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Anesthesia Pharm > Inhalation Agents (Dewan Part 5) > Flashcards

Inhalation Agents (Dewan Part 5) Flashcards

1
Q

Describe the difference between the immobilization function of inhaled agents versus the sedating effects

A

The immobilizing effect of inhaled anesthetics involves a site of action in the spinal cord, whereas sedation/hypnosis and amnesia involve supraspinal mechanisms

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2
Q

The potency of general anesthetics correlates with ____.

A

their solubility in oil, indicating the importance of their interaction with hydrophobic targets and cell membrane

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3
Q

General anesthetics act by ___

A

binding directly to amphiphilic cavities in proteins.

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4
Q

Volatile inhaled anesthetics enhance ___.

(Mechanism of Action)

A

inhibitory synaptic transmission in the following ways:

  • postsynaptically by potentiating ligand-gated ion channels activated by γ-aminobutyric acid (GABA) and glycine
  • extrasynaptically by enhancing GABA receptors and leak currents
  • presynaptically by enhancing basal GABA release.
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5
Q

What is the difference between volatile and non-volatile inhalational agents?

A

Their chemical properties

Non-volatile anesthetics have high vapor pressures and low boiling points, meaning they are in gas form at room temperature.

Whereas volatile anesthetics have low vapor pressures and high boiling points, meaning they are liquids at room temperature and so require vaporizers during administration.

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6
Q

Example of non-volatile gases

A

nitrous oxide (N2O)

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7
Q

Example of Volatile Gases

A

halothane, isoflurane, desflurane, sevoflurane

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8
Q

Inhaled anesthetics suppress ____.

A

excitatory synaptic transmission

  • presynaptically by reducing glutamate release (volatile agents)
  • postsynaptically by inhibiting excitatory ionotropic receptors activated by glutamate (gaseous agents).
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9
Q

General anesthetics cause a reduction in ___.

A

nerve transmission at synapses.

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10
Q

Volatile anesthetics primarily affect the function of ___.

A

ion channel and neurotransmitter receptor proteins in the membranes of nerve cells, which are lipid environments.

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11
Q

Inorganic agents (N2O) inhibit ___.

A

NMDA receptor (N methyl , N aspartate)

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12
Q

How does the spinal cord mediate immobility?

A

Inhibition of glutamate channels.

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13
Q

GABAa stimulation produces __.

A

supraspinal inhibition of transmission.

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14
Q

Inhalation Agents cause what effects?

A

dose dependent and reversible effects.

  • Loss of consciousness/amnesia/hynosis (hypocampus)
  • Analgesia (Spinal Thalamic tract)
  • Muscle relaxation
  • Immobility with stimulation (ventral horn)
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15
Q

Unconsciousness effect occurs from which area?

A

cerebral cortex, thalamus

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16
Q

Amnesia occurs from which area?

A

amygdala , hippocampus

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17
Q

Analgesia occurs from which area?

A

spinothalamic tract

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18
Q

Immobility occurs from which area?

A

spinal cord receptors

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19
Q

Guedel’s Stages of Anesthesia

A

I: Awake: amnesia, analgesia

II: Excitation * (stage two)

III: Surgical Anesthesia

IV: Overdose, lose life sustaining reflexes.

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20
Q

Describe Guedel’s Stage 1

A

Stage of Analgesia or disorientation

From the beginning of induction of anesthesia to loss of consciousness.

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21
Q

Describe Guedel’s Stage 2

A

Stage of Excitement or stage of delirium

  • From loss of consciousness to onset of automatic breathing.
  • Eyelash reflex disappears but other reflexes remain intact.
  • Coughing, vomitting, and struggling may occur.
  • Respirations can be irregular with breath-holding.
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22
Q

Describe Guedel’s Stage 3

A

Stage of Surgical Anesthesia: from onset of automatic respiration to respiratory paralysis. It is divided into four planes:

  • Plane 1- Eye reflex is lost, swallowing reflex disappears
  • Plane 2- Beginning of paralysis of intercostal muscles. Laryngeal reflex is lost although inflammation of the upper respiratory tract increases reflex irritability. Corneal reflex disappears. Secretion of tears increases (a useful sign of “light” anesthesia)
  • Plane 3- From beginning to completion of intercostal muscle paralysis. Diaphragmatic respiration persists but there is progressive intercostal paralysis.
  • Plane 4- Apnea
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23
Q

Describe Guedel’s Stage 4

A

From stoppage of respiration until death. Anesthetic overdose cause medullary paralysis with respiratory arrest and vasomotor collapse.

