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Duke Pharmacology- Hannah > IV Anesthetics > Flashcards

IV Anesthetics Flashcards

1
Q

What ideal drug property does propofol violate?
A. Pain on Injection
B. Context sensitive half-time is 40 minutes
C. Can cause bradycardia & hypotension
D. Two of the above
E. None of the above

A

D. It is water insoluble so causes pain on injection & can cause bradycardia & hypotension
These violate the 7 ideal drug principles: water soluble, no hypersensitivity reactions, fast on, fast off, quick return to mental baseline, limited CV and respiratory issues, steep dose-response relationship

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2
Q

What is the mechanism of action of propofol?

A

Binds allosterically to GABA, allows Cl- to come in and hyperpolarize the cell (inhibitory)

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3
Q

What are the ideal properties of a drug?

A
  1. Water soluble
  2. Limited CV & Respiratory Effects
  3. No hypersensitivity reactions
  4. Quick on (quick onset of action)
  5. Quick off (metabolized quickly)
  6. Steep dose-response relationship
  7. Quick return to baseline mental status
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4
Q

Chemical Structure of Propofol

A

“Snowman” Phenol with two arms

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5
Q

What is the pH and pKa of Propofol?

A

Diprivan: pH:7-8.5 pKa: 11
Propfol: pH: 4.5-6.4 pKa: 11
pH differs due to additives/manufacturing

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6
Q

What is a principle advantage of propofol?
A. it has antiemetic properties
B. antagonist is flumazenil
C. Rapid return to consciousness
D. Not influenced by renal or liver dysfunction

A

C. Rapid return to consciousness

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7
Q 
Which enantiomer of propofol produces bronchodilation?
A. S-enantiomer
B. R-enantiomer 
C. It comes in a racemic mixture
D. Propofol is non-chiral
A

D. Propofol is non-chiral

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8
Q

What is the stability of propofol?

A

Allows for bacterial growth so open vial must be thrown out after 6 hours

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9
Q

What is the best way to prevent pain on injection of any drug?

A

Large bore IV in large

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10
Q

What is the antagonist or reversal agent of propofol?

A

There is none! We are married to its effects

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11
Q

What is the clearance of propofol?

A

0.87, clearance exceeds hepatic blood flow

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12
Q

Propofol Clearance

A

Clearance exceeds hepatic blood flow
-Tissue uptake in the lungs- reduces initial conc. next round of blood comes in and diffuses from lungs back into blood
-extensive hepatic metabolism CYP450
Propofol is not influenced by hepatic or renal dysfunction
Decreased rate of plasma clearance in patients older than 60

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13
Q

Metabolite of propofol

active or inactive?

A

Active: 4-hydroxypropofol

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14
Q

Context sensitive half-time of propofol

A

<40 minutes

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15
Q

Hypersensitivity with propofol

A 
egg lecithin 
sulfite allergies (asthmatics)
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16
Q

What drugs would you not give to patients with porpyphria?

A

Barbiturates, diazepam, & etomidate

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17
Q

Protein binding with propofol

A

98% bound, 2% free (increased in pregnancy, severe hepatic and renal disease)

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18
Q

What drugs produce myoclonus?

A

methohexital, etomidate, propofol (rare)

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19
Q

Neuro effects of propofol

A

Good for neuroprotection (outside of high ICP)

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20
Q

CV effects of propofol

A

hypotension due to decrease in sympathetic tone and vasodilation (primarily)
CNS, cardiac, and baroreceptor depression

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21
Q

Your preceptors asks you why propofol causes hypotension. What do you tell them?

A

Propofol decreases sympathetic tone and vasodilation

Also has CNS, Cardiac & baroreceptor depression

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22
Q

What respiratory effects does propofol have?

A

Respiratory depression common in induction doses
-Dose dependent w/ infusions secondary to decreased sensitivity of respiratory center to CO2
Minimal bronchodilation

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23
Q

Induction dosage of propofol

A

Adult dose 1.5 to 2.5 mg/kg (decrease in elderly, increase in kids, effects exaggerated with CV disease)

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24
Q

When do you decide to give ideal vs. actual body weight dosage?

