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ANESTHESIA PHARM 2 > INHALED ANESTHETICS II > Flashcards

INHALED ANESTHETICS II Flashcards

1
Q

how is anesthesia different from every other aspect of medicine?

A

anesthesia is neither therapeutic nor diagnostic

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2
Q

what goals are we trying to accomplish with general anesthesia?

A
  • minimize deleterious direct and indirect effects of agents
  • sustain physiologic homeostasis during procedure
  • improve post outcomes
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3
Q

what are the components of general anesthesia?

A
  • analgesia
  • amnesia
  • hypnosis
  • muscle relaxation
    (inhaled anesthetics can do all four of these, including muscle relaxation, but there are better drugs for this)
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4
Q

what are the drawbacks of TIVA compared to GA?

A

pts on TIVA require a lot more propofol/remifentanil to maintain sedation, and pts will wiggle, because these drugs do not offer any muscle relaxation

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5
Q

how do inhaled anesthetics work?

A

NOT REALLY SURE!! no definitive answer as to what receptors they bind to, etc.

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6
Q

define pharmacodynamics

A

what the drug does to the BODY

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7
Q

define MAC

A

minimum alveolar concentration required to prevent movement in response to nociceptive stimulation in 50% of the population

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8
Q

how is MAC used as a measure of comparison?

A

allows comparison of potency

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9
Q

what MAC value will prevent movement in 95% of the population?

A

1.3 MAC prevents movement in 95% of the population

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10
Q

how does age affect MAC values?

A

MAC decreases 6% per decade of age after age 40

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11
Q

define MAC awake

A

end-tidal concentration of an anesthetic agent at which 50% o pts appropriately respond to verbal commands (like “open your eyes”)
* applies only to inhalation agents and is affected by adjunctive needs, age, hypothermia, and sedatives

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12
Q

what is the MAC awake value?

A

0.1 – 0.3 ET agent

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13
Q

define MAC bar

A

concentration required to block autonomic reflexes to nociceptive stimuli

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14
Q

what is the MAC bar value?

A

1.7 – 2.0 ET agent

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15
Q

what is the MAC amnesia value

A

0.4 – 0.6 ET agent

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16
Q

what factors will increase MAC requirements for a pt?

A
  • hyperthermia
  • drug-induced increase in catecholamines
  • hypernatremia
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17
Q

how does chronic alcohol abuse vs. acute alcohol intoxication affect MAC requirements?

A
  • chronic alcohol abuse will not alter MAC requirements, whereas * acute alcohol intoxication may decrease MAC requirements (due to GABA receptor flooding)
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18
Q

what factors will not alter MAC requirements?

A
  • gender
  • duration of anesthesia
  • PaCO2 15-95mmHg
  • PaO2 > 38mmHg
  • hyper/hypokalemia
  • thyroid dysfunction
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19
Q

what drugs will decrease MAC requirements?

A
  • opioids (also neuraxial opioids)
  • preop meds
  • alpha-2 agonists
  • lithium
  • lidocaine
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20
Q

what physiologic states will decrease MAC requirements?

A
  • increased age
  • hypothermia
  • PaO2
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21
Q

what surgical states will decrease MAC requirements?

A
  • pregnancy
  • immediate post-partum
  • cardiopulmonary bypass
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22
Q

what was the primary problem associated with the inhaled anesthetics introduced in the 1840s?

A

Nitrous oxide, ether, chloroform – PONV

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23
Q

what was the primary problem associated with the inhaled anesthetic introduced in 1951?

A

halothane – halothane induced hepatitis

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24
Q

what was the primary problem associated with the inhaled anesthetic introduced in 1960?

A

methoxyflurane – combustible

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25
Q

what was the primary problem associated with the inhaled anesthetic introduced in 1973?

A

enflurane – seizures

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26
Q

how do inhaled anesthetics affect cerebral blood flow?

A
  • increase vasodilation, so * decrease vascular resistance, therefore * increasing CBF and ICP
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27
Q

how can you counteract the increase in intracranial pressure associated with inhaled anesthetic use?

A

hyperventilate the patient – induces vasoconstriction

28
Q

how does halothane effect cerebral blood flow?

