Exam 3 Flashcards

1
Q

influences of age on the PK of volatiles

A

↓ lean body mass (muscle mas)
↑ fat mass = ↑ Vd for drugs (especially for more fat soluble)- in certain compartments
↓ clearance if pulmonary exchange is impaired
↑ time constraints due to lower cardiac output

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2
Q

Boyle’s Law

A

Given a constant temperature….
Pressure and volume of gas are inversely proportional

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3
Q

Fick’s Diffusion Law

A

Once the molecules get to the alveoli, they move around randomly and begin to diffuse into the pulmonary capillary

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4
Q

Diffusion depends on:

A

Partial pressure gradient of the gas
Solubility of the gas (diffusion)
Thickness of the membrane

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5
Q

Carbon dioxide vs oxygen molecular wt and solubility

A

Carbon dioxide, molecular wt 44 g
Oxygen, molecular wt 32 g

co2 is more soluble

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6
Q

Graham’s Law of Effusion

A

Process by which molecules diffuse through pores and channels without colliding
Smaller molecules effuse faster dependent on solubility (diffusion)

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7
Q

Alveolar pressure an indicator of:

A

Depth of anesthesia
Recovery from anesthesia- if brain is greater than amount to alveoli – waking up / loosing gas from vessel rich group to alveolis.

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8
Q

Solubility

A

A ratio of how the inhaled anesthetic distributes between 2 compartments at equilibrium (when partial pressures are equal)

***the relative capacity of each compartment to hold volatile

temperature dependent

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9
Q

Blood gas partition coefficient for Halothane

A

2.54

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10
Q

Blood gas partition coefficient for Enflurane

A

1.90

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11
Q

Blood gas partition coefficient for isoflurane

A

1.46

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12
Q

Blood gas partition coefficient for nitrous oxide

A

0.46

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13
Q

Blood gas partition coefficient for desflurane

A

0.42

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14
Q

Blood gas partition coefficient for sevo

A

0.69

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15
Q

des color

A

blue

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16
Q

sevo color

A

yellow

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17
Q

iso color

A

purple

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18
Q

halothane color

A

red

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19
Q

MAC: Minimum alveolar concentration:

A

“the concentration at 1 atm that prevents skeletal muscle movement in response to supramaximal, painful stimulation in 50% of patients”

partial pressure/ percentage of volatile anesthetic we will give.

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20
Q

MACawake

A

(0.3-0.5 MAC)

presumes that all we are giving is 1.3 mac when we turn the mac off and we let them wake up when they get to 0.3-0.5 = wake up.

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21
Q

MACBAR

A

(1.7-2.0 MAC)

blunts autonomic responses. If we had 2 mac of des on board w/ no pain and we intubated you, hr wouldnt respond, no sns response at mac bar. But will be very hypotensive. Mac bar = not used.

