Inhalation Agents Part 3 Flashcards

1
Q

What effects do inhaled agents have on MAP?

A

At equipotent doses all agents will have similar effects

  • MAP decreases with increased concentration of Sevo, Iso and Des in a dose dependent manner
  • SVR also decreases (vasodilation)
  • Exceptions *
  • Halothane decreases MAP by decreasing CO
  • N2O has either no change or mildly increases MAP
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2
Q

How are halogenated agents dosed compared to N2O?

A
  • N2O is based on flow (% x L/min)

- Halogenated agent based on MAC (% x MAC value)

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3
Q

How do halogenated agents effect HR?

A

Dose dependent and different for each agent
- Iso—> starting at .25 MAC, linear dose dependent increase in HR, especially with rapid increase in concentration
* Des—> ≥ 1 MAC- linear dose dependent increase in HR, especially with rapid increase in concentration
<1 MAC- min increase in HR
- Sevo—> no increase in HR until > 1.5 MAC

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4
Q

What is the rule of 24?

A

Total combined flow of Des x O2 flow if >24 will see tachycardia
- keep <24 to keep HR under control (have Des ~8 and flows ~3)

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5
Q

What type of patient must you be cautious with increasing agent slowly to prevent tachycardia?

A

Cardiac compromised

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6
Q

Is CI influenced by inhalation agents?

A

Minimally

- TEE shows Des to produce minor increase in EF compared to awake measurements

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7
Q

Rapidly increase the dose will rapidly increase HR with ________ and ________ when > _____MAC.

A

Iso and Des

1 MAC

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8
Q

Abrupt increase in HR is not observed with ______, ______, or _______ up to MAC 2.

A

Sevo, halo or enflurane

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9
Q

Do the newer agents predispose the heart to PVCs?

A

Not unless they are given in extremely high concentrations

—> halothane does d/t catecholamines and hypercarbia

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10
Q

How do the agents effect QT interval and what should be avoided?

A

Inhalation agents prolong QT interval
* avoid SEVO in patients with known congenital long QT syndrome (LQTS)
(Safe with beta blocker therapy)

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11
Q

How do inhalation agents effect CAD?

A

Data shows no difference between inhaled and IV opioid anesthetic
—> volatile anesthetics exert protective effect on the heart
- limit the area of myocardial injury and preserving function after exposure to ischemic insult

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12
Q

What is coronary steal?

A

ISO’s ability to dilate healthy coronary arteries and not stenotic arteries, thus stealing from diseased vessels

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13
Q

What is ischemic preconditioning?

A

Like inoculation or vaccination against ischemia

  • protective mechanism present in all tissues
  • exposure to brief episodes of ischemia confers protective effect on myocardium agains subsequent prolonged ischemic insult (reversible or irreversible)
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14
Q

What are the 2 periods of protection with ischemic preconditioning?

A

1st period: 1-2 hours after conditioning episode

2nd period: benefits reappear 24 hours later and can last as long as 3 days

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15
Q

What is the crucial event that confers protective activity with ischemia preconditioning?

A

Opening of mitochondrial ATP sensitive K+ channels

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16
Q

What effect do the agents have on chronic HTN?

A

BP will drop even lower with anesthesia
- vessels are always clamped down —> less blood volume- when gas vasodilates vessels are hypovolemia
—> IVF boluses help

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17
Q

What are the pulmonary effects of inhaled agents?

A
  • increase in RR and decrease in tidal volume (minute ventilation preserved)
  • as anesthesia deepens- gas exchange is less efficient (shallow breathing)
  • PaCO2 increases proportionately to depth of anesthesia
  • dose depended blunted response to hypercarbia
  • apnea threshold increased- higher CO2 level needed to stimulate breathing
  • hypoxic drive altered- O2 must be lower to stimulate breathing
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18
Q

How do the agents effect the chest wall?

A

Gas relaxes everything

  • cephalad displacement of diaphragm
  • inward displacement of rib cage from enhanced expiratory muscle activity—> decreases FRC
  • atelactasis in dependent lung zones
    • worse with spontaneous ventilation
    • increasing PEEP can help
  • limit HPV
  • Bronchodilation: greatest effect when bronchoconstriction present
    • will help with bronchospasm
19
Q

What are the effects of pungency?

A
  • Coughing- worse in asthma and smokers- use inhaler before (gas is irritating)
  • breath holding
  • laryngospasm
  • arterial desaturation
  • Des and Iso are pungent —> Des is the most pungent
    (Non-pungent gases are Sevo, Halo, Nitrous Oxide)
20
Q

What are the CNS effects of the agents?

A
  • decrease CMRO2
  • with normal CO2 levels- cerebral vasodilation with MAC > 0.6
    ≥1MAC vasodilation that increases flood flow -> be careful with increased ICP
21
Q

How does N2O effect CNS differently?

