Cardiac cycle

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

Dynamic geometry of the left ventricle

Abstract: Some instantaneous geometric changes of the left ventricle during the cardiac cycle have been discussed. The importance of involving size, shape and changes in wall thickness in mathematical manipulations designed to study ventricular mechanics has been stressed. It is suggested that changes of size, shape and wall thickness provide special mechanical advantages to the ventricle during the various phases of the cardiac cycle. It is proposed that the equivalent geometric model of the left ventricle is a thick-walled, nonprolate ellipsoid. Changes in size of the left ventricle alter the manner in which it contracts. Changes in shape of the ventricle during the cardiac cycle alter the relation from moment to moment between internal volume and surface area. Changes in wall thickness alter the stresses distributed across the ventricular wall and adjust the wall stress during the cardiac cycle within certain limits as yet undefined and for reasons which are as yet not understood. Thus it is clear that for any given heart rate, myocardial inotropic state and ventricular pressure, the stresses and tension within the ventricular wall are major functions of not only pressure but ventricular size, shape and wall thickness.

Using cardiac phase to order reconstruction (CAPTOR): A method to improve diastolic images

Abstract: A method is proposed to reconstruct multiphase images that accurately depicts the entire cardiac cycle. A segmented, gradient-recalled-echo sequence (FASTCARD) was modified to acquire data continuously. Images were reconstructed retrospectively by selecting views from each heartbeat based on cardiac phase rather than the time elapsed from the QRS complex. Cardiac phase was calculated using a model that compensates for beat-to-beat heart rate changes. Images collected using cardiac phase to order reconstruction (CAPTOR) depict the entire cardiac cycle and lack the temporal gap that is characteristic of prospectively reconstructed sequences. Time-volume curves of the left ventricle capture the contribution of atrial contraction to end-diastolic volume (EDV). Transmitral phase-contrast flow measurements show a second peak inflow (a wave) that is absent in the standard sequence. Because atrial contraction contributes to ventricular EDV, images using CAPTOR potentially may provide a more reliable measure of EDV, stroke volume, and ejection fraction than standard techniques.

Continuous Measurements of Left Ventricular Dimensions in Intact, Unanesthetized Dogs

Abstract: Left ventricular dimensions have been directly measured for extended periods of time in intact unanesthetized dogs under various conditions. The diameter of the left ventricle during diastole is very large in relation to the change in diameter during each cycle. Thus, considerable quantities of blood remain within the chamber at the end of systolic ejection. The stroke output can be increased by either more complete systolic ejection during exercise or by greater diastolic filling during a startle reaction. Accelerated heart rate occurs in both cases. Changes in left ventricular diameter occur very rapidly, often being manifest within the duration of a single cardiac cycle. Mechanisms by which changes in ventricular size can be directly affected by neural and hormonal influences are briefly considered.

Uniformity of transmural perfusion in anesthetized dogs with maximally dilated coronary circulations.

Abstract: In 14 beating hearts, coronary blood flow was measured electromagnetically in either the left circumflex or the left anterior descending coronary artery, and regional myocardial blood flow was computed from tissue uptake of 7-10^ radioactive microspheres. Metabolic dilation of the coronary circulation was induced by occluding the coronary artery for 10 or 90 seconds, and pharmacologic dilation was induced by infusing papaverine into the artery. In seven dogs, differently labeled microspheres were administered (1) before coronary artery occlusion, (2) at the peak reactive hyperemic response to a 10-second coronary artery occlusion, and (3) early in the rising phase of the hyperemic response following a 90-second coronary artery occlusion. Myocardial blood flow was distributed uniformly across the left ventricular free wall before occlusion and at peak hyperemia after the 10-second occlusion, but early in the hyperemic response to the 90-second occlusion coronary blood flow preferentially perfused subepicardial tissue. In another group of seven dogs, microspheres were administered (1) before coronary artery occlusion, (2) at the peak hyperemic flow after a 90-second occlusion, and (3) at the peak flow during local intracoronary infusion of papaverine. The left ventricular free wall was uniformly perfused under each condition. However, in 12 vented, fibrillating hearts with coronary circulations dilated maximally by perfusion with venous blood containing either papaverine or adenosine, left ventricular blood flow was preferentially directed to the subendocardium (endocardial-epicardial ratio averaged 1.37 ± 0.08 [SE]). We conclude that the coronary circulation of the normally functioning canine heart can dilate maximally without causing relative subendocardial ischemia because of a gradient of vascularity that favors the subendocardium and compensates for systolic flow limitation in that region. • Coronary blood flow is uniformly distributed across the left ventricular free wall of the normally perfused heart of the anesthetized dog (1-3), in spite of the observation that blood entering the left coronary circulation during the systolic phase of the cardiac cycle perfuses primarily the epicardial tissue (4). This nonuniform distribution of systolic flow is believed to be due to the transmural gradient of pressure generated by ventricular contraction (4). It would appear, therefore, that to perfuse the ventricular wall uniformly, diastolic coronary blood flow should be preferentially directed to the subendocardial area. Moir and DeBra (5) have postulated that autoregulatory adjustments in vascular tone are responsible for maintaining adequate subendocardial perfusion. If such an autoregulation is the only mechanism involved in adjusting blood flow to regional requirements, dilation of the coronary vasculature would result in