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Mar: Sem 4 - Principles II > Exam 2: Acute Pain & Opioid-Free Analgesia > Flashcards

Exam 2: Acute Pain & Opioid-Free Analgesia Flashcards

1
Q

What types of somatic pain are there?

A
  • Superficial: skin, SQ, mucous membranes
  • Deep: muscles, bones, tendons

S4

Examples are knife cut to finger or a deeper pain like extremity injury jumping from a burning building

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2
Q

What types of visceral pain are there?

A
  • Parietal: sharp, stabbing, localized organ pain.
  • Referred: Cutaneous pain from embryological development patterns and convergence of visceral and somatic afferent input to CNS.

S4

expanding bowel gas from injesting certain food. Parietal would be appendicits. Referred would be L shoulder pain from an MI

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3
Q

Is chronic nociceptive pain or neuropathic pain more abnormal?

A

Neuropathic pain

S7

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4
Q

Red flags for pain

A
  • Constitutional symptoms
  • Pain that wakes patient up from sleep
  • Immunosuppression
  • Severe or progressive neurologic deficit
  • Cold, pale mottled or cyanotic limb
  • New bowel/bladder dysfunction
  • Severe abdominal pain or signs of shock/peritonitis (bc there is so many different things in the abd and its hard to isolate the pain source)

S10

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5
Q

What are some possible cardiac consequences of poorly managed or acute pain?

A

↑ HR
↑ BP
↑ Cardiac workload

S11

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6
Q

What are some possible respiratory consequences of poorly managed or acute pain?

A
  • Splinting (resp muscle spasm)
  • ↓ VC
  • Atelectasis
  • Hypoxia
  • Pulmonary infection risk

S11

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7
Q

What are some gastrointestinal consequences of poorly managed pain?

A

Ileus

S11

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8
Q

What are some possible renal consequences of poorly managed pain?

A
  • Oliguria
  • Urine retention

S11

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9
Q

What are some possible coagulative consequences of poorly managed pain?

A

↑ clot risk

S11

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10
Q

What are some possible immunologic consequences of poorly managed pain?

A

Immunosuppression

S11

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11
Q

What are some possible musculoskeletal consequences of poorly managed pain?

A
  • Fatigue & weakness
  • Limited mobility = clotting

S11

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12
Q

What is the Specificity Theory?
Who came up with it?

A

Intensity of pain is directly related to the tissue injury - Rene Descartes

Pain is a specific sensation with its own sensory apparatus independent of touch and other senses

S12

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13
Q

What theory linked pain and emotion?

A

Intensity Theory (Plato)

Plato defined pain as an emotional experience, rather than a sensory one.

S13

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14
Q

What is the Gate Control theory of pain?

A
  • proposed by Ronald Melzack and Patric Wall
  • According to the Gate Control Theory, pain transmission is modulated by a balance of impulses transmitted to the spinal cord and these fibers terminate and inhibitory interneurons in the Substantia Gelatinosa and the cells in this area functions as a gate regulating transmission of impulses to the central nervous system

S14

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15
Q

Where is pain attenuated in the CNS according to gate theory?

A

Substantia Gelatinosa of the spinal cord

S14

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16
Q

Thermal, mechanical and chemical tissue damage activates nociceptors, which are____?

A

Free afferent nerve endings of myelinated A-delta and unmylenated C fibers

S15

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17
Q

What chemicals are released upon tissue injury that mediate pain?

A
  • Histamine
  • Bradykinin (peptide)
  • Prostaglandins (lipids)
  • Neurotransmitters like Serotonin

S15

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18
Q

Give an example of first order neurons.

A

Aδ and C (sensory free nerve endings)

S16

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19
Q

Where do first order Aδ and C fibers synapse at?

A

Dorsal Root of the spinal cord

S17

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20
Q

Where do second order neurons synapse at?

A

Crosses lamina X, ascend the spinothalamic tract and synapse at the Thalamus

S18

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21
Q

Where do the third order neurons project to?

A

Third Order neurons from the thalamus projects through the internal capsule and to the postcentral gyrus of the cerebral cortex

S19

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22
Q

What is the name of the process by which noxious stimuli are converted to action potentials?

A

Transduction

S21

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23
Q

What is the name of the process by which an action potential is conducted through the nervous system?

A

Transmission

S21

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24
Q

What is the name of the process by which pain transmission is altered along its afferent pathway?

