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92 PART II ANESTHESIA
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chemoreceptor trigger zone of the medulla, causing nausea and vomiting. Finally, rapidly administered
high doses can cause spasm of the thoracoabdominal muscles, resulting in hypoventilation.
29. What is remifentanil, and how does it differ from other opioids?
Remifentanilisanultrashort-actingopioidwithadurationof5to10minutes.Ithasacontext-sensitive
half-time of 3 minutes. It is metabolized by nonspecific plasma esterases. It is commonly used as a continuous infusion. Intravenous bolus administration has been associated with increased incidence of bradycardia and chest-wall rigidity. It also has been shown to induce hyperalgesia and acute opioid tolerance.
30. What are the pharmacokinetics among the commonly used opioids?
See Table7-5.
31. Which opioids stimulate the release of histamine?
Morphine,codeine,andmeperidine(Demerol)causehistaminerelease,resultinginvasodilationand
possible hypotension. Fentanyl, sufentanil, and alfentanil do not stimulate histamine release.
32. What opioid antagonist is most commonly used in clinical anesthesia?
Naloxoneisthepuremu-receptorantagonistthatisusedtoreversetheeffectsofopioids.Naloxone
will reverse overdoses and respiratory depressant effects; however, at the same time, it reverses
theanalgesiceffects.Normaldosagesmaycauseabruptreversal,whichcanresultintachycardia,
hypertension, pulmonary edema, and cardiac dysrhythmias. To avoid these adverse effects, naloxone
shouldbegivenindosesof40mg(0.1mL),repeatedeveryfewminutes.
33. Which intravenous induction agents are recommended for use in major trauma
or other hypovolemic states?
Etomidate is an agent commonly used because of its cardiac stability in patients with limited cardiac
reserve. Ketamine is recommended for patients who are hypovolemic because of the direct stimulationofsympatheticoutowfromtheCNS.However,patientswithdepletedendogenouscatecholamines may not be able to respond to the stimulation, resulting in more hypotension. The induction
doseofetomidateis2to3mg/kgandthatofketamineis1to2mg/kg.
34. Which induction agents alter ICP?
Thiopental,propofol,etomidate,andfentanylreduceICPbecausetheycausedecreasesincerebral
blood flow and cerebral metabolic consumption of oxygen. Ketamine increases cerebral blood flow,
cerebralmetabolism,andICP.
35. What are the roles of anticholinergic medicines in sedation and the differences
among the options?
Anticholinergic medications can be used as antisialagogues as well as in the management of
bradycardia.VariabilityoftheCNSeffectsrelatestothedifferentialabilitytocrosstheBBB.ScopolaminecrossestheBBBwithoutdifculty,causingCNSdepressionandamnesia.Atropinehasless
pronouncedCNSeffectsthanscopolaminebutproducesgreatertachycardia,whereasglycopyrrolate
Table 7-5. Pharmacokinetics among the Commonly Used Opioids
MORPHINE FENTANYL REMIFENTANYL MEPERIDINE
Potency (com-
pared with IV
morphine)
Dosage (sedation/
analgesic)
Onset (minutes) 5-15 1-3 1.5-2 15
Peak (minutes) 20-30 3-5 2 5-7
Duration (hours) 3-4 0.5-1 0.1-0.2 2-3
Clearance Renal Liver Esterases Liver
1 100 250 0.1
2-10mgIV Sedation:0.5mcg/
kg(load);0.01-
0.04mcg/kg/
min(maint)
0.5-1mcg/kgload
(infusedover
30-60seconds);
0.025-0.2mcg/kg/
min(maint)
50-150mgIV
q3-4hours
CHAPTER 7 INTRAVENOUSSEDATION 93
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does not readily cross the BBB. As a result, only scopolamine and atropine have a risk of central
anticholinergicsyndrome(CAS),andemergencedeliriumcanbetreatedwithphysostigmine0.01to
0.03mg/kg,whichmayberepeated.
36. What is the management of an inadvertent intraarterial injection?
• Inductionofanesthesia.Leavethecatheterinplace.
• Inductionofanesthesia.Administer2to10ccof1%procaine(vasodilationmayattenuatethe
arteriospasm).
• Inductionofanesthesia.Assessthepulse/coloroftheextremity.
