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DNAP 2027 > Spring 25 - Basics - Pharmacology of Anesthesia > Flashcards

Spring 25 - Basics - Pharmacology of Anesthesia Flashcards

1
Q

Primary effects of Dex.

A
  • sedation
  • analgesia
  • anxiolysis
  • reduced postoperative shivering and agitation
  • cardiovascular sympatholytic actions
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2
Q

Precedex onset/duration

A
  • Onset 10 - 20 minutes
  • Duration 10 - 30 minutes
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3
Q

Precedex loading dose/gtt

A
  • ld =1 mcg/kg over 10 minutes
  • gtt = 0.2 to 0.7 mcg/kg/hour
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4
Q

Dex. main side effects

A
  • Bradycardia
  • hypotension
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5
Q

Etomidate MOA

A
  • Hypnotic
  • GABA receptor modulator
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6
Q

Etomidate induction dose

A
    • 0.3 mg/kg
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7
Q

Etomidate duration/Half-life

A
  • Duration 5 - 15 minutes
  • half-life is 2 - 5 hours
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8
Q

Etomidate adverse effect

A
  • Nausea / Vomiting
  • Burn on injection
  • Thrombophlebitis
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9
Q

Etomidate Contraindications

A
  • Porphyria
  • Adrenal suppression
  • Known sensitivity to Etomidate
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10
Q

Key points of etomidate

A
  • Minimal cardiorespiratory depression
  • Reduced ICP
  • Myoclonia on induction
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11
Q

Ketamine MOA

A
  • NMDA receptors antagonist
  • Blocks signals of pain perception to the thalamus and cortex
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12
Q

Ketamine CNS effects

A
  • Increases ICP/CBF/CMRO
  • Dissociative state of anesthesia
  • Vivid illusions and confusional disturbances on emmergence
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13
Q

Ketamine CV effects

A
  • Increases BP/HR
  • Increased cardiac contractility CO/CVP
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14
Q

Ketamine Respiratory effects

A
  • minor and short-lived.
  • Ventilation is generally preserved,
  • Bronchodilation
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15
Q

Ketamine induction dosage IV/IM

A
  • 2-4 mg/kg IV
  • 4-6 mg/kg IM
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16
Q

Ketamine maintenance dose

A
  • 15 - 45 mcg/kg/min
  • 0.5 - 1 mg/kg
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17
Q

Ketamine sedation and analgesia dose

A
  • 0.2 - 0.8 mg/kg
  • 5 - 20 mcg/kg/min
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18
Q

Ketamine key points

A
  • Dissociative anesthesia
  • Increased ICP and IOP
  • Emergence delirium
  • Releases catecholamines
  • Moderate analgesic property
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19
Q

Propofol induction/maintenance/sedation doses

A
  • Induction 1-2 mg/kg
  • Maintenance 100-200 mcg/kg/min
  • Sedation 25-75 mcg/kg/min.
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20
Q

Propofol systemic effects

A
  • Rapid (10 - 50 secs) onset
  • Reduces ICP, IOP and CMRO
  • Decreased BP, CO and SVR
  • Respiratory depression/apnea
  • Mild anti-emetic properties
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21
Q

Midazolam uses

A
  • Anxiolysis
  • Anesthesia (at high doses)
  • Amnesia
  • Anticonvulsant
  • Muscle-relaxing properties.
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22
Q

Midazolam systemic effects

A
  • Anterograde amnesia
  • Minimal CV effects
  • Most respiratory depressive benzo
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23
Q

Flumazenil onset and duration

A
  • Onset 1 - 2 minutes
  • Duration 45 - 90 minutes
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24
Q

What receptors are targeted by opioids?

A
  • Mu
  • Delta
    Both are located in the respiratory center in the brainstem
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25
Q

Morphine order of action (Sedation vs analgesia)

A
  • Sedation first, followed by analgesia.
  • Induced sedation should not be considered an indicator of appropriate analgesia.
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26
Q

Morphine metabolism occurs in

A

Liver

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27
Q

Morphine Dose / Onset / Peak /Duration

A
  • IV 0.05 - 0.15 mg/kg
  • Onset 20 min
  • Peak 30 - 60 minutes
  • Duration 4 - 5 hours
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28
Q

Fentanyl duration

A

20 - 40 minutes

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29
Q

Fentanyl metabolism/elimination

A
  • first-pass uptake in the lungs
  • Termination of action reflects elimination and
    not redistribution (when given as gtt)
  • elimination is prolonged in the elderly and neonates.
  • Eliminated in the urine and bile
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30
Q

