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Advanced Pharmacology 2 > Exam 3 Kane > Flashcards

Exam 3 Kane Flashcards

1
Q

What does Boyle’s Law state?

A

Given a constant temperature, pressure and volume of gas are inversely proportional

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2
Q

What does Fick’s Diffusion Law state?

A

Once gas molecules get to the alveoli, they move around randomly and begin to diffuse into the pulmonary capillary

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3
Q

What are the 3 things that diffusion depends on?

A
  1. Partial pressure gradient of the gas (higher the better)
  2. Solubility of the gase
  3. Thickness of the memberane (thicker is slower)
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4
Q

What does Graham’s Law of Effusion state?

A

Smaller molecules effuse faster, but are dependent on solubility

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5
Q

What about anesthetics control the way we go to sleep and wake up?

A

Partial pressure gradients of the gases

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6
Q

4 Factors affecting gas movement from the anesthetic machine to alveoli

A
  1. Inspired partial pressure (higher = faster)
  2. Alevolar ventilation (faster = more uptake)
  3. Anesthetic breathing system (effects fresh gas)
  4. FRC
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7
Q

3 Factors affecting gas movement from the alveoli to blood

A
  1. Blood gas partition coefficient
  2. Cardiac output
  3. A-v partial pressure difference (alveolar:venous)
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8
Q

3 factors affecting gas movement from arterial blood to the brain

A
  1. Brain:Blood partition coefficient
  2. Cerebral blood flow
  3. a-v partial pressure difference (arterial-venous)
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9
Q

What is blood:gas partition coefficient?

A

The ratio of how much drug is in one compartment to another until gas movement ceases

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10
Q

What are the 4 things that effect Pharmacokinetics

A
  1. Reduced lean body mass
  2. Increased fat
  3. Increase volume of distrubtion, especially if more fat soluble
  4. Reduced hepatic function
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11
Q

4 things described by pharmacokinetics

A
  1. Uptake from alveoli into pulmonary capillary blood
  2. Distribution
  3. Metabolism
  4. Elimination via lungs
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12
Q

What is the age range for medium dose MAC?

A

30-50’s

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13
Q

What are the 3 things that alveolar pressure is an indicator of

A
  1. Depth of anesthesia
  2. Recovery from anesthesia (amount of drug in brain is reduced and alveolar content is increased)
  3. Potency (MAC)
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14
Q

When administering volatile anesthetics, what occurs when the brain gradient is less than the lungs?

A

We will see more uptake of the anesthetic in the brain

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15
Q

What does a higher PI (of a volatile) cause?

A

More rapid approach of PA to PI and more rapid induction of the patient

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16
Q

What is the basis of concentration effect when adminsitering volatile anesthetics?

A

The more concentrated the drug, the faster the induction

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17
Q

Describe the second gas effect with a high volume gas such as N2O

A
  1. High volume of N2O uptake into pulmonary capillary
  2. Increases concentration of 2nd gas
  3. Increased uptake of 2nd gas due to gradient
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18
Q

Describe solubility in regards to volatile anesthetics

A

A ratio of how the inhaled anesthetic distributes between 2 compartments at equilibrium

or

the relative capacity of each compartment to hold volatile

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19
Q

What is solubility dependent on?

A

Temperature, if temp increases, solubility decreases

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20
Q

Describe PA/Pa when blood solubility of a volatile anesthetic is low

A

Minimal amounts must be dissolved, equilibrium is rapid, induction is rapid

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21
Q

Describe PA/Pa when blood solubility of a volatile anesthetic is high

A

Large amounts must be dissolved, equilibrium is slow, induction is prolonged

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22
Q

When is nitrous oxide contraindicated?

A

Bowel sx, pneumothorax, and intraocular or inner ear sx

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23
Q

Where does nitrous diffuse into?

A

Air-filled cavities, up to 10L in the first 10 to 15 minutes

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24
Q

When would you see retinal artery damage and vision loss when using nitrouc for Intraocular s/p retinal repair?

A

1 hour of nitrous infusion

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25
Q

What does emergence depend on?

A

Partial pressure of the gas in the brain

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26
Q

What are the 4 things that effect emergence when using volatile anesthetics?

A
  1. Length of anesthetic
  2. When PI = 0 (gas is turned off)
  3. Muscle/fat maybe not at equilibrium
  4. Muscle/fat continue to take up anesthetic (helps PA)
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27
Q

List the inhaled anesthetics in order from most soluble to least

A

Halothane = isoflurane > sevoflurane > desflurane

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28
Q

What dose 1 Mac describe

A

The concetration at 1 atm that prevents skeletal muscle movement in repsonse to supramaximal (surgical), painful stimulus in 50% of patients

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29
Q

What is immobility d/t MAC mediated by?

A

The spinal cord

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30
Q

Describe 1.3 MAC

A

98% of people will not move

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31
Q

Describe MACawake

A

0.3-0.5 MAC, this helps predict when a patient will wake up

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32
Q

Describe MACBAR

A

1.7-2.0 MAC, this descibes blunting of autonomic reflexes such as increased heart rate and blood pressure

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33
Q

Give the numbers for the partition coeffecients of blood:gas, brain:blood, and fat:blood of isoflurane

A
  1. blood:gas = 1.46
  2. brain:blood = 1.6
  3. fat:blood = 44.9
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34
Q

Give the numbers for the partition coeffecients of blood:gas, brain:blood, and fat:blood of nitrous oxide

A
  1. blood:gas = 0.46
  2. brain:blood = 1.1
  3. fat:blood = 2.3
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35
Q

Give the numbers for the partition coeffecients of blood:gas, brain:blood, and fat:blood of desflurane

A
  1. blood:gas = 0.42
  2. brain:blood = 1.3
  3. fat:blood = 27.2
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36
Q

Give the numbers for the partition coeffecients of blood:gas, brain:blood, and fat:blood of sevoflurane

A
  1. brain:blood = 0.69
  2. brain:blood = 1.7
  3. fat:blood = 47.5
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37
Q

What are MAC values based on?

A

30-55 year olds, 37 degrees celsius (98.6 F), 760 mmhg (1 ATM)

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38
Q

What is the MAC % of Nitrous Oxide?

A

104%

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39
Q

What is the MAC % of Isoflurane?

A

1.17%

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40
Q

What is the MAC % of Desflurane?

A

6.6%

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41
Q

What is the MAC % of Sevoflurane?

A

1.8%

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42
Q

What are the two biggest factors that alter MAC?

A
  1. Body temp
  2. Age (6% change per decade above and below 30-55)
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43
Q

When does MAC peak?

A

at 1 years old

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44
Q

4 things that cause an increase in MAC

A
  1. Hyperthermia (higher metabolic rate)
  2. Excess pheomelanina production (red heads)
  3. Drug-induced increase in catecholamine levels (increased metabolic rate)
  4. Hypernatremia (more likely to depolarize)
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45
Q

Examples of things that Decrease MAC (basically slowed metabolic rates, there’s a bunch so good luck)

A
  1. Hypothermia
  2. Preop and intraoperative meds
  3. Alpha-2 agonists (clonidine)
  4. Acute alcohol ingestion
  5. Pregnancy
  6. Post-partum (13-72 hours)
  7. Lidocaine (inhibits depol and changes threshold)
  8. PaO2 <38 mmHg
  9. Mean BP <40 mmHg
  10. Cardiopulmonary bypass d/t hypothermia
  11. Hyponatremia
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46
Q

8 things that do not change MAC

A
  1. Chronic alcohol abuse
  2. Gender
  3. Duration of anesthesia
  4. PaCO2 15-95 mmHg
  5. PaO2 > 38mmHg
  6. Hyper/Hypokalemia
  7. Thyroid gland dysfunction
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47
Q

How does anesthesia cause Spinal Immobility?

