Week 7 Handout (2) Flashcards
1
Q
What are the three phases of anesthesia?
A
Induction Phase, Maintenance Phase, Emergence Phase
Each phase has distinct purposes and processes.
2
Q
What is the purpose of the Induction Phase in anesthesia?
A
Achieve a state of unconsciousness and prepare the patient for surgery.
3
Q
What does the Maintenance Phase aim to achieve?
A
Maintain a steady state of anesthesia and ensure patient comfort and safety.
4
Q
What is the objective of the Emergence Phase?
A
Safely bring the patient out of anesthesia.
5
Q
What are the challenges faced during the Induction Phase?
A
Managing potential complications like hypotension or airway obstruction.
6
Q
What techniques are used in the Maintenance Phase of anesthesia?
A
Adjusting anesthetic dosage and using a combination of agents for optimal effect.
7
Q
What is the process involved in the Emergence Phase?
A
Gradual reduction of anesthetic agents, allowing the patient to regain consciousness.
8
Q
What is Dexmedetomidine?
A
The S-enantiomer of medetomidine, used for sedation.
9
Q
What is the pharmacodynamics of Dexmedetomidine?
A
Produces dose-dependent sedation resembling natural sleep without causing respiratory depression.
10
Q
What are the cardiovascular effects of Dexmedetomidine?
A
Hypotension and bradycardia resulting from CNS α-receptor stimulation and systemic vasodilation.
11
Q
What is the onset of action for Dexmedetomidine when administered by loading infusion?
A
10 to 20 minutes.
12
Q
Fill in the blank: The loading dose of Dexmedetomidine is _______.
A
1 µg/kg infused over 10 minutes.
13
Q
What is the significance of the SPICE III trial in relation to Dexmedetomidine?
A
Found that early sedation with Dexmedetomidine is not associated with a reduction in mortality.
14
Q
What are the systemic effects of Dexmedetomidine on the CNS?
A
Dose-dependent sedation, does not cause respiratory depression, patients are readily arousable.
15
Q
What is Etomidate?
A
A carboxylated imidazole derivative used as an intravenous anesthetic.
16
Q
What are the primary uses of Etomidate?
A
Used in compromised patients with minimal cardiorespiratory depression.
17
Q
What is the induction dose of Etomidate?
A
Typically 0.2-0.3 mg/kg.
18
Q
What adverse effects are associated with Etomidate?
A
Pain on injection, thrombophlebitis, nausea, and vomiting.
19
Q
Fill in the blank: Etomidate causes dose-dependent _______ depression.
A
CNS
20
Q
What is a major disadvantage of the current formulation of Etomidate?
A
It results in burning and pain on injection in up to 90% of patients.
21
Q
What is the pharmacokinetics of Etomidate?
A
Rapidly metabolized in the liver, terminal half-life of 2 to 5 hours.
22
Q
What is the effect of Etomidate on cardiovascular stability?
A
Offers hemodynamic stability upon induction.
23
Q
What is one of the unique respiratory effects of Dexmedetomidine?
A
Maintains respirations and normal brain respiratory responsiveness to CO2.
24
Q
True or False: Dexmedetomidine interferes with neurologic monitoring.
A
False.
25
What formulation modifications have been made to Etomidate over time?
To reduce pain on injection and myoclonia.
26
What are the renal effects of Dexmedetomidine?
Exhibits mild diuretic effect mediated via α2-receptor stimulation.
27
What is the pKa of Dexmedetomidine?
7.1.
28
What is the chemical structure of Dexmedetomidine?
(-)-4-[1-(2,3-dimethylphenyl)ethyl]-1H-imidazole monohydrochloride.
29
What is thrombophlebitis?
A condition involving inflammation of a vein due to a blood clot
## Footnote
Commonly associated with intravenous therapy.
30
What are common side effects of propylene glycol in formulations?
Burning and pain on injection in up to 90% of patients
## Footnote
This is significant for patient comfort during administration.
31
What is the incidence of subsequent venous sequelae postoperatively?
50% up to 7 days postoperatively
## Footnote
Indicates a high rate of complications following certain procedures.
32
What is a common effect during the onset of etomidate use?
Myoclonia
## Footnote
Involuntary muscle jerks can occur during induction.
33
What enzyme does etomidate inhibit?
11β-hydroxylase
## Footnote
This enzyme is essential for the production of corticosteroids.
34
What are the contraindications for etomidate?
Known sensitivity, adrenal suppression, acute porphyrias
## Footnote
Patients with these conditions should not receive etomidate.
35
How does etomidate contribute to cardiovascular stability?
Acts as an agonist at α1B-adrenoceptors, increasing blood pressure
## Footnote
Helps maintain myocardial oxygen supply and demand balance.
36
What respiratory effect does etomidate have?
Decreases minute volume but increases respiratory rate
## Footnote
Respiratory depression is less significant than with propofol.
37
What is the chemical structure of ketamine?
2-(2-chlorophenyl)-2-(methylamino)cyclohexanone
## Footnote
Ketamine has a chiral center and exists as two optical isomers.
38
What is the pKa of ketamine?
7.5
## Footnote
Indicates its acid-base properties.
39
What are the primary pharmacodynamic effects of ketamine?
Antagonism at N-methyl-D-aspartate (NMDA) receptors
## Footnote
This action blocks pain perception signals.
40
What is the primary pathway for ketamine metabolism?
Demethylation to form norketamine
## Footnote
Followed by hydroxylation and conjugation to form more water-soluble compounds.
