Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Adv Pharm II > IV induction/Neuro monitoring/Inhalation hx/volatiles > Flashcards

IV induction/Neuro monitoring/Inhalation hx/volatiles Flashcards

1
Q

what are examples of adjunct medications to primary anesthetics

A

antihistamines
antipsychotics
benzodiazipines
opioids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is balanced anesthesia

A

premedication
light sedation
regional anesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is general anesthesia

A

balance of unconsciousness, analgesia, amnesia, suppression of stress response, immobility
-unarousable complete loss of consciousness
-inability to maintain airway control
-loss of eyelid reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what pathway do the majority of IV inductions agents on on

A

excitement of inhibitory signals through the gamma-aminobutyric acid type A (GABA) receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are MOA theories

A

-membrane protein binding sites
-alter signaling between neurons (charges)
-GABA: ligand gated ion channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what receptors does ketamine work on

A

NMDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

receptors contain multiple

A

subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the primary binding site on GABA, what is the effect

A

GABA 2, hyper polarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

GABA is an ______ neurotransmitter

A

inhibitory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are examples of excitatory neurotransmitters

A

acetylcholine
glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are examples of secondary IV induction agents

A

Antihistamines
antipsychotics
benzodiazepines
opioids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is general anesthesia

A

A balance of unconsciousness, analgesia, amnesia, suppression of the stress
response, and sufficient immobility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

T/F general anesthesia results in an unarousable state and complete loss of consciousness

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F general anesthesia results in an inability to maintain airway or controll reflexes

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

T/F general anesthesia results in the loss of eyelid reflexes

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the MOA theories for IV induction agents

A

-membrane protein binding sites

-altering signaling between neurons by altering ion channels

-GABA receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where do the majority of IV induction agents act (receptor)

A

enhancement of inhibitory signals through the gamma-aminobutyric
acid type A (GABA) receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what system do most IV induction agents have their action on

A

reticular activating system in brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does the reticular activating system control

A

consciousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what controls the signals coming into the reticular activating system? where does it send the message

A

thalamus
cerebral cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what neurotransmitter does the reticular activating system use

A

acetycholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what kind of feedback mechanism does the reticular activating system use

A

positive feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are examples of excitatory neurotransmitters

A

acetylcholine
dopamine
norepinephrine
glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are examples of inhibitory neurotransmitters

A

Gamma-aminobutyric acid (GABA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the most abundant inhibitory neurotransmitter in the brain

A

GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what does GABAa regulate

A

neuronal excitability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does GABAa mediate

A

unconsciousness, amnesia, suppression of spinal reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what channels does GABA work on

A

Ligand-gated ion cys-loop channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how many protein subunits make up a GABA receptor

A

5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what channel does the GABA receptor control? what is the affect of its activation?

A

Cl-
hyperpolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what controls the release of GABA

A

Ca++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what happens when GABA is activated

A

-increases Cl- conductance
-cell membrane hyperpolarization
-decreased neuronal excitability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

where on GABA receptor does the GABAa endogenous enzyme bind

A

alpha and beta subunit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

where on GABAa receptor do Benzodiazepines bind

A

alpha and gamma subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

where on GABAa receptor does propofol, etomidate, and barbituates bind

A

within or proximal to beta subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

suppression of NMDA receptors leads to

A

depression of neuronal activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Where are NMDA receptors found

A

pre, post, and extra synaptically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

how many subunits are in an NMDA receptor

A

4 around a central ion channel pore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what types of subunits are NMDA receptors made from

A

-an NR1 receptor
-4 types of NR2 subunits (A-d)
-NR3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what effects the onset of an NMDA receptor

A

presynaptic glutamate
voltage of membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what blocks the channel pore of an NMDA receptor if agonist is present

A

Mg++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

NMDA receptors play a significant role in CNS functions that require activity-dependent changes in cellular physiology such as

A

learning and processing of sensory information

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is an example of an NMDA antagonist

A

ketamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

IV induction agents that work on NMDA are

A

antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

IV induction agents that work on GABA receptors are

A

agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

does ketamine competitively or non-competitively bind to NMDA receptrs

A

non-competitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Ketamine can only bind to NMDA receptors that are in the _________ position

A

open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what are examples of barbituate IV induction agents

A

thiopental,
Methohexital (brevital),
Pentobarbitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

T/F brevital changes the seizure threshold

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what receptors do barbituates work on

A

GABA
block action of Glutamate at AMPA and Kainate
inhibits neuronal nicotinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

how do barbiturates affects GABAa receptor

A

Enhances GABAa receptor function and decreases the rate of disassociation of GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

T/F barbituates block glutamate at NMDA receptors

A

false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

how do high doses of barbiturates affect GABA receptors

A

directly activate GABA receptors (even in absence of GABA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

T/F barbiturates cause EEG changes

A

T, cause low to high frequency patterns on EEG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

the CNS depression caused by barbiturates is ________ dependent

A

dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

barbiturates ________ cerebral metabolic rate for O2 (CMRO2) by _____ %

A

decrease
55%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

which barbiturates have anticonvulsant properties

A

Thiopental
pentobarbital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

barbiturates cause veno____________

A

dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

barbiturates (increase/decrease) preload and CO

A

decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what conditions do you avoid barbiturates in and why

A

aortic stenosis/tamponade
decreased preload and CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

do you mix barbiturates with ROC

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

do you mix barbiturates with saline?
why?