A

Modulation

S21

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25
Q

What is the name of the process by which painful input is integrated in the somatosensory and limbic cortices of the brain?

A

Perception

S21

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26
Q

What is Allodynia?

A

Allodynia is a pain from a stimulus that does not normally evoke pain (thermal or mechanical)

S22

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27
Q

Hyperalgesia is the process by which tissue trauma releases ____ that produced augmented sensitivity to stimuli.

A

local inflammatory mediators

hyperalgesia is an exaggerated response to a normally small amount of painful stimuli

S22-23

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28
Q

What is primary hyperalgesia?

A

Augmented sensitivity to painful response.

or

Allodynia-style misinterpretation of non-painful stimuli.

S23

Primary hyperalgesia is caused by a combination of peripheral and central sensitization, while secondary hyperalgesia is primarily caused by central sensitization

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29
Q

What is secondary hyperalgesia?

A

Increased neuronal excitability due to glutamate activation of NMDA receptors.

S23

Primary hyperalgesia is caused by a combination of peripheral and central sensitization, while secondary hyperalgesia is primarily caused by central sensitization

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30
Q

What opioid will potentiate hyperalgesia?

A

Remifentanil

S23

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31
Q

What is the treatment for hyperalgesia that was mentioned in lecture?

A

Ketamine

Lecture S23

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32
Q

Differentiate Hyperalgesia and Allodynia.

In chart form.

A
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33
Q

What is the hallmark “negative” symptom of neuropathy?

A

numbness

The paradoxical part is that nerve trauma and disease are also frequently associated with positive signs and symptoms

S25

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34
Q

GI blood flow and motility increase as we age. T/F?

A

False.

S27

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35
Q

Gastric acid secretion ____ as we age thus ____ gastric pH.

A

Gastric acid secretion decreases ‐ elevated gastric pH

S27

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36
Q

What effect does aging have on nutrient absorption in the GI tract?

A

Minimal effect but pts have increased complaints about their GI symptoms

S27

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37
Q

What occurs to muscle and fat mass as a patient ages?

A

Muscle decreases while fat proportion increases

S29

Dr. M slide says fat also decreases and thats why we can’t thermoregulate - this one is the ratios (not contradictory)

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38
Q

A decrease in ____ and ____ affects your protein-bound drugs in aging.

A

decrease in total body water (for water soluble drugs) and
albumin for protein bound drugs

S29

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39
Q

What occurs with hepatic function in the aging patient?

A
  • ↓ hepatic blood flow
  • ↓ liver mass and metabolic activity

S30

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40
Q

What occurs with renal function due to aging?

A
  • ↓ GFR
  • ↓ blood flow, kidney mass & functioning nephrons

S31

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41
Q

WHO steps for the pain relief ladder

A
  1. pain persisting or increasing = non-opioid pain management (NSAIDS, heat/cold, movement/positioning)
  2. pain persisting or increasing = opioid for mild to moderate pain + non-opioid
  3. Relief from pain = opioid for moderate to severe pain + non-opioid

S32

hit multiple receptors
Regaurdless of pain level, always use non-opiods +/- narcs

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42
Q

Do opioids or non-opioids act peripherally?

A

Non-opioids act peripherally, opioids act centrally and contribute to sedation effects

S33 (table comparing narcotics and non-narcotics)

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43
Q

Do opioids or non-opioids have anti-inflammatory effects?

A

most non-opioids have anti-inflammatory effects

S33

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44
Q

Do opioids or non-opioid analgesics exhibit a ceiling effect?

A

Non-opioid analgesics

S33 (table comparing narcotics and non-narcotics)

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45
Q

The μ receptor is responsible for…

A

analgesia, respiratory depression, euphoria, and reduced GI motility

GEAR

S34

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46
Q

The Kappa receptor is responsible for….

A

Analgesia, dysphoria, psychosis, miosis, and respiratory depression

DR. MAP

S34

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47
Q

The Delta receptor is responsible for…

A

analgesia alone when bound by an agonist

S34

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48
Q

4 Characteristics all opioids share

A
  • Derived from opium
  • bind to opioid receptors (mu1, mu2, K and D)
  • Act directly on the CNS
  • reduce the perception of pain, they don’t treat the cause

S35

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49
Q

What drug is described by the following organic structure:

Substitution of methyl group for hydroxyl group on #3 carbon of morphine molecule.
- what is it’s scientific name?
- What is/are the trade names?