41
What is a key use of ketamine in anesthesia?
Induction of anesthesia, especially in high-risk patients
## Footnote
Effective in conditions like shock and cardiovascular instability.
42
What characterizes the CNS effects of ketamine?
Dissociative state of anesthesia
## Footnote
Includes catalepsy, open eyes, and intact corneal reflexes.
43
How does ketamine affect the cardiovascular system?
Acts as a circulatory stimulant, increasing blood pressure and heart rate
## Footnote
Different from other intravenous anesthetics.
44
What is a notable respiratory effect of ketamine?
Minor and short-lived effects
## Footnote
Generally preserves ventilation.
45
What are the bronchodilatory effects of ketamine?
Potent bronchodilator, preserving airway reflexes
## Footnote
Increases secretions and maintains respirations.
46
What emergence phenomena can occur after ketamine administration?
Vivid dreams, floating sensations, and delirium
## Footnote
More common in adults than children.
47
What is the impact of ketamine on intraocular pressure (IOP)?
Usually increases IOP, dose-dependent
## Footnote
Important for ocular surgeries.
48
What is the typical induction dose of ketamine?
2-4 mg/kg IV, or 4-6 mg/kg IM
## Footnote
Oral dose is 10 mg/kg.
49
What is the chemical structure of propofol?
2,6-diisopropylphenol
## Footnote
Prepared as a 1% solution in a lipid emulsion.
50
What is the pH range of propofol?
7 to 8.5
## Footnote
Its pKa is 11.
51
What is the primary pharmacodynamic action of propofol?
Interaction with GABA_A receptors
## Footnote
Potentiates actions of endogenous GABA.
52
What are the systemic effects of propofol on the CNS?
Rapid loss of consciousness and reduced cerebral blood flow
## Footnote
Also reduces metabolic rate of oxygen consumption.
53
What is the typical induction dose of propofol?
1-2 mg/kg
## Footnote
Followed by a maintenance infusion.
54
What is the maintenance infusion rate for propofol?
100-200 µg/kg/min
## Footnote
Used for ongoing sedation and anesthesia.
55
What is the elimination half-life of propofol?
1 to 2 hours
## Footnote
Influenced by patient age and condition.
56
What effects does propofol have on blood pressure?
Mild to moderate transient decrease
## Footnote
More pronounced than other agents.
57
What does ICP stand for?
Intracranial pressure
58
What EEG data patterns are associated with higher doses of Propofol?
Delta rhythm and burst suppression
59
What condition has Propofol been used to manage?
Status epilepticus
60
What cardiovascular effect does Propofol usually cause?
Mild to moderate transient decrease in blood pressure
61
True or False: The effects of Propofol on blood pressure are less pronounced than those seen with equivalent doses of etomidate or midazolam.
False
62
In which patients can Propofol cause significant hypotension?
Patients over 50 years old, with a baseline mean arterial pressure less than 70 mm Hg, or when coadministered with high doses of fentanyl
63
What respiratory effect is commonly associated with Propofol?
Transient respiratory depression
64
What is a common outcome of induction doses of Propofol?
Apnea
65
What role might Propofol play in neuroprotection?
Multimodal neuroprotection including preservation of cerebral perfusion, temperature control, prevention of infections, and tight glycemic control
66
What is the relationship between Propofol and seizure duration during electroconvulsive therapy (ECT)?
Propofol reduces the duration of seizures induced during ECT compared to barbiturates
67
What effect does Propofol have on intraocular pressure?
It decreases intraocular pressure
68
Fill in the blank: Propofol easily crosses the ______ barrier.
Placental
69
What adverse effect can Propofol cause in neonates when used for cesarean delivery?
Sedative effects and lower Apgar scores
70
What conditions contraindicate the use of Propofol?
Known hypersensitivity to Propofol or its components, disorders of lipid metabolism, and sulfite sensitivity
71
What serious condition is associated with the use of Propofol, especially in higher doses?
Propofol Infusion Syndrome
72
What are some symptoms of Propofol Infusion Syndrome?
* Metabolic acidosis
* Hyperkalemia
* Lipidemia disorders
* Hepatomegaly
* Elevated liver transaminases
73
What unique chemical structure does Midazolam contain?
An imidazole ring
74
What happens to Midazolam in physiological solutions with a pH greater than 4.0?
It becomes lipophilic
75
What is the primary effect of Midazolam at clinical doses?
Dose-dependent CNS depressant effects
76
What are the common uses of Midazolam?
* Preoperative medication
* Anxiolytic
* Sedative
* Amnestic
77
What cardiovascular effects can Midazolam have?
Minimal effects, but may cause a decrease in blood pressure when combined with opioids
78
What respiratory effect is most prominent with Midazolam?
Respiratory depression
79
True or False: Midazolam is the least respiratory depressing among benzodiazepines.
False
80
What is Flumazenil used for?
To reverse midazolam-induced sedation and suspected benzodiazepine overdose
81
What is the onset time for Flumazenil?
1 to 2 minutes
82
What effect do opioids have on the ascending transmission of nociception?
They inhibit it
83
How do opioids affect respiratory function?
They produce dose-dependent respiratory depression
84
What pupil effect is associated with opioids?
Miosis (pinpoint pupils)
85
What gastrointestinal effects are commonly associated with opioids?
* Constipation
* Urinary retention
86
What hormonal effects do opioids have?
* Release of vasopressin
* Inhibition of stress-induced release of corticotropin and gonadotropins
87
What is Morphine known for?