A

no
will precipitate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what order of kinetics do barbiturates go thorugh

A

first order unless there is a high concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

barbiturates are weak (acids/bases)

A

acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

barbiturates require a pH>_____ to remain aquas

A

10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what happens if you mix barbiturates in non-base solutions like N.S and L.R.

A

precipitate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

barbiturates become ________philic in plasma

A

lipophilic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is the onset of barbiturates? why?

A

30-60 seconds
readily pronate in plasma and become lipophilic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

60% of barbiturates are __________ (ionized/non-ionized) at body pH due to pKa being higher.
this results in (easy/difficult) passage through lipid membranes

A

non-ionized
easy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what terminates the initial dose of barbiturates

A

redistribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Vd of barbiturates is related to perfusion of what

A

vessel rich organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

muscles results in a _______ reservoir

A

large

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

fat results in a ______ reservoir

A

smaller, slow distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Barbiturates are (high/low) protein bound

A

highly 75-90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

if a patient has liver disease how does this effect your barbiturate dose

A

decrease it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

how are barbiturates metabolized

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

T/F barbiturates cause histamine release

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what are s/s histamine release

A

uticarial rash

anaphylaxis

Hives

Edema

Bronchospasm

Shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

which barbiturate causes pain on injection

A

methohexital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what happens with IV infiltration of barbiturates

A

severe tissue necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what can happen with intra-arterial injection of barbiturates

A

chemical endarteritis

destroys tissue

intense vasospasm

excruciating pain

necrosis/gangrene

permanent nerve damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what are signs of the intense vasospasm caused by intra-arterial injection of barbiturates

A

blanching of skin with disappearance of pulses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what is the induction dose of methohexital

A

1 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what is the sedation dose of methohexital

A

0.2-0.4 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what is the duration of induction dose of methohexital

A

5-10 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what is the 1/2 life methohexital

A

3.9 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what is the pediatric rectal dose of methohexital

A

25 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what conditions is etomidate useful for

A

cardiac (aortic stenosis, tamponade, sepsis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what IV induction agent has the greatest selectivity for GABAa

A

Etomidate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

how many enantiomer are in etomidate? why?

A

1
R(+) isomer having the greatest hypnotic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

T/F Etomidate is hydrophilic

A

F, it is lipophilic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

T/F Etomidate is highly protein bound

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

how long does it take Etomidate to reach peak brain levels

A

2 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

how is Etomidate metabolized

A

liver
Plasma esterases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

how is the end product of etomidate metabolism excreted

A

renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what can Etomidate inhibit

A

11b-hydroxylase in the adrenal cortex, causes adrenal corticol suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what is the induction dose of Etomidate

A

0.2-0.4 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what is the T1/2 of Etomidate

A

2.9 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what is the onset/peak/DOA of Etomidate

A

30s/1 min/3-10 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what is the Vd of Etomidate

A

2-4.5 L/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what is the CL of Etomidate

A

10-20 mL/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

how does etomidate affect EEG

A

EEG slows to burst suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

how does etomidate affect CMRO2

A

decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

how does etomidate affecrt resp

A

resp depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

which causes more resp depression prop or etomidate

A

propofol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

how does etomidate affect muscles, how do you mitigate this

A

myoclonus, inject slowly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

how does etomidate affect injection site

A

pain on injection
thrombophlebitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

how does etomidate affect venous system

A

minimal vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

in what conditions can etomidate still cause significant vasodilation

A

sepsis,
shock,
SVR <2500,
aortic stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

how does etomidate affect cardiac

A

minimal cardiac depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

how does etomidate affect GI

A

n/v

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

T/F etomidate is an anticonvulsant

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what is 2,6 diisopropylphenol

A

propofol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What is MOA of propofol

A

-Potentiates GABA-mediated responses
-directly activates GABAA receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What GABA subunits does etomidate bind to?

A

likely b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

T/F propofol is a weak base

A

false
its a weak acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

T/F propofol is lipophilic

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

T/F propofol is a chiral molecule

A

F, it is achiral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

propofol is formulated in a lipid emulsion to mitigate its

A

hydrophobia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

what is the lipid emulsion of propofol formulated from

A

soybean oil,
glycerol,
purified egg phospholipid (lecithin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

T/F egg allergy crossover is common in propfol

A

f its rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

how long can an open vial or syringe of prop be open before disposal

A

12 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

how long can propofol be in a syringe before it is thrown away

A

1-2 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

what is in prop to stop bacterial growth

A

an antimicrobial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

what are examples of antimicrobials in propofol

A

ethylenediaminetetraacetic acid or sodium metabisulfite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

what causes the pain in propofol injection

A

its free aqueous concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

how can you mitigate pain of propofol injection

A

use AC vein
coadmin with lidocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

what causes propofols rapid onset

A

lipid solubility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

young people require (more/less) propofol

A

more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

how is propofol metabolized

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

how is propofol excreted

A

renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

what is CL of propofol

A

25 ml/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

T/F moderate hepatic or renal impairment has a large effect on DOA of propofol

A

F, it is little effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

what causes the short DOA of propofol

A

rapid redistribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

what is the induction dose of propofol

A

2-2.5 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

what is the induction dose of propofol for >65 yo

A

1-1.5 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

what is the onset/peak/doa of propofol

A

60 s, 1 min, 5-10 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

what is the elimination 1/2 life of propofol

A

0.5-1.5 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

what is the Vd of propofol

A

2-10 L/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

do you use propofol in sepsis

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

how much do you lower propofol dose by in sever hypovolemia

A

80-90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

if you fluid resuscitate a hypovolemic patient patient how much do you decrease prop dose by