A

halothane increased cerebral blood flow by up to 200% vs. isoflurane

29
Q

how are cerebral metabolic oxygen requirements (CMRO2) affected by volatile anesthetics?

A

CMRO2 is decreased

30
Q

what gas (and how much) will produce burst suppression? what is the downside of this?

A

1.5 MAC isoflurane will cause burst suppression and EEG will become almost quiescent BUT MAC of iso is 1.4, therefore, NO BLOOD PRESSURE (no cerebral blood pressure)!!

31
Q

which agent is prone to producing seizure activity in pts?

A

enflurane

32
Q

how much MAC will you be able to use when doing big spine cases/ monitoring motor/sensory potentials/ evoked potentials

A

0.5 MAC is the most you can run when monitoring motor/sensory potentials

33
Q

how is CSF production affected by agents?

A

increased (increased ICP as a side effect – theoretical)

34
Q

if CBF is increased with volatile anesthetics, how is cerebral perfusion pressure affected?

A

cerebral perfusion pressure is decreased

35
Q

which volatile agent increases ICP more than others, and also increases metabolic demands?

A

nitrous oxide

36
Q

how is blood pressure affected by halothane and enflurane? by N2O? by other volatile agents?

A

blood pressure is reduced with almost all agents.

  • halothane and enflurane decrease myocardial contractility
  • nitrous oxide produces no change, or slight increase
  • other volatiles decrease SVR/vasodilate, thus lowering blood pressure
37
Q

how do volatile anesthetics affect HR?

A
  • sevo, iso, N2O cause reflex tachycardia in response to decreased BP (baroreceptor mediated) (halothane is the exception)
  • des induces tachycardia due to stimulation of SNS, esp with rapid increases in vapor concentrations (beginning of cases)
38
Q

how is cardiac output affected by volatile anesthetics?

A
  • halothane/enflurane – decreased CO due to decreased contractility
  • other volatiles decreased CO but to a lesser degree
  • N2O is sympathomimetic, so slight increase in CO, but at high doses will decrease CO
39
Q

how is systemic vascular resistance affected by volatile agents?

A

iso, des, sevo decrease SVR

40
Q

how is pulmonary vascular resistance affected by volatile agents?

A

all volatiles decrease/have no effect of PVR

41
Q

how is the hypoxic pulmonary vasoconstriction response affected by volatile agents?

A

volatile agents blunt the hypoxic pulmonary vascular resistance, but this happens more in vitro than in vivo

42
Q

what should you expect when using N2O in pts with pulmonary hypertension?

A

N2O will increase PVR in pts with pulmonary hypertension

43
Q

which volatile agent is a potent coronary vasodilator? what effects can this agent produce?

A

isoflurane is a potent coronary vasodilator

  • can cause coronary steal phenomenon
    • (studies do not show increase in ischemia with iso)
44
Q

describe coronary steal

A

path of least resistance – in the case of stenotic coronary arteries, a general signal for coronary vasodilation is expressed to get more blood through the stenotic vessels. however, the signal is not isolated to the stenotic vessels, and the clear vessels dilate as well. the stenotic vessels will continue to see decreased flow as the blood moves along the path of lease resistance

45
Q

which agents sensitive cardiac muscle to arrhythmias?

A

halothane (sensitized cardiac muscle to epi) and enflurane

46
Q

how is minute ventilation affected by volatile agents? PaCO2?

A

overall decrease in minute ventilation –decreased tidal volumes but less than compensatory increase in RR (dose dependent) – rapid, shallow breathing that causes increased PaCO2

47
Q

what is the theorized ventilatory target of volatile agents?

A

theorized that agents directly inhibit medullary ventilitory center

48
Q

at 1.5-2 MAC, which agents produce apnea?

A

des and sevo

49
Q

what chemoreceptor do volatile agents produce a ventilatory effect on?

A

carotid bodies – agents decrease the ventilatory response to hypoxemia

50
Q

differentiate between agents in relation to airway resistance

A
  • all volatiles (except desflurane) produce a decrease in airway resistance (bronchodilation)
  • NO des for asthmatics due to increased airway resistance
51
Q

how do volatiles affect FRC?