A

Codeine
- 3-Methoxymorphine
- Tylenol #3 and Tylenol #4

S39

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50
Q

____ is much more reliably absorbed than morphine.

A

Codeine

S39

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51
Q

How is codeine metabolized?

A

CYP2D6
- 10% of the dose is demethylated in the liver to morphine
- remainder is demethylated to inactive norcodeine

10% of the population is resistant to its analgesic effect

S40

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52
Q

What drug exhibits side effects (without concurrent analgesia) in children?
Why is this?

A

Codeine

Children lack enzymatic maturity needed to properly break down codeine.

S40

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53
Q

Codeine metabolism is variable due to more than ____ polymorphisms resulting in analgesic variability.

A

50

S40

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54
Q

What is the adult dose and max of codeine?

A

15 - 60 mg q4

360mg max per day

S41

Corn says: Tylenol #3=30mg
Tylenol #4 = 60mg

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55
Q

What is the pediatric dose and max of codeine?

A

0.5 - 1 mg/kg/dose

60mg max per day

S41

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56
Q

60mg of codeine (maximal dose) is equivalent to how much aspirin?
and how long is its ET1/2?

A

650mg
3-3.5 hours

S41

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57
Q

What drugs does codeine have interactions with?

A

Opioids, EtOH, and Anticholinergics

S42

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58
Q

What drug is described by the following:

Synthetic 4-phenylpiperidine analogue of morphine and codeine which is composed of a racemic mixture of two enantiomets + and -

A

Tramadol

S43

59
Q

Where does the + enantiomer of tramadol have affinity and what does it do?

A

Centrally acting opioid agonist:
- μ → moderate affinity
- K & δ → weak affinity
- Opposes serotonin reuptake

S43

60
Q

What does the - entantiomer of tramadol do?

A
  • Inhibits NE reuptake
  • Stimulates α2 receptors

S43

Dexmetatomadine will be potentiated

61
Q

What is tramadol metabolized into and what is the relevance of its metabolite?

A

Tramadol → CYP3A4 & 2D6 → O-desmethyltramadol (2-4 times more potent)

S44

62
Q

What is tramadol’s potency compared to morphine?

A

1/5 to 1/10 potency of morphine

S45

63
Q

What is the oral onset for tramadol?

A

1-2 hours

S45

64
Q

What is the half life of tramadol?

A

6.3 hours (7.4 hoursfor metabolite)

S45

65
Q

When is tramadol contraindicated?

A
  • Seizure Disorders
  • PONV (high incidence)

S46

66
Q

What are the benefits of tramadol vs other opioids?

A
  • Minimal respiratory depression
  • Minimal-none addiction
  • Minimal constipation

S46

67
Q

Oral morphine dose requirement is ____ times the IM or IV route.

A

3

S47

68
Q

What receptors are primary affected by morphine?

A

μ-1 and μ-2

S47

69
Q

What are the two principle active metabolites of morphine? (also list effects)

A
  • Morphine-6-glucuronide → analgesia
  • Morphine-3-glucuronide → neurotoxicity & hyperalgesia

S48

70
Q

How is morphine metabolized?

A
  • Hepatic → conjugation w/ glucuronic acid
  • Extrahepatic = Kidneys

S48

71
Q

What 3 factors contribute to morphine’s minimal CNS absorption?

A
  • poor lipid solubility
  • high protein binding
  • high Ionization at normal bodily pH

S48

72
Q

What is the IV/IM onset and peak of action for morphine?

A

Onset: 15-30 min
Peak: 45-90 min

S49

73
Q

What differences does morphine exhibit in women vs men?

A

In women:
↑ potency
↓ speed of offset

S49

74
Q

What is the protein binding of morphine?
What about the half-time?

A

35% protein binding
1.7 - 3.3 hours

S49

75
Q

What is released from morphine administration?
What is the result?

A

Histamine → vasodilation and hypotension

S50

76
Q

Morphine should be avoided in patients with ____ impairment as the metabolite morphine–6-glucuronide can accumulate and lead to _________ ________.

A

Renal : respiratory depression

S50

77
Q

What drug is a synthetic derivative of thebaine?

A

Oxycodone

S51

78
Q

What are the metabolites of oxycodone?

A

Oxymorphone (active)
Noroxycodone (inactive)

Oxycodone is primary a prodrug.

S52

79
Q

What is the site of action of oxycodone?