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22
Q

nitrous mac

A

104%

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23
Q

halothane mac

A

0.75%

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24
Q

mac enflurane

A

1.63%

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25
mac iso
1.17%
26
mac des
6.6%
27
mac values based on
Based on 30-55y/o average; 37 degrees C; 760mmHg pressure (1 ATM)
28
sevo mac
1.8%
29
Factors that alter MAC
Biggest… Body temperature Age…6% per decade MAC peaks at 1 y/o
30
Increases in MAC
Hyperthermia Excess pheomelanin (redhead) production Drug-induced increase in catecholamine levels Hypernatremia
31
Decreases in MAC
Hypothermia Preoperative medication, intraoperative opioids Alpha-2 agonists Acute alcohol ingestion Pregnancy Post partum (early…12-72 hours) Lidocaine PaO2 <38 mm Hg Mean BP < 40mm Hg Cardiopulmonary bypass Hyponatremia
32
No change in MAC
Chronic alcohol abuse Gender Duration of anesthesia PaCO2 15-95 mm Hg PaO2 > 38 mm Hg Blood pressure > 40 mm Hg Hyper/hypokalemia Thyroid gland dysfunction
33
(Spinal) Immobility by
Depress excitatory AMPA and NMDA (glutamate receptors) Enhance inhibitory glycine Act on sodium channels
34
Loss of consciousness by
Inhibitory transmission of GABA Potentiation of glycine activation in brainstem
35
Henry’s Law
”the amount of dissolved gas in a liquid is proportional to its partial pressure above the liquid”
36
Vapor pressure halothane
243 torr
37
vapor pressure enflurane
175 torr
38
iso vapor pressure
238 torr
39
sevo generic name
ultane
40
desflurane generic name
suprane
41
isoflurane generic name
forane
42
Sevo vapor pressure
157 torr
43
des vapor pressure
669 torr
44
Things that affect Anesthetic machine to alveoli- boyls law
Inspired partial pressure Alveolar ventilation- faster = more inhaled gas we take in Anesthetic breathing system (is there a lot of re-breathing?) FRC
45
Things that affect pressure gradient alveoli to blood
Blood: gas partition coefficient- Different for every gas Cardiac output A-v partial pressure difference
46
Things that influence Partial pressure gradient of arterial blood to brain
Brain: blood partition coefficient Cerebral blood flow (depends on CO) a-v partial pressure difference
47
The impact of PI on the rate of rise of PA
The higher the PI (of a volatile) the more rapidly PA approaches PI
48
“Over pressurization”
Way to force extreme contraction gradient on the vaporizer to the patient get asleep in a couple breaths= large increases in inspired pressure. A large increase in PI
49
1 vital capacity breath of high concentration Sevoflurane (7%)
loss of eyelash reflex= ready to intubate
50
Second gas effect
nitrous + VAA High volume of N2O uptake into pulmonary capillary concentrates alveolis = increased VAA partial pressure
51
Nitrous diffuses into
air-filled cavity Up to 10L in the 1st 10-15 minutes Compliant walls Non-compliant walls
52
cases we dont give nitrous to
bowel case, ear or eye cases, pntx
53
if temperature of the blood increase.....
solubility of the drug increases
54
Low blood solubility......
Minimal amounts must be dissolved; PA/Pa is rapid; induction is rapid
55
High blood solubility.....
Large amounts must be dissolved: PA/Pa is slow; induction prolonged
56
When does emergence begin?
When PI is zero (inhaled agent is turned off) Muscle/fat maybe not at equilibrium Muscle/fat continue to take up anesthetic (helps decrease PA and PBr)
57
1.3 mac
the concentration at 1 atm that prevents skeletal muscle movement in response to supramaximal, painful stimulation in 99% of patients
58
Vapor Pressure
Pressure at which vapor, and liquid are at equilibrium
59
Splitting ratio
how big the whole is/ sending to pass through vaporizer Large splitting ration = sending more 0 splitting ration = not dividing at all
60
high flow
FGF exceeds minute ventilation
61
MOA that vaa on relaxing airway smm
Block voltage-gated Ca++ Deplete Ca++ in SR= no bronchodilation Require intact epithelium; inflammatory processes, epithelial damage alters
62
VAA With bronchospasm with R/f and meds
Risk factors: COPD, cough response with ETT, age <10, URI Sevoflurane > Isoflurane at causing bronchodilation Desflurane may worsen especially in smokers due to pungency/irritation
