Final: adjunts, opioids Flashcards
what is a medication that may be co administered with primary anesthetic to create a more balanced anesthesia
adjuvant
what are the non-opioid adjuvants
ofirmev
ketamine
toradol
what is the max dose of ofirmev
4g in 24hrs
what is a drug included in ofirmev solution
mannitol
what is the doses for ofirmev <> 50kg
<50kg= 15mg/kg
>50kg= 1000mg
what are contraindications for ofirmev
liver impairment
mannitol allergy
what is an advantage of ofirmev over toradol
does not increase bleeding time
what are some se of ofirmev
vomit
headache
insomnia
is ketamine competitive or non competitive
non competitive
what is the moa of ketamine
inhibits nmda receptor
what part of brain does ketamine inhibit impulses to, which causes dissociation
limbic cortex
what is the only primary anesthetic that also provides analgesia
ketamine
ketamine has a ________________ effect with volatiles
synergistic
ketamine has an ___________________ effect with propofol/benzos
additive
which is a larger effect, additive or synergistic effect
synergistic
what is the dose of ketamine
iv: 1-2 mg/kg
im 4-8 mg/kg
what is the onset, peak, doa of ketamine
30 s, 1 min, 5-15 min
what is the half life of ketamine
2-3 hour
how is ketamine metabolized
redistribution
what are the se of ketamine
hallucinations
increased salivation
nystagmus
how can you decrease hallucinations/salivation with ketamine
versed/robinol
what conditions would you want to avoid giving toradol
asthma
nasal polyps
rhinitis
hypovolemia
how is toradol eliminated
kidneys
what drug works by inhibit prostaglandin synthesis
toradol
what is the peak, onset, doa of toradol
10 min, 1 hour, 4 hour
ponv occurs in what % of general surgery
30%
what are some risk factors of ponv
female
hx of ponv
non smoker
young age
volatiles
post op opioids
duration of anesthesia
surgery type
general vs regional
what are sx of anticholinergic syndrome
restlessness
hallucinations
somnolence
unconsciousness
which anti-emetic can cause anti cholinergic syndrome
scopolamine
what is the dose of scopolamine
1.5mg patch transdermal
place at least 4 hours before surgery
remove after 24 hours
do not touch eyes- mydriasis
what is zofran drug class
5 ht3 antagonist
what is dose of zofran
adult: 4mg pre emergence
ped: 0.15mg/kg
what is onset/peak/doa of zofran
30 min, 2 hr, 4-24 hr
what is the bb warning for zofran
qt prolongation
what are sx of anticholinergic od
blurred vision
dry/flushed skin
rash on feac/neck chest
dry mouth
bowel/bladder loses tone
tachycardia
what kind of patient should you monitor ecg when giving zofran
electrolyte imbalance
chf
taking other qt prolonging drugs
when is decadron given
prior to induction
what common operative med should be cautioned in diabetics
decadron- increases glucose
what is reglan usually given in combination with
pepcid
what are se of reglan
extrapyramidal sx: involuntary muscle contraction, tremor, rigid muscle, tardive dyskinesia
when is reglan indicated
gerd
gastroparesis
full stomach prior to emergency case
what drug enhance ach transmission on intestinal smooth muscle, which increases lower esophageal sphincter tone, speeding up gastric emptying
reglan
what antiemtic can cause perineal burning
decadron
what are the h1 receptor antagoinsts
benadryl
promethazine
dimenhydrinate
t or f- benadryl alone causes decreased ventilatory drive
false
what drug is often combined with opioids to potentiate analgesia
promethazine
what drug must be metabolized in diphenhydramine to be effective
dimenhydrinate
why does promethaine have a low bioavailability
extensive 1st pass effect in live
what alpha 2 agonist has local anesthetic effects on peripheral nerves
clonidine
what med is added to local anesthetic solutions to increase doa
clonidine
what drug decreases sns activity by reducing circulating catecholamines
clonidine
what are some se of clonidine
dizzy
bradycardia
dry mouth
do not abruptly stop
what is epidural dosing of clonidine
30mcg/hr in mixture of opioid or local
what types of analgesia does precedex supply
supraspinal and spinal
what are some se of precedex
decreased salivation
bradycardia
decreased shivering
variable htn/hotn
what is a main advantage of precedex
preserves resp drive
where is precedex mainly metabolized
liver
what is preferred for awake fiberoptic intubation: precedex or ketamine
precedex
what is the alpha 2 agonist class of precedex
imidazoline
what is the site of action of precedex
locus coeruleus
what are some of the moa of precedex specifically
decreases catecholamine releasing–>
inhibit ca and k channel activation–>
hyperpolarizes cell
push precedex as fast as possible for best effect