A

μ and κ receptors of the CNS

S52

80
Q

What are the two types of PO oxycodone?

A

IR = Immediate release
CR = Controlled release

S51

81
Q

What is the dose of oxycodone? and what is the morphine equlvalent?

A

Dose: 5mg PO
10 - 15mg is equilvalent to 10mg morphine (rough 1 to 1 equivalence with morphine)

S53 (dose comes from S88)

82
Q

What is the onset of action of oxycodone?

A

< 1 hour

S53

83
Q

Opioids (in general) exhibit an ____ effect with other drugs that are CNS depressants

A

additive

S54

84
Q

Why is methadone used for opioid addiction maintenance?
is it synthetic or natural?

A
  • 60-90% oral bioavailability
  • High potency
  • Long duration of action
  • Synthetic borad-spectrum

S55

85
Q

What should be known about methadone’s half life?

A

Very long and unpredictable ET1/2 (up to 36 hours)
Can accumulate w/ repeated doses

S55

86
Q

What various receptors affinities does methadone have?

A
  • Weak noncompetitive NMDA antagonist
  • Serotonin reuptake inhibitor
  • Monoamine reuptake inhibitor
  • High μ receptor affinity

S55

87
Q

What would occur with concurrent methadone and carbamazepine use?

A

Carbamazepine (Tegretol) is a CYP450 inducer thus methadone will be metabolized faster.

S56

88
Q

What agents can decrease the metabolism of methadone?

A

CYP450 Inhibitor:

  • Antiretrovirals
  • Grapefruit juice

S56

89
Q

How much is methadone clearance affected by hepatic and renal impairment?

A

Not much
* Excreted in urine and bile with small amounts of unchanged drug

S56

90
Q

What is the dose of methadone?

A

2.5 - 10 mg PO/IM/SC q4-12 hours

S57

91
Q

Why are standardized simple dosing guidelines unachievable for methadone?

A

High variable half life (8-80 hours)

S57

92
Q

What is the most severe and unpredictable medication interaction associated with methadone?

A

MAOI’s

S58

93
Q

What drugs are known to increase the concentration/effects of methadone?

A
  • Cipro
  • Diazepam
  • Acute EtOH use

S58

94
Q

What drugs are known to decrease concentration/effects of methadone?

A
  • Amprenavir
  • Phenobarbital
  • Phenytoin
  • Rifampin
  • MAOI’s

S58

95
Q

What cardiac complications can occur in rare cases with methadone usage?

A
  • Pause dependent dysrhythmia associated with bradycardia
  • QT prolongation
  • Torsades

S58

96
Q

What drug is fentanyl structurally similar to?

A

Meperidine

Fentanyl is a Phenylpiperidine-derivative synthetic opioid agonist

S59

97
Q

Fentanyl has ____ potency, ____ onset of action and ____ duration of action.

A

High potency
Rapid onset
Short duration

S59

98
Q

What is the priniciple metabolite of fentanyl?

A

Norfentanyl

Detectable in urine up to 72 hours after single dose.

S60

99
Q

Why is elimination of fentanyl slightly prolonged despite very short duration of action?

A

Lungs serve as large inactive reservoir (up to 75% of initial dose undergoes first pass pulmonary uptake).

S61

100
Q

Why is fentanyl more potent and rapid than morphine?

A

Greater lipid solubility

S61

101
Q

What is responsible for fentanyl’s short duration of action?

A

Rapid redistribution to fat and muscle

S61

102
Q

What is the protein binding of fentanyl? what is it’s ET1/2?

A

84%
3.1-6.6 hours

S61

103
Q

What is hydromorphone and how is it formed?

A

semi-synthetic agent and hydrogenated ketone of morphine formed by N-demethylation of hydrocodone

  • Dilaudid is hydrophilic but it is also 10x more lipophilic than morphine which increases its potency

S63

104
Q

Hydromorphone is ____ times as potent as morphine when administered orally.

A

3 - 5 times

S63

105
Q

Hydromorphone is ____ times as potent as morphine when administered parenterally.

A

8.5 times

S63

106
Q

What is hydromorphone’s primary metabolite?

A

Hydromorphone-3-glucuronide

S64

107
Q

What should be known about Hydromorphone-3-glucuronide?

A
  • Lacks analgesic effects
  • May potentiate neurotoxic effects (allodynia, myoclonus, seizures).