Being the prototype for opioid agonists
88
What is a common route of administration for Morphine?
* Intramuscular
* Intravenous
* Subcutaneous
* Oral
* Intrathecal
* Epidural
89
What is opium primarily used for?
The abatement of moderate to severe pain
90
Morphine is more effective in relieving which type of pain?
Continuous dull pain
91
List the routes of administration for Morphine.
* Intramuscular
* Intravenous
* Subcutaneous
* Oral
* Intrathecal
* Epidural
92
When administered intravenously, which effect occurs first: sedation or analgesia?
Sedation
93
True or False: Morphine-induced sedation indicates appropriate analgesia.
False
94
What is Morphine's lipophilicity characteristic?
Among the least lipophilic of the opioids
95
What phase of metabolism does Morphine undergo in the liver?
Phase 2 glucuronide conjugation
96
What is the active metabolite of Morphine?
Morphine-6-glucuronide (M6G)
97
What is the typical IV dose range for Morphine?
0.05 to 0.15 mg/kg
98
What is the onset time for Morphine when administered IV?
20 minutes
99
What is Fentanyl known for in anesthesia?
Profound dose-dependent analgesia, ventilatory depression, and sedation
100
What is the duration of action for a single dose of Fentanyl?
Approximately 20-40 minutes
101
How is Fentanyl primarily terminated when given in multiple doses?
Elimination
102
What is the primary route of administration for the transdermal application of Fentanyl?
Transdermal
103
What is the delivery range of the Fentanyl transdermal patch?
25 to 100 mcg/hour
104
Alfentanil has a more rapid onset and shorter duration than which drug?
Fentanyl
105
What is the percentage of the nonionized fraction of Alfentanil at physiological pH?
90%
106
How is Alfentanil metabolized?
By oxidative N-dealkylation and O-demethylation in the liver
107
What is a clinical consideration regarding the use of Alfentanil?
Significant patient-to-patient variability in response
108
What can Erythromycin do in relation to Alfentanil?
Prolong the metabolism of Alfentanil
109
What is Hydromorphone derived from?
Morphine
110
What is the onset of action for Hydromorphone when administered IV?
15 to 30 minutes
111
What is the recommended dose range for Hydromorphone?
0.01 to 0.02 mg/kg
112
Why is Hydromorphone often recommended for patients with renal failure?
It lacks any known active metabolites
113
Meperidine is structurally similar to which compound?
Atropine
114
What happens to Meperidine after demethylation in the liver?
It is partially metabolized to normeperidine
115
What effect can accumulation of normeperidine lead to?
CNS excitation characterized by tremors, muscle twitches, and seizures
116
What can significant drug interactions between Meperidine and MAO inhibitors lead to?
Hyperthermia, seizures, and death
117
What is one of the effects of Meperidine besides analgesia?
Reducing shivering
118
What has caused the decline in the use of Meperidine?
Availability of safer and more convenient techniques
119
What is the potency of Alfentanil compared to morphine?
Approximately 10-25 times more potent than morphine
120
What is the potency of Fentanyl compared to morphine?
About 50-100 times more potent than morphine
121
How much stronger is Hydromorphone compared to morphine?
Roughly 5-7 times stronger than morphine
122
What is the potency ratio of Meperidine to morphine?
Generally considered less potent than morphine, with a ratio of about 1:10
123
What is the potency of Remifentanil compared to morphine?
Extremely potent, with estimates ranging from 100-200 times more potent than morphine
124
How potent is Sufentanil compared to morphine?
Around 500-1000 times more potent than morphine
125
How does Alfentanil compare to Fentanyl in terms of potency?
Approximately 1/5 to 1/10 as potent as fentanyl
126
What is the potency of Hydromorphone relative to Fentanyl?
Around 1/10 to 1/20 as potent as fentanyl
127
How does Meperidine compare to Fentanyl in potency?
Significantly less potent than fentanyl, approximately 1/75 to 1/100 as potent
128
What is the general potency of Morphine compared to Fentanyl?
About 1/50 to 1/100 as potent as fentanyl
129
How does Remifentanil's potency compare to Fentanyl?
Roughly equivalent to fentanyl in potency
130
How much more potent is Sufentanil compared to Fentanyl?
About 5 to 10 times more potent than fentanyl
131
What type of opioid is Buprenorphine?
A potent partial agonist opioid
132
What is the duration of action for Buprenorphine?
Approximately 8 hours
133
What is a unique feature of Buprenorphine regarding respiratory depression?
Exhibits a ceiling effect for respiratory depression
134
What is Butorphanol's mechanism of action?
Acts as an agonist at kappa receptors and a weak antagonist at mu receptors
135
What is the clinical use of Butorphanol?
Used for migraine headaches and postoperative pain
136
What is Nalbuphine's effect on opioid receptors?
Acts as both an agonist and an antagonist at opioid receptors
137
What is the analgesic response of Nalbuphine compared to morphine?
Equal to that of morphine
138
What is Naloxone?
A pure opioid antagonist
139
What is the action of Naloxone?
Blocks opioid receptor sites, reversing respiratory depression and opioid analgesia
140
What is the duration of action of Naloxone?
Less than that of most opioid agonists
141
What is the primary use of Naltrexone?
Used in alcohol use disorder programs
142
What is the duration of action for Naltrexone?
Approximately 24 hours
143
What is a key characteristic of Nalmefene?
A long-acting parenteral opioid antagonist
144
What is the elimination half-life of Nalmefene?
Approximately 10 hours
145
What is the primary use of Ketorolac?
