Week 7 Flashcards
(337 cards)
1
Q
What is the goal of the Induction Phase in anesthesia?
A
Unconsciousness by administering IV or inhalational agents.
2
Q
What should be monitored closely during the Induction Phase?
A
Vitals.
3
Q
What are the complications of the Induction Phase?
A
Hypotension and airway obstruction.
4
Q
What is the goal of the Maintenance Phase in anesthesia?
A
Steady anesthesia, pain control, and homeostasis.
5
Q
How are agents managed during the Maintenance Phase?
A
Agents are titrated to needs with continuous monitoring.
6
Q
What is the goal of the Emergence Phase in anesthesia?
A
Wake-up safely.
7
Q
What is done during the Emergence Phase?
A
Taper anesthetics and monitor for delirium, pain, and nausea/vomiting.
8
Q
What are the 4 A’s in anesthesia?
A
Analgesia, Amnesia, Areflexia, Anxiolysis.
9
Q
What type of agent is Dexmedetomidine?
A
Alpha-2 agonist.
10
Q
What are the effects of Dexmedetomidine?
A
Sedation, analgesia, anxiolysis, sympatholysis, and decreased shivering.
11
Q
What cardiovascular effects can Dexmedetomidine cause?
A
Bradycardia and hypotension; rapid loading may cause hypertension.
12
Q
What is the respiratory effect of Dexmedetomidine?
A
No respiratory depression; good for COPD/asthma.
13
Q
What is the dosing for Dexmedetomidine?
A
Load 1 µg/kg over 10 min, then 0.2–0.7 µg/kg/hr.
14
Q
What is the onset of action for Dexmedetomidine?
A
10 to 20 minutes.
15
Q
What is the duration of action after stopping Dexmedetomidine infusion?
A
10 to 30 minutes.
16
Q
What type of agent is Etomidate?
A
GABA agonist.
17
Q
What are the benefits of using Etomidate?
A
Good for cardiovascular stability.
18
Q
What are the side effects of Etomidate?
A
Adrenal suppression, myoclonus, pain on injection, and nausea/vomiting.
19
Q
What is the dosing for Etomidate?
A
0.2–0.3 mg/kg IV.
20
Q
What is the terminal half-life of Etomidate?
A
2 to 5 hours.
21
Q
What is the awakening time after Etomidate bolus administration?
A
5 to 15 minutes.
22
Q
What type of agent is Ketamine?
A
NMDA antagonist.
23
Q
What is the primary analgesic site for Ketamine?
A
Thalamoneocortical system.
24
Q
What are the effects of Ketamine?
A
Analgesia and dissociative anesthesia.
25
What cardiovascular effects does Ketamine have?
Increases heart rate, blood pressure, cardiac output, and central venous pressure.
26
What are the side effects of Ketamine?
Emergence delirium, increased secretions, vivid illusions, and disturbances.
27
What is the metabolism process for Ketamine?
Demethylation by the cytochrome P-450 system to form norketamine.
28
What is the induction dosing for Ketamine?
2–4 mg/kg IV, 4–6 mg/kg IM.
29
What is the infusion dosing for Ketamine?
15–45 µg/kg/min.
30
What is the bolus dosing for sedation and analgesia with Ketamine?
0.2-0.8 mg/kg IV over 2-3 min.
31
What caution should be taken with Ketamine?
Increased intracranial pressure and decreased seizure threshold.
32
What is Propofol?
A GABA_A agonist with rapid onset/offset, antiemetic properties, and causes amnesia.
33
What are the effects of Propofol on cerebral blood flow and intracranial pressure?
It decreases cerebral blood flow (CBF), intracranial pressure (ICP), and blood pressure (BP), and can cause dose-dependent apnea/respiratory depression.
34
What cardiovascular effects does Propofol have?
It can cause hypotension, especially in older patients or those with hypovolemia.
35
What is the half-life of Propofol?
1-2 hours.
36
What is the dosing for induction of Propofol?
1–2 mg/kg.
37
What is the dosing for Propofol infusion?
100–200 µg/kg/min for general use and 25–75 µg/kg/min for conscious sedation.
38
What are the clinical uses of Propofol?
Used in general anesthesia and ECT (reduces seizure threshold), and to manage status epilepticus.
39
What is a significant risk when using Propofol during cesarean delivery?
It easily crosses the placental barrier, leading to sedative effects in the neonate and lower Apgar scores.
40
What are the contraindications for Propofol?
Avoid in patients with egg/soy allergy and disorders of fat metabolism.
41
What is Propofol Infusion Syndrome?
A risk associated with Propofol that includes metabolic acidosis, hyperkalemia, lipidemia disorders, hepatomegaly, and elevated liver transaminases.
42
What is Midazolam?
A benzodiazepine and GABA modulator with rapid onset and short duration.
43
What are the effects of Midazolam?
Provides anxiolysis, anterograde amnesia, sedation, anticonvulsant effects, and increases seizure threshold.
44
What is the most common adverse effect of Midazolam?
Respiratory depression, especially when combined with opioids.
45
What is the reversal agent for Midazolam?
Flumazenil, which has an onset of 1–2 minutes and a duration of 45–90 minutes.
46
What are the CNS effects of opioids?
They inhibit ascending nociceptive signals in the spinal dorsal horn and activate descending pain inhibition pathways from the midbrain.
47
What is the effect of opioids on respiratory function?
They cause dose-dependent respiratory depression via mu & delta receptors in the brainstem.
48
What causes miosis (pinpoint pupils) in opioid use?
