Exam 3 Kane Flashcards
(311 cards)
1
Q
What does Boyle’s Law state?
A
Given a constant temperature, pressure and volume of gas are inversely proportional
2
Q
What does Fick’s Diffusion Law state?
A
Once gas molecules get to the alveoli, they move around randomly and begin to diffuse into the pulmonary capillary
3
Q
What are the 3 things that diffusion depends on?
A
- Partial pressure gradient of the gas (higher the better)
- Solubility of the gase
- Thickness of the memberane (thicker is slower)
4
Q
What does Graham’s Law of Effusion state?
A
Smaller molecules effuse faster, but are dependent on solubility
5
Q
What about anesthetics control the way we go to sleep and wake up?
A
Partial pressure gradients of the gases
6
Q
4 Factors affecting gas movement from the anesthetic machine to alveoli
A
- Inspired partial pressure (higher = faster)
- Alevolar ventilation (faster = more uptake)
- Anesthetic breathing system (effects fresh gas)
- FRC
7
Q
3 Factors affecting gas movement from the alveoli to blood
A
- Blood gas partition coefficient
- Cardiac output
- A-v partial pressure difference (alveolar:venous)
8
Q
3 factors affecting gas movement from arterial blood to the brain
A
- Brain:Blood partition coefficient
- Cerebral blood flow
- a-v partial pressure difference (arterial-venous)
9
Q
What is blood:gas partition coefficient?
A
The ratio of how much drug is in one compartment to another until gas movement ceases
10
Q
What are the 4 things that effect Pharmacokinetics
A
- Reduced lean body mass
- Increased fat
- Increase volume of distrubtion, especially if more fat soluble
- Reduced hepatic function
11
Q
4 things described by pharmacokinetics
A
- Uptake from alveoli into pulmonary capillary blood
- Distribution
- Metabolism
- Elimination via lungs
12
Q
What is the age range for medium dose MAC?
A
30-50’s
13
Q
What are the 3 things that alveolar pressure is an indicator of
A
- Depth of anesthesia
- Recovery from anesthesia (amount of drug in brain is reduced and alveolar content is increased)
- Potency (MAC)
14
Q
When administering volatile anesthetics, what occurs when the brain gradient is less than the lungs?
A
We will see more uptake of the anesthetic in the brain
15
Q
What does a higher PI (of a volatile) cause?
A
More rapid approach of PA to PI and more rapid induction of the patient
16
Q
What is the basis of concentration effect when adminsitering volatile anesthetics?
A
The more concentrated the drug, the faster the induction
17
Q
Describe the second gas effect with a high volume gas such as N2O
A
- High volume of N2O uptake into pulmonary capillary
- Increases concentration of 2nd gas
- Increased uptake of 2nd gas due to gradient
18
Q
Describe solubility in regards to volatile anesthetics
A
A ratio of how the inhaled anesthetic distributes between 2 compartments at equilibrium
or
the relative capacity of each compartment to hold volatile
19
Q
What is solubility dependent on?
A
Temperature, if temp increases, solubility decreases
20
Q
Describe PA/Pa when blood solubility of a volatile anesthetic is low
A
Minimal amounts must be dissolved, equilibrium is rapid, induction is rapid
21
Q
Describe PA/Pa when blood solubility of a volatile anesthetic is high
A
Large amounts must be dissolved, equilibrium is slow, induction is prolonged
22
Q
When is nitrous oxide contraindicated?
A
Bowel sx, pneumothorax, and intraocular or inner ear sx
23
Q
Where does nitrous diffuse into?
A
Air-filled cavities, up to 10L in the first 10 to 15 minutes
24
Q
When would you see retinal artery damage and vision loss when using nitrouc for Intraocular s/p retinal repair?
A
1 hour of nitrous infusion
25
What does emergence depend on?
Partial pressure of the gas in the brain
26
What are the 4 things that effect emergence when using volatile anesthetics?
1. Length of anesthetic
2. When PI = 0 (gas is turned off)
3. Muscle/fat maybe not at equilibrium
4. Muscle/fat continue to take up anesthetic (helps PA)
27
List the inhaled anesthetics in order from most soluble to least
Halothane = isoflurane \> sevoflurane \> desflurane
28
What dose 1 Mac describe
The concetration at 1 atm that prevents skeletal muscle movement in repsonse to supramaximal (surgical), painful stimulus in 50% of patients
29
What is immobility d/t MAC mediated by?
The spinal cord
30
Describe 1.3 MAC
98% of people will not move
31
Describe MACawake
0.3-0.5 MAC, this helps predict when a patient will wake up
32
Describe MACBAR
1.7-2.0 MAC, this descibes blunting of autonomic reflexes such as increased heart rate and blood pressure
33
Give the numbers for the partition coeffecients of blood:gas, brain:blood, and fat:blood of isoflurane
1. blood:gas = 1.46
2. brain:blood = 1.6
3. fat:blood = 44.9
34
Give the numbers for the partition coeffecients of blood:gas, brain:blood, and fat:blood of nitrous oxide
1. blood:gas = 0.46
2. brain:blood = 1.1
3. fat:blood = 2.3
35
Give the numbers for the partition coeffecients of blood:gas, brain:blood, and fat:blood of desflurane
1. blood:gas = 0.42
2. brain:blood = 1.3
3. fat:blood = 27.2
36
Give the numbers for the partition coeffecients of blood:gas, brain:blood, and fat:blood of sevoflurane
1. brain:blood = 0.69
2. brain:blood = 1.7
3. fat:blood = 47.5
37
What are MAC values based on?
30-55 year olds, 37 degrees celsius (98.6 F), 760 mmhg (1 ATM)
38
What is the MAC % of Nitrous Oxide?
104%
39
What is the MAC % of Isoflurane?
1.17%
40
What is the MAC % of Desflurane?
6.6%
41
What is the MAC % of Sevoflurane?
1.8%
42
What are the two biggest factors that alter MAC?
1. Body temp
2. Age (6% change per decade above and below 30-55)
43
When does MAC peak?
at 1 years old
44
4 things that cause an increase in MAC
1. Hyperthermia (higher metabolic rate)
2. Excess pheomelanina production (red heads)
3. Drug-induced increase in catecholamine levels (increased metabolic rate)
4. Hypernatremia (more likely to depolarize)
45
Examples of things that Decrease MAC (basically slowed metabolic rates, there's a bunch so good luck)
1. Hypothermia
2. Preop and intraoperative meds
3. Alpha-2 agonists (clonidine)
4. Acute alcohol ingestion
5. Pregnancy
6. Post-partum (13-72 hours)
7. Lidocaine (inhibits depol and changes threshold)
8. PaO2 \<38 mmHg
9. Mean BP \<40 mmHg
10. Cardiopulmonary bypass d/t hypothermia
11. Hyponatremia
46
8 things that do not change MAC
1. Chronic alcohol abuse
2. Gender
3. Duration of anesthesia
4. PaCO2 15-95 mmHg
5. PaO2 \> 38mmHg
6. Hyper/Hypokalemia
7. Thyroid gland dysfunction
47
How does anesthesia cause Spinal Immobility?
