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Pharmacology for Anesthesia > 02 - IV Anesthetics > Flashcards

02 - IV Anesthetics Flashcards

0
Q

Mechanism of action - barbiturates

A

Depress Reticular Activating System
Suppress exciting neurotransmitters (Ach)
Enhance inhibitory neurotrans (GABA)

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1
Q

Ten criteria for the ideal IV anesthetic

A 
Water soluble and stable
Lack of pain on injection, no tissue damage with extravasation
Low incidence of histamine release or hypersensitivity
Rapid, smooth onset
Rapid metabolism to inactive metabolites
Steep dose-response curve
Minimal cardiac/respiratory depression
Decreases ICP/CMRO2
Rapid, smooth recovery
Minimal side effects
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2
Q

Solubility and acidity of barbiturates

A

Water soluble but alkaline (ph>10)

Weak acid with pka close to 7.4

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3
Q

Are barbiturates stable?

A

No, lasts only 2 to 6 weeks in the refrigerator

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4
Q

What does intra-arterial injection of thiopental cause? How is it treated?

A

Crystals that lead to thrombosis and necrosis

Papaverine, lidocaine, stellate ganglion block, heparin

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5
Q

Thiobarbiturates compared to oxybarbiturates?

A

Thiobarbiturates (thiopental, thiomylal) - higher lipid solubility -> greater potency, rapid onset, shorter duration

Oxybarbiturates (methohexital) - lower lipid solubility -> less potency, slower onset, longer duration

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6
Q

Which drug is used for lethal injection?

A

Thiobarbiturates

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7
Q

What causes methohexital to have a short duration of action unlike other oxybarbiturates?

A

The methyl group

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8
Q

Absorption of barbiturates

A

IV for general anesthesia

Rectal/IM for premedication

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9
Q

Onset and redistribution time of barbs

A 
Fast onset (30 sec) and rapid redistribution (10-20 min) after single dose
Due to lipid solubility
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10
Q

What causes higher plasma levels of barbiturates?

A

Hypovolemia
Hypoalbuminemia
Acidosis
Elderly

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11
Q

Why are barbiturates a poor choice for maintenance of anesthesia?

A

Multiple doses saturate peripheral compartments, meaning slower redistribution
Long elimination half life - 3 to 12 hours

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12
Q

Biotransformation of barbiturates

A

Almost complete hepatic oxidation

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13
Q

Difference in biotransformation between thiopental and methohexital?

A

Thiopental - low hepatic extraction -> capacity limited, longer elimination half life

Methohexital - high hepatic extraction -> perfusion limited capacity, shorter elimination half life

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14
Q

Liver disease is unlikely to cause prolonged effect of thiopental from

A

A single dose

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15
Q

Renal clearance is difficult for barbiturates because

A

They are protein bound and lipid soluble - biotransformation must occur first

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16
Q

Elimination half life of methohexital

A

3.9 hours

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17
Q

Elimination half life of thiopental

A

11.6 hours

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18
Q

Dosage of methohexital

A

1-1.5 mg/kg/hr

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19
Q

Dosage of thiopental

A

3-5 mg/kg

6-8 mg/kg for infants

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20
Q

2-4 mg/kg/hr of thiopental

A

Can treat intracranial hypertension or intractable seizures

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21
Q

CV effects of barbiturates

A

Decreased blood pressure, increased heart rate (central vagolytic effect)

Venous pooling

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22
Q

With barbs, CO is maintained except in pts with

A

Hypovolemia
CHF
Beta blockade (very decreased CO and BP)

