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Pharm I > Inhaled Anesthetics > Flashcards

Inhaled Anesthetics Flashcards

1
Q

Nitrous Oxide (chart)

A

Molecular weight: 44
Odor: sweet
Blood:gas partition coefficient: 0.46
MAC c 100 O2: 104

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2
Q

Halothane (chart)

A 
Molecular Weight: 197
Boiling Point: 50.2
Vapor Pressure: 244
Odor: Organic
Not stable in soda lime 
Requires a preservative
Blood: gas partition coefficient - 2.54 (Most soluble in blood)
MAC c 100% O2: 0.75
MAC c 60-70% N2O: 0.29
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3
Q

Enflurane (chart)

A 
Molecular Weight: 184
Boiling Point: 56.5
Vapor Pressure: 172
Odor: Ethereal
Blood:gas partition coefficient: 1.9
MAC c 100% O2: 1.63
MAC c 60-70% N20: 0.57
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4
Q

Isoflurane (chart)

A 
Molecular weight: 184
Boiling Point: 48.5
Vapor Pressure: 240
Odor: Ethereal
Blood:gas partition coefficient - 1.46
MAC c 100% O2: 1.17
MAC c 60-70% Nitrous: 0.5
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5
Q

Desflurane (chart)

A 
Molecular Weight: 168
Boiling Point: 22.8
Vapor Pressure: 669
Odor: Ethereal 
Blood:gas partition coefficient 0 0.42
MAC c 100% O2: 6.6
MAC c 60-70% N2O: 2.83
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6
Q

Sevoflurane (chart)

A 
Molecular Weight: 200
Boiling Point: 58.5
Vapor Pressure: 170
Odor: Ethereal
Not stable in soda lime
Blood:gas partition coefficient - 0.69
MAC c 100% O2: 1.8
MAC c 60-70% N2O: 0.66
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7
Q

Partial pressure

A

Dalton’s Law is the total pressures of a mixture of gases is the sum of the pressures each gas would exert if it were present alone

  • We want to get inhaled anesthetics to the brain
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8
Q

Minute Ventilation

A

Sum of all exhaled gas volume in 1 minute
Minute ventilation =Tidal volume x Breaths/min
= 5 L/min

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9
Q

Alveolar Ventilation

A

Volume of inspired gases actually taking part in gas exchange in 1 minute

PCO2

(Tidal Volume - Dead Space) x Breaths per min

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10
Q

Dead Space

A

Basically any volume of inspired breath which dose not enter the gas exchange areas of the lungs is dead space.

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11
Q

Anatomic Dead Space

A

The breath entering the mouth, pharynx, and tracheobronchial tree but does not enter into the alveoli

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12
Q

Alveolar Dead Space

A

the portion of a breath that enters alveoli which are ventilated but not perfused

AKA West Zone’s 1

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13
Q

Alveolar Partial Pressure (PA)

A

determined by input (delivery) of inhaled anesthetic into alveoli minus uptake (loss) of drug from alveoli into arterial blood

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14
Q

Determinants of PA

A 
alveolar ventilation
anesthetic breathing system
solubility
CO
Alveolar to Venous Partial Pressure Differences
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15
Q

Concentration Effect

A

The higher the inspired concentration of anesthetic agent, the more rapid the relative rise in alveolar concentration of the agent

Machine -> alveoli -> blood -> brain

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16
Q

Second Gas Effect

A

The ability of the large volume uptake of one gas (first gas) to accelerate

We use Nitrous to do this

More applicable to a gas with a higher blood:gas partition coefficient

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17
Q

Partition coefficient

A

reflects the relative capacity of each phase to accept anesthetic; is temperature dependent

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18
Q

Blood:gas solubility

A
  • states how soluble an anesthetic is in blood
  • inversely related to induction time
  • less soluble the gas is in blood = quicker induction of anesthesia
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19
Q

Tissue:Blood Partition Coefficient

A

Determines uptake of anesthetic into tissues and time necessary for equilibration of tissues with Pa

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20
Q

Tissue:Gas

A

Concerns lean tissues (muscles, vessel rich organs) affinity for a given anesthetic agent

Predicts emergence times from anesthesia

Lower ratios indicate the gas is relatively insoluble in tissues thus emergence will be more rapid

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21
Q

Stage I of Anesthesia

A

Begins with induction of anesthesia
Ends with loss of consciousness (no eye-lid reflex)
Still can sense pain

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22
Q

Stage II of Anesthesia

A

Delirium Excitement
Uninhibited excitation
Pupils dilated, divergent gaze

Potentially dangerous response to noxious stimuli:
   Breath holding
   Muscular rigidity
   Vomiting
   Laryngospasm
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23
Q

Stage III of Anesthesia

A

Surgical Anesthesia
Centralized gaze with constriction of pupils
Regular respirations

