Exam 3 Part IV Flashcards
what patients would be especially vulnerable to an increase in PVR 2/2 N2O use
- pts with pulmonary htn 2. neonates with bronchopulmonary dysplasia and/or RSV 3. those with congenital heart defects (–> R-to-L shunt)
respiratory effects of N2O
- mild decrease in Tv 2. mild increase in RR 3. hypoxic respiratory drive decreased 4. ventilatory response to increased CO2 affected
renal/hepatic effects of N2O
- no significant effects on kidney 2. mild decrease in hepatic blood flow
neuromuscular effects of N2O
- does NOT provide significant muscle relax 2. increased muscle tone with high concentrations 3. does NOT trigger MH
hematologic effects of N2O
- inhibits enzymes that are vitamin B12 dependent (methionin synthetase) 2. leads to bone marrow suppression 3. peripheral neuropathies 4. & pernicious anemia
T/F: N2O causes increase uterine smM contractility
false; no effect on uterine smM
fetal effects of N2O
- increased incidence of spontaneous abortion with chronic exposure to N2O 2. may be hazardous to fetus esp during 1st trimester
what anatomical areas are “compliant spaces” and would have an increase in volume with the use of N2O
- GI tract 2. pneumoperitoneum 3. pneumothorax 4. air emboli
principle objective of inhlational anesthesia
- achieve a constant and optimal partial pressure of the agent
partial pressure gradients that guide INH anesthetic uptake
- anesthesia machine 2. alveolar 3. blood 4. brain
the goal with INH partial pressure gradients is for the _______________ to = ______________
inspired pressure; alveolar pressure
input of INH agent into alveoli is dependent on
- anesthesia machine 2. inspired partial pressure 3. alveolar ventilation
uptake of INH agent from alveoli to blood is dependent on
- solubility of the gas 2. CO 3. alveolar to venous partial pressure gradient
order of pressure gradients for inhalational agents
Pressure device (PD) - pressure inspired (PI) - Pressure alveoli (PA) - pressure arterial (Pa) - pressure brain (Pbr) same order with fraction
doubling the CO _________________ the time to uptake of INH agent
doubles
Et of INH agent = ________________ of the agent
partial pressure
pt will have awareness at a MAC < ___________
0.7
factors that influence tissue uptake of INH agent
- tissue solubility 2. tissue blood flow 3. Pa-Pbr partial pressure difference
you should have equilibration of INH agent Pa with VRG within _______________min
8-Apr
you should have equilibration of INH agent Pa with muscle and skin group (MG) within ___________________
1-4 hours
you should have equilibration of INH agent Pa and fat group within ____________
> 24 hours
your MAC should not get below ___________ without reversing your muscle relaxant
0.7
elimination of INH agent is determined by?
- length of administration of agent 2. solubility of agent (elim time decreased with less plasma soluble agents)
rate of decrease of INH in Pbr is reflected by the ____________
PA
what is the effect of N2O is discontinued abruptly
- reversal of partial pressure gradients –> reverse concentration effect 2. high volume of N2O enters the alveoli from capillary flow –> displacing O2 from alveoli –> decreasing PaCO2 3. dilutes PaCO2 –> decreased stimulus to breathe all leads to diffusion hypoxia
how can you avoid diffusion hypoxia with N2O
filling lungs with 100% FiO2 at the end of a case
Tec6 heats the vaporizer to _______________ creating VP = ___________atm
39 C; 2
what is the MOA of all local anesthetics?