An intravenous nonsteroidal anti-inflammatory drug (NSAID) for mild to moderate pain
146
What are the advantages of Ketorolac over opioids?
Lack of significant GI and cardiovascular side effects
147
What is the usual dose of Ibuprofen administered intravenously?
400 to 800 mg over 30 minutes
148
What is Acetaminophen's mechanism of action?
Believed to involve central inhibition of prostaglandin synthesis
149
What is a significant concern with high doses of Acetaminophen?
Hepatotoxicity
150
What is the primary action of both Ketorolac and Ibuprofen?
Inhibiting cyclooxygenase enzymes
151
What factors affect Inspiratory Concentration (FI)?
Fresh gas flow rate, breathing system volume, circuit absorption
152
What is the effect of a higher fresh gas flow rate on inspiratory concentration?
Leads to a closer match between inspired gas concentration and fresh gas concentration
153
What happens to alveolar concentrations during induction?
Lag behind due to uptake by pulmonary circulation
154
What is the impact of lower absorption by the machine or breathing circuit?
Helps maintain inspired gas concentration closer to fresh gas concentration.
155
What happens to alveolar concentrations during induction of anesthetics?
They lag behind inspired concentrations due to uptake by pulmonary circulation.
156
How does solubility in blood affect anesthetic uptake?
Insoluble agents like nitrous oxide are taken up less avidly than more soluble agents like sevoflurane.
157
What effect does increased cardiac output have on anesthetic uptake?
Increases anesthetic uptake, slowing the rise in alveolar partial pressure and delaying induction.
158
What is the partial pressure difference in anesthetic uptake?
The gradient between alveolar gas and venous blood, which affects pulmonary circulation uptake.
159
What causes the arterial partial pressure to be less than expected?
Venous admixture, alveolar dead space, and nonuniform alveolar gas distribution.
160
What is the concentration effect in anesthesia?
Increasing inspired concentration not only increases alveolar concentration but also its rate of rise.
161
What is the primary route for elimination of inhalation anesthetics?
Through the alveolar membrane.
162
What is the recommended practice to prevent diffusion hypoxia after nitrous oxide?
Administer 100% oxygen for 5 to 10 minutes after discontinuing nitrous oxide.
163
What role does biotransformation play in anesthetic elimination?
It accounts for a minimal increase in rate of decline of alveolar partial pressure but has a greater impact on soluble anesthetics.
164
What factors speed recovery from anesthesia?
Elimination of rebreathing, high fresh gas flows, low circuit volume, low absorption, decreased solubility, high cerebral blood flow, increased ventilation.
165
What is diffusion hypoxia?
A relative state of hypoxia due to dilution of oxygen and carbon dioxide concentrations from rapid exhalation of nitrous oxide.
166
What are the physical properties of nitrous oxide?
Gas at room temperature, can be kept as liquid under pressure, relatively inexpensive.
167
What cardiovascular effects does nitrous oxide have?
Stimulates sympathetic nervous system, potentially unmasking myocardial depression in certain patients.
168
What are the respiratory effects of nitrous oxide?
Increases respiratory rate, decreases tidal volume, and significantly depresses hypoxic drive.
169
What cerebral effects does nitrous oxide have?
Increases cerebral blood flow and volume, mildly elevating intracranial pressure.
170
What neuromuscular effects does nitrous oxide have?
Does not provide significant muscle relaxation and can cause rigidity at high concentrations.
171
How does nitrous oxide affect kidney and hepatic blood flow?
Decreases kidney blood flow and glomerular filtration rate, may reduce hepatic blood flow.
172
What is the biotransformation and toxicity of nitrous oxide?
Primarily eliminated by exhalation; can oxidize cobalt in vitamin B12, inhibiting dependent enzymes.
173
What are the drug interactions with nitrous oxide?
Often used with more potent volatile agents, reducing their required concentrations.
174
In which conditions is nitrous oxide contraindicated?
Pneumothorax, bowel distention, or intracranial air.
175
What is Minimum Alveolar Concentration (MAC)?
The alveolar concentration of an inhaled anesthetic that prevents movement in 50% of patients.
176
What is a limitation of MAC in clinical practice?
It is a median value and has limited utility during periods of rapidly changing alveolar concentrations.
177
How are MAC values for combinations of anesthetic agents characterized?
They are roughly additive.
178
What factors influence MAC?
Physiological and pharmacological variables, including a 6% decrease per decade of age.
179
What are the cardiovascular effects of isoflurane?
Dilates coronary arteries, may unmask myocardial depression.
180
What are the respiratory effects of isoflurane?
Causes respiratory depression, less pronounced tachypnea, good bronchodilator.
181
What cerebral effects does isoflurane have?
Increases cerebral blood flow and intracranial pressure at concentrations greater than 1 MAC.
182
What neuromuscular effects does isoflurane provide?
Provides muscle relaxation.
183
What renal and hepatic effects does isoflurane have?
Decreases renal blood flow and may reduce total hepatic blood flow.
184
What is the primary cardiovascular effect of isoflurane?
Decreases systemic vascular resistance and arterial blood pressure
## Footnote
Isoflurane mildly depresses myocardial contractility.
185
What respiratory effect does isoflurane have?
Depresses respiration and acts as a bronchodilator
## Footnote
Less pronounced tachypnea.
186
What are the cerebral effects of isoflurane at concentrations greater than 1 MAC?
Increases cerebral blood flow (CBF) and intracranial pressure
## Footnote
Cerebral vasculature remains responsive to Paco2 changes.
