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1
Q

MAC

A

Minimum alveolar concentration at steady state of anesthetic to produce no response to surgical stimulus in 50% of patients.

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2
Q

MAC-aware

A

0.4. MAC necessary to prevent response to verbal/tactile stimulation

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3
Q

MAC-BAR

A

BAR: 1.6. MAC necessary to blunt the autonomic response to a noxious stimulus

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4
Q

MAC-EI

A

1.3 MAC necessary to prevent laryngeal response to endotracheal intubation

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5
Q

increased MAC

A

hyperthermia, hypernatremia, hyperthyroid by15%, chronic alcohol abuse, redhead, drugs that increase catecholamines (MAOI, TCA, acute cocaine/amphetaminme, epinephrine)

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6
Q

decreased MAC

A

acute alcohol intoxication, pregnancy after 1st trimester, hypothermia, hypotension, hypoxemia under 40mm Hg, hyponatremia, anemia, drugs decreasing central catecholamines (chronic amphetamine use, clonidine), hypothyroid

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7
Q

Nitrous oxide and closed spaces

A

Nitrous oxide (N2O) is 35x more soluble that nitrogen in blood so N gets trapped in air spaces. When giving N2O, it will enter space faster than N can get out, rapidly expanding. So contraindicated for intestinal obstruction, pneumothorax, eye surgery where they inject gas(no use for 30 days), ear surgery, VAE, COPD(can rupture

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8
Q

final volume N2O expands to

A

Final Volume/Initial Volume = 1/(1-FiN2O)

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9
Q

N2O MAC and blood:gas coefficient

A

MAC of 104

Blooåd: gas partition coefficient is 0.47

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10
Q

N20 on heart

A

up CO and SVR

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11
Q

N2O on lungs

A

does not inhibit hypoxic pulmonary vasoconstriction so be careful in pHTN pt

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12
Q

N2O on blood

A

Longer use can lead to megaloblastic anemia by oxidizing cobalt in vitamin b12 thereby inhibiting vitamin b12 dependent enzymes like methionine synthetase which is important in DNA synthesis

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13
Q

phase I block

A

Sux(2 ACh) bind to post synaptic membrane and cause depolarization. Because it is not degraded by acetylcholinesterases, it stays in the NMJ causing continuous depolarization and relaxation

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14
Q

phase II block

A

W/ increasing doses/repeated doses, sux can cause phase II block. Continuous activation of AChR leads to ongoing Na into cell, K out but if it occurs long enough, post synaptic membrane will move towards normal anyways because increased activity of Na-K ATPase pump resulting in prolonged block

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15
Q

diagnosis of phase II block

A

Suspect if sux tachyphylaxis or given as infusion. Will see fade with TOF instead of normal decreased strength but no fade TOF of phase I

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16
Q

tx for phase II block

A

prevent it. Given acetylcholinesterase inhibitor but it is unpredictable. Maintain ventilation until block resolves.

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17
Q

sux block termination

A

Block terminates by diffusion of sux away from NMJ. Metabolism by pseudocholinesterase which is made in the liver

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18
Q

onset and duration of sux

A

onset 30-90 seconds

duration 5-10min

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19
Q

SE sux

A

bradyarrythmias, MH, myalgias, increased ICP, hyperkalemai (ESRD, prolonged immobility, burns, neuromuscular disease, increased IOP)

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20
Q

pseudocholinesterase deficiency

A

difficulty metabolizing sux.

  • qualitative is genetic. test w/ dibucaine number: Normal 80, heterozygous 40-60, homozygous 20.
  • quantitative; pregnancy, hypothyroid, malignancy, malnutrition
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21
Q

Ca in hyperparathyroidism

A

up Calcium so may cause muscle weakness but it is unpredictable

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22
Q

NMB in hpyerparathyroidism

A

instead of decreasing NMB like you’d think, hyperparathyroidism can lead to antagonized effects of NMB so doesn’t last as long

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23
Q

volatiles on CV

A

all but halothane down SVR so down MAP. Halothane down CO so down MAP. HR up at 0.25 MAC iso, 1 MAC des and 1.5 MAC sevo. Rapid increase in des can cause rapid up HR and bp as well. All depress myocardial contractility. Sevo can prolong QT.

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24
Q

volatiles on resp system

A

rapid, regular and shallow breathing. Little effect on min. ventilation. Blunt ventilation response to hyopxia and hypercarbia. Bronchodilation.

