6: Inhalation Anesthetics 2 Flashcards

1
Q

CNS depression is _____ dependent.

A

dose

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2
Q

What is the effect of the common anesthetics on cardiac output/depression?

A

Halothane > sevo ~ iso ~ des

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3
Q

Cardiac output is preserved when MAC is _____.

A

<1.0

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4
Q

How does halothane reduce CO and ABP?

A

By depressing myocardial contractility

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5
Q

Halothane blunts the _____ reflex.

A

baroreceptor

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6
Q

Halothane sensitizes the myocardium to _____.

A

catecholamines

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7
Q

Io, sevo, and des provide minimal ____ at useful [].

A

depression

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8
Q

How do iso, sevo, and des cause hypotension?

A

By vasodilation

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9
Q

How is contractility affected with iso/sevo/des vs. halothane?

A

It is less affected

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10
Q

Inhalants are broncho_____.

A

dilators

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11
Q

What is the order in which anesthetics decrease hepatic blood flow and oxygen delivery?

A

Halothane >>> sevo/des > iso

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12
Q

What is the term for decreased hepatic function/hepatocellular damage that is caused by halothane?

A

halothane hepatitis - in people

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13
Q

What effect do anesthestics have on the renal system?

A

Mild, reversible, dose dependent decrease in RBF and GFR (related to CO)

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14
Q

Sevo degradation by strong alkali CO2 absorber makes _____.

A

compound A

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15
Q

Nephrotoxicity from sevo is documented in _____.

A

rats

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16
Q

Nitrous oxide is a _____ at room temp and at atm pressure.

A

gas

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17
Q

Nitrous oxide is given directly thru a _____ and does not require a _____.

A

flowmeter, vaporizer

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18
Q

Nitrous oxide can be give with oxygen and _____.

A

vapor anesthetic

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19
Q

T/F: Nitrous oxide has NMDA antagonistic effect.

What does this mean?

A

True; it is an analgesic

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20
Q

Nitrous oxide can be used as an anesthetic _____ to reduce _____ of vapor anesthetics.

A

adjunct, MAC (25%)

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21
Q

What are the CNS effects of nitrous oxide?

A
  1. Increased cerebral blood flow
  2. Increased intracranial pressure
  3. Increased cerebral metabolic rate of oxygen
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22
Q

Due to CNS effects, nitrous oxide should be avoided in patients with _____ diseases.

A

neurologic

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23
Q

What are the respiratory effects of nitrous oxide?

A
  1. Min change on minute ventilation (decrease tidal volume but compensatory increase in RR)
  2. Depresses response to hypoxia
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24
Q

What are the CV effects of nitrous oxide and which one dominates?

A
  1. Stim sympathetic nervous system (HR, BP, CO usually increase) –> dominates
  2. Directly induces myocardial depression
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25
Q

Nitrous oxide is 34x more soluble in _____ than nitrogen.

A

blood

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26
Q

Nitrogen is more soluble in _____ than nitrous oxide.

A

gas

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27
Q

Nitrous oxide enters a gas-filled space ___ times faster than nitrogen can leave that space.

A

34

28
Q

Under what conditions is use of nitrous oxide contraindicated?

A
  1. Pneumothrax
  2. Pneumoperitoneum
  3. Pneumocephalus
  4. Gas-filled GIT
  5. Tracheal tube cuff
  6. Air embolism during minimally-invasive procedures
29
Q

How does nitrous oxide cause diffusion hypoxia and how can this be mitigated?

A
  1. When it is discontinued, a large volume will diffuse back from blood to alveoli and displace oxygen
  2. Resulting gas in alveoli becomes hypoxic mixture

Mitigate by supplementing oxygen for ~10 min after discontinuation of nitrous oxide

30
Q

What US governmental agencies regulate waste anesthetic gases?

A

FDA, OSHA, NIOSH

31
Q

What is the recommendation for waste gases by government agencies?

A

Max exposure level = 2 ppm for volatile agents, 25 ppm for nitrous oxide

32
Q

What is the most important control for waste anesthetic gases?

A

Use of scavenge and ensuring minimal leaks

33
Q

What is the only way of eliminating waste anesthetic gases from the environment?

A

Room ventilation

34
Q

What are 3 potential adverse events related to waste gas exposure?

A
  1. Patient experienced adverse drug reactions
  2. Health care provider exposure
  3. Environmental adverse effects
35
Q

What are short-term effects of WAG exposure?

A

Fatigue, headache, drowsiness, nausea, depression, irritability

36
Q

What are long-term effects of WAG exposure and what causes them?