187
What neuromuscular effect does isoflurane provide?
Provides muscle relaxation.
188
How does isoflurane affect renal and hepatic blood flow?
Decreases renal blood flow and may reduce total hepatic blood flow, but maintains hepatic oxygen supply.
189
What is the biotransformation product of isoflurane?
Metabolized to trifluoroacetic acid.
190
What is the toxicity risk associated with isoflurane?
Limited oxidative metabolism minimizes hepatic dysfunction risk.
191
What are the cardiovascular effects of desflurane?
Similar to isoflurane, with a decline in systemic vascular resistance and arterial blood pressure.
192
What is a notable respiratory effect of desflurane?
Airway irritant.
193
How does desflurane affect cerebral blood flow?
Increases CBF and intracranial pressure; cerebral vasculature remains responsive to Paco2 changes.
194
What neuromuscular effect is associated with desflurane?
Dose-dependent decrease in response to peripheral nerve stimulation.
195
What renal and hepatic effects does desflurane have?
Does not cause significant nephrotoxic effects; hepatic function tests generally unaffected.
196
How is desflurane metabolized?
Undergoes minimal metabolism; degraded by desiccated CO2 absorbent into carbon monoxide.
197
What are the contraindications and drug interactions for desflurane?
Shares contraindications with other volatile anesthetics; potentiates nondepolarizing neuromuscular blocking agents (NMBAs).
198
What are the cardiovascular effects of sevoflurane?
Mildly depresses myocardial contractility; causes a slight decline in systemic vascular resistance and arterial blood pressure.
199
What respiratory effects does sevoflurane have?
Depresses respiration and reverses bronchospasm.
200
What are the cerebral effects of sevoflurane?
Causes slight increases in CBF and intracranial pressure; high concentrations may impair CBF autoregulation.
201
What neuromuscular effects does sevoflurane provide?
Produces adequate muscle relaxation for intubation.
202
How does sevoflurane affect renal and hepatic blood flow?
Slightly decreases renal blood flow; maintains total hepatic blood flow and oxygen delivery.
203
What is the biotransformation rate of sevoflurane?
Metabolized at a rate lower than halothane but higher than isoflurane or desflurane.
204
What toxic byproducts can sevoflurane degrade into?
Nephrotoxic compound A and hydrogen fluoride.
205
What are the shared contraindications among isoflurane, desflurane, and sevoflurane?
Similar contraindications to other volatile anesthetics; potentiates NMBAs without sensitizing the heart to catecholamine-induced arrhythmias.
206
What does a single twitch test assess?
Qualitative assessment of neuromuscular function.
207
What does Train-of-Four (TOF) consist of?
Four twitches at 2 Hz every 0.5 seconds for 2 seconds.
208
What does a double-burst stimulation (DBS) test involve?
Two short bursts of 50-Hz tetanus separated by 0.75 seconds.
209
What is the purpose of the tetanus test?
Rapid delivery of a 30, 50, or 100-Hz stimulus for deep block assessment.
210
What does Posttetanic Count (PTC) involve?
50-Hz tetanus for 5 seconds, followed by a 3-second pause and single twitches of 1 Hz.
211
Which nerve is preferred for determining the level of neuromuscular blockade?
Ulnar nerve.
212
What is the significance of the facial nerve in neuromuscular monitoring?
Used when access to the arm is not practical.
213
What is the minimum tidal volume necessary to assess neuromuscular function?
At least 5 mL/kg.
214
What does a single-twitch strength indicate?
Should be qualitatively as strong as baseline, indicating 75-80% receptor occupancy.
215
What does no palpable fade in TOF suggest?
70-75% receptor occupancy.
216
What is the definition of TOF?
Delivering four separate stimuli at a frequency of 2 Hz every 0.5 seconds for a total duration of 2 seconds.
217
How is the TOF ratio (TOFR) calculated?
The size of the fourth twitch (T4) is compared to the first twitch (T1).
218
What does the disappearance of T4 indicate?
A block of 75% to 80%.
219
What does the absence of T4 and T3 suggest?
An 80% to 85% block.
220
What does the absence of T4, T3, and T2 indicate?
A 90% to 95% neuromuscular block.
221
What signifies 100% paralysis?
No responses can be elicited.
222
What is the importance of TOF monitoring in clinical practice?
Avoiding residual paralysis and ensuring patient safety.
223
What is the chemical structure of succinylcholine?
Formed by the joining of two acetylcholine (ACh) molecules; chemical formula C14H30N2O4.
224
What is the significance of the quaternary ammonium structure in succinylcholine?
Makes it water-soluble in the body and prevents it from passing the blood-brain barrier.
225
What is the onset time for succinylcholine?
Effects usually within 3 minutes after administration.
226
What is the clinical duration of succinylcholine?
5 to 10 minutes.
227
How is succinylcholine metabolized?
Hydrolyzed by plasma cholinesterases into succinylmonocholine and choline.
228
What is the recommended dosage for succinylcholine?
A bolus of 0.5 to 1.5 mg/kg for adequate adult paralysis.
229
What is the injected dose range for succinylcholine?
0.5 to 1.5 mg/kg
## Footnote
This bolus is recommended for adequate adult paralysis and relaxation for intubation.
230
What is the effective dose for 95% of the population (ED95) of succinylcholine?
Approximately 0.30 mg/kg
## Footnote
This is the effective dose for achieving the desired neuromuscular block.
231
Does succinylcholine pass the blood-brain barrier?
