3. Premedication --> Maintenance of Anesthesia Flashcards
(132 cards)
1
Q
benzodiazepine drugs
A
midazolam (versed)
lorazepam
diazepam
2
Q
benzodiazepine mechanism
A
binds to GABA receptor
3
Q
benzodiazepine effects
A
anxiolysis
antegrade amnesia
anticonvulsant
minimal cardiac/resp depression
4
Q
benzodiazepine reversal agents
A
flumazenil (Romazicon)
5
Q
benzodiazepine side effects
A
increased apnea
increase risk of post-op cognitive dysfunction
6
Q
midazolam administration
A
IV
PO
intranaal
7
Q
midazolam IV dose
A
1-2mg
8
Q
midazolam PO (peds)
A
0.3-0.7 mg/kg
up to 20mg
9
Q
midazolam intranasal dose
A
0.2-0.5mg/kg
causes nasal burning
10
Q
midazolam onset IV
A
rapid
20-25 secs
11
Q
midazolam onset PO
A
10-15 min
12
Q
midazolam onset intranasal
A
5-10 min
13
Q
Pre-Induction Checklist
A
Machine
Suction
Monitors
Airway (+emergency devices)
Invasive lines
Drugs
Special items
14
Q
most common methods for inducing pt
A
IV
Mask
IM (ketamine dart)
15
Q
fresh gas flow (FGF)
A
how fast gas is flowing
(L/min)
16
Q
Inspiratory concentration factors
(Fi)
A
Fresh gas flow
breathing circuit volume
circuit absorption of agent
17
Q
when machine absorbs a high amount of agent…
A
the pt absorbs less agent
18
Q
FGF and Fi relationship
A
directly proportional
19
Q
FGF and circuit volume relationship
A
???
increase volume decrease delivery?
20
Q
alveolar concentration factors
(FA)
A
uptake (into blood)
minute ventilation
overpressurization
21
Q
we want FA to ______
A
increase as quickly as possible
22
Q
uptake (into blood)
A
incr uptake decr partial pressure
23
Q
uptake factors
A
blood:gas coefficient
pulmonary blood flow
difference in alveolar gas and blood
24
Q
blood: gas coefficient
A
tells us how soluble an agent is in the blood
more soluble = more uptake
= slower FA increase
25
high B:G
slower FA increase
26
low B:G
faster FA increase
27
pulmonary blood flow
decreased CO = decreased uptake
= faster FA
28
agent concentration in alveolar gas vs venous blood
want higher [agent] in aveoli vs blood
generates larger driving force
29
N2O B:G
0.47
30
Iso B:G
1.4
31
Des B:G
0.42
32
Sevo B:G
0.65
33
minute ventilation and FA relationship
increased minute ventilation replaces anesthetic taken up into pulmonary
we want higher minute ventilation
34
overpressurization effect
increase amt of agent inspired (Fi)
increase Fi = increased downstream concentration
35
Fi vs FA
increasing Fi leads to a greater increase FA
5x Fi = 6.2x FA
36
augmented inflow effect
add gas to replace absorbed agent
Patm > Palveoli
sucks gas into alveoli (high -- > low)
5xFi = 6.8x FA
37
second gas effect
soluble first gas (N2O) is given at high inspired concentrations
N2O leaves alveoli quickly
causes over pressurization of sevo
increases driving factor
==faster induction
the partial pressure of the gas left behind (sevo) is relatively greater than that of the remaining gases (over pressurization)
38
Arterial concentration (Fa) factors
Ventilation-Perfusion mismatch (V/Q)
39
ventilation-perfusion mismatch
(V/Q)
mismatched distribution of ventilation / perfusion of lung units
some receiving high ventilation
others receiving high perfusion
40
V/Q results in
alveolar dead space
incr deadspace
== decr induction speed
41
Procedures that may cause V/Q
bronchial intubation
R-L shunt
42
MAC
the end-tidal concentration necessary to prevent movement in 50% of pts
43
1.3 MAC
prevents movement in 95% of surgical pts
(1.2-1.3 MAC)
44
0.5 Nitrous + 0.5 Sevo =
1.0 MAC
MAC is additive
45
MAC-awake
end tidal concentration that allows pt to respond meaningfully to stimuli
0.3-0.5 MAC
46
MAC-Awake (N2O)
0.64 MAC
47
MAC - Amnesia
concentration to prevent recall in 50% of pts
0.25-0.4 MAC (up to 0.6)
48
MAC-BAR
concentration where 50% of population wont mount an adrenergic response
1.5-1.6 MAC
49
N2O MAC
105%
50
ISO MAC
1.2%
51
DES MAC
6.0%
52
SEVO MAC
2.0%
53
MAC and age relationship
inversely proportional
young age = higher MAC
54
N2O supports...
