Cardiac cycle

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

A Novel Left Heart Simulator for the Multi-modality Characterization of Native Mitral Valve Geometry and Fluid Mechanics

Abstract: Numerical models of the mitral valve have been used to elucidate mitral valve function and mechanics. These models have evolved from simple two-dimensional approximations to complex three-dimensional fully coupled fluid structure interaction models. However, to date these models lack direct one-to-one experimental validation. As computational solvers vary considerably, experimental benchmark data are critically important to ensure model accuracy. In this study, a novel left heart simulator was designed specifically for the validation of numerical mitral valve models. Several distinct experimental techniques were collectively performed to resolve mitral valve geometry and hemodynamics. In particular, micro-computed tomography was used to obtain accurate and high-resolution (39 μm voxel) native valvular anatomy, which included the mitral leaflets, chordae tendinae, and papillary muscles. Three-dimensional echocardiography was used to obtain systolic leaflet geometry. Stereoscopic digital particle image velocimetry provided all three components of fluid velocity through the mitral valve, resolved every 25 ms in the cardiac cycle. A strong central filling jet (V ~ 0.6 m/s) was observed during peak systole with minimal out-of-plane velocities. In addition, physiologic hemodynamic boundary conditions were defined and all data were synchronously acquired through a central trigger. Finally, the simulator is a precisely controlled environment, in which flow conditions and geometry can be systematically prescribed and resultant valvular function and hemodynamics assessed. Thus, this work represents the first comprehensive database of high fidelity experimental data, critical for extensive validation of mitral valve fluid structure interaction simulations.

Implantable stimulation device and method for determining atrial autocapture using PVC response

Abstract: A pacemaker programmer and diagnostic system retrieves information stored within a pacemaker and analyzes the retrieved data in real time. The stored information can be retrieved by means of a telemetry communication link. The pacemaker automatically lengthens a post-ventricular atrial refractory period (PVARP). The pacemaker determines atrial capture threshold by generating atrial stimulation pulses while maintaining the ventricular stimulation pulse amplitude at a level known to ensure ventricular capture, and by detecting loss of atrial capture. In response to loss of atrial capture, a processor automatically triggers a premature ventricular contraction (PVC) response to prevent a retrograde P-wave from initiating a pacemaker-mediated tachycardia. Also in response to loss of atrial capture, the processor sets the atrial stimulation pulse amplitude to a value above the atrial capture threshold in a subsequent cardiac cycle, and restores the PVARP to its pre-test value.

A study with the electrocardiograph of the mode of death of the human heart

Abstract: In four of the seven cases the ventricles remained active from one and a half to eighteen minutes after the electrocardiograms failed to show evidence of auricular activity. In two cases the auricles outlasted the ventricles and in one case only did the auricles and ventricles stop apparently at the same time. Complete dissociation occurred three times. Some delay in the conduction time was seen in five of the seven cases. In two cases the auricles ceased to beat before evidence of impaired conduction appeared. There was always marked slowing; the slowest independent ventricular rates varied from 13.6 to 47.0. The slowest rates at which the auricles beat regularly varied from 20 to 65 per minute. There was never evidence of auricular fibrillation, although in two cases the electrocardiograms give fairly conclusive evidence that ventricular fibrillation occurred. The ventricles reestablished a regular rhythm after a short period of ventricular fibrillation in one case, while in the other but one ventricular contraction occurred after the appearance of fibrillation. Characteristic changes in the ventricular complex of the electrocardiograms occurred in all the records. They consisted of a gradual fusion of the R- and T-waves, forming, when the fusion was complete, a large rounded or peaked wave. In some cases the identity of the two waves was not entirely lost. In spite of the marked change in shape of the ventricular complexes, there was often but little change in their duration. In some cases the ventricular systole was shortened at the end, while in others it was prolonged. The change in the form of the ventricular electrical complex indicates that the course of the stimulus and the manner of the contraction of the muscle were abnormal. The fact that the R-wave became gradually prolonged suggests that the conduction of the stimulus through the ventricular walls became delayed as the heart died. The fact that after death there is a continuation of cardiac muscular activity sufficient to cause a difference in electrical potential between the two sides of the body does not necessarily mean that a ventricular systole in the sense of muscular shortening takes place. It has been observed experimentally that well defined electrical complexes may be caused by cardiac activity which cannot be seen or recorded graphically. As the duration of the ventricular complexes characteristic of the dying heart usually does not differ markedly from the duration of the complexes before clinical death, it seems probable that the entire musculature of the ventricles participates in the contraction; as definite shortening, or at least a marked change in duration, would be expected if only a part of the ventricular musculature participated in the activity which produced the complex.

Assessment of left-ventricular function.

Abstract: There are three distinct phases of the cardiac cycle (contraction, active relaxation, and passive relaxation) which should be examined in order to perform a thorough assessment of global left-ventricular function. Accurate measurements of left-ventricular pressure and volume are necessary to assess these phases of the cardiac cycle. The ideal index of contractility is sensitive to the intropic state of the heart, but insensitive to loading conditions, heart rate, and cardiac size. Indices of contractility may be derived from various aspects of the phase of contraction including isovolumic contraction, the end-systolic pressure-volume relationship, the phase of ejection, and the stress-strain relationship. The indices of contractility most commonly employed and arguably closest to 'ideal' are preload recruitable stroke work, an ejection phase index; the dP/dt - end-diastolic volume relationship, an isovolumic contraction phase index; and end-systolic elastance, an index derived from the end-systolic pressure-volume relationship. The active phase of relaxation is most commonly assessed by the time constant (tau) of the exponential ventricular pressure decline that occurs during the isovolumic period of relaxation. The value for tau varies inversely with ventricular function and reflects the active, energy consuming process of relaxation. tau is influenced by many of the same factors which influence contractility. The end-diastolic pressure-volume relationship reflects the passive properties of the left ventricle and may be used to obtain a measure of diastolic stiffness. The end-diastolic pressure-volume relationship is curvilinear (exponential) when end-diastolic pressures are varied over a wide range, but may be approximated by a linear relationship during low filling pressures. Diastolic stiffness is influenced by the viscoelastic properties of the heart, pericardial constraint, the atrioventricular pressure gradient, and ventricular interaction. Knowledge of the indices of the three phases of the cardiac cycle and their interactions are important to the understanding and interpretation of ventricular function in health and disease.