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Anesthesia Pharmacology > Pharm Unit 2 > Flashcards

Pharm Unit 2 Flashcards

1
Q

What can be given for pre-eclampsia?

A

Magnesium sulfate

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2
Q

What organs are a part of the vessel rich group (VRG)? What % of CO goes to the VRG?

A

brain, heart, kidney, liver
75%

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3
Q

What is included in the muscle group? What % of CO goes to the muscle group?

A

skeletal muscle and skin
18%

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4
Q

How much of CO is administered to fat?

A

5%

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5
Q

What is included in the vessel-poor group? What % of the CO is used?

A

bone, tendon, cartilage
2%

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6
Q

What are the 5 components of anesthesia?

A

Hypnosis, analgesia, muscle relaxation, sympatholysis and amnesia

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7
Q

What are the 4 stages of anesthesia?

A
  1. Analgesia
  2. Delerium
  3. Surgical anesthesia
  4. Medullary paralysis
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8
Q

What stage of anesthesia includes laryngospasm?

A

Stage 2 - delirium

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9
Q

What stage of anesthesia includes responses to stimulation that are exaggerated and violent?

A

Stage 2 - delirium

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10
Q

Which stage of anesthesia includes absence of all reflexes and flaccid paralysis with hypotension and a weak pulse?

A

Stage 4 - medullary paralysis

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11
Q

What stage of emergence should you extubate in?

A

Stage 1 - analgesia

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12
Q

What are the 4 protective airway reflexes?

A

sneezing, coughing, swallowing, gagging

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13
Q

How do barbiturates exert their effect?

A

Potentiating GABA-a channels, also act on glutamate/adenosine/neuronal nicotinic ACh receptors

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14
Q

What do barbiturates do the CBF/CRMO?

A

Act as a cerebral vasoconstrictor, reduce CBF and CRMO by about 55%

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15
Q

Why do you want to avoid infusions of barbiturates?

A

Prolonged context-sensitive half time. They also rapidly redistribute into other tissues - fat and protein reservoir

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16
Q

What is the effect on redistribution if the drug has a high protein binding capacity?

A

Longer duration of action

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17
Q

How well do barbituates bind to protein? Which protein?

A

albumin 70-85%

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18
Q

What are the 2 types of barbiturates? Which one is more lipid soluble?

A

Oxybarbiturates and Thiobarbiturates (more lipid soluble)

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19
Q

Which drugs are Oxybarbiturates and Thiobarbiturates?

A

Oxybarbiturates: Methohexital, Phenobarbital, Pentobarbital
Thiobarbiturates: Thiopental, Thiamylal

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20
Q

Why is it that: “the greater the ratio of fat to body weightthe less is the blood volume (ml/kg)?” Adipose tissue has….

A

Decreased blood supply

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21
Q

The greater the ratio of fat to body weight→ the_____ is the blood volume (ml/kg).”

A

less

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22
Q

__________ describes the distribution of a given agent at equilibrium, between two substances at the same temperature, pressure, and volume

A

Partition coefficient

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23
Q

__________ describes the distribution of an anesthetic between blood and gas at the same partial pressure

A

Blood-gas coefficient

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24
Q

A higher blood-gas coefficient correlates with ______ solubility of anesthetic in blood and thus ______ the rate of induction

A

higher, slowing

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25
Q

Dose of Thiopental?

A

4 mg/kg IV

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26
Q

Dose of methohexital?

A

1.5 mg/kg IV

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27
Q

How does methohexital affect seizures?

A

Lowers seizure threshold = easier to have one, making it an ideal drug for ECTs

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28
Q

Basic effects of barbiturate’s on ventilation?

A

Dose-dependent depression (less sensitive to CO2) with slower frequency and lower tidal volume, similar to narcotics

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29
Q

What happens during intra-arterial injection of a barbiturate?

A

Immediate intense vasoconstriction and pain - permanent nerve damage
- Treat with vasodilators: lidocaine or papaverine

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30
Q

What medications are affected by barbiturates? Why?

A
  • Enzyme induction approx. 2 to 7 days of infusion
  • Accelerated metabolism of anticoagulants, phenytoin, TCAs, digoxin corticosteroids, bile salts, and vit. K.
  • May persist for 30 days
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31
Q

List the induction, conscious sedation and maintenance doses of propofol

A

Induction = 1.5 - 2.5 mg/kg IV
CS = 25 - 100 mcg/kg/min
Main = 100 - 300 mcg/kg/min

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32
Q

What are the disadvantages to propofol?

A
  • Support bacterial growth.
  • Causes increased plasma triglyceride concentrations (in prolonged IV infusions).
  • Pain on injection
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33
Q

Describe Ampofol and Aquavan relative to Propofol

A

Ampofol = low-lipid emulsion with no preservative, higher incidence of pain on injection (good d/t less effect on triglycerides)
Aquavan = prodrug that converts into active form, no pain on injection, by has unpleasant sensation related side effects

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34
Q

Describe Propofol MOA

A

Selective modulator of GABA-a = increased Cl conductance and hyperpolarized cell

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35
Q

What are the elimination and context-sensitive half-times of propofol?

