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Semester 2 TxWes > Pharm Unit 3 > Flashcards

Pharm Unit 3 Flashcards

1
Q

What is Boyle’s law? How does it apply to anesthesia?

A

If temperature is constant, pressure/volume are inversely proportional. The vent; + pressure created with bellows, pressure increases, gases flow from the high pressure (vent) to low pressure (patient lungs)

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2
Q

What factors related to aging can change the pharmacokinetics of inhaled anesthetics?

A

Decreased lean body mass, increased fat, increased Vd particularly for fat soluble drugs, decreased clearance if pulmonary exchange is impaired, increased time constraints d/t lower CO

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3
Q

Describe Fick’s law

A

Diffusion depends on the partial pressure gradient of the gas, solubility of the gas and how thick the membrane is

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4
Q

Describe Graham’s law of effusion

A

Process of how molecules diffuse through pores/channels without colliding. Smaller molecules effuse faster though this is also affected by solubility

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5
Q

Why does CO2, with a higher molecular weight of 44g diffuse almost 20x better than oxygen with a molecular weight of 32g?

A

Because CO2 is much more soluble than oxygen

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6
Q

In relation to anesthetic gases, what is PA and indicator of?

A

Anesthetic depth (given time to equilibrate, the PP of the alveoli should reflect the PP in CNS) and recovery from anesthesia

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7
Q

What are the 3 partial pressure gradients that can dictate how much gas gets to the brain?

A

The positive pressure gradient from the vent to the lungs (1L /min? 5L /min?), the alveoli to blood gradient (how much gas is in the alveoli relative to the capillary) and the arterial blood to brain gradient

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8
Q

What is the relationship of inspired concentration to uptake of a gas?

A

The higher the inspired concentration the faster it should move from the alveoli to the capillary (this is the concentration effect)

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9
Q

If your PA of sevo is 2.5%, assuming time to equilibrate has occurred, what is the partial pressure in the brain?

A

2.5%

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10
Q

Describe over pressurization, why could it be dangerous?

A

This is a method to offset slow induction from poorly soluble volatiles; you drastically increase PI, such as 7% Sevo, this allows for rapid induction of anesthesia. The dangerous part is sustained delivery of high concentration volatiles can quickly result in an OD

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11
Q

What is the second gas effect?

A

You combine a volatile with a high uptake gas like N2O which accelerates the delivery of the other volatile. The N2O quickly goes into the capillary, creating a gradient that shrinks the capillary which can then increase the concentration of the other volatile which then increases uptake

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12
Q

What must you be aware of with N2O administration?

A

It can easily get into air filled cavities. While not necessary dangerous in the stomach/intestines, it could bloat them making it hard to see what’s going on and royally pissing off the surgeon. An example of where it could be dangerous is if doing ocular surgery, N2O could increase pressure to the point that blood flow is lost to the eye. It can also contribute to a pneumothorax.

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13
Q

You have kept your Desflurane at a MAC of 7.0 your entire case, despite not changing the MAC at all, the partial pressure in the brain is fluctuating, not constant (assuming the patient is not intubated). Why is this? What would override this response?

A

As the brain goes to sleep, CRMO decreases and blood flow decreases. This slows gas delivery to the brain. Then with less gas, the brain wakes up a little, CRMO increases, blood flow increases which increases gas delivery and the brain falls back asleep. These changes are occurring very rapidly. If the patient was intubated, we would override this response of the brain to change ventilation.

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14
Q

What would hyperventilation do to the speed of induction?

A

Slow it down; hyperventilation decreases CBF

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15
Q

In general, what does hyper/hypothermia do to solubility in the liquid phase?

A

Hyper = decrease in solubility
Hypo = increase in solubility

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16
Q

What is the relationship of solubility to induction speed/recovery?

A

Low solubility = rapid induction/recovery
High solubility = slow induction/recovery

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17
Q

List in order of increasing solubility: Isoflurane, Desflurane, Halothane, Sevoflurane and N2O

A

N2O < Des < Sevo < Iso < Halothane

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18
Q

What is the least soluble gas used in anesthesia?

A

N2O

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19
Q

Halothane has a blood:gas coefficient of 2.54, in basic numbers, describe how much is in the blood and how is in the gaseous phase

A

2.54 halothane in dissolved in blood, 1 is left in gaseous state (once dissolved, halothane is NOT able to go to the brain, which is why low blood:gas coefficient anesthetics tend to knock you out faster)

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20
Q

What is the blood:gas coefficient of Halothane?

A

2.54

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21
Q

What is the blood:gas coefficient of Isoflurane?

A

1.46

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22
Q

What is the blood:gas coefficient of N2O?

A

0.46

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23
Q

What is the blood:gas coefficient Desflurane?

A

0.42

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24
Q

What is the blood:gas coefficient Sevoflurane?

A

0.69

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25
Q

What is the relationship of fat:blood coefficient to awakening time?

A

The greater the coefficient, the more awakening is delayed

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26
Q

In basic terms, what part of anesthesia does the BG coefficient and FB coefficients affect?