1. Depress excitatory AMPA and NMDA (glutamate) receptors
2. Enhance inhibitory glycine
3. Action on Na channels to block presynaptic release of glutamate, which reduces excitation
4. Timely use of NMB's
48
How does anesthesia cause loss of consciousness?
1. Inhibitory transmission of GABA in the brain and RAS (reticular activating system)
2. Potentiation of glycine activation in brainstem
3. No effect of volatiles on AMPA, NMDA, or karinate
49
What is the universal color of a bottle that contains: sevo, iso, des?
1. Sevo: Yellow
2. Iso: Purple
3. Des: Blue
50
What does Dalton's Law state about partial pressure of gases?
Gases exert the same amount of pressure on the wall of a container whether they are mixed with other gases or not
51
What is Vapor Pressure?
Highest partial pressure at a given temperature, meaning vapor and liquid are at equilibrium
52
What does Henry's Law describe?
The total number of gas molecules dissolved in liquid (blood) varies directly with partial pressure
53
What do we want to occur in a liquid to increase the partial pressure of gas (overpressurize)?
Want greater pressure in liquid form, this helps increase anesthetic depth
54
How does heating or cooling effect vapor pressure?
1. Heat increases vapor pressure, allowing more molecules to move into the patient
2. Cooling decreases vapor pressure
55
What would greater vapor pressure indicate?
1. More likely to evaporate
2. Considered to be more volatile
56
What is the vapor pressure and boiling point of Halothane?
1. VP: 243 torr
2. BP: 50.2 C
57
What is the vapor pressure and boiling point of Isoflurane (Forane)?
1. VP: 238 torr
2. BP: 48.5 C
58
What is the vapor pressure and boiling point of Desflurane (Suprane)?
1. VP: 669 torr
2. BP: 22.8 C
59
What is the vapor pressure and boiling point of Sevoflurane (Ultane)?
1. VP: 157 torr
2. BP: 58.5 C
60
What does it mean when we see that we are inspiring more gas than we are exhaling?
Brain is still taking up meds
61
What does a higher splitting ratio indicate?
Less fresh gas is by-passing volatile anesthetic and getting to patient
62
What would increasing the temp or amount of a gas do for us?
We will have a greater and faster uptake of the gas
63
What is the purpose of flow-over?
Increase gas-liquid interface and improves the efficiency of vaporaization by increasing surface area available to be exposed to fresh gas flow
64
What did adding wicks do to vaporizaton?
Improved it by increasing more SA for the volatile to interact with fresh gas flow
65
4 purposes of the anesthesia circuit?
1. Delivery of oxygen
2. Delivery of inhaled drugs
3. Maintains temp/humidity
4. Removal of carbon dioxide and exhaled drugs
66
3 types of gas delivery systems
1. Rebreathing (Bain)
2. Non-breathing (self-inflating BVM)
3. Circle systems
67
What 4 features does a Bain circuit have and what is it's limitation?
1. APL valve
2. Circuit connector
3. Reservoir Bag
4. Oxygen connection
Bain circuits are limited to transportation
68
6 Descriptors of Circle systems
1. Fresh gas inlet from tank or wall without expired gas
2. Inspiratory and expiratory limbs
3. Reservoir bag
4. CO2 absorbant
5. One-way valves
6. Y Piece
69
How do you calculate minute volume?
Tidal volume multiplied by respiratory rate
70
What is considered high flow anesthesia?
Fresh gas flow exceeds minute ventilation
71
What are 2 positives with high flow anesthesia?
1. Prevents rebreathing
2. Rapid changes in anesthetic helps facilitate induction or emergence
72
2 negatives of high flow anesthesia?
1. Wasteful
2. Cool/dries delivered volume
73
What happens if FGF does not exceed minute ventilation?
Patient could re-breathe some CO2
74
Describe low flow anesthesia
FGF is less than minute ventilation
75
2 positives of low flow anesthesia
1. low cost
2. less cooling/drying
76
What is a negative with low flow anesthesia?
Very slow changes in anesthetic, which is not good if we are in a hurry
77
What is not a concern with low flow anesthesia anymore due to current research?
Low flow anesthesia does not cause compound A production with sevoflurane
78
What are the three things that determine the cost of volatile anesthetics (cost of liquid/mL)?
1. Volume of vapor obtained/mL
2. Volume percent of anesthetic delivered (potency and solubility)
3. FGF rate
79
How much more expensive is Des than Sevo?
about 3x
80
What did Dr. Snow's experiements with chloroform give us?
solubility, vapor pressure, potency and stage of anesthesia
81
What are the targets of methyl-ether ethers (volatile anesthetics)
1. Stimulation of GABA and glycine receptors
2. Inhibits NMDA-glutamate and nAch receptors
3. Activate K+ leak channels
4. Inhibit Na voltage gated channels
82
How do volatile anesthetics cause bronchodilation?
1. Relax airway smooth muscles
2. Block voltage gated Ca++ channels
3. Deplete Ca++ in SR
83
What do volatile anesthetics require to cause bronchodilation?
An intact epithelium, inflammatory processes such as asthma and epithelial damage alters effectiveness
84
Describe volatile anesthetic effect of bronchodilation without bronchospasm (2)
1. Baseline pulmonary resistance unchanged by 1-2 MAC
2. Need histamine release or vagal afferent stimulation to allow volatile to dilate
85
List the volatile anesthetics by which drug causes relaxation of respiratory system resistance to decrease faster from the least to most (iso, halothane, sevo, des)
1. Des
2. Iso
3. Halothane
4. Sevo
86
Neuromuscular effects of volatile anesthetics?
1. Dose-dependent skeletal muscle relation, but not enough to prevent movement
2. Potentiate depolarizing and non-depolarizing NMBDs through synergistic effects
3. Nitrous oxide has no relaxant effect on skeletal muscles
87
What are the effects of volatile anesthetics on CNS activity?
Dose dependent reductions in CMRO2 and cerebral activity
88
When does reduced CNS activity begin to occur with volatile anesthetics? burst suppression? electrical silence?
1. begins at approv 0.4 MAC as wakefulness changes to unconcsousness
2. 1.5 MAC burst suppression
3. 2 MAC electrical silence
89
Which volatile anesthetics show anticonvulsant activity and when do they show it?
des, iso, sevo ; at high concentrations and with hypocarbia
90
What volatile anesthetic shows proconvulsant activity?
enflurane, especially above 2 MAC or PaCO2 \<30 mmHg
91
When do we see a reduction in amplitude and increased latency of SSEP's and MEP's wih volatile anesthetics?