Inhibition of GABA interneurons, which disinhibits the Edinger-Westphal nucleus.
49
What are the antitussive effects of opioids?
They depress the medullary cough center, useful for suppressing reflex coughing during anesthesia.
50
How do opioids affect nausea and vomiting?
They stimulate the chemoreceptor trigger zone (CTZ) in the area postrema, involving 5-HT3 and D2 receptors.
51
What cardiovascular effects do opioids have?
They can cause bradycardia due to vagal stimulation and dose-dependent vasodilation, potentially leading to hypotension.
52
What is a common effect of high doses of opioids?
Muscle rigidity, which may impair ventilation.
53
What is pruritus in the context of opioid use?
Common with neuraxial opioids, especially morphine, and is not histamine-related.
54
What are the gastrointestinal effects of opioids?
They decrease GI motility, leading to constipation, and can cause urinary retention.
55
What endocrine effects do opioids have?
They stimulate vasopressin release and inhibit stress-induced corticotropin & gonadotropin release.
56
What is the use of neuraxial opioids?
Administered intrathecally or epidurally for analgesia, with side effects including pruritus and urinary retention.
57
What is morphine?
A natural opioid and the most abundant alkaloid in raw opium.
58
What type of pain is morphine more effective for?
Moderate to severe pain, particularly continuous dull pain.
59
What are the routes of administration for morphine?
Intramuscular, intravenous, subcutaneous, oral, intrathecal, and epidural.
60
What is the onset and peak time for IV morphine?
Onset: 20 min; Peak: 30-60 min.
61
What is the typical dose range for IV morphine?
0.05–0.15 mg/kg.
62
What is a notable side effect of morphine?
Histamine release leading to hypotension.
63
What caution is advised with morphine?
Caution in renal failure due to the active metabolite M6G.
64
What is fentanyl known for?
Profound dose-dependent analgesia, ventilatory depression, and sedation.
65
What is the onset and duration of fentanyl?
Fast onset/short duration (20-40 mins).
66
What is a key characteristic of fentanyl regarding histamine?
No histamine release.
67
What is the typical intraoperative dose of fentanyl?
2-50 mcg/kg IV.
68
What is the transdermal dose range for fentanyl?
25–100 mcg/hr for 24 to 72 hours.
69
What is hydromorphone?
A semisynthetic opioid, 5–7× more potent than morphine.
70
What is the onset of action for hydromorphone?
15 - 30 minutes.
71
What is the duration of action for hydromorphone?
4 – 5 hours.
72
What is the half-life of hydromorphone?
1 - 3 hours.
73
What is the typical dose range for IV hydromorphone?
0.01–0.02 mg/kg.
74
Why is hydromorphone considered safer in renal failure?
It has no active metabolites.
75
What type of agonist is Meperidine?
Synthetic mu agonist (Atropine-like = antispasmodic), ↓shivering (kappa agonist)
76
What is the toxic metabolite of Meperidine?
Normeperidine (longer than parent) → seizures (lowers the threshold, induces CNS excitability)
## Footnote
Leads to CNS excitation characterized by tremors, muscle twitches, and seizures.
77
In which patients should Meperidine be avoided?
Avoid in renal failure, elderly, and chronic use in cancer patients who may require high doses = risk of accumulation.
78
What drug interaction is associated with Meperidine?
MAOIs → serotonin syndrome: hyperthermia, seizures and death.
79
What is the dosing range for Meperidine when used for shivering?
12.5–25 mg IV for shivering.
80
What is the metabolism characteristic of Remifentanil?
Moderate lipophilic, Ester link metabolism (blood/tissue esterases) metabolized by hydrolysis.
81
What is the duration of action for Remifentanil?
Ultra-short acting (T½: 8–20 min).
82
What should be done after using Remifentanil?
Must transition to long-acting opioid.
83
What is the risk of bolus administration of Remifentanil?
Avoid bolus: causes apnea/rigidity.
84
How should Remifentanil be administered?
Use in infusion only; due to potential glycine neurotoxicity, Remifentanil should not be administered epidurally or intrathecally.
85
What is a key characteristic of Alfentanil?
Rapid onset, short duration than fentanyl.
86
Is Alfentanil effective for epidural use?
Effective epidurally.
87
What effect does Erythromycin have on Alfentanil?
Erythromycin has been shown to prolong the metabolism.
88
When is Alfentanil useful?
Useful for brief painful stimuli (e.g., block placement).
89
What is a notable interaction with Alfentanil?
Variable response; interacts with erythromycin.
90
Opioid potency relative to Morphine: Sufentanil
500–1000× more potent
## Footnote
Highest potency among opioids.
91
Opioid potency relative to Morphine: Remifentanil
100–200× more potent
## Footnote
Significant potency.
92
Opioid potency relative to Morphine: Fentanyl
50–100× more potent
## Footnote
Commonly used in pain management.
93
Opioid potency relative to Morphine: Alfentanil
10–25× more potent
## Footnote
Moderate potency.
94
Opioid potency relative to Morphine: Hydromorphone
5–7× more potent
## Footnote
Effective for severe pain.
95
Opioid potency relative to Morphine: Morphine
Reference (1×)
## Footnote
Standard for comparison.
96
Opioid potency relative to Morphine: Meperidine
~1/10× as potent (weaker)
## Footnote
Less effective than morphine.
97
Opioid potency relative to Fentanyl: Sufentanil
5–10× more potent
## Footnote
Highly potent compared to fentanyl.
98
Opioid potency relative to Fentanyl: Fentanyl
Reference (1×)
## Footnote
Standard for comparison.