A
  • Elimination half-time: 0.5-1.5 hours
  • Context-sensitive half time: 40 minutes (8 hour infusions)
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36
Q

How does the liver metabolize propofol?

A

CP450 - converted to water-soluble sulfate and glucuronic acid metabolites to be excreted by kidneys

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37
Q

Describe the BP/HR changes with propofol, etomidate and ketamine

A

P = decreased BP and HR
E = no change to BP and HR
K = increased BP and HR

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38
Q

T/F: Propofol is safe for alcoholic patients?

A

T: awakening time does not change with healthy vs ETOH patients

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39
Q

How does the dose of Propofol change with children vs elderly?

A

Children = increased dose, elderly = decreased dose (by 25-50%)

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40
Q

Why is Propofol advantageous as a sedative?

A

Prompt recovery, low PONV, anti-convulsant, amnestic, anti-oxidant. Does not provide analgesia however

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41
Q

What is the sub-hypnotic dose of Propofol?

A

10-15 mg IV followed by 10 mcg/kg/min

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42
Q

Anti-pruritic dose of Propofol?

A

10 mg IV

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43
Q

What effect does Propofol have on the airway?

A

Bronchodilation

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44
Q

Anti-convulsant dose of Propofol?

A

1 mg/kg IV

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45
Q

Effects on CRMO with Propofol?

A

Decreases CRMO, CBF and ICP. D/t autoregulation, CBF and PaCO2 are maintained

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46
Q

Propofol doesn’t induce seizures but can result in involuntary muscle movements, aka ________

A

myoclonus

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47
Q

What kind of EEG waves do we want in anesthesia?

A

Delta

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48
Q

Black box warning for Propofol?

A

Profound bradycardia leading to asystole in healthy patients

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49
Q

How does propofol work as an anti-emetic agent?

A

Depresses subcortical pathways and has a direct depressant effect on the vomiting center

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50
Q

Effects of propofol on the CV system

A
  • decreased SBP - SNS inhibition, decreased SVR
  • bradycardia
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51
Q

Describe Propofol infusion syndrome including dose

A

Dose > 75 mcg/kg/min longer than 24 hours.
s/s: severe refractory bradycardia in children, lactic acidosis, brady-dysrhythmias, and Rhabdomyolysis; green urine

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52
Q

What medication can you give with propofol to prevent bradycardia and asystole?

A

Antimuscarinic agent - atropine

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53
Q

Propofol (does or does not) affect the hypoxic pulmonary vasoconstriction response

A

does not - stays intact

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54
Q

What does it mean when urine is green or cloudy with propofol administration?

A

No alteration in renal function/NBD
- green = phenols
- cloudy = uric acid crystallization

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55
Q

Propofol ______ IOP

A

decreases

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56
Q

Etomidate MOA?

A

Selective modulator of GABA-a

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57
Q

_______ is the only drug with direct systemic absorption in oral mucosa that bypasses hepatic metabolism

A

etomidate

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58
Q

Drugs that are highly protein bound have _____ duration of action

A

longer

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59
Q

Etomidate is a weak _____; it is _____ soluble at physiologic pH

A

base, lipid

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60
Q

Etomidate is 35% propylene glycol →

A

pain at injection and venous irritation

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61
Q

What % of PO medication is metabolized during hepatic first pass?

A

50%

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62
Q

Onset, peak, and half-life of etomidate?

A

onset - 1 min
peak - 2 min
half-life - 2-5 hours

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63
Q

Etomidate is metabolized via ______

A

Hydrolysis (hepatic microsomal enzymes & plasma esterases)

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64
Q

Etomidate is ___% albumin bound, but ______ is 5x faster than thiopental

A

76%, clearance (prompt awakening)

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65
Q

Etomidate elimination is ___% in urine and ___% in bile

A

85% in urine & 10-13% in bile

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66
Q

Dose for Etomidate?

A

0.3 mg/kg IV

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67
Q

Best indication for etomidate?

A

In an unstable CV patient (esp with little to no cardiac reserve)
- min changes to HR, SV, CO, contractility
- mild decrease MAP d/t ↓ SVR and PAP

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68
Q

Etomidate has ______ analgesic effects

A

no

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69
Q

What is the big side effect of etomidate?

A

Myoclonic movements, very common. Can be prevented with fentanyl 1-2 mcg/kg IV
- caution pt with seizure hx

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70
Q

Contraindication to etomidate?

A

Adrenal suppression - it makes it worse so you lose your stress response

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71
Q

How does etomidate cause adrenal suppression?

A

Dose-dependent inhibition of the conversion of cholesterol to cortisol → ✕ stress response
- Severe hypotension, longer mechanical ventilation hours, etc.

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72
Q

What patients should etomidate be used cautiously in?

A

seizure hx, sepsis, hemorrhage

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73
Q

Relationship of CRMO/CBF to etomidate?

A

Decrease CBF, CRMO and ICP by 35-45% via cerebral vasoconstriction
↓ ICP

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74
Q

Etomidate effects on ventilation?

A
  • Is a depressant but less so than barbiturates.
  • Vt decreases are offset by compensatory increases in RR (transient 3-5 min)
  • stimulates CO2 medullary centers
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75
Q

Minute ventilation =

A

Vt x RR

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76
Q

What are the advantages of ketamine over etomidate/Propofol? Cons?