It's dose-related but around 0.5-1.5 MAC
92
What is an adequate anesthetic strategy to use to reduce SSEP's and MEP's?
60% nitrous ad 0.5 MAC volatile
93
What effect do volatile anesthetics have on cerebral blood flow?
Dose dependent effects:
* Increases in CVF d/t decreased cerebral vascular resist.
* May increase ICP
* Onset \> 0.6 MAC
* Occurs within minutes despite lack of BP changes
94
Describe the potency of volatile anesthetics on CBF (des, iso, nitrous, halothane)
* Des = Iso
* Sevo has less vasodilatory effects
* Nitrous is a potent vasodilator but give \< 1 MAC
* Halothane is the worst
95
Which volatile anesthetic is the drug of choice for brain patients?
Sevoflurane
96
At what MAC do we expect to see some loss of cerebral autoregulation with halothane, sevo, iso or des?
* Halothane lose by 0.5 MAC
* Sevo preserves to 1 MAC
* Iso and Des lost by 0.5-1.5 MAC
97
Describe how increases in ICP parallels increases in CBF (4)
1. Pts with space-occupying lesions most at risk
2. Opposed by hyperventilation, which causes reduced PaCO2 and Vasoconstriction
3. Onset \> 0.8 MAC
4. ICP increases by 7mmHg
98
What dose-dependent effects of volatile anesthetics cause respiratory depression?
Dose-dependent increases in respiratory rate but reduction in tidal volume
99
Describe how volatile anesthetics produce respiratory depression
Direct depression of medullary ventilatory center and interference with intercostal muscles, diaphram descends so the chest wall collapses inward
100
At what MAC do we see apnea with volatile anesthetics?
1.5-2.0 MAC
101
Up to what MAC do we see dose-dependent increases in respiratory rate and reductions in tidal volume with isoflurane?
Up to 1 MAC
102
Describe volatile anesthetics and blunting the hypoxic ventilatory response
1. Normally mediated by carotid bodies
2. At 0.1 MAC initiated (50-70% depression) and 1.1 MAC (100% depression)
3. All volatiles including nitrous
4. Lasts for several hours postop
103
Describe volatile anesthetics and blunting hypercarbic ventilatory response
1. Dose dependent
2. Nitrous does not increase PaCO2, substitution for part of MAC and has less depression
104
Describe what occurs with hypoxic pulmonary vasoconstriciton
Normal contraction of pulmonary artery smooth muscle due to alveoli not being ventilated properly to prevent perfusing bad areas of the lung
105
What do we see with regional blood flow within 5 minutes of HPV? Max response?
1. at 5 minutes, blood flowis half
2. Max response lasts 2-4 hours
106
At what MAC do we see a reduction in Hypoxic Pulmonary Vasoconstriction?
2 MAC
107
When should we have the most concern when blunting HPV?
1 lung ventilation due to increased perfusion but decreased arterial oxygenation
108
5 cardiac effects of volatile anesthetics
1. Direct myocardial depression
2. Peripheral autonomic ganglion blockade
3. Attenuation of carotid sinus reflexes
4. Decreased formation of cAMP
5. Decreased calcium influx
109
What is the reductionin MAP associated with volatile anesthetics primarily due to?
Reduction in SVR
110
When is dose dependent myocardial depression of more importance?
With diseased hearts with already altered contractility
111
Which volatile shows the most reduction in MAP? Which has no effect?
Isoflurane has the most, nitrous has no cardiac depression
112
When do we see dose dependent increases in HR with Sevoflurane?
\> 1.5 MAC
113
Which volatile shows greater dose dependent tachycardia, especially with overpressurization?
Desflurane
114
When will there be more variablity with dose dependent increases in heart rate caused by volatile anesthetics? (4)
1. Anxiety
2. Opioids
3. Beta-blockade
4. Vagolytic admin (anticholinergics)
115
Which volatile shows a mild increase in CO due to being a sympathomimetic?
Nitrous
116
When does sevoflurane show recovery of CO?
at 2 MAC
117
Describe coronary steal syndrome
Re-directing blood flow from poorly perfused areas and giving to those who are better perfused ; This is due to coronary vasodilation and preferentially in distal vessels
118
Cardiac output, SVR, MAP and HR effects of Isoflurane
1. CO: decreased
2. SVR: decreased
3. MAP: Greatly decreased
4. HR: increased
119
Cardiac output, SVR, MAP and HR effects of Desflurane
1. CO: no effect
2. SVR: decreased
3. MAP: decreased
4. HR: increased
120
Cardiac output, SVR, MAP and HR effects Sevoflurane
1. CO: no change
2. SVR: reduced
3. MAP: reduced
4. HR: no change
121
Cardiac output, SVR, MAP and HR effects Nitrous Oxide
1. CO: reduced
2. SVR: increased
3. MAP: no change
4. HR: increased
122
Cardiac output, SVR, MAP and HR effects of Halothane
1. CO: reduced
2. SVR: no change
3. MAP: reduced
4. HR: greatly reduced
123
What cardiac arhythmia is common with volatile anesthetic use?
Prolonged QT interval in healthy patients
124
Which volatiles inhibit K+ current and potentially inreases risk of torsades?
Iso, des and Sevo
125
What is the proarrhythmic effect of nitrous
Minimal
126
What effect do iso and sevo show in ablation studies?
1. Iso increases refractoriness of accessory paths, leading to more episodes of arrythmias
2. Sevo shows no effect and is acceptable to use in ablation
127
Describe cardiac preconditioning
Brief periods of ischemia prior to longer periods which helps prevent reperfusion injury
128
Describe preconditioning mediated by adenosine
1. Increases protein kinase C activity
2. Phosporylates ATP sensitive K+ channels
3. Better regulate vascular tone
129
How low of a MAC can we see cardiac preconditioning?
0.25 MAC
130
What occurs when the ANS and HPA activates in response to volatile anesthetics?
Perioperative surge in catecholamines, ACTH and cortisol; leading to suppression of monocytes, macrophages, and T-cells
131
What does evidence show with GA and cancer?
increased tumor metastasis
132
What is the effect of volatile anesthetics on total hepatic blood flow? hepatic artery flow?
Both are maintained
133
What is the effect of volatile anesthetics on portal vein flow?
Increased at 1-1.5 MAC due to vasodilation
134
Which volatile anesthetic decreases hepatic blood flow?
Halothane
135
When should we be concerned with inadequate oxygenation of hepatocytes when utilizing volatile anesthetics?