Alfentanil metabolism

A
  • Metabolized in the liver by oxidative N-dealkylation and O-demethylation in the cytochrome P-450 system.
  • The inactive metabolites are excreted in the urine
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31
Q

Alfentanil notable drug interation

A

Erythromycin has been shown to prolong the metabolism of Alfentanil

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32
Q

Hydromorphone Dose/Onset/Peak/Duration

A
  • 0.01 - 0.02 mg/kg
  • Onset 15 - 30 minutes
  • Peak 30 - 90 minutes
  • Duration 4 - 5 hours
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33
Q

Meperidine key points

A
  • Same structural and antispasmodic effects as atropine
  • Effective in reducing shivering as precedex
  • Accumulation can lead to CNS excitation and seizures
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34
Q

Remifentanil key points

A
  • rapid onset,
  • ultrashort duration,
  • titratability
  • simple metabolism
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35
Q

Remifentanil elimination 1/2 life

A

8 - 20 minutes

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36
Q

Morphine Dose

A
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37
Q

Hydromorphone (Diluadid) Doses

A
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38
Q

Fentanyl Doses

A
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39
Q

Sufentanil Dose

A
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40
Q

Alfentanil Doses

A
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41
Q

Remifentanil Doses

A
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42
Q

Buprenorphine key points

A
  • Partial agonist opioid that binds to mu receptor
  • Duration about 8 hrs due to slow dissociation from receptor
  • Ceiling effect does not increase respiratory depression
  • Minimal effect on GI motility
  • USED in opioid use disorder treatment
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43
Q

Butorphanol key points

A
  • Highly lipophilic
  • Kappa agonist / Weak mu antagonist
  • More analgesia than morphine but has a ceiling effect (less respiratory depression)
  • USED for post-op pain and the treatment of migraines
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44
Q

Nalbuphine key points

A
  • Both agonist (kappa) and antagonist (mu) of opioid receptor
  • Equal analgesia as morphine
  • Ceiling effect but difficulty reversal with naloxone
  • USED antagonizing pruritus and respiratory depression induced by other opioids.
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45
Q

Which highly lipophilic opioid Can produce more analgesia than morphine but has a ceiling effect below that of mu-agonist

A

Butorphanol’s

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46
Q

Partial Agonists and Agonists-Antagonists
- Receptor affinity

A
  • Buprenorphine = High affinity for mu receptors
  • Butorphanol = Angonist at kappa and weak antagonist at mu receptors
  • Nalbuphine = Agonist effect at kappa and antagonist effect at mu receptors.
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47
Q

Partial Agonists and Agonists-Antagonists
- Clinical uses

A
  • Buprenorphine = opioid use disorder treatment and for cancer pain
  • Butorphanol for migraine and postoperative pain
  • Nalbuphine for antagonizing pruritus and respiratory depression induced by other opioids
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48
Q

Naloxone key points

A
  • Pure opioid antagonist
  • Competitive antagonism at mu, kappa,
    and delta receptors
  • Duration is less than other (possible return of respiratory depression)
  • Reverse the side effects of epidural opioids while preserving some analgesic effects
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49
Q

Naltrexone key points

A
  • Same receptor binding capabilities as naloxone but higher oral efficacy and lasts longer
  • USED in ETOH use disorder and for patients addicted to opioids to prevent the euphoric effects of opioids
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50
Q

Nalmefene key points

A
  • Structurally similar to naloxone but longer acting parenteral
  • 1/2 life about 10 hours
  • Duration 8 hours
  • USED in alcohol use disorder programs. In acute opioid overdose
  • Dose 0.5 - 1.6 mg IV
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51
Q

Narcotic Antagonists
- Duration of Action

A

Naloxone has the shortest duration of action, while Naltrexone and Nalmefene have longer durations, making them suitable for longer-term management of opioid addiction or overdose

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52
Q

Narcotic Antagonists
- Use in addiction

A

Naltrexone and Nalmefene are used in alcohol use disorder programs, whereas Naloxone is primarily used for the emergency treatment of opioid overdose

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53
Q

Narcotic Antagonists
- Metabolic pathway

A

Naltrexone produces an active metabolite, contributing to its longer duration of action,
while Nalmefene’s longer action is due to its inherent pharmacokinetic properties.