A
  1. Depress excitatory AMPA and NMDA (glutamate) receptors
  2. Enhance inhibitory glycine
  3. Action on Na channels to block presynaptic release of glutamate, which reduces excitation
  4. Timely use of NMB’s
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48
Q

How does anesthesia cause loss of consciousness?

A
  1. Inhibitory transmission of GABA in the brain and RAS (reticular activating system)
  2. Potentiation of glycine activation in brainstem
  3. No effect of volatiles on AMPA, NMDA, or karinate
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49
Q

What is the universal color of a bottle that contains: sevo, iso, des?

A
  1. Sevo: Yellow
  2. Iso: Purple
  3. Des: Blue
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50
Q

What does Dalton’s Law state about partial pressure of gases?

A

Gases exert the same amount of pressure on the wall of a container whether they are mixed with other gases or not

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51
Q

What is Vapor Pressure?

A

Highest partial pressure at a given temperature, meaning vapor and liquid are at equilibrium

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52
Q

What does Henry’s Law describe?

A

The total number of gas molecules dissolved in liquid (blood) varies directly with partial pressure

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53
Q

What do we want to occur in a liquid to increase the partial pressure of gas (overpressurize)?

A

Want greater pressure in liquid form, this helps increase anesthetic depth

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54
Q

How does heating or cooling effect vapor pressure?

A
  1. Heat increases vapor pressure, allowing more molecules to move into the patient
  2. Cooling decreases vapor pressure
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55
Q

What would greater vapor pressure indicate?

A
  1. More likely to evaporate
  2. Considered to be more volatile
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56
Q

What is the vapor pressure and boiling point of Halothane?

A
  1. VP: 243 torr
  2. BP: 50.2 C
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57
Q

What is the vapor pressure and boiling point of Isoflurane (Forane)?

A
  1. VP: 238 torr
  2. BP: 48.5 C
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58
Q

What is the vapor pressure and boiling point of Desflurane (Suprane)?

A
  1. VP: 669 torr
  2. BP: 22.8 C
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59
Q

What is the vapor pressure and boiling point of Sevoflurane (Ultane)?

A
  1. VP: 157 torr
  2. BP: 58.5 C
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60
Q

What does it mean when we see that we are inspiring more gas than we are exhaling?

A

Brain is still taking up meds

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61
Q

What does a higher splitting ratio indicate?

A

Less fresh gas is by-passing volatile anesthetic and getting to patient

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62
Q

What would increasing the temp or amount of a gas do for us?

A

We will have a greater and faster uptake of the gas

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63
Q

What is the purpose of flow-over?

A

Increase gas-liquid interface and improves the efficiency of vaporaization by increasing surface area available to be exposed to fresh gas flow

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64
Q

What did adding wicks do to vaporizaton?

A

Improved it by increasing more SA for the volatile to interact with fresh gas flow

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65
Q

4 purposes of the anesthesia circuit?

A
  1. Delivery of oxygen
  2. Delivery of inhaled drugs
  3. Maintains temp/humidity
  4. Removal of carbon dioxide and exhaled drugs
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66
Q

3 types of gas delivery systems

A
  1. Rebreathing (Bain)
  2. Non-breathing (self-inflating BVM)
  3. Circle systems
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67
Q

What 4 features does a Bain circuit have and what is it’s limitation?

A
  1. APL valve
  2. Circuit connector
  3. Reservoir Bag
  4. Oxygen connection

Bain circuits are limited to transportation

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68
Q

6 Descriptors of Circle systems

A
  1. Fresh gas inlet from tank or wall without expired gas
  2. Inspiratory and expiratory limbs
  3. Reservoir bag
  4. CO2 absorbant
  5. One-way valves
  6. Y Piece
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69
Q

How do you calculate minute volume?

A

Tidal volume multiplied by respiratory rate

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70
Q

What is considered high flow anesthesia?

A

Fresh gas flow exceeds minute ventilation

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71
Q

What are 2 positives with high flow anesthesia?

A
  1. Prevents rebreathing
  2. Rapid changes in anesthetic helps facilitate induction or emergence
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72
Q

2 negatives of high flow anesthesia?

A
  1. Wasteful
  2. Cool/dries delivered volume
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73
Q

What happens if FGF does not exceed minute ventilation?

A

Patient could re-breathe some CO2

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74
Q

Describe low flow anesthesia

A

FGF is less than minute ventilation

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75
Q

2 positives of low flow anesthesia

A
  1. low cost
  2. less cooling/drying
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76
Q

What is a negative with low flow anesthesia?

A

Very slow changes in anesthetic, which is not good if we are in a hurry

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77
Q

What is not a concern with low flow anesthesia anymore due to current research?

A

Low flow anesthesia does not cause compound A production with sevoflurane

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78
Q

What are the three things that determine the cost of volatile anesthetics (cost of liquid/mL)?

A
  1. Volume of vapor obtained/mL
  2. Volume percent of anesthetic delivered (potency and solubility)
  3. FGF rate
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79
Q

How much more expensive is Des than Sevo?

A

about 3x

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80
Q

What did Dr. Snow’s experiements with chloroform give us?

A

solubility, vapor pressure, potency and stage of anesthesia

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81
Q

What are the targets of methyl-ether ethers (volatile anesthetics)

A
  1. Stimulation of GABA and glycine receptors
  2. Inhibits NMDA-glutamate and nAch receptors
  3. Activate K+ leak channels
  4. Inhibit Na voltage gated channels
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82
Q

How do volatile anesthetics cause bronchodilation?

A
  1. Relax airway smooth muscles
  2. Block voltage gated Ca++ channels
  3. Deplete Ca++ in SR
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83
Q

What do volatile anesthetics require to cause bronchodilation?

A

An intact epithelium, inflammatory processes such as asthma and epithelial damage alters effectiveness

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84
Q

Describe volatile anesthetic effect of bronchodilation without bronchospasm (2)

A
  1. Baseline pulmonary resistance unchanged by 1-2 MAC
  2. Need histamine release or vagal afferent stimulation to allow volatile to dilate
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85
Q

List the volatile anesthetics by which drug causes relaxation of respiratory system resistance to decrease faster from the least to most (iso, halothane, sevo, des)

A
  1. Des
  2. Iso
  3. Halothane
  4. Sevo
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86
Q

Neuromuscular effects of volatile anesthetics?

A
  1. Dose-dependent skeletal muscle relation, but not enough to prevent movement
  2. Potentiate depolarizing and non-depolarizing NMBDs through synergistic effects
  3. Nitrous oxide has no relaxant effect on skeletal muscles
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87
Q

What are the effects of volatile anesthetics on CNS activity?

A

Dose dependent reductions in CMRO2 and cerebral activity

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88
Q

When does reduced CNS activity begin to occur with volatile anesthetics? burst suppression? electrical silence?

A
  1. begins at approv 0.4 MAC as wakefulness changes to unconcsousness
  2. 1.5 MAC burst suppression
  3. 2 MAC electrical silence
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89
Q

Which volatile anesthetics show anticonvulsant activity and when do they show it?