• Inductionofanesthesia.Consideravascularconsult.
BiBliography
AllenDM:Intravenousanestheticsandbenzodiazepines.InDukeJ, editor: Anesthesia secrets,ed3,Philadelphia,2006,
Mosby.
American Society of Anesthesiologists: Task force on sedation and analgesia by nonanesthesiologists: practice guidelines
for sedation and analgesia by non-anesthesiologists, Anesthesiology96:1004–1017,2002.
HathewayJ:Opioids.InDukeJ, editor: Anesthesia secrets,ed2,Philadelphia,2000,Hanley&Belfus.
HudsonRJ,StanskiDR,BurchPG:Pharmacokineticsofmethohexitalandthiopentalinsurgicalpatients,Anesthesiology
59:215–219,1983.
Malamed S: Sedation: a guide to patient management,ed5,Mosby,2009.
McDowellG:Intravenousinductionagents.InDukeJ, editor: Anesthesia secrets,ed2,Philadelphia,2000,Hanley&Belfus.
NabonsalJ:Preoperativemedications.InDukeJ, editor: Anesthesia secrets,ed2,Philadelphia,2000,Hanley&Belfus.
NuttDJ:NewinsightsintotheroleoftheGABAA—benzodiazepine receptor in psychiatric disorder, Br J Psychiatry
179:390–396,2001.
RevesJG,FragenRJ,VinikHR, et al.: Midazolam: pharmacology and uses, Anesthesiology62:310–324,1985.
StoeltingRK,MillerRD:Intravenousanesthetics.InStoeltingRD,MillerRD, editors: Basics of anesthesia,NewYork,1999,
ChurchillLivingstone.
Swank KM:Preoperativeevaluation.InDukeJ, editor: Anesthesia secrets,ed3,Philadelphia,2006,Mosby.
WinkelmannG:Benzodiazepines.InDukeJ, editor: Anesthesia secrets,ed2,Philadelphia,2000,Hanley&Belfus.
INHALATION ANESTHESIA
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AND NEUROMUSCULAR
BLOCKING AGENTS
CHAPTER 8
Matthew Cooke
1. What inhalational anesthetics are currently available, and how are they delivered
in clinical use?
Three volatile liquids (desflurane, isoflurane, and sevoflurane) and one gas (nitrous oxide) are used
clinically. The volatile liquids require a vaporizer for inhalational administration. Additionally, the
desflurane vaporizer has a heating component to allow delivery at room temperature.
Inhalational anesthetic delivery systems exist for the delivery of one or multiple agents. These
delivery systems have mandatory scavenging and fail-safe mechanisms to optimize safety. Inhalation
agents are administered in hospital operating rooms and outpatient environments, such as surgery
centers and dental offices.
2. What is the mechanism of action of inhalational anesthetics?
The mechanism of action of volatile anesthetics, along with their molecular and cellular actions,
remains elusive. Volatile anesthetics act on synaptic transmission in the central nervous system but
proof remains a matter of debate.
Inhalational anesthetics act in the central nervous system. They disrupt synaptic transmission,
interfere with the release of neurotransmitters from presynaptic nerve terminals, alter reuptake of
neurotransmitters, change binding of neurotransmitters to the postsynaptic receptor sites, and influence the ionic conductance.
The Meyer-Overton theory postulates that anesthesia occurs when a sufficient number of inhalation anesthetic molecules dissolve in the lipid cell membrane. However, the Meyer-Overton theory
does not describe why anesthesia occurs. The Critical Volume Hypothesis believes that the absorption
of anesthetic molecules could expand the volume of a hydrophobic region within the cell membrane
and subsequently distort channels necessary for sodium ion flux and the development of action
potentials necessary for synaptic transmission.
The protein interaction theory hypothesizes that anesthetics bind to specific proteins that affect
ion flux during membrane excitation, resulting in either potentiation of inhibitory neurotransmitters
(e.g., GABA, glycine) or inhibition of excitatory neurotransmitters (e.g., glutamate NMDA receptors).
This is supported by a steep dose response curve.
3. How long can oxygen at 2 L/min be delivered from an E cylinder with a reading of
500 psi?
A full E cylinder of oxygen (O2) contains approximately 600 L at a pressure of 2000 psi. At 2 L/min, a full
E cylinder will deliver O2 for approximately 300 minutes, or 5 hours. A reading of 500 psi will therefore
give you approximately 1 hour and 15 minutes of O2.