combustion
N2O --> 2N2 + O2
55
what gas agent does not trigger MH
N2O
56
N2O cardiovascular response
sympathomimetic
no change to HR (slight evelation)
57
N2O respiratory response
increase RR
decrease TV
increase PVR (pulm vasc. resistance)
58
N2O mechanism
NMDA receptor antagonist
may provide analgesia bc NMDA is involved in pain transmission
59
N2O contraindications
N2O will expand air filled spaces
60
Sevo properties
nonflammable
non-pungent
61
Sevo CV effects
decrease contractility
decrease SVR
decrease BP
no change HR
62
Sevo respiratory effects
increase RR
decrease TV
bronchodilator
63
Sevo cerebral effects
increase CBF
increase ICP
decrease CMRO2 (brain O2 consum)
64
Sevo and MH
triggers MH
65
Sevo metabolism
5% metabolized
flouride metabolite - nephrotoxicity
66
Compound A
produced by interactions w/Sevo and the barium hydroxide lime/soda lime
nephrotoxic
2LPM flow rate for sevo gas
67
Isoflurane properties
nonflammable
68
Iso CV effects
decrease contractility
decrease
SVR
decrease BP
increase HR
maintains CO (cardiac output)
vasodilation
69
Iso Respiratory effects
increase RR
decrease TV
bronchodilation
70
Iso Cerebral effects
increase CBF
increase ICP
decrease CMRO2
71
ISO and MH
triggers MH
72
coronary steal
Pt has blocked CA == vasodilation
if you give Iso:
Iso causes vasodilation of other arteries which "steal" blood from the blocked CA
73
Des properties
non-flammable
pungent airway irritant
20C vapor pressure = 681mmHg
(special vaporizer)
74
Des CV effects
increase HR
decrease SVR
decrease BP
maintain CO
75
Des respiratory effects
increase RR
decrease TV
bronchoconstriction (asthmatic pts)
76
Des cerebral effects
increase CBF
increase ICP
decrease CMRO2
77
Des and MH
triggers MH
78
how do we choose volatile agent?
type of surgery
cost/availability
fat:blood ratio
pt characteristics
79
N2O F:B
2.3
80
Iso F:B
45
81
Des F:B
27
82
Sevo F:B
48
83
why IV induction more common?
rapidly bypass stage 2
rapid recovery after bolus dose due to redistribution to tgt site
more portable
not greenhouse gases
84
Propofol mechanism
GABAa receptor agonist
85
propofol onset
rapid
86
Propofol duration of action
short
why?