A
  • No pain on injection and profound analgesia at subanesthetic doses.
  • Does have delirium concerns and abuse potential.
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77
Q

What preservative is used for ketamine?

A

Benzethonium Chloride

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78
Q

S/S of ketamine use

A
  • “Dissociative anesthesia”
  • resembles cataleptic state in which eyes remain open with slow, nystagmic gaze
  • non-communicative, but wakefulness is present; hypotonus and purposeful skeletal muscle mvmt
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79
Q

What is the street equivalent of ketamine?

A

PCP or angel dust

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80
Q

Compare isomers of ketamine

A

S (the left or -) = more intense analgesia, more rapid recovery, less salivation, lower incidence of emergence reactions
R = (right or +) = cocaine like effect, less fatigue, less cognitive impairment

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81
Q

Where does ketamine work?

A

NMDA receptors (prevents glutamate from activating them), all opioid receptors (mu, delta and kappa) and weak actions at GABA-a and sigma opioid receptors. Also affects calcium and neuronal nicotinic ACh channels (analgesic effect)

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82
Q

What is the peak, duration, and half-time of ketamine?

A

peak: 1 min
duration: 10-20 min (60-90 min to return to full orientation)
half-time: 2-3 hours

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83
Q

Ketamine has a Vd of ______

A

3 L/kg (large)

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84
Q

Does ketamine have inactive or active metabolites?

A

Norketamine: active metabolite (1/3 – 1/5 potency); prolonged analgesia

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85
Q

What is the hepatic clearance rate of ketamine? How is it excreted?

A

1 L/min
kidneys

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86
Q

Ketamine has _____ lipid solubility

A

high

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87
Q

Induction doses IV and IM of ketamine?

A

IV = 0.5 - 1.5 mg/kg
IM = 4 - 8 mg/kg
PO = 10 mg/kg

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88
Q

Maintenance doses of IV/IM ketamine?

A

IV = 0.2 - 0.5 mg/kg
IM = 4 - 8 mg/kg

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89
Q

Subanesthetic/analgesic dose of ketamine?

A

0.2 - 0.5 mg/kg IV

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90
Q

Post op sedation/analgesia dose of ketamine?

A

1 - 2 mg/kg hour

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91
Q

Neuraxial Analgesia dose for ketamine?

A
  • 30 mgs Epidural
  • 5 - 50 mg in 3 mLs of saline Intrathecal/Spinal/Subarachnoid
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92
Q

What anti-sialagogue do you give with ketamine?

A

Glycopyrrolate

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93
Q

Ketamine LOC to fill consciousness times

A
  • LOC effect: 30 secs – 1 min (IV); 2 to 5 mins (IM)
  • Return of consciousness (ROC): 10 to 20 minutes
  • Full consciousness: 60 to 90 minutes.
  • Amnesia persists after ROC: 60 to 90 minutes
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94
Q

What is the coronary artery disease cocktail (include dosages)?

A

Valium = 0.5 mg/kg IV
Ketamine = 0.5 mg/kg IV
Ketamine infusion of 15-30 mcg/kg/min

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95
Q

Avoid or caution use of ketamine in patients with

A
  • Pulmonary: Systemic/pulmonary HTN
  • Neuro: Increased ICP
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96
Q

Ketamine clinical uses

A
  • Acutely hypovolemic patients
  • Asthmatic & MH patients
  • CAD cocktail
  • pediatric induction
  • burn pts, reverse opioid tolerance
  • psych disorders - depression, PTSD, OCD, restless leg syndrome
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97
Q

How does ketamine affect ICP? At what dose does the ICP effect plateau?

A

Potent cerebral vasodilator = 60% increase in CBF, no further increase in ICP at 0.5 - 2 mg/kg IV
- myoclonus, increased amp SSEP, does not alter seizure threshold

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98
Q

Ketamine effects on CV system?

A

Increased CO, BP, HR, PAP, MRO2
- increases catecholamine levels

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99
Q

Decreased CO and BP in patients with ketamine can be treated with ______

A

epi - depleted catecholamine stores

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100
Q

Effects of ketamine on ventilation?

A

No depression of ventilation, airway reflexes are maintained, increase in salivary secretions, bronchodilator

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101
Q

Ketamine s/sx of emergence delirium

A
  • Psychedelic Effects in 5% to 30% of patients
  • S/Sx: visual, auditory, proprioceptive, and confusional illusions
  • Morbid & vivid dreams (in color) and hallucinations up to 24H
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102
Q

What is the MOA of how ketamine causes psychedelic effects?

A

MOA: depression of the inferior colliculus and medial geniculate nucleus

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103
Q

What can be given with ketamine to prevent emergence delerium?

A

Benzos, Clonidine and Dexmedetomidine

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104
Q

What are the side effects of ketamine on other systems?

A
  • Inhibits platelet aggregation
  • Inhibits cytosolic free calcium concentration - Enhances non-depolarizing NMBDs
  • Inhibit plasma cholinesterase’s - Prolongs apnea from sux
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105
Q

What is the relationship of ketamine to volatiles, NMBDs and Sux?