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24
Q

Anesthetic Neurotoxicity

A

Ongoing concern that early exposure to anesthetics can promote cognitive impairment later in life. Concern that exposure affects the development and elimination of synapses in the infant brain.

Volatile anesthetics have been shown to promote apoptosis by altering cellular calcium homeostatic mechanisms.

Anesthetic agents have also been suggested to contribute to tau protein hyperphosphorylation (associated with Alzheimer’s Disease).

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25
Q

Inhalational agents have been associated with ischemic pre-conditioning.

What is ischemic pre-conditioning?

A

Although inhalational agents have been suggested as contributing to neurotoxicity, they have also been shown to provide both neurological and cardiac protective effects against ischemia-reperfusion injury.

Ischemic preconditioning implies that a brief ischemic episode protects a cell from future, more pronounced ischemic events.

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26
Q

Who defined the concept of MAC?

A

Dr. Ted Eger

MAC is simply a measure of relative potency

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27
Q

What is MAC?

A

Minimum alveolar concentration

The MAC of an inhaled anesthetic is the alveolar concentration that prevents movement in 50% of patients in response to a standardized painful stimulus (surgical incision).

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28
Q

1.3 MAC of any volatile anesthetic has been found to ___

A

prevent movement in about 95% of patients

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29
Q

0.3-0.4 MAC is associated with ____

A

awakening from anesthesia (MAC awake) when the inhaled drug is the only agents maintaining anesthetic (a rare situation)

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30
Q

MAC is decreased by 6% for ___

A

every decade of age, regardless of volatile anesthetic

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31
Q

MAC is realtively unaffected by __

A

sex, length of surgery, thyroid function, or potassium level (but uptake increases over time)

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32
Q

What factors decrease MAC?

A
  • Age (Elderly)
  • Anemia
  • Hypothermia
  • Drugs (sedatives, narcotics, alpha agonists, lithium, local anesthetics)
  • Hypoxemia
  • Hyponatremia/hypercalcemia
  • Pregnancy
  • Acute use of alcohol/drugs except cocaine
  • Extreme hypercarbia
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33
Q

What factors increase MAC?

A
  • Youth
  • Hyperthermia
  • Hypernatremia
  • CNS Stimulants (Cocaine and Amphetamines)
  • Red hair (pheomelanin)
  • Chronic Alcohol
  • Ephedrine
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34
Q

Characteristics of Nitrous Oxide and class

A

NMDA receptor antagonist

Colorless, odorless, nonexplosive, nonflammable (but equally as capable as oxygen of combustion)

It can be kept at room temperature and ambient pressure. It can be kept as a liquid under pressure because its critical temperature lies above room temperature.

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35
Q

Cardiovascular Effects of Nitrous Oxide

A

stimulates the sympathetic nervous system

Slightly depresses myocardial contracility in vitro

arterial BP, CO and HR are relatively unchanged or slightly elevated due to stimulation of chatecholamines

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36
Q

Cerebral Effects of Nitrous Oxide

A

By increasing CBF and cerebral blood volume, NO produces a mild elevation of intracranial pressure.

Also increases cerebral oxygen consumption (CMRO2)

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37
Q

Concentrations of Nitrous Oxide below MAC may provide ___.

A

analgesia in dental durgery, labor, traumatic injury, and minor surgical procedures.

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38
Q

Neuromuscular and GI effects of Nitrous Oxide

A

Does not provide significant muscle relaxation. In fact, at high concentrations in hyperbaric chambers, NO causes skeletal muscle rigidity.