Pre-existing liver disease
136
Describe Type 1 Hepatotoxicity (4)
1. 20% of patients
2. 1-2 weeks after exposure
3. Direct toxic effect or free radical effect
4. Nausea, lethargy, fever (flu-like symptoms)
137
Describe Type 2 Hepatotoxicity (5)
1. Less common than Type 1
2. Immune-mediated response against hepatocytes
3. Prior exposure to any volatile anesthetics, but more common with halothane
4. High mortality; acute hepatitis, hepatic necrosis
5. 1 month exposure
138
List enflurane, isoflurane and desflurane in order from greatest to least of the drug being metabolized to acetyl halide
En\>iso\>des
139
Describe metabolism of enflurane, isoflurane and des to acetyl halide (3)
1. Oxidized by P450 to acetyl halide metabolites
2. Capable of causing antibody reaction
3. Most likely in patients sensitized by Halothane or Enflurane
140
Describe sevo metabolism (2)
1. Metabolized to vinyl halide
2. Not capable of stimulating antibody formation
141
What renal effects do volatile anesthetics have?
Dose dependent reduction in RBF, GFR and UO, not related to vasopressin release
142
How do we abolish the renal concerns when utilizing volatile anesthetics?
Preop hydration
143
What metabolite of volatile anesthetics causes increased creatinine, hypernatremia, hyperosmolality and decreased creatinine clearance?
fluoride
144
Which volatile anesthetic was removed from the market due to causing fluoride toxicity?
Methoxyflurane
145
What helps reduce nephrotoxicity with newer volatile anesthetics?
Lower solubility and being exhaled prior to metabolism and eliminated renally
146
What was removed from market because it lead to compund A formation?
Barium hydroxide (bara-lime)
147
What is Compound A?
A nephrotoxic vinyl halide
148
What volatile anesthetic was implicated for high incidences of compound A, but is now is not considered an issue?
Sevo (it is less renal toxic even in CKD)
149
What are the triggers of malignant hyperthermia?
All volatile anesthetics and succinylcholine
150
What is generally thought to be a predisposing factor of malignant hyperthermia?
Inherited, genetic traits
151
Describe malignant hyperthermia (4)
1. Hypermetabolic state of skeletal muscle
2. Excessive release of Ca++
3. Muscle rigidity
4. Rhabdo
152
What are the symptoms of malignant hyperthermia?
increased body temp, increased CO2 production and increased O2 consumption
153
Which volatile anesthetics are emetogenic?
All of them
154
When does GA cause PONV?
With volatile and opioid use 25-30% of the time
155
Metabolic effects of nitric oxide?
1. B12 deficiency due to oxidization of cobalt ion leading to inhibition of DNA synthesis
2. Megaloblastic bone marrow suppression (after 24 hours of exposure)
3. Increase plasma homocysteine levels (increases periop myocardial event)
156
What patient populaton do we avoid utilizing nitrous oxide in?
Pregnant moms, especially in the 1st trimester
157
What is the 1/2 time of nitric oxide?
45 minutes
158
What is increases in plasma homocysteine levels due to with nitric oxide use and which comorbidity increases risk associated?
Low plasma homocysteine levels are associated with low B vitamines and patients with atherosclerosis are more likely to increase periop MI
159
Obstetric effects of volatile anesthetics
1. Dose dependent (0.5-1.5 MAC) reuction in smooth muscle contractility and reduction in fetal blood flow
2. Useful in retained placenta but fan worsen blood loss in uterine atony
3. No effect with nitrous
4. Mom may have recall with emergent c-sections
160
5 Things associated with Halothane
1. It is a halogneated alkane
2. compatible with inhalation induction
3. sweet, non pungent
4. high potency, intermediate solubility
5. lower risk of N/v, non-flammable, good for vasodilation
161
4 concerns with halothane
1. Catecholamine-induced arrhythmias
2. Occasional hepatic necrosis
3. Pedatriac bradyarrhythmias
4. Decomposition to HCL acid, thymol preservative added
162
Describe enflurane (4)
1. Halogenated methyl ethyl ether
2. Clear, non-flammable, pungent odor
3. Intermediate solubility, high potency
4. Decreases seizure threshold
163
Describe Isoflurane (6)
1. An isomer of enflurane that is highly potent
2. Highly pungent, causes coughing and sputtering
3. Immediate solubility, high potency
4. Expensive to purify, cheaper if used more
5. Resistant to metabolism and unlikely to cause organ toxicity
6. Stable, no deterioration after 5 years
164
Describe Desflurane (5)
1. Fluorinated methyl ethyl ether identicle to isoflurane (F sub for Cl-)
2. Requires special vaporizer (would boil at OR room temp)
3. The most pungent
4. Over-pressurizing (SNS stimulation)
5. Will degrade to carbon monoxide if absorbent dehydrated
165
List the anesthetics in order from most likely to degrade into carbon monoxide to least
Des\>enflurane\>iso\>sevo(trivial)
166
What difference does desflurane show to isoflurane
Reduced solubilty and potency and increased vapor pressure
167
Describe Sevoflurane (5)
1. Fluroinated methyl isopropyl ether with low solubility
2. Sweet smelling, not pungent and least airway irrittion of modern volatiles
3. Metabolized to inorganic fluoride that is least likely to from carbon monoxide
4. The least cerebral vasodilation, so drug of choice for increased ICP
5. Suppresses lidocaine induced seizure activity
168
Describe Nitrous Oxide (4)
1. Usually not used alone
2. Low moleculare weight
3. sweet smelling/odorless
4. Good analgesic properties, has no delayed effects
169
Why is Nitrous Oxide not used alone for anesthesia?
1. Low solubility, low potency
2. Does not produce skeletal muscle relaxation
3. Can't deliver 1 MAC
170
Describe Xenon (6)
1. An inert gas, NMDA antagonist
2. MAC 63-71%, blood:gas coefficient 0.115
3. Odorless, non-pungent
4. Absence of metabolism
5. Very expensive
6. Favors air bubble expansion, neuro concerns and less bowel expansion than nitrous oxide
171
Describe Post-op cognitive dysfunction (4)
1. Alterations in Ca++ homeostasis, SIRS, acceleration of amyloid veta plaques
2. Iso, iso with nitrous, sevo and des
3. Hyoxia, hypothermia
4. Increased apoptosis
172
Describe anesthetic preconditioning (5)
1. Exposure to volatile PRIOR to ischemia
2. Iso 0.25 MAC
3. Production of reactive oxygen species (ROS)
4. Upregulate cell defense
5. Demonstrated in heart, brain, kidney and lung
173
Descibe volatile effect on immune function and cancer (3)
1. Suppress natural killer cells
2. Significant suppression increases patient mortality
3. Suppression from volatiles \< suppression from stress response of surgery
174
What is the main effect on nueromuscular blocking agents?
