Inhalation Anesthetics

Question 1

What is MAC?

Answer 1

MAC represents “the Mean Alveolar Concentration that
prevents movement in half of subjects in response to a surgical
incision.”
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 607.

Question 2

What is MAC-BAR?

Answer 2

MAC-BAR refers to the concentration of inhaled anesthetic that
prevents an adrenergic response to skin incision (increased
heart rate, blood pressure, plasma norepinephrine levels). MACBAR50
is the dose of volatile anesthetic that prevents the
adrenergic response in 50% of patients and MAC-BAR95 is the
dose that prevents an adrenergic response in 95% of patients.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 88.

Question 3

What is MAC-awake and how does it correlate to

MAC?

Answer 3

Mac-awake is defined as “the concentration of inhaled
anesthetic that inhibits appropriate responses to spoken
commands in half of patients”. It normally correlates to
approximately 0.35 MAC.
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 607.

Question 4

How does having red hair affect MAC?

Answer 4

It has been demonstrated that natural redheads have a
significantly higher anesthetic requirement for desflurane than
do non-redhead patients.
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 607.

Question 5

MAC and MAC-awake are reduced by neuraxial

blockade. How does this occur?

Answer 5

Even though neuraxial blockade doesn’t affect cranial nerve
function like other factors that decrease MAC (hypothermia,
hypnotics, opioids, antidepressants, anti-seizure medications,
etc) it decreases MAC by inhibiting the ascending spinal cord
signals that stimulate cortical arousal in the brainstem.
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 607-
608.

Question 6

How does body temperature affect MAC?

Answer 6

For each 1 degree Celsius drop in temperature, MAC
decreases by 5%.
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 607.

Question 7

What is ED95 and how does it relate to MAC?

Answer 7

The ED95 is the dose of a volatile anesthetic that is effective in
preventing movement in response to surgical incision in 95% of
patients and usually correlates to about 1.3 MAC.
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 607.

Question 8

Besides hypothermia and advanced age, what other

physiologic factors decrease MAC?

Answer 8

Besides hypothermia and advanced age, factors that decrease
MAC include alpha-2 agonists, acute ethanol ingestion,
hypoxemia, hyponatremia, metabolic acidosis, anemia,
hypotension, and pregnancy.
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 607.

Question 9

How does age affect MAC and at what age is MAC

highest?

Answer 9

MAC generally decreases with age. MAC is highest in patients
between the ages of 6 and 12 months.
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 607.

Question 10

What are the four groups tissues are divided into
when discussing the transfer of volatile anesthetics
to the tissues?

Answer 10

The four groups are the vessel-rich group, muscle, fat, and the
vessel-poor group.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 156.

Question 11

What tissues constitute the vessel-rich group, what
percentage of body weight do they account for, and
what percent of cardiac output do they receive?

Answer 11

The vessel-rich group consists of the brain, heart, liver, kidneys,
and endocrine organs. They constitute about 10% of body
weight, but receive about 75% of cardiac output.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 156.

Question 12

What tissues constitute the muscle group, what
percentage of body weight do they account for, and
what percent of cardiac output do they receive?

Answer 12

The muscle group consists of both muscle and skin. It is not as
well perfused as the vessel-rich group, comprising about 50% of
body weight but receiving only 19% of cardiac output.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 156.

Question 13

What tissues constitute the fat group, what
percentage of body weight do they account for, and
what percent of cardiac output do they receive?

Answer 13

Adipose tissue is the sole component of the fat group. It usually
is about 20% of bodyweight and receives 6% of the cardiac
output.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 156.

Question 14

What tissues constitute the vessel-poor group, what
percentage of body weight do they account for, and
what percent of cardiac output do they receive?

Answer 14

The vessel-poor group consists of teeth, hair, nails, bones,
ligaments, and cartilage. It comprises about 20% of body
weight and receives less than 1% of cardiac output.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 156.

Question 15

What is the Meyer-Overton rule?

Answer 15

The Meyer-Overton rule states that the lipid solubility of an
inhalation agent is directly proportional to its potency.
Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis,
MO: Elsevier Saunders Company; 2014: 86.

Question 16

What are the three factors that influence the uptake

of a volatile anesthetic?

