moribund (medical treatment cannot improve animal's condition, sx required immediately, not expected to live more than 24h with or without sx). Disease condition advanced.
ie extreme shock and dehydration, severe trauma, terminal malignancy or infection
Physical status, category E
Emergency operation, any physical status may be operated on as necessary. Greater risk than non-emergency status due to lack of time for full work-up.
Why use anticholinergics/parasympathetics as premedicants
reduce secretions
prevent bradycardia
reduce gastrointestinal motility
Why NOT use anticholinergics/parasympathetics as premedicants
decrease GI motility
slight increase in myocardial work load and cardiac dysrrhythmias
Tranquilizer/ataractic/neuroleptic
"a state of stoical indifference". Best in quiet environment, can be roused. Increased dose = NO increase in calming, just side effects.
neurolepanalgesic
tranquilizer plus opioid analgesic (acepromazine plus opioid)
Acepromazine
tranquilizer
slow onset, long duration.
Antiemetic, antihistaminic
decreases circulating catecholamines
may induce seizures?
Causes hypotension (alpha1 blocker, vasodilation in splanchnic bed and skin), hypothermia, decreased PCV, decreased ventilation, penile prolapse in horses
Droperidol - InnovarVet
Butyrophenone (tranquilizer), anti-emetic in InnovarVet
made dogs and cats bite owners 24h later. Not available in US.
Azaperone - Stresnil, Sui-calm
butyrophenone (major tranquilizer)
used in wildlife capture and to decrease stress in feeder pig introduction
susceptibility differs between species. Sheep get interstitial pulmonary edema, hypoxia.
normal family of side effects
shorter-lasting than detomidine (20-30 mins)
detomidine
alpha-2 agonist sedative
used in horses, cheap
more potent than xylazine
longer-lasting than xylazine (60+ minutes)
same family of side effects
medetomidine
alpha-2 agonist sedative, no longer available for domestic species, racemic mixure of isomers (only one works).
dogs and cats
lasts a LONG time
usu needs to be reversed with atipamazole
used for capture still
dexmedetomidine
alpha-2 agonist sedative, dextro-rotatory isomer (so twice as potent as medetomidine, except not)
used in CRI to supplement anesthesia, sedation in ICU, analgesia post-op. Clinically similar to medetomidine
Romifidine
alpha-2 agonist sedative
licensed for horses
good sedative and analagesia
intermediate duration of action (~45m?)
more specific at alpha-2 receptors than xylazine.
ANS and energy
sympathetic NS expends energy
parasympathetic accumulates energy
Principle site of ANS organization is the
hypothalamus
tonicity
holds organs in a state of intermediate activation, which can be increased or decreased
SNS preganglionic originate from the
thoracolumbar region, synapse at sympathetic trunk/ganglia (first is short, second is long). Preganglionic can also synapse directly on adrenal medulla to produce epi
Sympathetic response extent
DIFFUSE response because postganglionic outnumber preganglionic
augmented by release of EPI from adrenal glands.
adrenal gland acts as the
post-synaptic neuron. Pre-gang neurons contact the gland directly. Cells of adrenal come from neural cells.
preganglionic fibers (both divisions) are
Myelinated (faster)
Postganglionic fibers (both divisions) are
not myelinated (slower)
PNS preganglionic originate from
craniosacral - from brainstem and sacral spinal cord.
Vagus is ~75%, innervates heart, lungs, esophagus, stomach, SI, colon, liver, gallbladder, pancreas, ureters. Sacral is the rest.
Long preganglionic, short postganglionic
PNS postganglionic fibers
short, near or within viscera.
parasympathetic response extent
1:1 or 3:1, so focused, localized, discrete and limited response, not like mass effect SNS.
Vagal bradycardia occurs without changes in GI motility or salivation
Neurotransmitters
preganglionic of both release ACh
postganglionic of PNS release ACh
postganglionic of SNS release norepinephrine
Synthesized in neurons. Rate depends on ANS ACTIVITY
Cholinergic receptors
at effector organ in PNS, at ganglia of all ANS (presynaptic), at neuromuscular junction.
Muscarinic (ANS) and nicotinic (muscle), both respond to ANS
effects of muscarinic receptors (postganglionic PNS)
bradycardia, decreased inotropism (SA and AV nodes), bronchoconstriction, salivation, GI hypermotility, increased gastric secretion.