S64

108
Q

When is Hydromorphone-3-glucuronide’s neurotoxic side effects an actual concern?

A

Patients with renal insufficiency

S64

109
Q

What is the typical parenteral dose of parenteral Hydromorphone?

A

0.2-2mg Q3-5 min parenterally for post op pain

S65

110
Q

What is the typical oral dose of hydromorphone?

A

2 - 8 mg

S65

111
Q

What is the duration of action and ET1/2 of hydromorphone?

A

3 - 4 hours
ET1/2 if 2.3 hrs

S65

112
Q

What is hydrocodone derived from?

A

Codeine
- semi-synthetic opioid

S67

113
Q

How does the potency of hydrocodone and codeine compare?

A

Hydrocodone is 6 - 8 x more potent than codeine

S67

114
Q

What are the two most abused opioids?

A

1st = Oxycodone
2ⁿᵈ = Hydrocodone

Lecture S67

115
Q

What are the two metabolites of hydrocodone metabolism?

A
  • Hydromorphone (via CYP2D6)
  • Norhydrocodone (inactive) via CYP3A4 (catalyzed oxidation)

S68

116
Q

What is the morphine equivalent of hydrocodone?

A

1 mg morphine = 3 mg hydrocodone

S69

117
Q

What is typical hydrocodone dosing?

A

2.5 - 10mg Hydrocodone with 300 - 750mg acetaminophen
q4-6hours

S69

Hint: Same mg dosing as hydromorphone with tylenol added

118
Q

What receptors does buprenorphine have affinity to?

A

Semi-synthetic agonist-antagonist derived from alkaloid thebaine
μ - partial agonist (strong)
κ - antagonist (strong)
δ - agonist (weak)

S71

119
Q

What benefits does buprenorphine provide?

A
  • ↓ respiratory depression
  • ↓ immune suppression
  • ↓ constipation
  • No accumulation in renal patients

S71

120
Q

What is the primary metabolite of buprenorphine?

A

Norbuprenorphine from CYP3A4

S72

121
Q

What should be known about norbuprenorphine?

A
  • Full agonist at Mu, Delta and ORL-1 receptors and partial agonist at Kappa
  • 1/50th analgesic activity of buprenorphine
  • ↑↑↑ Respiratory depression

S72

122
Q

What is the IV/IM buprenorphine dose equivalence for morphine?

A

0.3mg IM buprenorphine = 10mg morphine

S73

123
Q

What is the half life of buprenorphine?

A

Long

20 - 73 hours

S73

124
Q

Should buprenorphine be avoided in patients with renal impairment?

A

No. Hepatic elimination primarily

S73

125
Q

What are the differences in side effects of buprenorphine compared to other agonists-antagonists?

A
  • may be resistant to naloxone
  • pulmonary edema has been observed
  • dysphoria unlikely compared to other agents

S74

126
Q

What receptors do NSAIDs bind to?

A

Trick question. NSAIDs inhibit COX pathway as their method of pain modulation.

S78

127
Q

What is the recommended dose for each NSAID:
- Ibuprofen
- Celecoxib
- Naproxen
- Diclofenac

A
  • Ibuprofen: 200mg three times daily
  • Celecoxib: 100 mg daily
  • Naproxen: 220 mg twice daily
  • Diclofenac: 50mg twice daily

S80

128
Q

How might antidepressants work as pain medication adjuvants?

A

Increase transmission in spinal cord to reduce pain signaling

doesn’t work right away, dizziness, decreased appetite and dry mouth

S81

129
Q

Whats the IV dose of fentanyl for pain?

A

20 - 50 mcg

S88

130
Q

What anticonvulsants are used as adjuvant medication to relieve pain?

A
  • Gabapentin (Neurontin): watch for sedation/ respiratory depression in older patients
  • Phenytoin (Dilantin)
  • Carbamazepine (Tegretol)
  • Topiramate (Topamax)

S81

131
Q

What skeletal muscle relaxants are used as adjuvant medication to relieve pain?

A
  • Baclofen (Lioresal®)
  • Carisoprodol (Soma®)
  • Cyclobenzaprine (Flexeril®)
  • Methocarbamol (Robaxin®)
  • Tizanidine (Zanaflex®)

S82

132
Q

What is Opioid Free Anesthesia?

A
  • Technique where no intra-operative systemic, neuraxial, or intracavitary opioid is administered during the anesthetic.

