Triggered activity must be added to spontaneous activity and to circus movement as a cause for extrasystoles and tachycardias of either atrial or ventricular origin. The activity of a triggerable focus requires phase 4 depolarization caused by an afterpotential; this distinguishes it from the activity seen in circus movement. A triggerable focus becomes rhythmically active only if driven at a critical rate or by a critically timed premature impulse; this distinguishes it from a focus of spontaneous or automatic activity. The ease of triggering a triggerable focus increases in the presence of catecholamines; triggerable foci in the atrium become quiescent when exposed to acetylcholine. At the present time, fibers within the coronary sinus provide the most persuasive example of triggered activity as a possible cause of arrhythmias of clinical significance. It is possible that the coupled extrasystoles of digitalis toxicity may be triggered; there is every reason to believe that further examples of triggered arrhythmias of possible clinical significance will be discovered.

A B S T R A C T In an appropriate ionic environment, the resting potential Of canine cardiac Purkinje fibers may have either of two values. By changing the external K concentration, [K]0, in small steps, it was shown that, in the low (1 mM) CI, Nacontaining solutions used in this study, the two levels of resting potential could be obtained only within a narrow range of [K]0 values; that range was usually found between 1 and 4 mM. Within the critical [K]0 range the resting potential could be shifted from either level to the other by the application of small current pulses. It was shown that under these conditions the steady-state current-voltage relationship was "N-shaped," and that a region of both negative slope, and negative chord, conductance lay between the two stable zero-current potentials. The negative chord conductance was largely due to inward sodium current, only part of which was sensitive to tetrodotoxin (TTX). Under appropriate conditions, the negative chord conductance could be abolished by several experimental interventions and the membrane potential thereby shifted from the lower to the higher resting level: those interventions which were effective by presumably diminishing the steadystate inward current included reducing the external sodium concentration, adding TTX, or adding lidocaine; those which presumably increased the steady-state outward current included small increases in [K]0, brief depolarizations to around -20 mV, or the addition of acetylcholine chloride.

Depressed excitability and responsiveness were created in excised bundles of canine Purkinje fibers. A segment 8 mm long was depressed by being encased in agar containing 47 mM K + , the ends of the bundle outside the agar remaining normal. Either normal end could be excited through extracellular electrodes. Action potentials were recorded by intracellular microelectrodes at each end and within the depressed segment. Conduction velocity within the depressed segment fell as low as 0.05 m/sec. Abnormalities of impulse transmission through the depressed segment included delay, 2:1 block, higher degrees of block, rate-dependent block, and block showing the Wenckebach phenomenon. Asymmetries of conduction seen included one-way block. Action potentials in the depressed segment were of low amplitude and showed slow upstrokes. Variations in action potential duration occurred in the depressed segment when conduction failed or was very slow and when impulses were dropped. Delay in conduction too great to result simply from a slow upstroke is attributed to summation of excitatory events across regions of block in a syncytium of cells. The results prove that conduction delays great enough to permit re-entry can occur in short segments of Purkinje fibers subjected to high K+.

No abstract

The mechanism of atrioventricular delay has been studied in isolated rabbit hearts. Multiple intracellular microelectrodes have been employed to obtain simultaneous records from single fibers of atrium, A-V node and His bundle. An appreciable delay in the transmission of excitation has been found only in the atrial portion of the A-V node. Action potentials recorded from single fibers in this area show a low resting potential, slow diastolic depolarization, slow upstroke and low amplitude. These action potentials frequently show one or more notches or steps on the rising phase. Action potentials recorded from fibers of the His bundle are similar in shape and amplitude to those of peripheral Purkinje fibers. Records obtained at several sites between the atrial portion of the node and the His bundle show a gradual transition in action potential shape. The mechanism of slow transmission across the A-V node is discussed in relation to the electrical activity of fibers at the atrial end of this structure.

No abstract

The action potentials recorded from heart muscle with a suction electrode have been compared to those recorded with an intracellular microelectrode. It has been found that if the suction electrode is properly used the monophasic potentials recorded with it may be taken as a reliable index of the time of arrival of excitation at the electrode and as a reliable index of the shape of the action potential during the entire phase of repolarization. The suction electrode potentials differ from the microelectrode potentials in showing a lower rise velocity, a smaller amplitude, a quantitatively different reversal or overshoot and, in the beating heart, ‘afterpotentials’ caused by mechanical effects. When the shape of the action potential, as observed with the microelectrode, is changed by ions such as K+ or Ca++ a similar change is observed in the potential recorded with the suction electrodes.

Thin canine cardiac Purkinje fibers in a fast flow chamber were exposed to K-free fluid for 15 s to 6 min to initiate "sodium loading," then returned to K-containing fluid to stimulate the sodium pump. The electrophysiological effects of enhanced pump activity may result from extracellular K depletion caused by enhanced cellular uptake of K or from an increase in the current generated as a result of unequal pumped movements of Na and K, or from both. The effects of pump stimulation were therefore studied under three conditions in which lowering the external K concentration ([K]0) causes changes opposite to those expected from an increase in pump current. First, the resting potential of Purkinje fibers may have either a "high" value of a "low" (less negative) value: at the low level of potential, experimental reduction of [K]0 causes depolarization, whereas an increase in pump current should cause hyperpolarization. Second, in regularly stimulated Purkinje fibers, lowering [K]0 prolongs the action potential, whereas an increase in outward pump current should shorten it. Finally, lowering [K]0 enhances spontaneous "pacemaker" activity in Purkinje fibers, whereas an increase in outward pump current should reduce or abolish spontaneous activity. Under all three conditions, we find that the effects of temporary stimulation of the sodium pump are those expected from a transient increase in outward pump current, not those expected from K depletion.