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54
Q

Ketorolac key points/contraindication

A
  • IV NSAID
  • Can be administered IV & IM
  • No CV and GI dysfunction
  • CONTRAINDICATION (Atopic/asthmatic patients/elderly/renal or GI dysfunction, or
    bleeding disorders)
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55
Q

Ibuprofen key points dosage / Onset / Duration

A
  • Similar effects to Ketorolac
  • Analgesic and antipyretic
  • Dosage 400 - 800 mg (IV Over 30 min)
  • Onset 30 minutes
  • Duration 4 - 6 hours
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56
Q

Acetaminophen (Not-Nsaid) key points

A
  • Analgesic and antipyretic
  • Adult > 13 yo dose 1000 mg (IV over 15 minutes)
  • Child <13 dose 15 mg/kg
  • Max daily dose 4000 mg
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57
Q

Non-Narcotic Analgesics
- Mechanism of action

A

Both Ketorolac and Ibuprofen are NSAIDs and work by inhibiting cyclooxygenase enzymes, whereas Acetaminophen’s mechanism is less clear but is believed to involve central inhibition of prostaglandin synthesis.

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58
Q

Non-Narcotic Analgesics
- Analgesic properties

A
  • Ketorolac and Ibuprofen are effective for mild to moderate pain
  • Acetaminophen is used for mild pain and fever
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59
Q

Non-Narcotic Analgesics
- Side effects

A
  • Ketorolac and Ibuprofen can have GI and CV side effects
  • Acetaminophen can cause hepatotoxicity at high doses.
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60
Q

Relationship between gas uptake in the blood and alveolar concentration

A

The greater the uptake, the slower the rate of rise of the alveolar concentration and the lower the FA: FI ratio

61
Q

Relationship between agent solubility and uptake (in the blood)

A
  • Insoluble agents like nitrous oxide are taken up less
    avidly by the blood.
  • More soluble agents like sevoflurane uptake is faster than non-soluble agents
62
Q

Relationship between cardiac output, alveolar partial pressure and uptake

A
  • An increase in cardiac output increases anesthetic uptake, slowing the rise in alveolar partial pressure
    and delaying induction
  • Low-output states can lead to overdosage with
    soluble agents.
63
Q

Relationship between partial pressure differences and agent uptake

A

The gradient between alveolar gas and venous blood, which depends on tissue uptake, also affects the uptake of anesthetic by the pulmonary circulation.

64
Q

Reason for discrepancy (Missmatch) between alveolar and arterial anesthetic partial

A
  • Venous admixture
    -Alveolar dead space
  • Nonuniform alveolar gas distribution
65
Q

What are the alveolar and arterial consequences of a mismatch between alveolar and arterial partial pressures?

A
  • Increase in alveolar partial pressure (especially for highly soluble agents)
  • Decrease in arterial partial pressure (especially for poorly soluble agents)
66
Q

Relationship between inspired concentration and alveolar concentration

A

Increasing the inspired concentration not only
increases the alveolar concentration but also its rate of rise.

67
Q

Factors that speed up induction and accelerate recovery

A
  • Elimination of rebreathing,
  • High fresh gas flows
  • Low anesthetic-circuit volume
  • Low absorption by the anesthetic circuit
  • Decreased solubility
  • High cerebral blood flow,
  • Increased ventilation.
68
Q

Diffusion Hypoxia
- Rapid Elimination of Nitrous Oxide

A

Nitrous oxide is quickly eliminated from the body through the alveolar membrane. This rapid elimination is one factor that speeds up recovery from anesthesia.

69
Q

Diffusion Hypoxia
- Dilution of Oxygen and Carbon Dioxide

A

Due to the rapid exhalation of nitrous oxide, the oxygen (O2) and carbon dioxide (CO2) concentrations in the alveolar gas are diluted. This can lead to a relative state of hypoxia.

70
Q

Diffusion Hypoxia
- Prevention of Diffusion Hypoxia:

A

To prevent diffusion hypoxia, it is recommended to administer 100% oxygen for 5 to 10 minutes after discontinuing nitrous oxide. This practice helps to maintain adequate oxygen levels in the alveoli and bloodstream, countering the dilution effect caused by the rapid exit of nitrous oxide.

