Cardiac Utilization of the Momentum of Blood

Sugawara, Motoaki; Uchida, Kenzo; Kondoh, Yukiyoshi; Jones, Christopher J.

doi:10.1007/978-4-431-66945-6_4

Cited by 3 publications

(1 citation statement)

References 6 publications

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“…The blood, once set in motion, will continue in motion because of its inertia until the heart stops it (28). In late systole, when LV muscle shortening has reached a limit but its tension-bearing ability is still maintained, the inertia of the blood flowing out of the LV causes swift end-systolic unloading of the LV, producing a much smaller LV end-systolic volume and much greater elastic recoil force (19,22,29). The schematic diagram that demonstrates the idea that inertia force of late systolic aortic flow enhances LV elastic recoil is shown in Figure 8.…”

Section: Discussionmentioning

confidence: 99%

Lack of Inertia Force of Late Systolic Aortic Flow Is a Cause of Left Ventricular Isolated Diastolic Dysfunction in Patients With Coronary Artery Disease

Yoshida

Ohte

Narita

et al. 2006

Journal of the American College of Cardiology

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Section: Discussionmentioning

confidence: 99%

Lack of Inertia Force of Late Systolic Aortic Flow Is a Cause of Left Ventricular Isolated Diastolic Dysfunction in Patients With Coronary Artery Disease

Yoshida

Ohte

Narita

et al. 2006

Journal of the American College of Cardiology

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A noninvasive method of measuring wave intensity, a new hemodynamic index: application to the carotid artery in patients with mitral regurgitation before and after surgery

et al. 1999

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Wave intensity (WI) is a new hemodynamic index, which is defined as (dP/dt)(dU/dt) at any site of the circulation, where dP/dt and dU/dt are the time derivatives of blood pressure and velocity, respectively. Arterial WI in normal subjects has two positive sharp peaks. The first peak occurs during early systole when a forward-traveling compression wave is generated by the left ventricle. The magnitude of this peak increases markedly with an increase in cardiac contractility. The second peak, which occurs towards the end of systole, is caused by generation of a forward-traveling expansion wave by the ability of the left ventricle to actively stop aortic blood flow. The interval between the R wave of the ECG and the first peak of WI (R-1st peak interval) and the interval between the first and second peaks (1st-2nd interval) are approximately equal to the preejection period and left ventricular ejection time, respectively. Using a combined Doppler and echo-tracking system, we obtained carotid arterial WI noninvasively. We examined the characteristics of WI in 11 patients with mitral regurgitation (MR) before and after surgery, and 24 normal volunteers. In the MR group before surgery, the second peak was decreased and the (1st-2nd interval)/(R-R interval) ratio was reduced, compared with the normal group (140 +/- 130 vs 750 +/- 290mmHg m/s3. P < 0.0083; 20.7% +/- 3.4% vs 26.7% +/- 2.8%, P < 0.083). There were no significant differences in the first peak between the normal group and the MR group before and after surgery. The second peak in the MR group was increased significantly (P < 0.016 vs before surgery) to 1,150 +/- 830mmHg m/s3 in the early period after surgery (stage I), and to 1,090 +/- 580mmHgm/s3 in the late period after surgery (stage II). These values did not differ significantly from that of the normal group. At stage I, the (R-1st peak interval)/ (R-R interval) ratio was increased from 13.4% +/- 2.7% to 20.6% +/- 5.6% (P < 0.016 vs before surgery). At stage II, this ratio decreased to 16.2% +/- 2.8% (P < 0.016 vs stage I). but was still significantly higher than that before surgery. The (1st-2nd interval)/(R-R interval) ratio increased significantly after surgery (P < 0.016 vs before surgery) to values (27.0% +/- 4.5% at stage I and 28.9% +/- 2.6% at stage II) which did not differ significantly from that of the normal group. The recovery of the second peak after surgery suggests that the left ventricle had recovered the ability to actively stop aortic blood flow. Wave intensity is useful for analyzing changes in the working condition of the heart.

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