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Certain benzodiazepine metabolites are pharmacologically active and have the potential to accumulate with repeated administration of the parent drug to anephric patients 12.5mg coreg fast delivery pulse pressure reference range. For example purchase 12.5mg coreg amex blood pressure medication overdose death, 60% to 80% of midazolam is excreted as its (active) α-hydroxy metabolite 25mg coreg with visa blood pressure drops when standing, which72 accumulates during long-term infusions in patients with renal failure. Volunteers with renal impairment receiving dexmedetomidine experienced a longer-lasting sedative effect than subjects with normal kidney function. The most likely explanation is that less protein binding of dexmedetomidine occurs in subjects with renal dysfunction. However, chronic administration results in accumulation of its 6-glucuronide metabolite, which has potent analgesic and sedative effects. Meperidine is remarkable for its neurotoxic, renally excreted metabolite (normeperidine) and is not recommended for use in patients with poor renal function. Hydromorphone is metabolized to hydromorphone-3-glucuronide, which is excreted by the kidneys. This active metabolite accumulates in patients with renal failure and may cause cognitive dysfunction and myoclonus. Codeine76 also has the potential for causing prolonged narcosis in patients with renal failure and cannot be recommended for long-term use. Small-to-moderate doses, titrated to effect, are well77 tolerated by uremic patients. Therefore, caution should be exercised in78 administering a loading dose, but the total dose and infusion dose should be similar to those for patients with normal renal function. Renal failure has no effect on the clearance of remifentanil, but elimination of the principal metabolite, remifentanil acid, is markedly reduced. Only succinylcholine, atracurium, cis-atracurium, and mivacurium appear to have minimal renal excretion of the unchanged parent compound. Most nondepolarizing muscle relaxants must be either hepatically excreted or metabolized to inactive forms in order to terminate their activity. Although the following discussion focuses on the pharmacology of individual muscle relaxants, coexisting acidosis and electrolyte disturbances as well as drug therapy (e. However, use of a continuous succinylcholine infusion raises concerns because the major metabolite, succinylmonocholine, is weakly active and excreted by the kidney. Use of the long- acting muscle relaxants doxacurium, pancuronium, and pipecuronium might also be questioned in patients with known renal insufficiency. Similar findings have been reported for the 3536 pharmacokinetics of pipecuronium. Atracurium and its derivative, cis-atracurium, undergo enzymatic ester hydrolysis and spontaneous nonenzymatic (Hoffman) degradation with minimal renal excretion of the parent compound. One potential concern is that an atracurium metabolite, laudanosine, may cause seizures in experimental animals and may accumulate with repeated dosing or continuous infusion. Table 50-4 Nondepolarizing Muscle Relaxants in Renal Failure Initial reports suggested that the pharmacokinetics of vecuronium are unchanged in renal failure, but it has subsequently emerged that its duration of action is prolonged as a result of reduced plasma clearance and increased elimination half-life. Rocuronium has a pharmacokinetic profile in normal subjects similar to that of vecuronium. Single-dose pharmacokinetic studies in patients with88 renal failure have reported conflicting results. The short-acting muscle relaxant mivacurium is enzymatically eliminated by plasma pseudocholinesterase at a somewhat slower rate than succinylcholine. Low pseudocholinesterase activity correlates with slower recovery from a bolus dose of mivacurium in anephric patients. The83 maintenance infusion dose has been reported to be both lower than and91 similar to that in normal control subjects. The anticholinergic agents atropine and glycopyrrolate, used in conjunction with the anticholinesterases, are similarly excreted by the kidney. Therefore, no dosage alteration of the anticholinesterases is required when antagonizing neuromuscular blockade in patients with reduced renal function. This agent is a modified γ-cyclodextrin that encapsulates aminosteroidal neuromuscular blocking agents (e. Edema results when Starling forces favor passage of fluid into the interstitial space. Fluid overload due to a variety of chronic conditions (congestive heart failure, renal failure, or hepatic cirrhosis) may be first recognized during preoperative assessment and may require that elective surgery be delayed for treatment to reduce operative risk.
Animal studies suggest that dexmedetomidine may be less neurotoxic than other traditionally used agents order 25 mg coreg with amex arterial hypertension, such as midazolam buy cheap coreg on-line hypertension 4019. Although much work remains43 to be done with this drug in the neonatal population cheap 12.5 mg coreg visa blood pressure limits, it is emerging as a viable sedative in neonates. The advantage of using opioids is their ability to maintain cardiovascular stability during major surgery. Infants who are on long-term doses of opioids may develop dependence and have to be placed on methadone, a longer-acting opioid. A dose of 2 to 4 μg/kg/hr can maintain hemodynamic stability in these infants during surgery. The45 use of fentanyl in association with benzodiazepines may lead to hypotension and hemodynamic instability. Caution must be exercised when the combination is administered during the perioperative period. Continuous infusions may predispose to respiratory depression more frequently than bolus doses. There is no significant maturational change in the brain associated with fentanyl, compared with morphine. Hence, the sensitivity to fentanyl will not significantly change as the infant matures significantly. Fentanyl still continues to be the mainstay in newborns for sedation and analgesia. Because of decreased48 clearance, dosing in neonates, especially premature infants, should occur on a 4- to 6-hour basis to allow for more predictable clearance of the drug. Morphine infusions in the perioperative period have resulted in minor prolongation of postoperative ventilation. However, increased incidence of apnea or hypotension was not observed in neonates despite prolonged morphine infusions after successful extubation. The sensitivity to morphine-6-glucoronide increases with age because of increased maturation of the neuronal receptors. The pharmacokinetics of remifentanil in neonates are similar to that of older children. Remifentanil can be used for maintenance of anesthesia with53 avoidance of volatile anesthetic agents. The use of remifentanil infusion facilitated tracheal extubation in infants in a randomized trial when compared with volatile agents. The pharmacokinetics of methadone are being studied in neonates; however, published data is not available. However, it is used frequently in managing opioid tolerance without significant complication. Factors that influence the choice of agent include the time of onset, duration of action, cardiovascular effects, drug availability, and mechanism of clearance/elimination. Thus, the recommended intravenous dose of succinylcholine for neonates and infants is 3 mg/kg, compared with 2 mg/kg in children, with an onset time of 30 to 45 seconds and duration of 5 to 10 minutes. The recommended intramuscular dose of succinylcholine is 4 mg/kg, with an onset time of 3 to 4 minutes and duration of approximately 20 minutes. Caution should be exercised when administering a second dose of succinylcholine because this can lead to vagally mediated bradycardia or sinus arrest. The reports of hyperkalemia with cardiac arrest in such children with unrecognized muscular dystrophy have led some clinicians to take the position that succinylcholine should not be used routinely for this group of patients. The occurrence of this problem is somewhere in the range of 1 in 250,000 anesthetics, with a mortality rate of 50%. Succinylcholine is still recommended in rapid- sequence situations, potential difficult airway, or if there are airway emergencies with progressive desaturation. When it is evident that a neonatal airway is obstructed by laryngospasm or other reason and no progress is made in ventilation, intramuscular or intravenous succinylcholine should be administered.
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