Inhalation Agents Flashcards

1
Q

Define inhalation agents

A

These are volatile and non-volatile gases used in the induction and maintenance of general anesthesia, as well as sedation

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2
Q

List some indications of inhalation agents

A

Indications can be classified as operative setting or ICU setting

Operative setting.
primary therapy for preoperative sedation.
Adjunctive anesthesia maintenance to Ivy anesthetic

ICU
Facilitate tolerance of endotracheal, intubation, mechanical ventilation, and different bedside procedures

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3
Q

What are the two main mechanism of action of inhalation agents?

A

1) depressed, excitatory, pathway
2) Augments inhibitory pathway

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4
Q

List three ways in which inhalation agents can depress excitatory pathways

A

By inhibiting acetylcholine at the muscarinic, and the nicotinic receptors

By inhibiting glutamate at the NMDA, receptors

By inhibiting serotonin at the 5-HT receptors

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5
Q

List two ways in which inhalation agents augment inhibitory pathways

A

By acting at the chloride channel GABA receptors

By acting on potassium channels (closing potassium channels will prevent the subsequent hyperpolarization that comes after depolarization)

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6
Q

What is the mechanism of action of volatile gases?

A

They act at the chloride channels by binding to GABA receptors

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7
Q

How do non-volatile inhalant agents work

A

They act at glutamate and MDA receptors by blocking the action of L-glutamate

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8
Q

List four properties of the ideal, inhaled agent

A

Ample potency.
Low solubility in blood and tissue
Resist physical and metabolic degradation.
Protects and does not injure vital tissues

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9
Q

Defined the term minimum alveolar concentration MAC

A

This is the fraction of volume of the anesthetic agent present in the inspired air that produces immobility to noxious stimuli in 50% of patients

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10
Q

True or false the lower the MAC value the more fat soluble the anesthetic

A

True

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11
Q

What are the three main factors that determine the speed of induction and rate a recovery of an inhalation agent?

A

Fi- inspired, gas, concentration
F A- alveolar gas concentration
Fa- arterial gas concentration

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12
Q

What are the factors that affect inspired gas concentration? Fi

A

1) FGF rates – fresh gas flow
2) breathing circuit volume
3) circuit absorption

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13
Q

True or false the patient receives. The concentration of inhalation agents set on the vaporizer.

A

False
this is because the inhalation agent mixes with gases in the breathing circuits before being inspired by the patient

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14
Q

Describe how fresh gas flow rates, breathing system volume, and circuit absorption affect the inspired gas concentration

A

The higher, the fresh gas fluid, the smaller, the breathing system, volume and the lower the circuits absorption. The closer of the inspired gas concentration will be to the fresh gas concentration.

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15
Q

What are the three factors affecting alveolar concentration?

A

Uptake.
Ventilation.
Concentration

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16
Q

Why is the alveolar partial pressure of an inhalation agent important

A

It is important because it determines the partial pressure of an anesthetic in the blood and ultimately in the brain similarly the partial pressure of anesthetic in the brain, is directly proportional to its brain tissue concentration, which determines the clinical effect

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17
Q

What is the relationship between the uptake of an anesthetic agent and the alveolar concentration and rate of induction

A

The greater the uptake of the anesthetic agent, the lower, the alveolar concentration and the lower the partial pressure of the inhalation agent, and the slower the rate of induction

Remember that the lower the partial partial of the inhalation agent, the lower the concentration in the brain

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18
Q

What are the three factors that affect the anesthetic uptake in the blood of an inhalation agent?

A

Solubility in the blood
Alveolar blood flow.
Difference in partial pressure between alveolar gas and venous blood

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19
Q

Which one of the following inhalation agents of like concentration rises faster, and hence has a faster induction onset

Nitrous oxide or halothane, why?

A

Nitrous oxide has a faster onset of induction because it has a lower solubility in blood, and therefore the alveolar concentration of nitrous oxide rises faster than that of halothane

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20
Q

How does cardiac output affect induction of an inhalation agent?

A

As cardiac output increases, anesthetic, uptake increases the rise in alveolar. Partial pressure slows, and induction is delayed.

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21
Q

How do low output states affect the dosage of inhalation agents that are soluble

A

Low-output states predispose patients to overdosage with soluble agents as the rate of rise in alveolar concentration will be markedly increased

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22
Q

How can you counter the lowering of alveolar partial pressure by uptake

A

The lowering of alveolar, partial pressure by uptake can be countered by increasing alveolar ventilation

In other words, constantly replacing the anesthetic taken up by the pulmonary bloodstream results in better maintenance of the alveolar concentration (and partial pressure and recall the higher the partial pressure the faster the induction/recovery)

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23
Q

What effect does increasing ventilation have on soluble versus insoluble inhalation agents?

