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anesthesia pharm II > inhalational agents: individual agents > Flashcards

inhalational agents: individual agents Flashcards

1
Q

when was halothane introduced?

A

1956

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2
Q

what are the properties of halothane?

A
  • blood:gas- 2.4
  • MAC- 0.76%
  • MAC awake- 55% of MAC
  • MW 197.4
  • vapor pressure- 244 torr at 20 C
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3
Q

what is the chemical name of halothane?

A

2-bromo-2-chloro-1, 1, 1,-trifluoroethane

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4
Q

describe halothane

A
  • sweet, non-pungent odor
  • nonflammable
  • stable in soda lime, but decomposes rubber products and most metals
  • requires storage in dark bottles and preservative, thymol, to prevent spontaneous oxidative decomposition
  • breaks down to hydrochloric acid, hydrobromic acid, chloride, bromide, and phosgene
  • thymol remaining in vaporizer after vaporization can cause vaporizer turnstiles or temp compensating devices to malfunction (high flows to flush out)
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5
Q

what are cardiac effects of halothane?

A
  • dose dependent myocardial contractility depression
  • decreased CO and BP
  • 2 MAC causes 50% drop in BP and CO
  • slow conduction through AV node to cause junctional rhythms, wandering pacemaker, bradycardia
  • inhibits baroreceptor reflex (no reflex tachycardia w/ drop in BP)
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6
Q

how does halothane cause myocardial depression?

A

interferes w/ Na-Ca exchange and intracellular Ca utilization
*depression accentuated by beta blocking agent, propranolol, and calcium channel blockers

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7
Q

if halothane is combined with aminophylline, what results?

A

serious ventricular arrhythmias

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8
Q

how does halothane effect myocardium’s response to catecholamines?

A
  • sensitizes the myocardium to catecholamines

* *hypercarbia enhances the sensitization

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9
Q

what is the maximum dose of epinephrine safe to use w/ halothane?

A
  • adults: 1.5 mcg/kg subq
  • add lidocaine 0.5% doubles max dose to 3 mcg/kg subq
  • children: 7.8-10 mcg/kg (w/ and w/o lidocaine)
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10
Q

what are respiratory effects of halothane?

A
  • excellent bronchodilator; reverses asthma-induced bronchospasm (best according to M&M; probably no difference from sevo)
  • works by inhibiting intracellular calcium mobilization
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11
Q

what are CNS effects of halothane?

A
  • direct cerebral vasodilation
  • cerebral autoregulation is attenuated
  • *must hyperventilate prior to initiation of halothane
  • *at 1.1 MAC and MAP of 80, halothane increases CBF by 190% (more than iso)
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12
Q

describe halothane hepatitis

A
  • no clear mechanism
  • possibly: antibody that binds to hepatocytes previously exposed to halothane
  • hepatotoxic metabolites are produced in hypoxic situation (enzyme induction), immune response, allergic reaction, familial factors
  • this antibody response may involve liver microsomal proteins that have been modified by trifluoroacetic acid as the triggering agents
  • incidence 1 in 35,000 fatal, hepatic necrosis (1 in 10,000 jaundice)
  • hepatitis d/t other inhaled agents only 1 in 1 million
  • incidence is higher if halothane exposure repeats within 28 days
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13
Q

what are risk factors of halothane hepatitis?

A
  • liver hypoxia (causes reductive metabolism v. oxidative)
  • sepsis
  • obesity
  • age over 40 y/o
  • female
  • enhanced metabolism/induced enzymes (smokers, alcoholics, poly-pharmacy pts.)
  • rarely reported in prepubescent children, even w/ preexisting liver disease
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14
Q

what are the effects of halothane on hematology?

A

-like sevo, may cause a decrease in platelet aggregation and increases in bleeding time

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15
Q

when was isoflurane introduced?

A

1981

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16
Q

what are the properties of isoflurane?

A
  • blood:gas- 1.4
  • MAC- 1.17%
  • MAC awake- 38% of MAC
  • MW- 184
  • vapor pressure 240 torr at 20 C
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17
Q

describe isoflurane

A
  • pungent, ether-type smell
  • isomer of enflurane
  • stable, nonflammable
  • no preservative necessary
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18
Q

what are cardiac effects of isoflurane?

