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Therapies
Published in Marc H. De Baets, Hans J.G.H. Oosterhuis, Myasthenia Gravis, 2019
Myasthenic weakness may worsen after surgery. Depolarizing neuromuscular blocking agents should not be used. Even low doses may lead to pronounced and long-lasting neuromuscular block. If application of a neuromuscular blocking agent is necessary, a nondepolarizing curare-like relaxant, such as alcuronium, vecuronium, or atracurium, is used at one tenth to one half the normal dose.113 It should be anticipated that patients with myasthenia occasionally require assisted respiration for longer than normal after surgery, even if myasthenia has been treated successfully before the operation. Assisted respiration is continued until the patient is able to cooperate and demonstrates adequate respiratory function. A detailed discussion of pre- and postoperative care of the myasthenic patient may be found in reference 114.
Pharmacokinetic-Pharmacodynamic Correlations of Anesthetic Agents
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
Virginia D. Schmith, Keith T. Muir
The kco, EC50, and s values may also be dependent on the muscle used as the site of monitoring. Figure 1 illustrates the plasma alcuronium concentration-effect relationship for the limb and diaphragm. Counterclockwise hysteresis is evident for both muscle groups; however, the T1/2kco was two-fold shorter in the diaphragm than in the limb (2.38 ± 1.27 and 4.36 ± 1.27 min, respectively). The EC50 was also greater in the diaphragm than in the limb (0.18 + 0.05 and 0.10 + 0.04 mg/ml, respectively).52 Bragg et al.31 also reported a shorter T1/2kco and a greater EC50 in the larynx and diaphragm than in the adductor pollicis muscle. Thus, the time course of paralysis varies depending on the muscle site studied, due to factors such as perfusion, partition, and receptor sensitivity. Knowledge of these differences can be applied in the anesthetic setting to optimize the timing of events (e.g., intubation, surgical incision) relative to NMB agent administration.
Classifications
Published in Fazal-I-Akbar Danish, Ahmed Ehsan Rabbani, Pharmacology in 7 Days for Medical Students, 2018
Fazal-I-Akbar Danish, Ahmed Ehsan Rabbani
Neuromuscular blocking agentsCompetitive blocking/nondepolarising agentsAlcuroniumAtracuriumDimethyl tubocurarineFazadiniumGallaminePancuroniumTubocurarineVecuroniumDepolarising agentsDecamethoniumSuxamethoniumSuxemethonium
Effect of cardiopulmonary bypass on cytochrome P450 enzyme activity: implications for pharmacotherapy
Published in Drug Metabolism Reviews, 2018
Santosh Kumar Sreevatsav Adiraju, Kiran Shekar, John F. Fraser, Maree T. Smith, Sussan Ghassabian
On the other hand, drugs that are not metabolized by liver are affected to a smaller extent compared with the previous group. Vancomycin, rocuronium, doxacurium, and alcuronium are drugs with low plasma protein binding (30–70% to albumin) and that are eliminated from the body unchanged in the urine (vancomycin (Zhao et al. 2014), teicoplanin (Roberts et al. 2014), daptomycin (Dvorchik et al. 2003)) or urine and bile (alcuronium (Miller et al. 1997), rocuronium (Khuenl-Brady and Sparr 1996), doxacurium (Cook et al. 1991; Asokumar et al. 1998)). A 20% increase in vancomycin CL with no change in t½β (Ortega et al. 2003) was underpinned by a 30% decrease in vancomycin renal CL during CPB which returned to the pre-CPB levels after CPB termination (Klamerus et al. 1988). Similarly, a 38% decrease in doxacurium t½β1/2 in hypothermic compared with normothermic CPB has been reported (Asokumar et al. 1998). The impact of CPB on the renal CL of drugs can be explained by two opposing factors: reduced kidney perfusion and reduced plasma protein binding. Teicoplanin and daptomycin are eliminated by the kidney (Dvorchik et al. 2003; Roberts et al. 2014), but have high plasma protein binding (Lee et al. 1991; Yano et al. 2007; Beer et al. 2009) with both factors potentially affected by initiation of CPB therapy. Altered plasma protein binding of important drugs is thought to be underpinned by changes in acid-base balance during CPB (Gedney and Ghosh 1995). Tranexamic acid is a drug with only 3% plasma protein binding and small metabolism (McCormack 2012) and its PK was not affected during cardiac surgery using CPB (Table 1).