PubMed · 10488298
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F Henderson. 1999. Ether anesthesia. 1913.. https://pubmed.ncbi.nlm.nih.gov/10488298/
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Recent qualms about the safety of aesthetic lipoplasty may be attributable more to support system flaws than to technical process deficiencies. The authors here focus on perfunctory patient monitoring when sedative or analgesic drugs are given, cavalier infiltration of mega-dose lidocaine, cursory intraoperative patient observation by team members with conflicting responsibilities, anesthesia providers unfamiliar with the unique surgical physiology of liposuction, hurried-discharge policies that virtually ignore the residual depressant effects of sedatives and analgesics, and compressive dressings that impair postoperative chest-wall expansion and venous return. Whereas pulmonary embolism remains the leading process cause of morbidity from liposuction, complications from austere resource allocation to dedicated patient monitoring should be largely preventable. Not all lipoplasties require an anesthesia provider but-when heavy sedation, mega-dose lidocaine, or both, are projected-a trained team member dedicated exclusively to patient safety and comfort should be a minimum patient care standard. The potential role of lidocaine cardiotoxicity in tumescent anesthesia is widely underappreciated and that of hypothermia goes mostly unrecognized. These, plus largely preventable or potentially correctable perioperative events such as pulmonary edema, fluid imbalance, or improperly administered sedative and analgesic drugs, demand upgrading and expansion of monitoring, resuscitative, and recuperative facilities in physician offices. In fact, ASPS guidelines urge that anesthesia services be engaged for dedicated patient care whenever "major" liposuction or conscious sedation is projected, because liposuction is neither as benign nor as simple a procedure as heretofore reputed. To assess objectively the operative and anesthetic risk of obesity, document body mass index for the preoperative record; morbid obesity (body mass index >/= 35.0), for instance, is a known risk multiplier for sedatives and analgesics. Other system issues such as the dynamic profile of high-dose lidocaine pharmacokinetics, the deportation of fat globules in the bloodstream, and the incidence of intraoperative hypothermia remain as unresolved topics for interdisciplinary, multi-institutional clinical research.
We investigated the effects of an L-type and N-type Ca(2+) channel blocker, cilnidipine, on neurally mediated chronotropic responses to clarify the anti-autonomic profile of cilnidipine in anesthetized dogs. Pretreatment with cilnidipine (0.3, 1.0 and 3.0 microg/kg, i.v.), which decreased mean blood pressure by 5 to 31 mm Hg, inhibited the changes in heart rate and plasma norepinephrine concentration induced by bilateral carotid artery occlusion, whereas it had no effect on vagal nerve stimulation-induced bradycardia. These results suggest that antihypertensive and antisympathetic doses of cilnidipine fail to influence chronotropic responses mediated by parasympathetic nerve activation in the in vivo canine heart.
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