4. How long can nitrous oxide (N2O) at 2 L/min be delivered from an E cylinder that
reads 750 psi?
N2O has a pressure of 750 psi, and approximately 1600 L of N2O is contained in an E cylinder. N2O is a
compressed liquid and not a compressed gas like O2. A compressed liquid does not show a linear correlation between volume and pressure as does a compressed gas. N2O pressure will remain at 750 psi
until all the liquid has been vaporized. Therefore an estimated time cannot be determined.
5. Why is N2O use contraindicated in patients with conditions involving closed gas
spaces?
N2O has a low blood-to-gas partition coefficient (0.46) and therefore low solubility. It can leave the
blood and enter air-filled cavities 34 times more quickly than nitrogen can leave the cavity to enter
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the blood. The use of N2O can increase the expansion of compliant cavities, such as a pneumothorax,
bowel gas in a bowel obstruction, and an air embolism. An increase in pressure will occur when N2O
is used with noncompliant cavities, such as the middle ear or sinuses.
The oral and maxillofacial surgeon needs to be cautious when treating the recent trauma patient (e.g.,
motor vehicle accident victim). An asymptomatic, undiagnosed closed pneumothorax can double in size
in 10 minutes after the administration of 70% N2O. Nitrous oxide-oxygen sedation should be postponed in
patients with gastrointestinal obstructions, middle ear disturbances, and, possibly, sinus infections.
6. Should a patient with an upper respiratory infection (URI) be given N2O via a nasal
hood?
Because a patient with a URI has nasal blockage, the delivery of the N2O is limited and the potential for
leakage of N2O around the hood is more likely. In addition, patients with a URI are also more likely to have
associated middle ear and sinus infections. Therefore the use of N2O with patients with URI is unwise.
7. Can inhalational anesthetics be administered to patients with chronic obstructive
pulmonary disease (COPD)?
Administration of volatile anesthetics (desflurane, isoflurane, and sevoflurane) is safe for patients
with COPD (asthmatic bronchitis, emphysema, and chronic bronchitis). Volatile anesthetics are potent
bronchodilators and, therefore, beneficial to patients with COPD.
N2O, however, should be used cautiously. Carbon dioxide (CO2) is a respiratory stimulus for patients
with normal respiratory physiology. Patients with COPD retain larger amounts of CO2 in their lungs and, over
time, lose their respiratory drive. COPD patients thus develop a hypoxic drive. The potential for the hypoxic
drive to cease with the severe chronic patient exists when O2 is >21% room air (i.e., N2O-O2 at 70/30%).
Patients with COPD have increased incidence of pulmonary bullae or blebs (combined alveoli).
Because of N2O’s low blood solubility, it can increase the volume and pressure of these lung defects,
which could create an increased risk of barotrauma and pneumothorax. Duration of exposure and
concentration of N2O must be considered.
During sedation with an open airway, keep patients breathing spontaneously, and do not take
away their respiratory drive. O2 supplementation should be used with caution in patients with severe
COPD. Supplemental O2 via nasal cannula delivers low FiO2, which should not affect hypoxic drive. It
is recommended that oxygen concentrations not exceed an FiO2 of 40. Remember, 4 L through a nasal
cannula equals 36% O2.
Nasal cannula (3 to 6 L/min): FiO2 = 20 + 4 × L/min
Face mask with reservoir (6 to 10 L/min): FiO2 = 10 × L/min
Asthma or reactive airways may occur at any age and could easily be encountered in the
office. Patients with debilitating emphysema and chronic bronchitis are often chronically ill and are
not seen commonly in an office setting. They may, however, be encountered in nursing homes and
hospitals.
8. When is administration of N2O sedation contraindicated in an asthmatic patient?
There are no absolute contraindications for the use of N2O sedation in asthmatic patients. Because
anxiety is a stimulus for an asthmatic attack, N2O sedation is actually beneficial for these patients.
9. What is the second gas effect?
This occurs when one gas speeds the rate of increase of the alveolar partial pressure of a second gas.
This effect is normally associated with an inhalational induction involving a large volume of N2O and a
volatile anesthetic. N2O’s low blood solubility allows it to be absorbed quickly by the alveoli, thus causing an increase in the alveolar concentration of the concomitantly administered volatile anesthetic.