A

NMBD = enhanced effect
Sux = prolonged
V = hypotension

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106
Q

Which induction agent has the highest analgesic properties?

A

ketamine

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107
Q

What is Ketafol?

A

mixing ketamine and propofol - not recommended bc propofol is not chiral and ketamine is (not stable - lipid bubbles)

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108
Q

Differentiate between the two components of pain

A
  1. sensory-discriminative - Ascending → spinothalamic & trigemino-thalamic tracts → cerebral cortex → perception of pain
  2. motivational-affective - attention/arousal, somatic/autonomic reflexes, endocrine responses, and emotional changes
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109
Q

_______ is the experience of pain with a series of complex neurophysiologic processes

A

Nociception

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110
Q

Define hyperalgesia and allodynia

A

Hyper = increased pain sensations to normally painful stimuli
A = perception of pain in response to non-painful stimuli

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111
Q

Where does transduction, transmission, modulation and perception occur in nervous system?

A

Transduction = signals starting at the nerve endings
Transmission = travel of the electrical impulses to the nerve body connecting to the dorsal horn
Modulation = process of altering pain (inhibitory/excitatory) transmission mechanisms at the dorsal horn
Perception = thalamus acting as the central relay station and discrimination of stimuli in the somatosensory cortex

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112
Q

What medication classes act at peripheral nociceptors or rather affect transduction?

A

LAs and NSAIDS

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113
Q

What medication classes act on transmission of nerve signals? Where?

A

LAs and on the a-delta and c-fibers

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114
Q

What medication classes act on modulation and where does this occur?

A

LAs, opioids, ketamine a2-agonists and in the spinal cord, primarily in the dorsal horn

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115
Q

What medication classes act on perception and where does this occur?

A

Opioids, a2-agonists, GAs. In the brain -> somatosensory cortex

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116
Q

Describe the process a stimulus would take to travel throughout the CNS

A

Stimulus→ Nociceptor → Resting Threshold → Transmission → Modulation → Interpretation

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117
Q

Describe the physiology of c-fibers and type 1 (a-beta) and type 2 (a-delta) fibers including speed

A

C-fiber (unmyelinated) = burning pain and sustained pressure pain (2 meters/second)
AB = heat, mechanical and chemical pain
AD = heat
Both alpha = much faster

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118
Q

What are the 7 chemical mediators of pain?

A
  • Peptides (substance P, calcitonin, bradykinin, CGRP)
  • eicosanoids
  • Lipids (PGAs, thromboxane, leukotrienes and endocannabinoids),
  • neutrophins
  • cytokines
  • chemokines
  • extracellular proteases/protons
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119
Q

What are peptide mediators of pain?

A

Substance P, calcitonin, bradykinin, CGRP

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120
Q

What are lipid mediators of pain?

A

PGAs, thromboxane, leukotrienes and endocannabinoids

121
Q

What are the receptors and ion channels of the dorsal root ganglion and peripheral terminals?

A
  • Purinergic
  • Metabotropic
  • Glutamatergic
  • Tachykinin
  • TRPV I
  • Neurotrophic
  • Ion channels
122
Q

Define primary vs secondary hyperalgesia

A

P = at the original site of injury, decreased pain threshold, increased response to stimuli, spontaneous pain and expansion of receptive field
SH = uninjured skin surrounding the injury that has been sensitized by central neuronal circuits

123
Q

Basic function of the dorsal horn

A

Relay center for nociceptive and other sensory activity

124
Q

What do the ascending pathways do?

A

Transmit sensations such as pain to the brainstem and forebrain

125
Q

What fibers would you find in lamina I (marginal layer)?

A

Afferent C-fibers

126
Q

What would you find in Lamina II (substantia gelatinosa)?

A

afferent c-fibers, also where opioids can exert their effect

127
Q

Where does substance P work?

A

Lamina III and IV - NKI receptor

128
Q

Where would you find myelinated fibers in the cord? What do they innvervate?

A

Lamina I, IV, VII and the ventral horn, and they innervate muscles and viscera

129
Q

Describe the gate theory of pain

A

If the gate is open, the pain is projected to supraspinal brain regions, if the gate is closed, pain is not felt with simultaneous inhibitory impulses

130
Q

What happens if you rub an injured area?

A

The a-beta fibers deliver information about the rubbing/touching which override the slower information from a-delta and c-fibers regarding pain

131
Q

What does the limbic cortex and thalamus do with pain information?

A

They are involved with perception of motivational-affective pain components

132
Q

What does the PAG and RVM (rostro-ventral medulla) do with pain information?

A

Depress or facilitate the integration of pain information in the spinal dorsal horn

133
Q

What does tissue injury release?

A

Substance P and glutamate

134
Q

What are things damaged cells can release that cause pain?

A

Bradykinin, histamine, PGAs, serotonin, hydrogen ions and lactic acid

135
Q

What are some excitatory impulses? Inhibitory?

A

E = glutamate, calcitonin, neuropeptide Y, aspartate, substance P
I = GABA, glycine, enkephalins, norepi, dopamine

136
Q

What information travels the spinothalamic tract? Lamina?

A

Pain, temperature and itch, I VII and VIII

137
Q

What information travels the spinobulbar tract? Lamina?

