Barb/Non-Barb EXAM REVIEW Flashcards

1
Q

What is a common side effect associated with the use KETAMINE? (MUPU)

A

-Unique in its ability to stimulate the CV system
-Unique in its ability to cause emergence delirium
- May ⇧ ICP placing pts with intracranial pathology at
risk
- Produces CV effects that resemble sympathetic
nervous system stimulation (INCREASES HR and BP)

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2
Q

What is a common side effect associated with the use ETOMIDATE?

A

CV stability is characteristic with 0.3mg/kg IV
induction dose
• Minimal changes in HR, stroke volume or cardiac
output
MYOCLONUS: Excitatory effects that manifest as spontaneous movements, dystonia and tremor
• ⇩ cerebral blood flow and CMRO2
• ⇩ ICP

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3
Q

What is a common side effect associated with the use PRECEDEX?

A

Hypotension, transient HTN
Nausea, bradycardia, fever, vomiting, hypoxia
Tachycardia, anemia, dry mouth, thirst

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4
Q

What is a common side effect associated with the use PROPOFOL?

A

CNS
⇩cerebral metabolic rate for oxygen (CMRO2)
⇩ ICP and cerebral blood flow
⇩burst suppression)
⇩ somatosensory evoked potentials (SSEP) and
motor evoked potentials (MEPs)

CV
⇩ in systemic BP( ⇩ preload) greater than
equivalent thiopental dose
⇩ BP often accompanied by changes in cardiac
output and SVR
BRADYCARDIA
- Relaxation of smooth muscle is due to inhibition of
sympathetic vasoconstrictor nerve activity
• Stimulation of laryngoscopy and intubation reverses
BP effects of propofol
• BP effects exaggerated in hypovolemic, elderly, & pt
with compromised LV function due to CAD
• Adequate hydration recommended prior to administering propofol

RESP
Maintenance doses of propofol ⇩ Vt and RR
• Causes bronchodilation and ⇩ incidence of
intraoperative wheezing in asthma pt
• ⇩Ventilatory response to CO2 & arterial hypoxemia

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5
Q

What is a common side effect associated with the use METHOHEXITAL?

A

High dose associated with seizures
Normovolemic pt- transient 10-20 mmHg ⇩ in BP
and offset by compensatory 15-20BPM ⇧ in HR
Overdose or large dose to ⇩ ICP may cause direct
myocardial depression
Induction- mild, transient ⇩ BP due to peripheral
vasodilation (mostly venous), reflecting depression
of the medullary vasomotor center and ⇩
sympathetic nervous system outflow

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6
Q

Propofol dose :_______equivalent _________ thiopental or __________Methohexital

A

• 1.5-2.5mg/kg IV is equivalent to 4-5mg/kg

thiopental or 1.5 mg/kg methohexital

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7
Q

What is the most likely mechanism of action for Ketamine?

A

• NMDA receptor, member of the glutamate receptor,
ligand gated ion channel
• Ketamine- inhibits activation of the NMDA receptor by
glutamate, ⇩presynaptic release of glutamate and
potentiates GABA
• Ketamine- noncompetitive antagonist of NMDA receptor
• Interacts with the phencyclidine-binding receptor site,
leading to inhibition of NMDA activity

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8
Q

What is the most likely mechanism of action of ETOMIDATE?

A

Binds GABA and enhances the affinity of the inhibitory
neurotransmitter (GABA) for these receptors
• Etomidate does not modulate other ligand gated ion channels at clinically relevantconcentrations

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9
Q

What is the most likely mechanism of action PRECEDEX?

A

• Highly selective, specific and potent full alpha 2
adrenergic agonist(1600 times the affinity for the
receptor)
• Indicated as an adjunct for anesthesia and ICU sedation
Produces hypnotic, sedative and analgesic effects
Produces pharmacologic effects similar to
clonidine-
clonidine is partial alpha 2 agonist

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10
Q

What is the most likely mechanism of PROPOFOL ?

A

Sedative-hypnotic effects via GABA activation
• Selective modulator of GABA receptors
• GABA receptor activated= ⇧chloride ions=
hyperpolarizes cell= functional inhibition
• Propofol may also ⇩ the rate of GABA dissociation
from the GABA receptor

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11
Q

What is the most likely mechanism of action METHOHEXITAL ?

A

Works on GABA in the CNS
• Produces sedative-hypnotic effects
• GABA hyperpolarizes postsynaptic cell
• Barbiturates and propofol ⇩ dissociation of GABA
from receptor and ⇧duration of GABA activated
opening of chloride channels

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12
Q

How does Ketamine affect ventilation and management of a patient’s airway?