A

Increasing ventilation has minimal effect on insoluble agents and has more effect on soluble agents

This is because soluble agents are more significantly affected by uptake than the insoluble agents so the partial pressure is more likely to decrease with soluble agents than insoluble agent .
RECALL ventilation increase, affects the partial pressure

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24
Q

List, one inhalation agent that depresses spontaneous ventilation

A

Halothane

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25
Q

How can concentration affect inhalation agent reduce the slowing of induction due to uptake from alveolar gas?

A

An increased inspired concentration of the inhalation agent can reduce the slowing of induction

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26
Q

Recovery from anesthesia of inhalation agents depends on what

A

Redistributing the concentration of anesthetic agent from brain tissue

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27
Q

How are anesthetic agents eliminated?

A

Biotransformation,
transcutaneous loss, or
exhalation

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28
Q

Why does halothane have faster elimination than isoflurane, even though halothane is more soluble than isoflurane

A

This is because Halane undergoes extensive biotransformation, and this account is for as fast elimination

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29
Q

Where is the most important route for elimination of inhalation anesthetics

A

The alveolus

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30
Q

Which inhalation anesthetic causes diffusion hypoxia, and why

A

Nitrous oxide causes diffusion hypoxia because it has a rapid elimination that so rapid that alveolar oxygen and carbon dioxide are diluted

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31
Q

How do you prevent diffusion hypoxia when a patient is recovering from nitrous oxide

A

This is prevented by administering 100% oxygen for 5 to 10 minutes after discontinuing nitrous oxide

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32
Q

True or false the rate of recovery is faster than induction for nitrous oxide

A

True

This is because tissues that have not reached maximum saturation of the inhalation agent will continue to take off the anesthetic agent until the alveolar partial pressure falls below the tissue, partial pressure. For example, fat will continue to take up, anesthetic agent and hasten, recovery until the partial pressure exceeds the alveolar, partial pressure

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33
Q

True or False
The speed of recovery from an inhalation agent is related to the redistribution

A

True

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34
Q

What is the maximum alveolar concentration (MAC) of nitrous oxide?

A

105

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35
Q

What is the maximum alveolar concentration of halothane?

A

0.75

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36
Q

What is the maximum alveolar concentration of isoflurane?

A

1.2

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37
Q

What is the maximum alveolar concentration of desflurane?

A

6.0

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38
Q

Sevoflurane MAC

A

2.0

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39
Q

State the MACs in order

Nitrous Oxide
Desflourane
Sevoflourane
Isoflourane
Halothane

A

105
6.0
2.0
1.2
0.75

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40
Q

Describe the properties of nitrous oxide

A

It is a colorless, odorless, nonexplosive, and non-flammable gas

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41
Q

How does alcohol affect minimum alveolar concentration?

A

Acute intoxication decreases the mean alveolar concentration, while chronic abuse increases the mean alveolar concentration

This is because when a person is acutely intoxicated, it requires less inhalation agent to produce anesthesia while for patients who are chronic alcohol abusers they have a high tolerance level, so you require more inhalation anesthetic to produce anesthesia

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42
Q

What is the mechanism of action of nitrous oxide?

A

It acts at the NMDA N- methyl D- aspartate for receptor and blocks L glutamate from exciting the neuron

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43
Q

List four volatile inhalation agents

A

Desflurane
Sevoflurane
Isoflurane
Halothane

44
Q

List one non volatile inhalation agent

A

Nitrous Oxide

45
Q

What is the means of elimination of nitrous oxide

A

Is eliminated on change by the lungs during exhalation

46
Q

Absolute contraindications for nitrous oxide use

A

Airway or breathing compromise.
Causes Expansion of gas filled air spaces.(pneumothorax, sbo/lbo)
Pulmonary hypertension associated with exercise intolerance

47
Q

List five relative contraindications for nitrous oxide

A

<6 mos old
Pregnancy
Pre-existing issues with B12, and folate metabolism
History of cvs
Bowel, middle ear, neurosurgery (non-compliant to expansion)

48
Q

What is the effect of nitrous oxide on the cardiovascular system?

A

Mild agenic stimulation.
Mild negative inotrope
Improves hemodynamic performance when used with volatile liquid

49
Q

What is the effect of nitrous oxide on the respiratory system?