GI: Increases the risk of post-op nausea/vomiting as a result of activation of chemoreceptor trigger zone in the medulla.

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39
Q

Renal and Hepatic Effects of Nitrous Oxide

A

Renal: Decrease kidney blood flow by increasing renal vascular resistance which leads to a drop in GFR and urine output.

Liver: Hepatic blood flow probably falls but to a lesser extent than with the volatile agents.

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40
Q

How is nitrous oxide eliminated? Biotransformation?

A

During emergence, almost all nitrous oxide is eliminated by exhalation. A small amount diffuses through the skin.

Biotransformation is limited to less than 0.01% that undergoes reductive metabolism in the GI tract by anaerobic bacteria.

41
Q

What is unique about nitrous oxide and B12?

A

By irreversibly oxidizing the cobalt atom in vitamin B12, NO inhibits enzymes that are vitamin B12 dependent. These enzymes include methionine synthetase, which is necessary for myelin formation, and thymidylate synthetase, which is necessary for DNA synthesis.

42
Q

Prolonged exposure to anesthetic concentrations of nitrous oxide can result in ___.

A

Bone marrow depression (megaloblastic anemia) and even neurological deficiences (peripheral neuropathies).

altered immunological response to infection by affecting chemotaxis and motility of polumorphonuclear leukocytes

43
Q

Why and when is nitrous oxide avoided in pregnancy?

A

It’s avoided before the 3rd trimester due to its possible teratogenic effects

44
Q

Contraindications for administering nitrous oxide

A

venous or air embolism, pneumothorax, acute intestinal obstruction with bowel distention, intracranial air (pneumocephalus following dural closure or pneumocephalography), pulmonary air cysts, intraocular air bubbles, and tympanic membrane grafting.

Nitrous oxide is of limited value in patients requiring high inspired oxygen concentrations.

45
Q

What is Nitrous Oxide typically used with and why?

A

Since Nitrous oxide has a high MAC, it prevents its use as a complete general anesthetic, and is frequently used in combination with the more potent volatile agents.

46
Q

Nitrous oxide and the environment

A

It is an ozone-depleting gas with greenhouse effects

47
Q

Decreasing the concentration of nitrous oxide (increasing oxygen concentration) increases ___.

A

the concentration of a volatile anesthetic being used in combination (second-gas effect).

48
Q

Halothane class and general facts.

A

Halogenated alkane

The carbon-fluoride bond are responsible for its nonflammable and nonexplosive nature. Thymol preservative and amber-colored bottles retard spontaneous oxidative decomposition. Rarely used in United States.

49
Q

Cardiovascular effects of Halothane

A

Dose-dependent reduction of arterial blood pressure due to direct myocardial depression; Coronary blood flow decreases because of the drop in systemic arterial pressure.

Cardiac depression- from interference with sodium-calcium exchange and intracellular calcium utilization- causes an increase in right atrial pressure.

Halothane blunts the baroreceptor reflex. Slowing of SA node conduction may result in juntional rhythm or bradycardia.

50
Q

What drug interaction should you be mindful of with Halothane?

A

Halothane sensitizes the heart to the arrythmogenic effects of epinephrine, thus doses of epinephrine above 1.5 mcg/kg should be avoided.

51
Q

Respiratory effects of Halothane

A

Rapid, shallow breathing. The increased respiratory rate is not enough to counter the decreased tidal volume, so alveolar ventilation drops, and resting PaCO2 is elevated. Apneic threshold also rises.

Potent bronchodilator.

Halothane’s respiratory effects are probably due to central (medullary depression) and peripheral (intercostal muscle dysfunction) mechanisms.

52
Q

What is the apneic threshold?

A

the highest PaCO2 at which a patient remains apneic

53
Q

What effect does Halothane have on hypoxic drive?

A

severely depressed by even low concentrations of halothane

54
Q

Describe Halothane’s bronchodilator mechanism

A

Halothane is a potent bronchodilator and often reverses asthma-induced bronchospasm. Halothane attenuates airway reflexes and relaxes bronchial smooth muscle by inhibiting intracellular calcium mobilization.