Interrupton of transmission of nerve impulses at neuromuscular junction (NMJ)
175
What is the main action of depolarizing muscular blockade agents?
Mimic acetylcholine
176
What is the main action of non-depolarizing neuromuscular blockade agents?
Intereferes with the action of acetylcholine
177
What is the purpose of neuromuscular blockage agents? (4)
1. Minimizes incidence of tissue trauma
2. Decreases airway trauma
3. Facilitates surgical exposure
4. Minimizes injury from patient movement
178
3 Signs showing airway trauma
1. airway edema
2. hoarseness
3. vocal cord injury
179
What class fo NMBD is succinylcholine?
depolarizing
180
Which non-depolarizing NMBD's are long acting?
1. Pancuronium
2. Doxacurium
3. Pipecuronium
181
Which non-depolarizing NMBD's are intermediate acting?
1. Atracurium
2. Vecuronium
3. Cisatracurium
182
Which non-depolarizing NMBD's are short acting?
Mivacurium
183
What are the 3 non-depolarizing NMBDs considered benzylisoquinoline?
**MAC**
* Mivacurium
* Atracurium
* Cisatracurium
184
Which non-depolarizing NMBDs are considered aminosteroids?
1. Pancuronium
2. Doxacurium
3. Pipercuronium
4. Rocuronium
5. Vecuronium
185
What does ED95 describe?
The dose necessary to produce 95% suppression of a single twitch in the presence of nitrous/barbs/opioid anesthesia
186
3 descriptors of the adductor policis muscle
1. Single twitch at Hz
2. Ulnar nerve stimulated
3. Thumb moves towards midline
187
What is the order of block dependent on?
1. # of presynaptic Ach containing vesicles released
2. # of postsynaptic Ach receptors
3. Blood flow to area
188
Which preferred testing site of neuromuscular blockade is a poor indicator of laryngeal relaxation?
Adductor pollicis
189
Which preferred site of neuromuscular blockade testing more closely reflects onset of blockade at diaphragm and why
Obicularis oculi because it tests CN 7, the facial nerve
190
What is the third favorite spot for neuromuscular blockade testing?
posterior tibial
191
Patient symptoms of neuromuscular blockade (6)
1. visual focus
2. mandibular muscle weakness
3. ptosis
4. diplopia
5. dysphagia
6. increased hearing acuity
192
Describe single twitch from peripheral nerve stimulators
1. Usually 1 Hz every 10 seconds, at the onset of block, will fade with each stimulus
2. Correlates with events at post-junctional membrane
193
Describe double burst assessment with peripheral nerve stimulators (4)
1. 2-3 short bursts followed by 2-3 short bursts
2. Developed to improve detection of residual block
3. Fade in 2nd response vs 1st
4. Qualitatively better than TO4
194
Describe the train of four
1. 4 stimuli at 2 Hz q 1/2 second
2. Reflects events at presynaptic membrane
3. Only 60% fade or \> is detected
4. Train of four ratio
195
Describe the train of four ratio (4)
1. Prior to NMBD 4/4 twitches showing TOFR 1
2. After administration return of 4 twitches
3. Amplitude of 4th twitch to 1st twitch
4. Amplitude of 4th is 50% of 1st, TOFR 0.5
196
Describe Tetanic stimulation
1. Very rapid, 50 Hz for 5 seconds
2. Sustained muscle response due to more Ca++ and Ach around = depolarizing block
3. Non-sustained response with non-depolarizing block
4. Phase 2 block with succs
197
What is fade related to with non-sustained response from tetanic stimulation
1. Presynaptic depletion of Ach or inhibition of release
2. Frequency and length of stimulation
198
Describe post-tetanic stimulation (3)
1. Tetanic stimulation then single twitch 3 seconds later
2. Occurs d/t accumulation of calcium during tetany
3. No response = intense blockade
199
What was the major side effect of Rapacurium (Raplon)
Increased Bronchospasm that could not be reveresed in young people
200
Describe the anatomy of a NMJ: Presynaptic (3)
1. Large, myelinated motor neurons from spinal cord or medulla
2. Unmyelinated motor nerve ending that innervates a single muscle fiber
3. Responsible for Ach synthesis, uptake and storage into vesicles; also release and reuptake of choline
201
Describe the Anatomy of NMJ: Synaptic cleft
1. Synaptic cleft filled with fluid, contains collagen and acetylcholinesterase
2. Calcium dependent
3. Acetylcholinesterase close by for hydrolysis of Ach to acetic acid and choline
202
Describe the anatomy of NMJ: Post-synaptic
1. Membrane with multiple folds
2. 90 mv resting membrane potential
3. Maintained by sodium/potassium (3 Na out, 2 K in)
4. nAch-R directly opposite
203
Describe the nAch-R subunit (2)
1. Pentameric unit with 2 alpha, beta, delta and epsilon on outside; transmembrane pore in the center
2. Conformational change if Ach binds to allow ions to flow
204
Describe what happens if NMBD bind to nAch-R
1. No conformational change
2. No ion flow
3. Probability of binding due to concentration of NMBD vs Ach
4. Succinylcholine only requires binding to 1 alpha subunit, this is thought to be why fasciculations occur
205
Describe Succinylcholine (4)
1. Only depolarizing NMBD in clinical practice
2. 2 unique characteristics showing intense, rapid paralysis, offset of effects prior to hypoxia
3. Useful for tracheal intubation and rapid sequence
4. Releases histamine
206
What is the dose, onset of action and duration of succinylcholine?
1. Dose: 1mg/kg at actual body weight
2. Onset: 30-60 seconds
3. Duration: 3-5 minutes
207
What is the MOA of succinylcholine (6)
1. Attaches to 1 or both alpha subunits
2. Mimics effects of Ach
3. Hydrolysis is slower than Ach
4. Sustained opening of receptor ion channels
5. Leakage of potassium ions causes a 0.5 mEq/liter serum increase
6. Depolarization called "Phase 1 block"
208
Which patients should we caution giving succinylcholine to?
Diabetics and chronic renal failure
209
What are the characteristics of a Phase 1 block (6)
1. Reduced contraction to single twitch stimulation
2. Reduced amplitude to continuous stimulation
3. TOF ratio \>0.7
4. Absence of post-tetanic faciculation
5. Augmented block after administration of anticholinesterase drug
6. Skeletal muscle fasciculations
210
What are the characteristics of Phase 2 block? (5)
1. Responses typical of non-depolarizing NMBD
2. Can be antagonized by anticholinesterase drug
3. Arupt transition with succ dosages of 2-4mg/kg
4. Lack of poorly functioning pseudocholinesterase
5. Relative "overdose"
211
What is the difference between Phase 1 and Phase 2 blocks?