63
Respiratory resistance comparison meds
thiopental and des more than halothane, sevo or iso
64
vaa nm effects
Dose-dependent skeletal muscle relaxation Potentiate depolarizing and non-depolarizing NMBDs nAch receptors at NMJ Enhance glycine (inhibitory nt) at spinal cord Nitrous oxide has no relaxant effect on skeletal muscles
65
VAA on cmro2 and cerebral activity mac to get there mac for burst supp and silence
⬇️ CMRO2 and cerebral activity Begins approx 0.4 MAC as wakefulness changes to unconsciousness 1.5 MAC: burst suppression 2 MAC: electrical silence Isoflurane=sevoflurane=desflurane
66
vaa on cbf, mac necessary. meds that affect and how
Dose dependent ; ⬆️ CBF due decreased cerebral vascular resistance May increase ICP Onset > 0.6 MAC Occurs within minutes despite lack of BP change Isoflurane= Desflurane Sevoflurane less vasodilatory effect Nitrous potent vasodilator (but give < 1MAC) Halothane worst
67
vaa effect on Autoregulation at what mac
Halothane lost by 0.5 MAC Sevo preserves to 1 MAC Iso and Des lost 0.5-1.5 MAC
68
vaa on Respiratory depression mac for apnea
Dose-dependent ↑ rate, ↓ Vt Apnea (1.5-2.0 MAC)
69
Type I: hepatotoxicity
20% of patients 1-2 weeks after exposure Direct toxic effect or free radical effect??? Nausea, lethargy, fever
70
Type II: hepatotoxicity
Less common Immune-mediated response against hepatocytes: eosinophilia, fever Prior exposure High mortality: acute hepatitis, hepatic necrosis 1 month after exposure
71
mivacurium reversal
reverses from plasma cholinesterase
72
Depolarizing action
Mimics the action of acetylcholine
73
Non-depolarizing Action
Interferes with the action of acetylcholine
74
Depolarizing meds
succinylcholine (Anectine)
75
Long acting non depolarizing
Pancuronium (Pavulon)
76
short acting non depolarizing
mivacrium (mivacron)
77
Intermediate acting non depolarizing
Atracurium (Tracrium) Vecuronium (norcuron) Rocuronium (zemuron) Cisatracrium (nimbex)
78
Chemical Classification for pancuronium (pavulon)
Aminosteroid
79
Chemical Classification for atracurium
Benzylisoquinolone
80
Chemical Classification Vecuronium
Aminosteroid
81
Chemical Classification rocuronium
aminosteroid
82
Chemical Classification cisatracurium
Benzylisoquinoline
83
Chemical Classification mivacruium
Benzylisoquinoline
84
ED95 for NMBD
Equal Potency: dose necessary to produced 95% suppression of single twitch In the presence of nitrous/barbiturate/opioid anesthesia-----GA.
85
Adductor pollicis muscle-
palm nerve that causes the thumb to adduct
86
NMB block depends on....
# of postsynaptic Ach receptors number of presynaptic Ach containing vesicles released # of postsynaptic Ach receptors. Fewer R than what we have ach released? Blood flow to area Drug potency
87
Orbicularis oculi reflects
facial nerve stimulation More closely reflects diaphragm and laryngeal muscle blockade Underestimate residual paralysis
88
Adductor pollicis indicates
Poor indictor of laryngeal relaxation Good indicator of peripheral recovery. Look for extubation Gold standard for recovery
89
Distal electrode
black
90
proximal electrode
red
91
Ulnar nerve side of arm
pinky side, closer to midline
92
Defasciculating dose
give 20% of normal intubating dose early / primer/ small dose as primer prior to intubating dose, pt still somewhat awake but they are still somewhat awake and if you give defasciculating dose = still have side effects ; blurred vision, feeling weak/ can’t take a deep breath tell them; will get sleepy, blurry eye, droopy eyeballs, encourage them to close their eyes. helps keeping them from being anxious.
93
Patient symptoms to nmb
Loss of visual focus Mandibular muscle weakness Ptosis Diplopia Dysphagia Increased hearing acuity; encourage quiet environment.
94
Single twitch and use
Usually 1 Hz/second decreasing to 0.1 Hz q 10 seconds Continuously/ gtt Onset of block = fade with each stimulus
95
Double Burst
3 short bursts followed by 3 short bursts; pause in between Use 50 Hz (supramaximal current)- more strength/ power Developed to improve detection of residual block Fade in 2nd response vs 1st Qualitatively better than TO4
96
Train of Four (TOF)
