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Advanced Pharmacology 2 > Exam 4 Castillo > Flashcards

Exam 4 Castillo Flashcards

1
Q

Intubating dose, time to maximum block and clinical duration of response for Rocuronium

A
  1. Intubating dose: 0.6mg/kg
  2. Max block: 1.7 min
  3. Duration of Response: 36 min
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2
Q

Intubating dose, time to maximum block and clinical duration of response for Vecuronium

A
  1. Intubating dose: 0.1mg/kg
  2. Max block: 2.4 min
  3. Duration of Response: 44 min
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3
Q

Intubating dose, time to maximum block and clinical duration of response for Atracurium

A
  1. Intubating dose: 0.5mg/kg
  2. Max block: 3.2 min
  3. Duration of Response: 46 min
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4
Q

Intubating dose, time to maximum block and clinical duration of response for Cisatracurium

A
  1. Intubating dose: 0.1mg/kg
  2. Max block: 5.2 min
  3. Duration of Response: 45 min
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5
Q

Intubating dose, time to maximum block and clinical duration of response for Mivacurium

A
  1. Intubating dose: 0.15mg/kg
  2. Max block: 3.3 min
  3. Duration of Response: 16.8 min
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6
Q

Intubating dose, time to maximum block and clinical duration of response for Pancuronium

A
  1. Intubating dose: 0.08 mg/kg
  2. Max block: 2.9 min
  3. Duration of response: 86 min
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7
Q

Intubating dose, time to maximum block and clinical duration of response for d-Tubocurarine

A
  1. Intubating dose: 0.6mg/kg
  2. Max block: 5.7 min
  3. Duration of response: 81 min
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8
Q

For the reversal of neuromuscular blockade purposes, what is the appropriate monitoring tool?

A

Acceleromyograph

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9
Q

The best time to establish a baseline for neuromuscular twitches and/or tetany is when?

A

Prior to administration of any neuromuscular blocking agent

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10
Q

The most common muscle monitored for assessment of twitches and/or tetany is what?

A

Adductor Pollicis

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11
Q

The most common nerve monitored when assessing for neuromuscular blockade is?

A

Ulnar nerve

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12
Q

The most common neuromuscular assessment technique utilized intraoperatively by anesthesia providers is?

A

Train of Four

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13
Q

4 drugs utilized for NMBD reversal? Which is the most common?

A
  1. Edrophonium (expensive)
  2. Neostigmine (most common)
  3. Pyridostigmine
  4. Physostigmine
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14
Q

Anti-cholinergic agents utilized in conjunction with NMBD reversal agents?

A
  1. Atropine sulfate

2. Glycopyrrolate

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15
Q

MOA of NMBD reversal agents?

A

Inhibit acetylcholinesterase, allowing for more acetylcholine to be available at the NMJ (dislodges the paralytics)

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16
Q

What type of antagonist are NMBD reversal agents?

A

Competitive antagonsits

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17
Q

What is the max range for Neostigmine before reaching the ceiling effect?

A

60 to 80 mcg/kg

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18
Q

What is the max range for Edrophonium before reaching the ceiling effect?

A

1 to 1.5 mg/kg

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19
Q

What 5 factors does reversal of neuromuscular blockade depend on?

A
  1. Depth of NM block
  2. AchE inhibitor choice
  3. Dose administered
  4. Rate of plasma clearance of NMBD
  5. Anesthesia agent choice and depth
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20
Q

Dose, onset of action and duration of action of Edrophonium?

A
  1. Dose: 0.5 to 1 mg/kg
  2. OOA: 1 to 2 mins
  3. DOA: 5 to 15 mins
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21
Q

Dose, onset of action and duration of action of Neostigmine?

A
  1. Dose: 40 to 70 mcg/kg
  2. OOA: 5 to 10 mins
  3. DOA: 60 mins
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22
Q

With NMBD reversal agents, which show similar elimination half times?

A
  1. Edrophonium
  2. Neostigmine
  3. Pyridostigmine
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23
Q

Which NMBD reversal agent shows prolonged elimination half time?

A

Physostigmine

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24
Q

Renal excretion percentage of neostigmine?

A

50%

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25
Q

Renal excretion percentage of pyridostigmine and edrophonium?

A

75%

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26
Q

How does renal failure effect NMBD reversal agents?

A

Decreases plasma clearance and prolongs the duration of action so we should give less of the drug

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27
Q

Hepatic clearance of NMBD reversal agents?

A

30 to 50% elimination if no renal function

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28
Q

What are the side effects of NMBD reversal agents due to?

A

Increased acetylcholine in all NMJ, leading to increased nicotinic or muscarinic activity

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29
Q

Cardiovascular side effects of NMBD reversal agents?