In theory, a high concentration of one gas (e.g., 70% N2O) could speed the induction of a second gas
(e.g., sevoflurane).
Inhalational inductions are normally used in energetic pediatric patients. Obtaining intravenous
access in children who cannot sit still is difficult, and a quick induction is desirable. The speed of
induction with sevoflurane should be increased when it is used concurrently with 70% N2O.
10. What is minimal alveolar concentration (MAC)?
MAC is the concentration of an inhaled anesthetic at 1 atm that prevents skeletal muscle movement
response to a painful stimulus (e.g., surgical skin incision) in 50% of patients (Table 8-1). A MAC of
1.3 prevents skeletal movement in approximately 95% of individuals undergoing surgery. The potency
of anesthetic gases can be compared using MAC.
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Table 8-1. Minimal Alveolar Concentration (MAC) of Commonly Used Agents
AGENT MAC
Nitrous oxide 104
Isoflurane 1.15
Halothane 0.77
Desflurane 6.0
Sevoflurane 1.71
11. What factors affect MAC?
Factors that decrease MAC: Factors that increase MAC:
Higher altitudes (Ø barometric pressure) Increased central neurotransmitter levels (MAOIs,
Pregnancy Cocaine, ephedrine, levodopa)
Hypothermia Hyperthermia
Hyponatremia Alcohol (chronic use)
Alcohol (acute use) Hypernatremia
Barbiturates
Calcium channel blockers
Opioids
12. How can MAC values be used to gauge awareness during surgery?
Intraoperative patient awareness is a concern with all patients undergoing a deep sedation or
general anesthesia. Volatile anesthetics have amnestic properties at an adequate MAC. Intravenous medications are often used in conjunction with volatile anesthetics, which often cause
a decrease in MAC. This decreased MAC may prevent an amnestic state. Although specific
concentrations of volatile agents have not been established for the elimination of intraoperative
recall, clinical studies show that awareness is eliminated between 0.4 and 0.6 MAC for isoflurane.
Attaining a MAC of 0.8 has been recommended to guarantee unconsciousness and, therefore, lack
of awareness.
Awareness precautions need to be taken with certain anesthetic techniques. An anesthetist may
be tempted to decrease the concentration of a volatile anesthetic when a paralytic has been used
because surgical stimulation has been eliminated. The addition of midazolam, an amnestic benzodiazepine, can be used in situations where MAC has been reduced below 0.8. MAC is often reduced in
patients who develop intraoperative hypotension because of volatile inhalational vasodilating properties. Vasopressors, such as ephedrine and phenylephrine, may be necessary to maintain a MAC of 0.8
when additional amnestic medications are not being used.
13. Why are additive values of MAC for inhalational anesthetics beneficial?
Additive values are beneficial when a decrease in volatile anesthetics is desired. MAC values are
additive; therefore the simultaneous administration of N2O with a volatile anesthetic will decrease the
MAC of both agents. For example, using 0.5 MAC N2O (approximately 50%) with 0.5 MAC isoflurane
(approximately 0.6%) results in a MAC of 1.0.
The only inhalational anesthetics that would be administered simultaneously would be a
volatile anesthetic (desflurane, halothane, isoflurane, and sevoflurane) and N2O. Fail-safe mechanisms exist on anesthetic machines to prevent the simultaneous administration of two volatile
agents.
N2O has a MAC >100% and therefore is not used as a sole anesthetic agent, because a minimum of 21% O2 is required at 1 atm. Typically, N2O concentrations of 20% to 70% are used.
14. What are the hemodynamic effects of volatile anesthetics?
Volatile anesthetics depress the cardiovascular system, which results in a reduced mean arterial
pressure. Desflurane, isoflurane, and sevoflurane cause primarily a decrease in systemic vascular
resistance, which is reflected by a reduced blood pressure.
CHAPTER 8 INHALATION ANESTHESIA AND NEUROMUSCULAR BLOCKING AGENTS 97
Oxygenation and Ventilation
Pulmonary Minute
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20
Conscious
(end-expiratory)
control
0.81%
Halothane
10
Volume (L/min)
40 60
End-Expiratory P
Figure 8-1. The CO2 response curve. Note the effects of inhalational anesthetics on the pulmonary minute volume.