Blocked by antimuscarinic/anticholinergic (atropine)
adrenergic receptor drug sensitivity
alpha sensitive to NE and Epi
beta sensitive to isoproterenol and epi
dopamine works with different receptor
alpha adrenergic receptors
alpha 1: found in vascular muscle, NE and Epi, activation = vasoconstriction, blockade = dilation (acepromazine is alpha blocker)
alpha 2: pre- and post-synaptic. Post = vasoconstriction, pre = blocks negative feedback for NE release, sedation
Beta adrenergic receptors
beta 1: myocardium, SA, ventricular conduction, + inotrope and + chronotrope
beta 2: smooth muscle of vessels and bronchi. stim = relaxation
dopamine is a precursor for epi and NE, activates alpha and beta as well as DA1.
adrenergic receptors
alpha1, alpha2, beta1, beta2, DA1
dynamic: synthesized or removed, internalized or externalized; inversely proportional to amt of catecholamines in plasma. More causes downregulation, chronic antagonist use causes upregulation (withdrawal)
baroreceptor reflex
baroreceptors in carotid bodies and aortic arch (stretch receptors) stim vagus and glossopharyngeal nerves to inhibit or increase SNS tone, change HR and BP.
sympathomimetic vs sympatholytic (and para)
mimetic mimics the SNS, lytic opposes, looks like PNS (but isn't). describes mechanism of action, not result (so sympathomimetic does not = parasympatholytic, dobutamine does not = atropine, but effects are similar)
ways autonomic drugs can work (modes of action)
Prejunction membrane: interfere with neurotransmitter release (alpha2 agonists), stimulate transmitter release (ephedrine), interfere with reuptake
Postjunction membrane: directly stimulate receptor or interfere with natural agonist of transmitter
antimuscarinic/anticholinergic drugs and MOA
block postjunctional receptors, prevent action of ACh on heart and vessels/bronchioles. Reverse or prevent vagally mediated bradycardia (increase HR, which increases ABP and CO)
reduced secretions, bronchodilation, slow GI motility, important in horses (and rabbits)
atropine and glycopyrrolate (antimuscarinic, no effect on nicotinic)
paradoxical bradycardia of atropine/glycopyrrolate
blocks negative feedback loop on presynaptic first, increases ACh so causes bradycardia (negative chronotrope and dromotrope) for a while before post-synaptic overwhelmed. Dose-dependent
sympathomimetic drugs and MOA
catecholamines (endogenous and synthetic, direct and indirect). Act on alpha and/or beta receptors
direct: activate receptors directly, work by themselves and don't depend on endogenous catecholamines
indirect (synthetic non-catecholamines): stimulate release of endogenous NE (CAN BE DEPLETED). Could also have direct effects. EPHEDRINE
clearance of catecholamines
rapid inactivation by MAO and COMT
fast uptake into prejunctional
cleared by lungs
SHORT duration (~5min)
not liposoluble so limited central effects, PERIPHERAL (airways, vessels)
used to increase HR in heart block, pacemaker implantation.
severe vasodilation (hypotension) and arrhythmias limit use
short duration (~5 mins) (all symp)
dobutamine
synthetic catecholamine
selective B1 agonist, weak B2 agonist
+ inotrope, modest vasodilation to increase CO and muscular perfusion
often used in horses to decrease postanesthetic myopathy
short duration (~5 mins) (all symp)
phenylephrine
direct agonist of alpha1 receptors
vasoconstriction causes increase in arterial BP
reflex bradycardia (baroreceptor reflex)
short duration (~5 mins) (all symp)
ephedrine
synthetic non-catecholamine
INDIRECT AND DIRECT alpha and beta agonist
activates receptors and releases NE (mostly this) (also releases epi since see B2?)
lasts longer than most catecholamines
increase HR, contractility, APT and CO
can deplete NE with repeated doses
beta adrenergic antagonists (beta blockers)
esmolol
suppress or reduce sympathetic tone, treat dysrrhythmias, antihypertensive, tx of pheochromocytoma
beta adrenergic agonists
albuterol (beta2 agonist)
mainly bronchodilators
vasopressin
not a catecholamine, but used for vasoconstriction
anticholinergics as premedication
PRO: reduce secretions, prevent bradycardia, reduce GI motility
CON: reduce GI motility, increase myocardial work and cardiac dysrrhythmias.