A

It is a non-irritant.
It has minimal effect on minute ventilation.
Reduces the ventilator depression that occurs with volatile agents 

50
Q

What are the effects of nitrous oxide on the central nervous system?

A

Increases cerebral perfusion.
Cerebral metabolic rate.
Intracranial pressure 

51
Q

What are the effects of of nitrous oxide on the blood?

A

It’s irreversibly oxidizes the cobalt iron at the center of vitamin B 12 and can cause megaloblastic anemia

52
Q

List six adverse effects of nitrous oxide

A

Increased risk of postoperative nausea and vomiting.
Diffusion hypoxia.
Hallucinations.
Teratogenic effect.
Hyper Homcy anemia, causing negative effects on CVS.
Potentiates respiratory depression

53
Q

How do you treat diffusion hypoxia caused by nitrous oxide?

A

Treat with five minutes of 100% O2 when emerging from anesthesia

54
Q

List two toxic effects of nitrous oxide

A

Megaloblastic anemia with neurologic dysfunction.
Increased risk of myocardial depression

55
Q

Which inhalation anesthetic agent is the most volatile of all the inhalation agents

A

Desflurane

56
Q

List for properties of desflurane

A

Non-flammable.
Colorless.
Pungent odor
Airway irritant

57
Q

What is the MAC of desflurane ?

A

6

58
Q

What is the onset time of desflurane

A

1-2 mins
This is because it has a low blood gas coefficient and and has a lower blood and tissue solubility, therefore has faster induction and recovery time

59
Q

How is DESFLURANE eliminated in the body

A

Majorities eliminated by Long in expired air. It has a rapid elimination because of its low solubility.

60
Q

List two indications for desflurane

A

Induction and maintenance

61
Q

What is the dosage for induction using DESFLURANE

A

3% inhaled increased by 0.5 to 1% increments every 2 to 3 breaths

62
Q

For maintenance of anesthesia and adults what is the dosage of DESFLURANE

A

2.5 to 8% with or without nitrous oxide

63
Q

List three absolutes contraindications specific to DESFLURANE

A

Severe hypovolemia.
Previous family history of malignant hyperthermia
Intracranial, hypertension

64
Q

List song drug reactions that pull as country indications for using DESFLURANE

A

Potentiates, non-depolarizing neuromuscular blocking, blocking agents

Increases the toxicity of epinephrine

65
Q

What is the effect of DESFELURANE on the cardio

A

Decrease in systemic, vascular resistance, and prayer for vasodilation.
Cardiac depression

66
Q

What is the effect of DESFLURANE on a respiratory system

A

It is extremely irritant to the airway, and hence not suitable for inhalation induction.
Decrease in tidal volume, decreased volume, and CO2 retention and increase in respiratory rates

67
Q

What is the effect of Desflurane on the CNS?

A

It increases intracranial tension more than isoflurane

68
Q

What is effect of DESFLURANE on the kidneys

A

It is not toxic, but there is a decrease in GFR and a urine output because of the decreased cardiac output

69
Q

What is the effect of DESFLURANE on the muscles

A

It causes skeletal muscle relaxation

70
Q

List for adverse and toxic effects of DESFLURENE

A

Highly irritable to airway.
Malignant hypothermia.
Postoperative nausea, vomiting.
Postoperative, shivering

71
Q

Describe the chemical and physical properties of SEVOFLURANE

A

It is a clear, colorless liquid, non-flammable and supplied in amber colored bottles to prevent oxidation

72
Q

What is the MAC of SEVOFLURANE?

A

2%

73
Q

What are the factors that affect the uptake of volatile anesthetic agents?

A

Solubility.
Cardiac output.
Concentration gradient between the alveoli and Venus blood

74
Q

What is the usual maintenance dose of SEVOFLURANE adults

A

0.5-3%

75
Q

List three specific contraindications for SEVOFLURANE

A

Severe hypovolemia.
Susceptible to malignant hypothermia.
Intracranial, hypertension

76
Q

What is the effect of SEVOFLURANE on the respiratory system

A

Respiratory depression.
Bronchodilation

77
Q

What is the effect of SEVOFLURANE on the cardiovascular system

A

Stable HR.
Mildly decreases contractility.
May prolong QT interval

78
Q

List five adverse effects of SEVOFLURANE

A

Potential nephrotoxicity.
Post operative, nausea vomiting.
Trigger agent for malignant hypothermia.
Rapid emergence in pediatric patients that may lead to agitational.
Pediatric patient with down syndrome made developed bradycardia

79
Q

Describe some chemical and physical properties of iso fluorine

A

Clear colorless liquid.
Nonflammable.
Pungent order
Supplied an amber colored bottles to prevent oxidation

80
Q

What is the MAC of isoflurane?