A

des, iso, sevo ; at high concentrations and with hypocarbia

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90
Q

What volatile anesthetic shows proconvulsant activity?

A

enflurane, especially above 2 MAC or PaCO2 <30 mmHg

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91
Q

When do we see a reduction in amplitude and increased latency of SSEP’s and MEP’s wih volatile anesthetics?

A

It’s dose-related but around 0.5-1.5 MAC

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92
Q

What is an adequate anesthetic strategy to use to reduce SSEP’s and MEP’s?

A

60% nitrous ad 0.5 MAC volatile

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93
Q

What effect do volatile anesthetics have on cerebral blood flow?

A

Dose dependent effects:

  • Increases in CVF d/t decreased cerebral vascular resist.
  • May increase ICP
  • Onset > 0.6 MAC
  • Occurs within minutes despite lack of BP changes
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94
Q

Describe the potency of volatile anesthetics on CBF (des, iso, nitrous, halothane)

A
  • Des = Iso
  • Sevo has less vasodilatory effects
  • Nitrous is a potent vasodilator but give < 1 MAC
  • Halothane is the worst
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95
Q

Which volatile anesthetic is the drug of choice for brain patients?

A

Sevoflurane

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96
Q

At what MAC do we expect to see some loss of cerebral autoregulation with halothane, sevo, iso or des?

A
  • Halothane lose by 0.5 MAC
  • Sevo preserves to 1 MAC
  • Iso and Des lost by 0.5-1.5 MAC
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97
Q

Describe how increases in ICP parallels increases in CBF (4)

A
  1. Pts with space-occupying lesions most at risk
  2. Opposed by hyperventilation, which causes reduced PaCO2 and Vasoconstriction
  3. Onset > 0.8 MAC
  4. ICP increases by 7mmHg
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98
Q

What dose-dependent effects of volatile anesthetics cause respiratory depression?

A

Dose-dependent increases in respiratory rate but reduction in tidal volume

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99
Q

Describe how volatile anesthetics produce respiratory depression

A

Direct depression of medullary ventilatory center and interference with intercostal muscles, diaphram descends so the chest wall collapses inward

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100
Q

At what MAC do we see apnea with volatile anesthetics?

A

1.5-2.0 MAC

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101
Q

Up to what MAC do we see dose-dependent increases in respiratory rate and reductions in tidal volume with isoflurane?

A

Up to 1 MAC

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102
Q

Describe volatile anesthetics and blunting the hypoxic ventilatory response

A
  1. Normally mediated by carotid bodies
  2. At 0.1 MAC initiated (50-70% depression) and 1.1 MAC (100% depression)
  3. All volatiles including nitrous
  4. Lasts for several hours postop
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103
Q

Describe volatile anesthetics and blunting hypercarbic ventilatory response

A
  1. Dose dependent
  2. Nitrous does not increase PaCO2, substitution for part of MAC and has less depression
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104
Q

Describe what occurs with hypoxic pulmonary vasoconstriciton

A

Normal contraction of pulmonary artery smooth muscle due to alveoli not being ventilated properly to prevent perfusing bad areas of the lung

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105
Q

What do we see with regional blood flow within 5 minutes of HPV? Max response?

A
  1. at 5 minutes, blood flowis half
  2. Max response lasts 2-4 hours
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106
Q

At what MAC do we see a reduction in Hypoxic Pulmonary Vasoconstriction?

A

2 MAC

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107
Q

When should we have the most concern when blunting HPV?

A

1 lung ventilation due to increased perfusion but decreased arterial oxygenation

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108
Q

5 cardiac effects of volatile anesthetics

A
  1. Direct myocardial depression
  2. Peripheral autonomic ganglion blockade
  3. Attenuation of carotid sinus reflexes
  4. Decreased formation of cAMP
  5. Decreased calcium influx
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109
Q

What is the reductionin MAP associated with volatile anesthetics primarily due to?

A

Reduction in SVR

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110
Q

When is dose dependent myocardial depression of more importance?

A

With diseased hearts with already altered contractility

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111
Q

Which volatile shows the most reduction in MAP? Which has no effect?

A

Isoflurane has the most, nitrous has no cardiac depression

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112
Q

When do we see dose dependent increases in HR with Sevoflurane?

A

> 1.5 MAC

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113
Q

Which volatile shows greater dose dependent tachycardia, especially with overpressurization?

A

Desflurane

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114
Q

When will there be more variablity with dose dependent increases in heart rate caused by volatile anesthetics? (4)

A
  1. Anxiety
  2. Opioids
  3. Beta-blockade
  4. Vagolytic admin (anticholinergics)
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115
Q

Which volatile shows a mild increase in CO due to being a sympathomimetic?

A

Nitrous

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116
Q

When does sevoflurane show recovery of CO?

A

at 2 MAC

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117
Q

Describe coronary steal syndrome

A

Re-directing blood flow from poorly perfused areas and giving to those who are better perfused ; This is due to coronary vasodilation and preferentially in distal vessels

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118
Q

Cardiac output, SVR, MAP and HR effects of Isoflurane

A
  1. CO: decreased
  2. SVR: decreased
  3. MAP: Greatly decreased
  4. HR: increased
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119
Q

Cardiac output, SVR, MAP and HR effects of Desflurane

A
  1. CO: no effect
  2. SVR: decreased
  3. MAP: decreased
  4. HR: increased
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120
Q

Cardiac output, SVR, MAP and HR effects Sevoflurane

A
  1. CO: no change
  2. SVR: reduced
  3. MAP: reduced
  4. HR: no change
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121
Q

Cardiac output, SVR, MAP and HR effects Nitrous Oxide

A
  1. CO: reduced
  2. SVR: increased
  3. MAP: no change
  4. HR: increased
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122
Q

Cardiac output, SVR, MAP and HR effects of Halothane

A
  1. CO: reduced
  2. SVR: no change
  3. MAP: reduced
  4. HR: greatly reduced
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123
Q

What cardiac arhythmia is common with volatile anesthetic use?

A

Prolonged QT interval in healthy patients

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124
Q

Which volatiles inhibit K+ current and potentially inreases risk of torsades?

A

Iso, des and Sevo

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125
Q

What is the proarrhythmic effect of nitrous

A

Minimal

126
Q

What effect do iso and sevo show in ablation studies?

A
  1. Iso increases refractoriness of accessory paths, leading to more episodes of arrythmias
  2. Sevo shows no effect and is acceptable to use in ablation
127
Q

Describe cardiac preconditioning

A

Brief periods of ischemia prior to longer periods which helps prevent reperfusion injury

128
Q

Describe preconditioning mediated by adenosine

A
  1. Increases protein kinase C activity
  2. Phosporylates ATP sensitive K+ channels
  3. Better regulate vascular tone
129
Q

How low of a MAC can we see cardiac preconditioning?

A

0.25 MAC

130
Q

What occurs when the ANS and HPA activates in response to volatile anesthetics?

A

Perioperative surge in catecholamines, ACTH and cortisol; leading to suppression of monocytes, macrophages, and T-cells

131
Q

What does evidence show with GA and cancer?

A

increased tumor metastasis

132
Q

What is the effect of volatile anesthetics on total hepatic blood flow? hepatic artery flow?

A

Both are maintained

133
Q

What is the effect of volatile anesthetics on portal vein flow?

A

Increased at 1-1.5 MAC due to vasodilation

134
Q

Which volatile anesthetic decreases hepatic blood flow?

A

Halothane

135
Q

When should we be concerned with inadequate oxygenation of hepatocytes when utilizing volatile anesthetics?