99
Opioid potency relative to Fentanyl: Remifentanil
~Equal potency, much shorter duration
## Footnote
Quick onset and offset.
100
Opioid potency relative to Fentanyl: Alfentanil
1/5 to 1/10 as potent
## Footnote
Weaker than fentanyl.
101
Opioid potency relative to Fentanyl: Hydromorphone
1/10 to 1/20 as potent
## Footnote
Less effective compared to fentanyl.
102
Opioid potency relative to Fentanyl: Morphine
1/50 to 1/100 as potent
## Footnote
Significantly weaker than fentanyl.
103
Opioid potency relative to Fentanyl: Meperidine
1/75 to 1/100 as potent
## Footnote
Very weak compared to fentanyl.
104
Buprenorphine
Partial agonist opioid, binds mainly to mu, long duration (8 hrs)
## Footnote
Used in opioid use disorder treatment.
105
Butorphanol
Kappa agonist/weak mu antagonist, can produce more analgesia than morphine
## Footnote
Used for migraines and postop pain.
106
Nalbuphine
Kappa agonist/mu antagonist; analgesia equal to morphine
## Footnote
Ceiling effect for respiratory depression.
107
Naloxone
Pure, competitive antagonist, short duration (30–90 min)
## Footnote
Reverses respiratory depression.
108
Naltrexone
Antagonist similar to Naloxone but with higher oral efficacy
## Footnote
Used for opioid/alcohol addiction.
109
Nalmefene
Long-acting IV antagonist (8–10 hr)
## Footnote
Used in ETOH disorder programs.
110
What is Ketorolac?
IV/IM NSAID inhibiting cyclooxygenase enzymes, good for moderate pain. Avoid in atopic/asthmatic, elderly, renal/GI issues, or bleeding disorders.
111
What is Ibuprofen (Caldolor)?
IV (or common oral) NSAID inhibiting cyclooxygenase enzymes, analgesic and antipyretic. Dosage: 400–800 mg IV over 30 min, duration 4-6 hrs.
112
What is Acetaminophen (Ofirmev)?
Intravenous analgesic and antipyretic drug (NOT NSAID, no anti-inflammatory). Dosage: 1000 mg IV over 15 mins (or 15 mg/kg), opioid-sparing, hepatotoxicity risk (4000mg/day).
113
What factors affect Inspiratory Concentration (FI) of inhaled anesthetics?
↑ Fresh Gas Flow Rate → Faster rise in FI, closer to vaporizer setting.
↓ Breathing Circuit Volume → Faster change in inspired concentration.
↓ Circuit Absorption → Less anesthetic loss to tubing, more delivered to patient.
114
What factors affect Alveolar Concentration (FA)?
↑ Uptake into blood → Slower rise in FA, ↓ FA/FI ratio.
↑ Blood Solubility (e.g., sevoflurane) → Slower FA rise.
↓ Blood Solubility (e.g., nitrous oxide) → Faster FA rise.
↑ Cardiac Output → More uptake → Slower FA rise.
↓ Cardiac Output → Less uptake → Faster FA rise (risk of overdose with soluble agents).
↑ Alveolar-Venous Gradient → Greater uptake → Slower FA rise.
115
What factors affect Arterial Concentration (Fa)?
V/Q Mismatch: ↑ V/Q mismatch → ↑ alveolar-arterial gradient.
↓ Arterial partial pressure despite normal end-expiratory gas.
Especially affects: Poorly soluble agents → ↓ Fa; Highly soluble agents → ↑ alveolar partial pressure.
Concentration Effect: ↑ Inspired concentration (especially with N₂O) → Faster rise in alveolar and arterial concentration (caused by: concentrating effect + augmented inflow).
116
What is the primary route of elimination for inhaled anesthetics?
Exhalation via alveoli is the main elimination route. Nitrous oxide eliminated rapidly → risk of diffusion hypoxia.
## Footnote
Prevent with 100% O₂ for 5–10 min after stopping N₂O.
117
What factors speed up recovery (and induction) of inhaled anesthetics?
High fresh gas flow, low breathing circuit volume, low circuit absorption, ↓ agent solubility, ↑ ventilation, ↑ cerebral blood flow, no rebreathing.
118
What is Diffusion Hypoxia?
A relative hypoxic state that occurs due to the rapid elimination of nitrous oxide (N₂O) when anesthesia is discontinued.
119
What causes Diffusion Hypoxia?
It occurs due to the rapid elimination of nitrous oxide (N₂O) through the alveoli when anesthesia is discontinued.
120
How does N₂O lead to hypoxia?
N₂O diffuses out of the blood quickly and in large volumes, entering the alveoli, which dilutes alveolar oxygen (O₂) and carbon dioxide (CO₂).
121
What are the effects of diluted O₂ and CO₂ due to N₂O?
↓ O₂ concentration leads to potential hypoxia, and ↓ CO₂ concentration results in reduced respiratory drive.
122
How can Diffusion Hypoxia be prevented?
By administering 100% oxygen for 5–10 minutes after discontinuing nitrous oxide.
123
What is Nitrous Oxide (N₂O)?
A gas at room temperature, liquid under pressure, inexpensive and commonly used in anesthesia.
124
What type of receptor does N₂O act on?
N₂O is an NMDA receptor antagonist.
125
What are the environmental concerns associated with N₂O?
N₂O contributes to ozone depletion and is a greenhouse gas.
126
What are the cardiovascular effects of N₂O?