A

1.2

81
Q

What compound is isoflurane metabolize to

A

Trifluroacetic acid

82
Q

What is the induction dose of iso fluorine?

A

1.5 to 3% can produce surgical anesthesia in 7 to 10 minutes

83
Q

What is the maintenance concentration of iso fluorine with nitrous oxide?

A

1-2.5%

84
Q

What is an indication for ISOFLURANE and SEVOFLURANE?

A

Potentiates the action of co-administer depolarizing and nondepolarizing muscle relaxants

85
Q

True or false the co-administration of nitrous oxide lowers the MAC of volatile anesthetic agents

A

True

86
Q

What is the effect of isoflurane on the cardiovascular system?

A

Decrease blood pressure and cardiac output, and increased heart rate

87
Q

What is the effect of isoFlurane on the respiratory system?

A

Decreased title volume.
Increase respiratory rate.
Bronchodilation.
Decreased response to carbon dioxide reflexes

88
Q

What are the chemical and physical properties of halothane?

A

Hallene is a colorless halogenated hydrocarbon with a pleasant order.
Non-flammable and non-irritant
Place in an amber bottle to prevent oxidative decomposition

89
Q

What is the MAC of Halothane

A

0.75

90
Q

How is Halane metabolized and eliminated

A

20% is metabolized in the liver by cytochrome P450 and the primary metabolites are trifluoroacetic acid, Br, Cl

60 to 80% is eliminated through exhaling unchanged

91
Q

What is the concentration of Halane for induction in adults?

A

2 to 4% in oxygen or nitrous oxide

1.5-2 in children

92
Q

What is the maintenance concentration of halothane?

A

0.5 to 1.5%

93
Q

List for contraindications for Halothane

A

History of liver dysfunction following previous anesthetic exposure.
Intracranial mass.
Hypovolemic patient. (Negative inotropic effect)
Pheochromocytoma (sensitizes myocardium to adrenaline)

94
Q

What is the drug interaction that Halothane has with beta or calcium channel blockers

A

Myocardial, depression

95
Q

What effect does halothane have an epinephrine?

A

Potentiates the action

96
Q

List three adverse or toxic effects of Hall

A

Malignant hypothermia.
Myocardial dysrhythmia.
Halothane hepatitis

97
Q

How does halothane cause halothane hepatitis?

A

It produces metabolic and products trichloracetic acid which react immunologically with hepatic cells

98
Q

What are the clinical features of Halothane hepatitis?

A

2 to 3 weeks onset.
Acute hepatitis feature is: jaundice, fever, vomiting, hepatomegaly, rash, arthralgia

99
Q

What investigations are used to diagnose Halothane hepatitis?

A

Lab Findings :
Increased eosinophil.
Serum transaminases
Bilirubin.
Alkaline phosphates increase

Biopsy:
Massive, centrilobular hepatic necrosis

100
Q

How is Halothane hepatitis treated?

A

It ranges from supportive treatments to liver transplantation, depending on the severity of the liver damage

101
Q

What is malignant hyperthermia ?

A

This is a myopathy in which general anesthesia triggers, an uncontrollable contraction in skeletal muscle leading to life-threatening, hyper catabolic state and increasing body temperature

102
Q

What is the gene mutation scene in malignant hyperthermia

A

Ryanodinevreceptor type 1
Autosomal dominant

103
Q

What is the pathophysiology of malignant hyperthermia?

A

Administering a triggering, volatile anesthetic agent and Senel Colleen causes accumulation of intracellular calcium in skeletal muscle, that leads to over activation and hyper metabolism

104
Q

What are the early signs of malignant hyperthermia?

A

Tachycardia.
Tachypnea.
Cyanosis.
Rigidity.
Rising end tidal CO2

105
Q

List some late signs of malignant hyperthermia

A

Elevated body temperature temperature.
Signs of secondary organ damage.
Complex arrhythmias
Bleeding and or thrombosis
Muscle pain, swelling and weakness of affective muscles

106
Q

How do you treat malignant hyperthermia

A

Dantrolene: it inhibits calcium ion release from the sarcoplasmic reticulum

1mg/kg every 4-6hrs