good for ophthalmic surgery, cervical spinal cord decompression, endoscopy, with large dose mu opioids and cholinesterase inhibitors
don't use with preexisting tachyarrhythmias, maybe alpha2 due to vasoconstriction, bradycardia, low CO
atropine
anticholinergic. Broken down (atropinase) slowest in dogs, fastest in rabbits.
pupil dilation (not in birds), reduced lacrimation, crosses BBB, transient bradycardia after IV (presynaptic ACh inhibits ACh release), crosses placenta.
reduced lacrimation, transient bradycardia after IV (presynaptic ACh inhibits ACh release), crosses bbb and placenta.
glycopyrrolate
anticholinergic
longer lasting than atropine, pupil dilation
DOES NOT cross BBB or placenta.
increases gastric pH, so aspiration causes less damage
drug that neutralizes stomach contents with non-particulate agent
sodium citrate
drugs that decrease gastric acid production
famotidine
patients at risk for gastric reflux include
emergency sx
pregnancy
morbid obesity
diabetic gastroparesis/full stomach
post-sx
pre-op fasting >24h (+ lower pH)
increased age (+ lower pH)
intra-abdominal surgery
esophageal strictures
post-surgical complication!
metoclopramide
pro-kinetic, decreases gastric volume or pH
antagonizes inhibitory neurotransmitter (dopamine), augments ACh release and sensitizes muscarinic of GI smooth muscle
crosses BBB, could cause acute dystonic rxns and extrapyramidal
famotidine/ranitidine
specific and competitive histamine H2-receptor antagonist at parietal cells
gastric pH raised, volume of secretions reduced
45-60mins pre-anesthesia
rapid IV = cardiac arrhythmias
sodium citrate
non-particulate (clear) antacid used as prophylaxis against aspiration pneumonitis
Ondansetron
antagonizes 5-HT3 receptors both centrally and peripherally to control nausea and/or vomiting
cerenia (maropitant)
neurokinin (NK1) receptor antagonist to block pharmacological action of substance P in CNS to control nausea and vomiting
noxious stimulus
one that is actually or potentially damaging to tissue.
one of intensity and quality adequate to stimulate nocioceptors.
pain
defined by IASP in 1979
An unpleasant sensory and EMOTIONAL experience associated with actual or potential tissue damage, or described in terms of such damage
neuropathic pain
pain due to damage to nervous system
less responsive to traditional analgesics
characterized by spontaneous paresthesia and paroxysms of pain, pain caused by normal movement, hyperalgesia and allodynia
nocioceptors
nonencapsulated receptor organs responding preferentially to noxious stimuli.
Attached to nocioceptive neurons/fibers (pseudounipolar)
widely distributed, high stimulus threshold (just noxious)
Includes A-delta vs C fibers
Nocioceptorsclassified by diameter, myelination, and conduction velocity of parent fibers. What are the two fiber types? Compare pain they cause, degree of myelination, thickness and conduction velocity (just who is faster)
C: slow pain, burning, smaller, non-myelinated so usu slower.
A-delta fibers
pricking, sharp, aching pain
lightly myelinated
2-5 microns
conduction velocity = highly variable
first pain
C fibers
burning pain
unmyelinated
<2 microns
conduction velocity of 0.5-2.0m/sec
most polymodal (heat, pressure, vibration, too)
more numerous in visceral tissues
four physiological processes involved in nocioception
transduction
transmission
modulation
perception
transduction and transducers
first physiological process of nocioception
translation of physical energy into electrical activity by nocioceptors via transducers (mechano-, chemo-, thermo-). Most are polymodal. Ionotropic (faster) or metabotropic (slower)
algogenic chemicals
inflammatory soup that is released from neurons (and non-neurons) upon tissue injury. Includes inflammatory mediators, cytokines and neurotrophins. Things like bacteria are also algogenic, so infection can cause pain.
