scholarly journals Servocontrolled Computation of Instantaneous Aortic Blood Flow from Aortic Blood Pressure

1970 ◽  
Vol 11 (1) ◽  
pp. 45-56
Author(s):  
Hiroyuki SUGA ◽  
Osamu OKAI
2018 ◽  
Vol 2 (1) ◽  
pp. 16
Author(s):  
Vijay Kumar Narayana ◽  
Rajeev Sharma ◽  
Niranjan Murthy

<p><strong>Background:</strong> Systemic hypertension, a common disorder with potentially serious complications, exerts ill effects through structural and functional modifications of arterial wall. Haemodynamics play an important role in the development of atherosclerosis. Local hemodynamic temporal pressure and wall shear stress are important for understanding the mechanisms leading to various complications in cardiovascular function.</p><p><strong>Objectives:</strong> Since we could not find such a study in literature involving Indian population, this prompted us to investigate and establish the relationship between the blood pressure and the ascending aortic pulse wave parameters in normal individuals and compare the same with hypertensives.</p><p><strong>Material and Methods:</strong> A case control study was done in a tertiary care hospital involving 25 hypertensive parents and further compared with 25 normotensive subjects of same age group acting as control. The GE ̶ P 100 Doppler echocardiography machine was used to study acceleration time, deceleration time, ejection time, ejection fraction, peak flow velocity and pressure gradient in hypertensives and compared the same with age matched normotensive. Also ascending aortic diameter was mapped at the annulus.</p><p><strong>Results:</strong> The results of our study confirmed our assumption that in hypertensive the ascending aortic haemodynamic parameters are abnormal and both systolic and diastolic blood pressure does exert a statistically significant influence on the Doppler parameters of ascending aorta. The acceleration time, deceleration time, pressure gradient and ejection time showed statistically significant increase in hypertensives when compared to normotensive. At the same time the ejection fraction and the ascending aortic diameter showed a statistically significant decrease than normotensive.</p><p><strong>Conclusion:</strong> We would conclude to say that the Doppler parameters of ascending aortic blood flow are abnormal in hypertensives. This altered haemodynamics may lead to further ill effects by way of altered peripheral haemodynamics. This Doppler evaluation of ascending aortic blood flow can be developed as a clinical tool for evaluating hypertensives and assessing the benefit of treatment of hypertension.</p>


2003 ◽  
Vol 95 (2) ◽  
pp. 751-757 ◽  
Author(s):  
A. S. Thakor ◽  
C. N. Brown ◽  
A. V. Edwards

Submandibular vascular and secretory responses to parasympathetic chorda-lingual (C-L) stimulation were investigated in anesthetized sheep before, during, and after an intracarotid (ic) infusion of endothelin-1 (ET-1). Stimulation of the peripheral end of the C-L nerve at 4 and 8 Hz produced a frequency-dependent reduction in submandibular vascular resistance (SVR) associated with a frequency-dependent increase in submandibular blood flow, salivary flow, and Na+, K+, and protein output from the gland. During stimulation at 4 Hz, ic ET-1 significantly increased SVR ( P < 0.01), without significantly affecting either the aortic blood pressure or heart rate. Submandibular blood flow (SBF) was reduced by 48 ± 4% and the flow of saliva by 50 ± 1%. The effect on blood and salivary flow persisted for at least 30 min after the infusion of ET-1. The reduction in SBF was associated with a diminution in the output of Na+,K+, and protein in the saliva ( P < 0.01). These effects persisted for 30 min after the infusion of ET-1 had been discontinued and were linearly related to the flow of plasma throughout.


2010 ◽  
Vol 109 (2) ◽  
pp. 484-490 ◽  
Author(s):  
Kevin S. Heffernan ◽  
James E. Sharman ◽  
Eun Sun Yoon ◽  
Eui Jin Kim ◽  
Su Jin Jung ◽  
...  

