Handbook of Clinical Anesthesia

Chapter 31

Monitored Anesthesia Care

During monitored anesthesia care, the continuous attention of the anesthesiologist is directed at optimizing patient comfort and safety (Hillier SC, Mazurek MS: Monitored anesthesia care. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 815–832).

  1. Terminology

It is important to distinguish between the terms monitored anesthesia care and sedation/analgesia. Monitored anesthesia care implies the potential for a deeper level of sedation than that provided by sedation/analgesia and is always administered by an anesthesiologist provider. The standards for preoperative evaluation, intraoperative monitoring, and the continuous presence of a member of the anesthesia care team are no different from those for general or regional anesthesia. Conceptually, monitored anesthesia care is attractive because it should invoke less physiologic disturbance and allow a more rapid recovery than general anesthesia.

  1. Preoperative Assessment

The preoperative assessment of a patient scheduled for surgery under monitored anesthesia care should be as comprehensive as that performed before a general or regional anesthetic is administered. Additional considerations in the preoperative assessment of the patient scheduled to undergo monitored anesthesia care include evaluation of the patient's ability to remain immobile and cooperative. Verbal communication between the anesthesiologist and patient is important in order to evaluate the level of sedation, reassure the patient, and provide a mechanism when the patient is required to cooperate. The presence of a persistent cough may

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make it difficult for the patient to remain immobile (attempts to attenuate the cough with sedation are not likely to be successful). Additionally, orthopnea may make it impossible for the patient to lie flat.

III. Techniques of Monitored Anesthesia Care

A variety of medications are commonly administered during monitored anesthesia care with the desired endpoints of providing patient comfort, maintaining cardiorespiratory stability, improving operating conditions, and preventing recall of unpleasant perioperative events.

  1. Monitored anesthesia care usually involves intravenous (IV) administration of drugs with anxiolytic, hypnotic, analgesic, and amnestic properties either alone or as a supplement to a local or regional anesthetic.
  2. The drug(s) selected should allow rapid and complete recovery with a minimal incidence of nausea and vomiting or residual cardiorespiratory depression.
  3. A level of sedation that allows verbal communication is optimal for the patient's comfort and safety. If the level of sedation is deepened to the extent that verbal communication is lost, most of the advantages of monitored anesthesia care are also lost, and the risks of the technique approach those of general anesthesia with an unprotected and uncontrolled airway.
  4. Increased patient agitation may be a result of pain or anxiety (Table 31-1).
  5. Pharmacologic Basis of Monitored Anesthesia Care Techniques: Optimizing Drug Administration
  6. The ability to predict the effects of drugs demands an understanding of their pharmacokinetic and pharmacodynamic properties (context-sensitive half-time, effect site equilibration time, drug interactions).
  7. To avoid excessive levels of sedation, drugs should be titrated in increments rather than administered in larger doses according to predetermined notions of efficacy.
  8. Continuous infusions (e.g., propofol) are superior to intermittent bolus dosing because they produce lessfluctuation in drug concentration, thus reducing the number of episodes of inadequate or excessive sedation and contributing to a more prompt recovery (Fig. 31-1).

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Table 31-1 Causes of Patient Agitation During Monitored Anesthesia Care

Pain or anxiety
Life-threatening factors
   Hypoxemia
   Hypoventilation
   Impending local anesthetic toxicity
   Cerebral hypoperfusion
Less ominous but often overlooked factors
   Distended bladder
   Hypothermia or hyperthermia
   Pruritus
   Nausea
   Positional discomfort
   Uncomfortable oxygen masks or nasal cannulas
   Intravenous cannulation site infiltration
   Member of surgical team leaning on the patient
   Prolonged pneumatic tourniquet inflation

 

Figure 31-1. Schematic depiction of the changes in drug concentration during continuous infusion of the drug (heavy line indicates maintenance of a therapeutic concentration) or intermittent bolus injection of the drug (lighter line indicates that the drug concentration is often above or below the desired therapeutic concentration).