1.11%
80 100
CO
(mm Hg)
2
15. What are the hemodynamic considerations of the combined use of a volatile
anesthetic and the intravenous anesthetic propofol?
The inhalational anesthetics desflurane, isoflurane, and sevoflurane and the intravenous agent
propofol are potent vasodilators. Additive effects causing hypotension from a decrease in systemic
vascular resistance occur with simultaneous administration of these two anesthetic groups. Combining these agents should be done cautiously in elderly patients and patients taking hypertensive
medications. Preoperative blood pressures are extremely important. Selection of an alternative
intravenous anesthetic agent may be indicated. If propofol is used along with a volatile anesthetic, then vasopressors (e.g., ephedrine, phenylephrine) should be prepared and made readily
available.
16. What are the respiratory effects of volatile anesthetics?
Volatile anesthetics will cause a dose-dependent decrease in ventilation. Volatile anesthetics cause a
decrease in tidal volume (TV) with a compensatory increase in respiratory rate (RR) but a net decrease
in minute ventilation (mV).
Volatile anesthetics: net ↓mV = ↑RR × ↓TV
This decreased minute ventilation causes an increase in CO2. An increase in CO2 stimulates the respi-
ratory drive in the unanesthetized patient. Inhalational anesthetics, however, shift the CO2 response
curve to the right and lessen the ventilatory response to hypercarbia and hypoxia (Fig. 8-1).
17. What is partition coefficient? How can it influence the speed of induction?
A partition coefficient is defined as a distribution ratio of a volatile anesthetic as it distributes itself
between two phases at equilibrium when the temperature, pressure, and volume are the same
(Table 8-2). A blood-to-gas coefficient therefore describes the distribution of anesthetic between blood
and gas. High blood solubility requires a greater concentration of inhaled anesthetic to be dissolved
in the blood before equilibrium can occur. The blood acts as an inactive reservoir that prevents the
anesthetic from reaching the site of action, thereby slowing induction.
Gases with low solubility in blood and adipose equilibrate more rapidly. Nitrous oxide has very
low solubility and therefore achieves equilibration most rapidly. This explains why nitrous oxide has
the fastest onset among inhalation agents (Fig. 8-2). Relative onset of effect is directly proportional
to solubility, when all other factors are equal (e.g., alveolar concentration, cardiac output). The lower
solubility of sevoflurane compared with isoflurane explains why sevoflurane is a more rapid induction
agent.
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1.0
Minutes
F
/ F
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0.8
I
0.6
A
0.4
0.2
Nitrous oxide
Desflurane
Sevoflurane
Isoflurane
0
Figure 8-2. Relative Onset of Effect. Gas tensions throughout body tissues equilibrate when the inspired gas tension (FI)
equals that in the alveoli (FA). (Becker D, Rosenberg M: Nitrous oxide and the inhalation anesthetics, Anesth Prog 55(4):
124–131, 2008 Winter.)
10 20
30
Table 8-2. Partition Coefficients for Inhaled Anesthetics
DESFLURANE ISOFLURANE N2O SEVOFLURANE
Blood:gas 0.42 1.4 0.46 0.68
Brain:blood 1.3 1.6 1.1 1.7
Muscle:blood 2.0 2.9 1.2 3.1
Fat:blood 27 45 2.3 48
Oil:blood 18.7 90.8 1.4 47.2
18. Which volatile anesthetic has the quickest wake-up potential after a long
(>5 hours) surgical procedure?
Anesthetics take time to be distributed from the blood to the tissues (e.g., muscle, fat). As the length
of time of a surgery increases and tissues become increasingly saturated with an anesthetic, wakeup times increase. The fat-to-blood partition coefficient for desflurane is the lowest for all volatile
anesthetics, and it provides the quickest wake-up. A common misconception is that sevoflurane has
a quick wake-up time because it has a quick onset. For short surgeries this is true, because tissue
saturation has not had time to occur. For long surgeries, however, sevoflurane does not provide a
quick wake-up. (See sevoflurane’s tissue:blood coefficients in Table 8-2.)