It stimulates the sympathetic nervous system, which can mask myocardial depression.
127
What happens in CAD or hypovolemia with N₂O use?
Cardiac depression may be unmasked.
128
What respiratory effects does N₂O have?
It increases respiratory rate and decreases tidal volume, with no major change in minute ventilation.
129
What cerebral effects are associated with N₂O?
It increases cerebral blood flow (CBF), cerebral blood volume (CBV), and intracranial pressure (ICP).
130
What are the neuromuscular effects of N₂O?
N₂O does not cause muscle relaxation; high doses may cause muscle rigidity.
131
How is N₂O eliminated from the body?
It is primarily eliminated via exhalation, with a small amount through the skin.
132
What risk is associated with prolonged use of N₂O?
It can oxidize cobalt in vitamin B12, inhibiting B12-dependent enzymes, leading to megaloblastic anemia and neuropathy.
133
What are the drug interactions with N₂O?
N₂O is used to lower MAC requirements of other volatile agents and alters anesthetic gas concentrations when passed through a vaporizer.
134
What are the contraindications for N₂O use?
Avoid in air-filled space expansion situations such as pneumothorax, bowel obstruction/distention, inner ear surgery, recent craniotomy with pneumocephalus, and intraocular gas.
135
What is MAC (Minimum Alveolar Concentration)?
MAC = concentration to prevent movement in 50% of patients. Reflects the partial pressure of the anesthetic in the brain.
136
How does MAC change with age?
MAC decreases by 6% per decade of life.
137
What is the significance of 1.3 MAC?
1.3 MAC is approximately 95% no movement (ED95).
138
What does 0.3-0.4 MAC indicate?
0.3-0.4 MAC corresponds to awakening.
139
How do you calculate additive MAC between agents?
For example, 0.5 MAC N₂O + 0.5 MAC sevo = 1 MAC.
140
What are the cardiovascular effects of Isoflurane?
Isoflurane dilates coronary arteries and may cause myocardial depression in vulnerable patients.
141
What are the cardiovascular effects of Desflurane?
Desflurane decreases systemic vascular resistance (SVR) and blood pressure (BP), similar to isoflurane.
142
What are the cardiovascular effects of Sevoflurane?
Sevoflurane causes mild myocardial depression and a slight decrease in SVR and BP.
143
What are the respiratory effects of Isoflurane?
Isoflurane depresses respiration but is a good bronchodilator.
144
What are the respiratory effects of Desflurane?
Desflurane is an airway irritant and not ideal for inhalation induction.
145
What are the respiratory effects of Sevoflurane?
Sevoflurane depresses respiration and reverses bronchospasm like isoflurane.
146
What are the cerebral effects of Isoflurane?
Isoflurane increases cerebral blood flow (CBF) and intracranial pressure (ICP) at >1 MAC.
147
What are the cerebral effects of Desflurane?
Desflurane increases CBF and ICP; autoregulation is preserved with changes in PaCO₂.
148
What are the cerebral effects of Sevoflurane?
Sevoflurane causes mild increases in CBF and ICP and may impair autoregulation at high concentrations.
149
What are the neuromuscular effects of Isoflurane?
Isoflurane provides muscle relaxation.
150
What are the neuromuscular effects of Desflurane?
Desflurane decreases response to peripheral nerve stimulation in a dose-dependent manner.
151
What are the neuromuscular effects of Sevoflurane?
Sevoflurane provides adequate muscle relaxation for intubation.
152
What are the renal/hepatic effects of Isoflurane?
Isoflurane decreases renal blood flow but maintains hepatic oxygen delivery.
153
What are the renal/hepatic effects of Desflurane?
Desflurane has minimal nephrotoxicity, and hepatic function tests remain normal.
154
What are the renal/hepatic effects of Sevoflurane?
Sevoflurane causes slight decreases in renal blood flow while maintaining hepatic blood flow and oxygen delivery.
155
What is the biotransformation of Isoflurane?
Isoflurane has limited metabolism to trifluoroacetic acid.
156
What is the biotransformation of Desflurane?
Desflurane has minimal metabolism and can produce carbon monoxide with dry CO₂ absorbents.
157
What is the biotransformation of Sevoflurane?
Sevoflurane undergoes more metabolism than the others, leading to the production of Compound A and HF (nephrotoxic potential).
158
What are the contraindications and interactions of Isoflurane?
Isoflurane has no unique contraindications but potentiates neuromuscular blocking agents (NMBAs).
159
What are the contraindications and interactions of Desflurane?
Desflurane has similar contraindications to other volatiles and also potentiates NMBAs.
160
What are the contraindications and interactions of Sevoflurane?
Sevoflurane has the same class effects as others, potentiates NMBAs, and does not cause catecholamine sensitization.
161
What is the Single Twitch neuromuscular monitoring test?
One supramaximal electrical stimulus at 0.1–1 Hz. Requires a baseline for comparison and is used for qualitative assessment only.
162
What is the Train-of-Four (TOF) neuromuscular monitoring test?
Four electrical pulses at 2 Hz over 0.5-2 seconds. Reflects 70–100% blockade and is commonly used to assess onset, maintenance, and emergence of blockade.
163
What does no palpable fade in TOF suggest?
No palpable fade suggests approximately 70–75% receptor occupancy.
164
What is the Double-Burst Stimulation (DBS) neuromuscular monitoring test?
Two bursts of 50 Hz tetanus separated by 0.75 seconds. It is better at detecting fade than TOF.
165
What is the Tetanus neuromuscular monitoring test?
