Deleterious hemodynamic effects of lidocaine in severe congestive heart failure.
Deleterious hemodynamic effects of lidocaine in severe congestive heart failure.
复制标题
利多卡因对严重充血性心力衰竭的有害血流动力学影响。
DOI:
10.1016/0002-8703(89)90278-0
复制
发表时间:
1989
影响因子:
4.8
通讯作者:
Packer,M
中科院分区:
文献类型:
--
作者:
Gottlieb,SS;Packer,M
Ventricular arrhythmias are extremely common in patients with congestive heart failure, and these patients are frequently considered to be candidates for antiarrhythmic drug therapy. Yet patients with left ventricular dysfunction are particularly likely to experience adverse hemodynamic and electrophysiologic effects from antiarrhythmic agents. Lidocaine is an antiarrhythmic drug that is thought to exert minimal (if any) proarrhythmic or cardiodepressant effects.‘, 2 Although this local anesthetic agent can decrease cardiac contractility in vitro, 3 the drug has not been reported to produce clinically significant changes in cardiac output or ventricular filling pressures in patients with heart disease, even in those with a history of congestive heart failure. 1’2 The risk of lidocaine-induced central nervous system toxicity is increased in patients with heart failure, however, since this disease state reduces the apparent volume of distribution and the hepatic clearance of the drug. 4 Accordingly, the administration of the usual therapeutic doses of lidocaine may produce very high serum levels of the drug. In spite of such altered pharmacokinetics, lidocaine has never been reported to produce worsening symptoms of heart failure in patients with left ventricular dysfunction. We observed a patient with severe chronic congestive heart failure whose circulatory status deteriorated repeatedly when he was treated with lidocaine and who improved rapidly upon withdrawal of the drug. In order to determine whether lidocaine caused these adverse clinical effects, we rechallenged the patient with lidocaine after the insertion of a balloon-flotation catheter in the right side of the heart.A 56year-old man with severe cardiomyopathy secondary to ischemic heart disease was referred to Mount Sinai Hospital for the treatment of severe chronic heart failure. Three years after coronary artery bypass surgery and a perioperative myocardial infarction, he had symptoms of dyspnea and fatigue at rest (New York Heart Association functional class IV) despite treatment with digitalis and diuretics. The left ventricular ejection fraction was 22% by