Phase 1 augmented by anticholinesterase drug but phase 2 block antagonized by anticholinesterase drugs with twitch differences
212
Describe the butyrylcholinesterase (plasma cholinesterase) that hydrolizes succinylcholine
1. Glycoprotein enzyme
2. Synthesized in liver
3. Terminated by diffusion of NMJ into plasma
4. Succinylmonocholine is less potent and choline
213
Describe pseudocholinesterase activity (6)
1. Descreased hepatic production, 75% beore apparent
2. Drug-induced decreases (Neostigmine, reglan, chemo, insecticides)
3. Genetically atypical
4. Chronic diseases (renal)
5. Pregnancy (high estrogen levels)
6. Obesity increases activity
214
Describe dibucaine
1. Local amide anesthetic
2. Inhibits breakdown of butyrylcholinesterase
3. % inhibiton = dibucaine number
215
What is a dibucaine number?
1. Reflects quality not quantity of enzyme
2. 20: SCh 1mg/kg lasts 3 hours
216
Side effects of Succinylcholine (8)
1. Cardiac dysrhythmias
2. Hyperkalemia
3. Myalgia
4. Myoglobinuria
5. Increased intragastric pressure
6. Increased intraocular pressure
7. Increased intracranial pressure
8. Sustained muscle contraction
217
Describe cardiac dysrhythmias associated with succinylcholine (3)
1. SB, JR, Sinus arrest
2. Action at cardiac muscarininc, cholingergic receptors
3. Action at ANS ganglia
218
What actions at cardiac muscarinic, cholinergic receptors causes cardiac dysrhythmias with succinylcholine?
1. mimics action of Ach
2. Most liley on 2nd dose, 5 minutes post 1st
3. Due to metabolites: succinylmonocholine and choline
219
What actions of succinylcholine at ANS ganglia cause cardiac dysrhythmias?
1. Increased heart rate and blood pressure
2. Mimics action of Ach
3. Usually occurs with large doses
220
What patients would we worry about causing hyperkalemia with succinylcholine admin. due to extrajunctional sites?
1. Unrecognized muscular dystrophy such as in duchenne's which is diagnosed at 2-6 years of age
2. Unhealed 3rd degree burns
3. Denervation of skeletal muscles (atrophy) that occurs within 96 hours to 6 months of stagnation
4. Skeletal muscle trauma
5. Upper motor neuron lesions
221
Can you alter hyperkalemia with succinylcholine if you pretreat with non-depolarizers?
no
222
Describe myalgia associated with succinylcholine admin (3)
1. Associated with young adults
2. Neck, back, abdomen
3. Confused with pharyngitis due to intubation
223
Describe myoglobinuria associated with succinylcholine admin
1. Damage to skeletal muscles, especially pediatrics
2. Fasiculations unlikely to cause
3. Usually found to later have MH or muscular dystrophy
224
Describe intragastric pressure and LES pressure with succinylcholine administration
1. Related to intensity of fasiculations
2. Related to direct increases in vagal tone
3. Not seen in children due to minimal fasiculations
4. Passage of gastric fluid into esophagus and pharynx can cause aspiration
225
Describe maximum incrase in intraocular pressure after administration of succinylcholine (5)
1. Occurs 2-4 minutes after admin
2. Lasts 5-10 minutes
3. MOA unknown
4. Contraction of EOM and globe distrortion
5. Resistance to outflow of aquous humor and dilation of vessels
226
When is succinylcholine contraindicated with eye surgery?
Open anterior chamber injury due to possibility of causing permanent blindness
227
Describe intracranial pressure in regards to succinylcholine admin
1. Increases with patients who have intracranial tumors or CHI
2. Not consistently observed in studies
3. Attenuated by hyperventilation prior to admin
228
Describe sustained skeletal muscle contraction with succinylcholine admin
1. Incomplete jaw relacation/masseter muscle spasm associated with halothane and succinylcholine in children
2. Considered normal response if inadequate dosage given
3. Differentil diagnonis with MH
229
Define malignant hyperthermia
Heriditart rhabdomyolysis associated with anesthetics that leads to muscle destruction, hyperkalemia, acidosis, dysrhythmias, renal failure, DIC
230
Triggers for malignant hyperthermia?
All volatile anesthetics and succinylcholine
231
What is thought to be the cause of malignant hyperthermia?
1. Mutation in skeletal muscle calcium release
2. RyR1 receptors in 50-70% of MH patients and native americans
3. Skeletal muscle caffeine contracture testing and muscle biposy can help pre-dx
232
Symptoms associated with MH?
1. Acute increased skeletal muscle metabolism
2. Increased oxygen consumption
3. Lactate formation
4. Heat production
5. Rhabdo
233
Clincial presentation of rhabdomyolysis?
1. increased ETCO2
2. increased temp 1 degree C q 5 minutes
3. Arrythmias
4. Skeletal muscle rigidity
234
What are the ABCD's of Malignant Hyperthermia?
* Agents = stop all triggering agents
* Administer non-triggering anesthetics
* Ask for help
* Ask for MH cart
* Breathing = hyperventilation with 100% oxygen
* Cooling procedures if patient is \>102.2 F (fluids and ice)
* Dantrolene continuous and rapid IV push
235
What is the effect and metabolism of Dantrolene?
1. Inhibits calcium release into SR
2. Metabolized in the liver into 5-hydroxydantrolene
3. 50% of patients complained of weakness of grip
236
What are the most common side effects of dantrolene? (4)
1. Weakness
2. Phlebitis
3. Respiratory failure
4. GI upset
237
What are the less common side effects of dantrolene? (3)
1. Confusion
2. Dizziness
3. Drowsiness
238
What is the dose of dantrolene in MH?
2mg/kg IV, repeat dose until symptoms subside or reach a total of 10mg/kg IV
239
Why must we be cautious in giving dantrolene to patients on other calcium channel blockers?
Synergistic effect can lead to hyperkalemia and cardiovascular collapse
240
Describe Myasthenia Gravis
Autoimmune disease associate with antibodies against Ach receptors causing a reduction in them
241
What are the signs of myasthenia gravis?
1. Increaesing weakness/fatigue s the day goes on
2. Diplopia
3. Ptosis
4. Extremity and respiratory muscle weakness
242
What NMDs are patients with myasthenia gravis sensitive to?
Non-depolarizers
243
How is myasthenia gravis related to administration of succinylcholine?