A

BG = how fast you go to sleep
FB = how fast you wake up

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27
Q

Both Sevo and Des can put you to sleep quickly, but you wake up much faster with Des. Why is that?

A

Des has a much lower FB coefficient, so less gets stored in the fat, meaning less overall is stored in the body. Des is also less soluble.

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28
Q

What can increase washout of anesthetics from the brain?

A

Increased CO

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29
Q

Why does length of anesthesia have an impact on emergence?

A

The longer anesthesia goes, the more gas that can go into other tissues which can eventually be released backwards across the gradient

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30
Q

Which modern volatile has the fastest emergence? Slowest?

A

Fast = Desflurane
Slow = Halothane

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31
Q

Which 2 volatiles are sensitive to length of surgery in relation to increased awakening time?

A

Halothane and Isoflurane

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32
Q

What is MAC-awake, MAC-BAR and 1.3 MAC?

A

1.3 = concentration at 1 atm that prevents movement in 99% of people

MAC-awake 0.3 - 0.5 = MAC at which 50% of people no longer respond to verbal command. Movement is still very likely however

MAC-BAR 1.7 - 2.0= autonomic reflexes are blunted/suppressed. You can have really bad HR/BP problems, very easy to kill someone if not careful

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33
Q

What is the MAC of N2O?

A

104

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34
Q

What is the MAC of Halothane?

A

0.75

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35
Q

What is the MAC of Isoflurane?

A

1.17

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36
Q

What is the MAC of Desflurane?

A

6.6

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37
Q

What is the MAC of Sevoflurane?

A

1.8

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38
Q

How does MAC change with age?

A

Decreases, 6% per decade

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39
Q

What can increase MAC?

A

Hyperthermia, excess pheomelanin (red heads), increase in catecholamines, hypernatremia

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40
Q

What can decrease MAC?

A

Hypothermia, medications, A2 agonists, acute ETOH ingestion, pregnancy, post partum, lidocaine, PaO2 of less than 38 mmHg, BP less than 40 mmHg, cardiopulmonary bypass, hyponatremia

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41
Q

What does not change MAC?

A

Chronic ETOH abuse, Gender, duration of anesthesia, PaCO2 of 15-95, PaO2 of greater than 38 mmHg, BP greater than 40 mmHg, hyper/hypokalemia, thyroid gland dysfunction

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42
Q

What mediates immobility with volatile administration?

A

The spinal cord; depress excitatory AMPA and NMDA receptors. Enhance inhibitory glycine receptors and acts on Na channels to block the release of glutamate

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43
Q

What mediates LOC with volatiles administration?

A

The brain, specifically the RAS by potentiating glycine activation in the brainstem.

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44
Q

What is vapor pressure?

A

The pressure at which vapor and liquid are at equilibrium

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45
Q

What is Henry’s law?

A

The amount of dissolved gas in a liquid is proportional to its partial pressure above the liquid. This is the concept behind over-pressurizing.

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46
Q

How does temperature affect vapor pressure?

A

Heat = increased vapor pressure = more likely to evaporate
Cold = decreased vapor pressure = more likely to stay in liquid phase

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47
Q

What is the vapor pressure of Halothane?

A

243 torr

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48
Q

What is the vapor pressure of Isoflurane?

A

238 torr

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49
Q

What is the vapor pressure of Desflurane?

A

669 torr

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50
Q

What is the vapor pressure of Sevoflurane?

A

157 torr

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51
Q

What is the relationship of vapor pressure to boiling point?

A

As vapor pressure increases, boiling point decreases

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52
Q

What are 3 types of gas delivery systems?

A

Rebreathing (Bain), non-breathing (self-inflating BVM) and circle systems

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53
Q

What changes would you expect to see if you increased FGF (fresh gas flow)?

A

If exceeding minute ventilation then you would see; rapid changes in anesthetic, prevents rebreathing, can cool/dry the delivered volume, more wasteful

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54
Q

What changes would you expect to see if you decreased FGF (fresh gas flow)?

A

If less than minute ventilation; lower cost, less cooling/drying, slow changes in anesthetic, potential concern about compound A

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55
Q

When do volatiles not cause bronchodilation?

A

If the patient is not broncho-spasming (pulmonary resistance unchanged by 1-2 MAC) or if the epithelium is not intact (such as an inflammatory disease process)

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56
Q

Which volatiles produces the most bronchodilation? Which one could have airway irritation concerns?

A

Dilation = Sevoflurane
Irritation = Desflurane

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57
Q

Which volatiles/drugs are notorious for causing bronchospasm?

A

Desflurane and thiopental

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58
Q

What is the only gas that has no dose-dependent skeletal muscle relaxation?

A

N2O

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59
Q

What is the relationship of volatiles to NMBD’s?

A

They potentiate them by enhancing glycine at the spinal cord

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60
Q

Describe ischemic preconditioning

A

With a small exposure to anesthetic gas, the body recognizes the benefit of the gas, and when you later give them a larger dose of the gas they are less likely to have ischemia. Valuable in heart patients.

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61
Q

How does ischemic preconditioning reduce the chance of reperfusion injury?