A

Liphophilic drug would give true body weight whereas drugs that stay in blood stream we’ll error on side of ideal body weight

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25
Q

What drug would you give to cause respiratory depression for induction?

A

Propofol causes more than etomidate and ketamine

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26
Q

Propofol dose of IV sedation:

A

25-100 mcg/kg/min
minimal/no analgesic properties (give something for pain!)
can be used in conjunction with anxiolytic and opioid
prompt recovery without residual sedation-great for endoscopy

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27
Q

Propofol dose for maintenance of anesthesia:

TIVA (total IV anesthetic) dosage

A

100-300 mcg/kg/min
associated w/ minimal postop n/v
used in conjunction w/ short-acting opioid

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28
Q

Other applications of propofol & dosages

A

Antiemetic: 10-15 mg IV; followed by 10 mcg/kg/min infusion
Antipruritic: 10 mg IV related to intrathecal opioids, cholestasis
Anticonvulsant: 1 mg/kg IV
Attenuate bronchoconstriction: effects intracellular Ca++ homeostasis
Analgesic (neuropathic pain)

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29
Q

Contraindications of propofol

A

Hypersensitivity (lethicin- found in eggs, peanuts, soybeans)
Lipid metabolism disorder
Sulfate allergy
Use caution in elderly, debilitated and cardiac-compromised patients

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30
Q

What does PRIS stand for & what is it?

A

Propofol infusion syndrome
seen in long-term, high dose infusions of propofol
associated with significant morbidity and mortality

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31
Q

Which of the following patients has a higher likelihood of developing PRIS?
A. 85 year old patient undergoing right hip fixation with active liver disease
B. Patient intubated in the ICU for shock receiving steroids
C. Older patient coming from ICU for intraop procedure who has been receiving propofol for 7 days
D. Child who is coming in for tonsillectomy

A

C.

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32
Q

Risk factors of PRIS:

A

> 4mg/kg/hr, >48 hr dose, critical illness, high fat-low carb intake, concomitant catecholamine infusion, steroid administration and inborn errors of mitochondrial fatty acid oxidation

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33
Q

Signs of PRIS:

A 
high anionic gap metabolic acidosis
cardiac failure
persistent bradycardia refractory to treatment
fever
severe hepatic and renal disturbances
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34
Q

Which of the patient’s is not experiencing a symptom of PRIS?
A. Patient is bradycardic to 45 and not responsive to atropine administration
B. Patient is in septic shock with fever of 104
C. Patient with a pH 7.0, pCO2: 35, bicarb: 14
D. Patient with high ALT/AST
E. Patient with drop in urine output to 10cc/shift
F. All patients are experiencing symptoms of PRIS

A

F.

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35
Q

What is happening in PRIS?

A

-Propofol is triggering agent (catechol & steroids already given)
Fatty acid and mitochondrial activity impaired- creates oxygen supply-demand mismatch causing tissue necrosis
Propofol inhibits oxidative phosphorylation preventing long-chain fatty acids into the cell, inhibits mitochondrial respiratory chain and blocks beta adrenoreceptors and calcium channels

36
Q

Extensive s/s of PRIS:

A

CV: hypotension, bradycardia, widening QRS, VTACH, VFIB, asystole, ischemic EKG, arrhythmia, heart failure
Respiratory: hypoxia, pulmonary edema
Renal: acute kidney injury, hyperkalemia
Musculoskeletal: rhabdomyolysis
Metabolic: hyperthermia, high anion gap met acidosis, urine discoloration
Hepatic: hepatomegaly, abnormal LFTs, Steatosis, lipidemia, hypertriglyceridemia

37
Q

Propofol Abuse

A

Not a controlled substance (facility dependent)
addictive properties to propofol b/c you can sleep for 10 minutes and wake up feeling refreshed
Can develop tolerance

38
Q

Etomidate pH, pKa

A

pH: 8.1, pKa 4.2, etomidate is also chiral (administered as single isomer-R+ isomer 5x more potent)

39
Q

Why we would use etomidate over propofol?