no- may cause hypertension because sns effect will occur before cns effects are able to kick in and overpower sns effects
what is the moa of benzos
gaba agonist
how is versed metabolized
cyp450
what are the 3 positive effects of versed
amnesia
sedation
anxiolysis
what drugs does versed have a synergistic effect with
prop and fent
what channel do gaba receptors effect and how
chloride- opens channels leading to hyperpolarization
what is a dopamine receptor blocker antipsychotic
droperidol
what disease would you want to avoid droperidol
parkinsons
how can droperidol effect ekg
prolong qtc
t or f- droperidol causes sedation and anti-emetic effects
true
what is a risk of droperidol admin
extrapyramidal effects
neuroleptic malignant syndrome
what receptors do opioids work on
mu, delta, kappa
what side effects will adjuvant opioids help decrease with volatile
myocardial depression
t or f- opioids causes spinal analgesia only
f- supraspinal and spinal
what can opioids do to muscles
muscle rigidity
what are the mu receptor prototypes
morphine
fent
what are the delta receptors prototypes
deltorphin
what are the kappa receptors prototypes
buprenoprhine
pentazocine
which opioid receptor does not cause resp depression/gi effects/sedation
delta
what receptor has endogenous ligands of beta endorphine, endomorphin
mu
what receptor has endogenous ligands leu/met enkephalin
delta
what receptor has endogenous ligands dynorphin
kappa
desflurane can be reduced by 85% by administering what
fent 1.5 mcg/kg 5 mins before incision
t or f- remifentanil is metabolized by liver
false
esterases
what opioid is best for rapid recovery
remifentanil
5-10 min DOA
what is the MOA of reglan
enhances ACH transmission on intestinal smooth muscle thereby increasing lower esophageal sphincter tone, speeding up gastric emptying, and lowering gastric fluid volume
what is the dose for reglan
10 mg IV 15-30 min prior to induction (push over 5 min)
what are SE of reglan
extrapyramidal symptoms (involuntary muscle contractions, tremors, rigid muscles, tardive dyskinesia)
what are the side effects of Decadron
increases BS
delays wound healing
perineal burning
what is the dose of diphenhydramine
25-50 mg (0.5-1.5 mg/kg) oral, IM, IV q3-6 hrs
what is the MOA of promethazine
antihistamine, antimuscarinic
what is the dose of promethazine
12.5-50 mg q4-12 hrs
what is a prodrug of diphenhydramine
Dimenhydrinate
What is the MOA of alpha 2 agonists?
Inhibit NE release, reducing sympathetic outflow
what are the effects of Clonidine
decreased sympathetic activity, enhance parasympathetic tone, reduced circulating catecholamine
what are epidural/caudal/PNB effects of Clonidine
adjunct for anesthesia and analgesia
treats chronic neuropathy pain to increase efficacy, Segmental
what are the side effects of Clonidine
sedation, dizziness, bradycardia, dry mouth
what can abruptly stopping clonidine lead to
rebound htn
agitation
sympathetic overactivity
what is dosing of clonidine
30 mcg/hr in mixture with opioid or local
what is MOA of precedex
G-Protein-Coupled receptors on presynaptic nerve endings
Inhibit the activation of Ca++ and K+ channels, thus hyperpolarizing the cell
what is the site of action of precedex
Pontine and locus coeruleus
what are some side effects of precedex
transient htn
minimal effects of resp drive
precedex effects picture
what is the 1/2 life of precedex
6-8min
how is precedex metabolized
liver
what does versed work synergistically with
propofol and opioids
what kind of drug is droperidol
antipsychotic
what is the blackbox warning on droperidol
prolong QTc
what are risks of Droperidol
> QTC
extrapyramidal effects
neuroleptic malignant syndrome
opioids effect picture
which opioid receptor causes resp depression, GI effects, and sedation
mu
opioid receptor chart
what is the parent compound for many sympathomimetics
B-phenylethlamine
what is a 3,4-hydroxyl substitution of B-phenylethylamine
dopamine
what is the metabolic precursor for norepinephrine and epinephrine
dopamine
what decreases the activity of norepi at B-receptors
lack of an N-substitution in the B-phenylethylamine
what classes of medications increase Ca++ interaction with cardiac actin and myosin
B-agonists
phosphodiesterase inhibitors
cardiac glycosides
what medications act on the B-1 receptor
epinephrine
dobutamine
dopamine
isoproterenol
to a lesser extent
-ephedrine
-norepinephrine
what the is physo of B1 activation
acts on cardiac myocyte sarcolemma
activates G3 protein
activates adenylyl cylclase
increased cyclic AMP
activates protein kinase A
increased opening of voltage gated Ca++ channels
What is the MOA of phosphodiesterase inhibitors?