19. What is diffusion hypoxia?
Although its existence has been questioned, diffusion hypoxia is postulated to occur when the admin-
istration of N2O has been discontinued with the spontaneous breathing of room air. The theory holds
that N2O’s low blood solubility allows it to leave the blood rapidly and enter the alveoli. Excessive
N2O in the alveoli dilutes the O2 and makes the patient hypoxic. This phenomenon has been refuted
by many studies. Nonetheless, because of side effects such as headaches, nausea, vomiting, and
lethargy, administering O2 for 3 to 5 minutes following N2O use is recommended.
20. What are the concerns to administration of N2O sedation to an obstetric patient?
N2O crosses the placenta and therefore has the potential to cause teratogenic effects to the fetus. The
greatest potential for problems exists during the first trimester when organs are forming. Significant
exposure during the first 6 weeks can inhibit DNA synthesis. Consequently, female surgeons and staff
who are not aware that they are pregnant may be at greater risk than patients.
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Recent research has refuted the claim that N2O is dangerous to the fetus. Although N2O has been
used safely for years in obstetrics, it would be wise to obtain a medical consult before its administration in pregnant women who are in their second or third trimesters. Even if N2O sedation is approved
by the patient’s obstetrician, it should be used only for short procedures, and no more than 50% N2O
should be administered.
21. What are neuromuscular blocking agents (NMBs)?*
NMBs, commonly called muscle relaxants, are drugs that interrupt transmission at the neuromuscular
junction. These drugs provide skeletal muscle relaxation and, consequently, can be used to facilitate
tracheal intubation, assist with mechanical ventilation, and optimize surgical conditions. Occasionally,
they may be used to reduce the metabolic demands of breathing; in the management of status epilepticus (although they do not diminish central nervous system activity), status asthmaticus, or tetanus;
and to facilitate the treatment of raised intracranial pressure.
These drugs inhibit the function of all skeletal muscle, including the diaphragm, and must be
administered only by personnel skilled in airway management. NMBs should never be given without
preparation to maintain the airway and ventilation. The concomitant use of sedative-hypnotic or
amnestic drugs is indicated, because NMBs alone achieve complete paralysis while allowing the
patient complete awareness.
22. How are NMBs classified?*
These drugs are classified into two groups according to their actions at the neuromuscular
junction:
1. Depolarizing NMB (succinylcholine [SCh]): SCh mimics the action of acetylcholine by depolarizing
the postsynaptic membrane at the neuromuscular junction. The postsynaptic receptor is occupied/
depolarized and remains refractory to further stimulation.
2. Nondepolarizing NMBs: These agents act by competitive blockade of the postsynaptic membrane,
so that acetylcholine is blocked from the receptors and cannot have a depolarizing effect.
23. What is the mechanism of action of SCh?*
SCh is the only depolarizing agent to be used widely in clinical anesthetic practice. The depolarizing
agent mimics the action of acetylcholine. However, because SCh is hydrolyzed by plasma cholinesterase (pseudocholinesterase), which is present only in the plasma and not at the neuromuscular
junction, the length of blockade is directly related to the rate of diffusion of SCh away from the
neuromuscular junction. Consequently, the resultant depolarization is prolonged when compared with
acetylcholine. Depolarization gradually diminishes, but relaxation persists as long as SCh is present at
the postsynaptic receptor.
24. What are the indications for using SCh?*
In clinical situations in which the patient has a full stomach and is at risk for regurgitation and
aspiration when anesthetized, rapid paralysis and airway control are priorities. Such situations include
diabetes mellitus, hiatal hernia, obesity, pregnancy, severe pain, and trauma.
SCh provides the most rapid onset of any NMB currently available. In addition, the duration of
blockade induced by SCh is only 5 to 10 minutes. Respiratory muscle function returns quickly should
the patient prove difficult to intubate. SCh is indicated for the treatment of laryngospasm unresponsive
to positive pressure ventilation.
25. What is the breakdown and elimination process of nondepolarizing NMBs?*
Atracurium and cisatracurium are unique in that they undergo spontaneous breakdown at physiologic
temperatures and pH (Hoffmann elimination), as well as ester hydrolysis. These properties allow safe
delivery in patients with compromised hepatic or renal function.
Aminosteroid relaxants (pancuronium, vecuronium, pipecuronium, and rocuronium) are
deacetylated in the liver, and their action may be prolonged in the presence of hepatic dysfunction.
