23.Anesthetic Drugs Flashcards
types of opioid receptors
mu, kappa, delta located in peripheral tissue and CNSG protein coupled receptors, upon activationinflux of K+ into cell and a decrease in IC CaDecreases release of NT (substance P, glutamate) in PREsynaptic cellshyperpolarizes POSTsynaptic cells
T/FAnalgesia supplied by opioid can reduce inhalant anesthesia requirement by 40-60%
TRUEAnalgesia supplied by opioid can reduce inhalant anesthesia requirement by 40-60% depending on the dose and type used
DEA class of opioids
mu opioids control II substances (hi abuse control)buprenorphine IIIbutorphenol, tramadol IV (low abuse control)
GI side effects of opioids
ileusnauseavomiting (SQ, IM)—stimulates CRTZpassive regurgitation under GA (morphine)mu opioids: incr bile duct sphincter of Oddi and pyloric sphincter tone
historically histamine release has been associated with IV administration of which opioids
meperidinemorphine (lesser extent)
reversal agent for mu opioids
naloxone 0.01 mg/kg IV (30-60 min DOA)butorphenol 0.01-0.05 mg/kg IVresolution of dysphoria occurs at much lower doses than would be associated with loss of analgesic effects of the primary opioid
non GI side effects of opioids
sedationdysphoriaminimal cardiovascular depressiondose dep resp depressionhyperthermia (cats–hydromorphone)urinary retention (Peterson et al JAVMA 2014 says IV bolus hydro sign assoc with UR not norphine epidural)
why is morphine the preferred opioid for epidurals
LOW lipophilicity stays in epidural space for a long time12-24 hr epidural DOA3-4 hr IV DOA
potency for mu receptorhydromorphone vs morphine vs oxymorphone vs fentanyl
potency of morphine prototype 1hydromorphone 8 x more potent than morphineoxymorphone 10 x more potent than morphinefentanyl 100 x more potent than morphine
major advantage of oxymorphone
10 x more potent than morphineBUT alsoless dysphoria, passive regurg than morphine$$$$$$
Unique to merperidine
SHORT DOA (1 hr)histamine releasepotency 10x LESS than morphinecontributes to serotonin syndrome
define serotonin syndrome
result of excessive serotonin in the CNSresults in hypothermia, anxiety, shock, seizures, rhabdomyolysis, acute renal failureMonoamine oxidase inhibitors (MAOIs)–>block enzyme that recycles serotonin, keeps serotonin around longer
unique to methadone
mu opioid that does NOT release histamine2 x more potent than morphine3-4 hr DOANMDA receptor antagonist (associated with less excitatory responses in cats)
fentanyl patch in dogs vs cats
cats: reliable therapeutic concentrations when placed on lateral thorax. Analgesic starts 12-16 hr post placement and up to 5 daysdogs: less reliable plasma concentrationsDO NOT use on anesthetized and/or hypothermic patients
unique to remifentanil
metabolized by plasma esterases NOT the liver/kidneylike fentanyl, has a short half life (CRI)
buprenorphine MOA and potency
40 x more potent than morphinePARTIAL mu agonistceiling effect: higher doses are NOT associated with increased analgesia or side effects but may result in increase duration of action!
bioavailability of buprenorphine in cats
pH feline mouth buprenorphine is more rapidly absorbed 100% transbuccal
MOA butorphenol
kappa AGONISTmu ANTAGONIST
T/FButorphenol as antiemetic properties
TRUE
Tramadol
WEAK mu agonisteffects are likely opioid INDEPENDENTeffects more likely due to inhibition of serotonin and NE reuptakepotential for serotonin syndrome in combo w MAOi
define neuroleptanalgesic
opioids combined with tranquilizer state of analgesia, sedationsynergistic effect
MOA of benzodiazepines
enhance effects of GABAGABA binds its receptor and allows CL- influx which hyperpolarizes and prevents propagation of the AP signalschedule III controlled substances DEAdiazepam and midazolam
reversal agent for benzodiazepines
flumazenil
MOA phenothiazines/acepromazine
depress dopamine in the reticular activating system (which is necessary to maintain arousal)antihistamine and antiemetic propertiesblocks alpha 1 receptors –>vasodilationNo analgesia, NO reversal agentlong lasting
T/FAcepromazine is contraindicated in seizure patients
FALSE(JAAHA 2006 Tobias et al disproved)acepromazine is NOT contraindicated in seizure patients
MOA alpha 2 agonists
ratio alpha 2: alpha 1tranquilizersdecr NE release in CNSwork on peripheral alpha 1 receptors (vasoconstriction,, hypertension, arrhythmogenic) may eventually lead to hypotensionrespiratory depression and bradycardiaprovide some analgesia
side effects with alpha 2 agonist xylazine
alpha 2:alpha 1 160:1induces vomiting in cats92 fold incr compl44 fold incr in cardiac arrest in dogs (generally contraindicated)
medetomidine alpha 2 agonist
alpha 2:alpha 11600:1 MUCH more alpha 2 specific vs xylazinereversal with atipamezoldexmedetomidine is isomer: less sedation, shorter DOA
T/Fanticholinergics should be administered carefully in cardiac patients or patients given alpha 2 agonists because the incr HR will decrease overall myocardial demand
