Anesthesia with local anesthetics like etidocaine and bupivacaine can lead to cardiac arrest, especially if they are inadvertently injected intravascularly. Despite the belief that oxygenation and blood pressure support can prevent such events, some patients are susceptible. The article discusses several cases of sudden cardiac arrest following regional anesthesia with these agents, emphasizing that hypoxia may not be the primary cause. Cardiac arrest often occurs immediately after rapid injection, with resuscitation being difficult and requiring prolonged cardiac massage. The cases involved various anesthetic techniques, including caudal, interscalene, and epidural blocks. The cardiovascular system is generally more resistant to local anesthetic toxicity than the central nervous system, but the relative toxicity of these agents does not always align with their respiratory effects. Studies show that the cardiovascular toxicity of these agents can be significantly higher when administered intravenously compared to absorption from injection sites due to their high lipid solubility. The article highlights the need for further research to understand the dose-response relationship between CNS and cardiac toxicity, and to determine the most effective methods of cardiac resuscitation in cases of local anesthetic toxicity. It also emphasizes the importance of evaluating the role of membrane stabilizers in treating such cases. The article concludes that the true incidence of this phenomenon needs to be determined, and that more cases may have occurred without being reported.Anesthesia with local anesthetics like etidocaine and bupivacaine can lead to cardiac arrest, especially if they are inadvertently injected intravascularly. Despite the belief that oxygenation and blood pressure support can prevent such events, some patients are susceptible. The article discusses several cases of sudden cardiac arrest following regional anesthesia with these agents, emphasizing that hypoxia may not be the primary cause. Cardiac arrest often occurs immediately after rapid injection, with resuscitation being difficult and requiring prolonged cardiac massage. The cases involved various anesthetic techniques, including caudal, interscalene, and epidural blocks. The cardiovascular system is generally more resistant to local anesthetic toxicity than the central nervous system, but the relative toxicity of these agents does not always align with their respiratory effects. Studies show that the cardiovascular toxicity of these agents can be significantly higher when administered intravenously compared to absorption from injection sites due to their high lipid solubility. The article highlights the need for further research to understand the dose-response relationship between CNS and cardiac toxicity, and to determine the most effective methods of cardiac resuscitation in cases of local anesthetic toxicity. It also emphasizes the importance of evaluating the role of membrane stabilizers in treating such cases. The article concludes that the true incidence of this phenomenon needs to be determined, and that more cases may have occurred without being reported.