A

Pre-existing liver disease

136
Q

Describe Type 1 Hepatotoxicity (4)

A
  1. 20% of patients
  2. 1-2 weeks after exposure
  3. Direct toxic effect or free radical effect
  4. Nausea, lethargy, fever (flu-like symptoms)
137
Q

Describe Type 2 Hepatotoxicity (5)

A
  1. Less common than Type 1
  2. Immune-mediated response against hepatocytes
  3. Prior exposure to any volatile anesthetics, but more common with halothane
  4. High mortality; acute hepatitis, hepatic necrosis
  5. 1 month exposure
138
Q

List enflurane, isoflurane and desflurane in order from greatest to least of the drug being metabolized to acetyl halide

A

En>iso>des

139
Q

Describe metabolism of enflurane, isoflurane and des to acetyl halide (3)

A
  1. Oxidized by P450 to acetyl halide metabolites
  2. Capable of causing antibody reaction
  3. Most likely in patients sensitized by Halothane or Enflurane
140
Q

Describe sevo metabolism (2)

A
  1. Metabolized to vinyl halide
  2. Not capable of stimulating antibody formation
141
Q

What renal effects do volatile anesthetics have?

A

Dose dependent reduction in RBF, GFR and UO, not related to vasopressin release

142
Q

How do we abolish the renal concerns when utilizing volatile anesthetics?

A

Preop hydration

143
Q

What metabolite of volatile anesthetics causes increased creatinine, hypernatremia, hyperosmolality and decreased creatinine clearance?

A

fluoride

144
Q

Which volatile anesthetic was removed from the market due to causing fluoride toxicity?

A

Methoxyflurane

145
Q

What helps reduce nephrotoxicity with newer volatile anesthetics?

A

Lower solubility and being exhaled prior to metabolism and eliminated renally

146
Q

What was removed from market because it lead to compund A formation?

A

Barium hydroxide (bara-lime)

147
Q

What is Compound A?

A

A nephrotoxic vinyl halide

148
Q

What volatile anesthetic was implicated for high incidences of compound A, but is now is not considered an issue?

A

Sevo (it is less renal toxic even in CKD)

149
Q

What are the triggers of malignant hyperthermia?

A

All volatile anesthetics and succinylcholine

150
Q

What is generally thought to be a predisposing factor of malignant hyperthermia?

A

Inherited, genetic traits

151
Q

Describe malignant hyperthermia (4)

A
  1. Hypermetabolic state of skeletal muscle
  2. Excessive release of Ca++
  3. Muscle rigidity
  4. Rhabdo
152
Q

What are the symptoms of malignant hyperthermia?

A

increased body temp, increased CO2 production and increased O2 consumption

153
Q

Which volatile anesthetics are emetogenic?

A

All of them

154
Q

When does GA cause PONV?

A

With volatile and opioid use 25-30% of the time

155
Q

Metabolic effects of nitric oxide?

A
  1. B12 deficiency due to oxidization of cobalt ion leading to inhibition of DNA synthesis
  2. Megaloblastic bone marrow suppression (after 24 hours of exposure)
  3. Increase plasma homocysteine levels (increases periop myocardial event)
156
Q

What patient populaton do we avoid utilizing nitrous oxide in?

A

Pregnant moms, especially in the 1st trimester

157
Q

What is the 1/2 time of nitric oxide?

A

45 minutes

158
Q

What is increases in plasma homocysteine levels due to with nitric oxide use and which comorbidity increases risk associated?

A

Low plasma homocysteine levels are associated with low B vitamines and patients with atherosclerosis are more likely to increase periop MI

159
Q

Obstetric effects of volatile anesthetics

A
  1. Dose dependent (0.5-1.5 MAC) reuction in smooth muscle contractility and reduction in fetal blood flow
  2. Useful in retained placenta but fan worsen blood loss in uterine atony
  3. No effect with nitrous
  4. Mom may have recall with emergent c-sections
160
Q

5 Things associated with Halothane

A
  1. It is a halogneated alkane
  2. compatible with inhalation induction
  3. sweet, non pungent
  4. high potency, intermediate solubility
  5. lower risk of N/v, non-flammable, good for vasodilation
161
Q

4 concerns with halothane

A
  1. Catecholamine-induced arrhythmias
  2. Occasional hepatic necrosis
  3. Pedatriac bradyarrhythmias
  4. Decomposition to HCL acid, thymol preservative added
162
Q

Describe enflurane (4)

A
  1. Halogenated methyl ethyl ether
  2. Clear, non-flammable, pungent odor
  3. Intermediate solubility, high potency
  4. Decreases seizure threshold
163
Q

Describe Isoflurane (6)

A
  1. An isomer of enflurane that is highly potent
  2. Highly pungent, causes coughing and sputtering
  3. Immediate solubility, high potency
  4. Expensive to purify, cheaper if used more
  5. Resistant to metabolism and unlikely to cause organ toxicity
  6. Stable, no deterioration after 5 years
164
Q

Describe Desflurane (5)

A
  1. Fluorinated methyl ethyl ether identicle to isoflurane (F sub for Cl-)
  2. Requires special vaporizer (would boil at OR room temp)
  3. The most pungent
  4. Over-pressurizing (SNS stimulation)
  5. Will degrade to carbon monoxide if absorbent dehydrated
165
Q

List the anesthetics in order from most likely to degrade into carbon monoxide to least

A

Des>enflurane>iso>sevo(trivial)

166
Q

What difference does desflurane show to isoflurane

A

Reduced solubilty and potency and increased vapor pressure

167
Q

Describe Sevoflurane (5)

A
  1. Fluroinated methyl isopropyl ether with low solubility
  2. Sweet smelling, not pungent and least airway irrittion of modern volatiles
  3. Metabolized to inorganic fluoride that is least likely to from carbon monoxide
  4. The least cerebral vasodilation, so drug of choice for increased ICP
  5. Suppresses lidocaine induced seizure activity
168
Q

Describe Nitrous Oxide (4)

A
  1. Usually not used alone
  2. Low moleculare weight
  3. sweet smelling/odorless
  4. Good analgesic properties, has no delayed effects
169
Q

Why is Nitrous Oxide not used alone for anesthesia?

A
  1. Low solubility, low potency
  2. Does not produce skeletal muscle relaxation
  3. Can’t deliver 1 MAC
170
Q

Describe Xenon (6)

A
  1. An inert gas, NMDA antagonist
  2. MAC 63-71%, blood:gas coefficient 0.115
  3. Odorless, non-pungent
  4. Absence of metabolism
  5. Very expensive
  6. Favors air bubble expansion, neuro concerns and less bowel expansion than nitrous oxide
171
Q

Describe Post-op cognitive dysfunction (4)

A
  1. Alterations in Ca++ homeostasis, SIRS, acceleration of amyloid veta plaques
  2. Iso, iso with nitrous, sevo and des
  3. Hyoxia, hypothermia
  4. Increased apoptosis
172
Q

Describe anesthetic preconditioning (5)

A
  1. Exposure to volatile PRIOR to ischemia
  2. Iso 0.25 MAC
  3. Production of reactive oxygen species (ROS)
  4. Upregulate cell defense
  5. Demonstrated in heart, brain, kidney and lung
173
Q

Descibe volatile effect on immune function and cancer (3)

A
  1. Suppress natural killer cells
  2. Significant suppression increases patient mortality
  3. Suppression from volatiles < suppression from stress response of surgery
174
Q

What is the main effect on nueromuscular blocking agents?

