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Pharm Semester 2 > Exam 3 > Flashcards

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
Q

mac iso

A

1.17%

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26
Q

mac des

A

6.6%

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27
Q

mac values based on

A

Based on 30-55y/o average; 37 degrees C; 760mmHg pressure (1 ATM)

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28
Q

sevo mac

A

1.8%

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29
Q

Factors that alter MAC

A

Biggest…
Body temperature
Age…6% per decade
MAC peaks at 1 y/o

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30
Q

Increases in MAC

A

Hyperthermia

Excess pheomelanin (redhead) production

Drug-induced increase in catecholamine levels

Hypernatremia

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31
Q

Decreases in MAC

A

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

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32
Q

No change in MAC

A

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

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33
Q

(Spinal) Immobility by

A

Depress excitatory AMPA and NMDA (glutamate receptors)

Enhance inhibitory glycine

Act on sodium channels

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34
Q

Loss of consciousness by

A

Inhibitory transmission of GABA
Potentiation of glycine activation in brainstem

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35
Q

Henry’s Law

A

”the amount of dissolved gas in a liquid is proportional to its partial pressure above the liquid”

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36
Q

Vapor pressure halothane

A

243 torr

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37
Q

vapor pressure enflurane

A

175 torr

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38
Q

iso vapor pressure

A

238 torr

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39
Q

sevo generic name

A

ultane

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40
Q

desflurane generic name

A

suprane

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41
Q

isoflurane generic name

A

forane

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42
Q

Sevo vapor pressure

A

157 torr

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43
Q

des vapor pressure

A

669 torr

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44
Q

Things that affect Anesthetic machine to alveoli- boyls law

A

Inspired partial pressure
Alveolar ventilation- faster = more inhaled gas we take in
Anesthetic breathing system (is there a lot of re-breathing?)
FRC

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45
Q

Things that affect pressure gradient alveoli to blood

A

Blood: gas partition coefficient- Different for every gas
Cardiac output
A-v partial pressure difference

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46
Q

Things that influence Partial pressure gradient of arterial blood to brain

A

Brain: blood partition coefficient
Cerebral blood flow (depends on CO)
a-v partial pressure difference

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47
Q

The impact of PI on the rate of rise of PA

A

The higher the PI (of a volatile) the more rapidly PA approaches PI

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48
Q

“Over pressurization”

A

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

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49
Q

1 vital capacity breath of high concentration Sevoflurane (7%)

A

loss of eyelash reflex= ready to intubate

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50
Q

Second gas effect

A

nitrous + VAA

High volume of N2O uptake into pulmonary capillary concentrates alveolis = increased VAA partial pressure

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51
Q

Nitrous diffuses into

A

air-filled cavity
Up to 10L in the 1st 10-15 minutes
Compliant walls
Non-compliant walls

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52
Q

cases we dont give nitrous to

A

bowel case, ear or eye cases, pntx

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53
Q

if temperature of the blood increase…..

A

solubility of the drug increases

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54
Q

Low blood solubility……

A

Minimal amounts must be dissolved; PA/Pa is rapid; induction is rapid

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55
Q

High blood solubility…..

A

Large amounts must be dissolved: PA/Pa is slow; induction prolonged

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56
Q

When does emergence begin?

A

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)

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57
Q

1.3 mac

A

the concentration at 1 atm that prevents skeletal muscle movement in response to supramaximal, painful stimulation in 99% of patients

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58
Q

Vapor Pressure

A

Pressure at which vapor, and liquid are at equilibrium

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59
Q

Splitting ratio

A

how big the whole is/ sending to pass through vaporizer

Large splitting ration = sending more
0 splitting ration = not dividing at all

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60
Q

high flow

A

FGF exceeds minute ventilation

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61
Q

MOA that vaa on relaxing airway smm

A

Block voltage-gated Ca++

Deplete Ca++ in SR= no bronchodilation

Require intact epithelium; inflammatory processes, epithelial damage alters

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62
Q

VAA With bronchospasm with R/f and meds

A

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

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63
Q

Respiratory resistance comparison meds

A

thiopental and des more than halothane, sevo or iso

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64
Q

vaa nm effects

A

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

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65
Q

VAA on cmro2 and cerebral activity
mac to get there
mac for burst supp and silence