A

Prevents cardiac dysrhythmias, contractile dysfunction, clinically apparent in delaying MI for PCI and CABG

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62
Q

What do all volatiles do to CRMO/cerebral activity?

A

All decrease CRMO and cerebral activity. Iso = Sevo = Des

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63
Q

At what MAC does CNS activity begin to change? Burst suppression? Electrical silence?

A

Change = 0.4 MAC
BS = 1.5 MAC
ES = 2.0 MAC

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64
Q

Which volatiles are pro-convulsant? Anti-convulsant? Which one has an exception?

A

PC = Enflurane
AC = Des, Iso and Sevo

Sevo does have seizure like activity in children at high concentrations and with hypocarbia

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65
Q

What do volatiles do to SSEPs and MEPs?

A

Suppress both; decrease in amplitude and increase in latency

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66
Q

What do all volatiles do to CBF?

A

Increase CBF, and therefore also increase ICP starting at 0.6 MAC

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67
Q

Which volatiles would have the greatest risk of increasing ICP? Least?

A

Greatest increase = Halothane, Least = Sevoflurane (has the least vasodilatory effect)

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68
Q

Why do you not go above 0.5 MAC in certain neuro surgeries?

A

Because at greater than 0.5 MAC, you lose the ability to monitor SSEP and MEP. You can still anesthetize the patient using Remi, propofol and precedex. If using MEP, avoid paralytics

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69
Q

In general, what volatile is a good choice for neuro patients?

A

Sevo

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70
Q

You are forced to use Halothane; your patient has a rapidly increasing ICP. Assuming you can’t switch the gas, what would be a quick way to drop ICP?

A

Hyperventilate the patient

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71
Q

What is the relationship of ICP to CBF?

A

Linear; if CBF goes up, ICP goes up

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72
Q

When do you lose auto-regulation with: Halothane, Iso/Des and Sevoflurane?

A

Halothane: 0.5 MAC
Iso/Des: 0.5 - 1.5 MAC
Sevo: 1 MAC

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73
Q

What affect do volatiles have on respiration?

A

Dose dependent decrease in VT but increase in RR. Not adequate enough to maintain minute ventilation -> hypercarbia a concern

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74
Q

At what MAC value does apnea occur?

A

1.5 - 2.0

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75
Q

What gases blunt the hypoxic response? Hypercarbic?

A

All blunt the hypoxic response, all but N2O blunt the hypercarbic response

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76
Q

What is the stimulus for a COPD patient to breathe? Normal patient?

A

COPD = too little oxygen
NP = too much CO2

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77
Q

What is the general trend of MAC to PaCO2?

A

As MAC increases, PaCO2 increases (except with N2O)

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78
Q

Which volatile increases PaCO2 the most? Concomitant administration of what would reduce this response?

A

Desflurane, and N2O administration. Combining the 2 can help reduce the amount of PaCO2 increase

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79
Q

How much of the HPV response is lost at 2 MAC?

A

50%

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80
Q

What effect do volatiles have on the heart? Which volatile is notorious for its depressant effects on the heart?

A

All volatiles (except N2O) directly depress the myocardial tissue (meaning contractility, SV, CO, MAP and SVR all drop). HR may reflexively increase. Halothane has the worst CV depressant quality.

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81
Q

What is the effect of volatiles on HR? Which gas is notorious at causing a rapid increase in HR?

A

Dose dependent increase in HR. Desflurane is notorious for a massive increase in HR if you over pressurize.

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82
Q

When does Sevo start to increase HR?

A

At MAC greater than 1.5

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83
Q

How does the body compensate to the drop in CO with volatiles?

A

By increasing HR

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84
Q

What volatile would be the best choice for an ablation? Worst?

A

Best = Sevoflurane
Worst = Isoflurane (increases refractory pathways)

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85
Q

What is a cardiac concern in healthy patients with volatile administration?

A

Prolonged QT interval

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86
Q

What gas has minimal proarrhythmic effects?

A

N2O

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87
Q

What is a potential cancer concern with volatiles?

A

That the altering of the hypothalamic/pituitary axis could make certain types of cancer reoccur

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88
Q

Liver blood flow is generally maintained except with what volatile?

A

Halothane

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89
Q

What are the 2 types of hepatotoxicity related to volatile administration?

A

Type I: more common, occurs in 20% of patients 1-2 weeks after exposure. Nausea, lethargy, fever

Type II: less common, an immune mediated response about a month later, high mortality and usually caused by Halothane. Acute hepatitis -> hepatic necrosis

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90
Q

What do most of our gases metabolize into? Which one metabolizes into something different? Why does this matter?

A

Acetyl halide. Sevo metabolizes into vinyl halide. Acetyl halide’s can cause an antibody reaction (fairly rare), whereas vinyl halides do not cause an antibody reaction, again, making Sevo a great choice for neuro patients

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91
Q

Which hepatic flow can be increased with volatiles? What happens to the others?

A

Portal vein flow d/t vasodilation. Hepatic artery flow and total hepatic flow is maintained but not changed

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92
Q

What are the general renal effects of volatiles? What can you do to minimize these effects?

