Exam 2 Flashcards

(180 cards)

1
Q

What is transduction?

A

Nerve/electrical impulses/signals start at the nerve endings. Damaged or not

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2
Q

What is transmission?

A

Travel of nerve/electrical impulses to the nerve body connecting to the dorsal horn of the spinal cord.

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3
Q

Where do peripheral nerve blocks work?

A

At the dorsal horn

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4
Q

What is modulation?

A

Process of altering (inhibitory/excitatory) pain transmission mechanisms at the dorsal horn to the PNS and CNS.

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5
Q

What are the locations of nociceptors?

A

Skin, muscles, joint, viscera, vascular

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6
Q

Describe unmyelinated & myelinated fibers?

A
  • Unmyelinated; C-fibers, burning pain from heat & pressure, travel at <2m/s.
  • Myelinated: Aβ & Aδ fibers, conduct heat, mechanical, chemical pain signals. Aδ fibers conduct fast heat pain. Travels >2m/s
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7
Q

What are the first chemical pain mediators?

A

Peptides: (Substance P, Calcitonin, Bradykinin, CGRP)

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8
Q

List chemical mediator groups?

A

Peptides, Eicosanoids, Lipids, Neutrophins, Cytokines, Chemokines, Extracellular proteases & protons

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9
Q

List all Lipid chemical mediators?

A
  • Prostaglandins
  • Thromboxanes
  • Leukotrienes
  • Endocannabinoids
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10
Q

List all receptors & Ion channels?

A

Dorsal Root Ganglion & Peripheral Terminals, Purinergic, Metabotropic, Glutamatergic, Tachykinin, TRPV I, Neurotrophic, Ion channels

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11
Q

Describe Hyperalgesia & Allodynia?

A
  • Hyperalgesia: Increased pain sensations to normally painful stimuli.
  • Allodynia: Perception of pain sensations in response to normally non-painful stimuli.
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12
Q

What is primary hyperalgesia & its 4 categories?

A
  • Pain at the original site of injury from heat and mechanical injury.
  • Decreased pain threshold, Increased response to suprathreshold stimuli, Spontaneous pain, Expansion of receptive field
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13
Q

What is Secondary Hyperalgesia?

A

Uninjured skin surrounding the injury (only from mechanical stimuli like pressure, inflammation). Sensitization of central neuronal circuits

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14
Q

Which Lamina do opioids work on?

A

Lamina II (substantia gelatinosa), on the afferent C-fibers

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15
Q

Which Laminae send innervating muscles & visceral pain?

A

Laminae I, IV, VII, & ventral horn

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16
Q

Which Lamia send substance P?

A

Laminae III & IV

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17
Q

Which Laminae are targeted for spinals & epidurals?

A

Laminae III & IV

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18
Q

Which laminae contains NKI receptors?

A

Laminae III & IV

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19
Q

Explain the Gate control theory of pain?

A

The gate is open & Aδ (small diameter, myelinated) & C fibers (unmyelinated) send pain signals. Then Aβ fibers (large diameter, myelinated: faster) deliver information about pressure and touch (rubbing) overriding Aδ signals.

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20
Q

What do the Periaqueductal gray -rostral ventromedial medulla (PAG-RVM) system do?

A

Depress or facilitate the integration of pain info in the spinal dorsal horn towards limbic cortex & thalamus.

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21
Q

List all Neuromodulators & which one is used by ketamine?

A
  • Substance P,
  • Glutamate
  • CGRP
  • NMDA (ketamine)
  • AMPA
  • BDNF
  • Cytokines
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22
Q

Injured tissues release what?

A

Nociceptors (Substance P & Glutamate)

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23
Q

Damaged cells, mast cells, and platelets release what mediators?

A

Bradykinin, Histamine, Prostaglandins, Serotonin, Hydrogen ion, Lactic acid

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24
Q

List all excitatory & inhibitory spinal modulators?