Anesthesia depth is sufficient for noxious stimuli when the noxious stimuli dose not cause increase sympathetic response

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24
Q

Stage IV of Anesthesia

A

Stay away from this stage. It is TOO DEEP

  • Apnea
  • Non reactive dilated pupils
  • Hypotension resulting in complete CV collapse if not monitored closely
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25
Q

Cardiac Output’s effect on Anesthesia

A
  • carries away either more or less anesthetic from alveoli

Increased: more rapid uptake—slowed induction
Decreased: speeds rate of rise in PA—less uptake—quicker induction

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26
Q

Recovery from Anesthesia

A
  • In soluble anesthestics: Duration of administration prolongs emergence
  • Exhaled gases will be rebreathed unless fresh gas flow rate is increased
  • rate of decrease in Pbr is relative to the decrease in PA
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27
Q

EEG Effects and Inhaled Anesthetics

A

MAC < 0.4 = same in all gases

Equal to 0.4 MAC = voltage shifts from posterior to anterior portions of the brain

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28
Q

Seizure Activity and Inhaled Anesthetics

A
  • Enflurane has high voltages and frequencies (most similar to seizure)
  • SUPPRESS convulsant Properties: Iso-, des-, sevo
  • N2O: increased motor activity; withdrawal in animals may indicate acute dependence
29
Q

Cerebral Blood Flow

A

Volatile anesthetics > 0.6 MAC produce cerebral vasodilation, decreased cerebral vascular resistance, dose-dependent increase

At 1.1 MAC: halothane > enflurane > isoflurane = Desflurane

N2O: increases

Increase occurs within minutes of administration of anesthetic

30
Q

Cerebral Metabolic O2 Requirements

A

Dose dependent decrease

Isoflurane = desflurane = sevoflurane > halothane

Decreases metabolic requirement– decreased CO2 production -> vasoconstriction that decreases CBF

31
Q

Cerebral Protection

A

Isoflurane shows protection from ischemia when used in carotid endarterectomy

32
Q

Effects on MAP

A

Decrease: Sevo, Iso, Des, (Decrease SVR)
Decrease: Halo decreases contractility

NO change: Nitrous

33
Q

Effects on HR

A

Increase: Des > Iso > Sevo (Sevo must be MAC > 1.5)
No change: Halothane

Des has highest increase

34
Q

Effects on CO/SV

A

Left SV : decreases with ALL anesthetics
Slight increase: Nitrous
Decrease: Halothane (dose dependent)
No change: sevo, des, iso

35
Q

Effects on SVR

A

Decrease: Iso > Des >Sevo
No change: Halothane, Nitrous

Iso has the most affect

36
Q

Effects on Pulmonary Vascular Resistance

A

Volatile Anesthetics: little to no effect

Increases: Nitrous (exaggerated in Pulm HTN, neonates and congenital heart disease)

37
Q

Cardiac Dysrhythmias

A
  • Anesthesia decreases the dose of Epi needed to potentiate produce Ventricular dysrhythmias
  • Effect is greatest with Halothane

Epi Dose: 6 mg/kg with Iso, Des, Sevo

38
Q

Effects on Coronary Blood Flow

A

Volatile anesthetics cause coronary vasodilation

39
Q

Ischemic Preconditioning (IPC)

A
  • Brief episodes of myocardial ischemia that occur before a longer period of ischemia provide protection against myocardial dysfunction and necrosis
    -protective mechanism against tissue injury
    -Occurs after 5 minutes of ischemia; effect lasts for 1-2 hours, disappears and reoccurs at 24 hours
    Second or late window may last as long as 3 day
40
Q

airway resistance

A

Anesthetics produce decreased airway resistance after antigen induced bronchoconstriction
Halothane—direct relaxing effects on airway smooth muscle (decreases vagal nerve traffic from CNS)

41
Q

Pattern of Breathing

A
  • dose dependent increase in frequency of breathing
  • tidal volume decreases with increased frequency—rapid and shallow breathing pattern
  • decreased minute ventilation, increased PaCO2 -> respiratory acidosis
  • isoflurane increases frequency of breathing at concentrations up to 1 MAC, then no further increase occurs
42
Q

Pulmonary Vascular Resistance

A

Nitrous causes a modest increase in the normal pt.