A

Dose dependent decrease in RBF, GFR and UOP. All occur d/t decreased CO not vasopressin release. These effects can be mostly abolished with preoperative hydration

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93
Q

When can volatiles be nephrotoxic?

A

With fluoride toxicity, most prevalent in methoxyflurane. It can theoretically occur in any fluorinated volatile (Des, Iso, Sevo, Halothane and Enflurane) but these are generally expired from the body before they can be metabolized

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94
Q

When does compound A formation occur? Why is it generally not a concern nowadays?

A

With CO2 absorbers and sevoflurane. Because with low FGF, we only reach 19.7 ppm of compound A, and in rats, fatal levels are 400 ppm, and ATN occurs at 100 ppm

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95
Q

What is the primary method that modern anesthesia uses to abolish compound A concerns?

A

The use of CaOH or LiOH rather than KOH or NaOH in our absorbers

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96
Q

What happens with Sevoflurane in a desiccated CO2 absorber?

A

More methanol and formaldehyde can be produced, which creates heat, which then further speeds up the reaction -> spontaneous combustion. We mitigate this by adding water to CO2 absorbers or by adding water to Sevo.

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97
Q

What can diagnose MH?

A

The caffeine contracture test or muscle biopsy

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98
Q

Which volatiles can cause PONV?

A

All of them

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99
Q

What are some metabolic effects of of N2O?

A

Vitamin B-12 deficiency, megaloblastic bone marrow suppression (after 24 hours of exposure with repeated exposure over several days), can increase plasma homocysteine levels (can increase atherosclerosis and increase myocardial events)

100
Q

What are some obstetric effects of volatiles?

A

Dose dependent (0.5 - 1 MAC) decrease in uterine smooth muscle contractility, useful with retained placenta but can worsen blood loss in uterine atony

101
Q

What are some general effects of Halothane?

A

Good for inhalation induction (sweet, non-pungent, high potency), lower risk of N/V. Concerns: catecholamine induced arrhythmias, hepatic necrosis, pediatric brady-arrhythmias and decomposition to HCL acid

102
Q

What are some general effects of Isoflurane?

A

Highly pungent, intermediate solubility and high potency. Expensive to purify, resistant to metabolism.

103
Q

What are some general effects of Desflurane?

A

Low solubility, potency and high vapor pressure. Requires a special vaporizer. Most pungent, over pressurizing can lead to massive SNS stimulation. Can degrade to CO if absorbent dehydrated.

104
Q

What are some general effects of Sevoflurane?

A

Low solubility, sweet smelling, not pungent, little airway irritation. Can metabolize into compound A. Has the least cerebral vasodilation (good for neuro patients).

105
Q

What are some general effects of N2O?

A

Low solubility/potency. Can’t give 1 MAC, no muscle relaxation, sweet smell to no odor. Good analgesic properties. 2nd gas effect is desirable. Very high incidence of N/V, can increase PVR and cause shunting in neonates.

106
Q

Per lecture, what is one undesirable effect or continuous administration of N2O over an hour?

A

Retinal artery occlusion leading to vision loss

107
Q

What is the definition of emergence? Effect of CO?

A

Rate of decrease in Pbr or rather the washout from the brain. High CO = faster emergence, slower CO = slower emergence

108
Q

What receptors in the brain do volatile have no effect on?

A

AMPA, NMDA or kainate

109
Q

What does this mean: FGF < VM

A

That fresh gas flow is less than minute ventilation, FGF > VM would mean that fresh gas flow is greater than minute ventilation

110
Q

What gas can cause vitamin B12 deficiency?

A

N2O

111
Q

List in order from least to most likely to degrade into CO if dehydrated: Des, Iso, Enflurane and Sevo?

A

Sevo < Iso < Enflurane < Des

112
Q

What is dTc?

A

D-tubocurarine or curare an early paralytic

113
Q

What is the basic MOA of all paralytics?

A

Interruption of transmission of nerve impulses at the neuromuscular junction

114
Q

What is the basic MOA of depolarizing and non-depolarizing NMBDs?

A

D: mimics ACh
ND: interferes with the action of ACh

115
Q

What are 3 reasons we use NMBDs?

A

To minimize airway trauma, facilitate surgical exposure and minimize injury form patient movement

116
Q

Which NMBDs are Benzylisoquinolines?

A

Atracurium, cisatracurium and mivacurium

the only -curium that is NOT a benzylisoquinoline is doxacurium

117
Q

What are the long acting paralytics?

A

Pancuronium, Doxacurium and Pipecuronium

118
Q

What are the intermediate acting paralytics?

A

(The ones we are most familiar with)
Atracurium, Vecuronium, Rocuronium and Cisatracurium

119
Q

What are the short acting non-depolarizing paralytics?

A

Mivacurium

120
Q

What paralytic is the isomer of atracurium?

A

Cisatracurium

121
Q

What is ED95?

A

The dose necessary to produced 95% suppression of single twitch

122
Q

What is the order of a block dependent on?

A

Reliant on the number of presynaptic ACh vesicles released, # of postsynaptic ACh receptors, blood flow to the area, and potency

123
Q

In general, what muscles will block first?