A
  • causes cerebral vasodilation
  • increases CMRO2
    • to counter these effects give opioids, barbs, or propofol. (Not ketamine—> bad for brains)
22
Q

What happens to ICP with ≥1MAC of all agents?

A

Increases ICP

In head trauma keep gasses < 1 MAC

23
Q

What happens to autoregulation of blood flow in the brain <1 MAC?

A

Impaired, worsens as MAC increases

24
Q

How do the agents effect evoked potentials?

A
  • depress amplitude and increase latency of SSEP in a dose dependent manner
    • both of these are signs of nerve damage…..
  • EPS abolished at 1 MAC
    • or N2O + o.5 MAC
  • even low concentrations (0.2-0.3) decrease reliability of MEPs
25
Q

Which gas do you avoid when your patient has a history of seizures?

A

SEVO— can induce seizures

So can ethrane

26
Q

How is the EEG effected by the agents?

A

Increases amplitude and synchrony as depth increases
Eventual burst suppression
- 1.5-2.0 MAC —> isoelectric EEG, stage 4, no brain activity

27
Q

How do the agents effect neuromuscular characteristics?

A
  • dose dependent skeletal muscle relaxation
  • enhances activity of NMB drugs
  • stopping agent enhances recovery from NMB
28
Q

Do all inhalation agents trigger MH?

A

Except N2O

Halo>iso>sevo>des

29
Q

How do the agents effect the liver?

A

Immune mediated liver injury
—> caused by trifluoroacetate metabolite
- mild liver injury
- more likely to occur after decreased blood flow and O2 to liver
- halothane > iso> des as far as metabolism is concerned
- from TFA and inorganic fluoride ions

30
Q

What should you do if patient has had previous liver dysfunction after receiving inhalation anesthesia?

A

Low risk, but avoid agents

31
Q

How do the agents effect the kidneys?

A

Sevo—> compound A—> nephrotoxic after prolonged exposure with O2 <1L/min

  • causes transient proteinurea, enzymurea, glycosurea
  • to avoid Compound A—> limit low FGF (<2L/min) to <2 MAC hrs of sevo anesthetic
32
Q

What is something to be aware of with N2O?

A
  • it inactivates methionine synthase—> enzyme that regulates B12 and folate metabolism
  • N2O contraindicated with pre existing B12 deficiency or underlying critical illness
33
Q

What is homocysteine?

A

Requires methionine synthase for conversion

  • increased levels associated with adverse coronary events
  • since N2O inactivates methionine synthase, homocysteine levels may increase
34
Q

What does N2O do to closed gas spaces?

A

Transfers to them rapidly, 34 x more than nitrogen diffuses out

  • compliant wall =increased volume
  • noncompliant wall= increased pressure
35
Q

What happens when the CO2 absorbent is fully dedicated?

A

Causes degradation and carbon monoxide production from all agents regardless of the temperature

36
Q

What accelerates desiccation of CO2 absorbants?

A

High FGF (exceeding normal minute ventilation)

37
Q

Degradation of soda lime is an exothermic process. What implications does this have?

A

May elevate temperature so high that it leads to explosion or fire in canister
*especially SEVO

38
Q

With desiccated soda lime:

A
  • Sevo—> compound A production is sped up

- Iso and Des—> produce carbon monoxide

39
Q

How do you prevent desiccated soda lime?

A
  • change CO2 absorbent frequently (q 1 week here)
  • limit FGF during cases
  • turn FGF off between cases
  • when in doubt change absorbent
40
Q

T/F

Immune response is depressed for a while after exposure to gas?

A

True

41
Q

How does a variable bypass vaporizer work?

A

(Seen with Sevo, Iso, halo)

  • 2 streams of inflowing fresh gas
    • 1 with reservoir to liquid anesthetic
    • 1 bypassing reservoir
  • concentration of gas leaving the vaporizer determined by relative flow to gas through reservoir channel vs bypass channel
    • controlled by adjusting dial
42
Q

What is true regarding a variable bypass vaporizer?

A
  • temperature compensated
  • calibrated for individual anesthetic d/t different vapor pressures
  • tilting/overfilling may lead to overdose
43
Q

What is true about the tec 6 heated vaporizer?

A

Used for des since the vapor pressure of des at 20C and 1 atm is 700mmHg (boils are room temp) and using a variable bypass vaporizer will deliver inaccurate amounts

  • heats des to 2 atms—> for accurate delivery
    • at high altitudes partial pressure of des is lower—> need to give higher dose to account for altitude
44
Q

What is the equation to account for altitude ?

A

Required vaporizer setting= (MAC desired x 760mmHg)/local barometeric pressure