A
  1. Bradycardia
  2. Dysrhythmias
  3. Asystole
  4. Decreased SVR
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30
Q

Pulmonary side effects of NMBD reversal agents?

A
  1. Bronchoconstriction
  2. Increased airway resistance
  3. Increased salivation
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31
Q

GI side effects of NMBD reversal agents?

A
  1. Hyperperistalsis

2. PONV (Castillo contradicts everyone and says this isn’t real)`

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32
Q

Dose of atropine?

A

7 to 10 mcg/kg

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33
Q

Effect on the eyes of atropine?

A

Mydrasis (Pupillary dilation)

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34
Q

Dose of glycopyrrolate?

A

7 to 15 mcg/kg

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35
Q

What drug dose atropine match the profile of?

A

edrophonium

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36
Q

What drugs does glycopyrrolate match the profile of?

A

Neostigmine and pyridostigmine

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37
Q

What drug is preferred to reverse NMBDs in patients with cardiac disease and how should it be administered with cardiac disease?

A

Glycopyrrolate may be preferred, administer it slowly, over 2 to 5 minutes

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38
Q

What NMBD did purified human plasma cholinesterase show effective reversal for?

A

Mivacurium

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39
Q

What NMBD did cystiene show effective reversal for?

A

Gantacurium

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40
Q

What NMBD did sugammadex show effective reversal for?

A

Selective relaxant binding agent with amino steroid (Rocuronium)

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41
Q

4 descriptors of Sugammadex?

A
  1. gamma-cyclodextrin
  2. Dextrose units from starch
  3. Highly water soluble
  4. Encapsulates the receptor
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42
Q

MOA of Sugammadex?

A

Intermolecular (Van der waal) forces, thermodynamic (hydrogen) bonds, and hydrophobic interactions lead to a very right reversal by encapsulation

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43
Q

Drugs in order from best to worst reversal with Sugammadex?

A

Roc > Vec > Pancuronium

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44
Q

What does Sugammadex bind to?

A

Free drug in the plasma

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45
Q

What is the major route of elimination for Sugammadex?

A

Urine, so avoid using it in renal failure and dialysis patients

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46
Q

How much Sugammadex is eliminated in 6 hours? 24 hours?

A
  1. 70% in 6 hours

2. 90% in 24 hours

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47
Q

What is the elimination half time of Sugammadex?

A

2 hours

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48
Q

Dose of Sugammadex for deep neuromuscular block?

A

8 to 16 mg/kg

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49
Q

Is Recurarization observed with Sugammadex use?

A

Not with appropriate dosages

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50
Q

How deep is the block and what dose of Sugammadex should you administer if spontaneous recovery has reached reappearance of the second twitch in response to train-of-four stimulation?

A

Moderate block, 2mg/kg

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51
Q

How deep is the block and what dose of Sugammadex should you administer if spontaneous recovery of the twitch response has reached 1-2 post-tetanic counts, no twitch response to TOF?

A

Deep block, 4mg/kg

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52
Q

Dose related side effects of Sugammadex?

A
  1. N/V
  2. Pruritus
  3. Urticaria
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53
Q

2 other side effects of Sugammadex?

A
  1. Anaphylaxis

2. Bradycardia

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54
Q

Re-dosing administration of Rocuronium 5 minutes after reversal agent?

A

1.2mg/kg

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55
Q

Re-dosing administration of Rocuronium and Vecuronium 4 hours after reversal agent?

A
  1. Roc: 0.6 mg/kg

2. Vec: 0.1 mg/kg

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56
Q

What drug should you administer if neuromuscular blockade is required before the recommended waiting time has elapsed?

A

Use a non steroidal neuromuscular blocking agent

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57
Q

3 Cautions with Sugammadex?

A
  1. It will bind with progesterone for 7 days, need to use other forms of contraception (Oral will not work)
  2. Toremifene (non-steroidal anti-estrogen) will displace NMBD from Sugammadex
  3. Patient will show elevated aPTT, PT and INR with patients on heparin/LMWH
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58
Q

3 uses of Local Anesthetics

A
  1. Treat dysrhythmias
  2. Analgesia for Acute and Chronic pain
  3. Anesthesia
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59
Q

What is the gold standard drug that all local anesthetics are compared to?

A

Lidocaine

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60
Q

Molecular structure of local anesthetics?

A
  1. Lipophilic portion
  2. Hydrocarbon chain
  3. Hydrophilic portion
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61
Q

What determines if a local anesthetic is an ester or an amide?

A

The bond between the lipophilic portion and the hydrophilic portion

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62
Q

What is added to epinephrine to make the drug more stable?