inhibits breakdown of cAMP by inhibiting PDE3,
what kind of drug is milrinone
phosphodiesterase inhibitor
what vasopressor acts on the V1 receptor to cause vasoconstriction
vasopressin
what drugs are in the catecholamine class of drugs
epi
norepi
dopamine
dobutamine
isoproterenol
t/f phenylephrine is a catecholamine
false
what sympathomimetic are excreted unchanged in the urine
ephedrine, milrinone
what metabolizes vasopressin
vasopressinases in the liver and kidney
what metabolizes most cathecholamines
COMT (catechol-o-methyltransferase)
MAO (monoamine oxidase)
which catecholamine is not metablized by MAO
dobutamine
where are alpha-1 receptors located
peripheral vasculature (vasc smooth muscle)
what do B1 receptors modulate
inotropy
chronotropy
lusitropy
where are B2 receptors located? what do they stimulate
-widely distributed in vasculature
-dilation of muscular, splanchnic, renal vasculature
-Bronchodilation
what is lusitropy
ventricles to relax
what receptors does dobutamine work on
B1 B2
what is the drug of choice septic shock with systolic dysfunction
dopamine
what is the drug of choice for stress echocardiography
dobutamine
what is the drug of choice for weaning from cardiopulmonary bypass
milrinone
what is the drug of choice for post-cardiopulmonary bypass vasoplegia
vasopressin
what cell synthesizes, stores, and releases epinephrine
chromaffin in adrenal medulla
how does epi effect mucosal edema
decreases
how does epi effect mast cells
stabilizes so decreased histamine, tryptase, other inflammatory mediators
how does epi effect CPP during codes
increased
what is the number one factor that increases myocardial oxygen consumption
HR
what medication do you give to treat hypotension with a decrease in HR and/or low cardiac output
EPI
what receptor does epi stimulate to cause bronchodilation and mast cell stabilization
B2
how does epi effect BS
hyperglycemia from
-increased liver glycogenolysis
-reduced uptake of glucose
-inhibits release of insulin
what are some adverse effects of epi
hyperglycemia
hypokalemia
lactic acidosis
myocardial ischemia
what can happen if you give epi to a patient with acute cocaine intoxication
Myocardial ischemia
stroke
what conditions is epi contraindicated in
cocaine intoxication
tetraology of fallot
hypertrophic obstructive cardiomyopathy
digitalis
halothane
BBs
what is the primary neurotransmitter of the sympathetic NS
norepi
where is norepi released from
postganglionic nerve endings
what are adverse effects of norepi
-severe HTN causes increased cardiac workload and cardiac ischemia
-organ dysfunction from lack of blood flow
where are D1 receptors located
mesenteric and renal vasculature
what two affects does dopamine have on renal function
diuresis
naturesis
when in low concentrations, what is the action of dopamine
D1 (renal, mesenteric, coronary vasc) vasodilation
increased GFR and renal blood flow
increased Na excretion and urine output
decrease SVR
what do high doses of dopamine do
directly stimulate B1 receptors
enhance release of norepi
increased contractility
increased HR
increases BP
alpha-1 vasoconstriction
what are adverse effects of dopamine
tachycardia
tachyarrhythmias
myocardial ischemia
decreased splachnic perfusion
gut ischemia
reduced ventilatory response
hypoxemia
decreased GH, prolactin, TSH
what kind of medication is dobutamine
direct-acting synthetic catecholamine
how does dobutamine effect cardiac filling pressures and PVR
decreases
what are adverse effects of dobutamine
tachy
arrhythmias
hypertension
exacerbate MI
what are end effects of milrinone
increases CI
reduces art pressure
reduces LVEDP
reduces PVR
why is milrinone effective in treatment of RHF
increases vent contractility
decreasing PVR
what is a possible issue with milrinone and RHF
decreases SVR, so combine with norepi or vasopressin
how does phenylephrine effect lungs
pulmonary vasoconstriction and pulmonary htn
what are adverse effects of phenylephrine
severe brady
brief asystole
reduced CO
pulme edema
arrhythmias
cardiac arrest
what do you give if phenylephrine causes severe hypertension
phentolamine (alpha-1 antagonist)