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

how does propofol affect EEG

A

slows to burst suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

how does propofol affect CMRO2

A

decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

how does propofol affect airway muscles

A

decreases reflexes and tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

how does propofol affect heart

A

myocardial depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

how does propofol affect muscles

A

rhabdomyolysis with infusion syndrome (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

how does propofol affect liver

A

hypertriglyceridemia with prolonged infusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

how does propofol affect injection site

A

pain on injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

how does propofol affect venous system

A

decreased vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

how does propofol affect lungs

A

bronchodilation, resp depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

how does propofol affect GI

A

antiemesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

T/F propofol is an anticonvulsant

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

what is the only IV induction drug that decreases pain

A

ketamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

what kind of drug is Ketamine

A

NMDA receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

what kind of mixture is ketamine

A

racemic mixture of R and S enantiomers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

T/F ketamine is competitive binding

A

false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

what other receptor does ketamine block

A

nicotinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

what gives ketamine its local anesthetic properties

A

Na+ channels and binds mu and k opioid receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

what are common clinical uses of ketamine

A

OB/C section

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

T/F Ketamine depresses RAS

A

false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

T/F ketamine dissociates thalamus from limbic cortex

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

how does ketamine affect CMRO2, CBF, and ICP

A

increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

T/F ketamine is a good drug for head trauma patients

A

F, it increases ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

what are emergence reactions from ketamine

A

unpleasant hallucination,
vivid dreams,
delirium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

how can you reduce the incidence of emergence reactions with ketamine

A

benzos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

how does ketamine affect IOP

A

increases, dont give in glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

do you use ketamine in open eye injuries

A

no, increases IOP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

T/F nystagmus is common in ketamine

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

what is the induction dose of Ketamine

A

1-2mg/kg IV or
4-8 mg/kg IM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

what is the onset/peak/doa of ketamine

A

30s/1min/5-15 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

what is the elimination 1/2 life of ketamine

A

2-3 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

what is the Vd of Ketamine

A

2.5-3.5 L/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

what is the CL of ketamine

A

17 ml/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

how does ketamine affect venous system

A

increased vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What are the CNS effects of ketamine?

A

dissociative sedation
possible emergence delirium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

how doe ketamine affect eyes

A

nystagmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

how does ketamine affect mouth

A

increased salivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

what drugs can you used to decrease salivation

A

glyco
IV scoplamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

how does ketamine affect lungs

A

bronchodilation with preserved resp drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

how does ketamine affect heart

A

indirect myocardial stimulation
direct myocardial depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

what are the “good” effects of ketamine

A

maintains SVR
increased HR
bronchodilation
awake intubations
maintain resp drive
local mac on sick patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

what are the “Bad” effects of ketamine

A

dont use on head traumas
dont use on eye traumas
dont use in cardiac or aortic stenosis 2/2 tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

what does too much muscle relaxant lead to

A

longer recovery phase
prolonged mechanical ventilation
increased expense to institution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

what is the last muscle to be paralyzed and the first to wake up

A

diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

can a muscle fiber partially contract?

A

no it is all or none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

the response of the entire muscle depends on

A

the # of nerves activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

what is a supramaximal stimulus

A

> 50 mA, +20-25% of necessary, so painful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

when do we use supramaximal stimulus

A

when patient is asleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

when do we use submaximal stimulus

A

when patient is awake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

what is the number of cycles/)second of electrical stimulation (how rapidly a stimulation occurs)

A

Hz (hertz)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

what is 0.1 Hz

A

one stimuli every 10 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

what is 1.0 Hz

A

one stimuli every second

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

the electricity during PNA stimulation is _______

A

constant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

what are the 2 variables of Peripheral nerve stimulator

A

Hz-how often stimuli is applied
mA- electrical output, how much electricity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

what percent of patients experience residual paralysis

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

what patients do not notice residual paralysis

A

young healthy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

what patients suffer from residual paralysis

A

obese, emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

what do you give patients suffering from residual paralysis

A

reversal like sugammadex or neostig

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

where do we place the red electrode for monitoring

A

directly over nerve, toward head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

where do we place the black electrode for monitoring

A

directly over nerve, distal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

what does an electrical current cause to be released

A

an action potential releases ACh at the synaptic cleft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

what are the different patterns of nerve stimulation

A

single twitch
TOF (train of four)
Tetanus
Post-tetanic count (PTC)
Double-burst stimulation (DBS)

204
Q

how do you use TOF

A

compare T1 to T4 and make ratio/percentage

205
Q

how do we use tetanus

A

constant shock, watch for fade

206
Q

in a phase 2 block if you do 5 seconds of tetany and there is no fade what does this tell you

A

you are safe to extubate

207
Q

what is benefit of DBS

A

more accurate supposedly

208
Q

when single twitch stimulation results in no twitches what muscles have been relaxed

A

laryngeal and diaphragm

209
Q

what do you have to do before using the single twitch stimulation method

A

require baseline stimulation prior to NMBA given

210
Q

how long does a single twitch stimulation last

A

0.2 msec

211
Q

how often does TOF give stimuli

A

every 0.5 seconds (2 Hz)