FALSEanticholinergics should be administered carefully in cardiac patients or patients given alpha 2 agonists because the incr HR will INCREASE overall myocardial demandreverse alpha 2 drugs first, then give anticholinergics
what induction agent also provides analgesia
KETAMINEpropofol, thiopental, etomidate do NOT provide analgesia
MOA propofol
agonism at GABA receptors–> increasing inhibition throughout CNSemulsion–>susceptible to bacT contaminationquick acting; extra hepatic metabolismapnea, hypotension/vasodilation, reflex tachycardia, pain on injection, myoclonusreduces intracranial pressure
T/Fpropofol may cause oxidative damage to feline RBC
TRUEpropofol may cause oxidative damage to feline RBCBUT NOT CLINICALLY ANEMIC
ketamine MOA
dissociative agent (dissociation btwn higher brain functions and unconscious function)antagonism at NMDA receptormild sympathomimetic effects if intact SNS (may increase myocardial work)muscle rigidity, increases salivation, inr intraocular and intracranial pressureSchedule III class DEA
barbiturates thiopental MOA for induction
modulate the effects of GABA at the GABA receptornarrow therapeutic index: cardio and reap depressant, arrhythmogenicliver metabolismthiopental: necrosis if extravascularly (use lidocaine/saline infusion w warm compress to tx)
breed of dog that should avoid thiopental
greyhounds (sighthounds)lack a critical enzyme for thiopental metabolism resulting in prolonged anesthesia recovery
etomidate MOA for induction
works at GABA receptormost significant benefit is minimal cardiovascular depressioncan cause muscle rigidity
why is etomidate contraindicated in patients with relative adrenocortical insufficiency
etomidate induces adrenal gland suppression for up to 6 hrin critical ill who may be at risk for adrenal insufficiency, etomidate is contraindicated
what is MAC
minimum alveolar concentration=concentration of anesthetic required to prevent movement in response to a stimuli in 50% of normal patientsusually 1.2-1.5 x higher to require a patient not to move to surgical stimuliit is a measure of spinal cord afferent and efferent transmissionSPECIES ISO SEVODOG 1.3% 2.1%CAT 1.7% 3.1%
absorption of inhalant depends on what factors
- blood/gas solubility of the inhalant2. CO3. minute ventilation4. difference btwn the alveolus and venous blood inhalant concentration
describe solubility btwn isoflurane and sevoflurane
sevo is LESS soluble than iso sevo has a HIGH MAC bc of lower solubility
MOA of local anesthetics
block fast Na channels on afferent nerveslidocaine: lipophilic (FAST onset 5 min; SHORT DOA 45-60min)bupivacaine: higher lipid solubility and protein binding (slower onset 45 min but LONGER DOA 6-8 hours)
T/FBupivacaine can be given IV like lidocaine
FALSEBupivacaine should NOT be given IV (risk sign cardiotoxicity); but can be given intrapleural post thoracotomylidocaine can be used IV for analgesia, anti arrhythmic
define Bier Block
local anesthetic (lidocaine) given IVApply Esmarch bandage to exsanguinate leg, place tourniquet, and give lidocaine distally
lidocaine vs bupivacaine toxicity doses based on species
LIDOCAINE BUPIVACAINEDOG >8 mg/kg >4 mg/kgCAT >6 mg/kg >2 mg/kg*lower therapeutic index of bupivacainelidocaine toxicities seen usually CRI or high IV boluses: initial GI, then neuro, final cardiac and death
depolarizing vs nondepolarizing NM blockers
depolarizing: succinylchloride (mimic Ach)nondepolarizing (more common): atracurium, vecuronium
reversal agents for non depolarizing NM blockers
atracurium is generally short acting and degrades via hoffman elimination (independent liver/kidney)1. neostigmine2. edrophoniumboth inhibit ACH-ase therefore incr ACH available may result in cholinergic crisis SLUDDE
anticholinergic agents
atropine and glycopyrrolateparasympatholyticsdecrease hi vagal tone
which prostaglandin is the MOST potent for transmission of pain associated with inflammation
PDE2Made from cyclocoxygenase pathway and AAimportant prostaglandin for vasodilation and kidney perfusion
how to combat anesthetic relative hypotension from vasodilation
lower inhalantIVF small bolusesalpha agonists (ephedrine, phenylephrine)dopamine (higher doses than for Beta effects)if not effective with above, vasopressin
anesthesia considerations for patients with cardiac disease
HCM (cats) with or without SAM–aim to slow HR, maintain volume without fluid overloadDCM (dobies)–require inotropic support; risk arrhthymiasValvular endocardiosis (old toy breeds)–aim to incr stroke volume and fwd flow; risk volume overload**lower surgical fluid volume rate, consider isotonic low sodium fluid (0.45% NaCl with 2.5% dextrose), monitor CVP, use benzos NOT alpha 2 agonists, etomidate >propofol (vasodilatory effects)
R-A-A-S system goals for compensatory patients
INCR BPRETAIN intravascular fluidHYPERvolemia
T/Fketamine is contraindicated in animals that may be sensitive to the effects of catecholamines or that have HCM
TRUERemember, ketamine also has a mild sympathomimetic effect in animals with an intact SNS. Can increase the work load on heart.