A

Doesn’t burn on injection, no CV swings

40
Q

Mechanism of action: etomidate

A

allosteric agonists

41
Q

Volume of Distribution: etomidate

A

0.6 mL/kg

42
Q

Etomidate drug class

A

sedative hypnotic, base

43
Q

Etomidate binding

A

75% bound to plasma albumin (decrease in albumin increases active fraction significantly)

44
Q

Etomidate metabolism

A

metabolized by hydrolysis: phase 1
Plasma esterases and microsomal enzymes in the
liver

45
Q

Onset of etomidate

A

rapidly; return to consciousness 5 to 15 minutes

46
Q

Etomidate CNS

A

CBF & CMRO2 decreased, decrease in ICP while maintaining CPP
Involuntary myoclonic movements common

47
Q

Why wouldn’t you want to use etomidate if monitoring neurofunction?

A

due to CNS effects it decreases amplitude and increases latency
also can cause myoclonus

48
Q

Etomidate CV/Resp

A

maintains hemodynamic stability (advantage over propofol)
acts on alpha 2-B adrenergic receptors which
mediates increased BP
Minute volume decreases but RR increases

49
Q

Clinical Usage/Induction dose

A

No longer used as infusion d/t adrenal cortical depression

Induction doses up to 0.2-0.4 mg/kg

50
Q

True or false: etomidate has analgesic properties

A

False; of our sedative hypnotics only ketamine has true analgesic properties (could argue that propofol blunts neuropathic pain)

51
Q

Side effects and complications of etomidate:

A
  • spontaneous myoclonus occurs in >50% of patients
    admin of benzos or fentanyl can decrease
    incidence
    -etomidate causes adrenocortical suppression
    -increased incidence of postoperative n/v
    -porphyrias
52
Q

How does etomidate cause adrenocortical suppression

A
  • inhibits conversion of cholesterol to cortisol (11B-hydroxylase)
  • lasts greater than 8 hours after induction dose
  • avoid in septic shock
53
Q

Dislikes about etomidate

A

Adrenal cortical suppression, postop N/V, could take 15 min. to wear off

54
Q

Ketamine (phenycylidine) pKa, PH

A

base: pH 3.5-5.5, pKa 7.5

55
Q

Function of Ketamine:

A

provides “dissociative anesthesia”
Potent amnestic and analgesic
cataleptic state where eyes remain open with a slow nystagmic gaze

56
Q

Chirality of ketamine

A

comes in racemic mixture

57
Q

Pharmacokinetics of ketamine

A

not significantly bound to plasma proteins (12%); rapid distribution to tissues
highly lipid soluble, rapid transfer to BBB

58
Q

How is ketamine metabolized?

A

Demethylation of ketamine by CYP450 microenzymes-phase 1

metabolism dependent on hepatic flow

59
Q

Metabolite of ketamine

A

Norketamine

60
Q

Elimination half-life of ketamine

A

2-3 hours (d/t active metabolite)

61
Q

Mechanism of action of ketamine

A

binds non-competitively to the phenylcyclidine site on NMDA receptors (antagonist- glutamate)
exerts effects on opioid, monoaminergic, muscarinic,
VG Na+ receptors, Ca2+ channels and nAChr
channels
weak actions on GABA receptors

62
Q

An elderly patient with HTN & asthma is coming in for a general anesthetic procedure involving the eye. What would be your drug of choice for intraop sedation?

A

Propofol (have good window d/t baseline CV status), do not use ketamine as contraindicated in intraocular procedures due to increased IOP

63
Q

Which drug is contraindicated in a patient with a closed head injury?

A

Ketamine b/c it raises CBF, CMRO2, and ICP although can be attenuated w/ opioid and benzodiazpines

64
Q

What drug may cause a more difficult airway placement?