A
  • minimal myocardial depression (less than halothane); decreased O2 demand more in heart than other organs
  • CO preserved by increased HR r/t baroreflexes (also partially preserved) (CO not affected by 1-1.8 MAC iso)
  • SV decreases, but CO remains nearly constant d/t compensation
  • rapid increase in concentration causes increases in HR, BP, and norepinephrine (more in young, healthy pt.)
  • heart remains efficient even up to 1.9 MAC
  • mild beta stimulation causes vasodilation, decreased SVR and BP
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19
Q

what are the effects of isoflurane on coronary artery perfusion?

A
  • decreases coronary vascular resistance w/ coronary blood flow increased or unchanged
  • unlike NTG which dilates larger vessels taking blood flow away from smaller areas needing it, isoflurane dilates small endocardial coronary arteries within the heart muscle
  • coronary artery steal: w/ studies that suggest the steal, MAP fell significantly (less than 60) and other suggest it doesn’t occur
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20
Q

how does isoflurane effect blood pressure?

A
  • BP is decreased based on dose; this is mainly d/t SVR reduction
  • hypovolemic pts. may not tolerate this reduction (trauma)
  • carotid sinus baroreceptor reflex is maintained at 1 MAC, but depressed at 2 MAC
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21
Q

describe respiratory effects of isoflurane

A
  • causes greater respiratory depression than halothane
  • tachypnea is less pronounced resulting in enhanced reduction in Vm (will usu. have decreased Vt compensated by increased RR)
  • pungent and irritating to some airway; however, overall good bronchodilator (not as good as halothane)
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22
Q

what are CNS effects of isoflurane?

A
  • greater than 1 MAC, increases CBF and ICP
  • hyperventilation that accompanies the introduction of isoflurane can minimize effect on ICP
  • when isoflurane is used for deliberate hypotension, it decreases cerebral O2 demand
  • At 2 MAC, isoelectric EEG; provides brain protection during episodes of cerebral ischemia
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23
Q

describe hepatic effects of isoflurane

A
  • hepatic oxygenation better maintained b/c hepatic artery perfusion and hepatic venous oxygen saturation are preserved
  • isoflurane metabolized to fluoride ions, trifluoroacetic acid (halothane hepatitis), and formic acid
  • no real concerns for inorganic fluoride levels
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24
Q

when was desflurane introduced?

A

1992

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25
Q

what are properties of desflurane

A
  • blood:gas- 0.42
  • MAC- 6.6%
  • MAC awake- 34%
  • MW- 168
  • boiling point: 22.8 degrees C (73 degrees F)
  • vapor pressure: 669 torr at 20 degrees C
  • boiling point significantly different from other agents (48-58 C)
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26
Q

what is the chemical name for isoflurane?

A

1-chloro-2,2,2-trifluoroethyl-difluoromethyl-ether

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27
Q

what is the chemical name for desflurane?

A

1-fluoro-2,2,2-trifluoroethyl-difluoromethyl-ether

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28
Q

describe desflurane

A
  • differs from isoflurane only in the substitution of a fluorine atom for a chlorine atom on the alpha ethyl carbon
  • low boiling point, high vapor pressure requires temp controlled vaporizer and special bottle to prevent vaporization during pouring; vaporizer heats liquid to form gas which is blended w/ diluent gas flow
  • stable in MOIST absorbent (dry absorbent causes CO)
  • requires no preservatives
  • pungent
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29
Q

what is the result of increased fluorination from isoflurane to desflurane?

A
  • increased vapor pressure
  • enhanced molecular stability
  • decreased potency
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30
Q

what are the effects of dry CO2 absorbent on desflurane?

A

degradation of desflurane into carbon monoxide

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31
Q

what are the effects of desflurane’s pungents odor on airway?

A
  • increased airway irritation
  • increased salivation
  • breath holding
  • coughing
  • laryngospasm
  • w/ concentration greater than 6% on induction
  • avoid in smokers w/ reactive airways
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32
Q

how does the decreased potency of desflurane affect its MAC?