A

Behavior towards pain, I V and VII

138
Q

What information travels the spinohypothalamic tract? Lamina?

A

Autonomic, neuroendocrine and emotional aspects of pain, I V VII and X

139
Q

Describe the descending inhibitory pain pathway

A

Originate in PAG → RVM → dorsolateral funiculus → synapse in dorsal horn

140
Q

What are the neurotransmitters used in the descending inhibitory tracts?

A

Endorphins, enkephalins, serotonin

141
Q

What happens when you hyperpolarize a-delta and c-fibers?

A

Decreased release of substance P via opening of K channels and closing of Ca channels

142
Q

What are the 2 descending pathways of pain modulation?

A
  • Descending Inhibition Pathway (DI)
  • Descending Facilitation Pathway (DF)
143
Q

What are the opioid receptors for the PAG-RVM system?

A

Mu, Kappa and Delta receptors

144
Q

Treatment for neuropathic pain?

A

Common to have allodynia and hyperalgesia, opioids, gabapentin, anti-depressants and cannabis

145
Q

Describe visceral pain

A

Diffuse and poorly localized, if it is referred to the muscle/skin it become somatic pain

146
Q

What are some causes of visceral pain?

A

ischemia, stretching of ligamentous attachments, spasms, distention

147
Q

________ are a variety of painful conditions following injury in a region with impairment of sensory, motor, and autonomic systems

A

Complex Regional Pain Syndromes

148
Q

When does pain become perceivable in an neonate?

149
Q

What are the CV responses to pain?

A

HTN, ↑HR, myocardial irritability, ↑ SVR, compromised LV (↓ CO, myocardial ischemia)

150
Q

What are the pulmonary responses to pain?

A
  • ↑ total body O2 consumption/CO2 production → ↑ Vm and work of breathing
  • Splinting
  • Decreased movement of chest wall →
    Atelectasis and Intrapulmonary shunting
  • Impaired coughing
151
Q

What are the GI/GU responses to pain?

A
  • Enhanced sympathetic tone, ↑ sphincter tone, and ↓ motility (Ileus and urinary retention)
  • Hypersecretion of acid (Stress ulceration and aspiration)
  • N/V
  • Abdominal distention
152
Q

What are some endocrine responses to pain?

A

↑ catabolic hormones (catecholamines, cortisol, glucagon)
↓ anabolic hormones (insulin, testosterone)
combined effects = negative nitrogen balance, carb intolerance, and increased RAAS

153
Q

What are the hematologic responses to pain?

A

Stress-related - platelet adhesiveness, reduced fibrinolysis, and hypercoagulability

154
Q

What are the immune responses to pain?

A

Stress-related - Leukocytosis and depressed reticuloendothelial system (increased infection)

155
Q

What are some examples of phenanthrenes?

A

Morphine, codeine and thebaine

156
Q

What are some examples of benzylisoquinolines?

A

Papaverine and noscapine

157
Q

How do opioid agonists work?

A

Inhibit ACh, dopamine, norepi and substance P, they increase K conductance (hyperpolarize), inactivate Ca channels and decrease neurotransmission

158
Q

Where would you find opioid receptors in the Brain, spinal cord and outside the CNS?

A

B = PAG, locus ceruleus, RVM and hypothalamus
SC = dorsal horn at the substantia gelatinosa (lamina II)
Outside CNS = sensory neurons and immune cells

159
Q

What is the only opioid receptor that is not supraspinal?

160
Q

What effects would you expect from Mu1 vs Mu2 receptors?

A

1 = analgesia, euphoria, low abuse, miosis, bradycardia, hypothermia and urinary retention
2 = analgesia, ventilatory depression, physical dependence, constipation

161
Q

Is there any difference in the agonists/antagonists of Mu1/Mu2?

A

No, they are all the same.
Ago = endorphins, morphine and synthetics. Antag = naloxone, naltrexone and nalmefene

162
Q

What effects occur at Kappa?

A

Analgesia, dysphoria/sedation, low abuse potential, miosis, diuresis

163
Q

What effects occur at delta?

A

Analgesia, depression of ventilation, physical dependence, constipation, urinary retention

164
Q

What are the body’s endogenous agonists of kappa and delta?

A

K = dynorphins, D = enkephalins

165
Q

What opioid receptors depress ventilation?

A

Mu2 and delta

166
Q

What opioid receptors have dependence issue?

A

Mu2 and delta

167
Q

What opioid receptors have low abuse potential?

A

Mu1 and kappa

168
Q

What opioid receptors cause miosis?

A

Mu1 and kappa

169
Q

What opioid receptors cause urinary retention?

A

Mu1 and delta

170
Q

What opioid receptor has the most effects?

171
Q

What opioid receptors cause euphoria? Dysphoria/sedation?

A

Eu = Mu1
Sedation = kappa

172
Q

What drug could you give to help reverse the opioid ventilation s/e but keep the analgesia going?

A

Physostigmine - increases ACh

173
Q

What are the CNS effects of opioids?

A
  • Decreased CBF and possibly ICP
    • Caution with head injury: wakefulness, miosis, PaCO2, BBB
  • Myoclonus with large doses
174
Q

Which opioids cause cough suppression?

