Effect of high K, low K, and quinidine on QRS duration and ventricular action potential

Abstract

Perfusion of isolated rabbit hearts with high potassium, low potassium, and quinidine solutions caused a diffuse widening of the QRS complex with no change in shape. These QRS changes were correlated with the magnitude and upstroke velocity of the ventricular transmembrane potential. An increase of QRS duration by 132% produced by high K was accompanied by a decrease of the action potential, resting potential, and upstroke velocity. A similar increase in QRS duration produced by quinidine was accompanied by a slow upstroke velocity but no change in magnitude of the action potential or resting potential. An increase of QRS duration by 49% produced by low K was accompanied by an increased action and resting potential, and upstroke velocity. We attributed the QRS changes produced by high K and quinidine, at least partly, to a slow conduction in the ventricle, caused by a slow upstroke velocity of the action potential. The QRS changes produced by low K could be explained by hyperpolarization. Early arrhythmias caused by low K were due to atrioventricular conduction disturbances.

Changes in extracellular K+ concentration modulate contractility of rat and rabbit cardiac myocytes via the inward rectifier K+ current IK1

“…to depolarize or hyperpolarize the resting potential is fairly consistent from one cell type to the next, the degree to which the membrane potential shifts away from the calculated Nernst potential for K + (E K ) varies significantly from one cell type to the next (Whalley et al 1994;Bailly et al 1998;Baczko et al 2003), depending upon the slope conductance for K + and input resistance (R input ) of the cell (Aronson & Nordin, 1988;Bridge et al 1990;McCullough et al 1990;Whalley et al 1994;Golod et al 1998) (Ng et al 1987) or decrease (Herzig, 1992) action potential duration in rat and rabbit atrial and ventricular muscle. Similar discrepancies have been observed following a reduction of [K + ] o in rabbit, human and bullfrog ventricular and atrial tissues (Gettes et al 1962;Goto et al 1977;Christe, 1983;White & Terrar, 1991).…”

Characterization of concentration- and use-dependent effects of quinidine from conduction delay and declining conduction velocity in canine Purkinje fibers.

“…A description ofthe kinetics ofrecovering should therefore be available from this interstimulus recovery interval. Blockade associated with the nth pulse of a train can be described recursively in terms ofblockade acquired during the preceding pulse by the relationship: an+ = ane-(\+Xt'r) + r(l e-r)e + a (l - (3) This defines the overall drug uptake rate, X*, as the weighted sum ofthe two state-dependent uptake rates which predicts a linear relationship between X*, determined from an exponential fit to declining 1/max or incremental conduction delay at any given interstimulus interval and tr, the recovery interval between pulses. For open-channel blockade as expected with quinidine (29,(31)(32), ta is presumed to be the mean channel open time, which is assumed to be constant during pulse train stimulation (66).…”

“…Declining conduction velocity (0) or other measures of conduction delay (CD) have been shown to accompany both the decline in Vma produced by a reduction in extracellular sodium concentration (1) and drug-induced sodium channel blockade (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Despite such qualita-Receivedforpublication 25 July 1988 and in revisedform 21 February 1989.…”

Spatial and Nonspatial Influences on the TQ-ST Segment Deflection of Ischemia

“…Potassium can (a) directly alter the transmembrane potential (depolarizes cells during diastole and shortens their action potential duration during systole [81]); (b) influence the rate of potassium leakage and accumulation in the extracellular apace (stimulates uptake by the cell of potassium ion [82]); and (c) increase potassium conductance (83). The precise mechanism by which potassium infusion reduced the magnitude of the TQ-ST segment deflections in this study cannot be ascertained without making simultaneous measurements of transmembrane potentials before and during coronary artery occlusion in the normal and ischemic regions.…”