71
Q

Nitrous oxide key points

A
  • NMDA antagonist
  • CV stimulant (Mask respiratory depression
  • Respiratory rate increased and decrease tidal volume
  • Depress hypoxic drive
  • Increased cerebral blood flow and ICP (Mildly)
  • No muscle relaxation
  • Decreased kidney and hepatic blood flow
  • PONV
72
Q

How is Nitrous oxide Eliminated? and contraindications

A
  • Primarily eliminated by exhalation
  • Small amount diffusing through the skin

-CONTRAINDICATED in conditions where rapid diffusion into air-containing cavities can be hazardous, such as pneumothorax, bowel distention, or intracranial air.

73
Q

Definition of MAC

A

The alveolar concentration of an inhaled anesthetic that prevents movement in 50% of patients in response to a standardized stimulus, such as a surgical incision

74
Q

Utility of MAC

A
  • It reflects the partial pressure of the anesthetic in the brain
  • Allows for comparisons of potency between different anesthetic agents
  • Serves as a standard for experimental evaluation
75
Q

Explain the Additivity of MAC Values

A

A mixture of 0.5 MAC of nitrous oxide and 0.5 MAC of isoflurane produces a similar effect in suppressing movement in response to surgical incision as 1.0 MAC of isoflurane alone.

76
Q

MAC Value ISO

A

Alone - 1.17
+ N2O - 0.56

77
Q

MAC Value Sevo

A

Alone - 2
+ N2O - 0.66

78
Q

MAC Value Des

A

Alone - 6
+ N2O - 2.38

79
Q

MAC Value Nitrous

80
Q

What is the effect of the 3 Main Gases
- On the cardiovascular system?

A

All three anesthetics have similar effects on the
cardiovascular system, primarily causing a decrease in systemic vascular resistance and arterial blood pressure.

81
Q

Which of the 3 Main Gases
- Causes airway irritation?

A

Desflurane is an airway irritant.

82
Q

What is the effect of the 3 Main Gases
- on the Brain?

A

All increase CBF and intracranial pressure, with sevoflurane and desflurane having similar effects on CBF autoregulation.

83
Q

Which of the 3 Main Gases
- Decrease peripheral nerve stimulation

A

Desflurane

84
Q

Which of the 3 Main Gases
- Has minimal nephrotoxic effects

A

Desflurane

85
Q

Which of the 3 Main Gases
- Has the highest rate of metabolism?

A

Sevoflurane has a higher rate of metabolism with potential nephrotoxic byproducts

86
Q

All three leading gases potentiate which class of meds?

A

All three anesthetics share similar contraindications and potentiate NMBAs.

87
Q

Progressive Disappearance of Twitches TOF

A
  • If T4 disappears (3 twitches) → 75% to 80% neuromuscular blockade
  • If T4 and T3 disappear (2 twitches) → 80% to 85% neuromuscular blockade
  • If T4, T3, and T2 disappear (1 twitche) → 90% to 95% neuromuscular blockade
  • If no twitches are seen (0 twitches) → 100% paralysis (complete neuromuscular blockade)
88
Q

Timing for Reversal of NMBA using TOF

A
  • 1 response to TOF = 30 minutes.
  • 2 to 3 responses = 4 to 15 minutes
  • 4 responses to TOF recovery can be achieved within 5 minutes of reversal with neostigmine or 2 to 3 minutes after using edrophonium.
89
Q

Succinylcholine MOA

A
  • Competitive agonist at nicotinic acetylcholine (nACh) receptors, causes depolarization without repolarization.
90
Q

Succinylcholine onset/half-life/duration/full recovery time

A
  • onset 30 - 60 secs
  • 1/2 life 2 - 4 minutes
  • duration 5 - 10 minutes
  • full recovery 12 - 15 minutes
91
Q

Succinylcholine dose

A
  • 0.5 to 1.5 mg/kg
  • ED95 is approximately 0.30 mg/kg
92
Q

Succinylcholine metabolism

A

Plasma cholinesterase produced in the liver.
Liver damage may prolong the effects of the drug

93
Q

Succinylcholine absolute contraindication

A
  • Patients with known or suspected MH or who have MH in their families
  • Indirect increase in ICP
  • Only in emergency for children under 8 years old
94
Q

Explain Phase I (intended) block

A

Succinylcholine initially acts by mimicking (ACh) at the neuromuscular junction, leading to depolarization. The muscle is depolarized and cannot be repolarized immediately, leading to paralysis.

