anesthesiology exam 2 - IV induction agents Flashcards

Intracranial pressure
Terms Definitions
what are the stages of anesthesia?
I: voluntary movement, II: involuntary movement/delirium, III: surgical anesthesia, IV: medullary death
what are the planes of stage III anesthesia?
1: eyeball movement present, 2: loss of laryngeal reflex, sluggish palpebral, analgesia, stable pulse and respiration, 3 decreased respiratory function, weak corneal reflex, centered and dilated pupil
what stage and plane of anesthesia is ideal for surgery?
stage III, plane 2
why use injectable induction agents?
IV drugs, rapidly depress the CNS, bypass or limit the time a patient spends during stage II-excitement (physically and emotionally unpleasant, dangerous)
what are some injectable induction agents?
barbiturates (thiopental), propofol, dissociative anesthetics (ketamine/tiletamine), etomidate
how are barbiturates classified?
duration of action (long, intermediate, short, ultrashort), chemical structure
what increases the lipid solubility of barbiturates?
substitution of sulfur for oxygen (ie thiobarbiturates vs oxybarbiturates)
what does increasesd solubility of barbiturates result in?
increased solubility resulting in decreased duration of action (shorter acting) with increased metabolic degradation and increased hypnotic potency
what are general features of barbiturates that require caution?
barbiturates are acids that are prepared as salts that are basic, so must be administered IV only and will cause perivascular skin sloughing (pH of thiopental is >10)
what are the CNS effects of barbiturates?
potentiating inhibitory effects and inhibiting excitatory effects (increase GABA binding, the main inhibitory neurotransmiter and block glutamate binding, the main excitatory neurotransmitter), depress the reticular activating system which controls arousal (results in calming and decreassed motor activity), anticonvulsant, awakeing due to redistribution into fat and msucle
what makes barbiturates 'cerebral-friendly'?
quiet the electroencephalogram (EEG), decrease cerbral metabolic demands (oxygen, glucose), decreases cerebral blood flow (CBF), lower intra-cranial pressure (ICP)
what are the cardiovascular effects of barbiturates?
in healthy dogs it decreases cardiac contractility and increases HR and systemic vascular resistance, in compromised dogs it increases cardiovascular depression, bigeminy
what is bigeminy?
a normal sinus beat followed by PVC, repeating
what are the respiratory effects of barbiturates?
respiratory depression and/or apnea, laryngospasm
what are the pharmacokinetics of barbiturates?
available drug is the unbound, unionized form (acidosis/hypoproteinemia increase the availabley drug), awakening is due to redistribution (animals with small fat stores can have exaggerated effects and risk overdose and repeated doses can accumulate in fat and muscle), extensively metabolized by liver, excreted unchanged by kidney, barbiturates cause microsomal enzyme induction (P450 system)
what is the metabolism of barbiturates in greyhounds?
greyhounds are deficient in enzyme neede for hepatic metabolism, minimal fat stores, easier to overdoes, longer to wake up, not recommended
what is the analgesic effect of barbiturates?
none, anesthetized brains do not 'feel' pain (the pain pathways are activated)
how are barbiturates administered?
to effect
what is an unusual effect of barbiturates?
sequestration of red blood cells in the spleen
what is the CNS effect of propofol?
binds to the inhibitory GABA receptor (separate from the binding site of the barbituarates)
why is propofol described as 'cerebral friendly'?
quiets the electroencephalogram (EEG), decreases cerebral blood flow (CBF), lowers intra-cranial pressure, decreases cerebral metabolic demands (oxygen/glucose)
what are the cardiovascular effects of propofol?
myocardial depression, no compensatory increase in HR (unlike barbiturates), vasodilation, does not sensitize myocardium to arrhythmias
what are the respiratory effects of propofol?
significant respiratory depression (rate related), not having the ability to intubate and ventilate a patient after propofol induction is malpractice
what is the analgesic effect of propofol?
no analgesia
what is the metabolism of propofol?
extensive liver metabolism, extensive extra-hepatic metabolism (metabolism exceed hepatic blood flow,elimination almost unchanged with liver failure)
what are the pharmacokinetics of propofol
duration of action (induction dose last ~8-10min, arousal is due to redistribution), route of administration (IV only, extravascular administration does not result in skin sloughing)
what are specifics unique to propofol?
no preservative and great culture medium, smooth induction and recovery (without pre-medicants), 'calming' agent at subanesthetic dose, anticonvulsant, heinz body formation with CRI in cats
what are examples of dissociative anesthetics?
what type of induction agent is ketamine/tiletamine/phencyclidine?
dissociative anesthetics
how do dissociative anesthetics work?