A

⬇️ 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

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66
Q

vaa on cbf, mac necessary. meds that affect and how

A

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

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67
Q

vaa effect on Autoregulation at what mac

A

Halothane lost by 0.5 MAC

Sevo preserves to 1 MAC

Iso and Des lost 0.5-1.5 MAC

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68
Q

vaa on Respiratory depression mac for apnea

A

Dose-dependent ↑ rate, ↓ Vt
Apnea (1.5-2.0 MAC)

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69
Q

Type I: hepatotoxicity

A

20% of patients
1-2 weeks after exposure
Direct toxic effect or free radical effect???
Nausea, lethargy, fever

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70
Q

Type II: hepatotoxicity

A

Less common
Immune-mediated response against hepatocytes: eosinophilia, fever
Prior exposure
High mortality: acute hepatitis, hepatic necrosis
1 month after exposure

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71
Q

mivacurium reversal

A

reverses from plasma cholinesterase

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72
Q

Depolarizing action

A

Mimics the action of acetylcholine

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73
Q

Non-depolarizing Action

A

Interferes with the action of acetylcholine

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74
Q

Depolarizing meds

A

succinylcholine (Anectine)

75
Q

Long acting non depolarizing

A

Pancuronium (Pavulon)

76
Q

short acting non depolarizing

A

mivacrium (mivacron)

77
Q

Intermediate acting non depolarizing

A

Atracurium (Tracrium)
Vecuronium (norcuron)
Rocuronium (zemuron)
Cisatracrium (nimbex)

78
Q

Chemical Classification for pancuronium (pavulon)

A

Aminosteroid

79
Q

Chemical Classification for atracurium

A

Benzylisoquinolone

80
Q

Chemical Classification Vecuronium

A

Aminosteroid

81
Q

Chemical Classification rocuronium

A

aminosteroid

82
Q

Chemical Classification
cisatracurium

A

Benzylisoquinoline

83
Q

Chemical Classification
mivacruium

A

Benzylisoquinoline

84
Q

ED95 for NMBD

A

Equal Potency: dose necessary to produced 95% suppression of single twitch

In the presence of nitrous/barbiturate/opioid anesthesia—–GA.

85
Q

Adductor pollicis muscle-

A

palm nerve that causes the thumb to adduct

86
Q

NMB block depends on….

A

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
Q

Orbicularis oculi reflects

A

facial nerve stimulation

More closely reflects diaphragm and laryngeal muscle blockade

Underestimate residual paralysis

88
Q

Adductor pollicis indicates

A

Poor indictor of laryngeal relaxation
Good indicator of peripheral recovery.
Look for extubation
Gold standard for recovery

89
Q

Distal electrode

A

black

90
Q

proximal electrode

A

red

91
Q

Ulnar nerve side of arm

A

pinky side, closer to midline

92
Q

Defasciculating dose

A

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
Q

Patient symptoms to nmb

A

Loss of visual focus
Mandibular muscle weakness
Ptosis
Diplopia
Dysphagia
Increased hearing acuity; encourage quiet environment.

94
Q

Single twitch and use

A

Usually 1 Hz/second decreasing to 0.1 Hz q 10 seconds

Continuously/ gtt
Onset of block = fade with each stimulus

95
Q

Double Burst

A

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
Q

Train of Four (TOF)

A

4 stimuli at 2 Hz in ½ second
Reflects events at presynaptic membrane

97
Q

TOF Ratio
Prior to NMBD:

A

4/4 twitches…TOFR 1

98
Q

TOF Ratio
After administration

A

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
Q

Tetanic stimulation

A

Very rapid, 50 Hz for 5 seconds

100
Q

Tetanic stimulation depolarizing block

A

Sustained muscle response

101
Q

Tetanic stimulation non-depolarizing block

A

Non-sustained response; fade

Phase II block with Succs

102
Q

Fade with tetanic stimulation related to

A

Presynaptic depletion of Ach or inhibition of release
Frequency and length of stimulation

103
Q

Post-tetanicstimulation

A

Single twitch 3 seconds after tetanic stimulation

Occurs d/t accumulation of calcium during “tetany”
Excess calcium stimulates Ach release

104
Q

no response to Post-tetanicstimulation

A

= intense blockade
Block is really strong and wont be unparalyzed.

105
Q

stimulation for reversing someone

A

TOF -> tetany and post tetanic stimulation.

Earlier response = more spontaneous reversal we have.