A
  • MAC changes w/ age, but d/t its decreased potency, desflurane MAC changes are much larger
  • 0.6-0.7 yrs.: 9.96%
  • 25 yrs.: 7.25%
  • 36-49 yrs: 6.0%
  • 65 yrs.: 5.17%
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33
Q

what is the fat:gas solubility of desflurane and what is the significance?

A
  • 13 compared to 70 for isoflurane

* does not like to be stored in fat, so good use w/ obese (esp. w/ sleep apnea) if cases are longer

34
Q

what is the significance of desflurane’s low blood:gas solubility?

A
  • blood:gas solubility of 0.42, very similar to N2O of 0.46
  • more rapid increase and decrease in alveolar concentration w/ lower soluble agents
  • faster recovery
  • wake up times approx. 50% faster than w/ isoflurane
35
Q

describe desflurane effect on heart rate

A
  • rapid increase in concentration above 6% can cause sympathetic stimulation w/ increased HR and BP
  • can double HR and BP w/ change from 4% to 8% in less than one minute
  • most commonly seen in young, healthy pts. w/ little opioid (max increases inverse w/ age; elderly, decreased change in HR but see increased change in BP)
  • occurs both w/ N2O and w/o
  • returns to normal with 5 minutes (if go back don’t and increase % fast again, wont see effect again)
  • beta blockers may block this effect
  • caution w/ CAD pts.
36
Q

what can help limit the change in HR and BP w/ desflurane?

A
  • fentanyl 1.5 mcg/kg prior to increasing concentration
  • don’t exceed 6%
  • increase (even above 6%) slowly minimizes changes
  • alfentanil, sufentanil, clonidine, beta blockers
  • esmolol affects the increase in HR, but doesn’t change increase in BP
  • lidocaine 1.5 mg/kg minimizes HR response, but not BP response
  • propofol and N2O have no effect
37
Q

how does desflurane effect SVR?

A

-decreases, but to lesser extent than w/ isoflurane (has a bigger increase in NE)

38
Q

how does desflurane effect coronary vascular resistance?

A
  • decreased resistance to coronary blood flow

- redistribution (coronary steal) not seen w/ CAD present

39
Q

what are respiratory effects of desflurane?

A
  • respiratory depression similar to isoflurane up to 1.66 MAC of desflurane
  • HPV preserved as it is w/ sevoflurane and isoflurane
40
Q

what are neuromuscular effects of desflurane?

A
  • causes fade w/ tetanus at 3% to 12%
  • potentiated pancuronium, vecuronium, rocuronium, and SCh in a dose dependent manner (steroid class non-depolarizers)
  • dose dependent: increased concentration, increased potentiation
41
Q

what are CNS effects of desflurane?

A
  • EEG changes similar w/ isoflurane
  • burst suppression at 1.24 MAC
  • no seizure activity
  • cerebral blood flow similar to isoflurane during 1 and 1.5 MAC
  • increases CBF and ICP in normocarbic, normotensive pt.
  • consider use during deliberate hypotension d/t rapid titratibility and reduction of CMRO2 and CPP
42
Q

describe metabolism of desflurane

A
  • least metabolized at 0.02%
  • minute amount of trifluoroacetic acid produced
  • no increase in serum inorganic fluoride
43
Q

when was sevoflurane introduced?

A
  • 1990 (Japan)

- 1995 (US)

44
Q

what are the properties of sevoflurane?

A
  • blood:gas- 0.69
  • MAC- 1.8%
  • MAC awake- 34%
  • MW- 200
  • vapor pressure- 170 torr at 20 C (lowest)
  • MAC at 0.6 yr.-25yrs: 2.5-2.6%
45
Q

what is the chemical name of sevoflurane?

A

Fluoromethyl-2,2,2 trifluoro-1-(trifluoromethyl) ethyl ether

46
Q

describe sevoflurane

A
  • nonpungent, sweet smelling
  • low solubility (more than des) blood:gas- 0.69, fat:gas 37
  • unstable
47
Q

describe how sevoflurane is unstable

A
  • can spontaneously degrade, must have water added as a preservative
  • reactive w/ CO2 absorbent to produce compound A
  • potential for fire w/ dry absorbent
  • can degrade to hydrogen fluoride w/ reaction w/ glass bottle packaging, anesthesia equipment and manufacturing impurities (water added and bottles changed to plastic)
  • hydrogen fluoride can cause acid burns to lungs and mucosa
48
Q

what is done to prevent effects of compound A

A
  • minimum of 1 L/min flow up to 2 MAC hrs
  • greater than 2 MAC hrs. use no less than 2 l/min
  • increased flow decreases CO2 being rebreathed and exposed to absorbent and keeps temp down
49
Q

describe effects of sevoflurane’s solubility

A
  • shorter cases, quicker emergence (similar to des)

- longer cases seems to act more like iso

50
Q

how does sevoflurane effect myocardium and HR?

