Effects of adrenaline and potassium on QTc interval and QT dispersion in man
Effects of adrenaline and potassium on QTc interval and QT dispersion in man
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DOI：
10.1046/j.1365-2362.2003.01123.x
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发表时间：
2003-02-01
影响因子：
5.5
通讯作者：
Heller, SR
中科院分区：
文献类型：
--
作者：
Lee, S;Harris, ND;Heller, SR
背景低血糖可急性改变心脏复极，心电图（ECG）上的心率校正QT（QTc）间期和QT离散度（QTd）增加;这些变化与交感-肾上腺反应的反调节有关。当输注到健康志愿者体内时，肾上腺素产生QTc延长和血浆钾（K+）下降。然而，低钾血症心脏复极独立，因此，我们的目的是确定肾上腺素诱导的复极变化是否介导直接或通过降低血浆K+。材料和方法10名健康男性进行了研究，在两个场合。在两次访视中，他们接受了相似的l-肾上腺素输注，但有一次还给予了钾;调整输注速率以维持基线时的循环K（+）。结果钾阻断前后QTc间期和QTd均延长，而无钾阻断时QTc间期和QTd均延长。在未进行K+置换的情况下，平均（SE）QTc从378（5）ms延长至最终最大值433（10）ms，QTd从36（5）ms增加至69（8）ms（均P < 0.001）。钾离子替代治疗时，QTc间期分别为385（7）ms和423（11）ms（P < 0.001），QTd 38分别为4 ms和63（5）ms（P = 0.001）。肾上腺素对心肌的直接作用似乎是最可能的机制。
Background Hypoglycaemia alters cardiac repolarization acutely, with increases in rate-corrected QT (QTc) interval and QT dispersion (QTd) on the electrocardiogram (ECG); such changes are related to the counterregulatory sympatho-adrenal response. Adrenaline produces both QTc lengthening and a fall in plasma potassium (K+) when infused into healthy volunteers. Hypokalaemia prolongs cardiac repolarization independently however, and therefore our aim was to determine whether adrenaline-induced repolarization changes are mediated directly or through lowered plasma K+.Materials and methods Ten healthy males were studied on two occasions. At both visits they received similar l- adrenaline infusions but on one occasion potassium was also administered; infusion rates were adjusted to maintain circulating K (+) at baseline. The QTc interval, QTd, peripheral physiological responses and plasma adrenaline and potassium concentrations were measured during both visits.Results The QTc interval and QTd increased both with and without potassium clamping. Without K+ replacement, mean (SE) QTc lengthened from 378 (5) ms to a final maximum value of 433 (10) ms, and QTd increased from 36 (5) ms to 69 (8) ms (both P < 0.001). During K (+) replacement, QTc duration at baseline and study end was 385 (7) ms and 423 (11) ms, respectively (P < 0.001), and QTd 38 was (4) ms and 63 (5) ms (P = 0.001).Conclusions These data suggest that disturbed cardiac repolarization as a result of increases in circulating adrenaline occurs independently of extracellular potassium. A direct effect of adrenaline upon the myocardium appears the most likely mechanism.