106
Q

twitches are what type of measurement

A

qualitative not quantitative

107
Q

What breaks down succ

A

butyrylcholinesterase (plasma cholinesterase)

108
Q

Purpose of Ache

A

hydrolysis of Ach

breaks down to acetic acid and choline

109
Q

resting membrane potential for post synaptic cleft of nmj

A

-90 mv

Maintained by sodium/potassium
nAChRs directly opposite

110
Q

Pentameric unit of nachr

A

2-alphas, beta, delta, gamma
Transmembrane pore

111
Q

If Ach binds to nachr subunit

A

Conformational change
Pores open, sodium/calcium/potassium flow

112
Q

If NMBD binds to nachr subunit

A

No conformational change
No ion flow
Probability of binding d/t concentration of NMBD vs Ach

113
Q

sch on nachr

A

*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
Q

Dose of sch

A

1 mg/kg IV

115
Q

Onset of sch

A

30-60 seconds; don’t ventilate after giving

116
Q

Duration of action of sch

A

3-5 min

117
Q

Hydrolysis of sch

A

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
Q

Depolarization called

A

phase 1 block

119
Q

Phase I block characteristics

A

⬇️ 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
Q

Phase II block typical

A

Responses typical of non-depolarizing NMBD

Can be antagonized by anti-cholinesterase drug

121
Q

other causes of phase 2 block

A

SCh dose 2-4 mg/kg
Lack of/poorly functioning pseudocholinesterase
Relative “overdose”….phase 1 transition to phase 2 characteristics ; desensitization

122
Q

butyrylcholinesterase

A

Synthesized in liver
Terminated by diffusion out of NMJ into plasma
Succinylmonocholine (less potent) and choline

123
Q

Pseudocholinesterase activity affected by….

A

-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
Q

Dibucaine-related variant

A

Get Dibucaine level
Reflects quality not quantity of enzyme
20: SCh 1mg/kg lasts 3 hours

125
Q

Dibucaine

A

-Amide local anesthetic
-Inhibits breakdown of butyrylcholinesterase
-% inhibition = dibucaine number

126
Q

normal dibucaine level

A

80 or above = normal breakdown

127
Q

Side effects of SCh

A

Cardiac dysrhythmias (SB, JR, Sinus arrest)
Hyperkalemia
Myalgia
Myoglobinuria
Masseter spasm
⬆️ intragastric pressure
⬆️ intraocular pressure
⬆️ intracranial pressure
Pretreatment with non-depolarizing NMBD

128
Q

Myoglobinuria from sch

A

Damage to skeletal muscles
Especially pediatrics

Usually found later to have MH or muscular dystrophy
Deuchenees.
No sux to peds

129
Q

Actions at cardiac muscarinic, cholinergic receptors
with sch

A

Mimics action of ACh
Most likely on 2nd dose, 5 minutes post 1st
Due to metabolites: succinylmonocholine and choline

130
Q

Sch Actions at ANS ganglia

A

⬆️ Heart rate and blood pressure
Mimics action of Ach
Usually occurs with large doses

131
Q

Hyperkalemia occurs in….

A

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
Q

Myalgia with sch

A

Young adults

Neck, back, abdomen
Phayngitis

Confused with pharyngitis d/t intubation

Muscle aches from muscle twitching

133
Q

Intraocular pressure from sch

A

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
Q

Intracranial pressure with sch

A

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
Q

Sustained skeletal muscle contraction with sch

A

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
Q

Malignant hyperthermia signs

A

Muscle destruction
Hyperkalemia
Acidosis
Dysrhythmia
Renal failure
DIC

Hereditary rhabdomyolysis associated with anesthetics

137
Q

Triggers for MH

A

ALL volatile anesthetics
Succinylcholine

138
Q

MOA of MH

A

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
Q

Symptoms of MH

A

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
Q

Treatment of MH

A

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
Q

Dantrolene dose

A

2mg/kg IV
Repeat doses until symptoms subside or 10mg/kg IV

142
Q

Dantrolene moa

A

Inhibits calcium release into SR
By affecting the ryanodine receptor

143
Q

Dantrolene metabolization

A

Metabolized in liver
5-hydroxydantrolene
Muscle relaxant properties
50% c/o weakness…grip strength
careful with; Verapamil, Cardizem->Cardiovascular collapse

144
Q

Dantrolene side effects

A

Most common
Weakness
Phlebitis
Respiratory failure
Gastrointestinal upset

Less common
Confusion
Dizziness
Drowsiness

145
Q

Myasthenia Gravis

A

Autoimmune disease
Antibodies against Ach receptor
↓ Ach receptors
Increasing weakness/fatigue
Diplopia
Ptosis
Extremity and respiratory muscle weakness
Tx with cholinesterase inhibitors