Continuous stimulation at 30–100 Hz for 5 seconds. Used for deep block assessment and can be painful; use sparingly in awake patients.
166
What is the Posttetanic Count (PTC) neuromuscular monitoring test?
50-Hz tetanus for 5 seconds followed by a pause and then single twitches at 1 Hz.
167
What is the most commonly used monitoring site for neuromuscular assessment?
The ulnar nerve is the most commonly used and accessible site, stimulating adductor pollicis (thumb movement) and is the best site for assessing recovery.
168
What is an alternative monitoring site when arm access is limited?
The facial nerve is an alternative, monitoring orbicularis oculi (eyelid) or corrugator supercilii (eyebrow).
169
What is the Train of Four (TOF)?
Four supramaximal electrical stimuli delivered at 2 Hz (every 0.5 seconds) over 2 seconds.
170
What does the Train of Four assess?
It assesses the degree or percentage of neuromuscular blockade (NMB).
171
In which paralysis range is TOF most sensitive?
TOF is most sensitive in the 70–100% paralysis range.
172
What does the TOF Ratio (TOFR) compare?
The size of the fourth twitch (T4) is compared to the first twitch (T1).
173
What does it indicate if T4 disappears?
It indicates approximately 75–80% blockade.
174
What does it indicate if T3 and T4 disappear?
It indicates approximately 80–85% blockade.
175
What does it indicate if only T1 remains?
It indicates approximately 90–95% blockade.
176
What does it indicate if there are no twitches?
It indicates approximately 100% blockade.
177
When is TOF used clinically?
TOF is used during the onset of blockade, maintenance, and emergence.
178
What is the TOFR guideline for safe extubation?
TOFR ≥ 0.9 indicates minimal residual blockade; safe for extubation.
179
What is the reversal time if TOF count is 1?
Reversal may take up to 30 minutes.
180
What is the reversal time if TOF count is 2–3?
Reversal in 4–15 minutes with intermediate NMBAs.
181
What is the recovery time with neostigmine if all 4 twitches are present?
Recovery in approximately 5 minutes.
182
What is the recovery time with edrophonium if all 4 twitches are present?
Recovery in approximately 2–3 minutes.
183
Why is TOF important in clinical practice?
It prevents residual paralysis, especially crucial in elderly or high-risk patients.
184
What risks are associated with inadequate reversal?
Inadequate reversal increases the risk for hypoxia, hypercarbia, atelectasis, airway obstruction, and delayed PACU recovery.
185
What is succinylcholine?
Only depolarizing neuromuscular blocker.
186
What is the mechanism of action of succinylcholine?
Mimics acetylcholine (ACh) → depolarizes motor endplate → paralysis.
187
What receptors does succinylcholine stimulate?
Stimulates nicotinic cholinergic receptors at neuromuscular junction; does not act on ganglionic nicotinic receptors.
188
What effect can succinylcholine have on the heart?
May activate muscarinic receptors in the heart → bradycardia.
189
What is the onset time for succinylcholine?
Rapid onset (≈30–60 sec); gold standard for rapid-sequence intubation.
190
How long do the clinical effects of succinylcholine last?
Clinical effect lasts 5–10 minutes, recovery in 12–15 minutes.
191
How is succinylcholine metabolized?
Rapidly hydrolyzed by plasma cholinesterase.
192
What percentage of the succinylcholine dose reaches the neuromuscular junction?
Only ~10% of the dose reaches neuromuscular junction.
193
What is the dosing for succinylcholine?
0.5–1.5 mg/kg IV bolus (intubation dose); ED95 ≈ 0.30 mg/kg.
194
Does succinylcholine cross the blood-brain barrier?
No, it does not cross the blood-brain barrier → no direct CNS effects.
195
What systemic effect can succinylcholine have on intracranial pressure?
Indirectly increases intracranial pressure (ICP).
196
What cardiovascular effects can succinylcholine cause?
Bradycardia (more common in children or repeated doses in adults); can cause arrhythmias.
197
How does liver dysfunction affect succinylcholine?
Liver dysfunction may prolong duration due to metabolism by liver-produced pseudocholinesterase.
198
Is succinylcholine safe for patients with normal potassium levels?
Safe if K⁺ normal; contraindicated in hyperkalemia.
199
What special considerations are there for elderly patients using succinylcholine?
Prolonged onset due to slower circulation.
200
How should succinylcholine be dosed in obese patients?
Use total body weight for dosing.
201
What is the recommendation for using succinylcholine in children?
Avoid routine use under 8 years old; use only in emergencies due to hyperkalemic rhabdomyolysis risk.
202
What are common postoperative complaints associated with succinylcholine?
Myalgias & fasciculations; can be reduced with pre-treatment (e.g., ND-NMBs, NSAIDs).
203
What effect does succinylcholine have on serum potassium levels?
Causes ↑ serum K⁺ by ~0.5 mEq/L; dangerous in burns, neuromuscular disease, trauma, prolonged immobility.
204
What are the contraindications for succinylcholine?
Malignant Hyperthermia (MH), elevated serum K⁺, neuromuscular disorders, burns, crush injuries (>24–48 hrs post).
205
What is pseudocholinesterase deficiency?
75 mutations reported; notable: Fluoride-resistant (F), Silent (S), and K variants; can cause prolonged apnea and delayed recovery.
206
What should be considered for bradycardia when using succinylcholine?
Consider pre-treatment with atropine, particularly in children or with repeat dosing.
207
What precautions should be taken regarding ICP when using succinylcholine?