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  1. Distribution, Elimination, Accumulation, and Duration of Action

After administration of IV drugs, the immediate distribution phase causes a rapid decrease in plasma levels as the drug is quickly transported to the vessel-rich group of rapidly equilibrating tissues. Accumulation of drug in poorly perfused tissues during prolonged IV infusion may contribute to delayed recovery when the drug is released back into the central compartment after drug administration is discontinued.

  1. Elimination half-lifeis often cited as a determinant of a drug's duration of action, when it is actually often difficult to predict the clinical duration of action from this value.
  2. The elimination half-life represents a single-compartment model in which elimination is the only process that can alter drug concentration.
  3. Most drugs used by anesthesiologists for monitored anesthesia care are lipophilic and much more suited to multicompartmental modeling than single-compartment modeling. In multicompartmental models, the metabolism and excretion of some IV drugs may make only a minor contribution to changes in plasma concentration compared with the effects of intercompartmental distribution.
  4. Context-sensitive half-timeis the time required for the plasma drug concentration to decline by 50% after an IV infusion of a particular duration is terminated. It is calculated by computer simulation of multicompartmental pharmacokinetic models of drug disposition.
  5. The context-sensitive half-time increases as the duration of the infusion increases (particularly for fentanyl and thiopental).
  6. This confirms that thiopental is not an ideal drug for continuous infusion during ambulatory procedures.
  7. The context-sensitive half-time of propofol is prolonged to a minimal extent as the infusion duration increases. (After the infusion ends, the drug that returns to the plasma from the peripheral compartments is rapidly cleared by metabolic processes and is therefore not available to slow the decay in plasma levels.)
  8. The context-sensitive half-times of drugs bear no constant relationship to their elimination half-times.

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Figure 31-2. The time to awakening is determined by the duration of infusion (context-sensitive half-time), the difference in the plasma concentration at the end of the procedure, and the plasma concentration below which awakening will occur.

  1. How Does the Context-Sensitive Half-Time Relate to the Time to Recovery?The context-sensitive half-time does not directly describe how long it will take for the patient to recover from sedation/analgesia but rather how long it will take for the plasma concentration or drug to decrease by 50%. The time to recovery depends on how far the plasma concentration must decrease to reach levels compatible with awakening (Fig. 31-2).
  2. Effect site equilibrationdescribes the time from rapid IV administration of a drug until its clinical effect is manifest. (A delay occurs because the blood is not usually the site of action but is merely the route via which the drug reaches its effect site.)
  3. Thiopental, propofol, and alfentanil have a short effect site equilibration times compared with midazolam, sufentanil, and fentanyl. This is an important consideration when determining bolus spacing of doses.
  4. A distinct time lag between the peak serum fentanyl concentration (which is an important consideration when determining bolus spacing of doses) and the peak electroencephalographic (EEG) slowing can be seen, but after administration of alfentanil, the EEG

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spectral edge changes closely parallel serum concentrations. If an opioid is required to blunt the response to a single, brief stimulus, alfentanil might represent a more logical choice than fentanyl.

  1. Drug Interactions in Monitored Anesthesia Care
  2. No one inhaled or IV drug can provide all the components of monitored anesthesia care. Patient comfort is usually maintained by a combination of drugs that act synergistically to enable reductions in the dose requirements of individual drugs.
  3. It is likely that a rapid recovery in the ambulatory setting can be achieved by using an opioid in combination with other drugs (especially a benzodiazepine) rather than using an opioid as the sole anesthetic.
  4. Opioid and benzodiazepine combinations are frequently used to achieve the components of hypnosis, amnesia, and analgesia.
  5. The opioid–benzodiazepine combination displays marked synergism in producing hypnosis. This synergism also extends to unwanted effects of these drugs. (Whereas midazolam alone produces no significant effects on ventilation, the combination with fentanyl produces apnea in many patients.)
  6. The advantage of synergy between opioids and benzodiazepines should be carefully weighed against the disadvantages of the potential adverse effect of this drug combination on the cardiovascular system and breathing.