hydralazine (direct arterial dilator)
T/F BB and CCB are effective ways to treat htn caused by phenylephrine
F, can cause cardiac depression and acute heart failure
where is vasopressin stored and released from
posterior pituitary gland
what effects the hemodynamic effects of vasopressin
presence/absence of sympathetic and renin-angiotensin systems
what are adverse effects of vasopressin
reduced mucosal perfusion
increases liver enzymes
total bilirubin concentrations
decreases platelet count
what is the physo effects of ephedrine
increase in systolic, diastolic, and MAPA
increased myocardial contractility
increases HR
increases CO
T/F ephedrine can cross the BBB
T, causes agitation and insomnia
what happens is a patient taking MAOIs take ephedrine
exaggerated hypertensive effect
what is the main center for neurogenic control of vascular tone
vasomotor center in midbrain
what are the two central neural systems that regulate bp
neurogenic control
baroreceptor reflexes
what are other humerol/endocrine control of BP
RAAS, ANP, renal Na/H2O secretion, eicosanoids, kallikrein-kinin system, adrenal steroids, endothelin system, medullipin
what are the three ways that drugs can treat high BP
1) effect ANS
2) inhibit RAAS
3) peripheral vasodilation
what are examples of arterial vasodilators
prazosin
phentolamine
phenoxybenzamine
tolazoline
hydralazine
diazoxide
CCBs
ACE inhibitors
what are examples of veno/arteriolar dilators
nitroprusside
what are examples of venodilators
nitroglycerine
name the alpha 1 blockers
doxazosin, prazosin, indoramin
name the a1,a2 blockers
phentolamine, phenoxybenzamine
what are the a1, b1 blockers
labetalol, carvedilol, nebivolol
what are examples of nitrovasodilators
nitric oxide
sodium nitroprusside
nitroglycerine
isosorbide dinitrate
isosorbide mononitrate
what is the MOA of CCBs
arterial vasodilation by blockade of Ca++ influx through L-type voltage gated Ca++ channels
may also reduce HR (chronotropy)
and contractility (inotropy)
what are the three types of CCBs
dihydropyridine
phenylalklamine
benzothiazepines
what are examples of dihydropyridines
nifedipine, nicardipine
what is site of action of dihydropyridines
resistance vessels with minimal effects on veins
what is the site of action of phenylalklamines
heart
what is the effect of CCBs on the heart
reduce HR and contractility thus decreasing CO and BP
(negative chronotropy and inotropy)
what is the site of action of benzothiazepines
vasculature
think diltiazem
how do B1 and B2 receptors have action
increase Camp
what does activation of B3 lead to
cardiodepression
what are the b1 selective blockers
acebutolol
atenolol
bisopropol
celiprolol
esmolol
xamoterol
what are the partial inverse agonists
metoprolol
nebicolol
how do BBs decrease BP
decreasing CO (by decreasing contractility and HR)
inhibiting the release of renin from the kidneys
what are the nonselective BBs
propranolol
timolol
Nadolol
Sotalol
what are the pharm effects of alpha-2 receptor agonists
sedation, analgesia, hypotension
what is the result of alpha-2 binding
decreased cAMP
hyperpolarization
decreased intracellular Ca++
How do alpha 1 antagonists work?
block receptor to prevent Ca++, causing smooth muscle relaxation AKA vasodilation
how does NO effect renal system
renal vasodilation= diuresis and natriuresis
what NO vasodilator releases NO spontaneously
sodium nitroprusside
what NO vasodilator need active reduction to have effect
organic nitrates like nitroglycerin
what kind of toxicity does sodium nitroprusside cause
cyanide
does nitroglycerin do more venous or arterial dilation
venous
what are the cardiac effects of nitroglycerin
decreased BP
reduced preload
reduced myocardial oxygen demand
coronary vasodilator
what phase of the AP does adenosine effect
phase one, calcium entry
what are the action of adenosine
stimulate NO=coronary vasodilation
activate K channels= hyperpolarize
blocks Ca entry= vascular relaxation
what is the MOA of hydralazine
promotes influx of K into vascular smooth muscle= hyperpolarize= muscle relaxation
-may inhibit Ca release from SR
What is dromotropy?