55
Q

What is a negative respiratory effect of Halothane for anesthesia recovery?

A

Halothane depresses clearance of mucus from the respiratory tract which promotes postoperative hypoxia and atelectasis.

56
Q

Cerebral effects of Halothane

A

By dilating cerebral vessels, halothane lowers cerebral vascular resistance and increases cerebral blood volume and cerebral blood flow.

Autoregulation is blunted. Autoregulation = the maintenance of CBF during changes in arterial BP

57
Q

How can we prevent increased intracranial pressure caused by Halothane?

A

Establishing hyperventilation prior to administration of halothane.

58
Q

Neuromuscular effects of Halothane

A

Relaxes skeletal muscle and potentiates nondepolarizing neuromuscular-blocking agents.

Like other potent volatile agents, it is a trigger for malignant hyperthermia.

59
Q

Renal and Hepatic Effects of Halothane

A

Renal: Reduces renal blood flow, GFR and urine output. Preoperative hydration limits these changes.

Hepatic: Hepatic blood flow decrease. Hepatic artery vasospasm has been reported. Metabolism of some drugs is impaired by Halothane.

60
Q

Metabolism of Halothane

A

Halothane is oxidized in the liver by a particular isozyme of CYP (2EI) to its principal metabolite, trifluoroacetic acid.

61
Q

Halothane Hepatitis is __

A

extremely rare.

Signs are mostly related to hepatic injury such as increased serum alanine and aspartate transferase, elevated bilirubin (leading to jaundice) and encephalopathy.

62
Q

Contraindications for Halothane

A

Patients with unexplained liver dysfunction following previous anesthetic exposure.

Intracranial mass lesions because of the possibility of intracranial hypertension secondary to increased cerebral blood volume and flow.

Hypovolemic patients and some patients with severe reductions in LV function may not tolerate Holathane’s negative inotropic effects.

63
Q

Drug interactions with Halothane

A

Myocardial depression is exacerbated by combining Halothane with B-adrenergic blocking agents and calcium channel blocking agents

TCAs and MAOIs (altreations in BP)

Aminophylline + Halothane has resulted in serious ventricular arrythmias

64
Q

Isoflurane general facts and class

A

Nonflammable volatile anesthetic with a pungent ethereal odor

65
Q

Cardiovascular Effects of Isoflurane

A
  • Minimal LV depression in vivo.
  • CO is maintained by a rise in heart rate due to preservation of carotid baroreflexes.
  • Mild beta-adrenergic stimulation increases skeletal muscle blood flow, decreases SVR, and lowers arterial blood pressure.
  • However, rapid administration of isoflurane can lead to transient increases in HR, BP and plasma levels of norepinephrine.
  • Dilates coronary arteries, but not nearly as much as nitroglycerin. But you can still have some concern for coronary “steal”.
66
Q

Respiratory effects of Isoflurane

A

Respiratory depression (like the other volatiles) except that tachypnea is less pronounced.

More pronounced fall in minute ventilation. Even low levels of isoflurane blunt the normal ventilatory response to hypoxia and hypercapnia.

Good bronchodilator even though it can irritate the upper airway reflexes.

67
Q

Cerebral Effects of Isoflurane

A

Increases CBF and intracranial pressure. Can be reversed by hyperventilation. In contrast to Halothane, the hyperventilation doesn’t have to be initiated prior to the use of the gas to prevent it.

Reduces cerebral metabolic oxygen requirements, and at 2 MAC, it produces an electrically silent EEG.

68
Q

Neuromuscular effects of Isoflurane

A

Relaxes skeletal muscle

69
Q

Renal and Hepatic effects of Isoflurane

A

Renal: Decreases renal blood flow, GFR and urine output

Hepatic: Total hepatic blood flow may be reduced during isoflurane anesthesia. Hepatic oxygen supply is generally better maintained than with Halothane because hepatic artery perfusion is preserved.

LFTs not usually affected.