A

overall decrease in FRC

52
Q

what effects do volatile anesthetics have on the renal system? (4)

A

agents do not have direct affect on renal system – effect is due to decreased MAP, SVR, myocardial function

  • decreased renal blood flow (due to decreased arterial pressure, SVR, myocardial function)
  • decreased GFR
  • decreased urine output
  • nephrotoxicity
53
Q

what effects do volatile anesthetics have on the hepatic system? (3)

A

agents do not have direct affect on renal system – effect is due to decreased MAP, SVR, myocardial function

  • decreased hepatic blood flow
  • decreased hepatic clearance
  • hepatic toxicity
54
Q

how are uterine smooth muscle contractility and blood flow affected by volatile agents?

A
  • decreases uterine smooth muscle contractility and blood flow, which could be helpful when removing retained placenta, but could increase blood loss after delivery (floppy uterus) when uterine fails to fully contract fully
55
Q

are there any deleterious effects to the fetus when inhaled anesthetics are delivered to pregnant women?

A

no. although inhaled anesthetics can cross the placenta an be delivered to the baby, the baby breaths them off

56
Q

what effects do volatile anesthetics have on skeletal muscle?

A
  • ether derived drugs (iso, sevo, des) produce muscle relaxation
  • nitrous oxide does not – may produce muscle rigidity
57
Q

how do volatile agents affect temperature?

A
  • lowers the core temp set point at which thermoregulatory vasoconstriction is activated
  • vasodilation redistributes blood flow from central to peripheral compartments
  • metabolic oxygen consumption is decreased, which decreases heat generation
58
Q

which volatiles trigger malignant hyperthermia? which is most/ least potent?

A
  • all volatiles trigger MH in genetically susceptible pts
  • halothane is most potent trigger
  • N2O is very weak trigger, if a trigger at all
59
Q

describe the nephrotoxic effect of inhaled agents and how we prevent it

A

*volatiles (specifically sevoflurane) can interact with CO2 absorbers to produce Compound A – shown to be a nephrotoxin in rates
( higher levels in baralyme vs. soda lime)
* flows > 2L/min will prevent formation of Compound A

60
Q

under what circumstances do you risk carbon monxide poisoning when using inhaled agents?

A
  • volatiles + bases in dry desiccated CO2 absorber
61
Q

which volatile has the following characteristics?

  • non-irritating
  • CV changes
  • high potency
  • thymol preservative
  • bronchodilator
  • metabolized up to 20%
A

halothane

* high metabolization responsible for halothane related hepatitis

62
Q

which volatile has the following characteristics?

  • highly potent
  • AW irritant
  • minimal metabolism – 0.2%
  • no toxic issues
  • minimal CV changes at 1 MAC
  • coronary vasodilator
  • great for neuro cases (2 MAC = isoelectric EEG)
A

isoflurane

* takes too long to wake up – more soluble

63
Q

which volatile has the following characteristics?

  • pungent – AW irritant (avoid with reactive AWs)
  • decreased potency (relative – can run at low flows and maintain high PA)
  • lowest volatile blood gas coefficient (0.47)
  • special vaporizers
  • easily titratable
  • carbon monoxide formation in desiccated CO2 absorbers
  • prompt recovery
A

desflurane

64
Q

which volatile has the following characteristics?

  • least AW irritant – minimal odor
  • good for inhalation induction
  • metabolized 2-5% (compound A formation leading to renal tubular injury)
  • prompt recovery (not as quick as des)
  • low flows for 2 MAC hours
A

sevoflurane

65
Q

which volatile has the following characteristics?

  • sweet smelling
  • highly insoluble
  • decreases MAC requirements of other gases in concert
  • little side effects
  • increased pulmonary vascular resistance/cerebral metabolic oxygen requirements
  • ANALGESIC EFFECTS
  • increased PONV
  • MAC > 100%
  • diffusion hypoxia
  • airspace expansion – no laparoscopic, ear, eye surgeries
A

nitrous oxide

ANESTHESIA PHARM 2 (4 decks)

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