A

Caused by metabolites:

  1. Repro disorders (infertility, abortion, teratogenesis in 1st trimester with nitrous oxide)
  2. Liver and kidney damage
  3. Bone marrow damage
  4. +/- carcinogenesis
37
Q

Why are iso and sevo less toxic than other WAG?

A

Lower levels of metabolism

38
Q

What are 2 environmental impacts that WAG can have?

A

Ozone depletion and greenhouse global warming

39
Q

What WAGs can cause ozone depletion?

A

halothane and iso (nitrous oxide also important)

40
Q

What WAG has the highest heat trapping effect for global warming? Which WAG is released in the greatest quantity?

A

Highest heat trapping = desflurane

Released in greatest qty = nitrous oxide

41
Q

What are 8 ways to prevent room pollution?

A
  1. Proper usage of scavenge equipment
  2. Inspect hoses and bags for holes and check machines for leaks
  3. Tighten all connections
  4. Empty reservoir bag into scavenger at end of anesthesia
  5. Reduce mask induction or chamber induction when possible
  6. Scavenge ventilators and gas analyzers
  7. Turn off flowmeters when not in use
  8. Turn of nitrous oxide cylinder when not in use
42
Q

What should you do when you spill a bottle of iso?

A
  1. Notify all personnel in vicinity and vacate room as much as possible
  2. Soak up as much liquid as possible in towels or litter and seal within a plastic bag
  3. Remove the bag to a well-ventilated area to allow evaporation
  4. Use fans to disperse the vapors indoors
43
Q

What is the genetic cause for malignant hyperthermia?

A

Mutation in the ryanodine Ca channel

44
Q

What metabolically causes malignant hyperthermia?

A

Hypermetabolic state due to high intracellular Ca level

45
Q

What things can trigger malignant hyperthermia?

A

Volatile anesthetics and depolarizing muscle relaxants

46
Q

What spp are prone to malignant hyperthermia?

A

Humans and swine

47
Q

What was wave 1 of the rise in opioid overdoses?

A

Rise in Rx opioid ODs (1999);

EX: natural and semi-synthetic, methadone

48
Q

What was wave 2 of the rise in opioid ODs?

A

Rise in heroin ODs (2010)

49
Q

What was wave 3 of the rise in opioid ODs?

A

Rise in synthetic opioid ODs (2013);

EX: Tramadol and Fentanyl

50
Q

Who controls controlled substances?

A

DEA

51
Q

How many schedules are there for controlled substances and what are they based on?

A

5; based on currently accepted medical use, abuse potential, and likelihood of causing dependence when abused

52
Q

_____ laws are always more strict than _____ laws.

A

State, federal

53
Q

What schedule has the highest abuse potential and dependence and which has the lowest?

A

1 = highest

5 = lowest

54
Q

What veterinary drugs are considered schedule II?

A

Full mu opioids, amphetamines, pentobarbital

55
Q

What is the abuse potential and dependence of schedule II drugs?

A

Abuse = high

Dependence = severe

56
Q

What veterinary drugs are considered schedule III?

A

Buprenorphine, ketamine

57
Q

What is the abuse potential and dependence of schedule III drugs?

A

Abuse = moderate

Dependence = moderate or low

58
Q

What veterinary drugs are schedule IV?

A

Benzodiazepines

59
Q

What is the abuse potential and dependence of schedule IV drugs?

A

Abuse = low

Dependence = low

60
Q

Where should controlled drugs be kept?

A

Securely locked cabinet of substantial construction

61
Q

What 5 factors should be considered when evaluating security of controlled drugs?

A
  1. # people who have access to them
  2. Location of storage safe
  3. Use of effective alarm system
  4. Quantity of controlled substances to be kept on hand
  5. Prior history of theft or diversion
62
Q

Where should blank Rx and DEA order forms be kept?

A

In a secure location

63
Q

What should be done if controlled drugs are lost?

A

Notify appropriate DEA field office of theft or significant loss promptly

64
Q

What was the policy for ambulatory practice regarding controlled drugs in 2006?

A

Per DEA, practicioners needed a separate registration for each state where they Rx’ed controlled substances

65
Q

What was the policy for ambulatory practice regarding controlled drugs in 2012?

A

The AVMA asked the DEA for discretion when investigating ambulatory veterinarians

66
Q

What was the policy for ambulatory practice regarding controlled drugs in 2014?

A

The Veterinary Medicine Mobility Act was created:

Allows vets to carry and dispense controlled substances as part of the usual course of their practice beyond the primary locations registered with the DEA (within the same state)