Cardiac cycle

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

Classification of supraventricular and ventricular cardiac rhythms using cross channel timing algorithm

Abstract: A system and method for classifying cardiac complexes sensed during a tachycardia episode. A first cardiac signal and a second cardiac signal are sensed, where the first cardiac signal has a voltage. A first cardiac complex and a second cardiac complex of a cardiac cycle are detected in the first and second cardiac signal, respectively. A predetermined alignment feature is identified in the second cardiac complex. A datum is defined, or positioned, at a specified interval from the predetermined alignment feature of the second cardiac complex. Voltage values are then measured from the first cardiac complex at each of two or more measurement intervals from the datum. The voltage values are then compared voltage values measured from NSR cardiac complexes to classify the first cardiac complex is either a ventricular tachycardia complex or a supraventricular tachycardiac complex.

Relationship between left ventricular wall thickness and left atrial size: Comparison with other measures of diastolic function

Abstract: We postulated that in patients with essential hypertension and normal left ventricular (LV) systolic function, left atrial (LA) size correlates with LV wall thickness by better reflecting the chronicity and duration of LA hypertension than the commonly used hemodynamic and Doppler measures of LV diastolic function. Accordingly, hemodynamic, Doppler, and two-dimensional echocardiographic measurements were performed in 30 subjects with no cardiovascular abnormalities other than essential hypertension (mean systolic blood pressure of 150±29 mm Hg). The mean LV wall thickness was 0.57±0.14 cm/m 2 and the mean LV ejection fraction was 0.62±0.12. Hemodynamic and Doppler measures including pulmonary capillary wedge and LV end-diastolic pressures, isovolumic LV pressure relaxation, LV chamber elastic stiffness, and E/A ratio (E and A waves on the pulsed Doppler signal of the mitral valve) correlated poorly ( r =0.01 to −0.52) with LV wall thickness. Both E/A ratio and isovolumic LV pressure relaxation correlated better ( p =0.05) with patient age than with LV wall thickness. In contrast, LA area (in the apical four-chamber view) had a good correlation ( r =0.77 for LA area in atrial diastole and r =0.86 for LA area in atrial systole) with LV wall thickness. Multiple regression analysis revealed LA area in atrial systole to be the best correlate of LA wall thickness. We conclude that because the left atrium is a thin-walled structure, its size may increase with an increase in LA pressure. In the absence of mitral valve disease and atrial fibrillation, LA size may reflect the chronicity and duration and thus the history of LA hypertension. LA size in the apical four-chamber view may, therefore, provide a simple noninvasive assessment of the degree of LV diastolic dysfunction.

Mitral anulus motion. Relation to pulmonary venous and transmitral flows in normal subjects and in patients with dilated cardiomyopathy

Abstract: The dynamics between mitral anulus motion, and, thus, motion of the base of the heart, and filling of the left atrium and ventricle were studied by Doppler echocardiography in 12 normal subjects and 28 patients with dilated cardiomyopathy. The normal motion of the mitral anulus is associated with two phases of inflow from the pulmonary veins. The first phase (J) of pulmonary venous inflow occurs during ventricular systole, concomitant with the descent of the mitral anulus toward the ventricular apex, the extent of which is 12.8 +/- 1.4 mm. The end of the descent of the anulus occurs at the cessation of aortic ejection. About 100 msec later, a rapid recoil of the mitral anulus toward the atrium coincides with the onset of transmitral filling. This rapid recoil contributes to the displacement of blood from the atria into the ventricles in early diastole. The second phase (K) of pulmonary venous flow begins in early diastole, with its peak occurring about 50 msec after the peak of transmitral flow. During atrial contraction, the mitral anulus moves slightly (2.4 +/- 0.7 mm) toward the atrium and then returns toward its initial position within 120 msec. This motion coincides with the A wave of transmitral flow. In patients with dilated cardiomyopathy, pulmonary venous flow and mitral anulus motion are markedly altered in comparison with normal subjects. In all patients, motion of the mitral anulus is either reduced or absent.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanics of Active Contraction in Cardiac Muscle: Part II—Cylindrical Models of the Systolic Left Ventricle

Abstract: Models of contracting ventricular myocardium were used to study the effects of different assumptions concerning active tension development on the distributions of stress and strain in the equatorial region of the intact left ventricle during systole. Three models of cardiac muscle contraction were incorporated in a cylindrical model for passive left ventricular mechanics developed previously [Guccione et al. ASME Journal of Biomechanical Engineering, Vol. 113, pp. 42-55 (1991)]. Systolic sarcomere length and fiber stresses predicted by a general "deactivation" model of cardiac contraction [Guccione and McCulloch, ASME Journal of Biomechanical Engineering, Vol. 115, pp. 72-81 (1993)] were compared with those computed using two less complex models of active fiber stress: In a time-varying "elastance" model, isometric tension development was computed from a function of peak intracellular calcium concentration, time after contraction onset and sarcomere length; a "Hill" model was formulated by scaling this isometric tension using the force-velocity relation derived from the deactivation model. For the same calcium ion concentration, the sarcomeres in the deactivation model shortened approximately 0.1 microns less throughout the wall at end-systole than those in the other models. Thus, muscle fibers in the intact ventricle are subjected to rapid length changes that cause deactivation during the ejection phase of a normal cardiac cycle. The deactivation model predicted rather uniform transmural profiles of fiber stress and cross-fiber stress distributions that were almost identical to those of the radial component. These three components were indistinguishable from the principal stresses. Transmural strain distributions predicted at end-systole by the deactivation model agreed closely with experimental measurements from the anterior free wall of the canine left ventricle.