Use caution in patients with brain injury or elevated ICP; consider pre-treatment or alternatives in neurosurgery.
208
What is Phase I Block in relation to succinylcholine?
Caused by initial succinylcholine administration; mimics acetylcholine → sustained depolarization of muscle membrane; muscle is paralyzed and unable to repolarize; no fade seen with TOF or tetanic stimulation.
209
What occurs during the transition to Phase II Block?
Occurs with high doses or prolonged/repeated use; membrane repolarizes but becomes desensitized to ACh; resembles nondepolarizing block.
210
What are the characteristics of Phase II Block?
Twitch response shows fade in train-of-four and tetanus stimulation; can be reversed with anticholinesterases (e.g., neostigmine); this is not effective in true Phase I block.
211
Why is it important to recognize Phase II Block during anesthesia?
TOF fade is the hallmark indicator of Phase II block.
212
What is the treatment for Phase II Block?
Use of anticholinesterases may be effective; must adjust management accordingly.
213
What are the prevention strategies for succinylcholine use?
Avoid excessive/repeated doses of depolarizing agents; use minimal effective dose; monitor with neuromuscular stimulation (TOF) to detect transition early.
214
What are Non-Depolarizing Neuromuscular Blockers (NDNMBs)?
NDNMBs are agents that induce skeletal muscle relaxation by competing with acetylcholine at nicotinic receptors.
215
What is Rocuronium?
Rocuronium is an aminosteroid non-depolarizing neuromuscular blocker with a rapid onset (60–90 sec) and intermediate duration (30–60 min).
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What is the mechanism of action of Rocuronium?
It competes with acetylcholine at nicotinic receptors, leading to skeletal muscle relaxation.
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What is the dose range for Rocuronium?
The dose for Rocuronium is 0.6–1.2 mg/kg IV.
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How is Rocuronium metabolized?
Rocuronium is primarily metabolized by the liver, with some renal metabolism.
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What is the reversal agent for Rocuronium?
Rocuronium can be reversed by Sugammadex.
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What are the cardiovascular effects of Rocuronium?
Rocuronium does not cause histamine release, leading to stable blood pressure and heart rate.
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What considerations are there for Rocuronium in elderly patients?
In elderly patients, Rocuronium has a slower onset and longer duration due to decreased clearance and increased volume of distribution.
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What is Vecuronium?
Vecuronium is an aminosteroid non-depolarizing neuromuscular blocker derived from pancuronium, with increased lipophilicity and faster onset.
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What is the dose for Vecuronium?
The dose for Vecuronium is 0.1 mg/kg IV.
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How is Vecuronium metabolized?
Vecuronium is metabolized by the liver and renally excreted, with an active metabolite that requires caution in renal dysfunction.
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What is Atracurium?
Atracurium is a competitive non-depolarizing neuromuscular blocker that is intermediate-acting.
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What is the metabolism of Atracurium?
Atracurium is metabolized through Hofmann elimination and ester hydrolysis.
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What are the potential side effects of Atracurium?
Atracurium can produce histamine release, leading to hypotension, bronchospasm, and tachycardia.
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What is the dose for Atracurium?
The dose for Atracurium is 0.5 mg/kg IV.
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What is Cisatracurium Besylate?
Cisatracurium Besylate is an isomer of atracurium that is more predictable and does not cause histamine release.
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What is the metabolism of Cisatracurium?
Cisatracurium is metabolized by Hofmann elimination and ester hydrolysis, making it ideal for renal/hepatic impairment.
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What is the dose for Cisatracurium?
The dose for Cisatracurium is 0.1 mg/kg IV.
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What considerations are there for Cisatracurium in pediatric patients?
In pediatric patients, the neuromuscular junction is immature in neonates, leading to variable responses.
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What do cholinesterase inhibitors do?
Inhibit acetylcholinesterase (AChE) → ↑ acetylcholine (ACh) at the neuromuscular junction.
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How do cholinesterase inhibitors affect nondepolarizing NMBs?
↑ ACh competes with nondepolarizing NMBs (e.g., rocuronium, vecuronium) → displaces them → restores muscle activity.
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What are the limitations of cholinesterase inhibitors?
Do NOT work for deep blockade (e.g., no twitches on TOF or PTC). Onset is slower than sugammadex. Must be paired with anticholinergic agents to prevent bradycardia and cholinergic side effects.
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What is Neostigmine?
The most commonly used anticholinesterase agent for reversal. Anticholinesterase (inhibits AChE → ↑ACh).
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What must Neostigmine be co-administered with?
Anticholinergic: Glycopyrrolate (preferred) or atropine.
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What is the maximum reversal effect of Neostigmine?
Max reversal ~TOF ≥ 2/4.
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What is the ceiling effect of Neostigmine?
Excess dosing doesn’t help.
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What is the pharmacokinetics of Neostigmine?
50% renal (unchanged). 50% hepatic metabolism and plasma esterases.
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What are the side effects of Neostigmine?
Bradycardia, bronchoconstriction, GI upset.
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What is the dose and onset of Neostigmine?
Dose: 25–75 mcg/kg IV. Onset: 5-15 minutes.
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What is the duration of Neostigmine?
Duration: 45-90 minutes.
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What is Edrophonium?
Used for faster onset, but its efficacy is less than neostigmine.
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What is the onset and duration of Edrophonium?
Fast onset (1–2 min), short duration.
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What must Edrophonium be paired with?
Atropine (rapid onset).
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What is Sugammadex?
Selective binding/rescue agent for aminosteroid NMBAs (roc > vec > pan).