A

Sodium Bisulfite

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63
Q

Potency, onset, DOA, and maximum single dose for infiltration of Procaine

A
  1. Potency: 1
  2. Onset: slow
  3. DOA: 40-60 min
  4. Max single dose for infiltration: 500mg
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64
Q

Potency, onset, DOA, and maximum single dose for infiltration of Chloroprocaine

A
  1. Potency: 4
  2. Onset: Rapid
  3. DOA: 30-45 min
  4. Max single dose for infiltration: 600mg
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65
Q

Potency, onset, DOA, and maximum single dose for infiltration of Tetracaine

A
  1. Potency: 16
  2. Onset: slow
  3. DOA: 60-180 min
  4. Max single dose for infiltration: 100 (topical)
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66
Q

Potency, onset, DOA, and maximum single dose for infiltration of Lidocaine

A
  1. Potency: 1
  2. Onset: rapid
  3. DOA: 60-120 min
  4. Max single dose for infiltration: 300mg
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67
Q

Potency, onset, DOA, and maximum single dose for infiltration of Prilocaine

A
  1. Potency: 1
  2. Onset: slow
  3. DOA: 60-120 min
  4. Max single dose for infiltration: 400mg
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68
Q

Potency, onset, DOA, and maximum single dose for infiltration of Mepivicaine

A
  1. Potency: 1
  2. Onset: slow
  3. DOA: 90-180 min
  4. Max single dose for infiltration: 300mg
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69
Q

Potency, onset, DOA, and maximum single dose for infiltration of Bupivicaine

A
  1. Potency: 4
  2. Onset: slow
  3. DOA: 240-480 min
  4. Max single dose for infiltration: 175mg
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70
Q

Potency, onset, DOA, and maximum single dose for infiltration of Levobupivicaine

A
  1. Potency: 4
  2. Onset: slow
  3. DOA: 240-480 min
  4. Max single dose for infiltration: 175 mg
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71
Q

Potency, onset, DOA, and maximum single dose for infiltration of Ropivacaine

A
  1. Potency: 4
  2. Onset: slow
  3. DOA: 240-480 min
  4. Max single dose for infiltration: 200mg
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72
Q

pK and protein binding % of Procaine

A
  1. pK: 8.9

2. Protein binding: 6%

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73
Q

pK and protein binding % of Chloroprocaine

A
  1. pK: 8.7

2. Protein binding: unknown

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74
Q

pK and protein binding % of Tetracaine

A
  1. pK: 8.5

2. Protein binding: 76%

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75
Q

pK and protein binding % of Lidocaine

A
  1. pK: 7.9

2. Protein binding: 70%

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76
Q

pK and protein binding % of Prilocaine

A
  1. pK: 7.9

2. Protein binding: 55%

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77
Q

pK and protein binding % of Mepivicaine

A
  1. pK: 7.6

2. Protein binding: 77%

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78
Q

pK and protein binding % of Bupivacaine

A
  1. pK: 8.1

2. Protein binding: 95%

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79
Q

pK and protein binding % of Levobupivacaine

A
  1. pK: 8.1

2. Protein binding: >97%

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80
Q

pK and protein binding % of Ropivacaine

A
  1. pK: 8.1

2. Protein binding: 94%

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81
Q

Which local anesthetics are liposomes utilized with?

A

lidocaine, tetracaine, and bipivacane

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82
Q

Why do we use liposomes with local anesthetics?

A

To upload higher amount of LA into a molecule and have a consistent release of LA in the tissues

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83
Q

What is the effect of using liposomes with local anesthetics?

A

prolonged duration of action and decreased toxicity

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84
Q

MOA of local anesthetics?

A

Blocks/inhibits Na+ passage in nerve membranes by binding to Na+ channels on the INSIDE of the cell to prevent action potentials

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85
Q

3 factors affecting blockade caused by local anesthetics?

A
  1. Lipid solubility or non-ionized form
  2. Repetitively stimulated nerve
  3. Diameter of the nerve, the large the diameter the more LA needed
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86
Q

3 other site of action targets for local anesthetics?

A
  1. Potassium channels
  2. Calcium ion channels
  3. G protein-coupled receptor
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87
Q

Why do we not see a block when using local anesthetics on infected areas?

A

the pH is too low for the local to work, it becomes ionized before entering the cell

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88
Q

Compare the requirement of LA for motor vs sensory nerves

A

Motor nerves have 2x the diameter and require higher concentration of LA

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89
Q

How many Nodes of Ranvier must be blocked for adequate blockade?

A

2, preferably 3 nodes blocked

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90
Q

Which are the fastest sensory fibers?

A

Preglangionic B fibers w/ the SNS

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91
Q

Which fibers are the usual targets of LAs?