MG patients are resistant to succ, ED95 is 2.5x greater to be effective, will need to use 1.5-2mg/kg IV
244
Describe Lambert-Eton disease
autoimmune disease associated with small cell lung cancer that produces antibodies against caclium channels and decreases release of Ach prejunctionally
245
What NMBds do patients with Lamber-Eton disease show increased sensitivity to?
depolarizers and non-depolarizers
246
MOA of non-depolarizing muscle relaxants (5)
1. Competively acts for alpha subunits (both) of post-junctional nAch-R
2. No conformational changes of the nAch receptor
3. Also act at pre-junctional sites
4. 70% post-juntional occupation = no blockade
5. 80-90% blocked receptors = neuromuscular transmission fails
247
Characteristics of blockade with NDMDs? (7)
1. Decreased twitch response to a single simulus
2. Unsustained response (fade) to continuous stimulus
3. TOF Ratio \<0.7
4. Post-tetanic potentiation
5. Potentiation of other non-depolarizing drugs
6. Antagonism by anticholinesterase drugs (neostigmine)
7. No fasiculations during onset
248
What does fade suggest?
Fade suggest some fibers are contracting while some are blocked
249
Main Adverse side effects of NDMDs? (3)
1. Cardiovascular effects
2. Critical illness myopathy
3. Altered responses
250
What are the cardiovascular effects associated with ND-NMBDs due to?
1. Release of histamine
2. Effects at cardiac muscarinic receptors
3. Effects on nAch-R at autonomic ganglia
251
What is the "autonomic margin of safety" when referring to cardiovascular effects of ND-NMBDs?
1. Difference between dose that produces blockade ED50 and dose that creates circulatory effects
2. Same dose for pancuronium
3. Very different dose for vec, roc, cis
252
Describe skeletal muscle weakness associated with when administering ND-NMBDs? (5)
1. Weeks to months after NMBD d/c
2. Usually an aminosteroid blocker
3. Glucocorticoids prior to NMBD may enhance risk
4. Nerve monitoring, sedation, analgesia, small doses of NMBD may be effective
253
What are altered responses associated with coadministration of ND-NMBDs and volatile anesthetics? (4)
1. Dose dependent enhancement
2. MOA leads to CNS depression and skeletal muscle tone
3. Decreased sensitivity of postjunctional membranes
4. Magnitude of intermediate NMBD \< long acting
254
Altered response of ND-NMBDs when associated with coadministration with local anesthetics?
1. Small doses enhance NMJ blockade
2. Large doses block NMJ transmission
255
MOA of local anesthetics?
1. Interfere with prejunctional Ach release
2. Stabilizes postjunctional membranes
3. Directly depress skeletal muscle fibers
4. Compete for plasma cholinesterases (ester LA)
256
Altered response of ND-NMBDs when coadmin with diuretics
1. Furosemide 1mg/kg enhances blockade do to inhibition of cAMP production and decreased Ach release
2. Large doses inhibit PDE1, makes more caMP, antagonism of blockade
3. Mannitol has no effect on blockade
257
Altered response of ND-NMBDs associated with coadmin of magnesium?
Enhances blockade of non-depolarizes and succinylcholine
258
MOA of magnesium
1. Decreased prejunctional releasr of Ach
2. Stabilization of postjunctional membranes
259
Altered response of ND-NMBDs with SNS drugs (2)
1. ephedrine prior to rocuronium decreases onset time by 22% and increases CO and skeletal muscle flow
2. Esmolol prior to induction delays onset of roc by 26%, can have reduction in HR and CO
260
Altered response of ND-NMBDs with hypothermia
1. Occurs with even mild hypothermia, will slow everything down
2. Temperature slowing of hepatic enzyme activity
3. Atracurium
4. Slows temperature dependent hoffman elimination and ester hydrolysis
261
Altered response of ND-NMBDs with hypokalemia?
1. Hyperpolarizes cell membrane
2. Resistance to depolarizing NMBDs
3. Increase sensitivity to non-depolarizing NMBDs
262
Altered respone of ND-NMBDs with acute hyperkalemia?
1. Decreases resting membrane potential
2. Increases effects of depolarizing NMBDs
3. Resitance to non-depolarizing NMBDs
263
Altered response of ND-NMBDs with burn patients?
1. Resistance begins approx 10 days post injury and declines after 60 days
2. Occurs with \> or equal to 30% BSA burnt
3. May be offset by using 1.2mg/kg dose of rocuronium
264
Which arm is more resistance to ND-NMBDs, the paretic arm or the unaffected side
The paretic arm, although the unaffected side is more resistant compared to normal patients
265
Altered response to ND-NMBDs and allergic reactions
1. More common with quaternary ammonium group (SANE)
2. Single quarternary : pan, vec and roc less likely
3. 1st exposure represent prior sensitization (soaps/cosmetics)
4. Cross sensitization possible
266
How does gender effect NMBDs?
women are more sensitive, 22% dose less than vec and 30% dose less than roc and duration of block is greater in women due to less skeletal muscle mass
267
Describe Pancuronium (Pavulon) (4)
1. Bisquaternary aminosteroid with vagolytic and butrylcholinesterase inhib properties
2. Intubating dose of 0.1mg/kg
3. Onset of action 3-5 minutes
4. Duration 60-90 minutes
268
Metabolism of Pancuronium (Pavulon)?
1. 40-60% cleared unchanged in urine
2. Renal failure can prolong effect due to 30-50% decreased plasma clearance
3. Liver disease causes an increase VD and prolongs elimination half time
4. Decreased plasma clearance with aging due to renal function reduction
269
Cardiovascular effects of Pancuronium (Pavulon) (5)
1. SNS activation do to release of NE presynaptically
2. Blockade of NE reuptake postganglionic
3. Increase HR/MAP/CO due to vagal blockade mostly at SA node
4. No changes in SVR or inotropy
5. No histamine release
270
Pros of intermediate acting NMBDs
1. Efficient clearance mechanism
2. Less accumulation with repeat doses or infusions
271
Intermediate acting NMBDs compared with long acting (5)
1. Similar onset of maximum blockade except high dose roc
2. Approx 1/3 duration of action
3. Minimal/absent cumulative effects
4. Minimal/absent cardiovascular effects
5. Antagonized by anticholinesterase drugs approx 20 minutes
272
Describe Atracurium (Tracrium)
1. Bisquaternary benzylisoquinolinium
2. Intubating dose of 0.2mg/kg
3. Onset 3-5 minutes
4. Duration 20-35 minutes
273
Metabolism of Atracurium (Tracrium)
1. Acts both presynaptic and postsynaptic cholinergic receptors may block nACH-R
2. Spontaneous in vivi degredation (Hoffman elim) = greater role
3. Ester hydrolysis by nonspecifici plasma esterases = lesser role
274
When would we see bp or hr changes with intermediate acting NMBDs?
