Neuraxial Flashcards

1
Q

What is the relationship between cardiac arrest and LA?

A

Patients may be refractory to treatment because local anesthetic-induced sympathetic nervous system blockade, which decreases circulating blood volume, may also cause a defective neuroendocrine response to stress

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2
Q

What is true about SNS blockade with LA?

A

Sympathetic nervous system blockade results in arteriolar dilatation but systemic BP does not decrease proportionally because of compensatory vasoconstriction in areas with intact sympathetic nervous system innervation

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3
Q

What is the most important CV response produced by spinal anesthesia?

A

Most important CV response produced by spinal anesthesia are those that result from changes in the venous circulation

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4
Q

What is the characteristics o the CV response from spinal anesthesia?

A

Unlike arterioles denervated by sympathetic nervous system blockade, venules do not maintain intrinsic tone and dilate maximally during spinal anesthesia

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5
Q

What is the result of increased vascular capacitance?

A

decreases venous return to the heart, leading to decreases in cardiac output and systemic BP

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6
Q

What are hypovolemic patients at risk for?

A

Risk of extreme systemic hypotension in patients who are hypovolemic

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7
Q

What is true regarding blockade of preganglionic cardiac accelerator fibers (T1 to T4) results in?

A

HR slowing, especially if decreased venous return and central venous pressure decrease stimulation of intrinsic stretch receptors in the right atrium (Bezold Jarisch reflex)

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8
Q

What is true regarding positioning and HR from blockade of T1 and T4?

A

The HR will increase with a head-down position that increases venous return and central venous pressure so as to stimulate these receptors

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9
Q

What is true about myocardial oxygen consumption?

A

requirements are decreased as a result of decreased HR, venous return, and systemic BP

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10
Q

What can occur with an excessive level of spinal anesthesia?

A

Apnea

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11
Q

What does apnea with spinal reflect?

A

Reflects ischemic paralysis of the medullary ventilatory centers due to profound hypotension and associated decreases in cerebral blood flow

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12
Q

What can produce analgesia when injected intravenously?

A

Lidocaine and procaine

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13
Q

Why is injection of Lidocaine and procaine limited in?

A

Use is limited by small margin of safety between IV analgesic doses and those that produce systemic toxicity

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14
Q

What is low dose of lidocaine infusion produce?

A

(to produce a plasma concentration of 1-2 ug/ml) decreases the severity of postoperative pain and decreases the requirements for opioids without producing systemic toxicity

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15
Q

Lidocaine IV also reduces anesthetic requirements for ________

A

volatile anesthetics

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16
Q

What is tumescent liposuction?

A

SQ infiltration of large volumes (5 or more liters) of solution containing highly diluted lidocaine (0.05 to 0.1%)

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17
Q

What is the dose of lidocaine with tumescent liposuction?

A

When highly diluted lidocaine solutions are administered, the dose of lidocaine may range from 35-55 mg/kg (mega-dose lidocaine)

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18
Q

Large volumes of lidocaine will peak in how many hours?

A

Slow and sustained release of lidocaine peak 12-14 hours after injection and declines gradually over the next 6-14 hours

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19
Q

What is true about epinephrine with lidocaine for tumescent liposuction?

A

Epinephrine peaks at 3 hours following injection and returns to normal after about 12 hours

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20
Q

What is high dose of lidocaine used for?

A

Commonly used in liposuction and reconstructive plastic surgery

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21
Q

What are related to increased mortality associated with tumescent liposuction?

A
  • Lidocaine toxicity

- Local anesthetic-induced depression of cardiac conduction and contractility

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22
Q

What classifies local anesthetics as a ester or amide?

A

Local anesthetics are classified as ester or amide type based on the linkage between the lipophilic phenyl ring and the hydrophilic tertiary amine

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23
Q

What is the difference between ester or amide LA reflected by?

A

This difference is reflected in their physiochemical and pharmacokinetic properties

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24
Q

What do local anesthetics bind to?

A

Local anesthetics bind to voltage gated Na+ channels and block depolarizing Na+ current through these channels

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25
Q

What effects LA speed of onset, potency and duration of action?

A

Properties such as lipid solubility, protein binding, and pKa of individual local anesthetics affect their speed of onset, potency, and duration of action

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26
Q

What is the characteristics of raising the pH of local anesthetic solutions?

A

favors the membrane-permeable neutral form and accelerates onset of action

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27
Q

What is true of voltage gated NA+ channels with LA?

A

Voltage gated Na+ channels transition between resting, activated (open), and inactivated states via coordinated conformational changes

28
Q

What do LA have a higher affinity for?

A

the activated and inactivated states than the resting state

29
Q

The same dose of local anesthetic can result in ____________________

A

higher plasma concentration and potential for systemic toxicity depending upon the type/location of block

30
Q

What is the metabolism of ester local anesthetics?

A
31
Q

What can increase risk of systemic toxicity with ester LA?