NMDA (N-methyl-D-aspartate) antagonists (NMDA receptors are excitatory), dissociate the thalamo-cortical and limbic systems (altered consciousness-wiggy, catealepsy, amnesia, analgesia), tiletamine (part of the combination telazol)
what are the CNS effects of ketamine?
increased cerebral oxygen demands, increased cerebral blood flow, increased intracranial pressure (caution with head injury/space occupying lesions), increased intra-ocular pressure, may alter seizure threshold
what are the cardiovascular effects of ketamine?
increases sympathetic tone-NE release (increase in HR, increase in BP, increase in CO), can lead to tachycardia and arrhythmias, cautions should be used with animals with cardiomyopathy or increaseed sympathetic tone (hyperthyroidism)
what are the respiratory effects of ketamine?
apneustic breathing (rapid breaths followed by breath-holding on inspiration), mild respiratory depression (mild hypercapnia, more severe with debilitated animals or when combined with other respiratory depressants), bronchodilation (Asthma patients)
what are the analgesic effects of ketamine?
analgesic, may also interact with opioid receptors (synergistic), disrupt windup of pain in dorsal horn, treat certain chronic pain states (interrupts central sensitization, amantadine is an oral NMDA antagonist), sub-anesthetic doses for analgesia (no behavioral effects)
what is the metabolism of ketamine?
dogs and horses (metabolized to active metaboline: norketamine which has 10-30% activity of ketamine), cats (excreted mostly unchanged through kidney), metabolites excreted through kidney, decreased renal excretion may prolong drug effects
what are the pharmacokinetics of ketamine?
used in wide variety of species with a large therapeutic index/high saftey margin, duration of action (dependent on species; dose and if used in combination with other drugs ~10-20min of anesthesia), route of administration (IM & IV, absorbed via mucous membranes, sometimes painful on injection)
what are general features of dissociatives?
poor muscle relaxation (use with benzodiazepines, alpha-2 agonists, phenothiazines), wake-up from solo drug is rough
what is telazol?
a dissociative, tiletamine + zolazepam
what is telazol contraindicated in?
new zealand white rabbits (renal necrosis)
what is the metabolism issues of telazol?
the metabolism of each drug may be different in different species; cats (T1/2 tiletamine =2.5h, T1/2 zolazepam=4.5h, wake up with benzodiazepine effects; slow, smooth), dogs (T1/2 tiletamine=2.5h, T1/2 zolazepam=1.5h, wake up with ketamine effect but more agitated, excited)
what is etomidate?
ultrashort non-barbiturate (imidazole compound)
what is the CNS effect of etomidate?
depresses CNS function (activating the inhibitory GABA receptors), decreases cerebral blood flow, decreases intracranial pressure, decreases cerebral metabolic rate, not as favorable as barbiurates and propofol
what are the cardiovascular effect of etomidate?
minimal to no changes in CV funciton (HR, BP, SV-unusual for an anesthetic), VERY heart friendly
what are the respiratory effects of etomidate?
brief apnea, mild decrease to tidal volume, respiratory rate rarely changed
what are the endocrine effects of etomidate?
decrease adrenocortical activitiy for 4-6h, inhibits 11-B hydroxylates which converts cholesterol to cortisol, decrease stress response, multiple doses/CRI may cause hypoadrenocorticism and death
what are the unique features of etomidate?
poor muscle relaxations (administer with muscle relaxant like benzodiazepine, has a lack of muscle relaxation resulting in muscle rigidity, myoclonus, vocalization, opisthotonus), emesis, 35% propylene glycol solution (pain on injection, hemolysis), expensive (~$4/ml so 4kg cat ~$8.00, 40kg dog ~$80.00)
how is etomidate administered?
duration of actions (5-10min of anesthetic effect), IV only
what is the effect of using opioids as induction agents?
CV friendly, slow induction, bradycardia, respiratory depression, poor muscle relaxation
what is the effect of using inhalents as induction agents?
face-mask/induction chamber, lots of waste gas exposure, slow induction, vasodilation, increased sympathetic tone
what is the best induction agent for patients with portosystemic shunts?
what is the best induction agent for a patient in heart failure?
what is the best induction agent for a patient with high ICP?
which induction agent increases CV function?
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