3x the ED95 dose, but they do release histamine
275
Describe vecuronium (norcuron)
1. Aminosteroid
2. Intubating dose 0.1mg/kg
3. Onset 3-5minutes
4. Duration 20-35 minutes
276
Describe the metabolism of Vecuronium (Norcuron)
1. Hepatic Metabolism is the principle organ of elimination
2. Renal excretion is prolonged with dysfunction
3. Repeated doses or infusion does show cumulative effects
277
Metabolism of Veucronium (Norcuron) in elderly and obstetrics (5)
1. Elderly show decreased volume of distribution and decreased plasma clearance
2. Elderly show delayed recovery with infusions
3. Obstetrics show insignificant side effects to fetus
4. Increased clearance in 3rd trimester (progesterone)
5. Prolonged duration early postpartum
278
Acid-base changes associated with Vecuronium (Norcuron) (3)
1. Dependent on when the acid-base status changes
2. If acidosis before NMBD, there will be no prolonged effect
3. If acidosis after NMBD, prolongs blockade
279
Cardiovascular effects of Vecuronium (Norcuron)
1. Essentially none
2. No histamine release
280
Describe Rocuronium (Zemuron) (4)
1. aminosteroid
2. Dose 0.6mg/kg, larger doses parallel onset of Sch but offset of pancuronium
3. Onset 3-5 minutes
4. Duration 20-35 minutes w/ intubating dose
281
Metabolism of Rocuronium (Zemuron) (3)
1. Excreted unchanged in bile (more liver metabolism than renal)
2. Longer duration of action in liver failure and elderly due to decreased clearance and an increased Vd
3. Only marginally affected in renal failure
282
Cardiovascular effects of Rocuronium (Zemuron) (2)
1. No histamine release
2. No cardiac effects
283
Describe Cisatracurium (4)
1. Benzylisoquinolinium
2. Intubating dose 0.1mg/kg
3. Onset 3-5 minutes
4. Duration of action 20-35 minutes
284
Metabolism Cisatracurium (Nimbex) (5)
1. Cis-isomer
2. Less histamine release
3. Recovery from infusion not affected by time
4. Hoffman elimination
5. No elimination 1/2 changes in CRF with bolus
285
Metabolism of Cisatracurium (Nimbex) in the elderly or obese
1. Elder show slight delays of about 1 min in onset due to slower CO
2. Obese show prolonged duratin of action if dosed at real body weight due to Vd
286
Cardiovascular effects of Cisatracurium (Nimbex)
1. No histamine release
2. Cardiovascular stability
287
Describe Mivacurium (Mivacron) (5)
1. Only clinically useful SA non-depolarizer
2. Benzylisoquinolinium
3. Intrubating dose 0.15 mg/kg
4. Onset 2-3 minutes
5. Duration of action 12-20 minutes
288
Metaboliosm of Mivacurium (Mivacron)
1. 3 stereoisomers with cis-trans and trans-trans showing the paralytic effects
2. NM blockade ability
3. Cleared by plasma cholinesterase
289
What would the effect of atypical plasma cholinesterases have on the metabolism of Mivacurium (Mivacron)
1. Decreases hydrolysis
2. Duration of action prolonged
3. Human plasma cholinesterase
290
Metabolism of Mivacurium (Mivacron) with renal dysfunction and hepatic disease
1. Renal dysfunction commmonly shows decreased cholinesterase activity
2. Hepatic disease shows increased volume of distribution, patients appear to be more resistant
291
Cardiovascular effects of Mivacurium (Mivacron) (4)
1. Minimal effects
2. Histamine release with 3x the ED95 dose shows transient MAP drop
3. MAP drop more in HTN patients than non-HTN patients
4. Possible bronchospasm concern
292
4 anti-cholinesterase drugs
1. Edrophonium
2. Neostigmine
3. Pyridostigmine
4. Physostigmine
293
Describe neostigmine (5)
1. Used to antagonize NMBD
2. Increases amount of Ach in NMJ
3. Increases chances of Ach instead of NMBD binding to alpha subunits
4. Dose dependent
5. When recovery of NMBD is occurring anyway
294
MOA of edrophonium and neostigmine
inhibition of acetylcholinesterase
295
Metabolism of Neostigmine and Edrophonium (3)
1. 50-70% of the drug is cleared renally
2. Elimination is 1/2 time is greatly prolonged in CRF
3. Hepatic clearance 30-50% if absence of renal function
296
Metabolism of Edrophonium and Neostigmine in elderly (4)
1. Edrophonium duration is not prolonged
2. Neostigmine duration is prolonged
3. Edrophonium requires a higher concentration in elderly
4. Neostigmine has no difference in concentration
297
Muscarinic effects of Neostigmine and Edrophonium (5)
1. Bradycardia
2. Salivation
3. Miosis (pupillary constriction)
4. Hyperperistalsis
5. Requires an anticholinergic drug prior to admin
298
GI/GU effects of edrophonium and neostigmine (3)
1. Enhance gastric fluid secretion
2. Increase mortality of GI tract
3. Increase PONV, especially if patient has severe predisposition
299
Dose, onset and duration of action of edrophonium
1. Dose: 1mg/kg
2. Onset: 1-2 minutes
3. Duration of action: 5-15 minutes
300
Dose of Atropine and initial effects
1. Dose: 7mcg/kg
2. Initial: Tachycardia with neostigmine
301
Dose, onset and duration of action of Neostigmine
1. Dose: 70mcg/kg with 5mg max
2. Onset: 5-10 minutes
3. Duration of action: 60 minutes
302
Dose of glycopyrolate
15 mcg/kg with 1 mg max
303
What contrinutes to persistent NM blockade?
Acetylcholinesterase is maximally inhibited and no further anticholinesterase is effective, patient will need to be on the vent postop
304
5 things that influence NMBD reversal
1. Intensity of block
2. Which NMBD did you use
3. Continued volatile anesthetic
4. Which reversal drug are you using
5. Patient condition
305
List the drugs Suggamadex reverses in order
1. Rocuronium
2. Vecuronium
3. Pancuronium
306
Describe Suggamadex (Bridion)
1. a cyclodextrin (starch)
2. very water soluble
307
MOA of suggamadex (bridion) (4)
1. Complexes with NMBD to decrease amount of available nAch-R
2. Binds free drug in plasma and creates concentration gradient
3. No metabolism, renal excretion
4. E 1/2 is 2 hours
308
Admin instructions of Suggamadex (Bridion)
1. Bolus over 10 seconds
2. Contraindicated in renal diseases requiring dialysis
3. Moderate block dose is 2mg/kg
4. Deep block dose is 4mg/kg
309
Dose related side effects of Suggamadex?
Nausea/vomiting, pruritius, urticaria
310
2 other side effects of suggamadex other than the dose related ones
Anaphylaxis, marked bradycardia
311
Cautions with suggamadex
1. Patients on Oral contraceptives will require a back-up method for 7 days
2. Toremifine or chemo drugs displaces vec/roc from suggamedex
3. Recurarization at lower than recommended doses
4. With heparanin and LMWH will have an elevate aPTT, PT, INR