A

ketamine b/c it causes increased secretions which may block view

65
Q 
Ketamine causes a \_\_\_\_ in the sympathetic nervous system to get a \_\_\_\_\_ in HR, BP, and SVR
A. Increased, decrease
B. Increase, Increase
C. Decrease, increase
D. Decrease, decrease
A

B.

66
Q

What patient would ketamine best drug to use for?
A. patient post MVA with a closed head injury
B. Patient with CAD
C. Patient with hypovolemic shock secondary to MVA
D. patient with chronic pain

A

C. good induction agent for patients in hypovolemic shock as it increases sympathetic nervous system and causes increase in BP, HR

67
Q

Induction dose of ketamine

A

1-2.5 mg/kg IV
4-8 mg/kg IM (<10 minutes)
10 mg/kg orally (10-20 minutes)

68
Q

What dose would you use to provide analgesia with ketamine?

A

0.2-0.5 mg/kg

69
Q

To provide more stable hemodynamic effects while avoiding unwanted emergence reactions

A

we could give subanesthetic doses of ketamine combined with propofol

70
Q

Side effects of ketamine:

A

potent cerebral dilator: avoid in patients where increased ICP would be concerning (intraocular)
tolerance can occur
-pulmonary arterial BP, HR, CO, Cardiac work, and myocardial O2 requirements increased
-increased oral secretions
-enhances non-depolarizing NMJ blockers
-Apnea after admin of succ is prolonged d/t inhibition of plasma cholinesterases

71
Q

emergence delirium

A

incidence: 5-30%; partially dose dependent
- associated w/ visual, auditory, proprioceptive, and confusional illusions
- could have morbid content and vivid color

72
Q

Which patient is at higher risk for emergence delirium?
A. 14 year old male undergoing baclofen pump placement
B. 60 year old male veteran undergoing a toe amputation
C. 46 year old cancer patient with history of depression undergoing mastectomy
D. Emergence delirium is rare & most likely will not be experienced

A

B.

73
Q

MOA of Dextromethorphan

A

low-affinity NMDA antagonist

74
Q

Dexmedetomidine mechanism of action

A

Alpha2 antagonist (more selective for A2 than A1)
high density of these receptors found in pontine locus ceruleus
-differs from GABA drugs in that it produces sedation by decreasing sympathetic nervous system activity
inhibits norepinephrine release

75
Q

What is the reversal of dexmedetomidine

A

Atipamezole

76
Q

Binding, metabolism and half-life of dexmedetomidine

A

highly protein bound
undergoes extensive hepatic metabolism
half-life 2-3 hours

77
Q

Clinical uses of dexmedetomidine:

A

pretreatment: attenuates hemodynamic response to tracheal intubation, decrease MAC & opioid requirements, increases hypotension

78
Q

Side effects of dexmedetomidine:

A

severe bradycardia/asystole

79
Q

Dosage of dexmedotimidine

A

TIVA: 0.5-1 mcg/kg bolus over 15 minutes

0.2-0.7 mcg/kg/hr infusion (up to 24 hours)

80
Q

Scopolamine Class

A

anticholinergic (only anticholinergic used for sedation)

81
Q

How does scopolamine cause sedation

A

decreases activity of the reticular activating system

82
Q

Preop sedation dosage

A

0.3-0.5 mg IV/IM

83
Q

Scopolamine pearls

A

strong antisialagogue effect-reduces rate of saliva
transdermal for N/V
Cross BBB and has least effect on HR
synergistic w/ opioids/benzos

84
Q

Scopolamine side effects

A

Mydriasis (Bella Donna) pupil dilation- check your pupils
Cycloplegia- inability to focus for near vision
Central anticholinergic symptom- can become unconscious
Overdose- characteristic of muscarinic cholinergic blockade (dry mouth, difficult swallowing, blurred vision, tachy, can’t sweat)

85
Q

Scopolamine reversal

A

Physostigmine- anticholinesterase
15-60 mcg/kg IV
Repeat as needed

Duke Pharmacology- Hannah (14 decks)

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