Answer 16

Alveolar blood flow, the blood:gas solubility of the anesthetic,
and the difference between the partial pressure of the
anesthetic in the alveoli and in venous blood.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 156.

Question 17

What is meant by an FA/FI ratio of 1.0?

Answer 17

The degree to which the alveolar concentration of an anesthetic
is becoming closer to the inspired concentration of an
anesthetic is often expressed as a ratio. If the alveolar
concentration equals the inspired concentration, then their ratio
= 1:1 or 1.0. Stating ‘the rate at which FA/FI = 1’ is just a
shortcut for stating ‘the rate at which the alveolar concentration
of the anesthetic equals the inspired concentration of the
anesthetic’.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 155-156.

Question 18

How does an increase in the uptake of a volatile

anesthetic affect the rate of induction?

Answer 18

The greater the rate of uptake, the greater the difference
between the alveolar concentration (FA) and the inspired
concentration (FI) and the slower the rate of induction.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 155.

Question 19

Besides the vaporizer dial setting, upon what three
factors does the composition of the inspired gas
mixture a patient receives depend?

Answer 19

The composition of the inspired gas mixture a patient receives
depends primarily upon the fresh gas flow rate, the volume of
the breathing circuit, and any absorption by the circuit. The
inspired gas concentration will be closer to the fresh gas
concentration if the circuit volume and level of absorption by the
circuit are low and the fresh gas flow is high.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 155.

Question 20

How is the uptake of volatile anesthetics related to

the rate of rise of the FA/FI ratio?

Answer 20

If there was no uptake of anesthetic gas by the body, the
concentration of anesthetic gas in the alveoli (FA) would rapidly
equal the concentration of anesthetic gas in the inspired gas
(FI). FA lags behind FI because the pulmonary circuit takes up
anesthetic gas and lowers the concentration in the alveoli. The
greater the amount of uptake, the slower the FA/FI ratio rises
toward 1. By definition then, uptake is inversely related to the
rate of rise of the FA/FI ratio.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 155.

Question 21

How does an increase in minute ventilation affect the

rate at which FA approaches FI?

Answer 21

As the minute alveolar ventilation increases, the rate at which
the alveolar concentration of a volatile anesthetic approaches
the inspired concentration increases. They are directly
proportional.
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 596.

Question 22

How does low blood solubility affect the pulmonary

uptake and elimination of a volatile anesthetic?

Answer 22

The lower the blood solubility, the faster pulmonary uptake and
elimination occurs.
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 596.

Question 23

What is overpressurization of a volatile anesthetic?

Answer 23

Overpressurization is the administration of 2-3 times the desired
alveolar concentration of a gas until the desired depth of
anesthesia is reached. At that point, the concentration of
inspired gas is reduced to a lower level.
Longnecker DE, Newman MF, Brown DL, Zapol WM.
Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 601.

Question 24

Why is the alveolar partial pressure of an anesthetic

agent important?

Answer 24

The alveolar partial pressure is important because it is the
factor that determines the partial pressure of anesthetic gas
within the blood. In turn, the partial pressure of anesthetic gas
in the blood determines the partial pressure of anesthetic gas
within the brain. Thus, the partial pressure of anesthetic gas in
the alveoli determines the concentration of gas within the brain
and this is the determinant of the clinical level of anesthesia.
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s
Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill;
2013: 156.

Question 25

How does the rate of rise in the FA/FI ratio compare | between soluble and insoluble anesthetic gases?

Answer 25

Anesthetic gases with low blood:gas solubility coefficients are not readily taken up by the bloodstream. Consequently, the alveolar partial pressure of these agents does not drop rapidly. Because the alveolar partial pressure does not drop due to the gas being taken up, it rapidly approaches the inspired concentration of the gas. Conversely, highly soluble agents are absorbed rapidly from the alveoli into the blood and the alveolar pressure drops substantially. Because of this absorption, the alveolar concentration rises much more slowly and takes a longer time to reach the inspired concentration. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 156-157.

Question 26

What are the factors that determine the rate at which the alveolar concentration (FA) of an anesthetic approaches the inspired concentration (FI)?