conduction velocity of AV node
what is the chemical structure of diltiazem
benzothiazepine
how does aging effect CCBs
reduced cardiac output leads to increased bioavailability and decreased clearance
what receptors does carvedilol block
Alpha 1, Beta 1, Beta 2
what are negative effects of BB
-negative inotropy
-worsened intermittent claudication, raynauds in patient with peripheral vasc disease
-bradycardia=synchopy
-nonselectives can cause bronchospasm and worsen asthma
-increased triglycerides
-lipophilic BBs can cause CNS depression, sleep disturbances, vivid dreams, and hallucinations
-sudden withdrawal can cause reflex tachy, htn, and palpatiation
how do BBs effect insulin
potentiate effects of insulin and other oral hypoglycemic agents
what kind of antiarrhhythmic is lidocaine
1b, sodium channel blocker
what kind of antiarrhhythmic is verapamil and clevidipine
4, CCB
what kind of antiarrhythmic is amiodarone
class 3, potassium channel blocker
what kind of antiarrhythmic is metoprolol, esmolol, labetalol
class 2, beta blocker
how do class 3 antiarrythmics effect EKG
QT prolongation
when do you not use BBS
diabetes-masks symptoms of hypoglycemia
tachycardia from phenylephrine
HF
asthma- if non selective
peripheral vasc disease- if non selective
what are the heart effects of CCBs
negative inotropy
negative chronotropy
negative dromotrope
all local anesthetics are weak __________
bases
3what are molecular components of all local anesthetics
aromatic ring
intermediate ester or amide link chain
tertiary amine end
the aromatic ring makes LA ________philic
lipo
what would make LAs hydrophilic
when there is an excess positive charge (protonated)
what LAs are in the Ester family
cocaine
procaine
2-chloroprocaine
tetracaine
what metabolizes most esters except cocaine
plasma cholinesterase
what metabolizes cocaine
liver (hepatic carboxylesterase)
which patients have an increased risk for LAST from ester LAs
plasma cholinesterase deficiency
what conditions decrease plasma cholinesterase
hepatic impairment
increased BUN
chemotherapeutic drugs
expectant mothers
which kind of LA has more allergic reactions
esters
how are amides metabolized
liver cyp450
which amide is not metabolized by CYP450
articaine, plasma carboxyesterase
agents with lower pKa are more ______________ at physiologic ph (7.4)
non ionized
which form of drug penetrates the lipid bilayer and has effect
nonionized
low pKa means (slower/faster) onset
faster
what is goal channel that LAs block
Na channels
what is definition of pKa
The pH at which the molecule is 50% ionized and 50% nonionized
why do LAs not work in infected, acidotic tissues
these tissues have a pH of 6, which means most of the LA is ionized
what can we add to LA to increase speed of onset
bicarb, because it is more basic, this brings the tissue pH closer to the LA pKa
what is the pKa of procaine
8.9
what is the pKa of tetracaine
8.6
what is the pKa of bupivicaine
8.1
what is the pKa of Ropivicaine
8.1
what is the pKa of Chloroprocaine
8.7
what is the pKa of Lidocaine
7.7
what is the pKa of Etidocaine
7.7
what is the pKa of Mepivicaine
7.6
increased lipid solubility correlates with _____________ penetration of the nueral membrane by local anesthetic
increased
what determines the potency of LAs
lipid solubility AKA oil:water partition coefficient
what molecular structure determines the lipophilicity of LAs
alkyl substituents on the aromatic ring and on or near the tertiary amine
the larger the alkly substituent of the LA the _____ the lipophilicity AKA potency
higher
a higher lipid solubility of LA increases what two aspect of pharmokinetic and decreases what aspect
potency
DOA
decreases onset
what are the two determinates of DOA of LA
protein binding and lipid solubility
the greater the protein binding the __________ the DOA
longer
what can we give with LAs to increase DOA
epi (vasoconstriction)
what are the four determininants of blood concentrations of LAs
-presence of a vasoconstrictor
-tissue blood flow
-concentration injected
-number and frequency of injection
what causes most of LA to be lost from injection site
vascular absorption
a site of LA injection with high rates of vascular uptake is (more/less) likely to have LAST
more
rank high to low vascular uptake sites for LA
IV
tracheal
intercostal
caudal
paracervical
epidural
brachial plexus
subarachnoid, sciatic, femoral