A

Interrupton of transmission of nerve impulses at neuromuscular junction (NMJ)

175
Q

What is the main action of depolarizing muscular blockade agents?

A

Mimic acetylcholine

176
Q

What is the main action of non-depolarizing neuromuscular blockade agents?

A

Intereferes with the action of acetylcholine

177
Q

What is the purpose of neuromuscular blockage agents? (4)

A
  1. Minimizes incidence of tissue trauma
  2. Decreases airway trauma
  3. Facilitates surgical exposure
  4. Minimizes injury from patient movement
178
Q

3 Signs showing airway trauma

A
  1. airway edema
  2. hoarseness
  3. vocal cord injury
179
Q

What class fo NMBD is succinylcholine?

A

depolarizing

180
Q

Which non-depolarizing NMBD’s are long acting?

A
  1. Pancuronium
  2. Doxacurium
  3. Pipecuronium
181
Q

Which non-depolarizing NMBD’s are intermediate acting?

A
  1. Atracurium
  2. Vecuronium
  3. Cisatracurium
182
Q

Which non-depolarizing NMBD’s are short acting?

A

Mivacurium

183
Q

What are the 3 non-depolarizing NMBDs considered benzylisoquinoline?

A

MAC

  • Mivacurium
  • Atracurium
  • Cisatracurium
184
Q

Which non-depolarizing NMBDs are considered aminosteroids?

A
  1. Pancuronium
  2. Doxacurium
  3. Pipercuronium
  4. Rocuronium
  5. Vecuronium
185
Q

What does ED95 describe?

A

The dose necessary to produce 95% suppression of a single twitch in the presence of nitrous/barbs/opioid anesthesia

186
Q

3 descriptors of the adductor policis muscle

A
  1. Single twitch at Hz
  2. Ulnar nerve stimulated
  3. Thumb moves towards midline
187
Q

What is the order of block dependent on?

A
  1. # of presynaptic Ach containing vesicles released
  2. # of postsynaptic Ach receptors
  3. Blood flow to area
188
Q

Which preferred testing site of neuromuscular blockade is a poor indicator of laryngeal relaxation?

A

Adductor pollicis

189
Q

Which preferred site of neuromuscular blockade testing more closely reflects onset of blockade at diaphragm and why

A

Obicularis oculi because it tests CN 7, the facial nerve

190
Q

What is the third favorite spot for neuromuscular blockade testing?

A

posterior tibial

191
Q

Patient symptoms of neuromuscular blockade (6)

A
  1. visual focus
  2. mandibular muscle weakness
  3. ptosis
  4. diplopia
  5. dysphagia
  6. increased hearing acuity
192
Q

Describe single twitch from peripheral nerve stimulators

A
  1. Usually 1 Hz every 10 seconds, at the onset of block, will fade with each stimulus
  2. Correlates with events at post-junctional membrane
193
Q

Describe double burst assessment with peripheral nerve stimulators (4)

A
  1. 2-3 short bursts followed by 2-3 short bursts
  2. Developed to improve detection of residual block
  3. Fade in 2nd response vs 1st
  4. Qualitatively better than TO4
194
Q

Describe the train of four

A
  1. 4 stimuli at 2 Hz q 1/2 second
  2. Reflects events at presynaptic membrane
  3. Only 60% fade or > is detected
  4. Train of four ratio
195
Q

Describe the train of four ratio (4)

A
  1. Prior to NMBD 4/4 twitches showing TOFR 1
  2. After administration return of 4 twitches
  3. Amplitude of 4th twitch to 1st twitch
  4. Amplitude of 4th is 50% of 1st, TOFR 0.5
196
Q

Describe Tetanic stimulation

A
  1. Very rapid, 50 Hz for 5 seconds
  2. Sustained muscle response due to more Ca++ and Ach around = depolarizing block
  3. Non-sustained response with non-depolarizing block
  4. Phase 2 block with succs
197
Q

What is fade related to with non-sustained response from tetanic stimulation

A
  1. Presynaptic depletion of Ach or inhibition of release
  2. Frequency and length of stimulation
198
Q

Describe post-tetanic stimulation (3)

A
  1. Tetanic stimulation then single twitch 3 seconds later
  2. Occurs d/t accumulation of calcium during tetany
  3. No response = intense blockade
199
Q

What was the major side effect of Rapacurium (Raplon)

A

Increased Bronchospasm that could not be reveresed in young people

200
Q

Describe the anatomy of a NMJ: Presynaptic (3)

A
  1. Large, myelinated motor neurons from spinal cord or medulla
  2. Unmyelinated motor nerve ending that innervates a single muscle fiber
  3. Responsible for Ach synthesis, uptake and storage into vesicles; also release and reuptake of choline
201
Q

Describe the Anatomy of NMJ: Synaptic cleft

A
  1. Synaptic cleft filled with fluid, contains collagen and acetylcholinesterase
  2. Calcium dependent
  3. Acetylcholinesterase close by for hydrolysis of Ach to acetic acid and choline
202
Q

Describe the anatomy of NMJ: Post-synaptic

A
  1. Membrane with multiple folds
  2. 90 mv resting membrane potential
  3. Maintained by sodium/potassium (3 Na out, 2 K in)
  4. nAch-R directly opposite
203
Q

Describe the nAch-R subunit (2)

A
  1. Pentameric unit with 2 alpha, beta, delta and epsilon on outside; transmembrane pore in the center
  2. Conformational change if Ach binds to allow ions to flow
204
Q

Describe what happens if NMBD bind to nAch-R

A
  1. No conformational change
  2. No ion flow
  3. Probability of binding due to concentration of NMBD vs Ach
  4. Succinylcholine only requires binding to 1 alpha subunit, this is thought to be why fasciculations occur
205
Q

Describe Succinylcholine (4)

A
  1. Only depolarizing NMBD in clinical practice
  2. 2 unique characteristics showing intense, rapid paralysis, offset of effects prior to hypoxia
  3. Useful for tracheal intubation and rapid sequence
  4. Releases histamine
206
Q

What is the dose, onset of action and duration of succinylcholine?

A
  1. Dose: 1mg/kg at actual body weight
  2. Onset: 30-60 seconds
  3. Duration: 3-5 minutes
207
Q

What is the MOA of succinylcholine (6)

A
  1. Attaches to 1 or both alpha subunits
  2. Mimics effects of Ach
  3. Hydrolysis is slower than Ach
  4. Sustained opening of receptor ion channels
  5. Leakage of potassium ions causes a 0.5 mEq/liter serum increase
  6. Depolarization called “Phase 1 block”
208
Q

Which patients should we caution giving succinylcholine to?

A

Diabetics and chronic renal failure

209
Q

What are the characteristics of a Phase 1 block (6)

A
  1. Reduced contraction to single twitch stimulation
  2. Reduced amplitude to continuous stimulation
  3. TOF ratio >0.7
  4. Absence of post-tetanic faciculation
  5. Augmented block after administration of anticholinesterase drug
  6. Skeletal muscle fasciculations
210
Q

What are the characteristics of Phase 2 block? (5)

A
  1. Responses typical of non-depolarizing NMBD
  2. Can be antagonized by anticholinesterase drug
  3. Arupt transition with succ dosages of 2-4mg/kg
  4. Lack of poorly functioning pseudocholinesterase
  5. Relative “overdose”
211
Q

What is the difference between Phase 1 and Phase 2 blocks?