A

More central and smaller/faster moving

124
Q

Describe the difference of how central muscles (laryngeal muscles) and peripheral (adductor pollicis) are paralyzed?

A

The central laryngeal paralyzes faster, but does not fully paralyze and recovers faster. The peripheral AP muscle takes slightly longer to paralyze, fully paralyzes and takes longer to fully recover

125
Q

What is the relationship of CO to a paralytics onset of action?

A

Linear; if an area gets high CO it should paralyze faster, if it gets less CO, it should take longer to paralyze

126
Q

What muscle is the gold standard to measure for recovery from a paralytic?

A

The adductor pollicis (ulnar nerve which stimulates the thumb)

127
Q

When setting up electrodes for a TOF, how do you position the electrodes?

A

The red (+) electrode should be proximal to the black (-) electrode

128
Q

Describe the characteristics of single twitch stimulation

A

1 Hz/sec decreasing to 0.1 Hz q/10 seconds.

129
Q

Describe the characteristics of double burst stimulation (DBS)

A

2-3 twitches followed by 2-3 short twitches, uses 50 Hz and the 2nd response should display a fade effect

130
Q

Describe the characteristics of TOF stimulation

A

4 stimuli at 2 Hz in 1/2 second. Before administration of a paralytic, all twitches should be equal

131
Q

What is TOFR? How would you use that number?

A

Train of 4 ratio comparing the first twitch to the fourth twitch. If the ratio is 1, then the amplitude of twitch 1 to twitch 4 is the same and the paralytic is reliably worn off (some judgement still needed if you give a reversal agent or not and if the patient is ready for extubation). If the ratio is 0.7-0.9, there is still SIGNIFICANT residual paralysis, and if questioning extubation, giving a reversal agent is likely indicated

132
Q

Describe the characteristics of tetanic stimulation

A

Rapid 50 Hz for 5 seconds creating a sustained muscle response, Common method is TOF -> tetany -> TOF to check depth of blockade

133
Q

What would be the difference in post-tetanic stimulation for a depolarized vs non-depolarized block?

A

D: there should be no difference in the amplitude of twitches
ND: the TOF after tetany should display increased amplitude

134
Q

What creates the larger amplitude in post-tetanic stimulation in a non-depolarized blockade?

A

The excess calcium release from tetany leads to a larger TOF twitch

135
Q

What would no response after tetanic stimulation indicate?

A

Intense blockade

136
Q

What is the basic difference in amplitude of twitches in depolarized vs non-depolarized blockade?

A

D: amplitude is equally depressed
ND: amplitude starts depressed and becomes progressively more depressed with subsequent stimulation

137
Q

What is the common to find in the synaptic cleft fluid?

A

Collagen and acetylcholinesterase

138
Q

Describe one theory as to why Sux creates fasiculations

A

The sux molecule can “bounce” from receptor to receptor which causes the fasciculation

139
Q

What sub-units do our paralytics bind to?

A

The alpha subunits (there are 2 total)

140
Q

What is our only depolarizing paralytic? What are its positive traits? Main indication?

A

Sux; that it creates intense rapid paralysis and wears off before extreme hypoxia occurs. Primary indication = RSI

141
Q

What is the dose, onset, and duration of Sux?

A

Dose: 1 mg/kg IV
Onset: 30-60 seconds
Duration: 3-5 minutes

142
Q

Why does sux cause increased K levels?

A

Because it is hydrolized slower than ACh allowing it to exert its effect longer, causing sustained K release from the cell

143
Q

A depolarization block is called what?

A

Phase I block

144
Q

How does a phase I block transition to a phase II block?

A

With sux over administration, such as 2-4 mg/kg or frequent subsequent doses. Lack of functioning pseudocholinesterase can also cause a phase II block

145
Q

What are characteristics of a phase I block?

A

Decreased contraction/amplitude, TOFR of greater than 0.7, absence of post-tetanic facilitation and skeletal muscle fasciculation

146
Q

What are characteristics of a phase II block?

A

Generally non-depolarized NMBD related, can be antagonized by an anti-cholinesterase drug

147
Q

Neostigmine is commonly used to reverse paralysis, would you use it for sux? Why or why not?

A

No. It has no effect on sux metabolism/reversal, sux is broken down by pseudocholinesterase hydrolysis (in fact, neostigmine would delay sux metabolism by inhibiting plasma pseudocholinesterase)

148
Q

What can decrease pseudocholinesterase activity?

A

Decreased liver function, drug induced decrease (Neostigmine, reglan, chemo, insectisides), genetics, chronic disease (renal most common), pregnancy

149
Q

What can increase pseudocholinesterase activity?

A

Obesity

150
Q

What does dibucaine related variant measure? Give values

A

A measurement of pseudocholinesterase quality and the response to Sux

80 = normal
75 = slightly prolonged
60 = slightly prolonged
45 = greatly prolonged
20 = greatly prolonged

151
Q

You are finishing a surgery for a patient who just took a Schmidt exam and their ICP is over 9000. Rocuronium was your paralytic. You are ready to try and reverse the patient. Your TOF is 0/4. Do you reverse the patient with neostigmine?

