Chapter 47 Monitored Anesthesia Care

Summarized by: Kyle Thompson, MD

 Monitored anesthesia care involves administering a combination of drugs for anxiolytic, hypnotic, amnestic, and analgesic effect. Ideally is should result less physiologic disturbance and allow for more rapid recovery than GA.
ASA definition of MAC is: "Monitored anesthesia care refers to instances in which an anesthesiologist has been called upon to provide specific anesthesia services to a particular patient undergoing a planned procedure, in connection with which a patient receives local anesthesia, or in some cases, no anesthesia at all. In such a case, the anesthesiologist is providing specific services to the patient and is in control of the patient's non-surgical or non-obstetrical medical care, including the responsibility of monitoring the patient's vital signs, and is available to administer anesthetics or provide other medical care as appropriate." Additional requirements are:
1. Performance of a preanesthetic examination and evaluation.
2. Prescription of anesthetic care.
3. Personal participation in, or medical direction of, the entire plan of care.
4. Continuous physical presence of the anesthesiologist or, in the case of medical direction, of the resident or nurse anesthetist being medically directed.
5. Proximate presence, or in the case of medical direction, availability of the anesthesiologist for diagnosis and treatment of emergencies.
 MAC does not necessarily imply the administration of sedatives. Facilities to secure the airway should always be immediately available.

 The preop should be no different than that for other patients. Additionally, the patient's ability to remain motionless and actively cooperate should be evaluated. Ability to verbally communicate with the patient is important as it:
1. assists in monitoring level of sedation and cardiorespiratory function
2. is a means of explanation/reassurance to the patient
3. allows requests for active participation by the patient.
 Cardiorespiratory disease is often the indication for MAC over GA. However, associated problems such as persistent cough or orthopnea may prevent immobility or prevent assumption of the supine position.

 The combination of agents used should provide analgesia, amnesia, and hypnosis with a minimum of side effects (PONV, prolonged sedation, cardiorespiratory sedation, dysphoria). Recovery ideally should be complete and rapid. The patient should be awake or rousable during the procedure, and able to communicate. The American Dental Association Council on Education has defined conscious sedation as a "minimally depressed level of consciousness that retains the patient's ability to independently and continuously maintain an airway and respond appropriately to physical stimulation and verbal commands." While patient agitation may be due to pain, anxiety it can also be caused by: hypoxia, hypercarbia, impending local anesthetic toxicity, and cerebral hypoperfusion. Other less severe causes are: bladder distention, hypothermia, hyperthermia, pruritus, nausea, positional discomfort, IV site infiltration, prolonged tourniquet inflation, or a member of the surgical team leaning on the patient.

•Distribution, Elimination, Accumulation, and Duration of Action
 The accumulation of drugs in the poorly perfused fatty tissues during a long case can contribute to a prolonged recovery as it is released back into the circulation over time. While the elimination half-time is often promoted as the guide to a drug's duration of action, it is often difficult to predict this duration based on elimination half-life alone. Only in a single compartment model does the elimination half-time represent the actual time required for a drug's plasma concentration to reach half its initial concentration.

•Context Sensitive Half-Time
 The effect of distribution on plasma drug concentration varies in magnitude and direction over time and is dependent on the drug concentration gradients present between compartments. The context-sensitive half-time describes the time required for the plasma drug concentration to decline by 50% after terminating an infusion of a particular duration and is calculated to by utilizing computer simulation of multicompartmental pharmacokinetic models of drug disposition. This reflects the combined effects of distribution and metabolism. The context-sensitive half-time of all drugs increases as duration of infusion increases, but markedly so in the cases of fentanyl and thiopental. While fentanyl's elimination is shorter than sufentanil's (462 vs 577 minutes), its context-sensitive half-time is twice that of sufentanil's at two hours and 8-10 times longer at five hours.
 There is no constant relationship between elimination half-life and context-sensitive half-time.

•Context-Sensitive Half-Time vs. Time to Recovery
 The context-sensitive half-time does not describe the time required for recovery. It estimates only the time required for a 50% reduction in plasma concentrations. While context-sensitive half-time is a reflection of plasma drug decay, the effect-site concentration is the important factor in determining rousability and wakefulness. Effect-site drug concentrations lag behind plasma concentrations as expected.

•Effect-Site Equilibration
 This is a concept very relevant to MAC. The delay between drug administration and initial drug effect is reflective of effect-site equilibration time as the plasma is merely the means of reaching the effect site for most drugs. If a parameter of drug effect can be measured, the half-time of equilibration between drug concentration in the blood and drug effect can the be determined. This is abbreviated as t1/2 keo. Smaller values correspond with rapidity of onset. Drugs with shorter values are:
thiopental, propofol, and alfentanil.
Drugs with longer values are:
midazolam (0.9-5.6m), sufentanil, and fentanyl (6.4m).
The t1/2 keo is a key factor in determining bolus spacing. Even using the shortest value for midazolam, 2.7 minutes is required for 87.5% effect-site equilibration of a bolus dose. Low cardiac output is another factor that will slow onset time.

