Kelly R A, Smith T W
Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Am J Cardiol. 1992 Jun 4;69(18):108G-118G; disc. 118G-119G. doi: 10.1016/0002-9149(92)91259-7.
The most important step in the management of toxicity due to any of the cardiac glycosides is its recognition. Despite the development of an accurate clinical assay for serum levels of digoxin greater than 20 years ago, digitalis toxicity remains common and difficult to confirm, even if suspected, due primarily to 2 factors. First, the signs and symptoms of digitalis toxicity, most commonly an abnormal electrocardiogram showing ventricular or atrial arrhythmias, with or without some degree of concurrent atrioventricular block, often also occur in patients with congestive heart failure (CHF) and underlying coronary atherosclerosis who are not receiving a cardiac glycoside. Second, due to digoxin's narrow therapeutic ratio, the marked degree of variability in the sensitivity of individual patients to its toxic effects, and the common problem of obtaining blood samples inappropriately during the early distribution phase following dosing, a serum digoxin concentration often does not serve as a reliable indicator of toxicity. Despite these difficulties in diagnosis, the management of digoxin toxicity has been made much more effective with the widespread availability of F(ab) fragments of anti-digoxin antibodies. This drug provides the clinician with a rapidly acting, safe antidote for all commonly used digitalis preparations. Conventional therapy for digoxin toxicity remains the maintenance of serum potassium levels greater than or equal to 4 mEq/liter, reversal of decompensated CHF or overt myocardial ischemia, attention to serum magnesium levels and the patient's acid-base status, appropriate antiarrhythmics in the event of ventricular arrhythmias, and a temporary pacemaker for high-grade atrioventricular block. Nevertheless, the high specificity and documented safety of the antibody preparation provides a needed safety net for the continuing use of cardiac glycosides as first-line inotropic agents in the modern therapy of chronic CHF.
对于任何一种强心苷类药物中毒的管理,最重要的步骤是识别。尽管20多年前就已开发出一种准确的地高辛血清水平临床检测方法,但洋地黄中毒仍然很常见且难以确诊,即使怀疑中毒,主要也是由于两个因素。首先,洋地黄中毒的体征和症状,最常见的是心电图异常显示室性或房性心律失常,伴有或不伴有一定程度的房室传导阻滞,在未接受强心苷类药物治疗的充血性心力衰竭(CHF)和潜在冠状动脉粥样硬化患者中也经常出现。其次,由于地高辛的治疗窗狭窄、个体患者对其毒性作用的敏感性差异很大,以及给药后早期分布阶段不恰当地采集血样这一常见问题,血清地高辛浓度往往不能作为中毒的可靠指标。尽管诊断存在这些困难,但随着抗地高辛抗体F(ab)片段的广泛可得,地高辛中毒的管理已变得更加有效。这种药物为临床医生提供了一种快速起效、安全的解毒剂,可用于所有常用的洋地黄制剂。地高辛中毒的传统治疗方法仍然是维持血清钾水平大于或等于4 mEq/升、纠正失代偿性CHF或明显的心肌缺血、关注血清镁水平和患者的酸碱状态、出现室性心律失常时使用适当的抗心律失常药物,以及为高度房室传导阻滞患者植入临时起搏器。然而,抗体制剂的高特异性和已证实的安全性为在慢性CHF现代治疗中继续将强心苷类药物作为一线正性肌力药物使用提供了必要的安全保障。