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Flashcards in Anesthesia Deck (32):
1

zero order

not constant and dependent upon plasma (constant mg/hr)

2

Clearance of drugs with first order kinetics

constant regardless of plasma concentration (%)

3

Phase 1 metabolism

Converts parent drug to more polar
(water soluble)

4

Phase II metabolism

Conjugate drug with polar moiety
making it more water soluble

5

Distribution of Cardiac Output

VRG= 10% body mass but 75% CO
Muscle = 40% body mass but 19% CO
Fat = 30% body mass but 6% CO
VPG = 20% body mass but 0.5% CO

6

Albumin binds _____ drugs?

Acidic I.e. Barbiturates

7

A1AG bind to _____ drugs?

Basic I.e. Local anesthetics

8

Which diseases decrease Albumin available to bind to drugs?

liver, kidney, CHF, Cancer which increase available drug

9

Which diseases decrease A1AG available to bind to drugs?

trauma, infection, MI, chronic pain

10

Volume of Distribution

total amount of drug in the body/drug blood concentration
– VD 0.7=total body water

11

Propofol Mech. of action?

Presumed interaction with GABA
– Delays the dissociation of GABA from receptors
• Increasing GABA activated opening of chloride ion channels
• Also acts as a sodium channel blocker
– Hyperpolarization of cell membranes.

12

Propofol Pharmacokinetics?

- 95-99% protein binding
- Metabolized via glucoronidation in the liver (up to 30% possibly in lungs
- Renal excretion

13

Dosing Propofol?

Induction - 1.5-2.5 mg/kg (adults) - decrease in elderly
- 2.5-3.5 mg/kg (kids)
Sedation (MAC) - 25-100mcg/kg/min
TIVA - 100-300 mcg/kg/min

14

Propofol effects on Cardio?

SBP ⇓d; MAP ⇓d; SVR ⇓d; HR ⇔
– Profound arterial and venous vasodilation ⇓s both preload and afterload.

15

Propofol effects on RESP and CNS?

RR depressed dose dependent—apnea after bolus
– Reduces airway reflexes

CBF ⇓d; ICP ⇓d; CMRO2 ⇓d; ⇓d IOP

16

What is Propofol infusion syndrome?

Acute refractory bradycardia (kids)
– RBBB is an early sign
– May lead to asystole if one or more:
• Metabolic acidosis
• Rhabdomyolisis
• Hyperlipidemia
• Enlarged or fatty liver
– Associated with propofol infusion >4mg/kg
for long duration (> 48 hours)

17

Fospropofol

Prodrug of Propofol
Longer onset
6.5 mg/kg (60-90kg)
Perianal paresthesia in 74%

18

Prop key points? - take home?

Awaken due to redistribution
• CV depression slightly > than NaP
• Resp effects similar to NaP but good
bronchodilator
• Does NOT cause hyperalgesia
• Reduces PONV and PDNV
• Good hypnotic
• Burns upon rapid injection in small vein
• Contraindicated with Egg Allergy

19

Etomidate Mech of action and Pharm?

Mechanism of Action
– Rapid onset of sleep--30-60 seconds
– Assumed to enhance the effects of GABA
– Rapid awakening
– 75% protein bound
– Hydrolyzed to inactive metabolites via ester
hydrolysis
– Elimination half life is 75 minutes
– Clearance is 5X faster than Sodium pentothal
– Excretion 85% renal, 15% biliary

20

Etomidate S/E Card, Pulm, CNS

CV effects
– SBP ⇔⇓d; HR ⇔⇑d ; SVR ⇔⇓d
• Pulmonary effects
– Minimal respiratory depression; increased
with opioids.
• CNS effects
– CBF ⇓d, ICP ⇓d, CMRO2 ⇓d

21

Etomidate Induction and maintenance dose?

.2-.4 mg/kg

NO REDOSING!!! Suppresses Adrenals!!!
- Inhibits 11β-hydroxylase and to a lesser extent 17α
hydroxylase

22

What to think about when giving Etomidate?

Beware of
– Myoclunus (spontaneous jerking)
– Adrenal Suppression
• Inhibits 11β-hydroxylase and to a lesser extent 17α
hydroxylase.
– ⇑d PONV versus NaP or Propofol
– No Analgesia

23

_______________ states that the potency of an anesthetic is proportional to its lipid solubility. This suggests a lipophilic site of action.

The Meyer-Overton rule

24

Ketamine works on which receptors?

NMDA; Opioid; Monoaminergic; muscarinic
receptors; & voltage gated Ca+ channels

25

Ketamine Pharmacokinetics?

Extremely lipid soluble (5-10X NaP)
– Metabolized in liver to norketamine
• 1/3 to 1/5 potency Ketamine
– Norketamine is hydroxylated and conjugated to
H2O soluble and excreted.
– Elimination half-life 2-3 hours
– Excretion >90% renal

26

Ketamine CV, Pulm, & CNS effects?

• CV effects
– SBP ⇑d; HR ⇑d ; SVR ⇑d
• Pulmonary effects
– No respiratory depression; increased with
opioids.
• CNS effects
– CBF ⇑d, ICP ⇑d, CMRO2 ⇑d (probably not good for neuro cases)

27

Ketamine induction dose IV & IM?

Induction of Anesthesia
– 1-3mg/kg IV or 4-8mg/kg IM
• Adjunctive Analgesic
– 0.2-0.5 mg/kg can provide profound analgesia

BEWARE OF:
– Emergence Delirium
• Visual, auditory, proprioceptive, and confusion
• Premedicating with Midazolam seems to help

28

Barbiturates Mech. of Action? (what receptors?)

Interact with GABAA (α subunit) receptor
• Different from the GABA or the BZD site
• Directly activate Cl-
ion channels, increase their duration
of opening.
– Increases the efficacy of GABA
• Hyperpolarize postsynaptic cell membranes.
– Also block the AMPA receptors (excitatory receptor)

29

Barbiturates elimination and protein bound?

NaP 83% protein bound (Albumin)
– Highly lipid soluble=rapidly into CNS
– Achieve CNS uptake in 30 seconds
– Prompt awakening after a single dose
– Hepatic metabolism (inactive) and eliminated by kidneys

30

Barbiturates CV, Pulm, & CNS effects?

CV effects
– SBP ⇓d; HR ⇑d (reflexive) ; SVR ⇓d
• Pulmonary effects
– Respiratory depression, APNEA, return with slow
respers and ⇓d tidal volumes.
• CNS effects
– CBF ⇓d, ICP ⇓d, CMRO2 ⇓d - neuro protective

31

Barbiturates effect on Renal & pH?

Modest decrease in GFR
– Metabolic acidosis ⇑s the effect of barbiturates
– Metabolic alkalosis ⇓s the effect of barbiturates
– Respiratory acidosis has much less effect

32

Barbiturates Key Points?

Awakening due to redistribution
• NaP causes dose dependent ⇓ SBP, SVR,
CO due to myocardial depression and
increased venous capacitance
• Potent respiratory depressants
• Poor analgesics-may cause hyperalgesia
• Contraindicated in Acute Intermittent
Porphyria
• Can cause histamine release
• Avoid SubQ and Intra-arterial injection