A

Phase 1 augmented by anticholinesterase drug but phase 2 block antagonized by anticholinesterase drugs with twitch differences

212
Q

Describe the butyrylcholinesterase (plasma cholinesterase) that hydrolizes succinylcholine

A
  1. Glycoprotein enzyme
  2. Synthesized in liver
  3. Terminated by diffusion of NMJ into plasma
  4. Succinylmonocholine is less potent and choline
213
Q

Describe pseudocholinesterase activity (6)

A
  1. Descreased hepatic production, 75% beore apparent
  2. Drug-induced decreases (Neostigmine, reglan, chemo, insecticides)
  3. Genetically atypical
  4. Chronic diseases (renal)
  5. Pregnancy (high estrogen levels)
  6. Obesity increases activity
214
Q

Describe dibucaine

A
  1. Local amide anesthetic
  2. Inhibits breakdown of butyrylcholinesterase
  3. % inhibiton = dibucaine number
215
Q

What is a dibucaine number?

A
  1. Reflects quality not quantity of enzyme
  2. 20: SCh 1mg/kg lasts 3 hours
216
Q

Side effects of Succinylcholine (8)

A
  1. Cardiac dysrhythmias
  2. Hyperkalemia
  3. Myalgia
  4. Myoglobinuria
  5. Increased intragastric pressure
  6. Increased intraocular pressure
  7. Increased intracranial pressure
  8. Sustained muscle contraction
217
Q

Describe cardiac dysrhythmias associated with succinylcholine (3)

A
  1. SB, JR, Sinus arrest
  2. Action at cardiac muscarininc, cholingergic receptors
  3. Action at ANS ganglia
218
Q

What actions at cardiac muscarinic, cholinergic receptors causes cardiac dysrhythmias with succinylcholine?

A
  1. mimics action of Ach
  2. Most liley on 2nd dose, 5 minutes post 1st
  3. Due to metabolites: succinylmonocholine and choline
219
Q

What actions of succinylcholine at ANS ganglia cause cardiac dysrhythmias?

A
  1. Increased heart rate and blood pressure
  2. Mimics action of Ach
  3. Usually occurs with large doses
220
Q

What patients would we worry about causing hyperkalemia with succinylcholine admin. due to extrajunctional sites?

A
  1. Unrecognized muscular dystrophy such as in duchenne’s which is diagnosed at 2-6 years of age
  2. Unhealed 3rd degree burns
  3. Denervation of skeletal muscles (atrophy) that occurs within 96 hours to 6 months of stagnation
  4. Skeletal muscle trauma
  5. Upper motor neuron lesions
221
Q

Can you alter hyperkalemia with succinylcholine if you pretreat with non-depolarizers?

A

no

222
Q

Describe myalgia associated with succinylcholine admin (3)

A
  1. Associated with young adults
  2. Neck, back, abdomen
  3. Confused with pharyngitis due to intubation
223
Q

Describe myoglobinuria associated with succinylcholine admin

A
  1. Damage to skeletal muscles, especially pediatrics
  2. Fasiculations unlikely to cause
  3. Usually found to later have MH or muscular dystrophy
224
Q

Describe intragastric pressure and LES pressure with succinylcholine administration

A
  1. Related to intensity of fasiculations
  2. Related to direct increases in vagal tone
  3. Not seen in children due to minimal fasiculations
  4. Passage of gastric fluid into esophagus and pharynx can cause aspiration
225
Q

Describe maximum incrase in intraocular pressure after administration of succinylcholine (5)

A
  1. Occurs 2-4 minutes after admin
  2. Lasts 5-10 minutes
  3. MOA unknown
  4. Contraction of EOM and globe distrortion
  5. Resistance to outflow of aquous humor and dilation of vessels
226
Q

When is succinylcholine contraindicated with eye surgery?

A

Open anterior chamber injury due to possibility of causing permanent blindness

227
Q

Describe intracranial pressure in regards to succinylcholine admin

A
  1. Increases with patients who have intracranial tumors or CHI
  2. Not consistently observed in studies
  3. Attenuated by hyperventilation prior to admin
228
Q

Describe sustained skeletal muscle contraction with succinylcholine admin

A
  1. Incomplete jaw relacation/masseter muscle spasm associated with halothane and succinylcholine in children
  2. Considered normal response if inadequate dosage given
  3. Differentil diagnonis with MH
229
Q

Define malignant hyperthermia

A

Heriditart rhabdomyolysis associated with anesthetics that leads to muscle destruction, hyperkalemia, acidosis, dysrhythmias, renal failure, DIC

230
Q

Triggers for malignant hyperthermia?

A

All volatile anesthetics and succinylcholine

231
Q

What is thought to be the cause of malignant hyperthermia?

A
  1. Mutation in skeletal muscle calcium release
  2. RyR1 receptors in 50-70% of MH patients and native americans
  3. Skeletal muscle caffeine contracture testing and muscle biposy can help pre-dx
232
Q

Symptoms associated with MH?

A
  1. Acute increased skeletal muscle metabolism
  2. Increased oxygen consumption
  3. Lactate formation
  4. Heat production
  5. Rhabdo
233
Q

Clincial presentation of rhabdomyolysis?

A
  1. increased ETCO2
  2. increased temp 1 degree C q 5 minutes
  3. Arrythmias
  4. Skeletal muscle rigidity
234
Q

What are the ABCD’s of Malignant Hyperthermia?

A
  • Agents = stop all triggering agents
  • Administer non-triggering anesthetics
  • Ask for help
  • Ask for MH cart
  • Breathing = hyperventilation with 100% oxygen
  • Cooling procedures if patient is >102.2 F (fluids and ice)
  • Dantrolene continuous and rapid IV push
235
Q

What is the effect and metabolism of Dantrolene?

A
  1. Inhibits calcium release into SR
  2. Metabolized in the liver into 5-hydroxydantrolene
  3. 50% of patients complained of weakness of grip
236
Q

What are the most common side effects of dantrolene? (4)

A
  1. Weakness
  2. Phlebitis
  3. Respiratory failure
  4. GI upset
237
Q

What are the less common side effects of dantrolene? (3)

A
  1. Confusion
  2. Dizziness
  3. Drowsiness
238
Q

What is the dose of dantrolene in MH?

A

2mg/kg IV, repeat dose until symptoms subside or reach a total of 10mg/kg IV

239
Q

Why must we be cautious in giving dantrolene to patients on other calcium channel blockers?

A

Synergistic effect can lead to hyperkalemia and cardiovascular collapse

240
Q

Describe Myasthenia Gravis

A

Autoimmune disease associate with antibodies against Ach receptors causing a reduction in them

241
Q

What are the signs of myasthenia gravis?

A
  1. Increaesing weakness/fatigue s the day goes on
  2. Diplopia
  3. Ptosis
  4. Extremity and respiratory muscle weakness
242
Q

What NMDs are patients with myasthenia gravis sensitive to?

A

Non-depolarizers

243
Q

How is myasthenia gravis related to administration of succinylcholine?

A

MG patients are resistant to succ, ED95 is 2.5x greater to be effective, will need to use 1.5-2mg/kg IV

244
Q

Describe Lambert-Eton disease

A

autoimmune disease associated with small cell lung cancer that produces antibodies against caclium channels and decreases release of Ach prejunctionally

245
Q

What NMBds do patients with Lamber-Eton disease show increased sensitivity to?