87
Propofol expiration
6 hrs post opening
88
Propofol CV
decrease BP
decrease SVR
decrease preload
decrease contractilioty
89
Propofol Respiratory
profound resp depression
depresses upper airway reflexes
90
Propofol Cerebral
decrease CBF
decrease ICP
decrease CMRO2
anticonvulsant (incr seizure thresh)
myoclonic movement
91
Proprofol misc effects
histamine release
antiemetic
92
Ketamine Mechanism
NMDA antagonist
93
Ketamine main effect
dissociative anesthesia
- diss sensory impulses from limbic cortex
- limbic system: awareness of sensation/emotions
94
Ketamine administration
IV
IM
Oral
Nasal
Rectal
low dose infusion for pain
95
Ketamine IV Onset/DOA
Onset: rapid
DOA: 5-10 min
96
Ketamine CV
incr BP
incr HR
incr CO
incr myocardial O2 demand
central sympathetic stimulant
(direct myocardial depressant)
97
Ketamine respiratory
no resp depression
bronchodilation
intact airway reflexes/muscle tone
98
Ketamine cerebral
incr CBF
incr ICP
incr CMRO2
99
Ketamine side effects
psychotomimetic (dreams/delirium)
seizures at low dose
anticonvulsant at high dose
incr secretions
100
Etomidate mechanism
GABA receptor agonist
depresses reticular activating system
(RAS)
- regulates sleep/arousal
101
Etomidate Onset
rapid
102
Etomidate metabolism
hepatic
plasma esteraseE
103
Etomidate side effects
PONV
myoclonus (30-60%)
injection pain
adrenal suppression (24-48 hrs post)
104
Etomidate CV effects
minimal
105
Etomidate Respiratory effects
mild resp depression
106
Etomidate Cerebral effects
decr CBF
decr ICP
decr CMRO2
maintains CPP (perfusion pressure)
increases SSEP amplitude (TOF?)
seizure potential
107
Lidocaine induction uses
reduce propofol burning
blunt airway response to DL
1mg/kg IV
108
Most common analgesic
fentanyl
109
fentanyl properties
fast acting
fat soluble =
crosses plasma membrane
long half life
110
Neuromuscular blocking agents
depolarizing
non-depolarizing
111
Succinylcholine mechanism
depolarizing
attached to ACh receptor causing random fasiculations and eventual paralysis
112
Sux onset/DOA
onset: 45 sec (IV)
duration: 10 min
113
Sux reversal
no reversal needed due to rapid recovery
114
Sux metabolism
plasma psuedocholinesterase
(butyrylcholinesterase)
115
Sux myalgia treatment
can treat w/ROC
(0.06-0.1 mg/kg IV)
116
Sux CV effects
bradycardia
(stimualtes cardiac postgang muscarinic receptors)
117
Sux and MH
triggers MH
118
Sux Contraindication
muscular dystrophy
-- sux can trigger rhabdo
hyperkalemia
--sux can incr [K+] by 0.5
-- burns/trauma
--spinal cord injuries
--sepsis
119
Pseudocholinesterase deficiency
AKA atypical plasma cholinesterase
AKA atypical Butyrylcholinesterase
genetic abnormality in psuedocholinesterase gene
120
Heterozygous atypical
pseudocholinesterase deficiency
20-30min blockade duration
dibucaine #: 40-60
121
Homozygous atypical
pseudocholinesterase deficiency
60min-8hr blockade duration
dibucaine #: 20-30
122
dibucaine number
test for pseudocholinesterase def
measures function not amount
less inhibitory to genetic changes
(homo: lower number)
(hetero: higher number)
(not mutated: highest)
123
Non-Depolarizing NMB categories
benzoisquinolone
steroidal
chlorofumarate
124
benzoisquinolone NMB drugs
cisatracurium
125
steroidal NMB drugs
vecuronium
rocuronium
126
chlorofumarate NMB drugs
gantacurium (experimental)
127
rocuronium onset/duration
onset: 60-90s
duration: 35-75 min
128
roc elimination
mostly biliary
some kidney
- not prolonged by kidney failure
129
vecuronium onset/duration
onset: 2-3 min
duration: 45-90 min
130
vec elimination
mostly biliary (small hepatic)
25% kidney
- mod prolong by kidney failure
131
cisatracurium onset/duration
onset: 2-3 min
duration: 40-75 min
132
cisatracurium elimination
hoffman elimination
- laudanosine metabolite
**use with kidney/liver failure pts
pH/temp sensitive drug