Inflammatorymediatorscauseperipheralsensitizationofneuronsby binding to _______ receptors and activating intracellular signaling cascades
Metabotropic
neurve transection leads to formation of a
Neuroma
hyperalgesia (3 characteristics)
sensitization of nocioceptors (decreased threshold, increased response, spontaneous activation) causes left shift on stimulus-response graph, so lower magnitude is painful
peripheral sensitization
inflammatory mediators bind to metabotropic receptors to increase probability that future stimulus will activate receptor. Preventing generation of inflammatory mediators helps prevent peripheral sensitization (PREEMPTIVE ANALGESIA)
transmission
2nd physiologic process in nocioception
propagation of an action potential along peripheral nocioceptive neurons and into/throughout CNS
The _______ appears to be the major nocioceptivepathway (except for the head) in carnivores
spinocervicothalamic
The ________ is the major nocioceptivepathway in the head
trigeminothalamic
T/F: pain in viscera is usually worse as a result of stimuli like ischemia or dissensionofa hollow viscous than as a result of surgical incision
True
T/F: nocioceptive neurons traveling from viscera to CNS travel to the CNS in EITHER the glossopharyngeal/vagus nerve and a pair of spinal nerves OR two pairs of spinal nerves
True
T/F: the RAS is responsible for making sure an organism pays attention to a noxious stimulus
True
Stimulation of hypothalamus by nocioceptive pathways causes release of catecholaminea and pituitary hormones
True
T/F: the Limbic System ensures an organism will link noxious stimuli with negative emotion
True
primary neurotransmitter released by first-order nocio neurons in spinal cord dorsal horn? Name two receptors to which it binds on post-synaptic membrane
GLutamate (excitatory), binds to AMPA, NMDA, G-protein coupled receptors
Spinal cord Dorsal horn is divided into how many laminae of Reed? Which are main sites of terminati of first-order A-delta and C nocio neruons?
A Is I and IV-V, C is I and II.
Spinal cord plasticity/ synaptic long-term potentiation (“central sensitization” or “wind-up”) is induced by an increase in intracellular _____ ions in the second-order neuron in the dorsal horn due to opening of the ion channel of the _____ receptor. Two things must happen for this ion channel to become permeable to these ions; name these two things.
Calcium due to NMDA receptors. Requires glutamate/glycinebindingand removal of Mg++ plug
excitatory: glutamate, involved in reflex arcs (withdrawal)
T/F: Synaptic long-term potentiation can be avoided by preventing noxious input into the spinal cord before it starts (with analgesic drugs), but NOT by general anesthesia alone (inhalant anesthesia).
True
With regard to interneurons and the Gate Theory: Stimulation of A-beta (innocuous touch) fibers can stimulate _____, which then inhibit second-order (projection) neurons. This is why transcutaneous electrical nerve stimulation (TENS), massage, and other therapies that stimulate A-beta fibers can decrease pain.
Inhibitory interneurons, serotonin and norepinephrine
T/F: Pain induces protein catabolism, which can interfere with healing of wounds or surgical incisions.
True
Gate theory: The ___ and the ___ (two areas in the brainstem) project to the dorsal horn of the spinal cord, where they inhibit first-order neurons, second-order neurons, and excitatory interneurons. They also release the neurotransmitters ___ and ___, which stimulate inhibitory interneurons; these inhibitory interneurons then inhibit first- and second-order nociceptive neurons.
PeriaqueductalGrey Matter and Rostral Ventromedial Medulla System, _______ and _______
Modulation
third physiological process in nocioception
modification of nocioception in the dorsal horn (protective). Interneurons (excitatory vs inhibitory)
Gate theory
inhibitory interneurons are "gate cells", a "closed gate" (stimulated) stops noxious signals from ascending to brain
massage relieves pain!
cognitive and emotional factors can control pain processing
periqueductal grey matter (PAG) gets input from higher structures to control pain processing - disinhibits nucleus raphe magnus of rostral ventromedial medulla
ways to stop nocioception
direct postsynaptic inhibition of second order (projection neurons)
inhibition of neurotransmitter release from first-order neurons
excitation of inhibitory interneurons (release endogenous opioids)
inhibition of excitatory interneurons
Perception
fourth physiological process of nocioception
nocio neurons project from thalamus to somatosensory cortex
changes in somatosensory and motor cortices due to unchecked pain (phantom limb pain)
destruction of cortex does not eliminate pain perception
retention of water and Na, excretion of K (RAAS activation, ADH release triggered by angiotensin II, stimulation of thirst center in hypothalamus)
respiratory effects (central hyperventilation and respiratory alkalosis, hypoventilation and respiratory acidosis if ventilation painful)
decreased GI motility
Urine retention
General anesthesia
drug-induced reversible condition including unconsciousness (hypnosis), amnesia, analgesia and immobility with simultaneous stability of the autonomic, CV, respiratory, and thermoregulatory systems.
hippocampus, amygdala, and cortex (learning and memory). GABA involved
Where does hypnosis work?
thalamus, hypothalamus, cortex and brainstem.