T/Flidocaine is contraindicated in patients with third degree heart block
TRUEthough lidocaine can help treat arrythmiasdo NOT want to treat third degree AV block because patients are dependent on life saving ventricular escape rhythms.
Branham reflex
after ligation of PDAdecrease HR and incr BPthis is due to a rapid drastic change and increase in after load after ligation. does not always require treatment with anticholinergic
criteria for treatment of ventricular arrythmias
Na channel blockers lidocaine , procainamidedo NOT give if hi 2nd degree or 3rd degree AV blockVtach with HR > 150 bpmmultiformR on THypotension during irregular ventricular beatsT wave is followed by immediate QRS without P
considerations of the thyroid patient dog vs cat
dog hypoT and thyroid neoplasia–consider potential surgical complications (hemorrhage, post op swelling, recurrent laryngeal damage and laryngeal paralysis), hypoCa if PTG removed, rarely myxedema coma, decr plateletscats hyperT–thyroid storm (release catecholamines); thyrotoxic cardiomyopathy (similar to HCM), hypertensive
induction agent of choice for animals with thyroid disease
propofolavoid thiopental in hypoT because it interfere with release of Tavoid ketamine in hyperT cats bc of thyroid storm and cardiomyopathy
considerations of patients with pheochromocytomas
tumors arising from chromaffin cells of adrenal medulla that secrete excessive catecholaminespretreatment with phenoxybenzamine (providing alpha adrenergic blockade) consider: blood loss, cross matching, hypertension (may need nitroprusside), tachycardia (may need beta blockers); avoid acepromazine bc may block control with phenoxybenzaminemay need pre or post corticoid/mineralocorticoid supplementation depending on disease process and removal of gland(s)
Herrera et al2008 JVIMpredictive factors and effect of phenoxybenzamine in dogs undergoing adrenalectomy for pheochromocytomas
pretx phenoxybenzamine (blocks alpha adrenergic receptos)0.6 mg/kg PO q12hr (median 20 days preop)mortality sign diff btwn groups 13% with treatment 48% without treatmentyoung age, decr surgical time, and lack of intraop arrhythmias also were prognostic for survival
5 mx of arterial hypoxemia
- decreased fraction of inspired air2. hypoventilation3. V/Q mismatch4. diffusion barrier impairment5. R to L shunting
one lung ventilation vs two lung ventilation
one lung ventilation results in decr oxygen levels and mild hypercarpia compared to two lung ventilation
6% hetastarch oncotic pressurevsnormal COP
6% HES 29-32 mm Hg (30)normal COP 18-22 mm Hg25% human albumin 200 mm Hg16 % canine albumin 98 mm Hg
laparoscopy and anesthetic considerations
IAP 14 cm H20 maximun allowableabove this, renal perfusion is compromisedCO2 insufflation and Trendelenburg fashion (head down) may exacerbate CO2 into blood and hypoventilation
air emboli
if any air is instilled into the arterial or venous systemcan result in tissue damage due to impaired perfusion or air lock in the R side of the heart that prevents blood from flowing into the lungssigns: sudden drop end tidal CO2, SPO2 and BP
how to tx air embolism
compressions to drive air out of right side and into the lungs so that it can be exhaledplace dog in LEFT lateral recumbency so air rises in right ventricle
what is the only anesthetic drug that has been shown to adversely affect neonatal survival
xylazine
T/F inflammed joints have an up regulation of opiate receptors
TRUEtherefore, IA dose of preservation free morphine can provide analgesia for up to 72 hours IA
methods of local anesthetics
- regional (Bier block, intrapleural/peritoneal)2. infiltrative (wound soaker catheters, ring blocks, line blocks)3. epidural4. peripheral nerve blocks5. intraarticular Na channel blockers and/or opioids
volumes for caudal epidurals for hindlimb sx vs body cavity surgery
hindlimb 0.2 ml/kgbody cavities 0.3 ml/kgaseptic, preservation free morphine, lidocaine/bupivacaine**avoid long lasting local anesthetic with cranial spread bc do not want to risk paralyzing respiratory musculature–consider lidocaine
induction agents for ophtho sx
least increase in IOP = thiopentalmost increase in IOP = ketamine, propofolinhalants overall decrease IOP
heat losses during anesthesia occur through 4 mx
- evaporation: lungs, feet (minimal)2. conduction: direct contact w cold surface3. convention: contact with cold air, water4. radiation: continual loss via infrared energy
what is the method of choice to minimize heat loss
forced air warming blankets–resist heat loss via convectionmore effective than 1 or 3 blankets or warm fluids