70
Q

Metabolism of Isoflurane

A

Metabolized to trifluoroacetic acid. Prolonged sedation with isoflurane has results in elevated plasma fluoride levels.

Nephrotoxicity is extremely unlikely. Its minimal oxidative metabolism also minimizes any possible risk of significant hepatic dysfunction.

71
Q

Contraindications and Drug Interactions of Isoflurane

A

No specific contraindications

Can be given with epinephrine doses up to 4.5mcg/kg. Nondepolarizing NMBAs are potentiated by isoflurane.

72
Q

Desflurane Structure

A

Very similar to that of isoflurane, the only difference is a substitution of a fluorine atom for isoflurane’s chlorine atom.

This impacts the vapor pressure of Desflurane at high altitudes and it boils at room temperature which means that a special vaporizer needed to be developed for it.

73
Q

Describe the solubility of Desflurane

A

Low solubility of Desflurane in blood and body tissues causes a very rapid induction of and emergence from anesthesia. Therefore alveolar concentrations of desflurane approaches the inspired concentration much more rapidly than with the other volatile agents, giving the anesthesiologist tighter control over anesthetic levels.

Wakeup times are approximately 50% less than those observed with isoflurane. This is due to its blood/gas partition coefficient (0.42) that is even lower than nitrous oxide.

74
Q

What are characteristic features of Desflurane?

A

High vapor pressure, an ultrashort duration of action, and moderate potency

75
Q

Cardiovascular Effects of Desflurane

A

Similar to isoflurane. Increase in concentration is associated with decline in SVR that leads to a fall in arterial BP. CO unchanged.

Moderate rise in heart rate, CVP, and pulmonary artery pressure that often does not become apparents at low doses.

76
Q

Rapid increases in Desflurane concentration leads to ___

A

transient but sometimes worrisome elevation in heart rate, BP, and catecholamine levels that are more pronounced than occur with isoflurane, particularly in patients with cardiovascular disease.

These cardiac effects can be decreased by fentanyl, esmolol or clonidine.

77
Q

Respiratory Effects of Desflurane

A

Decrease in tidal volume and increase in respiratory rate

Overall decrease in alveolar ventilation that cause a rise in resting PCO2

Depresses the response to PCO2

78
Q

What problems can arise due to the pungency of Desflurane?

A

Airway irritation during induction manifested by salivation, breath-holding, coughing, or laryngospasm

Airway resistance may increase in children with reactive airway susceptibility

These problems make Desflurane a poor choice for inhalational induction.

79
Q

Cerebral Effects of Desflurane

A

Directly vasodilates the cerebral vasculature, increasing CBF, cerebral blood volume, and intracranial pressure at normotension and normocapnia. The body counters this by decreasing the cerebral metabolic rate of oxygen (CMRO2) that tends to cause cerebral vasoconstriction and moderate any increase in CBF. The increased intracranial pressure can be lowered by hyperventilation.

Cerebral oxygen consumption is decreased.

EEG effects: initially frequency is increased but as the depth is increased, it slowly leads to burst suppression

80
Q

Renal and Hepatic Effects of Desflurane

A

Renal: No evidence of any nephrotoxic effects. However, as CO declines, so does renal perfusion (just to keep in mind).

Hepatic: Risk of anesthetic induced hepatitis is minimal.

81
Q

Metabolism of Desflurane

A

Minimal metabolism in humans

Significant percutaneous loss. Degraded by dessicated CO2 absorbent into potentially clinically important levels of carbon monoxide. Carbon monoxide poisoning may be difficult to diagnose under general anesthesia, but the presence of carboxyhemoglobin may be detectable from an ABG.

82
Q

With Desflurane, what can reduce the risk of carbon monoxide poisoining?

A

Disposing of dried out absorbent or use of calcium hydroxide can minimize the risk

83
Q

Contraindications for Desflurane

A

Severe hypovolemia, malignant hyperthermia, and intracranial hypertension

84
Q

In pediatric patients Desflurane is associated with __

A

emergence delirium

85
Q

Desflurane drug interactions

A

Potentiates nondepolarizing neuromuscular blocking agents

Epinephrine can be safely administered in doses up to 4.5 mcg/kg as desflurane does not sensitize the myocardium to the arrythmogenic effects of epinephrine.