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25
volatiles on CNS
up CBF, down CMRO2 except N2O, cerebral vasodilation. Des up CSF production. Up ICP.
26
vapor pressure of volatiles
Halothane 243, Iso 240, Des 681, servo 160 when at 20C.
27
amount of volatile liquid used
Amount of liquid volatile = 3 x Fresh gas flow (L/min) x %
28
T compensation variable bypass vaporier
metallic strip. T up then up vapor pressure so strip closes over volatile containing chamber more so less fresh gas flow passes volatile and more is bypassed.
29
desflurane vaporizer
two separate chambers. Des chamber is constantly heated to 39C, over boiling point.
30
desflurane and altitude
don't need to change the dial because it is pressure regulated
31
volatiles and altitude
all but des you need to adjust because they are temperature regulated, not pressure
32
alveolar gas equation
PAO2 = FiO2 (Pressure where you are - PH2O which is 47) - PaCO2/RQ which is 0.8
33
examples of acetylcholinesterase inhibitors
neostigmine, pyridostigmine (myasthenia gravis tx), organophosphates/insecticide, physostigmine (glaucoma tx)
34
tx of acetylcholinesterase inhibitor poisoning
Pralidoxime which increases acetylcholine at nicotinic (muscles) and muscarinic receptors. Atropine, glycopyrollate, scopolamine, ipatropium only increases acetylcholine at muscarinic
35
neostigmine SE
SLUDGE: salivation, lacrimation, urination, diarrhea, GI upset/emesis, erection, bradycardia, bronchoconstriction
36
acetylcholine up regulation causes
spinal cord injury, stroke, burns after 24hr and lasts 2 years, immobilization, MS, Guillain Barre
37
testing
one
38
SE local anesthetics
CNS: tinnitus, blurred vision, dizziness, tongue parasthesias, circumoral numbnesss then nerouvs/anxious, then seizure to unconsciousness Cardiac: block fast Na channels in Purkinje fibers so decreased rate of depolarization. Prolonged PR and widened QRS. Also arrhythmias and arrest
39
max dose lidocaine
4 w/o, 7 w/
40
max dose mepivacaine
4 w/o, 7 w/
41
max dose bupi
3
42
max dose ropi
3
43
LAST treatment
lipid emulsion 20% 1.5cc/kg over 1 min then infusion of 0.25cc/kg until hemodynamically stable
44
regional anesthesia bony landmarks
C2 1st you can feel, C7 big, T7 bottom of scapula, L4 top of iliac crest, PSIS S2
45
femoral block target
lateral to artery. Midpoint between ASIS and pubic symphysis
46
sciatic nerve distribution
L4-S3. divides in popliteal fossa to tibial and common peroneal
47
tibial n
from sciatic. sensory to sole of foot, motor posterior compartment lg and sole of foot
48
common peroneal n
motor to ant/lat lower leg and sensation to leg except medial(saphenous)
49
sciatic n block good for what
foot/ankle surgery. would also need to block saphenous for complete analgesia
50
ultrasound acoustic impedance
resistance to sound wave propagation (dense more impedance and whiter/echogenic)
51
higher frequency ultrasound means what
more resolution but doesn't go as deep
52
ultrasound frequency
above 20kHz
53
colors on M mode
BART. blue away, red toward
54
adductor canal contents
saphenous n, femoral a, femoral v
55
adductor canal borders
roof: sartorius. lateral border vastus medialis. posterior: adductor longus
56
ankle block
need 5: superficial/deep peroneal, sural, tibial, saphenous
57
where to inject for ankle block
line medial malleoli: deep/superficial peroneal and saphenous. b/w lateral malleolus and achilles: sural. posterior to post tib a is tibial n
58
superficial peroneal n
L4-S1 for sensory from dorsal foot except b/w toe 1-2
59
deep peroneal n
sensory b/w toe 1-2, extends toe
60
sural n job
S1-2 for posterolateral leg/lateral foot
61
tibial n job
sensory plantar foot and flexes toes
62
deep vs superficial ankle nerves
deep: deep peroneal and tibial. superficial: sural, superficial peroneal and saphenous
63
hip arthroplasty RA vs GA
2000 meta-analysis said less 1mo mortality and dvt w/ RA but equal at 3mo. 2016 RCT said equal mortality, surgery duration, infection, nerve palsies, pony and dvt(if use ppx)
64
knee arthroplasty RA
epidural or spinal needs to cover T8-S2. can use femoral block for pain
65
when to stop NOAC before RA
ticlopidine 14d, plavix 7d, abciximab 2d, epifabatide 8hours
66
when to stop LMWH before RA
remove catheter 2 hours before starting LMWH. If on it, 10 hours from last dose
67
IV heparin and RA
block must be 1 hour before starting heparin. remove 1 hour before starting or 4 hours after stopping
68
how are local anesthetics eliminated
esters are by pseudocholinesterase. amides by liver
69
potency of local anesthetics
more potent is more lipophilic
70
duration of local anesthetic factor
more protein bound lasts longer
71
speed of onset of local anesthetic determined by
pKa. closer pKa to physiologic means faster onset because more is unionized form and can cross cell membrane. concentration also has an effect
72
what pressers to avoid for ACLS due to LAST
avoid vasopressin because it causes pulmonary hemorrhage. give smaller doses of epi because it is more arrhythmogenic. don't give b blocker or ca blocker. amio

ITE 2017 (1 decks)

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