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ITE 2017 > keywords > Flashcards

keywords Flashcards

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
Q

volatiles on CNS

A

up CBF, down CMRO2 except N2O, cerebral vasodilation. Des up CSF production. Up ICP.

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26
Q

vapor pressure of volatiles

A

Halothane 243, Iso 240, Des 681, servo 160 when at 20C.

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27
Q

amount of volatile liquid used

A

Amount of liquid volatile = 3 x Fresh gas flow (L/min) x %

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28
Q

T compensation variable bypass vaporier

A

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.

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29
Q

desflurane vaporizer

A

two separate chambers. Des chamber is constantly heated to 39C, over boiling point.

30
Q

desflurane and altitude

A

don’t need to change the dial because it is pressure regulated

31
Q

volatiles and altitude

A

all but des you need to adjust because they are temperature regulated, not pressure

32
Q

alveolar gas equation

A

PAO2 = FiO2 (Pressure where you are - PH2O which is 47) - PaCO2/RQ which is 0.8

33
Q

examples of acetylcholinesterase inhibitors

A

neostigmine, pyridostigmine (myasthenia gravis tx), organophosphates/insecticide, physostigmine (glaucoma tx)

34
Q

tx of acetylcholinesterase inhibitor poisoning

A

Pralidoxime which increases acetylcholine at nicotinic (muscles) and muscarinic receptors. Atropine, glycopyrollate, scopolamine, ipatropium
only increases acetylcholine at muscarinic

35
Q

neostigmine SE

A

SLUDGE: salivation, lacrimation, urination, diarrhea, GI upset/emesis, erection, bradycardia, bronchoconstriction

36
Q

acetylcholine up regulation causes

A

spinal cord injury, stroke, burns after 24hr and lasts 2 years, immobilization, MS, Guillain Barre

37
Q

testing

A

one

38
Q

SE local anesthetics

A

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
Q

max dose lidocaine

A

4 w/o, 7 w/

40
Q

max dose mepivacaine

A

4 w/o, 7 w/

41
Q

max dose bupi

A

3

42
Q

max dose ropi

A

3

43
Q

LAST treatment

A

lipid emulsion 20% 1.5cc/kg over 1 min then infusion of 0.25cc/kg until hemodynamically stable

44
Q

regional anesthesia bony landmarks

A

C2 1st you can feel, C7 big, T7 bottom of scapula, L4 top of iliac crest, PSIS S2

45
Q

femoral block target

A

lateral to artery. Midpoint between ASIS and pubic symphysis

46
Q

sciatic nerve distribution

A

L4-S3. divides in popliteal fossa to tibial and common peroneal

47
Q

tibial n

A

from sciatic. sensory to sole of foot, motor posterior compartment lg and sole of foot

48
Q

common peroneal n

A

motor to ant/lat lower leg and sensation to leg except medial(saphenous)

49
Q

sciatic n block good for what

A

foot/ankle surgery. would also need to block saphenous for complete analgesia

50
Q

ultrasound acoustic impedance

A

resistance to sound wave propagation (dense more impedance and whiter/echogenic)

51
Q

higher frequency ultrasound means what

A

more resolution but doesn’t go as deep

52
Q

ultrasound frequency

A

above 20kHz

53
Q

colors on M mode

A

BART. blue away, red toward

54
Q

adductor canal contents

A

saphenous n, femoral a, femoral v

55
Q

adductor canal borders

A

roof: sartorius. lateral border vastus medialis. posterior: adductor longus

56
Q

ankle block

A

need 5: superficial/deep peroneal, sural, tibial, saphenous

57
Q

where to inject for ankle block

A

line medial malleoli: deep/superficial peroneal and saphenous. b/w lateral malleolus and achilles: sural. posterior to post tib a is tibial n

58
Q

superficial peroneal n

A

L4-S1 for sensory from dorsal foot except b/w toe 1-2

59
Q

deep peroneal n

A

sensory b/w toe 1-2, extends toe

60
Q

sural n job

A

S1-2 for posterolateral leg/lateral foot

61
Q

tibial n job

A

sensory plantar foot and flexes toes

62
Q

deep vs superficial ankle nerves

A

deep: deep peroneal and tibial. superficial: sural, superficial peroneal and saphenous

63
Q

hip arthroplasty RA vs GA

A

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
Q

knee arthroplasty RA

A

epidural or spinal needs to cover T8-S2. can use femoral block for pain

65
Q

when to stop NOAC before RA

A

ticlopidine 14d, plavix 7d, abciximab 2d, epifabatide 8hours

66
Q

when to stop LMWH before RA

A

remove catheter 2 hours before starting LMWH. If on it, 10 hours from last dose

67
Q

IV heparin and RA

A

block must be 1 hour before starting heparin. remove 1 hour before starting or 4 hours after stopping

68
Q

how are local anesthetics eliminated

A

esters are by pseudocholinesterase. amides by liver

69
Q

potency of local anesthetics

A

more potent is more lipophilic

70
Q

duration of local anesthetic factor

A

more protein bound lasts longer

71
Q

speed of onset of local anesthetic determined by

A

pKa. closer pKa to physiologic means faster onset because more is unionized form and can cross cell membrane. concentration also has an effect

72
Q

what pressers to avoid for ACLS due to LAST

A

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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