212
Q

what is the frequency of TOF

A

2Hz

213
Q

how is TOF evaluated

A

fade

214
Q

how is TOF ratio determined

A

twitches/4

T4/T1

215
Q

how do you determine TOF %

A

T4/T1

216
Q

if there is NO neuromuscular blockade the 4th twitch will feel the same as the ______

A

1st

217
Q

as neuromuscular blockade increases, 4th twitch__________ until it ________

A

decreases
disappears

218
Q

after 4th twitch is lost what twitch is lost next

A

3rd then 2nd

219
Q

what is the optimal # of twitches

A

1-2

220
Q

with deep neuromuscular blockade how many twitches are present

A

none

221
Q

when is TOF most sensitive

A

70-100% paralysis

222
Q

the 4th twitch in TOF disappears at _________ blockade

A

75-80%

223
Q

the 3rd twitch in TOF disappears at _________ blockade

A

80-85%

224
Q

the 2nd twitch in TOF disappears at _________ blockade

A

90-95%

225
Q

what is considered the ideal operative paralysis %

A

85-95% blockade, 1-2 twitches

226
Q

how many twitches are present at 75-80% blockade

A

3

227
Q

how many twitches are present at 80-85% blockade

A

2

228
Q

how many twitches are present at 90-95% blockade

A

1

229
Q

what percent block is this

A

<70%

230
Q

what percent block is this

A

75%

231
Q

what percent block is this

A

80

232
Q

what percent block is this

A

90%

233
Q

what percent block is this

A

100%

234
Q

what are advantages of TOF

A

less painful
degree of block in nondepolarizing block can be evaluated
good for assessing surgical relaxation

235
Q

what is a phase one block

A

depolarization

236
Q

what is a depolarizing drug

A

Succinylcholine

237
Q

what happens with a high dose of succs

A

phase 2 block

238
Q

how does train of four appear in depolarizing blocks

A

all twitches are the same so all strong, all weak, or all gone

239
Q

which block has muscle fasciculation

A

depolarizing/phase 1

240
Q

which block has sustained response to tetanic stimulation

A

depolarizing/phase 1

241
Q

which block has absence of posttetanic potentiation, stimulation, or facilitation

A

depolarizing/phase 1

242
Q

which block has a lack of fade to tetanus, train of four, and double burst stimulation

A

depolarizing/phase 1

243
Q

which block is antagonized by prior admin of nondeplarizer as pretreatment

A

depolarizing/phse 1

244
Q

which block is potentiated by anticholinesterase drugs

A

depolarizing/phase 1

245
Q

which block has an absence of muscle fasciculation

A

nondepolarizing/phase 2

246
Q

which block has the appearance of tetanic fade and posttetanic potentiation, stimulation, or facilitation

A

nondepolarizing/phase 2

247
Q

which block has TOF and double burst fade

A

nondepolarizing/phase 2

248
Q

which block is reversible with anticholinesterase drugs

A

nondepolarizing/phase 2

249
Q

which block can be produced by an overdose and desensitization with succs at doses greater than 6 mg/kg

A

nondeplarizing/phase 2

250
Q

what does a TOF with succs look like

A
251
Q

what order do twitches reappear in

A

same order the disappear

252
Q

what is the TOF response of non-depolarizing block

A
253
Q

what is TOF response of depolarizing block

A
254
Q

what TOF indicates adequate recovery

A

0.7

255
Q

what does a TOF ratio of 0.7 mean

A

4th twitch is 70% as strong as 1st twitch

256
Q

at a TOF of 0.7 patients should be able to maintain ___________

A

airway

257
Q

at TOF of 0.7 ther are enough unoccupied receptors to bind with

A

Ach

258
Q

at what Hz does can tetanic stimulation deliver shock

A

30, 50, or 100

259
Q

what is the most common shock for tetanic stimulation

A

50 Hz for 5 seconds or 100 Hz for 5 seconds

260
Q

what are we observing for in tetanic stimulation

A

fade

261
Q

what is the physiology behind fade

A

presynaptic event
at beginning of tetanus large Ach released from nerve terminal
as stores are depleted the rate of release of Ach is depleted

262
Q

what does the degree of fade depend on

A

degree of neuromuscular blockade
frequency (Hz)
length (seconds)
how often tetanic stimulation is applied

263
Q

what causes fade in tetany

A

receptors are still occupied by NDMR

264
Q

what is the best shock indicator for extubation

A

5 second tetany, fade is easy to see

265
Q

50 Hz is _________ shocks per second OR one shock every ___________

A

50
20 msec

266
Q

100 Hz is _________ shocks per second OR one shock every ___________

A

100
10 msec

267
Q

does fade occur in depolarizing muscle relaxant

A

no

268
Q

if a patient is completely blocked with succs how will tetanus appear

A

no contraction

269
Q

if patient is partially blocked with succs how will tetanus appear

A

weak contraction that does not get weaker

270
Q

what do you do if you blocked a patient with an NDMR and you get no response to TOF

A

count post tetanic twitches
-shock 50 Hz for 5 sec then wait 3 seconds then do a single twitch stimuli at 1 Hz

271
Q

post tetanic twitches will appear __________ the first twitch in TOF. This is called ________

A

before
post tetanic potentiation

272
Q

what is the Hz and interval of Double burst stimulation

A

two bursts of 50 Hz separated by 750 msec

273
Q

how does double burst stimulation appear in nonparalyzed muscle

A

2 equal contractions

274
Q

how does double stimulation appear in partially paralyzed muscle

A

2nd response is weaker than first

275
Q

how many receptors are occupied when a patient has a tidal volume of 5 ml/kg

A

80% (20% free)