No
## Footnote
Succinylcholine does not have direct CNS effects but can indirectly increase intracranial pressure.
232
What cardiovascular effects can succinylcholine cause?
* Slight tachycardia
* Bradycardia
* Various types of arrhythmias
## Footnote
These effects may vary, especially in children or with repeated dosing in adults.
233
How is succinylcholine metabolized?
By plasma cholinesterase produced in the liver
## Footnote
Liver damage may prolong the effects of the drug.
234
Is succinylcholine contraindicated in patients with elevated preoperative potassium levels?
Yes
## Footnote
Elevated potassium levels can lead to complications.
235
What is the recommended dose of succinylcholine for obese patients?
1.0 mg/kg based on total body weight
## Footnote
There is no contraindication for use in obese patients.
236
In which group of patients should succinylcholine be used only in emergency situations?
Children under 8 years old
## Footnote
Routine intubation is not recommended due to risks of cardiac arrest from hyperkalemic rhabdomyolysis.
237
What common side effect is associated with succinylcholine administration?
Myalgias and fasciculations
## Footnote
Postoperative muscle pain can occur, especially in certain muscle groups.
238
What condition is absolutely contraindicated for the use of succinylcholine?
Malignant Hyperthermia (MH)
## Footnote
MH is a pharmacogenetic skeletal muscle disorder triggered by certain anesthetics.
239
What genetic variants can affect the response to succinylcholine?
* Fluoride-resistant (F)
* Silent (S)
* K variants
## Footnote
These mutations can lead to prolonged response and apnea.
240
What is a Phase II block in relation to succinylcholine?
A desensitization block that occurs with large doses of depolarizing NMBAs
## Footnote
It is characterized by a change in muscle membrane response.
241
What characterizes the transition from Phase I to Phase II block?
The muscle membrane starts to repolarize but becomes less responsive to acetylcholine
## Footnote
This transition affects how the neuromuscular block is managed.
242
What indicates a Phase II block during tetanic or TOF stimulation?
Fade in response
## Footnote
This is different from a Phase I block where there is no fade.
243
How can Phase II blocks often be reversed?
With anticholinesterase drugs
## Footnote
This is not effective for Phase I blocks.
244
What is the elimination half-life of Remifentanil?
8 to 20 minutes
## Footnote
This allows for rapid recovery after discontinuation.
245
What precautions should be taken when administering Remifentanil?
Bolus dosing is not recommended
## Footnote
Due to the potential for respiratory depression and muscle rigidity.
246
What is the commercial preparation of Remifentanil?
A water-soluble, lyophilized powder containing a free base and glycine
## Footnote
It should not be administered epidurally or intrathecally due to potential neurotoxicity.
247
What is Rocuronium?
A neuromuscular blocker used in anesthesia
248
What factors delay the onset times of Rocuronium in elderly patients?
Slower circulation times and other kinetic changes associated with aging
249
What leads to prolonged dosing interval and duration of action of Rocuronium in elderly patients?
Decreased hepatic and renal clearance and increased volume of distribution
250
What special considerations are needed for the use of Rocuronium in obese patients?
Higher risk for gastroesophageal reflux disease and pulmonary aspiration
251
How does Rocuronium's metabolism occur?
Undergoes deacetylation via the liver
252
What is the elimination half-life of Rocuronium in elderly persons?
137 minutes
253
What is the priming technique in the context of Rocuronium?
Giving 10% of the calculated intubating dose before inducing anesthesia
254
What is the protein binding percentage of Rocuronium?
Approximately 46%
255
What is Vecuronium Bromide?
A monoquaternary aminosteroid neuromuscular blocker
256
How does Vecuronium differ in chemical structure from Pancuronium?
Altered from a bisquaternary to a monoquaternary compound
257
What is the potency of Vecuronium compared to Pancuronium?
1.5 times more potent
258
What is the typical induction dose of Vecuronium?
0.1 mg/kg
259
What cardiovascular effects does Vecuronium have at clinical doses?
No significant cardiac effects
260
What is the elimination half-life of Vecuronium in healthy adults?
51 to 90 minutes
261
What effect does hepatic disease have on Vecuronium's elimination half-life?
Prolonged elimination half-life
262
What is Cisatracurium Besylate?
A nondepolarizing muscle relaxant and stereoisomer of atracurium
263
How does Cisatracurium's potency compare to Atracurium?
Three times more potent
264
What is the typical intubating dose of Cisatracurium?
0.1 mg/kg
265
What is the pH range of Cisatracurium solution?
3.25 to 3.65
266
What unique elimination process does Cisatracurium undergo?
Hofmann elimination and ester hydrolysis
267
What advantage does Cisatracurium offer in patients with renal or hepatic impairment?
Nonorgan-dependent elimination
268
What is the duration of action of Vecuronium after a dose of 0.1 mg/kg?
36.2 ± 6.4 minutes
269
How does aging affect Cisatracurium's kinetics?
Not significantly changed in elderly patients
270
What is the main reason for preferring Cisatracurium in obese patients?
Lack of histamine release and reliable kinetics
271
What is succinylcholine used for?
It is given according to total body weight.
272
What is the elimination mechanism of Cisatracurium?
It undergoes Hofmann elimination and nonspecific esterases.
273
What percentage of total body clearance of Cisatracurium is due to Hofmann elimination?
77%
274
What is the half-life of Cisatracurium?
Approximately 26 to 36 minutes.
275
How does the response to neuromuscular blocking agents (NMBAs) differ in pediatrics compared to adults?