A

myelinated A-alpha and unmyelinated C fibers perceiving pain and temperature

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92
Q

What is the effector pregnancy on local anesthetics?

A

Increased sensitivity

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93
Q

Describe local anesthetics

A

Weak bases with pK values above physiologic pH

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94
Q

What is the lipid solubility of LA in the nonionized form?

A

50%

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95
Q

When do LA show the most rapid OOA?

A

pKs closest to physiologic pH

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96
Q

What intrinsic effect of LAs effect potency and DOA??

A

Intrinsic vasodilator activity

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97
Q

Which LA shows greater systemic absorption?

A

Lidocaine

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98
Q

4 factors that influence the aborption of local anesthetics?

A
  1. Site of injection
  2. Dosage
  3. Use of epinephrine
  4. Pharmacologic characteristics of the drug
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99
Q

How much epinephrine is in 1:200,000 solution?

A

5mcg/mL

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100
Q

What is the primary determinant of drug potency?

A

Lipid solubility

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101
Q

What factor of pharmacokinetics is effected by Cardiac Output?

A

Rate of tissue distribution and rate of clearance

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102
Q

What is the metabolism of Amide LAs?

A

Microsomal enzymes in the liver, these show slower metabolism than Esters

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103
Q

Which LA shows the most rapid metabolism?

A

Prilocaine

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104
Q

What is the metabolism of Ester LAs?

A

Hydrolysis by cholinesterase enzyme in plasma is greater than the liver except with Cocaine

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105
Q

What is the metabolite of Ester LAs that predisposes them to allergic reactions?

A

Paraminobenzoic Acid (PABA)

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106
Q

Which LA show first-pass pulmonary extraction?

A

Lidocaine, bupivicaine, and prilocaine

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107
Q

Renal elimination and clearance of LAs?

A

Poor water solubility

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108
Q

Which LA shows 10 to 12% elimination in the urine?

A

Cocaine

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109
Q

What is the effect of pregnancy on LA metabolism?

A
  1. Lower levels of plasma cholinesterases

2. Significant transplacental transfer

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110
Q

Which is the effect of LA from transplacental transfer?

A
  1. Amides, this is not significant with esters
  2. Ion trapping
  3. Protein binding = rate and degree of diffusion
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111
Q

When will we see more nonionized LAs?

A

with a basic pH

112
Q

When will we see more ionized LAs?

A

with acidic pH

113
Q

Metabolism of Lidocaine?

A

Oxidative dealkylation in liver, then hydrolysis; hepatic disease will affect metabolism and elimination

114
Q

What is the metabolite of Lidocaine?

A

Xylidide

115
Q

What is the effect of pregnancy induced hypertension on lidocaine?

A

Prolonged clearance

116
Q

What is the metabolite of Prilocaine?

A

Orthotoluidine

117
Q

What does the metabolite of Prilocaine cause?

A

Conversion of hemoglobin to methoglobin

118
Q

At what dose of Prilocaine would we see methemoglobinemia?

A

> 600 mgs

119
Q

Signs and symptoms of Methemoglobinemia?

A

Cyanosis due to decreased O2 carrying capacity

120
Q

What is the treatment for Methemoglobinemia?

A

Methylene Blue 1 to 2 mgs IV over 5 minutes, total dose not to exceed 7 to 8 mg/kg

121
Q

Compare Mepivacaine to Lidocaine

A
  1. Longer duration of action
  2. Lacks vasodilator activity
  3. Prolonged elimination in fetus and newborn do not give in OB patients
122
Q

Metabolism for Bupivacaine?

A

aromatic hydroxylation, N-dealkylation, amide hydrolysis and conjugation

123
Q

What dose Bupivacaine bind to?

A

alpha1-acid glycoprotein

124
Q

Metabolism of Ropivacaine?

A

P450 enzymes

125
Q

What can occur with Ropivacaine metabolites in uremic patients?

A

Accumulation with uremic patients, but lesser toxicity than Bupivacaine

126
Q

What does Ropivacaine bind to?

A

alpha1-acid glycoprotein

127
Q

Where is Dibucaine metabolized?

A

The liver

128
Q

MOA of Dibucaine?

A

Inhibit the activity of normal butyrylcholinesterase by more than 70%

129
Q

Metabolite of Procaine?

A

PABA, excreted unchanged in urine

130
Q

Metabolism of Chloroprocaine?

A

Plasma cholinesterase 3.5x faster (fastest of all the LA)

131
Q

Metabolism of Tetracaine when compared with Procaine?

A

Slower than procaine

132
Q

Rank the hydrolysis of chloroprocaine, procaine, and tetracaine from greatest to least?

A

Chloroprocaine > procaine > tetracaine

133
Q

What is unique about benzocaine?