A
  • myocardial depression comparable to isoflurane at equal MAC concentration (protectant effect; decreases work and O2 consumption)
  • rarely may see bradycardia; treat by decreasing concentration
  • prolonged QT interval; use w/ caution w/ pts. w/ previously prolonged QT (leads to torsades)
51
Q

what are the effects of sevoflurane on SVR?

A
  • reduces SVR in slightly less magnitude than isoflurane
  • different mechanism than iso: reduces resistance through the aortic arch (arterioles at higher concentrations and abruptly)
  • isoflurane reduces arteriolar resistance gradually and dose dependently
52
Q

what is the effect of sevoflurane on baroreflex?

A

-preserved to greater extent than w/ other agents

53
Q

what are effects of sevoflurane on respiratory?

A
  • bronchodilator
  • Stoelting states it causes least degree of airway irritation among available agents
  • good for smokers, irritable airways, COPD, etc.
54
Q

how does sevoflurane compare to halothane for inhalation inductions?

A
  • slightly faster (least soluble)
  • less pt. movement
  • quicker onset of immobility
  • fewer airway problems
  • some studies contradict
  • at high concentrations, sevo causes less myocardial depression than halothane
55
Q

describe sevoflurane effects during an inhalation induction on a healthy, unpremedicated adult

A
  • given capacity breaths of up to 7% sevo
  • loss of lash reflex in 1 min
  • acceptance of LMA in 1.7 min
  • laryngoscopy, intubation in 4.7 min
  • capacity breaths: asked to take big, deep breaths and blow all out (decreasing FRC by decreasing ERV) then take big vital capacity breaths to fill alveoli w/ sevo
56
Q

how does sevo effect HPV?

A

preserved as with des and iso

57
Q

what are neuromuscular effects of sevoflurane?

A
  • similar to other agents, enhanced intensity and duration of NMB
  • may prolong duration of rocuronium longer than isoflurane (but less than des)
58
Q

what are CNS effects of sevoflurane?

A
  • autoregulation preserved up to 1.5 MAC
  • cerebral vasodilation similar to that w/ isoflurane
  • EEG may have evidence of seizure activity (7% concentration)
59
Q

what are the effects of sevoflurane on platelet aggregation?

A
  • inhibited more strongly than w/ halothane, d/t the suppression of arachadonic acid, probably d/t inhibition of cyclooxygenase
  • not clinically evident
60
Q

describe metabolism of sevoflurane

A
  • 5-8% metabolized by C-P450 to produce inorganic fluoride
  • levels of serum fluoride greater than 50 mcm/L in 7% of pts., but no evidence of clinically significant renal dysfunction (no increase in BUN or creatinine)
  • metabolized by liver and some kidney; if just kidney would probably see damage
  • different from other agents since no trifluoroacetic acid produced
61
Q

when was nitrous oxide introduced

A

discovered by Priestly in 1772; used for analgesia/anesthesia in 1840s

62
Q

what are the properties of N2O?

A
  • blood:gas- 0.46
  • MAC- 104%
  • MAC awake- 64% of MAC
  • MW- 44
  • critical temp- 35.5 C
  • vapor pressure- gas form at 20 degree C
63
Q

what is the chemical structure of N2O?

