Certain temporal patterns of A-V and V-A transmission in experimental preparations resemble phenomena attributed to "supernormal" conduction in the clinic. Detailed study of the properties of the A-V transmission system in such experiments reveals alternative explanations in which supernormality is clearly eliminated. By application of similar principles, supernormality can be eliminated as a factor in most if not all of the published examples. Three major categories can be discerned: (1) occult 2:1 A-V block, in which an idioventricular beat "retracts" an otherwise refractory barrier within the A-V node; (2) alternation between dissociated intranodal transmission pathways; and (3) "ventriculophasic" (vagal) depression of nodal conductivity.

The electron microscopic structure of heart muscle and the ultrastructural basis of cardiac contraction have been reviewed. The relation between muscle length and developed tension has been explained in terms of the structure of the sarcomere, which is the basic unit of contraction. Using the derived length-tension curve of the sarcomere, developed tension has been attributed to the overlap of thick and thin filaments within the sarcomere, lending support to the "sliding" mechanism in heart muscle. It has been shown that initial sarcomere length is a function of ventricular filling pressure and that this relation explains the normal limits of the heart as a pump, including: (1) the Starling mechanism whereby increased diastolic volume (EDV) engenders an increased stroke volume (SV), (2) the upper limits to ventricular filling pressure and volume, and (3) the normal range to the ventricular ejection fraction (SV/EDV). Further, ultrastructure helps to define the processes which occur with acute and chronic ventricular dilatation. In this regard, the importance of sarcomere dispersion and "fiber slippage," which may lead to disordered ventricular function, have been discussed.