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How does Sugammadex work?
Forms tight complex → inactivates NMBA.
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Does Sugammadex affect acetylcholine or muscarinic receptors?
Does NOT affect acetylcholine or muscarinic receptors (No need for anticholinergics).
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What is the reversal capability of Sugammadex?
Rapid, complete reversal from deep block.
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What is the excretion route of Sugammadex?
Excreted renally → avoid in severe renal dysfunction (drug accumulates).
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What are the side effects of Sugammadex?
Rare anaphylaxis, bradycardia, bleeding, interaction with hormonal contraceptives.
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What is the dosing for Sugammadex based on depth of blockade?
TOF ≥ 2 twitches: 2 mg/kg. PTC 1–2, TOF 0: 4 mg/kg. Immediate reversal after RSI (1.2 mg/kg Roc): 16 mg/kg.
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What are common adverse effects of reversal agents?
Nausea, vomiting, headache, hypotension, hypertension.
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What are serious adverse effects of reversal agents?
Anaphylaxis (rare, but possible—typically occurs within 4 minutes).
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What interaction does Sugammadex have with oral contraceptives?
Sugammadex can bind estrogen/progestin → reduce contraceptive efficacy. Advise backup contraception for 7 days.
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What are anticholinergics used for?
Prevent parasympathomimetic (muscarinic) side effects from anticholinesterase drugs (neostigmine, edrophonium).
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What side effects can occur if anticholinergics are not used?
Bradycardia, arrhythmias, hypotension, bronchoconstriction, hypersalivation, diarrhea, postoperative nausea and vomiting (PONV).
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What is Glycopyrrolate?
Quaternary amine → doesn’t cross BBB. Use with neostigmine.
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What are the characteristics of Glycopyrrolate?
Less tachycardia (no CNS) than atropine. Vagolytic effect can persist for 2 to 3 hours.
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What is the dose and onset of Glycopyrrolate?
Dose: 10-20 mcg/kg IV. Onset IV: 1 min, Onset IM/SQ: 15-30 minutes.
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How is Glycopyrrolate excreted?
Unchanged in urine. Also eliminated via expired CO₂ and feces.
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What is Atropine?
Tertiary amine → crosses BBB (may cause central anticholinergic syndrome: restlessness, hallucinations, dry mouth, blurred vision, hyperthermia, delirium).
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What is the vagolytic effect of Atropine?
Blocks muscarinic receptors, counteracting ACh excess.
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What is the onset and dose of Atropine?
Rapid onset → ideal for edrophonium pairing. Dose: 15 mcg/kg IV.
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What is the combination dose of Atropine and Edrophonium?
7 mcg/kg IV atropine + edrophonium.
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How is Atropine metabolized?
Liver (hepatic transformation into several metabolites).
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What class does Ephedrine belong to?
Synthetic noncatecholamine sympathomimetic.
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What is the mechanism of action of Ephedrine?
Direct α and β receptor agonist; indirectly releases endogenous norepinephrine.
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What are the effects of Ephedrine?
↑ Blood pressure, heart rate, cardiac output, and systemic vascular resistance; bronchodilation via β₂-receptor stimulation.
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What is the duration of action for Ephedrine?
15 minutes to 1.5 hours (dose-dependent).
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What is the IV dose range for Ephedrine?
5–25 mg.
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What are the preferred uses for Ephedrine?
Hypotension during spinal/epidural anesthesia; OB anesthesia (historically).
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What routes can Ephedrine be administered?
IV, IM, SC, oral.
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What caution should be taken with Ephedrine?
Caution in patients with coronary artery disease; repeated dosing may lead to tachyphylaxis.
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What is Phenylephrine?
A pure alpha-agonist (α1) that causes potent vasoconstriction.
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What are the effects of Phenylephrine?
↑ Systemic vascular resistance leading to sharp ↑ BP; causes reflex bradycardia.
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What is the onset and duration of Phenylephrine?
Onset: Immediate (IV); Duration: 5–20 minutes.
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What is the IV dosing recommendation for Phenylephrine?
Titrate cautiously to avoid overshooting BP.
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What are the uses of Phenylephrine?
Maternal hypotension after regional anesthesia; nasal decongestion; ophthalmologic mydriasis.
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What is Esmolol?
A cardioselective β1-blocker with rapid onset/offset.
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What is the onset and duration of Esmolol?
Onset: ~2 minutes; Duration: 10–15 minutes.
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What is the IV dosing for Esmolol?
Loading: 500 mcg/kg; Infusion: 100–300 mcg/kg/min; Bolus: 10–20 mg PRN.
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What are the uses of Esmolol?
Used perioperatively for tachycardia, hypertension, or arrhythmias.
285
What is Metoprolol?
A selective β1-blocker with various cardiovascular actions.
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What are the uses of Metoprolol?
Used for HTN, angina, post-MI stabilization.
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What is the IV dosing for Metoprolol?
5 mg every 5 minutes up to 15 mg.
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What is the oral dosing range for Metoprolol?
50–200 mg/day (regular); 25–400 mg/day (extended release).
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What is Labetalol?
A nonselective β-blocker + α1-blocker (β:α = 7:1).
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What are the effects of Labetalol?
↓ BP with vasodilation (no reflex tachycardia).
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What is the IV dosing for Labetalol?
0.25 mg/kg boluses; infusion at 2 mg/min PRN.
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What are the contraindications for Labetalol?
Contraindicated in bradycardia.
293
What is Atropine?
A tertiary amine used for bradycardia, antisialagogue, NMBD reversal adjunct.