A

No, while the TOF is 0/4, reversal will not have any effect. You need to start seeing twitches before giving a reversal agent.

152
Q

What are the s/e of Sux?

A

Cardiac dysrhythmias, Hyperkalemia, Myalgia, Myoglobinuria, fasiculations, increase in intragastric/intraocular/intracranial pressure and masseter spasm.

153
Q

What could you give as a pre-treatment to help reduce the severity of Sux s/e?

A

A small dose of an non-depolarizing NMBD

154
Q

When do the cardiac s/e of Sux generally tend to occur?

A

With a 2nd dose d/t accumulation of Sux metabolites

155
Q

Sux has opposing cardiac side effects, why is this?

A

Because it mimics ACh, which can act on cardiac muscarinic ACh receptors (causing depressant effects, SB, JR or sinus arrest) and act at the ANS ganglia (causing increase in HR and BP).

156
Q

What conditions place someone at risk for profound hyperkalemia related to Sux administration?

A

Patients with extra-junctional sites (muscular dystrophy, 3rd degree burns, muscle atrophy, skeletal muscle trauma, upper motor lesions)

157
Q

Why is the increase in intragastric pressure related to Sux not generally viewed as concerning?

A

Because while intragastric pressure increases, it also increases lower esophageal pressure, and this increased tone above the stomach likely counters the increased pressure below it

158
Q

When does the intraocular effects of Sux become a concern?

A

Intraocular can transiently increase, usually not a problem unless there is globe injury/distortion or resistance to outflow of the aqueous humor.

159
Q

After giving Sux you notice the patient develops jaws of steel. What is this condition called? What could it be indicative of?

A

A masseter muscle spasm, and can be an early indicator of MH

160
Q

What is the initial dose of dantrolene? Max dose?

A

2 mg/kg IV, max of 10 mg/kg IV

161
Q

What medication class could severely complicate dantrolene administration?

A

CCBs. Dantrolene, by definition, functions as a CCB. If the patient is taking CCBs, and you give them dantrolene, profound cardiovascular collapse could occur

162
Q

Per lecture, what is the most common s/e of dantrolene?

A

Muscle weakness (just like other CCBs)

163
Q

What paralytics are MG patients resistant to? Sensitive to?

A

Resistant = depolarizing
Sensitive = non-depolarizing

164
Q

What causes Lambert-Eaton? How does it alter your anesthetic plan?

A

Auto-immune issues from small cell lung cancer that decreases the release of ACh pre-junctionally. This makes them more sensitive to both depolarizing and non-depolarizing paralytics

165
Q

What is Dalton’s law?

A

The total partial pressure of a gas is the sum of all the different species of the gas that make up the total mixture.

166
Q

What volatile would you give if you needed to avoid dose dependent increase tachycardia and give a MAC of 1.5?

A

Sevo

167
Q

What organ systems does volatile related preconditioning have a positive effect on?

A

The heart and kidneys

168
Q

What is the isomer of enflurane?

A

Isoflurane

169
Q

What muscle is a good indicator of laryngeal and diaphragmatic recovery from a paralytic?

A

Orbicularis oculi

note that it is a poor indicator of peripheral recovery

170
Q

What gas has no cardiac depressive effects?

A

N2O

171
Q

List theses gases by increasing tendency to metabolize into Acetyl Halide: Enflurane, Isoflurane and Desflurane

A

Des < Iso < Enflurane

172
Q

What is the most common CO2 absorber?

A

CaOH absorber

173
Q

List theses gases by tendency to degrade into CO if the absorbent is dehydrated: Sevo, Enflurane, Iso, Des

A

Sevo < Iso < Enflurane < Des

174
Q

What is the only chlorinated volatile?

A

Isoflurane

175
Q

How many air turnovers per hour occur in the OR?

A

10 - 15/hour

176
Q

Why was the usage of safer absorbents (CaOH) initially slow?

A

Higher cost and they have half the CO2 absorbent ability of standard soda lime

177
Q

What is the Myer-Overton hypothesis? Why did it need to be modified?

A

Anesthetic potency is directly related to lipophilicity (more lipophilic = more potent, less lipophilic = less potent)
It needed to be modified because some anesthetics act at the polar part of the membrane, indicating charge and violating the hypothesis. So, the modified meyer-overton hypothesis says that anesthetic target sites have both polar and non-polar components

178
Q

What are the receptors that do have relevance to anesthesia?

A

Glycine and glutamate, specifically NMDA

179
Q

Immobility is mostly mediated in the spinal cord, where is amnesia mediated?

A

In the brain, likely in the lipophilic portion of the membrane

180
Q

In anesthesia, if immobility is achieved, what else is achieved?

A

If immobility is achieved then amnesia is achieved, and vice versa

181
Q

Describe the difference in variable bypass and flow-over volatile administration?

A

VB: you have a splitting ratio of gas bypassing the vaporizing chamber and some oxygen going into the chamber to carry away volatile gas
FO: Same as above, but it increases the gas-liquid interface and improves efficiency of vaporization by including wicks

182
Q

What is the relationship of potency to volume percent of anesthetic delivered?