A
  • Excitatory: Glutamate, Calcitonin, Neuropeptide Y, Aspartate, Substance P.
  • Inhibitory: GABA, Glycine, Enkephalins, Norepinephrine, Dopamine
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25
List the 4 ascending pathways of nociceptive information?
- Spinothalamic - Spinomedullary - Spinobulbar - Spinohypothalamic
26
What is send thru the Spinothalamic pathway & which laminae are used?
Pain, temperature, and itch (Laminae I, VII, & VIII: All afferent fibers)
27
What is send thru the Spinobulbar pathway & which laminae are used?
Behavior toward pain (Laminae I, V, VII)
28
What is send thru the Spinohypothalamic pathway & which laminae are used?
Autonomic, neuroendocrine, and emotional aspects of pain (Laminae I, V, VII, & X)
29
What are the 6 Supra-spinal modulation of nociception areas?
Forebrain S1 & S2, Anterior cingulate cortex (ACC), Insular cortex (IC), ACC and IC, Prefrontal cortex, Thalamus, Cerebellum
30
What does the forebrain process?
Location & intensity of pain
31
What does the Insular cortex (IC) process?
Emotional & motivational aspects
32
Where do descending inhibitory tracts originate & its pathway?
Periaqueductal gray through the rostal ventromedial medulla (RVM) --> dorsolateral funiculus --> synapse in dorsal horn
33
What are the descending inhibitory neurotransmitters?
Endorphins, enkephalins, serotonin
34
What fibers & how are they affected during descending inhibition?
Hyperpolarize Aδ & C fibers, Decrease release of substance P. Opening of K+ channels/inhibition of Ca2+ channels.
35
What are the 2 Descending pathways of pain modulation?
Descending Inhibition Pathway (DI) & Descending Facilitation Pathway (DF)
36
What receptors are used by the PAG-RVM systems?
µ, κ, δ opioid receptors
37
Where does the pain impulse originate if it is pertaining to the descending inhibitory tract?
PAG-RVM
38
What is the Primary Objective for pain?
Tissue healing without repeated injury.
39
What are the time frames for Acute & Chronic pain?
- Acute: days to weeks after injury. - Chronic: >3-6 months, persists beyond tissue healing
40
What is Neuropathic pain, who is at increased risk & what is the treatment?
Persists after the tissue has healed ➔ allodynia and hyperalgesia Increased risk: Cancer patients d/t chemo and radiation therapy Treatment: symptomatic (opioids gabapentin, amitryptiline, cannabis)
41
Describe Visceral pain & its causes?
Diffuse & poorly localized (referred to somatic sites: muscle & skin) --> CT scan. Causes: ischemia, stretching of ligamentous attachments, spasms, distention.
42
What is Complex Regional Pain Syndrome & examples?
- A variety of painful conditions following injury in a region with impairment of sensory, motor, and autonomic systems. - Examples: Spontaneous pain, allodynia, hyperalgesia, edema, autonomic abnormalities, active and passive movement disorders, and trophic changes of skin & SQ tissues.
43
Describe pain in Neonate and Infant?
Pain perception starts at 23 weeks of gestation. Lower pain threshold & exaggerated pain responses.
44
Describe the cardiovascular response to pain?
Prominent: Hypertension, Tachycardia, Myocardial irritability, ↑ SVR, Compromised LV --> decreased CO, Myocardial ischemia
45
Describe the Pulmonary Response to pain?
↑ total body O2 consumption/CO2 production, ↑ Vm and work of breathing, Splinting, Decreased movement of chest wall, Atelectasis, Intrapulmonary shunting (VQ mismatch). Impaired coughing
46
Describe the GI/GU response to pain?
Enhanced sympathetic tone:↑ sphincter tone, and ↓ motility --> Ileus & Urinary retention. Hypersecretion of stomach acid --> Stress ulceration, Aspiration & Increased gastric contents. N/V & Abdominal distention
47
Describe the endocrine response to pain?
↑ catabolic hormones: Catecholamines, Cortisol & Glucagon. ↓ anabolic hormones: Insulin & Testosterone. Effects: Negative nitrogen balance, Carbohydrate intolerance & Increases renin, aldosterone, angiotensin
48
Describe the Hematologic response to pain?
Stress related --> Plt adhesiveness, reduced fibrinolysis & hypercoagulability
49
Describe the emotional & immune responses to pain?