95
Q

Explain Phase II block

A

With prolonged exposure to high doses or repeated dosing, the muscle membrane starts repolarizing but becomes less responsive to acetylcholine. This transition is what characterizes the Phase II block

96
Q

Treatment of phase II block

A

If a Phase II block is identified, it can often be treated with anticholinesterase drugs, similar to the treatment of a block induced by nondepolarizing NMBAs

97
Q

Rocuronium Bromide MOA

A

Competitive antagonist at nicotinic acetylcholine (nACh) receptors

98
Q

Rocuronium onset/duration/half-life(elimination)

A
  • Onset is dose dependant
  • duration 30 - 60 minutes
  • Elimination 1/2 life 60 - 120 minutes
99
Q

Rocuronium intubation dose and onset

A
  • 2nd most used RSI (after Succs)
  • 0.6 - 1.2 mg/kg
  • onset 45 - 90 seconds
100
Q

Rocuronium key points

A
  • Cardioprotective
  • Duration of action is prolonged in patients with hepatic disease
  • Prolonged elimination half-life in patients with renal disease.
101
Q

Rocuronium elimination 1/2 life children/adults/elderly

A
  • Children 38.3 minutes
  • Normal adults 56 minutes
  • Elderly 137 minutes
102
Q

Vecuronium Bromide MOA

A

Competitive antagonist at nicotinic acetylcholine (nACh) receptors

103
Q

Vecuronium dose/onset/duration

A
  • Dose 0.1 mg/kg
  • Onset 3 minutes
  • Duration 3 - 45 minutes
104
Q

Vecuronium elimination/metabolism

A
  • Eliminated via hepatic and renal mechanisms
  • The duration of action is prolonged in patients with decreases in renal and liver function
105
Q

Cisatracurium MOA

A

Competitive antagonist at nicotinic acetylcholine (nACh) receptors

106
Q

Cisatracurium dose/half-life

A
  • Dose 0.1mg/kg
  • Half-life 26 to 36 minutes
107
Q

Cisatracurium key points

A
  • Maintains cardiovascular stability and does not cause histamine release
  • Suitable choice for patients with renal or hepatic impairment
  • The kinetics of cisatracurium are not significantly changed in elderly patients.
  • Preferred in obese patients due to its lack of
    histamine release and reliable kinetics.
108
Q

Atracurium MOA

A

Competitive antagonist at nicotinic acetylcholine (nACh) receptors

109
Q

Atracurium dose/onset/duration

A

ED95 0.10 - 0.25 mg/kg
onset 1.2 - 2.8 minutes
duration 30 - 60 minutes

110
Q

Atracurium key points

A
  • Undergoes Hofmann elimination
  • Safe to use in patients with liver and kidney diseases
  • Can cause histamine release and may lead to hypotension and tachycardia
111
Q

Cholinesterase inhibitors MOA
- Edrophonium

A

A reversible inhibitor of cholinesterase

112
Q

Cholinesterase inhibitors MOA
- Neostigmine

A

Degrades ACh-cholinesterase complex, leaving AChE unable to hydrolyze ACh

113
Q

Edrophonium vs. Neostigmine Pharmacokinetic Profiles

A

Edrophonium binds reversibly with the negatively charged enzyme site, while neostigmine forms a more stable enzyme

114
Q

Neostigmine dose/onset/duration

A
  • 25-75 mcg/kg
  • Onset of 5-15 minutes
  • Duration 45-90 minutes
115
Q

Sugammadex 3 doses

A
  • 2 mg/kg for patient with 2 or more twitches, spontaneous recovery
  • 4 mg/kg for 1 -2 PTC and no response to TOF
  • 16 mg/kg to reverse NMB soon after administration of a single dose of 1.2 mg/kg of rocuronium
116
Q

Sugammadex common reactions

A
  • Nausea/vomiting
  • Allergy, hypertension, and headache
  • Anaphylaxis
117
Q

Sugammadex and oral contraception

A

Binds oral contraceptives, and women of childbearing age should be counseled about using alternative contraceptive methods for 1 week after exposure to sugammadex

118
Q

Two most used anticholinergics

A

Atropine and Glycopyrolate

119
Q

Specific Anticholinergic Agents
- Atropine + Edrophonium: Dose

A

Atropine + edrophonium give 7 mcg/kg.