Of note, switching from isoflurane to desflurane at the end of a case does not make the patient emerge any faster.

86
Q

Sevoflurane general facts

A

Sevoflurane is halogenated with fluorine

Solubility in blood is greater than desflurane

Nonpungency and rapid increases in alveolar anesthetic concentrations make sevo an excellent choice for smooth and rapid inhalational inductions in both adults and pediatrics.

87
Q

Inhalation induction with 4% to 8% sevoflurance in a 50% mixture of nitrous oxide and oxygen can be acheived within ____.

A

1 minute

88
Q

What quality about Sevoflurane results in a more rapid emergence?

A

Its low blood solubility results in a rapid fall in alveolar anesthetic concentration upon discontinuation and more rapid emergence compared with isoflurane (although not an earlier discharge from PACU).

89
Q

What type of vaporizer do you need for Sevoflurane?

A

Sevoflurane’s modest vapor pressure permits the use of conventional variable bypass vaporizer.

90
Q

Cardiovascular effects of Sevoflurane

A

Mildly depresses myocardial contractility

SVR and arterial BP decline slightly less than deslurane or isoflurane

Causes little rise in HR so CO is not maintained as well as with isoflurane or desflurane.

May prolong QT interval

91
Q

QT prolongation in infants

A

QT prolongation may manifest 60 min following anesthetic emergence in infants

92
Q

Respiratory and Neuromuscular Effects of Sevoflurane

A

Resp: Depresses respiration and reverses bronchospasm to an extent similar to that of isoflurane.

Neuromuscular: Produces adequate muscle relaxation for intubation following an inhalational induction, although most practitioners will deepen anesthesia with various combinations of IV agents.

93
Q

Cerebral Effects of Sevoflurane

A

Slight increases in CBF and intracranial pressure at normocarbia

High concentrations of Sevo (>1.5 MAC) may impair autoregulation of CBF, thus allowing a drop in CBF during hemorrhagic hypotension. This effect tends to be less pronounced than with isoflurane

Cerebral metabolic oxygen requirements decrease, no seizure acivity has been reported.

94
Q

Renal and Hepatic Effects of Sevoflurane

A

Renal: Slightly decreases renal blood flow.

Hepatic: Decreases portal vein flow, but increases hepatic artery blood flow, thereby maintaining total hepatic blood flow and oxygen delivery. Generally, it is not associated with immune-mediated anesthetic hepatotoxicity.

95
Q

Metabolism of Sevoflurane

A

The liver micosomal enzyme P-450 metabolizes Sevoflurane at a rate one-fourth that of halothane but 10 to 25 times that of isoflurane or desflurane and may be induced with ethanol or phenobarbital pretreatment.

Serum fluoride concentrations exceed 50 millimole/L in approximately 7% of patients who receive Sevoflurane, yet clinically significant kidney dysfunction has not been associated with Sevo anesthesia.

96
Q

Soda lime or barium hydroxide lime can ___

A

degrade Sevoflurane, producing a nephrotoxic end product.

This isn’t really an issue anymore since our newer anesthesia machines don’t have soda lime

97
Q

Sevoflurane can be degraded into hydrogen fluoride by ___.

A

Metal and environmental impurities present in manufacturing equipment, glass bottle packaging, and anesthesia equipment.

98
Q

Contraindications of Sevoflurane and Drug Interactions

A

Severe hypovolemia, susceptibility to malignant hyperthermia, and intracranial hypertension

Sevoflurane potentiates NMBAs. It does not sensitize the heart to catecholamine-induced arrythmias.

99
Q

General Facts about Xenon

A

Inert element that does not form chemical bonds

Very costly process to scavenge it

Odorless, nonexplosive, fast onset and emergence, no hemodynamic effects and has been found to be protective against neuronal ischemia

Anesthesia Pharm (18 decks)

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