A

It is a weak acid with pK of 3.5

134
Q

Uses of benzocaine?

A

Topical anesthesia of mucous membranes for tracheal intubation, endoscopy, TEE, and bronchoscopy

135
Q

OOA, Duration and Dose of Benzocaine?

A
  1. OOA: rapid
  2. DOA: 30 to 60 minutes
  3. Dose: 200 to 300 mgs of 20% spray
136
Q

Metabolism of Cocaine?

A

Plasma and liver cholinesterases

137
Q

When is the metabolism of cocaine decreased?

A

Parturients, neonates, elderly, severe hepatic disease

138
Q

Peak and duration of cocaine?

A
  1. Peak: 30 to 45 minutes

2. Duration: 60 minutes after peak

139
Q

Cautions with Cocaine use? (5)

A

Coronary vasospasm, ventricular dysrhythmias, HTN, tachycardia, CAD

140
Q

Average pKa of LA?

A

8

141
Q

What is the purpose of alkalinizing LAs?

A

alkalization increases the % of lipid-soluble form

142
Q

Benefits of Alkalization of LAs? (3)

A
  1. Shortens onset of action (epidural by 3 to 5 minutes)
  2. Enhance the depth
  3. Increases the spread
143
Q

Effect of administering dexmedetomidine with LAs?

A

Increases the duration of both motor ands sensory blocks, providing a longer time between the spinal and first request for analgesic meds

144
Q

Effect of administering magnesium with LAs?

A

Increases duration with SAB or with opioids

145
Q

Effect of administering dexamethasone with LAs?

A

Increased duration of either IV or mixed with LA

146
Q

What 2 effects does mixing Chloroprocain and Bupivacaine show?

A
  1. Produces rapid onset

2. Tachyphylaxis

147
Q

Describe the mixing of Sodium Bicarbonate to LAs? (3)

A
  1. 8.4% of Sodium Bicarb
  2. 1mL only added
  3. Mixed with 30mL of local anesthetics
148
Q

Are the toxic effects of LAs additive or synergistic?

A

Additive

149
Q

What is the duration of action of LA proportional to?

A

The time the drug is in contact with nerve fibers

150
Q

What is the benefit of Vasoconstrictors administered with LAs? (3)

A
  1. Limit systemic absorption and maintain drug concentration in the vicinity of the nerve fibers
  2. Increased neuronal uptake of LA
  3. alpha-adrenergic effect may have some degree of analgesia
151
Q

What effect do vasoconstrictors have on the onset rate of LAs?

A

none, just keeps them localized

152
Q

Effect on cardiac irritability of vasoconstrictors administered with LAs and inhaled anesthetics?

A

enhanced cardiac irritability

153
Q

What is the expected side effect if vasoconstrictors administered with LAs are systemically absorbed?

A

HTN

154
Q

Recommended topical single max dose Lidocaine?

A

300mg

155
Q

Recommended single max dose Lidocaine for infiltration?

A

300mg or 500mg with epi

156
Q

Recommended single max dose Lidocaine for PNB?

A

300mg or 500mg with epic

157
Q

Recommended single max dose Lidocaine for IVRA (IV regional anesthesia)?

A

300mg

158
Q

Recommended single max dose Lidocaine for epidural?

A

300mg or 500mg with epi

159
Q

Recommended single max dose Lidocaine for spinal?

A

100mg

160
Q

Recommended single max dose Bupivacaine for infiltration?

A

175mg or 225mg with epi

161
Q

Recommended single max dose Bupivacaine for PNB?

A

175mg or 225mg with epi

162
Q

Recommended single max dose Bupivacaine for epidural?

A

175mg or 225mg with epi

163
Q

Recommended single max dose Bupivacaine for spinal?

A

20mg

164
Q

What places can LAs be applied for topical anesthesia?

A

Mucous membranes of the nose, mouth, tracheobronchial tree, esophagus, or GU tract

165
Q

Benefits of using cocaine for topical anesthesia?

A

Localized vasoconstriction, decreases blood loss and improves surgical visualization

166
Q

Benefits of using lidocaine for topical anesthesia?

A

Great with surface anesthesia, inhalation does not alter airway resistance but does cause vasodilation

167
Q

Which two LA are ineffective as topical agents?

A

Procaine and chloroprocaine due to poor penetration of mucous membranes

168
Q

Give an example of a eutectic mixture of LA? (EMLA)

A

Lidocaine 2.5% + prilocaine 2.5% = 5% LA (additive effects, not synergistic)

169
Q

Dose of EMLA?

A

1 to 2gms/10cm^2 area

170
Q

Onset of Action of EMLA?

A

45 minutes

171
Q

Readiness of EMLA for skin grafting?

