{'fraction_non_alphanumeric': 0.014905149051490514, 'fraction_numerical': 0.0027100271002710027, 'mean_word_length': 5.718181818181818, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Models and Mechanisms of Local Anesthetic Cardiac Toxicity: A Review

Abstract Cardiovascular collapse, even death, may occur after intoxication with bupivacaine or related amide local anesthetic agents. The problem has been studied in myriad laboratories for more than 20 years. Nevertheless, there is consensus neither regarding which animal model best mimics this clinical catastrophe nor as to which ion channel, enzyme, or other local anesthetic binding site represents the point of initiation for the process. This review aimed to define the various credible mechanisms that have been proposed to explain cardiovascular collapse and death after administration of local anesthetics, particularly after bupivacaine and related agents.