There are several differences in sensitivity and neuromuscular junction maturity.
276
What is the chemical structure classification of Atracurium?
It is classified as a benzylisoquinoline.
277
What is the degradation rate of Atracurium when refrigerated at 5°C?
6% per year.
278
What is the recommended shelf life of Atracurium when unrefrigerated?
14 days.
279
What is the ED95 of Atracurium?
0.10 to 0.25 mg/kg.
280
What is the onset time of Atracurium related to dosage?
Inversely proportional.
281
What is the average duration of action for Atracurium?
30 to 60 minutes.
282
What happens during Hofmann elimination of Atracurium?
Temperature- and pH-dependent breakdown occurs.
283
What are the primary metabolites of Atracurium excreted in?
Bile and urine.
284
What cardiovascular effects can Atracurium cause?
Histamine release leading to hypotension and tachycardia.
285
Does aging affect the duration of Atracurium and Cisatracurium?
No, it is not affected by aging.
286
How does Atracurium perform in obese patients compared to normal weight patients?
No differences in recovery indices or times.
287
What is the role of Neostigmine in reversal of neuromuscular blockade?
It is the most commonly used anticholinesterase agent.
288
What is a key consideration when administering Neostigmine?
Ensure a TOF count of at least 4 before administration.
289
What is Sugammadex known for?
High efficacy in reversing neuromuscular blockade.
290
What factors influence postoperative residual neuromuscular blockade?
* Type of anesthesia used
* Type and dose of NMBD administered
* Type and dose of reversal drug
* Duration of anesthesia
* Use of neuromuscular monitoring
* Patient factors
291
What is the mechanism of action for cholinesterase inhibitors?
They inhibit acetylcholinesterase, increasing endogenous ACh concentration.
292
How do Edrophonium and Neostigmine differ in their action?
* Edrophonium: reversible inhibitor, short duration
* Neostigmine: forms stable carbamyl-ester complex
293
What is the clinical application of cholinesterase inhibitors?
Reversal of neuromuscular blockade by increasing ACh concentration.
294
What is the mechanism of action of Neostigmine?
Neostigmine forms a carbamyl-ester complex at the esteratic site of cholinesterase, preventing hydrolysis of acetylcholine (ACh)
## Footnote
Neostigmine degrades similarly to the acetylcholine-cholinesterase complex.
295
What is the elimination half-life of Neostigmine?
70 to 80 minutes, increasing to 181 to 183 minutes in anephric patients
## Footnote
This indicates the time it takes for the concentration of Neostigmine in the bloodstream to reduce by half.
296
What is the common clinical application of Neostigmine?
Reversal of neuromuscular blockade
## Footnote
It increases the concentration of endogenous ACh around cholinoreceptors.
297
What is the recommended dose range for Neostigmine?
25-75 mcg/kg
## Footnote
It is important to adjust dosage based on the patient's condition.
298
True or False: Neostigmine can reverse deep neuromuscular blockade.
False
## Footnote
Administration in such cases can lead to incomplete reversal.
299
What is the clearance rate of Sugammadex?
Approximately 120 L/min
## Footnote
This indicates how quickly Sugammadex is eliminated from the body.
300
What is the recommended dosage of Sugammadex for spontaneous recovery of the second twitch?
2 mg/kg
## Footnote
This is for when recovery has reached the reappearance of the second twitch in response to TOF stimulation.
301
List some common adverse effects of Sugammadex.
* Nausea
* Vomiting
* Allergy
* Hypertension
* Headache
## Footnote
Anaphylaxis has also been reported, which initially delayed FDA approval.
302
What special consideration should be made for women of childbearing age after exposure to Sugammadex?
They should use alternative contraceptive methods for 1 week
## Footnote
Sugammadex binds oral contraceptives.
303
What are the effects of anticholinergics like Atropine?
Prevent parasympathomimetic side effects of anticholinesterase drugs
## Footnote
These effects include bradycardia, hypotension, and increased postoperative nausea.
304
What is the usual recommended dose of Atropine with Edrophonium?
7 mcg/kg
## Footnote
Atropine acts faster than Glycopyrrolate.
305
What is Glycopyrrolate's primary route of excretion?
Primarily in feces and urine, mostly as unchanged drug
## Footnote
It has limited gastrointestinal absorption due to its ionization.
306
What is the recommended dose range for Glycopyrrolate?
10-20 mcg/kg
## Footnote
It is often administered with neostigmine to prevent muscarinic effects.
307
What is the pharmacological classification of Ephedrine?
Synthetic noncatecholamine sympathomimetic
## Footnote
It stimulates both alpha and beta receptors.
308
What is the duration of action of Ephedrine?
15 minutes to 1.5 hours, depending on the dose
## Footnote
This is important for managing hypotension during anesthesia.
309
True or False: Ephedrine significantly increases serum glucose concentrations.
False
## Footnote
It has moderate effects compared to epinephrine.
310
What should be considered when using Ephedrine in patients with questionable coronary perfusion?
It can dramatically increase myocardial oxygen consumption
## Footnote
Caution is advised due to potential adverse cardiovascular effects.
311
What is the effect of ephedrine on myocardial oxygen consumption?
It can dramatically increase myocardial oxygen consumption.
312
What is the primary pharmacological action of phenylephrine?
Phenylephrine is a pure alpha-agonist with strong alpha-stimulating effects.
313
What are the clinical applications of phenylephrine?
* Prevention of nosebleeds during nasal intubation
* Reducing bleeding during ear, nose, and throat surgery
* Mydriatic in ophthalmology
* Addressing maternal hypotension after regional anesthesia
314
What is the usual IV dosage for phenylephrine?