Conscious involves arousal (RAS, reticular formation and locus coerulus) and awareness (cortex).
Where does immobility come from
inhibition of spinal reflex pathways - SPINAL CORD
what does brainstem control
ventilation and cardiac function (Isofluorane and propofol augment inhibition of GABA)
Anatomical location of anesthesia
SC and brainstem: immobility and autonomic homeostasis
hippocampus: amnesia
hypnosis: cortical and subcortical structures and brianstem
Meyer-Overton Rule
all anesthetics act at same molecular site -- the lipid bilayer. MORE LIPID SOLUBLE IS MORE POTENT!!!
3 exceptions: many lipid-soluble don't cause anesthesia, cutoff phenomenon (most lipid soluble stop working all together), isomers/enantiomers are not equally potent, but are equally soluble.
So not a great rule
Protein theories of general anesthesia
meyer-overton rule exceptions explained by lipid pockets in proteins. How much light it produces = potency. Too large or isomer, won't fit in pocket of protein, so better theory.
Ways general anesthesia affects CNS function (2)
neuronal excitability, communication between neurons (synapsis)
excitability
the propensity of a neuron to generate and propagate an action potential.
Determined by resting membrane potential, threshold potential, size/propagation of action potential
anesthetics hyperpolarize cortical and motor spinal neurons
hyperpolarization correlates with anesthetic potency
inhibits initiation of action potential, but too small to stop propagation
major excitatory neurotransmitter in CNS
glutamate
release decreased by general anesthesia (inhibition of RELEASE), maybe mediated by Na, K channels
N2)O and Xenon and Ketamine inhibit POSTSYNAPTIC response to glutamate on NMDA receptors
major inhibitory neurotransmitter in CNS
GABA
increase Cl- conductance, hyperpolarizes cell
2 effects of general anesthesia on GABA-A receptors
potentiation: increases current elicited by low concentrations of GABA
direct action: ability to activate GABA-A in the absence of GABA
general anesthesia increase affinity of GABA to GABA-A. Do not affect conductance, just increase frequency of opening or time to open
Leak channels
background K+ channels (voltage independant).
General anesthetics activate these channels. Silences spontaneous firing of some neurons.
Na channels
ion channels that change based on membrane potential
we used to think they were insensitive to general anesthetics but now it looks like isofluorane and halothane decrease some subtypes. Small inhibition of channels causes large inhibition of synaptic function
anesthetics inhibit these channels and reduce amplitude
more resistant to propofol and ketamine
laryngeal mask
ET tube with little cup on end that sits over larynx, not inserted into trachea. Can't protect from aspiration, can't suction deeply.
murphy eye
hole in the end of ET tube
pre-oxygenation
increases time to desaturation if something goes wrong.
T/F: opioids can cause hyperthermia in some species, such as cats, due to increased locomotion and/or central hypothalamic mechanism
True
name the three endogenous opioid peptides
Enkephalins, dynorphins, beta-endorphins
narcotic
Potent morphine-like analgesic drug
opioid
All exogenous substances that bind to opioid receptors and produce some agonist activity
Opioid MOA
CNS Presynaptic (main): increased K+ efflux and Ca++ channel inactivation = inhibition of neurotransmitter release, inhibition of adenylyl cyclase = decrease in neurotransmitter production
Name the contraindications for NSAID administration
concurrent NSAID or corticosteroid administration, coagulopathy, renal disease, hepatic disease, GI disease, hypovolemia, mast cell tumors
Which NSAID has a warning against multiple dosing in cats
Meloxicam
newly licensed oral NSAID for dogs and cats
rofenacoxib/onsior
Most common NSAID given to horses for orthopedic pain and the one for horses with colic
Ortho: phenylbutazone
colic: flunixin/banamine
Name the only NSAID that is FDA-approved for use in cattle
Flunixin
Morphine
Full Mu agonist opioid analgesic
24+ hours epidural (more hydrophilic than others), topical to corneas, intra-articular
releases histamine
nauseating and emetic
Hydromorphone and oxymorphone
synthetic full mu agonist opioids
dogs and cats
nauseating and emetic
methadone
Synthetic full mu agonist and NMDA antagonist, alpha-2 agonist.