they block voltage gated sodium channels
uses of local anesthetics
- local infiltration (hernia repair) 2. peripheral/regional blocks 3. neuraxial blocks 4. acute or chronic pain 5. IV injection for arrhythmias
all currently available LA consists of a _______________ ring + ___________
lipophillic phenyl ring; tertiary (majority)/quaternary amine
what determines whether a LA is an amide or an ester
the bond btween the benzene ring and the carbon group
tertiary amine LA have more _______________ effects than those that are quaternary
toxic CNS
which LA are esters
- procaine (novicaine) 2. chloroprocaine** (nesacaine) 3. tetracaine (pontocaine) 4. cocaine 5. benzocaine**
_______________ is available commercially as ambesol and origel
benzocaine
which LA are amides
- lidocaine (xylocaine)** 2. mepivacaine (carbocaine) 3. prilocaine 4. bupivacaine** (marcaine, sensorcaine) 5. levobupivicaine (chirocaine) 6. ropivicaine (naropin)** 7. articaine
which LA has the highest risk of toxicity
bupivicaine
metabolism of ester LA
- catalyzed by plasma tissue cholinesterases via hydrolysis 2. occurs throughout the body in the blood 3. rapid metabolism
which ester is NOT metaboized by plasma and tissue cholinesterases
cocaine
what is the longest acting ester
tetracaine
DOA of ester LA
short due to rapid metabolism
which category of LA is more likely to have allergic potential
esters; and is due to metabolism into PABA
if someone has an allergy to an amide LA, it is probably an allergy to what _______________
preservatives
an allergy to one ______________ is an allergy ALL, but an allergy to one ____________ is NOT an allergy to all
ester; amide
what are your low potency, short DOA LA
- procaine (novocaine) 2. chloroprocaine (nesacaine)
what are your intermediate potency, intermediate DOA LA
- mepivacaine (carbocaine) 2. lidocaine (xylocaine)
what are your high potency long DOA LA
- tetraine (pontocaine) 2. bupivicaine (marcaine) 3. ropivacaine (naropin)
which LA have a fast onset
- chloroprocaine 2. mepivacaine 3. lidocaine
which LA have a slow onset
- procaine 2. tetracaine 3. bupivacaine 4. ropivacaine
DOA of procaine
60-90 min
DOA of chloroprocaine
30-60 min
DOA of mepivacaine
120-240 min
DOA of lidocaine
90-120 min
DOA of tetracaine, bupivacaine, and ropivacaine
180-600 min
all LA are _______________ (weak acid, weak base, strong acid, strong base)
weak bases
what is pKa
the pH at which 50% of the drug is ionized (water soluble form) and 50% in non-ionized (lipid soluble) form
LAs are mostly ionized at a pH that is signifcantly ___________ its pKa
less
LA with increased pKa have _________ ionization at normal pH
increased (which slows the onset)
decreased pKa = ______________ onset
faster
what is the exception to pKa with LA onset
chloroprocaine, has a fast onset, but due to the dose not the pKa
rate of diffusion of LA depends on:
- chemical structure 2. lipid solubility 3. state of ionization (**most important characteristic)
a base in a in an alkaline environment is _______________, ___________, & ______________ across the bilipid membrane
non-ionized, lipid soluble, and easily diffusible
T/F: if the tissue you are trying to inject LA into is infected, the block will be potentiated
false; block will not work because infected tissue = acidic environment
T/F: the further away the pKa is from physiologic pH the more it will be ionized at injection
TRUE
LA provide analgesic as long as they __________________________
are in the site of deposition
target site of action of LA
NAME?
potency of LA is related to _____________
lipid solubility (which is dependent on pH and pKa)
onset of LA depends on ________ & _______
route and dose
DOA of LA depends on ____________ & ____________
protein binding; vascular uptake
increased protein binding of LA = __________ DOA; increased vascular uptake = _____________ DOA
increased; decreased
how does epi affect DOA of LA
they vasoconstrict which slows the vascular uptake rate, just prolonging the DOA
epidural requires ____________x more of the dose of LA to produce the dense block achieved with a spinal
10
a ________________ block has no nerve sheaths, has direct access to the nerves thus gives a fast onset
subarachnoid block
if you do a spinal block but your patient becomes hypotensive and nauseated, this is a sign of _____________
high spinal block
describe the chemical structure effect on MOA: (starting with drug in the vial)
- weak LA + slightly acidic solution = ionized 2. inject LA into tissues (more basic solution) –> protonating (picking up charge) –> unionization 3. unionized LA crosses lipid bilayer 4. intracellular pH is lower –> ionization of LA (so it cannot leave) 5. antagonizes the voltage gated ion channel
_____________ = extension of a centrally located neuron & is the functional unit of peripheral nerves
axon
axolemma of axon
Specialized bilipid plasma membrane surrounding the axoplasm containing proteins and ion channels
on the nerve cells where are the voltage gated ion channels located?