A
  • Codeine
  • Dextromethorphan: no analgesia
175
Q

What are the ventilation effects of opioids?

A
  • Decreased responsiveness of ventilation centers to CO2
    • increased in resting PaCO2 (Shift to the right)
      • Depression (mu2): rhythm (decreased rate with compensatory increase in tidal volume), pauses, periodic breathing
        • APNEA, aka overdose: miosis, hypoventilation & coma
176
Q

What are the CV effects of opioids?

A
  • Decreased SNS tone in peripheral veins
    • decrease in venous return, CO, & BP
    • orthostatic hypotension & syncope
  • Bradycardia or Histamine release → decreased BP
    • N20 or benzo = CV depression (CO & BP)
  • Benefit: cardioprotective from myocardial ischemia
177
Q

What skeletal issues do opioids have?

A

Can make the muscles rigid, treat with a muscle relaxer or naloxone

178
Q

What is spasm of biliary smooth muscle called?

A

Sphincter of oddi spasms

179
Q

What is the primary concern with Oddi spasms?

A

delayed gastric emptying and constipation, N/V, inc GI secretions

180
Q

Treatment for sphincter of Oddi spasm?

A

Glucagon 2 mg, naloxone 40 mcg, atropine 0.2 mg, Nalbuphine 10 mg, NTG (nitroglycerin) 50 mcg

181
Q

How long does tolerance generally take to occur?

182
Q

What are initial symptoms vs after 72 hours of opioid withdrawal?

A
  • Initial symptoms: yawning, diaphoresis, lacrimation, or coryza. Insomnia and restlessness.
  • 72 hrs: Abdominal cramps, N/V, and diarrhea.
183
Q

What opioids have the shortest onset, peak intensity and duration?

A

Demerol and fentanyl

184
Q

What opioid(s) have the longest onset, peak intensity and duration?

185
Q

Intraop and postop doses for morphine

A

I = 1 - 10 mg
P = 5 - 20 mg

186
Q

Intraop dose of fentanyl?

A

1.5 - 3 mcg/kg

187
Q

Intraop dose of sufentanil?

A

0.3 - 1 mcg/kg

188
Q

Intraop dose of remifentanil?

A

load 0.5-1 mcg/kg over 1 min

189
Q

Intraop and postop dose of dilaudid

A

I = 1-4 mg
P = 1.5 - 5 mg

190
Q

Infusion rate for sufentanil?

A

0.5 - 1 mcg/kg/hr

191
Q

Infusion rate for remifentanil?

A

0.125 - 0.375 mcg/kg/min

192
Q

What type of pain does morphine relieve?

A

Visceral/skeletal, joints, and integumental, dull > sharp, intermittent pain

193
Q

_______ is the gold standard of opioids

194
Q

_______ is the greek god of dreams

195
Q

IV onset and peak of morphine?

A

O: 10-20 min
P: 15 - 30 min

196
Q

How is morphine metabolized?

A

Via glucuronidation into 2 metabolites: Morphine-3 (75-95% but inactive) and morphine-6 (active)

197
Q

Compare the analgesic potency and speed of offset of morphine in women vs men

A

Women > men:analgesic potency and slower speed of offset

198
Q

Compare demerol potency to morphine

A

Demerol 1/10th the potency,

199
Q

Dose for demerol in post-op shivering?

200
Q

What receptors does demerol hit?

A

kappa and A2 receptors

201
Q

What is the metabolism and elimination of demerol?

A
  • Duration: 2 to 4 hours
  • Hepatic 1st pass: 80%
  • Metabolism: 90% hepatic → normeperidine
  • Protein-bound: 60% (elderly considerations)
  • Elimination: renal, acidic urine can speed elimination
    • Elimination ½ time: 3 to 5 hours (35 hours with renal failure)
202
Q

What are the signs of Demerol toxicity?

A

delirium (confusion, hallucinations) myoclonus & seizures

203
Q

Compare fentanyl to morphine

A

75 - 125x potency

204
Q

Fentanyl has lung-first pass of ___% and a _____ Vd

A

Lung-first pass: 75%
large Vd

205
Q

List the context sensitive half times of all fentanyl’s from least to greatest

A

Remifentanil -> sufentanil -> alfentanil -> fentanyl

206
Q

List the analgesia, induction and inhaled anesthetic doses of fentanyl

A

A = 1 - 2 mcg/kg IV
Ind = 1.5 - 3 mcg/kg IV
Inh = 2 - 20 mcg/kg IV

207
Q

What is the surgical anesthesia dose of fentanyl?

A

50 - 150 mcg/kg IV

208
Q

Intrathecal dose of fentanyl?

209
Q

Transdermal dose of fentanyl?

A

75 - 100 mcg over 18 hours

210
Q

Transmucosal (oral) dose of fentanyl?

A
  • 5 to 20 µg/kg
    Rapid dissolving film/lozenge in peds
  • 2 to 8 yo: 15-20 µg/kg PO 45 minutes prior
  • 1 mg of PO Fentanyl = 5 mgs of IV Morphine
211
Q

Advantage of fentanyl vs morphine in terms of s/e?

A

No histamine release, no significant bradycardia though can decrease BP and CO

212
Q

Fentanyl CNS s/e?