Prolonged duration (12h) after SQ, trans-mucosal in cats
less emetic (but still nausea)
fentanyl
Synthetic opioid full mu agonist in dogs and cats, small rumenants and camelids
patches and long-acting transdermal also available
tramadol
Weak mu agonist and serotonin/norepinephrine reuptake inhibitor, may cause serotonin release in CNS
ORAL, but dogs produce little of active metabolite.
NOT WITH MAO INHIBITORS OR SEROTONERGIC DRUGS or will get serotonin syndrome
butorphanol
Mu antagonist (competitive), kappa agonist
little analgesia
ceiling effect on side effects
Best opioid sedative.
Also mild pain, CRI for colic in horses, antitussive
buprenorphine
Semisynthetic Mu partial agonist, binds TIGHTLY and dissociates slowly. HARD TO ANTAGONIZE
6-8h
oral-transmucosal in cats
Simbadol is extended-release for cats, 24h
opioid receptor antagonists
Naloxone, naltrexone
displace mu and kappa agonists but don't activate receptors
reverse side effects as well as analgesia
NSAID MOA
inhibit eicosanoid production by inhibiting COX (3 isoforms)
COX1
Produces PGE2 (vasodilation, nocioceptor sensitization, beneficial GI effects) and TXA2 (vasoconstriction, platelet aggregation)
COX2
Produces PGE2 (vasodilation, nocioceptor sensitization, beneficial GI effects) and PGI2 (vasodilation, inhibition of platelet aggregation, only in inflamed tissues, expressed in GI tract).
Stimulates renin release and alters renal blood flow
ONLY "SAFER" DUE TO DECREASED GI EFFECTS IN HEALTHY GI TISSUES
Carprofen
COX2 preferential NSAID
approved for dogs (also in cats, horses, cattle in Europe)
Limb stretched causally, feel for pectineus (HARD) and femoral artery, femoral nerve is just cranial. There will be a POP when you go through fascia, otherwise you'll get electrical stimulation but NO BLOCK
under vastus medialis, between rectus femoris and pectineus
Sciatic block
Nerve between greater trochanter and ischiatic tuberosity, under biceps femoris and cranial to semiten, semimem. There are perineal/fibular and tibial branches
Bleeding disorders (could hit the internal vertebral venus plexus)
uncorrected hypovolemia (vasodilation)
infection at injection site, sepsis or bacteremia (venous plexus puncture, seeding infection into epidural space, abscess)
most common drugs for local anesthetic
Local like lidocaine, bupivicaine, opioids and alpha-2 agonists, or combinations
equipment for epidural injection
Tuohy needle is dull and bent, lets you feel the pop and hanging drop
DON'T USE A SPINAL NEEDLE
placement for epidural
lumbosacral space: between spinous process of L7 and median sacral crest, big dip you fall into
Coxococcigeal space: between Cd1 and Cd2
You know you're right because of "pop" from ligamentum flavum or hanging drop
Types of dead space
Alveolar
anatomical
machine
functional residual capacity
volume of gas left in the lungs at the end of a passive expiration
closing volume
Volume of gas left in the lungs when the airways start to close
minimum alveolar concentration
concentration of anesthetic vapor in the alveoli at 1 atm that produces immobility in 50% of patients exposed to a painful stimulus
ventilatoryvariable guidelines for domestic
Tidal volume: 10 mls/kg
minute volume: 150 mls/kg-min
metabolic oxygen: mls/kg-min
ways to increase CO2 in a P
Wrong gas in (don't change soda lime)
decreased alveolar ventilation(decreased central drive (drugs), increased resistance (ET tube), decreased compliance (obesity, pregnant))
diffusion limitation
increased venous admixture (PDA, heart defect)
mixed venous oxygen (less O2 coming back than should be, like anemia, Pyrexia)
V/Q values
Ventilationwithout perfusion = infinity
1 = perfect
0 = perfusion without ventilation
Gas vs vapor and significance
N2O is a gas, rest are vapors
vapors are liquid at room temp, must be mixed with gas, need vaporizer. Agent and temp dependent. Saturated vapor pressure is the MAX pressure you can get.
Gas can be 0-100% , we can give a max of ~70% to avoid hypoxia. Gas at room temp.
MAC
Minimum alveolar concentration at which 50% don't respond to surgical incisions. 50% don't move in response to noxious stimuli.