Answer 26

The rate at which FA approaches FI depends upon minute ventilation, cardiac output, and the blood:gas coefficient of the anesthetic. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 596.

Question 27

How do changes in cardiac output affect the rate at which the alveolar concentration of a volatile anesthetic approaches the inspired concentration?

Answer 27

They are inversely proportional. As cardiac output increases, the rate at which FA approaches FI decreases and vice versa. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 596.

Question 28

Anesthetic A has an blood:gas partition coefficient of 0.5 and anesthetic B has a blood:gas coefficient of 0.75. All other factors being equal, which one will lead to a slower induction and why?

Answer 28

Anesthetic B will exhibit a slower induction. The higher the blood:gas coefficient, the greater the uptake of the anesthetic and the longer it will take for the FA/FI to equal 1.0 Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 157.

Question 29

How does the blood:gas coefficient affect the rate at which the alveolar concentration of a volatile anesthetic approaches the inspired concentration?

Answer 29

They are inversely proportional. The higher the blood:gas solubility coefficient, the slower the rate at which FA approaches FI. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 596.

Question 30

How does a right to left shunt affect the speed of | induction?

Answer 30

If a right to left shunt is present, an inhalation induction proceeds more slowly because the anesthetic concentration of arterial blood increases more slowly. The opposite is true with a left to right shunt because the rate of transfer of anesthetic from the lungs to the blood is more rapid. This effect is rarely evident in the clinical setting, however. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 159.

Question 31

Which agent would have a faster onset at induction, a highly soluble anesthetic agent or a poorly soluble agent?

Answer 31

A poorly soluble agent would not be absorbed from the alveoli into the blood as quickly, therefore, its alveolar partial pressure would rise more quickly. Because the alveolar partial pressure determines the partial pressure of the gas in the brain where it exerts its clinical effect, the poorly soluble agent would have a faster onset than a highly soluble agent. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 156-157.

Question 32

What is the primary way in which volatile anesthetics | are eliminated from the body?

Answer 32

Although metabolism accounts for a very small amount of the elimination, the vast majority is eliminated via the alveoli. The gases are exhaled unchanged. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 159.

Question 33

To what extent are desflurane, isoflurane, and | sevoflurane metabolized?

Answer 33

Remember the rule of Two's: Desflurane = 0.02%, isoflurane = 0.2%, and sevoflurane = 2% Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 598.

Question 34

What is the primary way in which all volatile | anesthetics are metabolized?

Answer 34

The biodegradation of all volatile anesthetics is via phase I oxidation in the liver. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 88.

Question 35

How do the volatile anesthetics affect cardiac | conduction?

Answer 35

Sevoflurane, isoflurane, and desflurane all prolong the QT interval. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 612.

Question 36

How do volatile anesthetics affect hepatic blood flow?

Answer 36

All volatile anesthetics reduce hepatic blood flow primarily by decreasing portal blood flow. Isoflurane decreases it the least because it allows for compensatory increases in flow via the hepatic artery. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 613.

Question 37

How do volatile anesthetics affect pulmonary | vascular resistance?

Answer 37

While the vascular smooth muscle throughout the body is decreased, the effects on the pulmonary vasculature is minimal. The combination of changes in cardiac output counteract the vasodilatory actions of the volatile anesthetics resulting in no significant changes in pulmonary artery pressures. Nitrous oxide is capable of increasing pulmonary vascular resistance to a small degree, but this is not considered significant except in patients with pre-existing pulmonary hypertension. Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC, Ortega R. Clinical Anesthesia. 7th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2013: 469.

Question 38

What is hypoxic pulmonary vasoconstriction and how | do volatile anesthetics affect it?

Answer 38

Although volatile anesthetics exert little effect on pulmonary blood flow, they do exert a significant effect on hypoxic pulmonary vasoconstriction, which is the localized vasoconstriction that occurs in response to regional hypoxia in the lung. It occurs due to alveolar hypoxia, not arterial hypoxemia. HPV normally serves to improve V/Q characteristics within the lung to maximize the interface between oxygen and pulmonary blood flow. All of the volatile anesthetics have been shown to attenuate HPV in high doses in animal models, but the effect has not been demonstrated as clearly in clinical doses in humans yet. HPV can also be inhibited by very high or very low pulmonary artery pressures, hypocapnia, beta-adrenergic agonists, vasodilators such as nitroglycerin and nitroprusside, pulmonary infection, high or very low mixed venous PO2, and calcium channel blockers. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 674-676.