120
Q

Specific Anticholinergic Agents
- Glycopyrrolate: Dose/benefit(s) over atropine

A
  • Dose10 - 20 mcg/kg
  • Less initial tachycardia, no CNS effects
121
Q

Neostigmine Dose/Onset (min)/Duration

122
Q

Edrophonium Dose/Onset (min)/Duration

123
Q

Atropine Dose/Onset (min)/Duration

124
Q

Glycopyrrolate Dose/Onset (min)/Duration

125
Q

Sugammadex Dose/Onset (min)/Duration

126
Q

Ephedrine MOA

A
  • sympathomimetic
  • Stimulates alpha and beta receptors
  • Effects similar to epinephrine but moderate, no hyperglycemia
  • longer duration of action than epinephrine
127
Q

Ephedrine dose/onset/duration

A
  • Dose 5 to 25 mg,
  • Onset immediate
  • Duration 15 - 90 minutes
128
Q

Ephedrine caution

A

Patient with questionable coronary perfusion it can increase myocardiac oxygen requirement

129
Q

Phenylephrine MOA

A
  • Purely Alpha, no beta stimulation
  • Sharp rise in blood pressure
130
Q

Phenylephrine onset/duration

A
  • Onset immediate
  • Duration 5 - 20 minutes
131
Q

Phenylephrine other clinical uses

A

You can stick it in
- Eyes (Mydriatic)
- Ears
- Nose (prevent/reduce bleeding)
- Throat (reduce bleeding during ENT sx)

132
Q

Esmolol loading dose/infusion/boluses

A
  • Loading 500 mcg/kg
  • Infusion 100 - 300 mcg/kg/min
  • boluses 10 - 20 mg
133
Q

Esmolol onset/half-life/duration

A
  • onset 2 minutes
  • 1/2 life 9 minutes
  • duration 10 - 15 minutes
134
Q

Metoprolol MOA

A

Beta-blocking effects, which include negative chronotropic, dromotropic, inotropic,
antiarrhythmic, and antiischemic actions

135
Q

Metoprolol doses

A
  • IV 5-mg Q5 minute maximum dose of 15 mg.
  • po 50 - 200 mg daily
  • po XL 25 - 400 daily
136
Q

Labetalol MOA

A
  • Nonselective beta-blocker but is unique in that it
  • Also possesses an alpha-blocking component
  • 7:1 beta to alpha-blockade ratio.
137
Q

Labetalol dose bolus/gtt/duration

A
  • Bolus 0.25 mg/kg,
  • gtt 2 mg/min
  • Duration 2 - 6 hours
138
Q

Anticholinergics
- Atropine summary

A
  • Antisialagogue effects,
  • Prevention or treatment of bradycardia
  • Used in conjunction with Edrophonium
  • HR increase dose 0.4 to 0.6 mg onset 1 - 2 minutes
139
Q

Anticholinergics
- Scopolamine

A
  • Bella Dona alkaloid
  • Periop used for sedation, amnesia and PONV
  • 1.5 mg patch applied behind the ear 4 hours pre-op and last up to 3 days post-po
140
Q

Anticholinergics
- Glycopyrrolate

A
  • Most antisialagogue effect
  • Use in conjunction with Neostigmine
  • Prevents Bradycardia without creating tachycardia
141
Q

Cefazolin MOA

A

a β-lactam antibiotic works primarily via time-dependent killing

142
Q

Cefazolin dose

A

Adults 2g IV (Q4 hours for longer procedures)

143
Q

Antiemetics
- Dexamethasone (Decadron) Dose/ Duration

A
  • Dose 4 or 8 mg
  • Duration 72 hours
144
Q

Antiemetics
- Methylprednisolone (Solu-Medrol) Dose

A

40 mg prophylactic treatment

145
Q

Antiemetics
- Ondansetron dose/duration

A
  • Dose 4mg IV (at the end of the case)
  • Duration 4 - 6 hours
146
Q

Antiemetics
- Droperidol dose/contraindication

A
  • 0.625 to 1.25 mg IV
  • Parkinson Disease
    CAUSE QT prolongation
147
Q

Antiemetics
- Haloperidol dose

A

1 - 2 mg
SAME QT effect as. Droperidol

148
Q

Antiemetics
- Midazolam:

A

Recent studies suggest a significant antiemetic effect. Decreases dopamine’s emetic effect in the chemoreceptor trigger zone and decreases serotonin release by binding to the GABA receptor complex
USE MAY DELAY RECOVERY DUH!!

149
Q

Antiemetics
- Metoclopramide dose/half-life

A
  • Dose 20 mg
  • half-life 30 - 45 minutes (Weak one)
    DO NOT GIVE IN PARKINSON’S disease

DNAP 2027 (8 decks)

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