A

depolarizers and non-depolarizers

246
Q

MOA of non-depolarizing muscle relaxants (5)

A
  1. Competively acts for alpha subunits (both) of post-junctional nAch-R
  2. No conformational changes of the nAch receptor
  3. Also act at pre-junctional sites
  4. 70% post-juntional occupation = no blockade
  5. 80-90% blocked receptors = neuromuscular transmission fails
247
Q

Characteristics of blockade with NDMDs? (7)

A
  1. Decreased twitch response to a single simulus
  2. Unsustained response (fade) to continuous stimulus
  3. TOF Ratio <0.7
  4. Post-tetanic potentiation
  5. Potentiation of other non-depolarizing drugs
  6. Antagonism by anticholinesterase drugs (neostigmine)
  7. No fasiculations during onset
248
Q

What does fade suggest?

A

Fade suggest some fibers are contracting while some are blocked

249
Q

Main Adverse side effects of NDMDs? (3)

A
  1. Cardiovascular effects
  2. Critical illness myopathy
  3. Altered responses
250
Q

What are the cardiovascular effects associated with ND-NMBDs due to?

A
  1. Release of histamine
  2. Effects at cardiac muscarinic receptors
  3. Effects on nAch-R at autonomic ganglia
251
Q

What is the “autonomic margin of safety” when referring to cardiovascular effects of ND-NMBDs?

A
  1. Difference between dose that produces blockade ED50 and dose that creates circulatory effects
  2. Same dose for pancuronium
  3. Very different dose for vec, roc, cis
252
Q

Describe skeletal muscle weakness associated with when administering ND-NMBDs? (5)

A
  1. Weeks to months after NMBD d/c
  2. Usually an aminosteroid blocker
  3. Glucocorticoids prior to NMBD may enhance risk
  4. Nerve monitoring, sedation, analgesia, small doses of NMBD may be effective
253
Q

What are altered responses associated with coadministration of ND-NMBDs and volatile anesthetics? (4)

A
  1. Dose dependent enhancement
  2. MOA leads to CNS depression and skeletal muscle tone
  3. Decreased sensitivity of postjunctional membranes
  4. Magnitude of intermediate NMBD < long acting
254
Q

Altered response of ND-NMBDs when associated with coadministration with local anesthetics?

A
  1. Small doses enhance NMJ blockade
  2. Large doses block NMJ transmission
255
Q

MOA of local anesthetics?

A
  1. Interfere with prejunctional Ach release
  2. Stabilizes postjunctional membranes
  3. Directly depress skeletal muscle fibers
  4. Compete for plasma cholinesterases (ester LA)
256
Q

Altered response of ND-NMBDs when coadmin with diuretics

A
  1. Furosemide 1mg/kg enhances blockade do to inhibition of cAMP production and decreased Ach release
  2. Large doses inhibit PDE1, makes more caMP, antagonism of blockade
  3. Mannitol has no effect on blockade
257
Q

Altered response of ND-NMBDs associated with coadmin of magnesium?

A

Enhances blockade of non-depolarizes and succinylcholine

258
Q

MOA of magnesium

A
  1. Decreased prejunctional releasr of Ach
  2. Stabilization of postjunctional membranes
259
Q

Altered response of ND-NMBDs with SNS drugs (2)

A
  1. ephedrine prior to rocuronium decreases onset time by 22% and increases CO and skeletal muscle flow
  2. Esmolol prior to induction delays onset of roc by 26%, can have reduction in HR and CO
260
Q

Altered response of ND-NMBDs with hypothermia

A
  1. Occurs with even mild hypothermia, will slow everything down
  2. Temperature slowing of hepatic enzyme activity
  3. Atracurium
  4. Slows temperature dependent hoffman elimination and ester hydrolysis
261
Q

Altered response of ND-NMBDs with hypokalemia?

A
  1. Hyperpolarizes cell membrane
  2. Resistance to depolarizing NMBDs
  3. Increase sensitivity to non-depolarizing NMBDs
262
Q

Altered respone of ND-NMBDs with acute hyperkalemia?

A
  1. Decreases resting membrane potential
  2. Increases effects of depolarizing NMBDs
  3. Resitance to non-depolarizing NMBDs
263
Q

Altered response of ND-NMBDs with burn patients?

A
  1. Resistance begins approx 10 days post injury and declines after 60 days
  2. Occurs with > or equal to 30% BSA burnt
  3. May be offset by using 1.2mg/kg dose of rocuronium
264
Q

Which arm is more resistance to ND-NMBDs, the paretic arm or the unaffected side

A

The paretic arm, although the unaffected side is more resistant compared to normal patients

265
Q

Altered response to ND-NMBDs and allergic reactions

A
  1. More common with quaternary ammonium group (SANE)
  2. Single quarternary : pan, vec and roc less likely
  3. 1st exposure represent prior sensitization (soaps/cosmetics)
  4. Cross sensitization possible
266
Q

How does gender effect NMBDs?

A

women are more sensitive, 22% dose less than vec and 30% dose less than roc and duration of block is greater in women due to less skeletal muscle mass

267
Q

Describe Pancuronium (Pavulon) (4)

A
  1. Bisquaternary aminosteroid with vagolytic and butrylcholinesterase inhib properties
  2. Intubating dose of 0.1mg/kg
  3. Onset of action 3-5 minutes
  4. Duration 60-90 minutes
268
Q

Metabolism of Pancuronium (Pavulon)?

A
  1. 40-60% cleared unchanged in urine
  2. Renal failure can prolong effect due to 30-50% decreased plasma clearance
  3. Liver disease causes an increase VD and prolongs elimination half time
  4. Decreased plasma clearance with aging due to renal function reduction
269
Q

Cardiovascular effects of Pancuronium (Pavulon) (5)

A
  1. SNS activation do to release of NE presynaptically
  2. Blockade of NE reuptake postganglionic
  3. Increase HR/MAP/CO due to vagal blockade mostly at SA node
  4. No changes in SVR or inotropy
  5. No histamine release
270
Q

Pros of intermediate acting NMBDs

A
  1. Efficient clearance mechanism
  2. Less accumulation with repeat doses or infusions
271
Q

Intermediate acting NMBDs compared with long acting (5)

A
  1. Similar onset of maximum blockade except high dose roc
  2. Approx 1/3 duration of action
  3. Minimal/absent cumulative effects
  4. Minimal/absent cardiovascular effects
  5. Antagonized by anticholinesterase drugs approx 20 minutes
272
Q

Describe Atracurium (Tracrium)

A
  1. Bisquaternary benzylisoquinolinium
  2. Intubating dose of 0.2mg/kg
  3. Onset 3-5 minutes
  4. Duration 20-35 minutes
273
Q

Metabolism of Atracurium (Tracrium)

A
  1. Acts both presynaptic and postsynaptic cholinergic receptors may block nACH-R
  2. Spontaneous in vivi degredation (Hoffman elim) = greater role
  3. Ester hydrolysis by nonspecifici plasma esterases = lesser role
274
Q

When would we see bp or hr changes with intermediate acting NMBDs?