A

2 hours

172
Q

Procedures where EMLA is ready in 10 minutes? (4)

A
  1. Cautery of genital warts
  2. Venipucture, lumbar puncture
  3. Arterial cannulation (Nitroglycerine)
  4. Myringotomy
173
Q

3 factors associated with EMLA?

A
  1. Caution with methemoglobinemia d/t prilocaine
  2. Not recommended for skin wounds d/t vasodilation
  3. Contraindicated with amide allergies
174
Q

What kind of injection is used for extravascular placement of LA?

A

SubQ

175
Q

Concentration of lidocaine for inguinal operative site?

A

1% or 2%

176
Q

Concentration of ropivacaine and bupivacaine for inguinal operative site?

A

0.25%

177
Q

How do we double the duration of action when administering local anesthetics for infiltration?

A

by adding epinephrine 1:200,000

178
Q

When is local infiltration of LA contraindicated?

A

Not intracutaneously or into tissues at end arteries

179
Q

Examples for areas where we do not administer LA for local infiltration? (5)

A

fingers, toes, ears, nose, penis

180
Q

How is a PNB achieved with LA?

A

Injection of LA into tissues surrounding individual peripheral nerves or nerve plexuses

181
Q

MOA of PNB?

A

LA diffusion from outer mantle to central core of nerve along a concentration gradient

182
Q

What is affected first with PNB administration?

A

peripheral affected first then central, which is the site of action wanted

183
Q

What sensation comes back first with PNB?

A

Peripheral comes back first and then central

184
Q

Which fibers come back first after PNB?

A

Smallest sensory and ANS fibers first, and then larger motor and proprioceptive axons

185
Q

What is the OOA of PNB dependent on?

A

LA pKa

186
Q

OOA of lidocaine PNB?

A

3 minutes

187
Q

OOA of bupivacaine PNB?

A

15 minutes

188
Q

What does the duration of PNB depend on?

A

The dose of the LA

189
Q

What is the DOA of bipivacaine with epi/fentanyl/clonidine?

A

12 to 18 hours

190
Q

2 factors associated with Continuous infusion PNB?

A
  1. improved pain control, less nausea, and greater satisfaction
  2. Additives are used
191
Q

4 types of peripheral nerve blocks

A
  1. interscalene
  2. axillary
  3. femoral
  4. sciatic
192
Q

mA used for nerve stimulator with PNB?

A

0.1-1

193
Q

What benefit does ultrasound guided PNB give?

A

in plane vs out of plane

194
Q

Describe the (August) Bier Block

A

IV injection of LA into an extremity isolated from the rest of the systemic circulation with a tourniquet

195
Q

What does sensation and muscle tone depend on with Bier Block?

A

Tourniquet

196
Q

What is the most commonly used LA for Bier Block? Which shows greater effect?

A

Lidocaine is the most common, but mepivacaine shows a greater effect

197
Q

Where do we inject the LA for spinal anesthesia block (SAB)

A

Subarachnoid

198
Q

What confirmation do we look for before administering a SAB?

A

CSF

199
Q

Principle site of action for SAB?

A

preganglionic fibers

200
Q

Where is the sensory effect when administering a SAB?

A

same level of denervation

201
Q

Where is the SNS effect when administering SAB?

A

2 spinal segments cephalad of sensory

202
Q

Where is the MOTOR effect when administering SAB?

A

2 spinal segments below sensory

203
Q

5 most common LA for SAB?

A
  1. Tetracaine
  2. Lidocaine
  3. Bupivacaine
  4. Ropivacaine
  5. Levobupivacaine
204
Q

What is the dosage of SAB according to? (3)

A
  1. Height of patient (volume of SA space)
  2. Segmental level of anesthesia desired
  3. Duration of anesthesia desired
205
Q

What is more important in SAB, dose, concentration of the drug or volume of drug injected?

A

Dose is more important

206
Q

How many mL of LA do we give per every inch above 5 ft?

A

0.1mL up to 2 cc totally for 1.5 to 2 hours

207
Q

What is important in determining the spread of LA in SAB?

A

Specific gravity of the LA

208
Q

Describe hyperbaric SAB (3)

A
  1. LA specific gravity is > CSF
  2. Glucose 5% is the additive
  3. If Left hip arthroscopy is wanted site of action, want it below the injection site
209
Q

Describe hypobaric SAB (3)

A
  1. LA specific gravity is < CSF
  2. Distilled water is the additive
  3. If left hip arthroscopy, want left hip up
210
Q

What is the target of SAB, anterior or dorsal nerves?

A

anterior

211
Q

What is the most common LA used for Epidural anesthesia?

A

Lidocaine

212
Q

Which drugs used for epidurals are like bupivcaine but have less cardiac and CNS toxicity?