VII. Specific Drugs Used During Monitored Anesthesia Care (Table 31-2)

  1. Propofolhas many of the ideal properties of a sedative-hypnotic for use in sedation/analgesia.
  2. The context-sensitive half-time of propofol remains short even after prolonged IV infusions (in contrast to midazolam), and the short effect site equilibration time makes propofol an easily titratable drug that has an excellent recovery profile.
  3. The prompt recovery combined with a low incidence of nausea and vomiting make propofol well suited to ambulatory sedation/analgesia procedures.

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Table 31-2 Dose Ranges for Drugs Used to Produce Sedation/Analgesia

Drug

Typical Adult Intravenous Dose (Titrated to Effect in Increments)

Benzodiazepines

Midazolam

1–2 mg before propofol or remifentanil infusion

Diazepam

2.5–10.0 mg

Opioids

Alfentanil

5–20 µg/kg bolus 2 minutes before stimulus

Fentanyl

0.5–2 µg/kg bolus 2 minutes before stimulus

Remifentanil

0.1 µg/kg/min infusion 5 minutes before stimulus and then weaned to 0.05 µg/kg/min as tolerated (adjust up or down in increments of 0.025 µg/kg/min; decrease dose accordingly when coadministered with midazolam or propofol)

Propofol

250–500 µg/kg boluses
25–75 µg/kg/min infusion

Ketamine

4–6 mg/kg PO
2–4 mg/kg IM
0.25–1 mg/kg IV

Dexmedetomidine

0.5–1.0 µg/kg over 10–20 minutes followed by 0.2–0.7 µg/kg/hr

IM = intramuscular; IV = intravenous; PO = per os.

  1. Propofol in typical sedation/analgesia doses (25–75 µg/kg/min IV) has minimal analgesic properties and does not reliably produce amnesia.
  2. Benzodiazepinesare commonly used during sedation/analgesia for their anxiolytic, amnestic, and hypnotic properties.
  3. Midazolam has many advantages over diazepam and is the most commonly used benzodiazepine for sedation/analgesia (Table 31-3).
  4. Despite a short elimination half-time, there is often prolonged psychomotor impairment after sedation/analgesia techniques using midazolam as the main component.

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Table 31-3 Comparison of the Important Properties of Midazolam and Diazepam

Midazolam

Diazepam

Water soluble (does not require propylene glycol for solubilizing)

Lipid soluble (requires propylene glycol for solubilizing)

Not a veno-irritant (usually painless on injection)

Venoirritant (pain on injection)

Thrombophlebitis is rare

Thrombophlebitis is common

Short elimination half-time (4 hours)

Long elimination half-time (>20 hours)

Clearance is unaffected by H2 antagonists

Clearance is reduced by H2 antagonists

Inactive metabolites (1-hydroxy midazolam)

Active metabolites (desmethy-diazepam, oxazepam)

Resedation is unlikely

Resedation is more likely

  1. Midazolam may be better used in a modified role by administering lower doses before the start of a propofol infusion to provide the specific amnestic and anxiolytic component of a balanced sedation technique.
  2. The analgesic component of a balanced sedation technique could be provided by regional/local techniques or opioids. (There is a risk of significant respiratory depression when a benzodiazepine is combined with an opioid.)
  3. The dose of benzodiazepine required to reach a desired clinical endpoint is decreased in elderly patients compared with younger patients (reflecting pharmacodynamic factors) (Fig. 31-3).
  4. Flumazenil Antagonism of Benzodiazepines(Table 31-4). Routine use of flumazenil-antagonized benzodiazepine sedation is not cost effective.
  5. Opioids.The analgesic component of “balanced sedation/analgesia” is provided by an opioid, and sedation is provided by drugs (propofol, midazolam) with specific and potent hypnotic and amnestic properties (Tables 31-2 and 31-5).
  6. Remifentanilis a µ opioid agonist with a rapid onset (brain equilibration time, 1.0–1.5 minutes) and offset (ester hydrolysis) that facilitate titration to effect during monitored anesthesia care (MAC).

