{"title":"心脏装置患者房室结药物毒性的复杂管理:永久性起搏器患者大量钙通道拮抗剂过量","authors":"Patric W Gibbons, Peter R Chai, T. Erickson","doi":"10.15761/jccr.1000175","DOIUrl":null,"url":null,"abstract":"We present a unique case of a massive calcium channel antagonist overdose in a patient with a permanent pacemaker. Upon presentation after the acute overdose, the patient’s cardiac device was found to be pacing to an adequate rate (75 beats per minute) and she was admitted to the cardiac intensive care unit. Approximately 24 hours after her ingestion, she acutely decompensated and became hypotensive. The patient was started on infusions of norepinephrine, epinephrine, phenylephrine, and vasopressin. Her mean arterial pressure was unresponsive to multi-vasopressor therapy. She was then given a bolus of methylene blue and high-dose insulin euglycemic therapy. Despite these treatments, the patient remained hypotensive Therefore, intralipid emulsion therapy and IV epinephrine pushes were also administered. As a result of her shock and hemodynamic instability, her course was further complicated by hypoxemic respiratory failure for which she required ventilatory support and developed oliguric renal failure for which she was initiated on continuous veno-venous hemofiltration. This case emphasizes the challenges in managing complex physiology associated with nodal agent toxicity and is the first, to our knowledge, to describe management in a patient who already had a pacemaker, though it was ultimately ineffective in avoiding the patient’s profound decompensation.","PeriodicalId":73637,"journal":{"name":"Journal of cardiology case reports","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Complex Management of AV Nodal Agent Toxicity in Patients with Cardiac Devices: Massive Calcium Channel Antagonist Overdose in a Patient with a Permanent Pacemaker\",\"authors\":\"Patric W Gibbons, Peter R Chai, T. Erickson\",\"doi\":\"10.15761/jccr.1000175\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"We present a unique case of a massive calcium channel antagonist overdose in a patient with a permanent pacemaker. Upon presentation after the acute overdose, the patient’s cardiac device was found to be pacing to an adequate rate (75 beats per minute) and she was admitted to the cardiac intensive care unit. Approximately 24 hours after her ingestion, she acutely decompensated and became hypotensive. The patient was started on infusions of norepinephrine, epinephrine, phenylephrine, and vasopressin. Her mean arterial pressure was unresponsive to multi-vasopressor therapy. She was then given a bolus of methylene blue and high-dose insulin euglycemic therapy. Despite these treatments, the patient remained hypotensive Therefore, intralipid emulsion therapy and IV epinephrine pushes were also administered. As a result of her shock and hemodynamic instability, her course was further complicated by hypoxemic respiratory failure for which she required ventilatory support and developed oliguric renal failure for which she was initiated on continuous veno-venous hemofiltration. This case emphasizes the challenges in managing complex physiology associated with nodal agent toxicity and is the first, to our knowledge, to describe management in a patient who already had a pacemaker, though it was ultimately ineffective in avoiding the patient’s profound decompensation.\",\"PeriodicalId\":73637,\"journal\":{\"name\":\"Journal of cardiology case reports\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-01-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of cardiology case reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.15761/jccr.1000175\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of cardiology case reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15761/jccr.1000175","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Complex Management of AV Nodal Agent Toxicity in Patients with Cardiac Devices: Massive Calcium Channel Antagonist Overdose in a Patient with a Permanent Pacemaker
We present a unique case of a massive calcium channel antagonist overdose in a patient with a permanent pacemaker. Upon presentation after the acute overdose, the patient’s cardiac device was found to be pacing to an adequate rate (75 beats per minute) and she was admitted to the cardiac intensive care unit. Approximately 24 hours after her ingestion, she acutely decompensated and became hypotensive. The patient was started on infusions of norepinephrine, epinephrine, phenylephrine, and vasopressin. Her mean arterial pressure was unresponsive to multi-vasopressor therapy. She was then given a bolus of methylene blue and high-dose insulin euglycemic therapy. Despite these treatments, the patient remained hypotensive Therefore, intralipid emulsion therapy and IV epinephrine pushes were also administered. As a result of her shock and hemodynamic instability, her course was further complicated by hypoxemic respiratory failure for which she required ventilatory support and developed oliguric renal failure for which she was initiated on continuous veno-venous hemofiltration. This case emphasizes the challenges in managing complex physiology associated with nodal agent toxicity and is the first, to our knowledge, to describe management in a patient who already had a pacemaker, though it was ultimately ineffective in avoiding the patient’s profound decompensation.