subcutaneous
the higher the concentration of LA at site, the _______ the conduction block
longer
the lower the blood flow to site of LA injection site the _______ the conduction block
longer
what areas do we not add epi to LA
lacking collateral vessels (terminal circulation)
fingers
nose
toes
ear
what is a steroidal adjuvent to prolong LA block
dexamethasone
what alpha-2 agonist can we add to increase duration of both motor and sensory blocks
precedex
what alpha-2 agonist cab be added to epidural and intrathecal to produce more analgesic effects
clonidine
what opioid can prolong action of LA
ketamine
what analgesic adjuvent can be given to increase the duration of SAB
mg
what drug can be given with LA to speed onset
sodium bicarb
what benzo can be given with LA to increase DOA of SAB
versed
LA prevent _________ influx into the nerve axon
Na
what electric process do LA inhibit
action potential
what state of the sodium channels to LA bind with
open and inactivated more than the resting
what type of nerve fibers do LA bind with most easily
faster conduction velocities such as small myelinated A-gamma motor and A-delta sensory
then A-alpha and A-beta
then the small nonmyelinated C fibers
why do LA bind to nerves with faster conduction velocities
1) more binding sites are available during activated states
2) LA binding last longer on previously inactivated sites than on resting sites
what is it called when LA in epidural/spinal cuase autonomic blockade but not sensory/motor blockade
differential blockade
how much higher is sympathetic blockade then motor/sensory blockade in neuraxial block
6 dermatomes
how many nodes of ranvier must be blocked in a myelinated nerve to stop nerve conduction
2-3 nodes
the greater the frequency of APs the ________ the onset of the LA block
faster
where are voltage gated sodium channels found
only in axon
what LA concentrations are decreased when it passes through pulmonary circuit
lidocaine
bupivicaine
priolocaine
what metabolizes ester LA
plasma psuedocholinesterase
what metabolizes amide LA
cyp450
what population has a prolonged elimination of amides
neonates and infants
what causes the neonatal toxicity from lidocaine
accumulation of its major metabolite, monoethylglycineexylidide
what two diseases cause a exteneded half life clearance of lidocaine
CHF
liver disease
what is the goal of liposomal LA
increase amount of LA in the liposome and have a consistent release of LA into tissues
what LA can be incorporated into liposomes
Lidocaine
tetracaine
bupivacaine
what is the max dose of bupivacaine
mg:
mg/kg:
175 mg
2 mg/kg (2.5 mg/kg with epi)
what is the max dose of ropivacaine
mg:
mg/kg:
200 mg
3 mg/kg
what is the max dose of lidocaine
mg:
mg/kg
300 mg
4.5 mg/kg (7 with epi)
what is the max dose of mepivacaine
mg:
mg/kg:
300 mg
7 mg/kg
what is the max dose of prilocaine
mg:
mg/kg:
400 mg
6 mg/kg
increased dose ________ doa while ________ time of onset
increases
decreases
T/F when you reach the max dose of lidocaine, you can then switch an use prilocaine
F, they are additive
what is ED95
effective dose in 95% of patients
what are the two onset of last
immediate
delayed 2/2 redistribution/absorption from highly vascular tissues
which occurs first, CNS or cardiovascular signs of last
CNS
what is the initial CNS patho of LAST
-blockade of inhibitory pathways in the cerebral cortex
-unopposed release of the excitatory neurotransmitter glutamate
OR
suppression of both inhibitory and excitatory circuits leading to profound CNS depression
how does CNS depression from LAST effect lungs
resp depression leads to resp acidosis, elevated CO2 causes cerebral vasodilation, which delivers more LA to brain, then resp failure (this is a positive feedback loop)
how does elevated CO2 levels in LAST prolong LAST effects
CO2 enters cells, causing acidosis, more LA is in ionized form which cannot exit the cell, this leads to ion trapping of LA intracellularly and further CNS effects
how does increased CO2 effect LA protein binding
plasma protein binding of LA is decreased, leading to higher concentrations of unbound and further CNS toxicity
how do you avoid all the issues caused by resp depression/acidosis in LAST
adequately ventilate patient,
what three ways does LAST effect cardiovascular pathophysiology
directly
sympathetic blockade
parasympathetic blockade
what causes the profound hypotension in last