A

Levobupivacaine and ropivacaine

213
Q

Why is lidocaine good for epidurals?

A

good diffusion through tissues and safer

214
Q

General onset of action of epidurals?

A

15 to 30 minutes

215
Q

Why does adding epi not show an advantage with epidurals?

A

because the epidural space is not that vascular

216
Q

Between bupivacaine and lidocaine, which will cross the placental barrier more?

A

Lidocaine because bupivacaine shows higher protein binding

217
Q

How long does the effect of LA last on the fetus?

A

24 to 48 hours

218
Q

Difference between SAB and epidural?

A
  1. No differential zone of SNS, sensory and motor blockade with epidural
  2. Large doses required for epidural
219
Q

What type of effect do opioids show when administering concurrently with SAB or epidural?

A

Synergistic effect

220
Q

What volume of fluid is infiltrated during Tumescent Liposuction?

A

SQ infiltration of 5L or more

221
Q

Solution for SQ infiltration for Tumescent Liposuction?

A
  1. Doluted lidocaine 0.05% or .10%

2. Epinephrine 1:100,000

222
Q

What does SQ infiltration of fluid during tumescent liposuction cause?

A

Causes taut stretching of overlying blanched skin d/t large volume and vasoconstriction

223
Q

Plasma peak of LA for tumescent liposuction?

A

12 to 14 hours s/p injection

224
Q

Site of tumescent liposuction?

A

Thigh, abdomen, hips, buttocks

225
Q

Recommended dose of regional anesthesia lidocaine with epi?

A

7mg/kg with 500mg max

226
Q

Recommended dose of highly diluted lidocaine with epic for tumescent liposuction?

A

35 to 55 mg/kg

227
Q

How much lidocaine is absorbed by 1 gm SQ?

A

1 mg of lidocaine

228
Q

What are allergic reactions to LAs attributed to?

A

Manifestations of excess plasma levels

229
Q

Which type of LA are we more likely to have an allergic reaction to and why?

A

Esters due to PABA

230
Q

Do we see cross sensitivity between esters and amides?

A

no

231
Q

What do allergic reactions to LA look like? (6)

A
  1. Rash
  2. Urticaria
  3. Laryngeal edema
  4. Hypotension
  5. Bronchospasm
  6. IgE anaphylaxis
232
Q

What test do we use to determine if the allergic reaction was due to LA or not?

A

Intradermal test using preservative free LA

233
Q

Describe LA system toxicity (3)

A
  1. Due to excess plasma concentration of the drug
  2. Entrance into the systemic circulation from inactive tissue redistribution and clearance metabolism
  3. Accidental direct IV injection
234
Q

Other factors that could have a hand in LA toxicity? (5)

A
  1. Patient co-morbidities
  2. Medications
  3. Location and technique
  4. LA use
  5. Dose
235
Q

What does the magnitude of systemic absorption of LA depend on? (4)

A
  1. Dose
  2. Vascularity of site
  3. Epinephrine use which reduces systemic absorption by 1/3
  4. Physicochemical properties
236
Q

List the sites of highest blood concentration risk for LA admin from greatest to least (8)

A
  1. IV
  2. Tracheal
  3. Caudal
  4. Paracervical
  5. Epidural
  6. Brachial
  7. Sciatic
  8. SQ
237
Q

CNS effects of LA toxicity?

A

Drowsiness, facial twitch prior to seizure, seizure

238
Q

What metabolic abnormality promotes seizures with LAs?

A

hyperkalemia

239
Q

At what dose of lidocaine epidural should we monitor plasma levels?

A

> 900 mgs

240
Q

What type of treatment is hyperventilation for LA CNS toxicity?

A

temporary measure

241
Q

What is the effect of high plasma levels of Lidocaine on the heart?

A

Slows conduction of cardiac impulses due to blockade of Na+ channels, which leads to prolonged PR interval and QRS widening

242
Q

Effects of accidental IV injection of Bupivacaine?

A
  1. Precipitous hypotension
  2. AV block
  3. Almost immediate cardiac dysrhythmias including SVT, PVC, widened QRS and V-tach
243
Q

4 predisposing factors for cardiovascular system toxicity from LA?

A
  1. Pregnancy
  2. Arterial hypoxemia, acidosis, or hypercarbia
  3. Beta blockers, digitalis, Ca+ Channel Blockers
  4. Epinephrine and phenylephrine use
244
Q

Compare Lidocaine, Bupivacaine and Ropivacaine for CNS toxicity risk

A

Bupivacaine > Ropivacaine > Lidocaine

245
Q

Goals of treatment for systemic toxicity of LAs?

A
  1. Prompt airway management
  2. Circulatory support
  3. Removal of LA from receptor sites
246
Q

Treatment of seizures caused by systemic toxicity from LAs?