276
Q

how many receptors are occupied when a patient has no palpable fade to TOF stimulation

A

70-75% (25-30% free)

277
Q

how many receptors are occupied with sustained tetanus at 50 Hz for 5 sec

A

70% (30% free)

278
Q

how many receptors are occupied with vital capacity of 20 ml/kg

A

70% (30% free)

279
Q

how many receptors are occupied when there is no palpable fade with double-burst stimulation

A

60-70% (30-40% free)

280
Q

how many receptors are occupied when inspiratory force reaches -40 cm H2O

A

50% (50% free)

281
Q

how many receptors are occupied when patient can lift head for 5 sec

A

50%

282
Q

how many receptors are occupied with sustained hand grip

A

50%

283
Q

how many receptors are occupied with sustained bite and jaw clench on tongue blade

A

50%

284
Q

what peripheral nerves are used for stimulation

A

ulnar nerve
orbicularis oculi
corrugator supercilii
orbicularis oris
posterior tibial nerve
common peroneal nerve
median nerve

285
Q

T/F ulnar nerve is well correlated with larynx and diaphragm

A

false

286
Q

what response are you looking for when shocking ulnar nerve

A

thumb adduction

287
Q

what response are you looking for when shocking facial nerves

A

eyelid and eyebrow movement

288
Q

what is benefit of ulnar nerve site

A

easy access

289
Q

what is benefit of facial nerve site

A

easily accessed when arm not available
best site to measure onset (paralyzed first)

290
Q

which is more resistant to relaxants corrugator supercilli or orbicularis oculi

A

corrugator supercilii (eyebrow muscle)

291
Q

the diaphragm requires ________ times the amount required to black the adductor pollicis muscle

A

1.4-2x

292
Q

which recovers faster the diaphragm or adductor pllicis

A

diaphragm

293
Q

a surgeon is complaining that the patient is pushing, so you check twitches on the adductor pollicis and the patient is blocked, what is happening

A

diaphragm takes more drug to paralyze and comes off faster

294
Q

list muscles from the most to least sensitive to blockade

A

abd
orbicularis oculi
geniohyoid
masseter
upper airway muscles
peripheral limbs
laryngeal
diphragm

295
Q

where should red electrode be placed on arm

A

ulnar groove

296
Q

the inner eyebrow is _________ sensitive than the outer eyebrow

A

less

297
Q

facial stimulation sites

A
298
Q

when does intense blockade happen after giving an intubating dose of a NDMR

A

3-6min

299
Q

do you reverse during total blockade?

A

no

300
Q

what is another name for surgical blockade

A

moderate blockade

301
Q

how many twitches are present during an intense blockade

A

none

302
Q

when does moderate/surgical blockade begin

A

when 1st twitch of TOF returns

303
Q

how many twitches are present during surgical blockade

A

1-2

304
Q

T/F patients cannot cough or buck during surgical blockade

A

false

305
Q

can you reverse during surgical/moderate blockade

A

yes

306
Q

how many receptors are blocked with complete paralysis, 0/4 TOF

A

99-100

307
Q

how many receptors are blocked when diaphragm moves 0/4 TOF

A

95

308
Q

how many receptors are blocked with abdominal relaxation is adequate 1/4 TOF

A

90

309
Q

how many receptors are blocked when TV and VC are normal and 4/4 TOF

A

75% (25% free)

310
Q

how many receptors are blocked when patient can inspire -20 cm H2O and head lift is sustained

A

50%

311
Q

how many receptors are blocked when hand grasp is sustained

A

30% (70% free)

312
Q

sevoflurane belongs to which anesthetic drug class

A

ethers (C-O-C)

313
Q

vapor pressure

A

the pressure exerted by a vapor in equilibrium with its liquid or solid phase inside of a closed container

directly proportional to temp
increased temp= increased vapor pressure

314
Q

vapor pressure is _____(less than/greater than) atmospheric pressure

A

less than

315
Q

what occurs when vapor pressure is equal to atmospheric pressure?

A

boiling

316
Q

what can transform volatile anesthetics into toxic compounds?

A

CO2 absorbent and the liver

317
Q

what is not stable in hydrated soda lime

A

sevo

produces compound A

318
Q

what does des and iso make if they become unstable in desiccated soda lime

A

carbon monoxide (des>iso)

319
Q

vapor pressure of sevo

A

160

320
Q

vapor pressure of des

A

660

321
Q

vapor pressure of iso

A

238

322
Q

vapor pressure of N2O

A

38,770

323
Q

boiling point of sevo

A

59*C

324
Q

boiling point of des

A

22*c

325
Q

boiling point of iso

A

49*C

326
Q

boiling point of N2O

A

-88*c

327
Q

what is the molecular weight of sevo

A

200g

328
Q

molecular weight of des

A

168g

329
Q

molecular weight of iso

A

184g

330
Q

molecular weight of N2O

A

44g

331
Q

what anesthetics are stable in hydrated CO2 absorber

A

des
iso
N2O

332
Q

what anesthetics are stable in dehydrated CO2 absorber

A

N2O

333
Q

what is the blood:gas partial coefficient of des

A

0.42

334
Q

what is the blood:gas partial coefficient of N2O

A

0.47

335
Q

what is the blood:gas partial coefficient of sevo

A

0.6

336
Q

what is the blood:gas partial coefficient of iso

A

1.4

337
Q

define the blood: gas coefficient

A

the ability of the anesthetic agent to dissolve into the blood and tissues;

the relative solubility of an inhalation anesthetic in the blood vs alveolar gas when partial pressures between the two compartments are equal