- Emotional: Anxiety, sleep disturbances, depression. - Immune: Stress related Leukocytosis & depressed Reticuloendothelial system --> increased infection
50
What medication classes work @ perception & what is the MOA?
- Meds: Opioids, alpha 2-agonists, general anesthetics. - MOA: activate descending inhibitory pain pathways & memory.
51
What medication classes work @ Modulation & what is the MOA?
- Meds: Local anesthetics, opioids, ketamine, & alpha 2-agonists. - MOA: modulation of afferent signals in the dorsal horn of spinal cord & production of reflex reaction.
52
What medication classes work @ Transmission & what is the MOA?
Local anesthetics & transmission of action potentials via Aδ & C fibers
53
What medication classes work @ Transduction & what is the MOA?
- Meds: Local anesthetics, NSAIDs. - MOA: transduction of mechanical, chemical & thermal stimuli into an action potential.
54
Delineate the pathway of pain signals?
Stimuli --> dorsal horn --> afferent thru medulla --> thru midbrain --> thalmic nuclei --> forebrain.
55
What two populations have a higher fat component?
Geriatric & older women
56
What is myoclonus & what drug has a high incidence of it?
Involuntary movements, be careful before giving more meds. & Etomidate
57
When is Etomidate water soluble & lipid soluble?
Water soluble at acidic pH & lipid soluble at physiologic pH.
58
What structure does only Etomidate have?
Carboxylated imidazole
59
What is the MOA of Etomidate?
Selective modulator of GABA-a receptors
60
What are the pharmacokinetics of Etomidate (Onset, clearance, metabolism, elimination, excretion)?
- Onset= within 1min IV. 76% Albumin bound, Large Vd. - Clearance is 5x faster than Thiopental= prompt awakening. - Metabolism: Hydrolysis by hepatic microsomal enzynmes & plasma esterases. - Elimination: 85% urine & 10-13% in bile. - E ½ time: 2-5hrs
61
How long should someone not drive after Etomidate?
24hrs
62
What is the IV dose for Etomidate?
0.3mg/kg
63
When is Etomidate especially useful?
In Pt’s with unstable CV systems & little to no cardiac reserve
64
What type of med must/should be given in conjunction with Etomidate for induction?
Opioids as Etomidate does not have analgesic effects
65
What are the CV side effects of Etomidate?
- Minimal changes to HR, SV, CO & contractility. - Mild decrease in MAP d/t decreased SVR. - Sudden hypotension with hypovolemia especially with high 0.45mg/kg induction doses.
66
What are Etomidate’s ventilation side effects?
- Less depressant than barbs. Apnea with rapid injection. - Transient 3-5mins decreased Vt, offset by increased RR. - Stimulates CO2 medullary centers.
67
What is the MOA of Gabapentin?
Binds to V-G calcium channels —> enhances descending inhibition & inhibits excitatory neurotransmitter release
68
Gabapentin is lipid soluble/nonsoluble & binds/does not bind to protein?
Soluble & does not bind
69
What are the drug interactions with gabapentin?
None
70
What is the Pre-op dose for gabapentin?
300-1200 mg PO 1-2hrs prior to Sx
71
What are Gabapentin’s contraindications?
MG, myoclonus
72
What are the side effects of Gabapentin?
Somnolence, fatigue ataxia vertigo constipation abrupt withdrawal in seizure Pts weight gain
73
What are the MOA, dose, peak, duration & C/I of ofirmev?
- MOA: reduces prostaglandin metabolites - Dose: 1000mg Q4-6hr Max 3000-4000mg QD. - Peak: IV 30-60mins & 1-3hrs PO - Duration: 6-8hrs C/I: hepatic dysfunction
74
What are the MOA, dose, peak of ketorolac?
- MOA: inhibits PG synthesis by inhibiting COX1 & 2 - Dose: 15-30mg Q6h Max 60-120mg QD - Peak: 45-60mins
75
What are the contraindications of ketorolac?
Severe renal impairment bleeding CAD CABG pregnancy NSAID allergy
76
What are the MOA, dose, peak & excretion of ibuprofen?
- MOA: anti-inflammatory, analgesic, antipyretic (inhibits COX1 & 2) - Dose: 200-800mg IV over 30mins Q6H Max 3200mg QD. - Peak: 1-2hrs. - Excretion: urine & bile
77
What are the contraindications of ibuprofen?
NSAID allergy CABG bleeding ulcers
78
What is the MOA of Magnesium?
- Anti-nociceptive effects - NMDA receptor antagonist - Regulates calcium access into cell, neurotransmission, cell signaling & enzyme function.