A
  1. Supplemental oxygen
  2. Benzo (midazolam or diazepam)
  3. Propofol: if hemodynamically stable
  4. Muscle relaxant (succinylcholine or NMDA)
  5. Intralipid: Lipid emulsion
247
Q

Intralipid, lipid emulsion dose for treatment of systemic toxicity of LAs? (bolus and infusion doses)

A

Bolus: 1.5 mL/kg of 20% lipid emulsion
Infusion: 0.25 mL/kg/minute for at least 10 minutes

248
Q

What dose of lipid emulsion should be administered within the 1st 30 minutes of LA systemic toxicity?

A

3.8mL/kg (1.2 to 6 mL/kg)

249
Q

Epinephrine dose for treatment of LA systemic toxicity?

A

10 to 100mcg

250
Q

What is the last resort for treatment of systemic toxicity due to LAs?

A

cardiopulmonary bypass

251
Q

3 categories of neural tissue toxicity

A
  1. Transient neurologic symptoms
  2. Cauda Equina Syndrome
  3. Anterior Spinal Artery Syndrome
252
Q

Describe neural tissue toxicity

A

either transient or permanent neurologic injury

253
Q

Describe transient neurologic symptoms associated with neural tissue toxicity from LAs

A

Moderate to severe pain (lower back, buttocks and posterior things) within 6 to 36 hours after uneventful single shot SAB

254
Q

What LA shows greater risk of transient neurologic symptoms?

A

Lidocaine

255
Q

Treatment for transient neurologic symptoms with LA neural tissue toxicity?

A

Trigger point injections and NSAIDS as well as a neuro consult

256
Q

Recovery time for transient neurologic symptoms from LA neural tissue toxicity?

A

1 to 7 days

257
Q

Describe Cauda Equina Syndrom

A

Diffuse injury at lumbosacral plexus with varying degrees of sensory anesthesia, bowel and bladder sphincter dysfunction, and paraplegia

258
Q

Associated risk factors for Cauda Equina Syndrome? (2)

A

Large lumbar disc herniation, prolapse or sequestration with urinary retention

259
Q

Describe anterior spinal artery syndrome

A

Lower extremity paresis with a variable sensory deficit

260
Q

Cause of anterior spinal artery syndrome?

A

uncertain if its thrombosis or spasm of the bilateral anterior spinal artery

261
Q

3 other etiologies thought to cause anterior spinal artery syndrome (3)

A
  1. Effects of HTN or vasoconstrictor drugs
  2. PVD
  3. Spinal cord compression due to epidural abscess or hematoma
262
Q

Describe Methemoglobinemia

A

Potentially life-threatening complication due to decreased carrying capacity (metHgb >15%)

263
Q

Causes of Methemoglobinemia? (6)

A
  1. Prilocaine
  2. Benzocaine
  3. Lidocaine
  4. Nitroglycerine
  5. Phenytoin
  6. Sulfonamides
264
Q

Treatment for Methemoglobinemia?

A

Methylene blue 1 to 2 mg/kg over 5 min with a max 7 to 8mg/kg

265
Q

What is the reversal from metHgb (Fe 3+) to Hgb (Fe 2+) timing?

A

within 20 to 60 minutes

266
Q

What effect does lidocaine have on the ventilatory response to arterial hypoxemia?

A

lidocaine depresses it

267
Q

Which patients are susceptible to depression of ventilatory centers with lidocaine administration?

A

CO2 retainers

268
Q

What is the cause of hepatotoxicity due to LAs?

A

continuous or intermittent epidural bupivacaine to treat postherpetic neuralgia

269
Q

What do we wait for after stopping LA infusion that causes hepatotoxicity?

A

Normalization of liver transaminase enzymes

270
Q

MOA of Cocaine?

A

SNS stimulation by blocking presynaptic uptake of NE and dopamine, causing increased postsynaptic levels

271
Q

Adverse effects of Cocaine can last for how long?

A

up to 6 weeks

272
Q

CV side effects of cocaine? (5)

A
  1. HTN
  2. Tachycardia
  3. Coronary vasospasm
  4. Myocardial infarction or ischemia
  5. Ventricular dysrhythmias including Vfib
273
Q

Parturient side effects of cocaine?

A

Decreased uterine blood flow and fetal hypoxemia

274
Q

What could hyperpyrexia from cocaine use lead to?

A

Seizures

275
Q

Patients taking which medication should be shown extra caution if they are also taking cocaine?

A

Patients taking MAO-inhibitors

276
Q

Medication for myocardial ischemia caused by cocaine use?

A

IV nitroglycerine

Advanced Pharmacology 2 (5 decks)

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