Opioid slides S2

133
Q

Opioids acting on the Mu receptor will produce these unwanted effects.

A
  • Respiratory depression
  • Decrease GI motility/ constipation
  • Urinary retention
  • Prurititis
  • Physical dependence

Opioid free S4

134
Q

Opioids acting on the Kappa receptor will produce these unwanted effects.

A
  • Respiratory depression
  • Dysphoria

Opioid Free S4

135
Q

Opioids acting on the Delta receptor will produce these unwanted effects.

A
  • Respiratory depression
  • Urinary retention
  • Prurititis
  • Physical dependence

Opioid Free S4

136
Q

In general, all opioids can cause these side effects

A
  • Respiratory depression
  • dysphoria
  • N/V
  • Skeletal musle rigidity
  • Smooth muscle spasm
  • constipation
  • Urinary retention
  • biliary spasm (treat with glucagon remember?)
  • Pruritus
  • histamine release
  • Chronic: tolerance
  • chronic: physical dependence
  • Chronic: constipation

opioid free S5

137
Q

What is opioid-induced hyperalgesia (OIH)?

A
  • State of nociceptive sensitization caused by exposure to opioids.
  • The condition is characterized by a paradoxical response whereby a patient receiving opioids for the treatment of pain might actually become more sensitive to certain painful stimuli.

Opioid free S10

138
Q

Absolute and relative contraindications for using opioid free techniques

A
  • Absolute: Allergy to any adjuvant drugs
  • Relative
    • Disorders of autonomic failure
    • Cerebrovascular disease
    • Critical coronary stenosis acute coronary ischemia
    • Heart block / extreme bradycardia
    • Non-stabilized pypovolemic shock or polytrauma patients
    • Controlled hypotension for minimal blood loss
    • Elderly patients on beta-blockers

S13

139
Q

Opioid free toolbox: Ketamine (doses and highlights)

A
  • Doses less than 0.5 mg/kg reduces postoperative analgesic needs and especially seen in opioid-tolerant patients
  • It has anti-hyperalgesic and anti-allydonic and anti-tolerance effects.
  • decreases PONV

S14

140
Q

Opioid Free toolbox: Gabapentinoids (dosing and highlights)

A
  • Act on alpha-2-deta-1 subunit of presynaptic calcium channels and inhibit neuronal calcium channel influx. Results in reduction in release of excitatory neurotransmitters such as glutamate, substance P and calcitonin
  • Pregabalin: 225-300mg (lowest effective dose)
  • Gabapentin: we see ceiling effect at 600mg (this was on last year’s test)

S15

141
Q

Opioid free toolbox: IV lidocaine (dose and highlights)

A
  • Na-channel blocker
  • Analgesia: supresses nerve fiber impulses
  • anti-inflammatory: neural transmission blockade
  • anti-hyperalgesic: suppression of peripheral and central sensitzation
  • Dose: bolus of 100mg or 1.2-2mg/kg followed by infusion 1.33-3mg/kg/hr

S16

142
Q

Opioid free toolbox: magnesium (dose and highlights)

A
  • noncompetative NMDA antagonist on glutamate receptors: decreases Ca and Na ion entry and prevents efflux of K
  • prevents depolarization and transmission of pain signals: blunts somatic, autonomic and endocrine reflexes
  • Dose: loading dose of 30-50mg/kg then maintance of 6-20mg/kg/hr

S17

143
Q

Opioid Free toolbox: Alpha2 agonists (doses and highlights)

A
  • both presynaptic (inhibits NE negative feedback loop) and postsynaptic activity (sympathectomy) in CNS and PNS
  • activated G1-K channels causing hyperpolarization of neurons
  • reduces Ca conductance at voltage gated Ca channels
  • Dose for dexmetatomadine: 0.5mgc/kg loading dose over 10 min
    • then 0.1-0.3 mcg/kg/hr

S18

8x more specific at the alpha2 receptor than clonadine

144
Q

opioid free toolbox: beta blockers (highlights)

A
  • Esmolol is a selective β1-adrenoreceptor antagonist that controls HR, contractility and conduction - but may also be a good opioid-sparing adjunct (reasons specifically unclear)
    • One theory: Esmolol does slow heart rate; thereby it decreases cardiac output, which decreases hepatic blood flow, so this may slow metabolism of other drugs that are hepatically metabolized, such as fentanyl.

S19

Mar: Sem 4 - Principles II (27 decks)

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