A

• Upper airway skeletal tone is well maintained
• ⇧ salivary secretions=need to protect airway
• Bronchodilator activity- successful treatment of
status asthmaticus has been reported with
ketamine

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13
Q

How does Ketamine affect ventilation and management of a patient’s airway?

A

NO SIGNIFICANT RESPIRATORY DEPRESSION
• Upper airway skeletal tone is well maintained
• ⇧ salivary secretions=need to protect airway
• Bronchodilator activity- successful treatment of
status asthmaticus has been reported with
ketamine

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14
Q

What are major warnings, disadvantages and contraindications with the use of Barbiturates?

A

High dose = hypotension = ⇩ cerebral perfusion
pressure ‘•
Intra-Arterial Injection –>Immediate, intense vasoconstriction and excruciating pain that radiates along the distribution of the artery

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15
Q

What are major warnings, disadvantages and contraindications with the use of Barbiturates?

A

High dose = hypotension = ⇩ cerebral perfusion
pressure ‘•
Intra-Arterial Injection –>Immediate, intense vasoconstriction and excruciating pain that radiates along the distribution of the artery
(Gangrene and permanent nerve damage may result
• Risk ⇧ with ⇧ drug concentrations)
Venous thrombosis
Cross placenta
This ⇧ production of Heme, and may exacerbate
acute intermittent porphyria

For induction of anesthesia, barbs produce a dose
dependent depression of the medullary and pontine
ventilatory centers
• Leads to ⇩ response to hypercarbia
• Low RR and Low tidal volumes
⇧Apnea risk when used with other CNS depressant
drugs used for preop medication
Large doses needed to suppress laryngeal reflexes
& cough
Laryngospasm or bronchospasm may occur during
intubation attempts- no LMA

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16
Q

Barbiturate use is declining due to

A

• Lack specificity of effect in the CNS
• Lower therapeutic index than benzodiazepines
• Result in tolerance more easily than benzodiazepines
• Greater liability for abuse
• High risk for drug interaction
• Paradoxical excitation especially in the elderly
• ⇩ in pain threshold with small doses
• Hangover effect
• No skeletal muscle relaxation- to be effective
clinically

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17
Q

What IV induction agent should be avoided in a hypovolemic patient?

A

BARBITURATES

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18
Q

What are the cardiovascular effects of Methohexital?

A

⇩ in BP and offset by compensatory 15-20BPM

⇧ in HR

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19
Q

What are the cardiovascular effects Propofol ?

A

⇩ in systemic BP( ⇩ preload) greater than
equivalent thiopental dose
⇩ BP often accompanied by changes in cardiac
output and SVR
BRADYCARDIA

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20
Q

What are the cardiovascular effects PRECEDEX?

A

Hypotension
Transiet HTN
Brady/Tachy

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21
Q

What is a common concern regarding the use of etomidate?

A

MYOCLONUS• Can ⇩ myoclonus incidence with 1-2mcg/kg fentanyl or a benzodiazepine prior to etomidate
injection

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22
Q

What are all the advantages with the use of propofol?

A

• Rapid and complete awakening compared to other induction agents
• Minimal residual CNS effects
• No MH activation
• Doesn’t affect steroid synthesis or ACTH response
• Does not alter hepatic or fibrinolytic function
• Does not cause histamine release
• Context sensitive half time is minimally influenced by
duration of infusion (<40 minutes for up to 8hr infusion)
• Antiemetic and antipruritic effects

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23
Q

What are all the disadvantages with the use of propofol?

A

Dose dependent ventilatory depression
• Allergic reaction to phenol nucleus and diisopropyl
side chain
• May lead to anaphylaxis
May lead to bronchoconstriction
• Prolonged myoclonus has been reported in pt with
meningismus
• Potential for bacterial contamination. Propofol
strongly supports the growth of E-coli and
pseudomonas aeruginosa
• Use aseptic technique
• Discard unused portion in 6 hours
• Change infusion line q 12 hours
• HIGH abuse potential- high risk of death
Propofol infusion syndrome
• s/s Lactic acidosis, bradycardia unresponsive to
treatment, fat infiltrated liver, rhabdomyolysis
Pain at injection site

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24
Q

How is the primary action of barbiturates terminated?

A

Redistribution terminates action of methohexital (barb)

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25
Q

How is the primary action of propofol terminated?

A

Redistribution terminates action of propofol

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26
Q

How is the primary action of ketamine terminated?

A

Redistributed

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27
Q

How is the primary action of etomidate terminated?

A

Prompt awakening is the result of REDISTRIBUTION to

inactive tissues

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28
Q

How is the primary action of precedex terminated?

A

?