338
Q

a polar solute will be more soluble in a ____

A

hydrophilic solvent

339
Q

a non polar solute will be more soluble in a ______

A

lipophilic solvent

340
Q

an anesthetic gas with low blood:gas solubility is _____ likely to be taken up in the blood

A

LESS

341
Q

oil : gas sevo

A

50

342
Q

oil : gas des

A

18.7

343
Q

oil : gas iso

A

99

344
Q

oil : gas N2O

A

1.4

345
Q

what three factors determine anesthetic uptake into the blood

A

agent solubility

partial pressure difference between alveoli and the blood

cardiac output

346
Q

low solubility = _____ equilibration of FA/FI

A

faster
this means faster onset

347
Q

high solubility = _____equilibration of FA/FI

A

slower
means slower onset

348
Q

FA is determined by what two factors

A

delivery from anesthesia machine to alveoli

rate of transfer from alveoli to the blood

349
Q

what affects the delivery from anesthesia machine to alveoli

A

setting on the vaporizer

time constant of delivery system

anatomic dead space

alveolar ventilation

volume of the FRC

350
Q

what affects the rate of transfer from alveoli to the blood

A

blood: gas solubility
cardiac output

351
Q

what factors increase FA/FI

A

increase wash in:
-high FGF
-high alveolar ventilation
-low FRC
-low time constant
-low anatomic dead space

352
Q

what factors decrease FA/FI

A

decrease uptake:
-low solubility
-low cardiac output

353
Q

what are determinants of tissue distribution

A

tissue blood flow

solubility of anesthetic in tissue

arterial blood to tissue gradient

354
Q

what does the VRG include

A

heart, brain, kidney, liver, and endocrine glands

represents 10% of body mass
receives 75% of cardiac output
1st group to saturate with anesthetic gas

355
Q

what is responsible for the majority of anesthesia continued uptake after VRG is saturated?

A

the muscle group

then fat once muscle is saturated

356
Q

what are the ways volatile agents are eliminated

A
  1. ventilation
  2. hepatic biotransformation
    -des 0.02%
    -iso 0.2%
    -sevo 2-5%
357
Q

define FI

A

concentration gradient that pushes anesthetic agent from the vaporizer towards the alveoli

358
Q

define FA

A

The anesthetic washes into the alveoli and establishes a partial pressure

359
Q

what is uptake

A

the buildup of anesthetic partial pressure inside the alveoli is being opposed by continuous uptake of the agent into the blood

360
Q

FA/FI curve for inhaled anesthetics

A
361
Q

what metabolites are produced from des halothane and iso

A

trifluoroacetic acid (TFA)

small risk of immune mediated hepatic dysfunction

362
Q

what metabolites are produced from sevo

A

free fluoride ions

theoretical risk of high output kidney failure

363
Q

what are signs of high output renal failure

A

polyuria
hypernatremia
hyperosmolarity
increased plasma creatinine
inability to concentrate urine

364
Q

what accelerates the production of compound A

A

desiccated soda lime

365
Q

that is the recommended gas flow for sevo

A

1L/min for up to 2 MAC hrs

2L/min after 2 MAC-hrs

<1L/min not recommended at anytime

366
Q

what is a MAC-hr

A

one times the minimum alveolar concentration that prevents movement in response to a noxious stimulus in 50% of subjects (MAC) administered for 1 hour

367
Q

which P450 enzyme is chiefly responsible for halogenated anesthetic metabolism in the liver

A

CYP2E1

368
Q

what by product of halothan metabolism has been implicated in causing halothane hepatitis

A

TFA
trifluoroacetic acid

369
Q

concentration effect

A

the higher the concentration of inhalation anesthetic delivered to the alveolus (FA) the faster its onset of action (aka overpressuring)

370
Q

what are the two components of the concentration affect

A

concentrating affect
augmented gas inflow effect

371
Q

what is the concentrating effect

A

alveolus shrinks reducing the alveolar volume and causes relative increase in FA

372
Q

what is augmented gas inflow effect

A

the concentrating effect causes an increased inflow of tracheal gas containing the anesthetic agent to replace the lost alveolar volume

this increase in alveolar ventilation augments FA

alveolar volume is restore quickly, so very temporary phenomenon

373
Q

how does the concentration effect affect the rate of rise on the FA/FI curve

A

the higher the concentration of inhalation anesthetic delivered to the alveolus, the faster its onset of action

374
Q

which concept best explains why N2O has faster onset than desflurane

A

concentrating effect

375
Q

what is the ventilation effect

A

changes in alveolar ventilation affect the rate of rise in FA/FI

376
Q

what is second gas effect

A

describes the consequences of the concentration effect when a second gas is co-administered with N2O

