Facebook
Twitter
LinkedIn
Email
 |
Checking for direct PDF access through Ovid | |
Excerpt
The results are provocative, but any broad conclusions should be tempered by methodologic and, more importantly, pathophysiologic considerations, many of them discussed by the authors. The use of erythrocytes as surrogates for [K+]i in the ventricular myocardium must be validated. The mechanisms governing transmembrane potassium flux are different in these two tissues, and, therefore, [K+]i may not react in the same way to short-term, rapid changes in [K+]e. The inclusion in the study mainly of patients with normal left ventricular function may have diminished the likelihood of finding an association, because myocytes from failing hearts may be more sensitive to the effects of [K+]e (see below). Finally, even a strong statistical association in an observational study between lower potassium concentrations and ventricular arrhythmia does not imply a causative mechanism. Circulating epinephrine is important in the short-term regulation of plasma potassium concentrations, because it promotes the entry of potassium to muscular fibers and other cells. The effect is mediated by β2 receptors and appears to result from the activation of the Na+/K+-ATPase (sodium pump) (5). Therefore, an increased adrenergic drive after cardiac surgery could lower potassium concentrations and promote ventricular arrhythmias at the same time. A similar consideration applies to studies showing increased risk of primary ventricular fibrillation in patients with acute myocardial infarction with lower plasma potassium at admission (6, 7).
Much progress has been made since the days in which ventricular premature beats (VPBs) were proposed as harbingers of more serious arrhythmias and their pharmacologic suppression recommended (8). It is now accepted that the relevance of VPBs to more serious arrhythmias (ventricular tachycardia and fibrillation) varies according to substrate and mechanism. Aggressive treatment of VPBs with antiarrhythmic drugs in the setting of acute myocardial infarction or chronic coronary disease may, in fact, be detrimental. This may also apply to patients recovering from coronary artery surgery, in whom ventricular ectopy is common but also in whom ventricular tachycardia or fibrillation occurs in <1% (9).
Ventricular arrhythmias associated with prolonged repolarization appear the most susceptible to manipulation of potassium concentrations. Increases in [K+]e shorten action potential duration. The effect is mediated (at least partially) by an increase in the rapid component of the delayed rectifier potassium current (Ikr) (10), which is encoded by HERG. In patients with the congenital long-QT syndrome type 2 (secondary to mutations in HERG), modest potassium supplementation can dramatically shorten the QT interval (and ideally suppress arrhythmias) (11). Similar findings occur in patients with the acquired counterpart of this syndrome caused by drugs with class III activity. Clinically, drug-induced torsades de pointes frequently occurs in patients with lower potassium concentrations.
