Causes blood to pool in viscera → decreases flow to the brain
Accumulation results in l onger recovery → patients feel groggy
- is partial dose is administered it is liekly to cause excitement as opposed to induction
Relationship between barbiturates and pain
barbiturates are NOT analgesics, they actually enhance pain sensitiveity
explain the structure of the GABA A receptor and drug bdingin sites
- pentameric, each of 5 subunits is one of 3 predominant subtypes α, β, or γ.
- activation reuqires the simultaneous binding of two GABA molecules to the receptor, one to each of the two binding sites at the interface of the α and β subunits
- each subunit of teh GABAA receptor has 4 membrane spanning regions and a cysteine loop in the extracellular N terminal domain (blue segment and a dashed line)
- drug binding sites on GABAA receptor depicted in B: + indicates agonist of allosteric moedulator at the GABAA receptor, - inducates competitive or non competitive antagonist action