79
What are the contraindications for magnesium?
- MG - renal failure
80
What is the dose for lidocaine & when is it stopped?
- 1-2mg/kg IV (initial bolus) over 2-4mins - Then 1-2 mg/kg/hr (Qtt) - Stopped in 12-72hrs
81
What is monitored with lidocaine infusions?
- Cardiac - hepatic - renal dysfunction
82
What are the first signs of lidocaine toxicity?
- Tinnitus - circum-oral numbness - muscle twitching - hypotension - myocardial depression
83
What is the magnesium pre-op dose?
50mg/kg IV
84
What is the magnesium intraop dose?
8 mg/kg/hr
85
Magnesium significantly reduces the use of?
Fentanyl
86
What is the plasma ½ life of Zofran?
4hrs
87
What is the pediatrics dose for Zofran?
0.1 mg/kg IV
88
What increases the effectiveness of Zofran?
Corticosteroids
89
What is the MOA of decadron?
- Anti-inflammatory - Inhibition of phospholipase - Cytokines
90
What are the equilibration times for Fentanyl, Sufentanil, Alfentanil & remifentanil?
6.8mins 6.2mins 1.4mins 1.1mins
91
Which opioid agonists have the lowest & highest clearance in ml/min?
Lowest= Alfentanil Highest= Remifentanil
92
Which opioid agonists have the lowest & highest % nonionized?
Lowest= Meperidine (7) Highest= Alfentanil (89)
93
What are the opioid effects on Mu1 receptors?
Analgesia bradycardia euphoria hypothermia miosis urinary retention low abuse potential
94
What are the opioid effects on Mu2 receptors?
- Dependence - ventilation depression - constipation - Analgesia
95
What are the opioid effects on Kappa receptors?
- Analgesia - dysphoria - diuresis - low abuse potential - miosis - sedation
96
What are the opioid effects on Delta receptors?
- Analgesia, - ventilation depression - dependence - constipation - urinary retention
97
What are the Mu1 receptor agonists?
Endorphins, morphine, synthetic opioids
98
What are the Mu2 receptor agonists?
Endorphins, morphine, synthetic opioids
99
What are the Kappa receptor agonists?
Dynorphins
100
What are the Delta receptor agonists?
Enkephalins
101
What are the Mu1, Mu2, Kappa & Delta receptor antagonists?
Naloxone, naltrexone, nalmefene
102
What are the uses for naloxone?
- Opioid OD - dependence - hypovolemic/septic shock, - can reverse general anesthesia with high doses.
103
What are the Naloxone doses for Intraop & post op?
Intraop & Postop= 40-80mcg
104
What are the onset & duration of action of naloxone?
- Onset= 1-5mins - Duration= 30-45mins
105
What are the side effects of naloxone?
- N/V - crosses placenta - increased SNS - pulmonary edema - dysrhythmias (V-fib)
106
What is the use & duration of Naltrexone?
Used for alcoholism & duration is 24hrs PO
107
What is the dose & E1/2 time of Nalmefene?
- Dose: 15-25mcg IV - E 1/2: 10.8hrs
108
What is methylnaltrexone used for?
Gastric emptying, antagonizes N/V, & in peripheral
109
Which opioid antagonist does not reverse centrally mediated analgesia?
Methylnaltrexone
110
What receptors does Alvimopan affect?
Mu1 & Mu2
111
What is Alvimopan used for?
Post-op ileus
112
Where is Alvimopan metabolized?
Gut flora
113
What are Alvimopan’s limitations?
Longterm use can lead to CV events
114
What is Suboxone?
- Buprenorphine plus naloxone - Su(b)o(xone)= b=buprenorphine; xone= naloxone
115
What is Embeda?
- Extended release morphine plus naltrexone - (E)(m)beda= E=xtended & m=morphine
116
What is OxyNal?
Oxycodone plus naltrexone
117
Sufentanil, Alfentanil, & Remifentanil decrease MAC by how much?
Sufentanil= 70-90%, Alfentanil= 70%, Remifentanil= 50-91%
118
Butorphanol, Nalbuphine, & Pentazocine reduce MAC by how much?
- Butorphanol= 11% - Nalbuphine= 8% - Pentazocine= 20%
119
What is the main receptor for opioids in the spinal cord?
Substantia gelatinosa (laminae 2)
120
Why is epinephrine used in epidurals?
To avoid systemic absorption through the venous plexi
121
What are the epidural CSF peak times for fentanyl & sufentanil & morphine?
- Fentanyl= 20mins - Sufentanil= 6mins - morphine= 1-4hrs
122
What are the epidural plasma peak times for morphine, fentanyl & sufentanil?
- Morphine= 10-15mins - Fentanyl= 5-10mins - Sufentanil= <5mins