Vecuronium and rocuronium also have significant biliary excretion, and their action may be prolonged
with extrahepatic biliary obstruction.
Relaxants with significant renal excretion include tubocurarine, metocurine, doxacurium, pancuronium, and pipecuronium.
* Reprinted from Warnecke DE: Neuromuscular blocking agents. In Duke J, editor: Anesthesia secrets, ed 2, Philadelphia,
2000, Hanley & Belfus.
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Table 8-3. Neuromuscular Blocking Reversal Agents
DRUG DOSE (MG/KG) ONSET (MIN) DURATION (MIN)
Edrophonium 0.5-1.0 2 45-60
Neostigmine 0.035-0.07 7 60-90
Pyridostigmine 0.15-0.25 11 60-120
26. Is it possible to reverse the effects of the nondepolarizing NMBs?*
Just as competition at the receptor sites of the neuromuscular junction allows the relaxant to
overcome the effects of acetylcholine, medications that increase the amount of acetylcholine at the
neuromuscular junction facilitate reversal of relaxation. Reversal agents are acetylcholinesterase
inhibitors and include neostigmine, pyridostigmine, and edrophonium (Table 8-3). These drugs inhibit
the enzyme that breaks down acetylcholine, making more of this neurotransmitter available at each
receptor. Physostigmine, another acetylcholinesterase inhibitor, crosses the blood-brain barrier and
is not used for reversal of muscle relaxants. Pyridostigmine is used in the management of patients
with myasthenia gravis. The acetylcholinesterase inhibitors possess positively charged quaternary
ammonium groups, are water-soluble, and are renally excreted.
27. NMB reversal agents cause an increase in available acetylcholine. Is this a
problem?*
It is important to remember that the muscarinic effects of these drugs at cholinergic receptors in the
heart must be blocked by atropine or glycopyrrolate to prevent bradycardia. The degree of bradycardia
may be significant. Even asystole has been noted. The most common doses used for this purpose are
0.01 mg/kg of atropine and 0.005 to 0.015 mg/kg of glycopyrrolate.
To prevent bradycardias associated with the anticholinesterases, it is important to administer
an anticholinergic with a similar onset of action. Atropine is administered with edrophonium and
glycopyrrolate with neostigmine.
28. The heart is a muscle. Do muscle relaxants decrease contraction of the
myocardium?*
The NMBs have their primary effect at nicotinic cholinergic receptor sites. The myocardium is a
muscle with nerve transmission accomplished via adrenergic receptors using norepinephrine as the
transmitter. Consequently, muscle relaxants have no effect on cardiac contractility. NMBs also have no
effect on smooth muscle.
29. How do we make muscle relaxants work faster if we need to secure the airway
sooner?*
By overwhelming the sites of action (receptors in the neuromuscular junction), one can provide a
competitive advantage for the blocking drug over acetylcholine. This is exactly what is done with the
standard intubating dose of a nondepolarizing relaxant. The usual intubating dose is approximately
three times the ED95 (the dose expected to show 95% reduction in twitch height on electrical stimulation). For relaxants with cardiovascular stability, further increases in initial dose can provide some
decrease in onset time without producing side effects. However, with the exception of the nondepolarizing NMB rocuronium, it is very difficult to decrease the onset time to that of SCh. For drugs with side
effects such as histamine release, increases in dose usually increase side effects as well.
Another method of decreasing onset time is the priming technique. By giving one-third of the
ED95 at 3 minutes before the intubating dose, one can decrease onset time by as much as 1 minute.
However, sensitivity to the paralyzing effects of these agents varies greatly among patients, and some
patients may become totally paralyzed with a priming dose. Other patients may experience distressing
diplopia, dysphagia, or the sensation of not being able to take a deep breath. For this reason, the practice of administering “priming” doses of relaxants is discouraged by many anesthesiologists. Once
relaxants are administered at any dose, the anesthetist should be in the position to assist ventilation.
* Reprinted from Warnecke DE: Neuromuscular blocking agents. In Duke J, editor: Anesthesia secrets, ed 2, Philadelphia,
2000, Hanley & Belfus.
CHAPTER 8 INHALATION ANESTHESIA AND NEUROMUSCULAR BLOCKING AGENTS 101
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30. What is plasma cholinesterase (pseudocholinesterase)?*
Plasma cholinesterase is produced in the liver and metabolizes SCh as well as ester local anesthetics.