Question 39

How does the administration of a volatile anesthetic affect renal perfusion and the glomerular fitration rate?

Answer 39

Autoregulation of blood flow through the kidneys remains largely intact when volatile anesthetics are used. As the mean arterial pressure decreases from the effects of volatile anesthetics, the renal vasculature dilates to increase blood flow. This compensatory reduction in renal vascular resistance can, however, lead to a decrease in the glomerular filtration rate. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 95.

Question 40

How can volatile anesthetic agents be used to treat | status asthmaticus?

Answer 40

Because they exert a powerful bronchodilating characteristic, induction of general anesthesia with high concentrations of volatile anesthetics has been used in the treatment of refractory status asthmaticus. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 94-95.

Question 41

Which of the inhalation anesthetics trigger malignant | hyperthermia?

Answer 41

All of the volatile agents trigger malignant hyperthermia. Nitrous oxide is considered at most to be a weak trigger of malignant hyperthermia and is often combined with an intravenous anesthetic for patients with malignant hyperthermia. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 96.

Question 42

Which volatile anesthetic decreases CMRO2 the | most?

Answer 42

Isoflurane decreases CMRO2 the most. The effects of sevoflurane and desflurane are roughly equivalent. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 582.

Question 43

Which volatile agent increases cerebrospinal fluid | absorption?

Answer 43

Isoflurane is unique in that it is the only volatile agent that facilitates CSF absorption and has a favorable effect on CSF dynamics. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 581.

Question 44

In reference to the volatile anesthetics, what is luxury | perfusion?

Answer 44

The use of volatile anesthetics can result in luxury perfusion, a potentially beneficial effect during global ischemia which is characterized by a decrease in CMRO2 with a simultaneous increase in cerebral blood flow. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 582.

Question 45

How do volatile anesthetics affect neuromuscular | function?

Answer 45

All volatile agents produce a dose-dependent relaxation of skeletal muscle and a potentiation of the effects of nondepolarizing muscle relaxants. This is predominantly due to effects at the postsynaptic neuromuscular junction membrane. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 96.

Question 46

How do volatile anesthetics affect heart rate?

Answer 46

All volatile anesthetics increase heart rate by a direct vagolytic effect on the heart and via a baroreceptor response to the decrease in blood pressure they produce. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 612.

Question 47

How do inhalation anesthetics affect the hypoxic ventilatory drive? In what situations might this be significant?

Answer 47

Concentrations as little as 0.1 MAC of a volatile anesthetic can abolish the body's ventilatory response to hypoxia. This may become significant in patients whose minute ventilation is largely determined by their hypoxic drive, such as patients with emphysema. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 94.

Question 48

What inhalation anesthetic can increase the | intracranial pressure substantially?

Answer 48

Nitrous oxide can increase intracranial pressure substantially, especially in patients with mass lesions. Desflurane can also increase intracranial pressure in a small but steady manner, probably due to altered cerebrospinal fluid dynamics. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 878.

Question 49

How do inhalation anesthetics affect tidal volume | and respiratory rate?

Answer 49

The tidal volume is decreased as the concentration of the agent increases. The respiratory rate increases, however, and this is typically sufficient to prevent increases in arterial CO2 due to hypoventilation. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 94.

Question 50

How do volatile anesthetics affect the respiratory | response to carbon dioxide?

Answer 50

The response to CO2 is diminished. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 94.

Question 51

What is the only volatile agent capable of producing | an isoelectric EEG at clinical doses (1-2 MAC)?

Answer 51

Isoflurane is the only volatile agent capable of producing an isoelectric EEG at clinical doses. Desflurane and sevoflurane can produce burst suppression at doses greater than 1.2 and 1.5 MAC respectively, but not electrical silence. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 169.

Question 52

How do inhalation agents affect myocardial | contractility?