123
What are the intraop & post op doses for morphine?
- Intraop= 1-10mg - Postop= 5-20mg
124
What are the onset, peak & duration of morphine?
- Onset= 10-20mins - Peak= 15-30mins - Duration= 4-5hrs
125
What is the intraop dose for fentanyl?
Intraop= 1.5-3 mcg/kg
126
What are the onset & duration of fentanyl?
- Onset= 30-60sec - Duration 1-1.5hrs
127
What is the intraop dose for sufentanil?
0.3-1mcg/kg
128
What are the onset & duration of sufentanil?
- Onset= 30-60sec - Duration= 1-1.5hrs
129
What are the intraop & postop dose for hydromorphone?
- Intraop= 1-4mg - Postop= 1.5-4mg
130
What are the onset & duration of hydromorphone?
- Onset= 5-15mins - Duration= 2-4hrs
131
What is the infusion rate for sufentanil?
0.5-1 mcg/kg/hr
132
What is the infusion rate for Remifentanil?
0.125-1mcg/kg/hr
133
What is the intraop dose for Remifentanil?
0.5-1mcg/kg/hr
134
What are the onset & duration of Remifentanil?
- Onset= 30-60sec - Duration=6-8mins
135
What is the duration of meperidine?
2-4hrs
136
What are the effects of meperidine?
- Sedation - euphoria - N/V - ventilation depression
137
What is the E1/2 time for meperidine?
3-5hrs (35hrs with renal failure)
138
What are the toxicities of meperidine?
- Delirium - myoclonus - seizures
139
Which opioid receptor causes Diuresis?
Kappa
140
Which opioid receptors cause urinary retention?
Mu1 & Delta
141
Which opioid receptors cause constipation?
Mu2 (marked) & Delta (minimal)
142
Which opioid receptors have a low abuse potential?
Mu1 & Kappa
143
What are the advantages of opioid agonist-antagonists?
- Analgesia - low ventilation depression - low dependence - ceiling effect
144
What are the intrathecal/CSF times of fentanyl, sufentanil & morphine?
- Fentanyl & sufentanil are minimal & - morphine= 1-5hrs
145
What is the most common side effect of neuraxial opioids & the cause?
- Pruritus in the face, neck & upper thorax. - Caused by cephalad migration to trigeminal nucleus
146
What are the treatments for neuraxial pruritus?
- Naloxone - antihistamines - propofol - gabapentin
147
What are the side effects of neuraxial opioids?
- Ventilation depression (from 2 to 12hrs) - Depressed LOC from hypercarbia, sedation - CNS excitation (tonic skeletal muscle rigidity like seizures) - Herpes reactivation (2-5 days after epidural - Neonatal morbidity (negligible in breast milk)
148
What is the onset, Vd, metabolism, elimination & E1/2 time for Etomidate?
- Onset: 1min - Vd: Large w/ prompt awakening - Metabolism: Hydrolysis by hepatic enzymes & plasma esterases - Elimination: 85% urine, rest in bile - E1/2 time: 2-5hrs
149
What is the dose for etomidate?
0.3mg/kg
150
When is it wise to use etomidate & what else must be given?
- Has no or little CV effects - Must give opioid in conjunction
151
What are the side effects of Etomidate?
- Myoclonic movements - alteration of inhibitory & excitatory thalamocortical tract (balance) - attenuated by opioids or benzos - caution in seizure patients - adrenocortical suppression
152
Who should not receive etomidate & why?
- Septic or hemorrhaging Pt’s due to inhibition of cholesterol to cortisol conversion --> severe hypotension, longer ventilation. - Inhibition can last 4-8hrs.
153
What are the CNS side effects of etomidate?
- Decreased CBF & CMRO2 (direct cerebral vasoconstrictor, decreased ICP) - EEG changes (excitatory spikes) may activate foci seizure
154
What are the CV effects of etomidate?
- Minimal decrease in MAP d/t decreased SVR. - Sudden hypotension w/ hypovolemia w/ high >0.45mg/kg induction doses
155
What are etomidate’s ventilation side effects?
- Apnea with rapid injection, transient 3-5mins decrease in Vt, stimulates CO2 medullary center
156
Ketamine is derived from?
Phencyclidine
157
Ketamine causes amnesia & intense___?
Analgesia
158
What does someone look like that received ketamine?
- Noncommunicative but wakefulness - hypertonus & purposeful skeletal muscle movements
159
What are ketamine’s advantages & disadvantages over propofol & etomidate?
- Advantage: no injection pain, profound analgesia. - Disadvantage: frequency of emergence delirium, abuse potential