377
Q

does the second gas effect have a more meaningful impact on iso or sevo and why

A

it produces more meaningful benefit with agents of higher blood: gas solubility

iso>sevo>des

378
Q

what is the best way to mitigate diffusion hypoxia after N2O is discontinued

A

increase the FiO2 for 3-5 min after d/c N2O

it does not have to be 100% FiO2

379
Q

how does right to left shunt affect FA/FI

A

slower induction with volatile agent (less soluble agents are affected to a greater extent)

faster induction with an IV agent

380
Q

how does left to right shunt affect FA/FI

A

no meaningful impact on induction with a volatile agent

slower induction with an IV agent

381
Q

what is the MAC value for iso

A

1.15

382
Q

what is the MAC value for sevo

A

2.10

383
Q

what is the MAC value for des

A

7.25

384
Q

what is the process of converting liquids/solids to vapor

A

vaporization

385
Q

what is the temperature of a liquid at which point the majority will be converted to vapor

A

boiling point

386
Q

what determines the rate of vaporization

A

temp
vapor pressure of liquid
partial pressure of the vapor above the evaporating liquid

387
Q

what is gas molecules exerting kinetic energy as a pressure measured in mmHg

A

vapor pressure

388
Q

vapor pressure is dependent only on

A

temp

389
Q

as temp increased, vapor pressure

A

increases

390
Q

what is the vapor pressure of isoflurane

A

238 mmHg

391
Q

what is the vapor pressure of sevo

A

160 mmhg

392
Q

what is the vapor pressure of des

A

660 mmhg

393
Q

all liquids that exert high vapor pressure are known as a

A

volatile liquid

394
Q

if des is placed in an iso vaporizer, concentration will be -________ than expected

A

higher

395
Q

if iso is placed in a des vaporizer, the concentration will be _________ than expected

A

less

396
Q

what is the MAC vol% of Iso

A

1.15

397
Q

what is the MAC vol% of Sevo

A

2.10

398
Q

what is the MAC vol % of Des

A

7.25

399
Q

what is the Pmac1 of iso at atmosphere

A

8.7 mmHg

400
Q

what is the partial pressure of sevo at atmosphere

A

16

401
Q

what is the Pmac1 of Des at atmosphere

A

55

402
Q

what is the constant in charles law

A

pressure

403
Q

what are the variables in the charles law

A

temp
volume

404
Q

according to charles law as temp increases, volume _______________

A

increases

405
Q

what is henrys law

A

at a constant temperature, the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas at equilibrium above the gas-liquid interfaces

406
Q

what is the solubility constant for O2

A

0.003ml/100ml

407
Q

what is the constant for CO2

A

0.067 ml/100ml

408
Q

what is grahams law

A

the rate of effusion of a gas is inversely proportional to the square root of its molecular weight
(the bigger the molecule the slower)

409
Q

what is 1 MAC

A

the amount of gas where 50% of patients do not move under surgical stimulation

410
Q

what is MAC based on

A

sea level,

no other sedatives/narcotics,
40 yo male

411
Q

what factors increase MAC (meaning you need more gas)

A

-hyperthermia (henrys law)
-alcohol abuse
-drug-induced central nervous system activity (MAOIs)
-Hypernatremia
-age <40

412
Q

what factors decrease MAC (so you need less gas)

A

hypothermia
age over 40
A2 agonists
acute alcohol ingestion
sedatives narcotics

413
Q

factors increase MAC

A

hyperthermia
drug induced increases in central nervous system activity
hypernatremia
chronic alcohol abuse

414
Q

factors decrease MAC (from naglehaut)

A

-hypothermia
-increasing age
-preopsedatives
-drug-induced decreases in central nervous system activities
-alpha2 agonists
-acute alcohol ingestion
-pregnancy
-postpartum
-lithium
-lidocaine
-hypoxia
-hypotension
-cardiopulmonary bypass
-hyponatremia

415
Q

what does blood gas partition coefficient tell us

A

speed of uptake and elimination

416
Q

the lower the blood gas coefficient the ________ the onset/offset

A

faster

417
Q

blood gas partition tells you how much gas in is _______ as compared to tissues

A

blood

418
Q

the _______ the blood solubility the slower the uptake to the brain, so the slower the onset/elimination

A

higher

419
Q

what is the BG coefficient of ISO

A

1.4

420
Q

what is the BG coefficient of SEVO

A

0.6

421
Q

what is the BG coefficient of DES

A

0.42

422
Q

what is the BG coefficient of N2O

A

0.47

423
Q

what is the fastest gas in practice

A

N2O

424
Q

what does a BG coefficient of 1.4 mean

A

1.4x as much drug stay in blood rather than the tissue

425
Q

blood gas partition coefficients

A
426
Q

how does an MV affect onset/offset of gases

A

increased MV increases onset/offset

427
Q

what order of tissues do inhaled gases enter

A

vessel rich to vessel poor
Muscle>Fat>cartilage>bone

428
Q

what is the concentration affect

A

filling the breathing tube with gas to give a “loading dose” of gas

429
Q

what type of gas works best with concentration effect

A

higher BG coefficients like iso

430
Q

how does concentration effect affect onset

A

increase speed of onset

431
Q

when do we usually use concentration effect

A

with kids (ear tubes, tonsillectomy)

432
Q

what is the second gas effect

A

volatile + N2O speeds onset or emergence
N2O acts a a carrier

433
Q

what happens with second gas effect and emergence

A

N2O brings gas back into lungs causing a dilutional hypoxia (decreased O2 in alveoli)