A

3x the ED95 dose, but they do release histamine

275
Q

Describe vecuronium (norcuron)

A
  1. Aminosteroid
  2. Intubating dose 0.1mg/kg
  3. Onset 3-5minutes
  4. Duration 20-35 minutes
276
Q

Describe the metabolism of Vecuronium (Norcuron)

A
  1. Hepatic Metabolism is the principle organ of elimination
  2. Renal excretion is prolonged with dysfunction
  3. Repeated doses or infusion does show cumulative effects
277
Q

Metabolism of Veucronium (Norcuron) in elderly and obstetrics (5)

A
  1. Elderly show decreased volume of distribution and decreased plasma clearance
  2. Elderly show delayed recovery with infusions
  3. Obstetrics show insignificant side effects to fetus
  4. Increased clearance in 3rd trimester (progesterone)
  5. Prolonged duration early postpartum
278
Q

Acid-base changes associated with Vecuronium (Norcuron) (3)

A
  1. Dependent on when the acid-base status changes
  2. If acidosis before NMBD, there will be no prolonged effect
  3. If acidosis after NMBD, prolongs blockade
279
Q

Cardiovascular effects of Vecuronium (Norcuron)

A
  1. Essentially none
  2. No histamine release
280
Q

Describe Rocuronium (Zemuron) (4)

A
  1. aminosteroid
  2. Dose 0.6mg/kg, larger doses parallel onset of Sch but offset of pancuronium
  3. Onset 3-5 minutes
  4. Duration 20-35 minutes w/ intubating dose
281
Q

Metabolism of Rocuronium (Zemuron) (3)

A
  1. Excreted unchanged in bile (more liver metabolism than renal)
  2. Longer duration of action in liver failure and elderly due to decreased clearance and an increased Vd
  3. Only marginally affected in renal failure
282
Q

Cardiovascular effects of Rocuronium (Zemuron) (2)

A
  1. No histamine release
  2. No cardiac effects
283
Q

Describe Cisatracurium (4)

A
  1. Benzylisoquinolinium
  2. Intubating dose 0.1mg/kg
  3. Onset 3-5 minutes
  4. Duration of action 20-35 minutes
284
Q

Metabolism Cisatracurium (Nimbex) (5)

A
  1. Cis-isomer
  2. Less histamine release
  3. Recovery from infusion not affected by time
  4. Hoffman elimination
  5. No elimination 1/2 changes in CRF with bolus
285
Q

Metabolism of Cisatracurium (Nimbex) in the elderly or obese

A
  1. Elder show slight delays of about 1 min in onset due to slower CO
  2. Obese show prolonged duratin of action if dosed at real body weight due to Vd
286
Q

Cardiovascular effects of Cisatracurium (Nimbex)

A
  1. No histamine release
  2. Cardiovascular stability
287
Q

Describe Mivacurium (Mivacron) (5)

A
  1. Only clinically useful SA non-depolarizer
  2. Benzylisoquinolinium
  3. Intrubating dose 0.15 mg/kg
  4. Onset 2-3 minutes
  5. Duration of action 12-20 minutes
288
Q

Metaboliosm of Mivacurium (Mivacron)

A
  1. 3 stereoisomers with cis-trans and trans-trans showing the paralytic effects
  2. NM blockade ability
  3. Cleared by plasma cholinesterase
289
Q

What would the effect of atypical plasma cholinesterases have on the metabolism of Mivacurium (Mivacron)

A
  1. Decreases hydrolysis
  2. Duration of action prolonged
  3. Human plasma cholinesterase
290
Q

Metabolism of Mivacurium (Mivacron) with renal dysfunction and hepatic disease

A
  1. Renal dysfunction commmonly shows decreased cholinesterase activity
  2. Hepatic disease shows increased volume of distribution, patients appear to be more resistant
291
Q

Cardiovascular effects of Mivacurium (Mivacron) (4)

A
  1. Minimal effects
  2. Histamine release with 3x the ED95 dose shows transient MAP drop
  3. MAP drop more in HTN patients than non-HTN patients
  4. Possible bronchospasm concern
292
Q

4 anti-cholinesterase drugs

A
  1. Edrophonium
  2. Neostigmine
  3. Pyridostigmine
  4. Physostigmine
293
Q

Describe neostigmine (5)

A
  1. Used to antagonize NMBD
  2. Increases amount of Ach in NMJ
  3. Increases chances of Ach instead of NMBD binding to alpha subunits
  4. Dose dependent
  5. When recovery of NMBD is occurring anyway
294
Q

MOA of edrophonium and neostigmine

A

inhibition of acetylcholinesterase

295
Q

Metabolism of Neostigmine and Edrophonium (3)

A
  1. 50-70% of the drug is cleared renally
  2. Elimination is 1/2 time is greatly prolonged in CRF
  3. Hepatic clearance 30-50% if absence of renal function
296
Q

Metabolism of Edrophonium and Neostigmine in elderly (4)

A
  1. Edrophonium duration is not prolonged
  2. Neostigmine duration is prolonged
  3. Edrophonium requires a higher concentration in elderly
  4. Neostigmine has no difference in concentration
297
Q

Muscarinic effects of Neostigmine and Edrophonium (5)

A
  1. Bradycardia
  2. Salivation
  3. Miosis (pupillary constriction)
  4. Hyperperistalsis
  5. Requires an anticholinergic drug prior to admin
298
Q

GI/GU effects of edrophonium and neostigmine (3)

A
  1. Enhance gastric fluid secretion
  2. Increase mortality of GI tract
  3. Increase PONV, especially if patient has severe predisposition
299
Q

Dose, onset and duration of action of edrophonium

A
  1. Dose: 1mg/kg
  2. Onset: 1-2 minutes
  3. Duration of action: 5-15 minutes
300
Q

Dose of Atropine and initial effects

A
  1. Dose: 7mcg/kg
  2. Initial: Tachycardia with neostigmine
301
Q

Dose, onset and duration of action of Neostigmine

A
  1. Dose: 70mcg/kg with 5mg max
  2. Onset: 5-10 minutes
  3. Duration of action: 60 minutes
302
Q

Dose of glycopyrolate

A

15 mcg/kg with 1 mg max

303
Q

What contrinutes to persistent NM blockade?

A

Acetylcholinesterase is maximally inhibited and no further anticholinesterase is effective, patient will need to be on the vent postop

304
Q

5 things that influence NMBD reversal

A
  1. Intensity of block
  2. Which NMBD did you use
  3. Continued volatile anesthetic
  4. Which reversal drug are you using
  5. Patient condition
305
Q

List the drugs Suggamadex reverses in order

A
  1. Rocuronium
  2. Vecuronium
  3. Pancuronium
306
Q

Describe Suggamadex (Bridion)

A
  1. a cyclodextrin (starch)
  2. very water soluble
307
Q

MOA of suggamadex (bridion) (4)

A
  1. Complexes with NMBD to decrease amount of available nAch-R
  2. Binds free drug in plasma and creates concentration gradient
  3. No metabolism, renal excretion
  4. E 1/2 is 2 hours
308
Q

Admin instructions of Suggamadex (Bridion)

A
  1. Bolus over 10 seconds
  2. Contraindicated in renal diseases requiring dialysis
  3. Moderate block dose is 2mg/kg
  4. Deep block dose is 4mg/kg
309
Q

Dose related side effects of Suggamadex?

A

Nausea/vomiting, pruritius, urticaria

310
Q

2 other side effects of suggamadex other than the dose related ones

A

Anaphylaxis, marked bradycardia

311
Q

Cautions with suggamadex

A
  1. Patients on Oral contraceptives will require a back-up method for 7 days
  2. Toremifine or chemo drugs displaces vec/roc from suggamedex
  3. Recurarization at lower than recommended doses
  4. With heparanin and LMWH will have an elevate aPTT, PT, INR

Advanced Pharmacology 2 (5 decks)

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