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23
Q

Respiratory effects of barbiturates

A

Decreased hypoxic/hypercapnia drive
Airway obstruction
Bronchospasm/laryngospasm

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24
Neuro effects of barbiturates
``` Decreased CBF, ICP Very decreased CMRO2 to burst suppression on EEG Anti analgesic? Anti epileptic Tolerance/dependence ```
25
Why do barbs cause decreased renal blood flow?
Hypotension
26
Hepatic - barbs
Decreased hepatic blood flow Induction of enzymes (CYP) Porphyrin formation
27
What is porphyria and what can drug can cause it?
Disorder of enzyme in heme biosynthetic pathway Caused by barbs
28
Acute porphyria
Overproduction and accumulation of porphyrin
29
Neuro effects of acute porphyria
Abdominal pain, Vomiting, Neuropathy, Weakness, Seizures, Hallucinations, Depression, Anxiety, Paranoia, cardiac arrhythmia, pain, diarrhea
30
May evoke histamine release
Sulfur (thio) containing compounds
31
Mechanism of propofol
Inhibitory transmission of GABA
32
What is intralipid?
Brand name of fat emulsion made from soybean oil, glycerol, and egg lecithin
33
Lecithin
In egg yolks while most allergies to eggs are from the white
34
Propofol supports bacterial growth
Opened vials should be discarded after six hours
35
Phospropofol (Aquavan)
A water soluble prodrug | Side effect of perineal burning
36
Absorption of propofol
IV
37
Distribution - propofol
Highly lipid soluble | Very fast redistribution
38
Redistribution time of propofol
Less than eight minutes
39
Why is propofol suggested to have extrahepatic metabolism?
Biotransformation exceeds HBF
40
Biotransformation of thiopental or propofol is faster?
Propofol is up to ten times faster than thiopental
41
Biotransformation - propofol
Liver conjunction (inactive metabolites) but not affected by moderate cirrhosis
42
What is propofol infusion syndrome and what causes it?
Lactic acidosis after prolonged (>24 hrs) of high dose infusion (>75 mcg/kg/min)
43
Symptoms of propofol infusion syndrome
Lipemia Rhabdomyolysis Metabolic acidosis Death
44
Excretion of propofol
Renal, but not affected by chronic renal failure
45
Dosage - propofol
1.5-2.5 mg/kg 25-75 mcg/kg/min for sedation 100-200 mcg/kg/min for GA - target of 4-6 mcg/ml
46
Risks of using propofol as a sole agent for GA
Risk of awareness | Higher incidence of movement
47
CV effects - propofol
Very decreased SVR, contractility, and preload Hypotension due to above Potential for bradycardia Coronary sinus lactate production
48
What can cause greater CV effects with propofol?
Rapid injection Old age LV failure
49
Respiratory effects of propofol
Profound depression of upper airway reflexes Apnea Decreased hypoxic/hypercapnia drive
50
Does thiopental or propofol produce less wheezing?
Propofol
51
Neuro effects of propofol
Decreased CBF, ICP, CMRO2 Antiemetic, antiepileptic Occasional myoclonus, hiccough
52
What is bradykinin?
Protein produced by propofol and its lipid solvent Vasodilates and increases contact between aqueous phase of propofol and free nerve endings
53
What part of propofol causes burning?
The phenol (present in aqueous phase)
54
Ways to prevent propofol burn
Lidocaine and tourniquet (Bier block) Pretreat with IV opioid (alfentanyl) Mixing with lidocaine to acidify
55
How might lidocaine help with propofol burn?
Inhibits bradykinin
56
Why does propofol have potential for abuse and addiction?
Produces euphoria on emergence, intense dreaming, and amorous behavior
57
Mechanism of etomidate
Depresses reticular activating system | Mimics GABA
58
Reduces the effect of disinhibition of motor activity (myoclonus) from etomidate
Premedications (benzos, opioids)
59
Solubility of etomidate
Highly lipid soluble Dissolved in propylene glycol (burns) Available in fat emulsion (no burn)
60
Absorption of etomidate
IV
61
Distribution of etomidate
Highly protein bound, but highly lipid soluble | Rapid distribution
62
Biotransformation - etomidate
Hepatic hydrolysis and plasma esterases | Impaired in severe liver disease
63
Excretion - etomidate
Urine
64
Dose of etomidate
0.2-0.3 mg/kg
65
What medication is the first line induction agent in trauma or unstable patients? Why?
Etomidate | Minimal CV and respiratory effects
66
Neuro effects - etomidate
Decreased CMRO2, ICP, CBF Myoclonus Antiepileptic PONV
67
Which drug can enhance EEG signal?
Etomidate | Ketamine
68
What kind of EEG signals does etomidate produce in epileptic patients?