A
  • Seizure like activity
  • SSEP and EEG (>30 µg/kg IV)
  • Modest increase in ICP (6 to 9 mmHg)
213
Q

What was morphine originally derived from?

A

Poppy (Papaver Somniferum)

214
Q

Why is fentanyl discouraged in cardiopulmonary bypass?

A

You can lose some to the circuit

215
Q

How much does fentanyl increase ICP?

216
Q

What is fentanyl synergistic with?

A

Benzo’s and Propofol (this can be a good thing, combined you could lower the dose of the propofol)

217
Q

List the fentanyl in order of least to most potent

A

Alfentanil < Remifentanil and Fentanyl (both the same) < Sufentanil

218
Q

Which is more potent, fentanyl or sufentanil?

A

Su: 5 - 12x more potent than fentanyl

219
Q

Lung first pass and protein binding of sufentanil

A
  • 60% lung first-pass uptake
  • 92.5% protein binding (smaller Vd < fentanyl)
220
Q

What does sufentanil bind to (not receptors)?

A

A1-acid glycoprotein

221
Q

Give the analgesia, induction, intra-op and infusion doses of sufentanil

A

A = 0.1 - 0.4 mcg/kg IV
Ind = 18.9 mcg/kg IV
Intraop = 0.3 - 1 mcg/kg IV
Inf = 0.5 - 1 mcg/kg/hr IV

222
Q

Compare and contrast potency and onset of fentanyl and alfentanil

A

Alfentail is 1/5 less potent, but has a faster onset of 1.4 minutes

223
Q

Which 2 fentanyl’s have the same protein binding?

A

Alfentanil and sufentanil

224
Q

What is the induction, induction alone and maintenance dose of alfentanil?

A

Ind = 15 - 30 mcg/kg IV (90 sec prior)
Ind A = 150 - 300 mcg/kg IV
M = 25 - 150 mcg/kg/hour IV

225
Q

Alfentanil is ___% nonionized at normal pH

A

90% -> low lipid solubility

226
Q

What is a contraindication to alfentanil?

A

Parkinsons and other neuromuscular disorders (MG, muscular dystrophy etc)

227
Q

Remifentanil is a selective ___ opioid agonist

228
Q

Remifentanil potency compared to alfentanil and fentanyl

A

15 to 20 times as potent as alfentanil (same as fentanyl)

229
Q

Remifentanil has an _____ structure; hydrolysis by _______

A

ester
Hydrolysis by nonspecific plasma and tissue esterases
- rapid onset and offset

230
Q

What fentanyl is dosed in IBW?

A

Remifentanil

231
Q

Which fentanyl rapidly reaches steady state?

A

Remifentanil

232
Q

Give the induction and maintenance dose of remifentanil

A

I = 0.5 - 1 mcg/kg IV
M = 0.25 - 1 mcg/kg IV or 0.005 - 2 mcg/kg/min IV

233
Q

Which fentanyl is not recommended for spinal/epidural use?

A

Remifentanil

234
Q

Remifentanil has synergistic depression of ventilation with ________

235
Q

Remifentanil clearance and elimination half-time?

A

Clearance: 3L/min (8x more rapid > alfentanil)
Elimination half-time: 6.3 minutes (99.8%)

236
Q

Before stopping Remifentanil, give what?

A

longer-acting opioid

237
Q

Compare hydromorphone and morphine

A

Hydromorphone is 5x more potent, less hydrophilic, no histamine release and does have an active metabolite

238
Q

Dose range for dilaudid?

A

0.5 - 4 mgs IV

239
Q

Why is codeine not given IV?

A

histamine-induced hypotension

240
Q

Elimination half-time of codeine?

A

3-3.5 hours

241
Q

Cough suppressant and analgesia dose range for codeine?

A

CS = 15 mg
A = 60 - 120 mg

242
Q

Dose of tramadol? Primary drug interaction?

A

3mg/kg PO and interacts with coumadin

243
Q

Which opioids have the greatest and least context sensitive half times?

A

Greatest = fentanyl
Least = remifentanil

244
Q

Which opioids have the highest protein binding? Least?

A

High = Su, al and remifentanil
Low = morphine

245
Q

Which opioids have the highest and lowest Vd?

A

High = fentanyl
Low = alfentanil

246
Q

Which opioids have the highest/lowest VD?

A

High = fentanyl
Low = alfentanil

247
Q

Which opioids have the highest/lowest partition coefficient?

A

High = sufentanil
Low = morphine

248
Q

Which opioids have the highest/lowest E1/2?

A

High = fentanyl
Low = remifentanil

249
Q

Which opioids have the highest/lowest blood/brain equilibration times?

A

High or longest = fentanyl
Low or shortest = remifentanil

250
Q

What are the advantages of opioid agonist-antagonists?

A

Provide analgesia, limited depression of ventilation, low chance of dependence and ceiling effect prevents additional responses

251
Q

What receptors does pentazocine work on?

A

Delta and kappa

252
Q

Describe pharmacokinetics of pentazocine

A

1/5th as potent as nalorphine, antagonized by naloxone, may have withdrawal s/sx

253
Q

What OAA crosses the placental barrier?