A

Decreased activity or absence of plasma cholinesterase can increase the risk for systemic toxicity with ester type local anesthetics

32
Q

What is the metabolism of amide LA?

A

undergo biotransformation mainly in the liver

33
Q

What can increase risk of systemic toxicity with amide LA?

A

Patients with decreased hepatic or renal function have longer elimination times and are at an increased risk for systemic toxicity

34
Q

What limits the clinical use of la?

A

systemic and local toxicity of local anesthetics

35
Q

What is the manifestation of la?

A

Systemic toxicity manifests primarily in CNS and and cardiovascular effects and local toxicity by nerve degeneration (neurotoxicity)

36
Q

What is the key components of treatment of LAST?

A

Lipid emulsion infusion and avoidance of hypoxia and acidosis are recognized as crucial in the treatment of local anesthetic toxicity

37
Q

What is true about lipid emulsion?

A

should be available whenever local anesthetics are administered in large doses such as during placement of PNBs and neuraxial blocks

38
Q

What is neuraxial opioids?

A

Placement of opioids in the epidural or subarachnoid space to manage acute or chronic pain occurs by diffusion of opioid to mu receptors in substantia gelatinosa of spinal cord

39
Q

What is neuraxial opioids not associated with?

A

Analgesia produced by neuraxial opioids not asso. w/sympathectomy, sensory block, or motor block

40
Q

What is true about opioid epidurals?

A

undergo uptake into epidural fat, systemic absorption, & diffusion into CSF; produces CSF concentration of drug; penetration into dura influenced by lipid solubility of opioid drug

41
Q

What is the CSF concentration peak of fentanyl?

A

20 minutes

42
Q

What is the CSF concentration peak of sufentanil?

A

6 minutes

43
Q

What is the CSF concentration peak of morphine?

A

1-4 hours

44
Q

What is the characteristics of the epidural space?

A

Extensive venous plexus; extensive vascular absorption of opioids

45
Q

What is the examples of extensive vascular absorption of opioids from the epidural space?

A
  • Blood concentration of fentanyl peak in 5-10 minutes
  • Even less time with sufentanil
  • Blood concentration of morphine peaks after 10-15 minutes
46
Q

What decreases systemic absorption of neuraxial opioids?

A

Epinephrine added to solution w/ LA & opioid placed epidural space decreases systemic absorption

47
Q

What are the side effects of neuraxial opioids?

A

Pruritis, urinary retention, sedation

48
Q

What is the characteristics of pruritis?

A

caused by cephalad migration of opioid in CSF; interaction w/opioid receptors in trigeminal nucleus

49
Q

What is the treatment of pruritis?

A

Tx w/opioid antagonist naloxone

50
Q

What is a safety issue with neuraxial opioids?

A

Obstructive sleep apnea

51
Q

What is OSA?

A

OSA characterized by recurrent episodes of apnea/hypopnea due to upper airway collapse during sleep

52
Q

What impact do OSA and opioids have?

A

Opioids pose risk to OSA patients d/t effects on ventilation

53
Q

What is true about patients with OSA?

A

OSA patients have increased sensitivity to respiratory depressant effects of opioids

54
Q

What is the recommendations for patients with OSA?

A

minimize amount of opioid; highest risk for postop opioid-induced respiratory depression on 1st postop day; may peak on 3rd postop night & persist up to 7 days

55
Q

What is the types of depression of ventilation?

A

Early depression of ventilation and Delayed depression of ventilation

56
Q

What are the components of early depression of ventilation?

A
  • occurs within 2 hours of neuraxial injection
  • d/t systemic absorption of lipid-soluble drug and/or cephalad migration of opioid in CSF
  • early depression of vent unlikely w/morphine
57
Q

What is the medications most commonly associated with early depression of ventilation?

A

epidural admin of fentanyl or sufentanil

58
Q

What are the components of delayed depression of ventilation?

A

occurs more than 2 hours of neuraxial injection; d/t cephalad spread of opioid in the CSF & interaction w/opioid receptors in medulla

59
Q

What is the medications most commonly associated with delayed depression of ventilation?

A

Typically involves morphine which occurs 6-12 hours after epidural or intrathecal injection; coughing may affect movement of CSF & increase likelihood of depression of ventilation

60
Q

________ reliably detects opioid-induced arterial hypoxemia

A

Pulse oximetry

61
Q

What is the treatment of hypoxemia of neuraxial opioids?

A

Supplemental O2 an effective tx for hypoxemia but may mask hypercarbia & significant hypoventilation

62
Q

What is the most reliable clinical sign of depression of ventilation?

A

depressed level of consciousness

63
Q

What is the late sign of hypoventilation, in patients receiving supplemental O2?

A

hypoxemia

64
Q

Pulse oximetry of limited value in detection of _______________

A

opioid-induced respiratory depression

65
Q

What may need to be done in some situations for neuraxial opioids?

A

Continuous respiratory rate or carbon dioxide monitoring may be indicated in some settings