A reduced quantity of plasma cholinesterase may be the result of liver disease, pregnancy, malignancies, malnutrition, collagen vascular disease, and hypothyroidism. This reduction could result in a
prolonged duration of blockade with SCh.
31. What is the importance of a dibucaine number?*
The dibucaine number is used to identify individuals at risk for prolonged paralysis following adminis-
tration of SCh. Dibucaine number is the percent of pseudocholinesterase (PChE) enzyme activity that
is inhibited by dibucaine. Dibucaine inhibits normal plasma cholinesterase by 80%, whereas atypical
plasma cholinesterase is inhibited by only 20%. A patient with normal SCh metabolism will have a
dibucaine number of 80. If a patient has a dibucaine number of 40 to 60, then that patient is heterozygous for this atypical plasma cholinesterase and will have a moderately prolonged block with SCh. If
a patient has a dibucaine number of 20, the patient is homozygous for atypical plasma cholinesterase
and will have a very prolonged block with SCh.
It is important to remember that a dibucaine number is a qualitative, and not quantitative, measurement. Consequently, a patient may have a dibucaine number of 80 but have prolonged blockade
with SCh related to decreased levels of normal plasma cholinesterase.
32. Are clinicians accurate in determining arterial desaturation by “visual oximetry”
(how red is the blood)?
†
No. Pulse oximetry should be regarded as the fifth vital sign.
33. Can any other environmental or clinical conditions result in inaccurate pulse
oximetry values?
†
Reliability depends on a strong arterial pulse plus good light transmission. Inaccuracy results with
hypotension (mean arterial pressure <50 mm Hg), hypothermia (<35° C), vascular disease
(poor peripheral perfusion), and vasopressor therapy (vasoconstriction). Bright lights, intravenous dyes,
nail polish, and excessive motion each may produce bad information.
34. What is the relationship between oxyhemoglobin saturation (SaO2) and partial
pressure of oxygen (PaO2)?
†
Proper interpretation of pulse oximetry requires recall of the oxyhemoglobin dissociation curve
(Fig. 8-3). A rightward shift (decreased hemoglobin affinity for oxygen) facilitates oxygen unloading at
the tissue level. Increasing temperature, increasing PaCO2, increasing 2,3-diphosphoglycerate, and
increasing hydrogen ion concentration—all “increases”—shift the curve to the right. When the PaO2
is >100 mm Hg, however, the curve is virtually flat. Consequently, a large drop in PaO2 (e.g., from 200
to 100 mm Hg) may occur with no discernible change in SaO2.
35. How should a hypoxic event be managed?
†
Before you even start trying to make the diagnosis, give oxygen. The first maneuver for intubated
patients is to hand-ventilate with an Ambu bag. A ruptured endotracheal tube cuff is self-evident,
whereas difficult bagging implies airway obstruction, bronchospasm, or tension pneumothorax.
Inability to pass a suction catheter confirms endotracheal tube obstruction. If the obstruction is not
reversible by changing head position or by cuff deflation, the endotracheal tube must be replaced
immediately. If there is difficulty with bagging and no evidence of airway obstruction, listen to the
chest for breath sounds to exclude a tension pneumothorax. The mechanical ventilator and breathing
circuit must be examined for malfunction. Send arterial blood gases to confirm hypoxia (low PO2) and
rule out hypoventilation (high PCO2).
Next, get a chest X-ray (to rule out a pneumothorax and to confirm the correct position of the
endotracheal tube) and review recent medications, interventions (e.g., suctioning, position changes,
nursing care), and changes in clinical status. Most acute hypoxic events in the intensive care unit are
the result of easily identified and reversible mechanical problems, such as disconnects from oxygen
delivery systems or mucus plugging that requires suctioning.
* Reprinted from Warnecke DE: Neuromuscular blocking agents. In Duke J, editor: Anesthesia secrets, ed 2, Philadelphia,
2000, Hanley & Belfus.
†
Reprinted from Haenel J, Johnson JL: Oxygen monitoring and assessment. In Harken AH, Moore EE, editors: Abernathy’s
surgical secrets, ed 5, Philadelphia, 2005, Mosby.
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