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Figure 31-3. The plasma concentration of midazolam at which 50% of subjects will fail to respond to verbal command (Cp50) is a function of age.

  1. The likelihood of depression of ventilation or chest wall rigidity is decreased by administering remifentanil over 30 to 90 seconds or using a continuous IV infusion technique.
  2. A bolus dose (1 µg/kg IV) administered over 30 seconds administered 90 seconds before placement of a retrobulbar block is effective in preventing pain during subsequent placement of the block.
  3. Administration of midazolam (2 mg IV) in combination with remifentanil results in decreased dose requirements for the opioid and relieves patient anxiety.

Table 31-4 Recommended Regimen for Use of Flumazenil

The initial recommended dose is 0.2 mg IV.
If the desired level of consciousness is not achieved within45 seconds, repeat 0.2 mg dose IV.
If necessary, repeat 0.2 mg IV every 60 seconds to a maximum of1.0 mg.
Recognize the potential for resedation.

IV = intravenous.

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Table 31-5 Indications for Administration of an Opioid During Monitored Anesthesia Care

Initial injection of a local anesthetic
Retrobulbar block
Patient discomfort unrelated to the procedure
Uncomfortable position
Propofol injection
Pneumatic tourniquet pain

  1. Because most painful stimuli are of unpredictable duration and because the risk of depression of ventilation is increased after bolus administration, the most logical method for administration of remifentanil during monitored anesthetic care is by adjustable IV infusion (see Table 31-2).
  2. Discontinuation or accidental interruption of the remifentanil infusion will result in abrupt offset of effect, which may result in patient discomfort, hemodynamic instability, and patient movement.
  3. Ketamineis an intense analgesic that is frequently used as a component of pediatric sedation techniques (0.25–0.5 mg/kg IV produces minimal respiratory and cardiovascular depression) (see Table 31-2).
  4. Increased oral secretions make laryngospasm more likely (an antisialagogue should be administered).
  5. Ketamine is frequently combined with a benzodiazepine to reduce the incidence of hallucinations.
  6. Patient movement may make ketamine less than ideal for procedures requiring the patient to remain motionless.
  7. Dexmedetomidinestimulates α-2 receptors to produce sedation, analgesia, decreases in sympathetic outflow, and an increase in cardiac vagal activity (bradycardia and hypotension) (see Table 31-2).
  8. Respiratory function is not depressed to the same extent as with other sedatives, and patients sedated with dexmedetomidine are more easily aroused from a given level of sedation. However, airway intervention to relieve obstruction and apnea may be required during dexmedetomidine administration, particularly when used in combination with other respiratory depressants.

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Table 31-6 Comparative Properties of Propofol and Dexmedetomidine

 

Propofol

Dexmedetomidine

Pain upon injection

Yes

Minimal

Analgesic properties with subhypnotic doses

Minimal

Yes

Amnestic properties with subhypnotic doses

Significant

Insignificant

Time of onset with typical administration

Rapid

5–10 minutes

Restrictive regulations on use by non-anesthesiologist providers

Yes

No

Potential for significant bradycardia

Minimal

Significant

  1. Episodes of bradycardia and sinus arrest have been associated with dexmedetomidine administration in young healthy volunteers with a high vagal tone, particularly during rapid IV injection.
  2. Dexmedetomidine may be used for pediatric magnetic resonance imaging and computed tomography studies.
  3. Amnesia During Sedation with Dexmedetomidine or Propofol(Table 31-6). All sedative-hypnotics have the potential to impair memory formation. In contrast to propofol and benzodiazepines, it is unlikely that dexmedetomidine has amnestic properties at subhypnotic doses.