A

Pentazocine

254
Q

Dosage of PO and IV pentazocine?

A

IV = 10 - 30 mg
PO = 50 mg

255
Q

General CV effects of pentazocine?

A

Increased HR, BP, PA and LV-EDP

256
Q

Compare butorphanol and pentazocine potency

A

Butorphanol is 20x more potent agonist and 10 - 30x more potent antagonist relative to pentazocine

257
Q

Describe receptor affinity for pentazocine

A

low affinity for Mu and sigma, moderate for kappa
so low antagonism and dysphoria, but can produce analgesia and anti-shivering effects

258
Q

What is the caution for use of Butorphanol?

A

Do not use with other opioid agonists

259
Q

What is the only OAA that does not increase CV effects?

A

Nalbuphine

260
Q

What OAA would you use in cardiac cath lab?

A

Nalbuphine

261
Q

List the OAA from least to most potent

A

Nalbuphine < Pentazocine < Nalorphine < Butorphanol

262
Q

Which OAA has 50x more affinity for mu receptors relative to morphine?

A

Buprenorphine

263
Q

Why isn’t Nalorphine used?

A

High incidence of dysphoria (sigma receptor)

264
Q

Which OAA is more potent than morphine?

A

Buprenorphine

265
Q

Which antagonist can increase myocardial contractility?

266
Q

Dose of Naloxone?

A

1 - 4 mcg/kg IV
(40-80 mcg)

267
Q

Duration of Naloxone?

268
Q

Dose of Naloxone in continuous infusion, shock and epidural

A

CI = 5 mcg/kg IV
S = greater than 1 mg/kg IV
E = 0.25 mcg/kg/hour IV

269
Q

Use of naltrexone?

A

ETOH, lasts for 24 hours

270
Q

Dose of Nalmefene? potency relative to naloxone?

A

15 - 25 mcg q 2-5 min, same potency

271
Q

What is methylnaltrexone used for?

A

Gastric emptying and antagonizing N/V

272
Q

What is Alvimopan used for?

A

Post-op ilieus

273
Q

What is the only drug listedin lecture here to be metabolized by the gut flora?

274
Q

What are some of the tamper or abuse resistant opioids?

A

Suboxone (buprenorphine and naloxone), Embeda (ER morphine and naltrexone) and Oxynal (oxycodone and naltrexone)

275
Q

How much does fentanyl reduce MAC of Iso or des?

276
Q

How much does su, al and remifentanyl reduce mac?

A

Su = 70 - 90%
Al = up to 70%
Remi = 50 - 91%

277
Q

With neuraxial opioids, what are you targeting?

A

The opioid receptors in the substantia gelatinosa

278
Q

How much more drug do you give with an epidural relative to a spinal?

A

5 - 10x more

279
Q

What can you do to prevent systemic absorption of an epidural?

A

Add epinephrine

280
Q

List in order of increasing lipid solubility: sufentanil, fentanyl, morphine

A

Morphine < fentanyl < sufentanil

281
Q

If you had a left hip replacement with the hip up, right hip down, would you want a high or low baracity (hypobaracity) epidural?

A

Low so that it would float

282
Q

If you had a left hip replacement with the hip down and right hip up, would you want a high or low baracity epidural?

A

High so that it would sink down to the hip

283
Q

Which opioid would experience the most cephalad movement in the CSF?

284
Q

Common s/e of neuraxial opioids?

A

Pruritis, N/V, urinary retention (more so in males)

285
Q

What is the most reliable sign of decreased ventilation with neuraxial opioids? Treatment?

A

Decreased LOC secondary to hypercarbia. 0.25 mcg/kg/hour IV of naloxone

286
Q

What do you base barbiturate dosing on?

A

Lean body weight due to its propensity to go into other tissues

287
Q

Why are barbiturates no longer used as a pre-medication in pre-op?

A

They are notorious for having a bad hangover effect

288
Q

Which isomer of barbiturates are more potent?

A

S-isomers, though they are only marketed as a racemic mixture

289
Q

How much do barbiturates generally decrease HR/BP?

A

10 - 20 mmHg drop in BP, 15 - 20 reduction in HR

290
Q

For what drug class is SSEP monitoring required?

A

Barbiturates

291
Q

What are the plasma levels of unconscious vs awake of propofol?

A

Unconscious = 2-6 mcg/ml
Awake = 1 - 1.5 mcg/ml

292
Q

Where would you find nociceptors?

A

Skin, muscles, joints, viscera and vasculature

293
Q

Where would you find the NKI receptor where substance P would act?

A

Lamina III and IV

294
Q

Which opioids have the highest incidence rates of spasm of the oddi sphincter?

A

Fentanyl > Demerol > Morphine

295
Q

All the fentanyl’s are derivatives of what opioid?

296
Q

Which fentanyl’s bind to A1-Acid glycoprotein?

A

Al and Sufentanil

297
Q

Which fentanyl has a very rapid onset/offset with minimal tissue accumulation?

A

Remifentanil

298
Q

What is the common reason to use an OAA?

A

If the patient cannot tolerate a pure opioid agonist

299
Q

What OAA is resistant to narcan?

A

Buprenorphine

Anesthesia Pharmacology (11 decks)

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