146
Q

Care for MG

A

Resistant to Sch… 1.5-2.0 mg/kg
fewer receptors….ED95 2.5 times higher

pt should go first case

147
Q

Lambert-Eton

A

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
Q

“autonomic margin of safety”

A

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
Q

Volatiles that cause dose dependent enhancement of NMBD

A

Desflurane>Sevoflurane>Isoflurane
Onset as early as 30 minutes

150
Q

loop DiureticsCorticosteroidsMetocloproideLAs
w/ nmd

A

Enhances or prolong blockade;
↑ acetylcholine release
Depression of cholinesterase activity
Depression of nerve conduction

151
Q

Magnesium on non depol and sch and moa

A

Enhances blockade

MOA (for non-depolarizers);
Decreases prejunctional release of Ach
Decreases sensitivity to postjunctional membranes

152
Q

Ephedrine prior to non-depolarizers

A

Decreases onset time d/t⬆️ CO and skeletal muscle flow

153
Q

Esmolol prior to induction

A

Delays onset

154
Q

Hypothermia on ndmb and moa

A

Even mild hypothermia
Vecuronium, Pancuronium (doubles the duration)

MOA; Temperature slowing of hepatic enzyme activity

155
Q

Atracurium/Cisatracurium metabolism

A

MOA: temperature and ph dependent elimination processes
Hoffman elimination
Ester hydrolysis

156
Q

Burns on ndmb and moa

A

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
Q

Stroke of ndmb and moa

A

paretic arm; Resistance compared to unaffected side

Unaffected side; Resistance compared to normal patients

MOA; Proliferation of extrajunctional nAChRs

158
Q

Allergic reactions

A

Succinylcholine more likely
Pavulon, Vecuronium, Rocuronium < Succinylcholine
Cisatracurium least likely

cross-sensitivity with quaternary ammonia

159
Q

Gender effect on ndmb

A

Women more sensitive
Need 22% less (vecuronium)- less muscle
Need 30% less (rocuronium)

duration of block greater in women

160
Q

Intubating Dose for Pancuronium(Pavulon)

A

0.1 mg/kg

161
Q

Onset for pancuronium

A

3-5 min

162
Q

duration of pavulon

A

60-90 minutes

163
Q

Metabolism of pavulon

A

80% eliminated unchanged in urine

164
Q

renal failure with pavulon

A

30-50% decreased plasma clearance
10-40% deasacetylpancuronium metabolite ½ as active (by liver)

165
Q

liver disease with pavulon

A

Increased VD
Larger initial dose is needed
Prolonged elimination ½ time

166
Q

Pavulon cv effects

A

↑ 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
Q

Compared with Long Acting NMBDs intermediate acting…..

A

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
Q

Vecuronium(Norcuron) dose onset duration

A

Intubating Dose: 0.1 mg/kg

Onset: 3-5 minutes

Duration: 20-35 minutes

169
Q

Vec metabolism

A

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
Q

the cumulative effect of vec

A

Repeated doses or infusion: cumulative effects

171
Q

vec metabolism for OB

A

Increased clearance in 3rd trimester (progesterone)
Prolonged duration early postpartum (give IBW)

172
Q

Vec on elderly

A

Decreased volume of distribution (less muscle mass)
Decreased plasma clearance (less hepatic flow)
Single dose mechanics unchanged
Delayed recovery with infusions

173
Q

Respiratory acidosis
Following NMBD

A

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
Q

Rocuronium(Zemuron) dose onset duration

A

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
Q

Metabolism for roc

A

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
Q

Cisatracurium(Nimbex), dose, onset, duration

A

Intubating Dose: 0.1 mg/kg

Onset: 3-5 minutes

Duration of action 20-35 minutes

177
Q

Metabolism of nimbex

A

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
Q

nimbex in obese

A

Duration of action prolonged IF dosed at actual body weight
d/t Vd

179
Q

Mivacurium(Mivacron) dose onset duration

A

Intubating Dose: 0.15 mg/kg

Onset: 2-3 minutes
Conditions less desirable

Duration of action: 12-20 minutes

180
Q

nimbex metabolism

A

Cleared by plasma cholinesterase

181
Q

nimbex histamine release

A

> 3 x ED95… transient MAP drop
More common with rapid, large doses
MAP drop more in HTN pts than non-HTN pts

182
Q

Dose succ based on….

A

actual body wt

183
Q

resistance

A

harder to block / need more to get effect

Pharm Semester 2 (6 decks)

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