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29
Q

How is naloxone classified?

A

Opiod antagonist

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30
Q

What is mechanism of action of the neurotransmitter GABA?

A

GABA hyperpolarizes postsynaptic cell

Major INHIBITORY NEUROTRANSMITTER IN the BRAIN

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31
Q

What is mechanism of action of the neurotransmitter GABA?

A

GABA Major INHIBITORY NEUROTRANSMITTER IN the BRAIN
GABA receptor is a CHLORIDE ION CHANNEL –> When GABA binds to the receptor , CHLORIDE IONS enters cell
GABA hyperpolarizes postsynaptic cell
Decrese NEURON’s action potential

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32
Q

Which of the neurotransmitters are excitatory? Which of the neurotransmitters are inhibitory?

A

Excitatory: GLUTAMATE

Inhibitory : GABA

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33
Q

Which IV induction agents lead to severe tissue damage when given intra-arterially? How can those be prevented? How can this be treated?

A

Methohexital,
• Gangrene and permanent nerve damage may result
• Risk ⇧ with ⇧ drug concentrations

Treatment
Immediate attempts to dilute drug, prevention of arterial spasm, general measures to maintain blood flow
–>Lidocaine, papaverine, phenoxybenzamine
–>sympathectomy of the upper extremity
produced by a brachial plexus block

Prevented by using dilute concentrations
• 1% methohexital

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34
Q

Explain differences between thiobarbiturates and oxybarbiturates?

A

• Oxybarbiturates metabolized only in hepatocytes
Thiobarbiturates are more potent than oxybarbiturates as they are more lipid soluble (the exception is methohexital which is an oxybarbiturate & is actually more potent than thiobarbiturates d/t ionization and physiologic pH)

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35
Q

EXTRA Avantageous characteristic/characteristics of thiopental (Pentothal) and methohexital (Brevital):

A

Short duration

Rapid onset of action

36
Q

EXTRA: Barbiturate pharmacology: pulmonary effects

A

Respiratory depression

Laryngospasm

37
Q

EXTRA: Avoid in pt with Acute Intermittent Porphyria

A

Methohexital

38
Q

Barbiturate causes

A

Vasodilation

39
Q

EXTRA: Enhancement of neuronal inhibition by barbiturates occur at synapses using this neurotransmitter.

A

GABA

40
Q

How do barbiturates affect ICP and CMRO2?

A

DECREASE BOTH

• Barbs used to ⇩ ICP, along with hyperventilation &
diuresis
• ⇩ ICP by ⇩ cerebral blood volume through drug
induced cerebral vasoconstriction and associated ⇩
in cerebral blood flow
• Barbs ⇩ metabolic oxygen requirements (CMRO2)
• Isoelectric EEG=max barb effect and ⇩ CMRO2 55%
• No improved outcomes for head trauma pt

41
Q

In patients with what comorbid conditions would it be recommended to decrease the dose of methohexital?

A

Uremic
Cirrhosis
LIVER ISSUES

42
Q

What IV induction agent would be best for placing an LMA?

A

PROPOFOL

43
Q

What is expected next if a patient yawns while increasing the dose of propfol?

A

APNEA

44
Q

What clinical effects are expected with induction doses of ketamine?

A

Eyes remain open
nystagmic gaze
Increased oral secretions
amnesia, bronchodilation, increased HR and CO, increased ICP and emergence delerium.

45
Q

How does propofol affect ventilation

A

Dose dependent depression of ventilation
• Apnea occurring in 25-35% of pts after induction
• Effect enhanced with preoperative opioids
• Painful stimuli may counteract this effect
• Maintenance doses of propofol ⇩ Vt and RR
• Causes bronchodilation and ⇩ incidence of
intraoperative wheezing in asthma pt
• ⇩Ventilatory response to CO2 & arterial hypoxemia

46
Q

How are barbiturates classified? What drugs fall into each class?

A

Oxybarbiturates: Methohexital,phenobarbital and pentobarbital
Thiobarbiturates: Thiopental, thiamylal

47
Q

What are the IV/IM induction doses of Ketamine?

A

1-2mg/kg IV

4-8mg/kg IM

48
Q

What is the mechanism of action of ketamine? Where in the CNS does ketamine work?

A

Ketamine- inhibits activation of the NMDA receptor by glutamate, ⇩presynaptic release of glutamate and potentiates GABA
• Ketamine- noncompetitive antagonist of NMDA receptor
• Interacts with the phencyclidine-binding receptor site,
leading to inhibition of NMDA activity
Works on Mu, Kappa and Delta receptors

49
Q

What are the IV induction doses of methohexital, propofol, precedex, etomidate?