294
What is the IV dosing for Atropine?
0.4–0.6 mg.
295
What is Scopolamine?
A tertiary amine used preop for PONV prevention.
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What is the patch dose for Scopolamine?
1.5 mg behind ear, 4 hrs before surgery.
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What are the side effects of Scopolamine?
Sedation, dry mouth, blurred vision.
298
What class does Ephedrine belong to?
Synthetic noncatecholamine sympathomimetic.
299
What is the mechanism of action of Ephedrine?
Direct α and β receptor agonist; indirectly releases endogenous norepinephrine.
300
What are the effects of Ephedrine?
↑ Blood pressure, heart rate, cardiac output, and systemic vascular resistance; bronchodilation via β₂-receptor stimulation.
301
What is the duration of action for Ephedrine?
15 minutes to 1.5 hours (dose-dependent).
302
What is the IV dose range for Ephedrine?
5–25 mg.
303
What are the preferred uses for Ephedrine?
Hypotension during spinal/epidural anesthesia; OB anesthesia (historically).
304
What routes can Ephedrine be administered?
IV, IM, SC, oral.
305
What caution should be taken with Ephedrine?
Caution in patients with coronary artery disease; repeated dosing may lead to tachyphylaxis.
306
What is Phenylephrine?
A pure alpha-agonist (α1) that causes potent vasoconstriction.
307
What are the effects of Phenylephrine?
↑ Systemic vascular resistance leading to sharp ↑ BP; causes reflex bradycardia.
308
What is the onset and duration of Phenylephrine?
Onset: Immediate (IV); Duration: 5–20 minutes.
309
What is the IV dosing recommendation for Phenylephrine?
Titrate cautiously to avoid overshooting BP.
310
What are the uses of Phenylephrine?
Maternal hypotension after regional anesthesia; nasal decongestion; ophthalmologic mydriasis.
311
What is Esmolol?
A cardioselective β1-blocker with rapid onset/offset.
312
What is the onset and duration of Esmolol?
Onset: ~2 minutes; Duration: 10–15 minutes.
313
What is the IV dosing for Esmolol?
Loading: 500 mcg/kg; Infusion: 100–300 mcg/kg/min; Bolus: 10–20 mg PRN.
314
What are the uses of Esmolol?
Used perioperatively for tachycardia, hypertension, or arrhythmias.
315
What is Metoprolol?
A selective β1-blocker with various cardiovascular actions.
316
What are the uses of Metoprolol?
Used for HTN, angina, post-MI stabilization.
317
What is the IV dosing for Metoprolol?
5 mg every 5 minutes up to 15 mg.
318
What is the oral dosing range for Metoprolol?
50–200 mg/day (regular); 25–400 mg/day (extended release).
319
What is Labetalol?
A nonselective β-blocker + α1-blocker (β:α = 7:1).
320
What are the effects of Labetalol?
↓ BP with vasodilation (no reflex tachycardia).
321
What is the IV dosing for Labetalol?
0.25 mg/kg boluses; infusion at 2 mg/min PRN.
322
What are the contraindications for Labetalol?
Contraindicated in bradycardia.
323
What is Atropine?
A tertiary amine used for bradycardia, antisialagogue, NMBD reversal adjunct.
324
What is the IV dosing for Atropine?
0.4–0.6 mg.
325
What is Scopolamine?
A tertiary amine used preop for PONV prevention.
326
What is the patch dose for Scopolamine?
1.5 mg behind ear, 4 hrs before surgery.
327
What are the side effects of Scopolamine?
Sedation, dry mouth, blurred vision.
328
What is Glycopyrrolate?
A quaternary ammonium compound with no CNS penetration.
## Footnote
Uses include bradycardia, antisialagogue, and use with neostigmine. It has less tachycardia than atropine and a longer duration.
329
What is Cefazolin?
A β-lactam antibiotic that is bactericidal via time-dependent killing.
## Footnote
Dose is 2g IV (adults) within 60 min before incision, redose every 4 hrs for long cases or >1500 mL blood loss, and used in various surgeries.
330
What are the SCIP Guidelines for Cefazolin?
Emphasize timing, selection, and discontinuation of prophylaxis.
331
What is Dexamethasone used for?
A glucocorticoid that inhibits the nucleus tractus solitarius and reduces serotonin in the CNS.
## Footnote
Dose is 4–8 mg IV after induction with a long duration (~72 hrs) and caution in diabetics.
332
What is Ondansetron?
A 5-HT3 antagonist effective for vomiting more than nausea.
## Footnote
Dose is 4 mg IV at the end of the case with a short duration (4–6 hrs) and risk of QT prolongation at high doses.
333
What is Palonosetron?
A 5-HT3 antagonist with a long half-life (44 hrs) and preferred for PDNV.
334
What is Aprepitant?
An NK-1 antagonist FDA-approved for PONV.
335
What is Droperidol?
A butyrophenone that blocks dopamine receptors.
## Footnote
Dose is 0.625–1.25 mg IV with QT prolongation warning and contraindicated in Parkinson's disease.
336
What is the antiemetic effect of Midazolam?
It has an anti-nausea effect via GABA/dopamine modulation.
## Footnote
May prolong recovery if used near the end of the case.
337
What are the best practices for antiemetic use?
Use multimodal prophylaxis in moderate/high-risk PONV, combine 5-HT3 antagonist + steroid or NK-1 antagonist, and use rescue therapy from a different drug class.
## Footnote
Do not repeat the same drug if PONV recurs <6 hours post-op.