A

Inverse; if you have low potency you will have a high volume% of gas delivered, or higher MAC. High potency = low volume% of gas delivered or lower MAC

183
Q

What are some risk factors for bronchospasm?

A

COPD, cough response with ETT, age less than 10, URI

184
Q

What mediates the hypoxic response? At what MAC does 50% suppression occur? 100?

A

The carotid bodies. 50 - 70 = 0.1 MAC, 100% suppression at 1.1 MAC

185
Q

What are the 2 primary factors that alter MAC?

A

Body temperature and age

186
Q

What mediates ischemic preconditioning?

A

Adenosine, increased protein kinase C activity, phosphorylation of ATP sensitive K channels, production of reactive oxygen species and better regulation of vascular tone

187
Q

What volatiles may actually start to increase CO after the initial drop with subsequent increase in MAC?

A

Des and Sevo

188
Q

When giving Sux, what can cause a masseter muscle spasm?

A

Inadequate dose (especially in children)

189
Q

What volatile can suppress lidocaine induced seizure activity?

A

Sevoflurane

190
Q

What are some basic considerations when choosing a paralytic?

A

Onset, duration, rate of recovery and metabolism (liver vs kidney most important)

191
Q

What do our paralytics compete with and what do they compete for?

A

Compete with ACh and compete for the alpha subunits of the nACh receptors sites

192
Q

A TOFR of less than 0.7 indicates what kind of block?

A

Non-depolarized

193
Q

A TOFR of greater than 0.7 indicates what kind of block?

A

Depolarized

194
Q

What are 3 general categories of adverse effects to monitor with non-depolarizing paralytics?

A

CV effects, critical illness myopathy and altered responses

195
Q

What causes the CV effects of non-depolarizers?

A

Histamine release, effects at either the cardiac muscarinic receptors or the nACh receptors at the autonomic ganglia

196
Q

Are the CV effects of non-depolarizers concerning?

A

Generally no because they are rarely clinically significant

197
Q

What non-depolarizer has a very narrow to no autonomic margin of safety?

A

Pancuronium

198
Q

Describe critical illness myopathy

A

A patient has been on a non-depolarizer for an extended period of time, and subsequently develops myopathy weeks to months after DC of the non-depolarizer was DC’d.

199
Q

What can potentiate critical illness myopathy?

A

Glucocorticoids prior to starting the paralytic

200
Q

List these volatiles by how much they are potentiated by the addition of an ndNMBD: Des, Sevo and Iso

A

Iso < Sevo < Des

201
Q

Which drugs can shorten a ndNMBD?

A

Corticosteroids

202
Q

What is the MOA of an nd-NMBD prolonged blockade? Drugs that can cause this?

A

Depression of cholinesterase activity, depression of nerve conduction. Diuretics, reglan, LAs

203
Q

What is the effect of magnesium on all NMBDs?

A

Enhances blockade.

NdMBDs = decrease prejunctional release of ACh and decrease sensitivity to postjunctional membranes

Sux = MOA unclear, theory that it more rapidly shifts to a phase II block

204
Q

What would the effect of giving ephedrine prior to administration of a n-dNMBD be?

A

Increase CO = faster onset time

205
Q

What would the effect of giving esmolol prior to administration of a n-dNMBD be?

A

Decrease CO = slower onset time

206
Q

What would the effect of hypothermia have on Vec/Pancuronium?

A

Double the duration via temperature related slowing of hepatic enzyme activity

207
Q

What would the effect of profound hypothermia have on atracurium/cisatracurium metabolism?

A

Slows; both are eliminated by hoffman elimination and ester hydrolysis and both are temperature/pH sensitive processes

208
Q

How does hypokalemia affect our NMBDs?

A

Hyperpolarize the cell membrane (K leave, membrane is more negative, harder to excite) = resistant to Sux but sensitive to n-dNMBDs

209
Q

How does hyperkalemia affect our NMBDs?

A

Increase resting membrane potential (more K comes in, cell is partially depolarized and easier to excite) = more sensitive to Sux but resistant to n-dNMBDs

210
Q

How does a burn affect our NMBDs?

A

No effect on depolarizers but our n-dNMBDs are affected. If BSA burn is greater than 30%, from day 10 - 60 they are more resistant to n-dNMBDs and may require higher doses.

211
Q

What is the only n-dNMBD that can double its intubation dose and mirror the timing/onset of Sux?

A

Rocuronium; 1.2 mg/kg

212
Q

Describe the trend of response to a n-dNMBD relative to someone who has had a stroke with residual weakness and a healthy person

A

In terms of resistance to the drug;
Paretic arm > unaffected side > than a healthy patient
MOA: proliferation of extra junctional nACh receptors

213
Q

List our common paralytics from least to most likely to have an allergic reaction

A

Cisatracurium < Pavulon = Vecuronium = Rocuronium < Sux

214
Q

What population is more sensitive to 1st exposure to NMBDs?

A

Women (quaternary ammonium compounds are commonly present in soaps/skin care products)

215
Q

What are the paralytic effects in women relative to men?

A

Women are more sensitive to NMBDs and the blocks last longer relative to men

216
Q

What is the only bisquaternary aminosteroid?