4 stimuli at 2 Hz in ½ second Reflects events at presynaptic membrane
97
TOF Ratio Prior to NMBD:
4/4 twitches…TOFR 1
98
TOF Ratio After administration
return of 4 twitches Amplitude of 4th twitch to 1st twitch If amplitude of 4th 50% of 1st…. TOFR 0.5 Experienced anesthetists’ unable to detect fade TOFR > 0.4 (40%)
99
Tetanic stimulation
Very rapid, 50 Hz for 5 seconds
100
Tetanic stimulation depolarizing block
Sustained muscle response
101
Tetanic stimulation non-depolarizing block
Non-sustained response; fade Phase II block with Succs
102
Fade with tetanic stimulation related to
Presynaptic depletion of Ach or inhibition of release Frequency and length of stimulation
103
Post-tetanic stimulation
Single twitch 3 seconds after tetanic stimulation Occurs d/t accumulation of calcium during “tetany” Excess calcium stimulates Ach release
104
no response to Post-tetanic stimulation
= intense blockade Block is really strong and wont be unparalyzed.
105
stimulation for reversing someone
TOF -> tetany and post tetanic stimulation. Earlier response = more spontaneous reversal we have.
106
twitches are what type of measurement
qualitative not quantitative
107
What breaks down succ
butyrylcholinesterase (plasma cholinesterase)
108
Purpose of Ache
hydrolysis of Ach breaks down to acetic acid and choline
109
resting membrane potential for post synaptic cleft of nmj
-90 mv Maintained by sodium/potassium nAChRs directly opposite
110
Pentameric unit of nachr
2-alphas, beta, delta, gamma Transmembrane pore
111
If Ach binds to nachr subunit
Conformational change Pores open, sodium/calcium/potassium flow
112
If NMBD binds to nachr subunit
No conformational change No ion flow Probability of binding d/t concentration of NMBD vs Ach
113
sch on nachr
*Sch only requires binding at 1 alpha subunit Other alpha either Sch or Ach Channel remains open longer Can leave 1 receptor and attach to other nAChRs till hydrolyzed….fasiculations
114
Dose of sch
1 mg/kg IV
115
Onset of sch
30-60 seconds; don’t ventilate after giving
116
Duration of action of sch
3-5 min
117
Hydrolysis of sch
Hydrolysis is slower than Ach Sustained opening of receptor ion channels Leakage of potassium ions = 0.5 mEq/liter serum increase Dialysis patients? Safe if dialyzed recent. Check K+ before giving
118
Depolarization called
phase 1 block
119
Phase I block characteristics
⬇️ contraction height to single twitch stimulation ⬇️ amplitude to continuous stimulation TOF ratio > 0.7; don’t have a fade and no change from first to last twitch Absence of post-tetanic facilitation; same amplitude Skeletal muscle fasciculations
120
Phase II block typical
Responses typical of non-depolarizing NMBD Can be antagonized by anti-cholinesterase drug
121
other causes of phase 2 block
SCh dose 2-4 mg/kg Lack of/poorly functioning pseudocholinesterase Relative “overdose”….phase 1 transition to phase 2 characteristics ; desensitization
122
butyrylcholinesterase
Synthesized in liver Terminated by diffusion out of NMJ into plasma Succinylmonocholine (less potent) and choline
123
Pseudocholinesterase activity affected by....
-Decreased hepatic production (⬇️ 75% before apparent) -Drug-induced decreases (Neostigmine, Reglan, chemo, insectides) -Genetically atypical; less quality of functioning pseudocholinesterase. -Chronic diseases (renal): ↓ activity (quality of function) -Pregnancy (high estrogen levels): ↓activity -Obese: ↑ activity of plasma cholinesterase. If giving in real life; give sux then based on actual body wt not ideal body wt because obesity increase hydrolysis ability. Get rid of sux faster.
124
Dibucaine-related variant
Get Dibucaine level Reflects quality not quantity of enzyme 20: SCh 1mg/kg lasts 3 hours
125
Dibucaine
-Amide local anesthetic -Inhibits breakdown of butyrylcholinesterase -% inhibition = dibucaine number
126
normal dibucaine level
80 or above = normal breakdown
127
Side effects of SCh
Cardiac dysrhythmias (SB, JR, Sinus arrest) Hyperkalemia Myalgia Myoglobinuria Masseter spasm ⬆️ intragastric pressure ⬆️ intraocular pressure ⬆️ intracranial pressure Pretreatment with non-depolarizing NMBD
128
Myoglobinuria from sch
Damage to skeletal muscles Especially pediatrics Usually found later to have MH or muscular dystrophy Deuchenees. No sux to peds