relaxation of vascular smooth muscle in the arterial tree
how does LAST effect EKG
lengthened PR interval
lengthened QRS complex
how does LAST effect ventricular function
slows rate of depolarization of purkinje fibers and ventricular muscle by blocking fast Na channels
what rhythms occur in LAST
bradycardia
cardiac arrest
2/2 dampened pacemaker activity in the sinus node
how does LAST effect contractility
negative inotropy
inhibits Ca++ from SR
inhibits Na and Ca currents
what three lab values increase the negative inotropic and chronotropic effects while increasing arrhythmias in LAST
hypercapnia
acidosis
hypoxia
what three medications decrease the threshold for cardiac toxicity in LAST
BBs
CCBs
Digoxin
what is treatment for LAST
Airway-intubate
Breathing-Ventilate
Circulation
Drugs:
intralipid (lipid emulsion)
benzodiazipines: for seizures
muscle relaxants to secure airway
cardiovascular support/resuscitation
what medications do we avoid in LAST
vasopressin
CCBs
BBs
LAs
reduce epi doses to 1 mcg/kg
what is method for lipid emulsion for LAST
1.5 ml/kg bolus then continuous infusion of 0.25 ml/kg/min
IF STILL UNSTABLE
another bolus then infusion of 0.5 ml/kg/min
how can we prevent LAST
-gentle aspiration
-aspirate frequently(every 5ml) /continuous
- monitor EKG for QRS changes
what happens with a lidocaine plasma concentration of 1-5 mcg/ml
analgesia
what happens with a lidocaine plasma concentration of 5-10 mcg/ml
light-headedness
tinnitus
visual disturbances
numbness of tongue
muscle twitching
seizures
convulsions
what happens with a lidocaine plasma concentration of 10-15 mcg/ml
seizures/convulsions
what happens with a lidocaine plasma concentration of 15-25 mcg/ml
unconsciousness
coma
resp arrest
what happens with a lidocaine plasma concentration of >25 mcg/ml
cardiovascular suppression
what are early CNS s/s LAST
dizziness, lightheadedness, facial n/t, auditory/visual disturbances, ringing in ears, slurred speech, drowsiness, disorientation
what are progressive CNS s/s LAST
tremors, twitching, shivering, tonic-clonic sz,
what are late CNS s/s LAST
sz activity stops
resp arrest
what are CV s/s LAST
hypotension
bradycardia
tachycardia
arrhythmias (Vtach, Vfib)
arrest
how does prolonged use of edrophonium, physostigmine and echothiophate effect LA
depressed psuedocholinesterase leasts to prolonged ester LA activity
what kind of LA has PABA (para-aminobenzoic acid) as a metabolite
esters
how does cocaine differ from other ester LAs
its a vasoconstricor
its naturally occuring
T/F ester LAs accumulate in the blood
F, they are metabolized by plasma psuedocholinesterase
what LA is good for pregnant patient
chloroprocaine (fast metabolism)
which ester LA is most likely to have LAST
tetracaine
what LA is used to assess plasma cholinesterase activity
dibucaine (high incidence of LAST)
what is normal dibucaine result
70-85% depression or 80%
what dibucaine number means homozygote atypical pseudocholinesterase
20
what dibucaine number is heterozygotic atypical pseduocholinesterase
30-70
what LAs are effected by atypical psuedocholinesterase
esters
what LA can cause methemoglobinemia
prilocaine, bupivicaine
what is treatment for methemoglobinemia
methylene blue
ester local anesthetics are derivatives of ________
benzoic acid
what causes bradycardia in subarachnoid injection
blockade of cardiac sympathetic preganglionic fibers, which arise from segments T1-T4
compared to sensory blockade, motor blockade occurs _______ segments lower
2-3
compared to sensory blockade, sympathetic blockade occurs __________ segments higher
2-6
your patient becomes nauseous 5 minutes after a spinal anesthetic, what is likely the cause
hypotension
how much do you reduce LA admin in parturient epidural
25-50%
what causes the hypotension associated with spinal and epidural anesthesia
blockage of sympathetic preganglionic nerves
what is an immune system response to a foreign, environmental antigen that causes an altered T cell and antibody response
hypersensitivity
what is the time frame for. a type 1 hypersensitivity reaction
15-30min
what antibodies act in type 1 hypersensitivity
IgE
where do IgE antibodies bind to in type 1 hypersensitivity
mast cells and basophils
what does a second exposure to the antigen do in type 1 hypersensitivity
-cross linking of two IgE antibodies on mast cells and basophils
-increased Ca++ inflyx
