scholarly journals Doppler Echocardiographic Method to Determine Early and Late Diastolic Filling Volume Separately. Validation and Relationship between Filling Velocity and Volume.

1998 ◽  
Vol 39 (4) ◽  
pp. 489-501
Author(s):  
Shingo KUROKAWA ◽  
Haruhiko OKURI ◽  
Taishi SASAOKA ◽  
Yohji MACHIDA ◽  
Kazuyuki OSADA ◽  
...  
1983 ◽  
Vol 55 (2) ◽  
pp. 323-328 ◽  
Author(s):  
M. Matsuda ◽  
Y. Sugishita ◽  
S. Koseki ◽  
I. Ito ◽  
T. Akatsuka ◽  
...  

To evaluate the effect of exercise on left ventricular diastolic filling, the following were measured at rest and during exercise in 14 control subjects and 15 athletes, using digitized M-mode echocardiography: the peak early diastolic lengthening rate of the left ventricular dimension and the filling volume and the filling fraction during the first 0.10 s of diastole. During ergometer exercise performed at a level that increased the heart rate to 100 beats/min, there were significant increases in the peak normalized lengthening rate of the left ventricular dimension (control subjects, 4.2 +/- 1.3 vs. 6.1 +/- 1.1 s-1, mean +/- SD, P less than 0.001; athletes, 5.3 +/- 0.9 vs. 7.4 +/- 1.1 s-1, P less than 0.001), filling volume (control subjects, 15 +/- 12 vs. 33 +/- 10 ml, P less than 0.001; athletes, 21 +/- 12 vs. 63 +/- 18 ml, P less than 0.001), and filling fraction (control subjects, 21 +/- 14 vs. 42 +/- 17%, P less than 0.005; athletes, 21 +/- 13 vs. 54 +/- 12%, P less than 0.01). The peak lengthening rate of the left ventricular dimension, the filling volume, and the filling fraction were significantly greater in athletes than in control subjects during exercise (P less than 0.005, P less than 0.001, and P less than 0.05, respectively). Augmented early diastolic filling may be a mechanism to provide adequate filling for the ventricle at high heart rates produced by exercise, especially in athletes.


1985 ◽  
Vol 249 (3) ◽  
pp. H604-H619 ◽  
Author(s):  
J. S. Meisner ◽  
D. M. McQueen ◽  
Y. Ishida ◽  
H. O. Vetter ◽  
U. Bortolotti ◽  
...  

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.


2006 ◽  
Vol 5 (1) ◽  
pp. 89-89
Author(s):  
I CLEMENTS ◽  
D HODGE ◽  
S SCOTT

Cardiology ◽  
2014 ◽  
Vol 128 (4) ◽  
pp. 352-354
Author(s):  
Steven J. Lavine

In August, 1903, I published a paper in the ‘Journal of Pathology’(1) in which I demonstrated a method experimentally producing uncompensated hear disease in an animal, which was compatible with life. This method consisted in diminishing the size of the pericardial sac by stitches, so that the diastolic filling of the heart was impeded. The main symptoms of this condition were dropsy and diminution in the amount of urine excreted. As the immediate result of this interference with the action of the heart, there occurred a rise of pressure throughout the whole systemic venous system extending as far back as the capillaries, and a fall of the mean arterial blood-pressure. Further, I found that the pressure in all the veins fell to the normal limit again within the space of about one hour, and that subsequently when dropsy was being produced, the vanous pressure in all parts of the body was normal, and the arterial pressure had almost recovered itself.


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