129
Actions at cardiac muscarinic, cholinergic receptors with sch
Mimics action of ACh Most likely on 2nd dose, 5 minutes post 1st Due to metabolites: succinylmonocholine and choline
130
Sch Actions at ANS ganglia
⬆️ Heart rate and blood pressure Mimics action of Ach Usually occurs with large doses
131
Hyperkalemia occurs in....
Patients with extrajunctional sites Unrecognized muscular dystrophy (Duchenne’s) Unhealed 3rd degree burns Denervation of skeletal muscles (atrophy) Skeletal muscle trauma Upper motor neuron lesions
132
Myalgia with sch
Young adults Neck, back, abdomen Phayngitis Confused with pharyngitis d/t intubation Muscle aches from muscle twitching
133
Intraocular pressure from sch
Maximum increase 2-4 minutes after administration -Lasts 5-10 minutes -MOA unknown -Contraction of EOM and globe distortion -Resistance to outflow of aqueous humor and dilation of vessels sch Contraindicated in open anterior chamber injury Efficacy of pre-curarization controversial
134
Intracranial pressure with sch
In patients with intracranial tumors or CHI Not consistently observed in studies Attenuated by hyperventilation prior to SCh Co2 decreases = cerebral blood flow decreases/constrict= decrease ICP RSI not ventilated
135
Sustained skeletal muscle contraction with sch
Incomplete jaw relaxation/masseter muscle spasm Muscles contract and don’t relax Spasm = cant intubate-> wait for sux to wear off Inadequate dosage given (children) Early indicator of Malignant Hyperthermia
136
Malignant hyperthermia signs
Muscle destruction Hyperkalemia Acidosis Dysrhythmia Renal failure DIC Hereditary rhabdomyolysis associated with anesthetics
137
Triggers for MH
ALL volatile anesthetics Succinylcholine
138
MOA of MH
Mutations in skeletal muscle calcium release Ryanodine receptor (RyR1) Ca release of SR 50-70% of MH patients Native Americans Skeletal muscle caffeine contracture testing Muscle biopsy
139
Symptoms of MH
Acute increased skeletal muscle metabolism Increased oxygen consumption Lactate formation Heat production Rhabdomyolysis ↑ ETCO2 ↑ temp 1 degree C/5 minutes Arrhythmias Skeletal muscle rigidity
140
Treatment of MH
Agent; stop triggering agent, adnimister non triggering anesthetics, ask for help, ask for MH cart Breathing- hyperventilate w/ 100% oxygen C= cooling if pt is >102.2 D=dantrolene, continous Rapid IV push
141
Dantrolene dose
2mg/kg IV Repeat doses until symptoms subside or 10mg/kg IV
142
Dantrolene moa
Inhibits calcium release into SR By affecting the ryanodine receptor
143
Dantrolene metabolization
Metabolized in liver 5-hydroxydantrolene Muscle relaxant properties 50% c/o weakness…grip strength careful with; Verapamil, Cardizem->Cardiovascular collapse
144
Dantrolene side effects
Most common Weakness Phlebitis Respiratory failure Gastrointestinal upset Less common Confusion Dizziness Drowsiness
145
Myasthenia Gravis
Autoimmune disease Antibodies against Ach receptor ↓ Ach receptors Increasing weakness/fatigue Diplopia Ptosis Extremity and respiratory muscle weakness Tx with cholinesterase inhibitors
146
Care for MG
Resistant to Sch… 1.5-2.0 mg/kg fewer receptors….ED95 2.5 times higher pt should go first case
147
Lambert-Eton
Autoimmune disease Small-cell lung cancer Antibodies against calcium channels Decreases release of Ach pre-junctionally Increased sensitivity Depolarizers Non-depolarizers give less; 20% of normal dose.
148
“autonomic margin of safety”
Difference between dose that produces blockade (ED95) and dose that creates circulatory effects Same dose for pancuronium Very different dose for vec, roc, cis
149
Volatiles that cause dose dependent enhancement of NMBD
Desflurane>Sevoflurane>Isoflurane Onset as early as 30 minutes
150
loop Diuretics Corticosteroids Metocloproide LAs w/ nmd
Enhances or prolong blockade; ↑ acetylcholine release Depression of cholinesterase activity Depression of nerve conduction
151
Magnesium on non depol and sch and moa
Enhances blockade MOA (for non-depolarizers); Decreases prejunctional release of Ach Decreases sensitivity to postjunctional membranes
152
Ephedrine prior to non-depolarizers
Decreases onset time d/t⬆️ CO and skeletal muscle flow