VIII. Patient-Controlled Sedation and Analgesia

  1. Techniques that allow the patient some direct control of the level of sedation increases patient satisfaction and eliminates the unpredictable variability in dose requirements between patients.
  2. A conventional patient-controlled analgesia delivery system that is set to deliver 0.5 mg midazolam and 25 µg fentanyl with a 5-minute lockout interval is useful. Alfentanil as a 5-µg/kg IV bolus with a 3-minute lockout period results in patient acceptability and an outcome comparable to physician-controlled analgesia.

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  1. Respiratory Function and Sedative-Hypnotics

During monitored anesthesia care, there is a risk of depression of ventilation as a result of drug-induced effects (with opioids, there is the potential for hypotension resulting in brainstem hypoperfusion). During sedation, it is likely that protective upper airway reflexes will be attenuated.

  1. Sedation and the Upper Airway
  2. The coordinated activation of the diaphragm and upper airway muscles (important for maintaining airway patency) is extremely sensitive to sedative-hypnotic drug administration.
  3. Elderly patients and those with pre-existing chronic obstructive pulmonary disease often have limited respiratory reserve and are unable to increase their respiratory muscle activity in response to the increased work of breathing induced by sedation; they may become hypercarbic, acidotic, and hypoxemic.
  4. Sedation and Protective Airway Reflexes
  5. Protective laryngeal and pharyngeal (swallowing) reflexes are depressed by drugs that produce sedation.
  6. Aspiration of gastric contents may occur either in the operating room or during recovery, particularly if oral intake is allowed before the return of adequate upper airway protective reflexes.
  7. Advanced age and debilitation may compromise the protective upper airway reflexes, placing these patients at increased risk for aspiration during sedation.
  8. Ideally, patients should be awake enough to recognize the regurgitation of gastric contents and be able to protect their own airways.
  9. Sedation and Respiratory Control
  10. It is likely that during regional anesthesia, there is a degree of deafferentation that will potentiate the respiratory depressant effects of sedative-hypnotic drugs, especially opioids.
  11. When used in combination, opioids and benzodiazepines appear to have the potential to produce marked depressant effects on respiratory responsiveness.
  12. Supplemental Oxygen Administration
  13. Arterial hypoxemia as a result of alveolar hypoventilation is a risk after the administration of sedatives, hypnotics, or analgesics.

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  1. In the absence of significant lung disease, the administration of only modest concentrations of supplemental oxygen is usually effective in restoring oxygenation to an acceptable level.
  2. A patient who is receiving minimal supplemental oxygen may have acceptable oxygenation despite significant alveolar hypoventilation.
  3. Before making the decision to discharge a patient to a less well-monitored environment without supplemental oxygen, it is useful to measure oxygen saturation with a pulse oximeter while the patient is breathing room air.
  4. Monitoring During Monitored Anesthesia Care
  5. American Society of Anesthesiologists (ASA) Standards for Basic Anesthetic Monitoringare applicable to all levels of anesthesia care, including monitored anesthesia care.
  6. Communication and Observation
  7. The presence of a vigilant anesthesiologist is the single most important monitor in the operating room.
  8. The effectiveness of this vigilance is enhanced by monitoring techniques and devices (Table 31-7).
  9. It is important that the anesthesiologist continually evaluates the patient's response to verbal stimulation to titrate the level of sedation and to allow the early detection of neurologic or cardiopulmonary dysfunction.
  10. Preparedness to Recognize and Treat Local Anesthetic Toxicity
  11. Because monitored anesthesia care is often provided in the context of regional or local anesthetic techniques, it is important that the anesthesiologist maintains a high index of suspicion for the risk of local anesthetic toxicity, especially in elderly and debilitated patients.
  12. Even if the anesthesiologist does not perform the block, he or she is in a unique position to advise the surgeon about the most appropriate volume, concentration, and type of local anesthetic drug or technique to be used.
  13. The clinically recognizable toxic effects of local anesthetics on the central nervous system and the

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cardiovascular system are concentration dependent. Cardiovascular toxicity usually occurs at a higher plasma concentration than neurotoxicity, but when it does occur, it is usually more difficult to manage than neurotoxicity.