Seizure like signals
69
Etomidate transiently inhibits
Cortisol/aldosterone synthesis (lasts 4-8 hours after one dose)
70
Fentanyl ___________ of etomidate
Increases levels and prolongs action
71
Produces dissociative analgesia
Ketamine
72
Mechanism of ketamine
Dissociates thalamus from limbic cortex = "cataleptic state" Inhibition + excitation NMDA antagonist
73
Produces hallucinations
Phencyclidine analogue (ketamine)
74
Absorption of ketamine
IV/IM
75
Solubility of ketamine
Water soluble
76
Distribution of ketamine
Rapid uptake and redistribution
77
Biotransformation - ketamine
Liver metabolism (some active) with high extraction (HBF dependent)
78
Excretion of ketamine
Urine
79
Dose of ketamine
Analgesia: 0.1-0.5 mg/kg Induction: 1-2 mg/kg IV or 4-8 mg/kg IM Mixed with propofol: 1 mg ketamine per 10 mg propofol
80
CV effects of ketamine
Increased HR, BP, CO
81
How does ketamine increase HR, BP, and CO?
By inhibiting the reuptake of norepinephrine
82
Respiratory effects of ketamine
Bronchodilator | Salivation
83
T or F. Ketamine decreases ventilation.
False. Minimal effect
84
Neuro effects of ketamine
Increased CMRO2, CBF, ICP Hallucination Myoclonus, but probably anti epileptic
85
Infusion of which drug can be used to treat chronic pain syndrome?
Ketamine
86
Ketamine potentiates
Neuromuscular blockers
87
Ketamine used with _________ can cause seizures?
Theophylline
88
Ketamine with sympathetic antagonists
Unmasks cardiac depression
89
Ketamine with _____________ inhibits norepinephrine uptake, causing
Tricyclic antidepressants Hypotension HF Ischemia
90
Mechanism of benzos
Enhance GABA in cerebral cortex
91
Benzos soluble in water
Midazolam
92
Benzos insoluble in water
Lorazepam (Ativan) | Diazepam (Valium)
93
Absorption of benzos
IV/IM PO Nasally SL
94
Why are benzos a poor choice for GA?
IV required | Significant first pass hepatic effect
95
Distribution of midazolam
Moderately lipid soluble Rapid redistribution Protein bound
96
Duration of benzo effect
18-20 min
97
Onset and peak effect of midazolam
30-60 sec onset | Pam effect in 5 min
98
Biotransformation of benzos
Hepatic (CYP3A4)
99
Which benzo has a long elimination half life, low hepatic extraction, and active metabolites?
Diazepam
100
Which benzo has medium elimination?
Lorazepam due to lower lipid solubility
101
Which benzo has the fastest elimination?
Midazolam, high hepatic extraction
102
Excretion of benzos
Urine
103
Dose of midazolam
Premed: 0.04-0.08 mg/kg IV, 0.4-0.8 mg/kg PO Induction: 0.1-0.3 mg/kg IV (slow recovery) Infusion: 0.02-01 mg/kg/hr
104
Can reduce hallucinations from ketamine
Benzos
105
CV effects of benzos
Minimal depression
106
Respiratory effects of benzos
Small decrease in hypercapnic drive
107
Neuro effects of benzos
``` Decreased CMRO2, CBF, ICP Anterograde amnesia Anxiolysis Anti seizure Muscle relaxation ```
108
Barbs or benzos decrease ICP more?
Barbs Benzos do not cause burst suppression
109
Symptoms of benzo withdrawal
Irritability Tremulousness Insomnia Death
110
Slows diazepam clearance
Cimetidine
111
Benzos and heparin
Displaces diazepam from protein binding
112
Slows midazolam clearance
Erythromycin
113
Benzos interact synergistically with
Volatiles, opioids, ethanol, barbs, CNS depressants
114
Why is flumazenil used as a reversal for other benzos? Dose?
High affinity for receptor with minimal activity 0.01 mg/kg up to 0.2 M IV bolis
115
Max dose of flumazenil
1 mg 0.2 mg repeated every minute up to five doses Resedation likely - redoes at 20 min intervals
116
T or F. Flumazenil decreases MAC.
False, no effect
117
Mechanism of decmetetomidine (precedex)
Highly selective alpha 2 receptor agonist
118
Which is more selective for the alpha 2 receptor? Dexmedetomidine or clonidine?
Dexmedetomidine
119
Used for sedation of ventilated ICU patients
Dexmedetomidine
120
Uses for dex
Anxiolysis MAC Anesthesia adjuvant Awake intubations
121
Dose of dex
0.2-0.7 mcg/kg/hr | TIVA 5-10 mcg/kg/hr (I've never seen it)
122
CV effects of dex
Hypotension | Bradycardia
123
Respiratory effects of dex
Minimal
124
At high doses, dex can reduce the MAC of volatiles by
90%
125
Why can dex be used for awake intubation?
Calm sedation with rousability
126
Which induction agent can decrease CMRO2 to burst suppression on EEG?
Barbs
127
Which barb can cause neuro excitation?
Methohexital

Pharmacology for Anesthesia (9 decks)

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