Careful titration is necessary to avoid large changes in blood pressure.
315
What is the onset and duration of action for intravenous phenylephrine?
Immediate onset with a duration ranging from 5 to 20 minutes.
316
What is the primary pharmacological property of esmolol?
Esmolol is a beta-blocker with a rapid onset and short duration of action.
317
What is the elimination half-life of esmolol?
Approximately 9 minutes.
318
What is the recommended IV loading dose of esmolol?
500 mcg/kg followed by an infusion of 100 to 300 mcg/kg/min as needed.
319
What are the clinical applications of metoprolol?
* After myocardial infarction (MI)
* In some types of angina and hypertension once the patient is stable
320
What is the usual IV administration for metoprolol?
5 mg doses at 5-minute intervals to a maximum dose of 15 mg.
321
What is the unique property of labetalol compared to standard beta-blockers?
Labetalol possesses an alpha-blocking component along with beta-blockade.
322
What is the typical IV dose of labetalol?
0.25 mg/kg, which can be repeated every few minutes as indicated.
323
What are the three anticholinergics used in anesthesia practice?
* Atropine
* Scopolamine
* Glycopyrrolate
324
What is the usual adult IV dose of atropine for increasing heart rate during anesthesia?
0.4 to 0.6 mg.
325
What is the duration of action for a scopolamine patch applied before anesthesia?
3 days.
326
What is the mechanism of action for cefazolin?
Cefazolin works primarily via time-dependent killing.
327
What is the usual adult dosage of cefazolin for surgical procedures?
2g IV.
328
What are the considerations for redosing cefazolin during surgery?
Additional doses should be given at intervals of about two times the half-life of the drug (every 4 hours).
329
What is the recommended dose of dexamethasone for PONV prevention?
4 mg IV after anesthesia induction.
330
What is the mechanism of action of dexamethasone for PONV prevention?
May involve central inhibition of the nucleus tractus solitarius, reduction of serotonin in the CNS, and inhibition of prostaglandin synthesis.
331
What is the recommended dose of a specific antiemetic after anesthesia induction?
4 mg IV, with some clinicians preferring 8 mg IV
## Footnote
The specific antiemetic is not named but refers to a commonly used medication in PONV prophylaxis.
332
What is the duration of action for the recommended antiemetic?
Approximately 72 hours
## Footnote
This duration indicates the effectiveness of the antiemetic in preventing PONV.
333
What is the mechanism of action of the recommended antiemetic?
Unclear, but may involve:
* Central inhibition of the nucleus tractus solitarius
* Reduction of serotonin in the CNS
* Inhibition of prostaglandin synthesis
334
What potential side effects can the recommended antiemetic cause in certain patients?
Can increase blood glucose in patients with:
* Impaired glucose tolerance
* Type 2 diabetes
* Obesity
335
What is the standard dose of Ondansetron for PONV?
4 mg IV at the end of the procedure
## Footnote
Ondansetron is a 5-HT3 receptor antagonist.
336
What are the notable characteristics of Ondansetron?
More effective for vomiting than nausea, known for minimal side effects
## Footnote
Higher doses can affect the QT interval.
337
What is a limitation of Ondansetron's effectiveness?
Short duration of action (4-6 hours) limits effectiveness for PDNV
338
Which drug is preferable for Post Discharge Nausea and Vomiting (PDNV)?
Palonosetron
## Footnote
Palonosetron has a longer half-life of 44 hours.
339
Name two examples of Neurokinin 1 Receptor Antagonists.
Aprepitant and fosaprepitant
## Footnote
Other examples include netupitant/palonosetron and rolapitant.
340
What is the primary action of Aprepitant?
Suppresses activity at the NST, where vagal afferents from the GI tract converge with brain inputs that initiate emesis
341
What is the primary method of elimination for Rocuronium?
Biliary elimination of unchanged drug
## Footnote
Renal excretion accounts for 33% of elimination.
342
What is the intubating dose range for Rocuronium?
0.6 to 1.2 mg/kg
## Footnote
This dosage provides good to excellent intubating conditions within 45 to 90 seconds.
343
What adverse effects may Droperidol cause?
Extrapyramidal side effects
## Footnote
Droperidol is contraindicated in Parkinson's disease.
344
What is the action of Rocuronium?
Competes with acetylcholine for binding to nicotinic receptors at the motor endplate, leading to muscle relaxation
345
What is a key characteristic of Rocuronium's pharmacokinetics?
Rapid onset, making it suitable for rapid sequence intubation (RSI)
346
What is the impact of hepatic disease on Rocuronium's duration of action?
Prolonged duration of action in patients with hepatic disease
347
What is the role of Midazolam in antiemetic therapy?
Decreases dopamine's emetic effect in the chemoreceptor trigger zone
348
What is the significance of using multimodal PONV and PDNV prophylaxis?
Should be considered for patients at moderate to high risk
349
True or False: Rescue therapy for PONV should come from the same therapeutic class as prophylactic drugs.
False
350
Fill in the blank: Rocuronium bromide is a ______ neuromuscular blocker.
monquaternary aminosteroid
351
What side effects are associated with Transdermal Scopolamine?
Sedation, blurred vision, dizziness, dry mouth
352
What is the half-life of Rocuronium?
60 to 120 minutes
353
What is the recommended combination for children at moderate or high risk for PONV?
Combination therapy using a 5-HT3 antagonist and a second drug
