Neuromuscular Blockers and Reversal Drugs

Pharmacology and Physiology for Anesthesia: Foundations and Clinical Application

Volumn , Issue , 2013, Pages 325-348

  Lien, Cynthia A ^a   Eikermann, Matthias ^b,c,d  

^a WEILL CORNELL MEDICAL COLLEGE   (United States)

^b HARVARD MEDICAL SCHOOL   (United States)

^c MASSACHUSETTS GENERAL HOSPITAL   (United States)

^d UNIVERSITY OF DUISBURG ESSEN   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 84887982709     PISSN: None     EISSN: None     Source Type: Book    
DOI: 10.1016/B978-1-4377-1679-5.00019-3     Document Type: Chapter

References (215)

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206. Donati F, Meistelman C, Plaud B Vecuronium neuromuscular blockade at the adductor muscles of the larynx and adductor pollicis. Anesthesiology 1991, 74:833-837. In this study, time to maximal effect of and recovery from vecuronium-induced neuromuscular block, 0.4 or 0.7 mg/kg, was determined at the adductor pollicis and the laryngeal adductors in 20 adult patients. While vecuronium had a more rapid effect in the laryngeal adductors, maximal depth of block was less profound than it was at the adductor pollicis. Recovery occurred more quickly in the larynx than at the adductor pollicis. (Ref. 13).
207. Eikermann M, Fassbender P, Malhotra A, et al. Unwarranted administration of acetylcholinesterase inhibitors can impair genioglossus and diaphragm muscle function. Anesthesiology 2007, 107:621-629. Administration of neostigmine to rats that had completely recovered from vecuronium-induced neuromuscular block resulted in impaired function of the genioglossus muscle and the diaphragm. With administration of the largest dose of neostigmine (1.2 mg/kg), tidal volume was significantly reduced and respiratory rate increased so that minute ventilation was unchanged from baseline. (Ref. 188).
208. Fuchs-Buder T, Meistelman C, Alla F, et al. Antagonism of low degrees of atracurium-induced neuromuscular blockade: dose-effect relationship for neostigmine. Anesthesiology 2010, 112:34-40. Administration of 10, 20, or 30 μg/kg neostigmine at TOFR of 0.4 or 0.6, when fade is likely not palpable in the TOF response, results in effective antagonism of residual atracurium-induced block. Neostigmine, 20 μg/kg will restore the TOFR to 0.9 or more within 10 minutes. Administration of these small doses of neostigmine does not augment existing neuromuscular block. (Ref. 190).
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211. 7 acetylcholine receptor, which is activated by choline, acetylcholine, and succinylcholine, has a prolonged depolarization in the presence of agonist and may, in clinical situations wherein there is upregulation of acetylcholine receptors, have a significant role in the hyperkalemic response to succinylcholine. (Ref. 71).
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213. Murphy GS, Szokol JW, Marymont JH, et al. Residual neuromuscular blockade and critical respiratory events in the postanesthesia care unit. Anesth Analg 2008, 107:130-137. An assessment of critical respiratory events in almost 7500 patients who had received general anesthesia. Just under 1% of patients had a critical respiratory event within 15 minutes of admission to the postanesthesia care unit. The majority of patients with a critical respiratory event (74%) had a TOFR of less than 0.7. Seventeen percent had a TOFR between 0.7 and 0.9. (Ref. 147).
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215. Sundman E, Witt H, Olsson R, et al. The incidence and mechanism of pharyngeal and upper esophageal dysfunction in partially paralyzed humans: pharyngeal videoradiography and simultaneous manometry after atracurium. Anesthesiology 2000, 92:977-984. A volunteer trial demonstrating that pharyngeal dysfunction occurred with increased incidence at TOFR equal to 0.6, 0.7, and 0.8. Pharyngeal coordination was decreased at TOFR equal to 0.6 and 0.7, and partial neuromuscular block was associated with as much as a fivefold increase in misdirected swallows. (Ref. 154).