Mechanisms and dynamics of episodes of progression of 2:1 atrioventricular block in patients with documented two-level conduction disturbances.

Twenty episodes of progression of 2:1 atrioventricular (AV) block were identified during incremental atrial stimulation in 7 patients with documented (2-level) block in the AV node and His-Purkinje system. All occurred at cycle lengths shorter than those at which stable 2:1 HV block had been detected. Thirteen episodes were typical since 2:1 increased to 3:1 AV block when an atrio-His (AH) Wenckebach period was completed with an atrial impulse that otherwise would have been conducted. These episodes occurred with dynamic A(M): V(N) ratios similar to those seen at the AV node. Seven atypical episodes were identified (while AH Wenckebach periods were occurring): (1) 2:1 increasing to 3:1 AV block and then to 4:1 AV block resulting from prolonged refractoriness in the His-Purkinje system subsequently followed by concealed conduction in the latter structure; (2) conversion of 3:2 directly into 3:1 AV block due to block of the next-to-last atrial impulse in the His-Purkinje system with completion of AH Wenckebach period with the following atrial impulse; and (3) 4:2 AV block presumably due to supernormal conduction in a transversely dissociated His-Purkinje system. These episodes occurred with A(M): V(N) ratios, which in other structures would have been indicative of different degrees of AV block. In conclusion, progression of 2:1 AV block during documented 2 level conduction disturbances (1) can be explained by mechanisms different than those currently known, and (2) has rich, but different dynamics from those observed exclusively in the AV node and exclusively in the His-Purkinje system.

[Depressed conduction and increased automaticity in acute septal myocardial infarction]. / Conducción deprimida y automatismo aumentado en el infarto de miocardio agudo septal.

A patient with an established LBBB suffered an acute septal myocardial infarction complicated with a 2:1 infranodal AV block. As the ventricular rate decreased, the preexisting LBBB disappeared, and, in its place, a RBBB bradycardia-dependent appeared. Later on, an escape rhythm emerged, and competition between the two rhythms evolved. These disturbances were short-lived, and took place in the first 24 h. It is postulated that an increase in the rate of diastolic depolarization, ischemia related, may cause, in the same area, impairment of conduction and increased automaticity accounting for the findings previously mentioned. In an acute septal infarction conduction disturbances usually are progressive; ischemia rarely may induce hypopolarization rise giving to complex, but reversible, phenomena.

[Acute myocardial infarct in the setting of a hyperpotassemia: electrocardiographic findings]. / Infarto agudo de miocardio en el seno de una hiperpotasemia: hallazgos electrocardiográficos.

Graded hyperkalemia and acute myocardial ischemia are remarkably reflected (and can even be predicted) in the surface ECG when they occur alone. If, however, acute ischemia supervenes in the setting of previous hyperkalemia, the ECG changes are less known. We describe a patient who suffered an acute septal myocardial infarction while his extracellular potassium was high. Changes in the ECG waveform brought about by both acute ischemia and hyperkalemia are emphasized. The origin of a sine-wave ventricular activation pattern, the supraventricular origin and likely sinoventricular conduction, versus ventricular tachycardia is, as well, discussed. Correction of hyperkalemia and other metabolic disturbances, as the first and most important therapeutic target, is critical when the origin and nature of the rhythm are controversial.

[Paroxysmal AV block induced by atrial flutter in acute inferior myocardial infarction]. / Bloqueo AV paroxístico inducido por flutter auricular en el infarto de miocardio agudo inferior.

Conduction disturbances in the acute phase of an inferior myocardial infarction are frequent. Paroxysmal AV block and ventricular standstill is, on the other hand, an unusual event. We describe a case of paroxysmal AV block precipitated by, and dependent on, the presence of atrial flutter. Concealed conduction of atrial impulses to the AV node is the likely cause of this form of AV block. The transient development, ischaemia related, of a longitudinal and transverse dissociation of the AV node, increased the concealed penetration of atrial impulses and its effect on subsequent impulse formation, given rise to a form of paroxysmal AV block.