Cardiac cycle

About: Cardiac cycle is a research topic. Over the lifetime, 3290 publications have been published within this topic receiving 96159 citations.

Dependence of left ventricular twist-radial shortening relations on cardiac cycle phase

Abstract: Cardiac models have proposed tight coupling between the systolic twisting motion of the left ventricle about its longitudinal axis and muscle shortening. Whether a similar relationship holds during...

End-systolic and end-diastolic ventricular interaction.

Abstract: Right ventricular volume affects left ventricular volume via direct interaction across the interventricular septum and series interaction because the right and left hearts are connected in series through the lungs. Because it is difficult to sort out complex physiological mechanisms in the intact circulation, the relative importance of these two effects is unknown. We used statistical analyses of transient changes in left and right ventricular pressures and dimensions following pulmonary artery and venae caval constrictions to separate and quantitate the direct (immediate) from the series (delayed) interaction effects on left ventricular size at end systole and end diastole. With the pericardium closed, direct interaction was one-half as important as series interaction at end diastole and was one-third as important at end systole. With the pericardium removed, direct interaction was one-fifth as important as series interaction at end diastole and one-sixth as important at end systole. These results suggest that differences between transient and steady-state end-systolic pressure-volume relationships are largely explained by direct interaction and that direct end-systolic interaction is important for maintaining balanced right and left heart outputs.

The three‐dimensional arrangement of the myocytes in the ventricular walls

Abstract: The arrangement of the myocytes aggregated together within the ventricular walls has been the subject of anatomic investigation for more than four centuries. The dangers of analyzing the myocardium on the basis of arrangement of the skeletal myocytes have long been appreciated, yet some still described the ventricular myocardium in terms of a unique band extending from the pulmonary trunk to the aorta. Another current interpretation, with much support, is that the ventricular myocytes are compartmentalized in the form of sheets, albeit that the extent of division, and interrelations, of the sheets is less well explained. Histological examination, however, shows that the only muscular unit to be found within the myocardial walls is the cardiac myocyte itself. Our own investigations show that, rather than forming a continuous band, or being arranged as sheets, the myocytes are aggregated together as a three-dimensional mesh within a supporting matrix of fibrous tissue. Within the mesh of aggregated myocytes, it is then possible to recognize two populations, depending on the orientations of their long axes. The first population is aligned with the long axis of the aggregated myocytes tangential to the epicardial and endocardial borders, albeit with marked variation in the angulation relative to the ventricular equator. Correlation with measurements taken using force probes shows that these myocytes produce the major unloading of the blood during ventricular systole. The second population is aligned at angles of up to 40 degrees from the epicardium toward the endocardium. The correlation with measurements from force probes reveals that these intruding myocytes produce auxotonic forces during the cardiac cycle. The three-dimensional arrangement of the mesh also serves to account for the realignment of the myocytes that must take place during ventricular contraction so as to account for the extent of systolic mural thickening.

Paradoxical Effect of Vagus Nerve Stimulation on Heart Rate in Dogs

Abstract: In the anesthetized, open-chest dog, electrical stimulation of the cardiac ends of the transected cervical vagus nerves produced effects on heart rate and A-V transmission that were dependent upon the P-St interval, i.e., the-time from the beginning of the P wave to the beginning of the stimulus. When one vagal stimulus was delivered per cardiac cycle, the pacemaker response curve (curve of the P-P interval as a function of the P-St interval) was sinusoidal in configuration, with a maximum at a P-St interval of 135 msec and a minimum at 349 msec. The mean P-P interval was 568 msec, and the mean amplitude of the pacemaker response curve was 58 msec. In any given experiment, the range of P-P intervals encompassed by the pacemaker response curve defined a range of frequencies over which S-A nodal rhythm became synchronized with the activity in the vagus nerves. Over such a range, increases in the frequency of vagal stimulation evoked paradoxical increases in heart rate. On either side of this range of synchronization, vagal stimulation elicited pronounced rhythmic oscillations of P-P and P-R intervals. The frequency of such oscillations was equal to the difference between the vagal stimulation frequency and the mean heart rate. The oscillations in P-R interval were approximately 180° out of phase with the oscillations in P-P interval.