Answer 52

Desflurane, isoflurane, and sevoflurane reduce myocardial contractility, delay the relaxation of the cardiac chambers, and can impair the synchronization between the left atrial and left ventricular contractions. Nitrous oxide reduces myocardial contractility by decreasing cardiac myocyte calcium levels. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 612.

Question 53

How do volatile anesthetics affect cerebral | metabolism?

Answer 53

How do volatile anesthetics affect cerebral | metabolism?

Question 54

How do inhaled anesthetic gases affect cerebral | blood flow and intracranial pressure?

Answer 54

All the inhaled anesthetic gases decrease cerebrovascular resistance, increase cerebral blood flow and, as a result, increase intracranial pressure. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 165.

Question 55

How do volatile anesthetics affect mean arterial | pressure?

Answer 55

All volatile anesthetics decrease the MAP in a dose-dependent fashion by decreasing vascular resistance, increasing vascular compliance, and depressing the myocardium. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 611.

Question 56

What is the vapor pressure of sevoflurane?

Answer 56

157 Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 597.

Question 57

What is the vapor pressure of desflurane?

Answer 57

664 Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 597.

Question 58

What is the vapor pressure of isoflurane?

Answer 58

238 Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 597.

Question 59

What are the blood:gas partition coefficients of isoflurane, desflurane, sevoflurane, and nitrous oxide?

Answer 59

Isoflurane = 1.43, desflurane = 0.42, sevoflurane = 0.68, and nitrous oxide = 0.47 Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 86.

Question 60

How many fluorides do desflurane, isoflurane, and | sevoflurane each possess?

Answer 60

Isoflurane has 5 fluorides, desflurane has 6, and sevoflurane is the most fluorinated with 7 fluoride atoms. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 597.

Question 61

What are the oil:gas partition coefficients for isoflurane, desflurane, sevoflurane, and nitrous oxide?

Answer 61

Isoflurane = 99, desflurane = 19, sevoflurane = 50, and nitrous oxide = 1.4 Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 86.

Question 62

What are the molecular weights of nitrous oxide, | isoflurane, desflurane, and sevoflurane?

Answer 62

Nitrous oxide is 44 daltons, isoflurane is 184.5, desflurane is 168, and sevoflurane is 200.1. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 597.

Question 63

What is the MAC of sevoflurane in a healthy, 30-60 | year old with a normal body temperature?

Answer 63

2.0 Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 88.

Question 64

What is the MAC of desflurane in a healthy, 30-60 | year old with a normal body temperature?

Answer 64

6 Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 88.

Question 65

What is the MAC of isoflurane in a healthy, 30-60 | year old with a normal body temperature.

Answer 65

1.17 Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 88.

Question 66

Between desflurane, isoflurane, sevoflurane, and nitrous oxide, which inhaled anesthetic is the most potent?

Answer 66

Isoflurane is the most potent. The oil:gas solubility coefficient provides an indication to the potency of an inhalation anesthetic. The higher the oil:gas solubility, the greater the potency. The oil:gas partition coefficient of isoflurane is 99, for sevoflurane it is 50, for desflurane it is 18.7, and for nitrous oxide it is 1.4. Nagelhout JJ, Plaus K. Nurse Anesthesia. 4th ed. Philadelphia, PA: WB Saunders Company; 2010: 94.

Question 67

How can desflurane affect the heart rate in high | concentrations?

Answer 67

Desflurane produces a small increase in sympathetic activity. When the concentration of desflurane is increased rapidly, catecholamine release is more pronounced and can result in increases in heart rate and blood pressure. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 170.

Question 68

Comparing desflurane, sevoflurane, nitrous oxide and isoflurane, an increase in cardiac output would slow the onset of which inhalation anesthetic the most?

Answer 68

Isoflurane. The effect is greatest in agents with a high blood:gas partition coefficient. The blood:gas partition coefficient of desflurane is 0.42, for nitrous oxide it is 0.47, for sevoflurane it is 0.6, and for isoflurane it is 1.4. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 81.

Question 69

What is compound A and what volatile anesthetic is | associated with it?

Answer 69

Compound A is a vinyl ether that is formed from the degradation of sevoflurane in carbon dioxide absorbents. It has been linked to renal damage in animal studies. No adverse effects have been demonstrated in humans at clinical doses, but the general recommendation is to use at least 2L/min fresh gas flow rate when using sevoflurane as a dilutional measure to prevent the accumulation of compound A in any significant concentration. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 172.