Increases may be clinically significant in the pt with pre-existing Pulmonary HTN

Volatile Agents decrease
Des which increases at a MAC of 1.6

43
Q

Hypoxic Pulmonary Vasoconstriction

A
  • The ability of the pulmonary vasculature to constrict in response to regional hypoxemia.
  • Mild by Volatile Anesthetics
  • Nitrous inhibits this, so it is avoided in thoracic surgery
44
Q

Hepatic Blood Flow

A

Iso @ 1.5%: dilates portal vein -> increased hepatic oxygenation
Halothane: vasoconstrictor

45
Q

LFTs

A
  • Transient increase with Des and enflurane

- surgical stimulation increases all

46
Q

Fluoride-Induced Nephrotoxicity

A

Polyuria, hypernatremia, hyperosmolarity,  serum creatinine, inability to concentrate urine

47
Q

Vinyl Halide Nephrotoxicity

A
  • CO2 absorbents (Baralyme, soda lime) react with sevoflurane and eliminate hydrogen fluoride from its isopropyl moiety to form breakdown products, including Compound A , a vinyl ether
  • Compound A is a dose dependent nephrotoxin in rats
  • Need to use at least 2L/minute fresh gas flow rate with sevoflurane to minimize concentration of Compound A that may accumulate in anesthesia breathing circuit
48
Q

Neuromuscular junction

A
  • Skeletal muscle relaxation with ether-derived fluorinated anesthetics
  • N2O—no relaxation, maybe rigidity
  • Ability to sustain contractions in response to continued stimulus is impaired with ether derivatives but not with halothane or N2O
  • Ether derivatives can cause dose dependent enhancement of NM blockers
49
Q

Malignant Hyperthermia

A
  • genetic predisposition (tested by muscle biopsy)
  • Halothane is highest trigger
  • acute disorder developing during or after GA
  • you have a constant leak of SR Ca++ through ryanodine receptor
  • Caused by: Volatile Anesthetics or Succinylcholine
50
Q

S/Sx of MH

A

Hypermetabolic state
Increased HR
Unexplained increase in End-Tidal Co2
-Respiratory and metabolic acidosis, rhabdomyolysis, arrhythmias, hyperkalemia and sudden cardiac arrest

Increased Temp is a LATE sign

51
Q

Treatment of MH

A
  1. notify MD as soon as you suspect it
  2. Stop triggering agents (gas)
  3. Hyperventilate c 100% O2 (Use fresh tank instead of circuit)
  4. abort procedure
  5. Give IV dantrolene
  6. Bicarb
  7. Cooling
  8. Insulin for Hyperkalemia
  9. Monitor core temp
  10. Monitor UO to prevent shock
52
Q

Nitrous Metabolism

A

Very little metabolism—mainly by anaerobic bacteria in GI tract
O2 concentration > 10% inhibits metabolism

53
Q

Halothane Metabolism

A
  • 15-20% metabolized by cytochrome P-450 enzymes
  • Oxidation with ample O2, reduction when PaO2 decreased
  • Oxidative metabolism produces trifluoroacetyl halide metabolite that may acetylate hepatic proteins resulting in formation of antibodies
  • Reductive metabolism in hepatocyte hypoxia produces inorganic fluoride (below level to produce nephrotoxicity)
54
Q

Enflurane Metabolism

A
  • 3% metabolized by cytochrome P-450 enzymes
  • Oxidative metabolism may produce fluoroacetylated hepatic protein-Ab complexes
  • Chemical stability, low solubility in tissues; most exhaled unchanged
  • Isoniazid increases nephrotoxic potential due to increased metabolism and defluorination
55
Q

Isoflurane Metabolism

A
  • 0.2% metabolized by cytochrome P-450 enzymes
  • Oxidative metabolism to trifluoroacetic acid; possibility of production of acetylated hepatic protein-Ab complexes
  • Chemical stability, low solubility; most exhaled unchanged
  • Metabolism, concentration of inorganic fluoride produced is less than with enflurane
56
Q

Desflurane Metabolism

A
  • 0.02% metabolized by cytochrome P-450 enzymes
  • Oxidative metabolism to trifluoroacetic acid; possibility of production of acetylated hepatic protein-Ab complexes
  • Chemical stability, low solubility; most excreted unchanged
57
Q

Metabolism of Sevoflurane

A
  • 5% metabolized by cytochrome P-450 enzymes
  • Oxidative metabolism—does not produce acetyl halides no possibility of hepatic protein-Ab complexes
  • Degraded by CO2 absorbents to potentially nephrotoxic Compound A (Baralyme > soda lime); amount of Compound A produced is less than the toxic level
  • Plasma fluoride concentration is higher after administration of sevoflurane than enflurane, but exposure of renal tubules to fluoride is limited because most elimination is through the lungs; hepatic production of fluoride may be less toxic than intrarenal production of fluoride
58
Q

Carbon Monoxide Toxicity

A
  • CO formation is a product of degradation of anesthetics with a CHF2 moiety by strong bases present in CO2 absorbents
    -Desflurane > enflurane > isoflurane
    -Halothane, sevoflurane have no vinyl group—no CO production
    -Increases intraoperative carboxyhemoglobin concentration
    -CO detection difficult because pulse oximetry can’t distinguish between carboxyhemoglobin and oxyhemoglobin
    =Delayed neurophysiological sequelae—cognitive defects, personality changes, gait disturbances—can occur up to 3-21 days later
59
Q