Table 31-7 Monitoring Techniques and Devices Used During Monitored Anesthesia Care

Visual, Tactile, and Auditory Assessment
Rate, depth, and pattern of breathing
Palpation of the arterial pulse
Peripheral perfusion based on temperature of the extremitiesand capillary refill
Diaphoresis
Pallor
Shivering
Cyanosis
Acute changes in neurologic status
Auscultation
Heart and breath sounds (precordial stethoscope)
Pulse Oximetry (an ASA standard)
Capnography (most effective in intubated patients but can beadapted [side stream] to MAC)
Electrocardiography
Temperature (forced-air heating is an effective means ofmaintaining normothermia)
Bispectral Index (value <80 minimizes the possibility of recall during sedation)

ASA = American Society of Anesthesiologists; MAC = minimum alveolar concentration.

  1. At low plasma concentrations, sedation and numbness of the tongue and circumoral tissues and a metallic taste are prominent features of local anesthetic toxicity.
  2. As plasma concentrations increase, restlessness, vertigo, tinnitus, and difficulty in focusing may occur.
  3. Higher plasma concentrations may result in slurred speech and skeletal muscle twitching, which often herald the onset of tonic-clonic seizures.

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  1. Cardiotoxicity may manifest before neurotoxicity when bupivacaine local anesthetic toxicity occurs.
  2. The conduct of monitored anesthesia care may modify the individual's response to the potentially toxic effects of local anesthetic administration and adversely affect the margin of safety of a regional or local anesthetic technique.
  3. Any decrease in cardiac output and hepatic blood flow during sedation may decrease the clearance of local anesthetics that are dependent on metabolism in the liver.
  4. Drug-induced depression of ventilation during sedation leads to acidosis, which increases delivery of local anesthetic to the brain via increases in cerebral blood flow, increases intracellular concentrations of the active non-ionized form of the local anesthetic, and potentiates the cardiovascular toxicity of local anesthetics.
  5. Administration of sedative-hypnotic drugs may interfere with the patient's ability to communicate the symptoms of impending local anesthetic.
  6. The anticonvulsant properties of benzodiazepines and barbiturates may attenuate the seizures associated with local anesthetic toxicity.

XII. Sedation and Analgesia by Non-Anesthesiologists

  1. The ASA has developed practice guidelines to guide the level of sedation and analgesia that should be provided by non-anesthesiologist providers.
  2. Four levels of sedation are defined in the ASA practice guidelines: minimal sedation, moderate sedation, deep sedation, and general anesthesia (Table 31-8).
  3. These practice guidelines emphasize that sedation and analgesia represent a continuum of sedation in which patients can easily pass into a level of sedation that is deeper than intended.
  4. Certain high-risk patient groups (extremes of age, severe comorbid diseases, morbid obesity, sleep apnea, pregnancy, alcohol abuse) should be evaluated by appropriate physician consultation before administration of sedation and analgesia by non-anesthesiologists.

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Table 31-8 Continuum of Depth of Sedation

 

Minimal Sedation

Moderate Sedation

Deep Sedation

General Sedation

Responsive-ness

Normal response to verbal stimulation

Purposeful response to verbal or tactile stimulation

Purposeful response after repeated or painful stimulation

Unarousable, even with a painful stimulus

Airway

Un-affected

No intervention is required

Intervention may be required

Intervention is often required

Spontaneous ventilation

Un-affected

Adequate

May be inadequate

Frequently inadequate

Cardiovascular function

Unaffected

Usually maintained

Usually maintained

May be impaired

  1. Controversy exists regarding the level of training required for non-anesthesiologists to be credentialed to provide moderate and deep sedation. The ASA recommends that practitioners should complete formal training in the safe administration drugs used to establish a level of moderate sedation and rescue of patients who exhibit adverse physiologic consequences of a deeper-than-intended level of sedation.

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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