Question 70

What is the most common arrhythmias seen with | sevoflurane? With nitrous oxide?

Answer 70

The most common arrhythmias seen with the use of sevoflurane are isolated supraventricular ectopic beats. Nitrous can produce atrioventricular nodal rhythms. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 612.

Question 71

Isoflurane has been demonstrated to cause coronary | steal in some cases. What is meant by this?

Answer 71

Isoflurane dilates coronary arteries. Diseased vessels with fixed, stenotic lesions, however cannot dilate as effectively as normal vessels. As the normal vessels dilate, blood is shunted towards the normal areas of the heart and away from the areas suplied by the already diseased vessels. This can result in worsening of ischemia. Desflurane and sevoflurane do not cause this effect. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 612.

Question 72

Why is desflurane not used for inhalation inductions | in pediatric patients?

Answer 72

Compared to sevoflurane and nitrous oxide, desflurane acts as a respiratory irritant in concentrations above 6% and can result in breath-holding, coughing, and laryngospasm during induction. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 94.

Question 73

Despite having a lower blood:gas solubility coefficient, the rate of rise of the FA/Fi ratio is higher for nitrous oxide than for desflurane. Why is this?

Answer 73

Agents with a lower blood:gas partition coefficient exhibit a faster rate of rise in the FA/Fi ratio. The exception is that nitrous oxide will exhibit a faster rate of rise than desflurane despite the fact that it has a blood:gas partition coefficient of 0.47 and desflurane has a blood:gas partition coefficient of 0.42. The increase with nitrous oxide is due to the fact that it is administered in doses of 50-70% compared to 3-9% for desflurane. This is referred to as the concentration effect. Nagelhout JJ, Plaus K. Nurse Anesthesia. 4th ed. Philadelphia, PA: WB Saunders Company; 2010: 94-95.

Question 74

Nitrous oxide is 35 times more soluble in blood than | nitrogen. What are the implications of this?

Answer 74

Because nitrous oxide is so much more soluble that nitrogen, it can diffuse into an air-filled space faster than the nitrogen can diffuse out of it, resulting in increased pressure, volume, or both in the space it enters. If the air-filled space is in the stomach or intestines, it can result in distention. If it is a pneumothorax or air embolus, the effects can be disastrous. Nitrous is even capable of diffusing into an endotracheal tube balloon, increasing the pressure it exerts against the tracheal wall. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 166.

Question 75

What is diffusion hypoxia?

Answer 75

The alveolar elimination of nitrous oxide occurs at such a rapid rate that alveolar oxygen and carbon dioxide are diluted. As a result, alveolar oxygen levels can drop below 21%. The administration of 100% oxygen after the discontinuation of nitrous oxide prevents this from occurring. Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail's Clinical Anesthesiology. 5th ed. New York, NY: McGraw-Hill; 2013: 159.

Question 76

What is methionine synthetase and how does nitrous | oxide affect it?

Answer 76

Methionine synthetase is a cobalamin-dependent enzyme necessary for nerve myelination, homocysteine degradation, and DNA synthesis. Nitrous oxide oxidizes the cobalt atom found on vitamin B12 (cobalamin) which can inhibit the formation of methionine synthetase. This would exert little effect on normal, healthy patients, but may warrant consideration of the use of nitrous oxide in patients with severe B12 deficiency. Longnecker DE, Newman MF, Brown DL, Zapol WM. Anesthesiology. 2nd ed. New York: McGraw-Hill; 2012: 613.

Question 77

According to the Occupational Safety and Health Administration (OSHA), operating room personnel should not be exposed to more than how many parts per million of a halogenated agent? What if nitrous oxide is used?

Answer 77

If nitrous oxide is also used, the maximum exposure to halogenated agents allowed by OSHA is 0.5 ppm. If nitrous oxide is not used, then the maximum exposure is 2 ppm. The maximum exposure to nitrous alone is 25 ppm. Nagelhout JJ, Plaus KL. Nurse Anesthesia. 5th ed. St. Louis, MO: Elsevier Saunders Company; 2014: 280.