Action potentials, afterpotentials, and arrhythmias.

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.

[1]  T. Saito,et al.  Electrophysiological Studies on the Mechanism of Electrically Induced Sustained Rhythmic Activity in the Rabbit Right Atrium , 1978, Circulation research.

[2]  A. L. Wit,et al.  Triggered and automatic activity in the canine coronary sinus. , 1977, Circulation research.

[3]  M. Vassalle,et al.  Circulation Research an Official Journal of the American Heart'association Brief Reviews the Relationship among Cardiac Pacemakers Overdrive Suppression the Effect of a Sudden Cessation of the Activity of a Dominant Pacemaker , 2022 .

[4]  P. Cranefield,et al.  Two Levels of Resting Potential in Canine Cardiac Purkinje Fibers Exposed to Sodium‐Free Solutions , 1976, Circulation research.

[5]  R. Myerburg,et al.  Eelctrophysiologic and ultrastructural characteristics of the canine tricuspid valve. , 1976, The American journal of physiology.

[6]  A. L. Wit,et al.  Triggered Activity in Cardiac Muscle Fibers of the Simian Mitral Valve , 1976, Circulation research.

[7]  B. Surawicz.  The Conduction of the Cardiac Impulse: The Slow Response and Cardiac Arrhythmias , 1975 .

[8]  G. Isenberg,et al.  Is potassium conductance of cardiac Purkinje fibres controlled by [Ca2+]i? , 1975, Nature.

[9]  P. Cranefield,et al.  Initiation of Sustained Rhythmic Activity by Single Propagated Action Potentials in Canine Cardiac Purkinje Fibers Exposed to Sodium‐Free Solution or to Ouabain , 1974, Circulation research.

[10]  G. Moe,et al.  Effect of Calcium on Acetylstrophanthidin‐Induced Transient Depolarizations in Canine Purkinje Tissue , 1973, Circulation research.

[11]  W. Trautwein,et al.  Membrane Currents in Cardiac Muscle Fibers , 1973 .

[12]  A. L. Wit,et al.  Electrophysiological Properties of Cardiac Muscle in the Anterior Mitral Valve Leaflet and the Adjacent Atrium in the Dog: POSSIBLE IMPLICATIONS FOR THE GENESIS OF ATRIAL DYSRHYTHMIAS , 1973, Circulation research.

[13]  G. Ferrier,et al.  A Cellular Mechanism for the Generation of Ventricular Arrhythmias by Acetylstrophanthidin , 1973, Circulation research.

[14]  Larry D. Davis.  Effect of Changes in Cycle Length on Diastolic Depolarization Produced by Ouabain in Canine Purkinje Fibers , 1973, Circulation research.

[15]  M. Rosen,et al.  Correlation between Effects of Ouabain on the Canine Electrocardiogram and Transmembrane Potentials of Isolated Purkinje Fibers , 1973, Circulation.

[16]  A. L. Wit,et al.  Conduction of the Cardiac Impulse III. Characteristics of very slow conduction , 1972 .

[17]  A. L. Wit,et al.  Slow Conduction and Reentry in the Ventricular Conducting System: II. SINGLE AND SUSTAINED CIRCUS MOVEMENT IN NETWORKS OF CANINE AND BOVINE PURKINJE FIBERS , 1972, Circulation research.

[18]  B. Hoffman,et al.  Reentry: Slow Conduction, Summation and Inhibition , 1971, Circulation.

[19]  E. Sonnenblick,et al.  An Intrinsic Neuromuscular Basis for Mitral Valve Motion in the Dog , 1967, Circulation research.

[20]  B. Hoffman,et al.  An Analysis of Arrhythmias Induced by Ouabain in Intact Dogs , 1963, Circulation research.

[21]  W. Trautwein.  Generation and conduction of impulses in the heart as affected by drugs. , 1963, Pharmacological reviews.

[22]  K. Matsuda,et al.  EFFECTS OF ACONITINE ON THE CARDIAC MEMBRANE POTENTIAL OF THE DOG , 1959 .

[23]  L. Cabrera.  [Ventricular fibrillation]. , 1956, Neurocirugia.

[24]  J. Dudel,et al.  [The action current of the myocardial fibers in oxygen deficiency]. , 1954, Pflugers Archiv fur die gesamte Physiologie des Menschen und der Tiere.

[25]  G. Dawes.  Experimental cardia arrhythmias and quinidine-like drugs. , 1952, Pharmacological reviews.

[26]  D. Scherf,et al.  Experimental parasystole. , 1951, American heart journal.

[27]  E. Bozler.  TONUS CHANGES IN CARDIAC MUSCLE AND THEIR SIGNIFICANCE FOR THE INITIATION OF IMPULSES , 1943 .

[28]  E. Bozler.  THE INITIATION OF IMPULSES IN CARDIAC MUSCLE , 1943 .

[29]  M. Segers.  L'accommodation Du Rythme Cardiaque , 1940 .

[30]  C. J. Rothberger.  Normale und pathologische Physiologie der Rhythmik und Koordination des Herzens , 1931 .

[31]  C. J. Rothberger,et al.  Experimentelle Beiträge zur Kenntnis der Strophantin-Extrasystolen , 1931 .

[32]  D. Scherf.  Untersuchungen über die Entstehungsweise der Extrasystolen und der extrasystolischen Allorhythmien , 1929 .

[33]  K. F. Wenckebach,et al.  Die unregelmässige Herztätigkeit , 1927 .