between the nodes of ranvier
for a LA to block saltatory conduction __________ nodes of ranvier have to be blocked
3
what are the three layers of connective tissue on the nerve that are barriers to LA
- endoneurium 2. perineurium 3. epineurium
LA preferentially bind to the ___________ & ____________ states of the voltage gated sodium ion channel
open; inactivated
resting membrane potential of a neural cell
-70 to - 90 mV
axolemma is relatively permeable to outward diffusion of __________, but is impermeable to __________
K+; Na
describe the action potential of a neural cell
- sodium channels are open (below threshold) 2. at threshold (~50 mV) potassium channels open 3. at peak sodium channels close (inactive) –> repolarization 4. potassium channels close just below - 50 mV
what is the guarded receptor/modulated receptor hypothesis
that LA’s preferentially bind to both the open & inactivated states of the voltage gated Na channels
if a LA goes through the pore interior to get to the binding site this is the ______________ pathway
hydrophillic
if LA goes through the lipid membrane to get to the binding site this is the _______________ pathway
hydrophobic
intracellular Na channel pore receptors have an increased affinity for the ____________ form of LA
ionized
what is the use dependent (phasic block/inhibition) of LA
- LAs work faster as the voltage gated sodium channel is repetitively depolarized 2. leads to greater number of Na channels being in the inactivated & open state 3. increases the opportunity for LA binding = accumulation of LA bound Na
describe the sequence of what gets blocked when you administer a LA (i.e. differential block)
- vasodilation –> autonomic function block 2. pain 3. touch 4. temperature 5. motor fx 6. proprioception
T/F: with LA non-myelinated fibers are generally blocked before myelinated fibers
false; myelin increases the diffusion barrier, but only need to block 3 nodes of ranvier and NOT the entire length of the nerve like with unmyelinated
T/F: there is a strong correlation btwn potency and lipid solubility of LA
TRUE
characteristics of larger LA molecules
- more lipophillic/relatively water insoluble 2. highly protein bound –> prolonged DOA 3. less easily absorbed systemically 4. bind to Na channels with a higher affinity that lower soluble agents 5. increased incidence of CV toxicity 6. higher potency = lower dose
duration of action of LA is determined by _______________ & ______________
protein binding; vascular uptake
the more protein bound a LA is –>
- more CV effects 2. longer duration of Action 3. higher affinity for voltage gated sodium channels
sx of horners syndrome
- miosis 2. ptosis 3. anhydrosis 4. epopthalamus
rate the sites of LA absorption from greatest absorption to least (after LA is IV)
- interpleural (greatest) 2. intercostal 3. caudal 4. epidural 5. brachial plexus 6. femoral/subarachnoid 7. sciatic 8. subcutaneous
factors that affect LA absorption (i.e. into vasculature away from site of injection)
- site of injection (greater vasculaturity = greater absorption) 2. dose 3. pKa 4. additives: epi & ketamine (decreases absorption via VC), alpha2 agonist and opioids (increase absorption via VD)
lipid solubility effect of LA on systemic absorption
more lipid soluble decreased systemic solubility
the safe & recommended dose for one type of block could result in ______________ for another type of block
systemic toxicity
w/ LA the faster the (systemic) absorption = the ______________ the DOA and the the ________________ risk of toxicity
shorter; increased