153
Esmolol prior to induction
Delays onset
154
Hypothermia on ndmb and moa
Even mild hypothermia Vecuronium, Pancuronium (doubles the duration) MOA; Temperature slowing of hepatic enzyme activity
155
Atracurium/Cisatracurium metabolism
MOA: temperature and ph dependent elimination processes Hoffman elimination Ester hydrolysis
156
Burns on ndmb and moa
Resistance Begins approx. 10 days post injury Declines after 60 days 30% BSA or > May be offset by using 1.2 mg/kg dose of Rocuronium-- use more ? MOA??? Altered affinity of nAChRs? Not related to altered density (# of receptors)
157
Stroke of ndmb and moa
paretic arm; Resistance compared to unaffected side Unaffected side; Resistance compared to normal patients MOA; Proliferation of extrajunctional nAChRs
158
Allergic reactions
Succinylcholine more likely Pavulon, Vecuronium, Rocuronium < Succinylcholine Cisatracurium least likely cross-sensitivity with quaternary ammonia
159
Gender effect on ndmb
Women more sensitive Need 22% less (vecuronium)- less muscle Need 30% less (rocuronium) duration of block greater in women
160
Intubating Dose for Pancuronium (Pavulon)
0.1 mg/kg
161
Onset for pancuronium
3-5 min
162
duration of pavulon
60-90 minutes
163
Metabolism of pavulon
80% eliminated unchanged in urine
164
renal failure with pavulon
30-50% decreased plasma clearance 10-40% deasacetylpancuronium metabolite ½ as active (by liver)
165
liver disease with pavulon
Increased VD Larger initial dose is needed Prolonged elimination ½ time
166
Pavulon cv effects
↑ HR, MAP, CO d/t vagal blockade Mostly at SA node BP increase d/t HR d/t SNS activation Release of NE presynaptically Blockade of NE reuptake
167
Compared with Long Acting NMBDs intermediate acting.....
Similar onset of maximum blockade (except high dose roc) Approximately 1/3 duration of action Minimal/absent cardiovascular effects Antagonized by anticholinesterase drugs approx 20 min.
168
Vecuronium (Norcuron) dose onset duration
Intubating Dose: 0.1 mg/kg Onset: 3-5 minutes Duration: 20-35 minutes
169
Vec metabolism
Hepatic metabolism Principle organ of elimination 3-desacetylvecuronium 50-80% as potent (but rapidly converted to metabolite with 1/10 the effects) Renal excretion Approx 30% appears unchanged (*70% metabolized in liver) Renal dysfunction Elimination ½ time prolonged
170
the cumulative effect of vec
Repeated doses or infusion: cumulative effects
171
vec metabolism for OB
Increased clearance in 3rd trimester (progesterone) Prolonged duration early postpartum (give IBW)
172
Vec on elderly
Decreased volume of distribution (less muscle mass) Decreased plasma clearance (less hepatic flow) Single dose mechanics unchanged Delayed recovery with infusions
173
Respiratory acidosis Following NMBD
prolongs blockade Activity inversely proportional to bound drug…acidosis decreases the bound amount Change in ionization at receptor increases attachment time Concern postop with hypoventilation
174
Rocuronium (Zemuron) dose onset duration
intubation: 0.6 mg/kg or RSI; 1.2 mg/kg (parrallel onset of sch) Onset: 3-5 minutes; 1-2 minutes (with sux) Duration: 20-35 minutes
175
Metabolism for roc
Excreted unchanged in bile Longer duration of action in liver failure and elderly d/t decreased clearance and an increased Vd 10-30% renal excretion Only marginally affected in renal failure
176
Cisatracurium (Nimbex), dose, onset, duration
Intubating Dose: 0.1 mg/kg Onset: 3-5 minutes Duration of action 20-35 minutes
177
Metabolism of nimbex
Recovery from infusion NOT affected by time Degradation Hoffman elimination (ph and temperature dependent) Doesn’t use non-specific plasma cholinesterases as much as Atracurium
178
nimbex in obese
Duration of action prolonged IF dosed at actual body weight d/t Vd
179
Mivacurium (Mivacron) dose onset duration
Intubating Dose: 0.15 mg/kg Onset: 2-3 minutes Conditions less desirable Duration of action: 12-20 minutes
180
nimbex metabolism
Cleared by plasma cholinesterase
181
nimbex histamine release
> 3 x ED95… transient MAP drop More common with rapid, large doses MAP drop more in HTN pts than non-HTN pts
182
Dose succ based on....
actual body wt
183
resistance
harder to block / need more to get effect