Pros and Cons of MAC
Pros: reproducible throughout species; End-tidal levels of anesthetic are in equilibrium with pressure in brain and plasma
cons: quantal (yes or no, anesthesia is not), only counts 50%(populations), depends on choice of end-point, represents no MOVEMENT, not no pain or hypnosis.
Things that affect MAC
other drugs: additive or synergistic (pre-anesthetics like opioids, sedative, N2O)
temperature: hyperthermia increases mac
Age: decreases with age
thyroid: Increase equals increase?
pregnancy: decreases MAC
Effects of inhalational aesthetics on the CNS (5), CV (5), resp (4)
CNS: Dose-dependent depression of CNS. Increase cranial blood flow and intracranial pressure, blunts autoregulation. Decrease brain's requirement for oxygen (CMRO2)
CV: dose- and agent-dependent depression. Halothane depresses myocardial contractility (reduces CO and ABP, blunts baroreceptor, sensitizes heart to catecholamines). Rest are minimal, better for baro, cause vasodilation (hypotension, not contractility), don't sensitize to catecholamines
resp: reduction of tidal volume, normal response to CO2 depressed, blunt response to hypoxia, bronchodilators
dif between halothane and other vapors
More prominent increase of cerebral blood flow and intracranial pressure
depresses myocardial contractility (rather than vasodilation like the others)
blunts baroreceptor function
sensitizes heart to catecholamines
N2O
Need 200% to anesthetize, we can't give more than 70%. But causes NMDA block so we give for analgesia. Multi-modal, decreases need for ISO to decrease vasodilation.
Increases cerebral blood flow and intracranial pressure and CMRO2, cerebral metabolic requirement for oxygen
minimal change in minute ventilation but depresses response to hypoxia
CV: DIRECT is myocardial depression, INDIRECT is catecholamine stim like ketamine. Net is SNS but can run out of catecholmamines and see depression
MOVES INTO HOLLOW CAVITIES, avoid in pneumothorax, GDV etc.
Diffusion hypoxia: displaces O2, so after discontinuation will move back into alveoli from blood and cause hypoxia, give O2 for 10 mins after.
Diffusion hypoxia
N2O discontinued, diffuses quickly into alveoli to equilibrate and can cause massive hypoxia, keep giving O2 for 10 minutes after discontinuing
T/F: Propofol (unless it’s Propoflo 28TM) must be discarded six hours after the bottle is opened because it supports bacterial growth.
True
What is propofol’s mechanism of action?
Decreases rate of dissociation of GABA from GABA-A receptors
Name two reasons why propofol has a short duration of action
Rapid redistribution to other tissues like fat and rapid metabolism (liver, lungs)
What are the CNS effects of propofol
Decreases cerebral metabolic rate for O2, cerebral blood flow and intracranial pressure
What are the CV effects of propofol
Decreased myocardial contractility and vasodilation = hypotension, blunts baroreceptor reflex
T/F: Propofol stimulates ventilation
True
what effect does propofol have on intraocular pressure
Decrease
Propofol can cause which hematological condition if given repeatedly over days?
Oxidative injury to RBC = Heinz body anemia
The dissociative anesthetics are antagonists at the _________ receptor but appear to have other effects too
NMDA
T/F: The dissociative anesthetics produce intense analgesia, and ketamine is used as a CRI for pain
True - ketamine
What is special about ketamine in the cat
Excreted unchanged by kidneys mostly
What are the CNS effects of the dissociative anesthetics
Seizures, increased cerebral blood flow and intracranial pressure, emergence delirium/hallucinations
What are the CV effects of dissociative anesthetics
Indirect CV stimulation, direct myocardial depression
What are the respiratory effects of the dissociative anesthetics
Don't depress ventilation as much as protocol, bronchodilator, pharyngeal/laryngeal reflexes maintained
what is the MOA of etomidate
Enhances affinity of GABA for GABA-A (no analgesic)
Name the two ways etomidate is metabolized
Hydrolysis by hepatic microsomes like enzymes and plasma set erases, excreted in urine and bile
Main clinical use of etomidate
IV induction of general anesthesia
especially good for CV patients (also renal, hepatic, hypovolemic)
T/F: Etomidate can cause hemolysis because it is dissolved in propylene glycol
True
What is the major endocrine side effect of etomidate
Adrenocortical suppression
Which induction agent is classified as a neurosteroid?
