Cardiac cycle

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

Comparison of echocardiographic and necropsy measurements of ventricular wall thicknesses in patients with and without disproportionate septal thickening.

Abstract: In several patients with asymmetric septal hypertrophy (ASH) diagnosed by echocardiography (septal-free wall thickness ratios greater than or equal to 1.3), we have discovered marked discrepancies between the echocardiographic and necropsy measurements of wall thicknesses that led to uncertainty regarding the actual cardiac diagnosis. To resolve these apparent incongruities, the echocardiograms and hearts of 17 patients with cardiac disease were studied. Six of nine patients with abnormal septal-free wall ratios greater than or equal to 1.3 during life had septal-free wall ratios that were not diagnostic of disproportionate septal thickening at necropsy. Such discrepancies may be explained as follows: 1) echocardiographic measurements during life were made in diastole (as per convention), but measurements at necropsy were made in hearts that appeared to have been in the systolic phase of the cardiac cycle; 2) the left ventricular free wall thickens considerably more than the ventricular septum in systole, as determined by echocardiography. This latter phenomenon resulted in septal-free wall ratios in systole that were consistently smaller than those in diastole. Furthermore, septal-free wall ratios obtained at necropsy corresponded most closely to those obtained by echocardiography in systole.

Effects of timing of atrial systole on LV filling and mitral valve closure: computer and dog studies

Abstract: Atrioventricular (AV) delay that results in maximum ventricular filling and physiological mechanisms that govern dependence of filling on timing of atrial systole were studied by combining computer experiments with experiments in the anesthetized dog instrumented to measure phasic mitral flow Ventricular filling volume is maximized at AV delay of 100 ms in the computer study and 80 ms in the dog study At any time in diastole atrial contraction accelerates mitral flow, opening the mitral valve widely; atrial relaxation then decelerates mitral flow, moving the valve leaflets toward closure The time the valve remains closed following atrial systole varies inversely with AV delay When AV delay is optimal, the mitral valve is moving rapidly toward closure but is not yet closed at onset of ventricular systole The decline in filling volume as AV delay decreases below its optimum value is primarily the result of premature termination of atrial ejection by ventricular systole As AV delay increases above its optimal value, filling volume progressively decreases because of premature mitral valve closure that limits effective diastolic filling period There is no significant retrograde mitral flow at any point in diastole for any AV delay

Methods and apparatus for assisting cardiac resynchronization therapy

Abstract: A method for assisting the planning of an interventional biventricular pacing procedure includes segmenting an image dataset of a heart of a patient to extract a surface of a left ventricle (LV) and a LV myocardium of the patient's heart, utilizing the segmented image dataset to divide the LV into myocardial segments or into a plurality of short axis slices, and detecting wall motion of each short axis slice of phases of a cardiac cycle of the patient's heart with respect to a reference phase. The method also includes localizing a region most recently attaining maximum displacement and a region most recently attaining maximum velocity, and generating 2D or 3D renderings including renderings indicating at least one of time delays of contraction, a maximum displacement, or a maximum velocity.

Dynamic Determinants of Left Ventricular Filling: An Overview

Abstract: The left ventricle fills through dynamic changes in its compliance as it relaxes (by altering its wall stress), through elastic recoil from a nonequilibrium shape, and through passive acceptance of blood during diastole. The driving force necessary to accelerate the blood and to overcome dissipative energy losses is provided by the pressure in the left atrium which acts as a passively compliant reservoir (whose potential energy is provided by the right ventricular contraction), and by the active generation of force during atrial systole. The efficiency of ventricular filling, and its ability to determine the subsequent stroke volume, is in part determined by the ability of the valve to open widely and to stay open during filling, to close competently at systole, and to remain closed without leakage.