A

N=N=O

*only inorganic agent (no carbon)

64
Q

describe N2O

A
  • inorganic
  • low molecular weight
  • odorless (sweet smelling)
  • low solubility; equilibrates rapidly (inspired 70% achieves 90% equilibration in 15 min)
  • low potency (cant get to MAC unless in hyperbaric chamber)
  • nonflammable; but supports combustion
  • N2O stored in a liquid-gas equilibrium in blue cylinder
  • 745 psi liquid in equilibrium w/ gas
  • stable in soda lime
  • impurities in N2O: N2, NO, NO2, water vapor
  • does not combine w/ hgb, carried in solution in blood
  • induces hepatic enzymes
65
Q

describe metabolism of N2O

A
  • less than 0.004% metabolized by intestinal flora (pseudomonas)
  • not metabolized by human body (liver/kidneys)
66
Q

what are cardiac effects of N2O?

A
  • myocardial depression directly
  • young healthy: sympathetic stimulation and increased SVR d/t increased endogenous catecholamines
  • increased PVR, esp. if PVR already slightly elevated (pulm. HTN, congenital heart w/ shunts) *avoid N2O
  • preexisting CV disease (LV dysfunction), myocardial depression enhanced (less than MAC equivalent of potent agents) *avoid
  • *although myocardial depressant effects directly, often see increased BP, CO, and HR d/t stimulation of catecholamines
67
Q

what are respiratory effects of N2O?

A
  • at concentrations less than 50%, no increase in PaCO2
  • increases RR more than other agents (maintains Vm better than other agents)
  • response to hypoxia is reduced w/ even small amount of N2O (like potent agents, not dose dependent)
68
Q

what are neuromuscular effects of N2O?

A
  • does not potentiate NMB

- at high concentrations, causes skeletal muscle rigidity

69
Q

what are CNS effects of N2O?

A
  • produces analgesia and amnesia
  • analgesia d/t increase in enkephalins produced
  • nystagmus occurs w/ 50% nitrous
  • cerebral vasodilation less than potent agents (helps to decrease increase in CBF w/ other agents)
  • increases CMRO2
70
Q

describe GI effects of N2O

A
  • gas in the bowel will increase in size w/ the use of N2O

- increased incidence of PONV

71
Q

what are uterine/reproductive effects of N2O?

A
  • does not effect uterine tone

- weak teratogen when used in high concentrations for prolonged time frame (just don’t use w/ pregnant women)

72
Q

describe N2O effect on vitamin B12 dependent enzymes

A
  • N2O inhibits methionine synthetase, which is necessary for myelin formation, and thymidylate synthetase, which is necessary for DNA synthesis
  • prolonged exposure can result in bone marrow depression- megaloblastic anemia, and even neurological deficiencies- peripheral neuropathies and pernicious anemia
73
Q

how long after exposure to N2O are critically ill pts. ability to synthesize DNA decreased?

A

up to 6 days after exposure

74
Q

w/ one study, what did the results show d/t no use of N2O?

A
  • decreased PONV
  • decreased wound infection
  • decreased fever
  • decreased pneumonia
  • decreased atelectasis
75
Q

describe the diffusion of N2O

A
  • 34x more soluble than nitrogen in the blood
  • absorbed into air-filled spaces faster than nitrogen moves back into the blood causing expansion of the “bubble”
  • no N2O use w/ GI, pneumothorax, tympanoplasty, CVL placements, ect.
76
Q

what are the immunologic effects of N2O?

A
  • affects chemotaxis and motility of polymorphonuclear leukocytes for phagocytosis, which is necessary for the inflammatory response to infection
  • decreased wound healing and increased infection
77
Q

describe diffusion hypoxia associated w/ N2O

A
  • Nitrous is so insoluble that it returns to alveoli so rapidly in such volumes that it dilutes other gases including O2
  • the hypoxia that can occur can be avoided if supplemental O2 is administered for the first 5-10 min after N2O is discontinued
78
Q

describe the 2nd gas effect associated w/ N2O

A
  • administering high concentrations of N2O will cause an increase of the alveolar concentration of a second gas
  • Fick’s Law
  • theoretic
79
Q

what caution should be taken with N2O in regards to O2?

A
  • when N2O is utilized, the O2 concentration must be decreased
  • care must be taken to avoid hypoxia, esp. in special populations
  • C-section: common practice to deliver no more than 50% N2O prior to the delivery of the infant
80
Q

what are occupational risks of N2O?

A
  • with no scavenging, reduced fertility

* w/ scavenging, no difference in fertility and birth defects w/ general population

anesthesia pharm II (5 decks)

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