160
What is ketamine’s preservative?
Benzethonium chloride
161
What are the benefits of S-ketamine?
- More analgesia (2x> racemic, 4x> R isomer) - more rapid metabolism & recovery - less salivation - lower incidence of emergence reactions.
162
What are the benefits of racemic ketamine?
- Less fatigue - less cognitive impairment
163
Which receptors does ketamine bind to?
- Noncompetitively to NMDA - All opioid receptors - muscarinic - V-G Na+ & L-type calcium channels - neuronal nACh - GABAa receptors.
164
What are ketamine’s CNS side effects?
- Potent cerebral vasodilator - no increase in ICP - Myoclonus - Does not alter seizure threshold
165
What are ketamine’s CV side effects?
- SNS like stimulation --> increases plasma Epi & Norepinephrine levels, which is blunted by benzos or inhaled anesthetics.
166
What does it mean if someone has a sudden drop in SBP & CO after ketamine & what do you do?
- Depleted catecholamine stores. - Give Neo
167
Fentanyl decreases MAC by how much?
50% for Isoflurane & desflurane
168
Who should NOT receive propofol (6)?
- Hypovolemic Pt’s - Pt’s w/ compromised LV function - Pediatric strabismus Sx d/t increased incidence of oculocardiac reflex - Bradycardic Pt’s unless treating w/ direct beta agonist - Pt’s w/ Hx of allergies to soy, glycerin, yolk lecithin & Na+ edetate d/t bronchoconstriction - Parkinson’s Pt undergoing stereotactic neurosurgery d/t temporary abolition of tremors
169
Who should/can receive propofol? What does propofol not affect?
- Renal dysfunction d/t no influence on clearance - Cirrhosis. Similar to alcoholics - Pregnant – crosses placenta but rapidly cleared - Malignant hyperthermia Pt’s - Asthmatics d/t bronchodilation effects - Pt’s with seizures - Pt’s w/ Hx of PONV - Pt’s with gastric emptying issues as it does not inhibit emptying but also not a prokinetic - Neuraxial pruritis - Pt’s w/ increased ICP d/t decrease in CMRO2 & CBF - Pt’s w/ abnormal rhythms d/t lack of effect on SA & AV nodes - Pt’s undergoing laparoscopic Sx d/t decreasing intraocular pressure - Acute lung injury d/t peroxynitrite-scavenging activity of propofol - CABG Pt’s d/t attenuation of lipid peroxidation
170
Pt's with what kind of diseases or disorders should NOT receive ketamine (5 should not & 4 are possible but need other interventions)?
- Pulmonary HTN - Increased ICP, increases CBF & CRMO2 - Eye exams or Sx d/t nystagmus effects - MG Pt’s d/t enhancement of NDMB & Scc - Pt’s w/ Hx of bleeding disorder if going for Sx d/t platelet aggregation inhibition - Not useful in neuraxial anesthesia unless combined with epinephrine - Pt’s with CAD due to increased MVO2. Unless preceded w/ 0.5mg/kg diazepam - Cardiac unstable Pt’s d/t increase in SNS activity unless blunted by pre-administration of benzos - Delirious Pt’s unless pre medicated with midazolam
171
o Who should/can receive ketamine?
 Burn Pt’s for dressing changes, skin grafts, debridement  Chronic pain Pt’s due to inhibition of spinal NMDA receptors  Pregnant women  Peds post cardiac Sx  Asthmatics d/t its bronchodilation effects  Malignant hyperthermia Pt’s  Traumatic brain injury w/ mechanical ventilation  significant decrease in ICP  Seizure Pt’s, does not alter seizure threshold  Pt’s with bronchospasms  Renal impaired Pt’s
172
What is the MOA for propofol?
Acts on GABAa --> increase chloride into cell --> hyperpolarize
173
Which induction drug can cause lactic acidosis?
Propofol infusion syndrome --> fatal bradycardia in children
174
Which induction drug should not be used in septic or hemorrhaging Pt's?
Etomidate: It causes Adrenocortical suppression (sepsis or hemorrhage= need cortisol response)
175
Which induction drug is great for hypovolemic Pt's?
Ketamine
176
Which induction drug should not be used in Neuro or pulmonary HTN Pt's?
Ketamine
177
Which induction drug does not cause histamine release & does not cause intra-arterial damage?
Etomidate
178
Which induction drug does not cause seizures or myoclonus?
Propofol
179
Which induction drug causes a decrease in SBP?
Propofol
180
Which induction drug causes decreased SNS & baroreceptor reflex?
Propofol