-Ca++ degranulates mast cells releasing mediators
what mediators are released from mast cell degranulation in type 1 hypersensitivity
-histamine
-heparin
-proteolytic enzyme
-chemotactic factors
what other mediators are activated by mast cell degranulation in type 1 hypersensitivity
bradykinin, leukotrienes, interleukins, serotoinin, prostaglandins, thromboxane
what is the most important mediator of type 1 hypersensitivity reaction
histamine
what results from binding of Histamine to H1 receptors in type 1 hypersensitivity
bronchoconstriction, increased vasc permeability, vasodilation, urticaria, pruritis, increased gut permeability, increased mucus
T/F type one hypersensitivity happens on first exposeure
F, happens on second
what can a severe allergic reaction lead to
angioedema
systemic vasodilation
hypotension
extravasation of protein and fluid
bronchospasm
dysrhythmias
how fast does anaphylaxis occur
within min
how do we treat type 1 hypersensitivity reaction
-antihistamine (benadryl)
-cromolyn sodium (inhibit mast cell)
-bronchodilators like B2 agonists (albuterol)
-leukotriene receptor blocker (singulair)
-inhibitors of cyclooxygenase pathways (zileutoin)
how do you diagnose a type 1 hypersensitivity individual
skin tests with allergen
immunoassays to measure IgE
tryptase
what medications can cause intraop anaphylasxis
anesthetics, antibiotics, antiseptics, blood products
what are the most frequent cause of anaphylactic reactions intraop
NMBA
1-succs
2-vec
3-atracurium
4-pancuronium
5-mivacurium
6-cisatracurium
what molecular strucutres cause anaphylactic reaciton is NMBs
quatinary ammoniums
what are the second and third leading causes of anaphylaxis intraop
abx
latex
what are the most common symptoms of anaphylaxis in intraop patient
hypotension
tachy
bronchospasm
THEN
hypovolemia
shock
hypoxemia
what is the definitive treatment for anaphylaxis intraop
epi
what do you do for anaphylactic patient intraop
epi
IV fluids
vasopressin
what is an example of an H2 antagonists
ranitidine
what are examples of b2 agonists
albuterol, terbutaline,
what medication can we give or airway edema
corticosteroids
what are s/s grade 1 anaphylaxis
Cutaneous signs: generalized erythema, urticaria, angioedema.
what are s/s grade 2 anaphylaxis
Cutaneous signs, hypotension, tachycardia, cough, difficult ventilation.
what are s/s grade 3 anaphylaxis
Hypotension, tachycardia or bradycardia, arrhythmias, bronchospasm.
what are s/s grade 4 anaphylaxis
Cardiac and/or respiratory arrest, pulseless electrical activity (PEA).
what mediates type 2 hypersensitivity reactions
IgM or IgG
what are examples of type 2 reactions
type 1 DM
myasthenia gravis
drug-induced hemolytic anemia
granulocytopenia
thrombocytopenia
transfusion reactions
goodpastures nephritis
what is treatment for type 2 reactions
anti-inflammatory
immunosuppressants
what is another name for type 3 reaction
immune complex hypersensitivity
what medaites type 3 reactions
IgG, IgM
what differentiates type 2 and type 3 reactions
in type 3 antigen is soluble and not attached to tissue
where are antibody-antigen complexes depositied in type 3 reactions
kidneys, skin, eyes
how long does it take for type 2 reaction
minute to hours
how long does it take for type 3 reaction
hours to weeks
what are examples of type 3 reactions
serum sickness
systemic lupus erythematosus
RA
what is another name for type 4 hypersensitivity
cell mediated or delayed type hypersensitivity
what is onset of type 4 reaction
24 hours to 14 days
what are the primary mediators of type 4 reactions
T lymphocytes
monocytes
macrophages
what are examples of type 4 reactions
poison Ivy
TB
leprosy
PPD test
what mediates type 5 hypersensitivity
autoantibodies that bind and stimulate specific target cells
what is an example of type 5
graves (stimulates TSH receptor)
why do we give FFP in angioedema
kininase 2 catalyzes the degredation of excessive bradykinin
what are some anesthetic considerations for intubating angioedema
do not delay intubation
-use video/fiberoptic technique
-use precedex and ketamine for intubation to maintain resp drive
-give succs once you see cords
what do you pretreat a protamine reaction wtih
pepcid
benadryl
calcium
what are the first signs of protamine reaction
increased peak airway and severe vasodilation
what is treatment for amniotic fluid embolism
A-OK
atropine
ondansetron
ketoralac