434
Q

how does the addition of N20 affect the concentration of other gases

A

increases concentration

435
Q

N20 is _____x more soluble than nitrogen

A

34

436
Q

how do you correct dilutional hypoxia

A

give 100% O2

437
Q

What does the oil:gas partition coefficient correlate with

A

potency

438
Q

what agent was oil/gas coefficient tested in

A

olive oil

439
Q

the higher the oil:gas coefficient, the ________ the potentency

A

higher

440
Q

the higher the oil:gas coefficient the _________ agent able to penetrate the BBB

A

more

441
Q

a gas with _______ MAC # has more potency

A

lower

442
Q

oil: gas coefficiency is like

A

lipid solubility

443
Q

the higher the oil:gas the _______- the MAC

A

lower

444
Q

MAC/ BG/ OG coefficients

A
445
Q

what is the MAC % of SEVO

A

2

446
Q

what is the BGC of SEVO

A

0.6

447
Q

what is the OGC of SEVO

A

50

448
Q

what is the MAC % of ISO

A

1.15

449
Q

what is the BGC of ISO

A

1.4

450
Q

what is the OGC of ISO

A

99

451
Q

what is the MAC% of N2O

A

105

452
Q

what is the BGC of N2O

A

0.47

453
Q

what is the OGC of N2O

A

1.4

454
Q

what is the BGC of DES

A

0.42

455
Q

what is the OGC of DES

A

18.7

456
Q

what is stage one of anesthesia

A

analgesia

mild cortical center depression

loss of sensation to pain

skeletal muscle movement intact

457
Q

T/F we often see stage 1 anesthesia

A

F, usually skip straight to 3

458
Q

what is stage two of anesthesia

A

excitement

central depression of motor centers, involuntary system is dominant

urinary incontinence

tachy

htn

tachypnea

eyes divergent

459
Q

T/F we extubate in stage 2

A

false

460
Q

T/F we should stimulate patients in stage 2

A

false
do not stimulate

461
Q

what is stage 3 anesthesia

A

surgical anesthesia

462
Q

what is stage 4 anesthesia

A

OD, dead, resp paralysis, severe CV/resp depression

463
Q

what is stage 3 plane 1

A

loss of spinal reflexes (spontaneous breathing)

464
Q

what is stage 3 plane 2

A

decreased muscle reflexes

465
Q

what is stage 3 plane 3

A

paralysis of intercostal muscles (true deep sx anesthesia)

466
Q

what is stage 3 plane 4

A

loss of muscle tone
decreased BP, dont want to be here

467
Q

vaporizer delivery output calculation

A
468
Q

what is the volume of breathing circuit

A

8L

469
Q

what is Fa

A

alveolar gas concentration

470
Q

what is an indicator of brain concentration

A

FA

471
Q

what process allows gas to move from blood to tissues

A

simple diffusion

472
Q

1 time constant is equal to what percentage

A

63%

473
Q

2 time constants is equal to what percentage

A

86%

474
Q

3 time constants is equal to what percentage

A

95%

475
Q

4 time constants is equal to what percentage

A

98%

476
Q

what is the formula for time constant

A

T= volume of circuit (8L) / fresh gas flow

477
Q

if fresh gas flow is 2L/min what is your time constant

A

4 min

478
Q

what is Fi

A

Concentration of anesthetic exiting the vaporizer

479
Q

what factors affect Fa/Fi fraction

A

Fi
inspired concentration
fresh gas flow
circuit volume
dead space
mv

FRC
Fa
solubility
CO
partial pressures

480
Q

what causes an increase in Fa/Fi

A

low solubility
low CO
high fresh gas flows
high MV

481
Q

what causes a decreased Fa/Fi

A

high solubility
high CO
low fresh gas flows
low MV

482
Q

What anesthetics are ethers

A

Des
Iso
Sevo
Enflurane
Methoxyflurane
Ether

483
Q

What anesthetics are alkanes

A

Halothane
Chloroform

484
Q

What anesthetics are gases

A

Nitrous oxide
Cyclopropane
Xenon

485
Q

IUPAC name for desflurane

A

Difluoromethyl 1,2,2,2-tetrafluoroethyl ether

486
Q

IUPAC name for sevo

A

Fluoromethyl 2,2,2-trifluoro-1-(trifluoromethyl) Ethyl ether

487
Q

IUPAC name for iso

A

1-Chloro 2,2,2-trifluoroethyl difluoromethyl ether

488
Q

IUPAC name for halothane

A

2-bromo-2-chloro-1,1,1-trifluoroethane

489
Q

What’s another term for pseudocholinesterase

A

Butyrylcholinesterase

490
Q

What are the steroidal NDNMB

A

Roc
Vec
Pancuronium

491
Q

what is this

A

sevoflurane

492
Q

what is this

A

desflurane

493
Q

what is this

A

isoflurane

494
Q

what is this

A

halothane

495
Q

what is this

A

nitrous oxide

496
Q

high vapor pressure agent in a low vapor pressure agent vaporizer would result in

A

higher concentration than desired

497
Q

vapor pressure is solely dependent on

A

temp

498
Q

standard conditions

A

760 atm
760 mmHg
29.92 inch pressure

499
Q

Higher blood solubility =

A

Slower uptake to the brain

Slower onset and elimination

500
Q

Blood: gas represents

A

Onset

501
Q

Oil :gas represents

A

Potency

502
Q

Thiopental induction dose

A

3-6 mg/kg

503
Q

Thiopental sedation dose

A

0.5-1.5mg/kg

504
Q

Thiopental DOA

A

5-8 min

505
Q

Thiopental 1/2 life

A

11 hrs

506
Q

Drug chloride is a weak

A

Base

507
Q

Weak acid drugs have what in the name

A

Na Mg or Ca

Adv Pharm II (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions