Adrenaline infusion increased QTc interval (to 423 ms; P<0.001) and QT dispersion (to 63 ms; P=0.001) even during potassium clamping, indicating a direct effect independent of hypokalemia.
Does l-adrenaline infusion with potassium replacement prevent QTc interval and QT dispersion prolongation compared to l-adrenaline infusion without potassium replacement in healthy males?
Adrenaline prolongs cardiac repolarization and increases QT dispersion through a direct myocardial effect, independent of its hypokalemic effects.
Absolute Event Rate: 423% vs 433%
p-value: p=<0.001
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.
Lee et al. (2003) studied Healthy volunteers (n=10). l-adrenaline infusion with potassium clamping vs. l-adrenaline infusion without potassium clamping was evaluated on QTc interval (p=<0.001). Adrenaline infusion increased QTc interval (to 423 ms; P<0.001) and QT dispersion (to 63 ms; P=0.001) even during potassium clamping, indicating a direct effect independent of hypokalemia.