A

Methohexital dose 1-1.5mg/kg

Propofol dose is 1.5-2.5 mg/kg

50
Q

What are the IV induction doses PRECEDEX?

A

Precedex
Initial dose 1mcg/kg IV, load over 10 minutes then 5-10mcg/kg/hour= TIVA without ventilatory
depression
0.2-1.5mcg/kg/hr -postop sedation

51
Q

What are the IV induction doses of ETOMIDATE

A

0.2-0.4 mg/kg

52
Q

What patients are at risk for emergence reactions? How can this be prevented?

A
  • Pts treated with ketamine dose > 2mg/kg
  • > 15 years of age
  • female
  • Hx of personality disorder or frequent dreaming
53
Q

What IV induction agent has anticholinergic side effects

A

KETAMINE

54
Q

What are advantages of the iv induction agent ketamine

A

Increases SVR, PVR, and SBP 20-40 mmHg.
No significant depression of ventilation and upper airway skeletal tone is well maintained.
Useful for burn dressing changes and hypovolemic patients.

55
Q

PREVENTION OF EMERGENCE DELIRIUM -KETAMINE

A

Benzodiazepine- most effective
Midazolam > diazepam
Give benzo 5 min prior to induction Inclusion of thiopental or inhalational agents may⇩incidence
ATROPINE or DROPERIDOL may ⇧ incidence of
emergence delirium with ketamine

56
Q

Methohexital vs thiopental

A

Methohexital has higher hepatic clearance than thiopental because of a Higher extraction ratio (3-4X more)

57
Q

Methohexital vs thiopental recovery of motor function

A

Earlier return to psychomotor recovery than thiopental

58
Q

Non-ionization of thiopental vs Methohexital

A

Thiopental 65

59
Q

Thio vs Metho reflecting less lipid soluble

A

More rapid metabolism than thiopental,

60
Q

Distribution half time of thiopental vs Methohexital

A

Methohexital 5.6 mins

Thiopental 8.5mins

61
Q

Elimination half time of Methohexital vs Thiopental

A

Methohexital 3.9 hours

Thiopental 11.6 hours

62
Q

Clearance Methohexital vs Thiopental

A

Methohexital 2.2 L/kg

Thiopental 2.5 L/kg

63
Q

Oxybarbiturates

A

Oxygen in the pyrimidine nucleus at carbon 2 position’

Methohexital

64
Q

Thiobarbiturates

A

Sulfur atom at the Carbon 2 position (Thiopental)

65
Q

Barbiturates are

A

Sodium salts

66
Q

You cannot mix barbiturates with

A
  • Acidic solution
  • LR
  • water soluble drugs
    Can lead to precipitation and occlusion of an IV line
67
Q

Use to induce seizures

A

Barbiturates and methohexital

68
Q

2 major contraindications to Barbiturates

A

Porphyrias

Hypovolemia

69
Q

Intra arterial injection

A

Thiopental or Methohexital

70
Q

Methohexital redistribution

A

Redistribution- terminates action- about 8.5

minutes

71
Q

Intra-arterial Injection immediate treatment

A

Treatment-immediate attempts to dilute drug,
prevention of arterial spasm, general measures to
maintain blood flow
Lidocaine, papaverine, phenoxybenzamine
sympathectomy of the upper extremity
produced by a brachial plexus block

72
Q

Cirrhosis , renal failure and barbiturates

A

Increase concentration of free barbiturates, RECUE DOSE by 50%

73
Q

Acidosis and BARBITURATES

A

Acidosis will INCREASE the NONIONIZED fraction and favor transfer of these agents into the brain

74
Q

ALKALOSIS and Barbiturates

A

Increase the dose.

75
Q

What induce oxidative microsomal enzymes

A

Chronic Use of barbiturates

76
Q

Reason why people awaken more quickly from Methohexital infusion relates to

A

Higher rate of hepatic clearance

77
Q

Barbiturates metabolism

A

Conjugated into water soluble metabolites , excreted in urine

78
Q

First order

A

a constant fraction

79
Q

Zero order

A

a constant amount

80
Q

Barbiturates are (acids vs bases)

A

Weak acids

81
Q

Barbiturates toxicity

A

Sodium bicarbonate to accelerate elimination

82
Q

High doses of methohexital associated with

A

Seizures

83
Q

Barbiturates on Pulmonary system

A

Brief period of apnea lasting 30-45 sec
60-90 second after admin
Full recovery in 15 mins

84
Q

Capable of brain protection

A

Barbiturates

85
Q

Focal cerebral ischemia protection

A

Barbiturates

86
Q

Barbiturates contraindicated in

A

Acute porphyria