Medical Education Department, Children's Hospital, Oakland, CA, USA.
Crit Care Med. 2012 Jul;40(7):2223-6. doi: 10.1097/CCM.0b013e318250a870.
To illustrate the challenges of managing patients with acute, undiagnosed arrhythmias through a case that demonstrates a possible association between catecholaminergic polymorphic ventricular tachycardia, a genetically determined severe arrhythmia disorder that often presents as either syncope or sudden death, and 3,4-Methylenedioxymethamphetamine ("Ecstasy") combined with marijuana, which are often considered safe drugs by users.
Case report.
Pediatric intensive care unit.
A 15-yr-old male collapsed suddenly after ingesting an unknown substance and smoking marijuana. He was successfully resuscitated by first-responder chest compressions and rescue breaths along with a single 100-J shock by paramedics. He was intubated and transferred to a pediatric intensive care unit. Initial cardiac workup was negative but severe instability on vasopressors and a family history of intermittent palpitations and syncope in his brother raised suspicion for catecholaminergic polymorphic ventricular tachycardia. Identification of the unknown substance required coordination with a toxicology laboratory.
The patient had extremely labile cardiovascular responses to vasopressors. On day 5, his blood pressure was stable and he was extubated. A full cardiac workup, including a catheterization (preadmission to pediatric intensive care unit), electrocardiogram, cardiac magnetic resonance imaging were done to screen out most structural arrythmogenic diseases. A specific genetic test for catecholaminergic polymorphic ventricular tachycardia was sent.
The patient's methylenedioxymethamphetamine blood level was 87 ng/mL approximately 12 hrs after ingestion. Given the 3-8 hr half-life of methylenedioxymethamphetamine, it is likely that levels were toxic at the time of ingestion (>110 ng/mL). Marijuana may have provided a synergistic critical catecholamine release to trigger an arrhythmia. Genetic testing showed a ryanodine receptor-2 mutation that was consistent with catecholaminergic polymorphic ventricular tachycardia.
While an initial cardiac workup for an acute, undiagnosed arrhythmia may be negative, family history may be a simple, essential component of patient management and disease diagnosis. This case demonstrates a possible association between methylenedioxymethamphetamine, marijuana, and catecholaminergic polymorphic ventricular tachycardia. All genetic and structural arrythmogenic disorders should be considered when working up a patient with presumed toxin-induced arrhythmias.
通过一个病例说明管理急性、未确诊心律失常患者的挑战,该病例表明儿茶酚胺多形性室性心动过速(一种由遗传决定的严重心律失常疾病,常表现为晕厥或猝死)与 3,4-亚甲二氧基甲基苯丙胺(“摇头丸”)和大麻之间可能存在关联,而这些药物常被使用者视为安全药物。
病例报告。
儿科重症监护病房。
一名 15 岁男性在摄入未知物质并吸食大麻后突然晕倒。急救人员通过第一反应者进行胸外按压和复苏呼吸,并使用除颤仪给予 100J 单次电击成功复苏。患者被插管并转入儿科重症监护病房。初始心脏检查结果为阴性,但升压药效果不稳定,且其哥哥有间歇性心悸和晕厥的家族史,这引起了对儿茶酚胺多形性室性心动过速的怀疑。确定未知物质需要与毒理学实验室协调。
患者对升压药有极其不稳定的心血管反应。第 5 天,患者血压稳定,拔管。进行了全面的心脏检查,包括导管插入术(入儿科重症监护病房前)、心电图、心脏磁共振成像,以排除大多数结构性心律失常疾病。还进行了特定的儿茶酚胺多形性室性心动过速基因检测。
患者摄入甲基苯丙胺后约 12 小时,血液中的甲基苯丙胺水平为 87ng/ml。鉴于甲基苯丙胺的半衰期为 3-8 小时,因此在摄入时(>110ng/ml)很可能存在毒性水平。大麻可能提供了协同的关键儿茶酚胺释放,引发心律失常。基因检测显示 Ryanodine 受体 2 突变,与儿茶酚胺多形性室性心动过速一致。
尽管急性、未确诊心律失常的初始心脏检查可能为阴性,但家族史可能是患者管理和疾病诊断的一个简单而重要的组成部分。本病例表明甲基苯丙胺、大麻和儿茶酚胺多形性室性心动过速之间可能存在关联。在处理疑似毒素诱导心律失常的患者时,应考虑所有遗传和结构性心律失常疾病。