Factors that Increase the magnitude of Carbon Monoxide (CO) Production

A
  • Dryness of CO2 absorbent—hydration prevents
  • High temperature of absorbent—occurs during low fresh gas flows and/or increased metabolic production of CO2
  • Prolonged high fresh gas flows—contributes to dryness of absorbent
  • Type of absorbent (Baralyme > soda lime)
60
Q

CO2 Absorber fires

A
  • Sevoflurane reacts with desiccated CO2 absorbents to produce CO and flammable organic compounds (methanol, formaldehyde)
  • Reaction produces heat, which increases chemical reaction speed so that sevoflurane breaks down rapidly
  • Flammable metabolites can spontaneously combust at high temperatures
  • Most often associated with Baralyme
61
Q

Minimal Alveolar Concentration (MAC)

A
  • A MAC (or 1 MAC) is the % of anesthetic agent (gas) which ceases movement in response to noxious stimuli in 50% of patients
  • An increase to a MAC of 1.3 will prevent movement in ~95% of pts
  • no change in gender
  • increased in women with natural red hair presumably d/t mutations of melano-cortin-1 receptor gene and increased pheomelanin concentrations
62
Q

Nitrous Oxide (N20)

A
  • “laughing gas”
  • Noninflammable, odorless,
  • Low blood solubility -> rapid onset of action
  • Fast induction and recovery time
  • Low potency
  • Combine with opioids or volatile anesthetics to produce general anesthesia
  • Good analgesic effects (short lived; dissipates after ~ 20 min.), sedative effect persists after even after analgesic effect dissipates; minimal skeletal muscle relaxation
63
Q

Nitrous Oxide Side Effects

A
  • Post-operative—causes nausea and vomiting (controversial)
  • Within closed body cavities, N2O can increase the volume -> pneumothorax or increased pressure e.g. in sinuses
  • Inactivates Vit B12
64
Q

Halothane

A
  • Halogenated alkane
  • Clear, nonflammable liquid with sweet non-pungent odor
  • acceptable for inhalation induction
  • Intermediate blood solubility (intermittent onset), high potency, rapid onset and recovery
  • Stored in amber colored bottles; thymol added as preservative to prevent oxidative decomposition. Thymol can cause vaporizer to malfunction
  • Possibility of hepatotoxicity
65
Q

Enflurane

A

-Halogenated methyl ethyl ether
-Clear, nonflammable liquid; pungent odor
Intermediate blood solubility, high potency, intermediate onset and recovery
- Decreases threshold for seizures
- Oxidized in the liver to inorganic fluoride ions which can be nephrotoxic
-Used in cases where low seizure threshold is desirable such a electroconvulsive therapy

66
Q

Isoflurane

A
  • Halogenated methyl ethyl ether
  • Clear, nonflammable liquid; pungent odor
    Intermediate blood solubility, high potency, intermediate onset and recovery
  • Isomer of enflurane
    -Extreme physical stability; no preservative required. No deterioration during 5 years of storage, carbon dioxide absorbents, or sunlight
67
Q

Desflurane

A
  • Fluorinated methyl ethyl ether (fluorine substituted for Cl in isoflurane)
  • high vapor pressure, increased molecular stability, decreased potency
  • would boil at room temperature; is converted to gas in vaporizer and mixed with diluent fresh gas flow
  • Potency is 5-fold less than isoflurane
  • Pungent odor causes airway irritation, salivation, breath-holding, coughing, or laryngospasm when >6% is used in the awake patient
68
Q

Sevoflurane

A
  • Fluorinated methyl isopropyl ether
  • Vapor pressure resembles that of halothane and isoflurane permitting delivery of anesthetic with an unheated vaporizer
  • Non-pungent, minimal odor; least irritating to airways—acceptable for inhalation induction
  • blood:gas partition coefficient 0.69) prompt induction and recovery
69
Q

Xenon

A
  • Inert gas
    MAC 63 - 74% in humans; more potent than N2O (MAC 104%)
  • MAC is gender dependent being less in females
    Nonexplosive, non-pungent, odorless, unreactive, causes minimal cardiac depression
  • High cost: Needs more studies to prove morbidity and mortality with Xenon
    -Has lowest blood:gas coefficient of 0.115
    -Does have tendency of bubble expansion like nitrous
    -does not contribute to MH
    -Emergence is 2-3 times faster than nitrous or Sevo
    -Potent hypnotic and analgesic resulting in suppression of hemodynamic and catecholamine responses to surgical stimulation

Pharm I (1 decks)

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