A

Pancuronium (Pavulon)

217
Q

What is the most common long acting n-dNMBD?

A

Pancuronium (Pavulon)

218
Q

What is the intubating dose, onset and duration of Pancuronium (Pavulon)?

A

ID: 0.1 mg/kg
Onset: 3-5 minutes
Duration: 60-90 minutes

219
Q

What metabolizes pancuronium (pavulon)?

A

Primarily renal, 80% is excreted unchanged via urine. In liver disease, d/t increased Vd an larger initial dose is needed and elimination may be delayed

220
Q

CV effects of Pancuronium (Pavulon)?

A

Increase in HR/MAP/CO d/t vagal blockade at the SA node. There is also no histamine release

221
Q

What are the intermediate acting n-dNMBDs?

A

Vec, Roc, Atracurium and Cisatracurium

222
Q

What are some differences between long-acting and intermediate n-dNMBDs?

A

Similar onset (except in high dose Roc), approximately 1/3 duration, minimal to no CV effects and can be antagonized by anticholinesterase drugs around the 20 minute mark

223
Q

What is the class, intubating dose, onset and duration of Vecuronium (Norcuron)?

A

Aminosteroid
ID: 0.1 mg/kg
Onset: 3-5 minutes
Duration: 20-35 minutes

224
Q

What is the primary route of metabolism of Vecuronium (Norcuron)?

A

Liver, approx 30% is renal

225
Q

Would Vecuronium (norcuron) be safe for an OB patient?

A

Yes; minimal effects to fetus, though does have increased clearance in 3rd trimester

226
Q

What would happen to Vecuronium blockade if the patient became acidotic after administration? Acidotic before administration?

A

If acidotic after administration the blockade prolongs
If acidotic before administration, no change to length of blockade

227
Q

CV effects of Vecuronium (Norcuron)?

A

None, no histamine release either

228
Q

What is the class, intubating dose, onset and duration of Rocuronium (Zemuron)?

A

Aminosteroid
ID: 0.6 mg/kg
Onset: 3-5 minutes
Duration: 20-35 minutes

229
Q

What would be the dose and onset of Rocuronium (Zemuron) to mimic Sux?

A

Dose: 1.2 mg/kg
Onset: 1-2 minutes

230
Q

What metabolizes Rocuronium (Zemuron)?

A

Primarily the liver with 10-30% renally excreted

231
Q

You have to administer Rocuronium or Vecuronium to a patient with kidney dysfunction, which one do you give?

A

Rocuronium; it is less renally excreted than Vec

232
Q

CV effects of Rocuronium (Zemuron)?

A

None, though it may have a very slight vagolytic effect

233
Q

What is the class, intubating dose, onset and duration of Cisatracurium (Nimbex)?

A

Benzylisoquinolone
ID: 0.1 mg/kg
Onset: 3-5 minutes
Duration: 20-35 minutes

234
Q

What is Cisatracurium’s relationship to recovery from infusion to length of infusion?

A

None; length of infusion has no effect on recovery

235
Q

What degrades Cisatracurium?

A

Primarily hoffman elimination, doesn’t use plasma cholinesterase as much as atracurium

236
Q

When does Cisatracurium have a prolonged action?

A

If dosed at actual body weight in someone who is obese d/t larger Vd

237
Q

CV effects of Cisatracurium?

A

None

238
Q

What is the class, intubating dose, onset and duration of Mivacurium (Mivacron)?

A

Benzylisoquinolone
ID: 0.15 mg/kg
Onset: 2-3 minutes
Duration: 12-20 minutes

239
Q

What is the only short acting n-dNMBD?

A

Mivacurium (Mivacron)

240
Q

How many isomers does Mivacurium (Mivacron) have and which have paralytic effects?

A

3; cis-cis, cis-trans and trans-trans
cis-trans and trans-trans have paralytic effects

241
Q

What metabolizes Mivacurium (Mivacron)?

A

Plasma cholinesterase

242
Q

CV effects of Mivacurium (Mivacron)?

A

Minimal, however at large doses 3x ED95 there can be a drop in MAP, especially with large/rapid doses that is more significant in pts with HTN than those without HTN

243
Q

(Unit 2 throwback) What is the relationship of lipid solubility to cephalad movement?

A

The more lipid soluble (or less water soluble) the less cephalad movement there is. The less lipid soluble (or more water soluble) the more cephalad movement there is. Morphine is more water soluble than fentanyl, so morphine would have more cephalad movement. This is because if its more water soluble it is more likely to stay in the CSF.

244
Q

When choosing Vecuronium or Rocuronium, which do you choose for renal dysfunction? Liver?

A

Renal = Rocuronium
Liver = Vecuronium

245
Q

What does hyper/hypokalemia do to NMBDs?

A

Hyper = sensitive to Sux, resistant to nd-NMBDs
Hypo = resistant to Sux, sensitive to nd-NMBDs

246
Q

What were the earliest NMBDs? Newest?

A

Early = dTc and Sux
Newest = Cisatracurium and Mivacurium. Rapacurium is the newest but not in use.

Semester 2 TxWes (16 decks)

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