Recovery from anesthesia begins in the operating room following discontinuation of the anesthetic drugs. Times to awakening and the quality of early recovery following general anesthesia may vary greatly, depending upon the properties of selected anesthetic drugs (inhaled anesthetics, sedative-hypnotics, opioid analgesics, and neuromuscular blocking drugs) as well as their additive and/or synergistic interactions ( StanskiiiiiaindiiShafe£i1995). The speed of recovery from inhaled anesthetics is influenced by four main factors: the solubility coefficient of the drug, the concentration administered and the duration of anesthesia, patient sensitivity, and drug interactions. The recent introduction of two new inhaled anesthetics, desflurane and sevoflurane, may ensure even more rapid and predictable recovery compared with regimens employing halothane, enflurane, or isoflurane (Table 1).
Table 1 Duration of the clinical effect of anesthetic drugs
Several recent developments have affected the factors determining speed of recovery from intravenous anesthetics. First, the introduction of new short-acting agents, including propofol, have had an enormous impact on the practice of anesthesia. Propofol is an effective induction agent and is also an effective hypnotic for maintenance of anesthesia when administered by continuous infusion. Propofol is further indicated for both monitored anesthesia care sedation and ICU sedation (titrated to a target level of sedation at rates between 25 and 75 pg/kg/min). The main advantages of this drug include its rapid, predictable, and pleasant recovery, even after prolonged administration (hours to days), and its antiemetic properties. Its disadvantages include insolubility, requiring formulation in intralipid, and a relatively high cost. Midazolam may be less costly when used either by continuous infusion or intermittent boluses for postoperative sedation of mechanically ventilated patients (titrated to a target level of sedation at rates between 0.5 and 1.5 pg/kg/min). However, recovery times are somewhat longer (30 min to several hours) and vary depending upon the duration of drug therapy, the depth of sedation during maintenance, and patient-related factors. Recent trends in cardiovascular anaesthesia have been directed towards early extubation (within 4-6 h of completion of surgery, rather than routinely ventilating patients overnight), a cost-effective practice which tends to be facilitated by the use of the shorter-acting sedatives ( M.il.l.e.Ll996).
A second recent advance in intravenous anesthesia has been the development of pharmacokinetic modeling procedures which provide a quantitative description of the relative contributions of distribution and elimination processes during recovery from intravenous anesthetic drugs ( Sch0id.e.La0d..S.h§.feLl995). The definitions of these new descriptors of clinical recovery are presented in Table^..
Table 2 Clinical predictors of recovery from intravenous anesthetics
Recovery from the effects of neuromuscular blocking drugs is influenced by a number of factors, including the duration of action of the drug ( Table 1), the dose, and the status of renal and hepatic function. In addition, the dose of anticholinesterase for reversal, patient temperature, acid-base status, and use of drugs that increase the neuromuscular block (e.g. inhaled anesthetics, aminoglycoside antibiotics) are also important determinants of recovery. Careful clinical evaluation of recovery from the effects of neuromuscular blocking drugs is essential, as residual paralysis has been shown to exist in 5 to 40 per cent of patients upon arrival in the PACU. Recovery of neuromuscular function can be confirmed by several simple tests, including observation of a sustained muscle contraction (without fade) to tetanic stimulation of the ulnar nerve at the wrist or noting the patient's ability to sustain a head lift for more than 5 s. If signs of persistent residual neuromuscular block persist, an additional dose of anticholinesterase and an antimuscarinic drug should be given immediately (e.g. neostigmine 50 Mg/kg plus atropine 20 Mg/kg intravenously).
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