 Cpss50 is the plasma concentration at a steady state required to abolish purposeful movement upon skin incision in 50% of patients. For example, when used as the sole agent, opioid requirements are tenfold higher than when used in conjunction with a N2O/potent inhaled vapor technique.
 Drug interactions can vary over the clinical dose range used. E.g., the greatest reduction of isoflurane MAC occurs within the analgesic dose range of fentanyl, 1-2 ng/ml. At 1.7ng/ml there is a 50% reduction, and at 3ng/ml a ceiling effect is reached with a 80% reduction in isoflurane MAC.
 The opioid-benzodiazepine combination displays marked synergism in producing hypnosis, extending also to the unwanted side effects of these drugs. A trial of midazolam 0.05mg/kg and fentanyl 2.0mcg/kg alone and in combination was performed. Midazolam alone produced no significant respiratory effects and the fentanyl alone produced hypoxemia in half the subjects. In combination however, they caused hypoxemia in 11 of 12, and apnea in 6 of 12 subjects. Our standard "two and two" premedication with midazolam and fentanyl would result in these doses in a 50kg patient.

 It has a context-sensitive half-time that is short even after prolonged infusions, and a short effect-site equilibration time. While the elimination half-time of midazolam is relatively short, the context-sensitive half-time is roughly twice that of propofol, and is associated with prolonged postop sedation and psychomotor impairment. Propofol does not reliably produce amnesia in subhypnotic doses. The addition of low dose midazolam could reliably create amnesia and simultaneously allow for rapid recovery.
 The purported proconvulsive properties of propofol were found to be absent upon monitoring the EEG of epileptic patients receiving a propofol infusion for a dental procedure.
 GA with propofol is generally associated with less PONV than other techniques, and there is evidence that a single 10mg dose possesses direct antiemetic properties.

 While midazolam has a short elimination half-time, there is often significant and prolonged psychomotor impairment following conscious sedation techniques using midazolam as their main component.
 The Cpss50 decreases significantly as a function of age, reduced threefold in an 80 year-old compared to a 40 year-old.
 Flumazenil has a very short elimination half-life of only 60 minutes, shorter than that of most clinically used benzodiazepines. In one study the effects of midazolam recurred 90 minutes following the administration of flumazenil.

 Currently available opioids do not reliably produce an acceptable or controllable degree of sedation in the absence of significant respiratory depression. The use of opioids is associated with a significant increase in the incidence of nausea and vomiting in ambulatory patients.

•Sedation and the Upper Airway
 During normal inspiration is subatmospheric creating a tendency to collapse. This tendency is opposed by upper airway muscles which contract just prior to diaphragmatic contraction. This upper airway motor control appears extremely sensitive to sedative-hypnotic drug administration. Sedative doses of midazolam have been reported to increase upper airway resistance three to fourfold, an effect exaggerated in the elderly.

•Sedation and Protective Airway Reflexes
 Protective pharyngeal and laryngeal reflexes are depressed by sedation, debilitation, and advanced age. Complete recovery of the swallowing reflex occur approximately 15 minutes after the return of consciousness from propofol anesthesia. It is depressed for up to two hours after midazolam despite the return to a normal state of consciousness. In otherwise healthy adult male volunteers the inhalation of 50% N2O was associated with marked depression of the swallowing reflex.

 In an otherwise normal man whose PCO2 is increased by hypoventilation secondary to opioid administration, the alveolar gas equation predicts a PAO2 of approximately 50mm Hg (SpO2 75%). If a modest FIO2 increase to 28% is made, the PAO2 increases to 100mm Hg (SpO2 100%).
 In isolated hypoventilation, modest increases in inspired O2 are remarkably effective at restoring oxygen saturation. Conversely, a patient receiving minimal O2 supplementation may have undetected alveolar hypoventilation.

•Communication and Observation
 The patient's response to verbal stimulation should be continually evaluated for effective titration of sedation. The patient should be observed for diaphoresis, pallor, shivering, cyanosis, and acute changes in neurologic status.

 Use the precordial stethoscope - inexpensive, effective, essentially risk-free.

•Pulse Oximetry
 In addition to sedation's potential hypoxic effects, other predisposing factors include obesity, preexisting upper airway obstruction and respiratory disease, age extremes, and the lithotomy position. The ASA Committee on Professional Liability analysis of closed claims revealed that respiratory events constituted the single largest source of adverse outcomes.

 Sidestream capnographs have been adapted for use with face masks, nasal airways, and nasal cannulae.

•Cardiovascular System
 The ECG must continuously be displayed and BP measured and recorded at least every five minutes.  The pulse should be monitored palpation, oximetry, or auscultation.

 There is still the opportunity for inadvertent hypothermia, particularly during regional and conscious sedation techniques in the elderly. Malignant hyperthermia is rare during MAC because the common triggering agents are rarely used. Hyperthermia can still occur as a result of thyroid storm or malignant neuroleptic syndrome.

•Preparedness to Recognize and Treat Local Anesthetic Toxicity
 The clinical recognizable effects are concentration dependent. Symptoms at different levels of toxicity:
Low - sedation, tongue and circumoral numbness, metallic taste
Medium - restlessness, vertigo, tinnitus, difficulty focusing
High - slurred speech, skeletal muscle twitching heralding the onset of tonic-clonic seizures
 A patient with compromised cardiovascular function with lowered cardiac output during sedation will have less hepatic perfusion and lowered metabolism of local anesthetics. Respiratory depression resulting in hypercarbia increases cerebral blood flow thereby increasing the amount of local anesthetic delivered to the brain. The more acidic pH of an acute hypercarbic state leading to a degree of intracellular ion trapping, increasing the intracellular concentration further. Cardiovascular toxicity is also increased by hypercarbia, as well as by hypoxia and acidosis. Cardiotoxicity is usually preceded by neurotoxicity but may occur first in a toxic overdose of bupivacaine.
 Local anesthetics also have an effect themselves on respiratory function according to two studies. In one, lidocaine was found to depress the ventilatory response to hypoxia. In two others lidocaine and bupivacaine have both been shown to increase the ventilatory response to carbon dioxide.