In the present study, we examined the influence of preload augmentation via passive leg elevation (PLE) on synthesized aortic blood pressure, aortic augmentation index (AIx), and aortic capacitance (a reflection of aortic reservoir function). Central and peripheral hemodynamics were measured via tonometry with a generalized transfer function in 14 young, healthy men (age = 24 yr). Aortic blood flow was calculated from the left ventricular outflow tract (LVOT) velocity-time integral (VTI) using standard two-dimensional echocardiographic-Doppler techniques. Measures were made in the supine position at rest (Pre), during PLE, and during recovery (Post). There was a significant increase in LVOT-VTI, synthesized aortic systolic blood pressure (BP) and AIx from Pre to PLE, with values returning to baseline Post ( P < 0.05). There was a reduction in aortic capacitance from Pre to PLE, with values returning to baseline Post ( P < 0.05). There was no change in heart rate, systemic arterial compliance, aortic elastance, aortic wave travel timing, or vascular resistance ( P > 0.05). Change in AIx from Pre to PLE was associated with change in LVOT-VTI ( r = 0.66, P < 0.05) and inversely associated with change in aortic capacitance ( r = −0.73, P < 0.05). These data suggest that in a setting of isolated augmented preload with minimal changes in other potential confounders, the morphology of the synthesized aortic BP waveform and AIx may be related to changes in aortic reservoir function.


2012 ◽  
Vol 112 (11) ◽  
pp. 1832-1838 ◽  
Author(s):  
Tatsuya Arai ◽  
Kichang Lee ◽  
Robert P. Marini ◽  
Richard J. Cohen

The purpose of this study was to introduce and validate a new algorithm to estimate instantaneous aortic blood flow (ABF) by mathematical analysis of arterial blood pressure (ABP) waveforms. The algorithm is based on an autoregressive with exogenous input (ARX) model. We applied this algorithm to diastolic ABP waveforms to estimate the autoregressive model coefficients by requiring the estimated diastolic flow to be zero. The algorithm incorporating the coefficients was then applied to the entire ABP signal to estimate ABF. The algorithm was applied to six Yorkshire swine data sets over a wide range of physiological conditions for validation. Quantitative measures of waveform shape (standard deviation, skewness, and kurtosis), as well as stroke volume and cardiac output from the estimated ABF, were computed. Values of these measures were compared with those obtained from ABF waveforms recorded using a Transonic aortic flow probe placed around the aortic root. The estimation errors were compared with those obtained using a windkessel model. The ARX model algorithm achieved significantly lower errors in the waveform measures, stroke volume, and cardiac output than those obtained using the windkessel model ( P < 0.05).


1993 ◽  
Vol 264 (5) ◽  
pp. R963-R971 ◽  
Author(s):  
M. Axelsson ◽  
A. P. Farrell

The effects of adrenergic agonists on dorsal aortic blood pressure, cardiac output, and coronary blood flow were studied in unrestrained coho salmon, Oncorhynchus kisutch. Resting coronary blood flow was 0.43 ml.min-1.kg body mass-1, which represented 1.1% of cardiac output or approximately 0.5 ml.min-1.g-1 compact ventricular mass calculated on 40% of total ventricle mass. Coronary blood flow was phasic and continuous throughout the cardiac cycle; flow seems to be affected by the ventricular contraction, with a peak flow occurring during diastole and a nadir in early systole. Epinephrine injections into the dorsal aorta resulted in a rapid increase in coronary blood flow in association with a rapid increase in dorsal aortic blood pressure. Subsequently there was also a slower increase in coronary vascular resistance, which could be blocked by phentolamine, indicating an alpha-adrenergic vasoconstriction. Isoprenaline injection produced an increase in coronary blood flow and a large reduction in coronary vascular resistance. The coronary vasodilatation was blocked by propranolol, indicating that it may be partly due to a beta-adrenergic vasodilatation. Preliminary results showed a marked increase in coronary blood flow associated with exposure to environmental hypoxia.


1978 ◽  
Vol 55 (s4) ◽  
pp. 243s-246s
Author(s):  
Chang-Seng Liang ◽  
Haralambos Gavras ◽  
H. R. Brunner

1. Salt depletion was produced in five dogs by a low salt diet and daily administration of frusemide for 5 days; a control group of five dogs was placed on the same diet, to which 2·5 g of sodium chloride was added. 2. Saralasin infusion (0·5 μg min−1 kg−1) reduced mean aortic blood pressure and total peripheral vascular resistance and increased cardiac output in salt-depleted dogs, but did not affect the heart rate and left ventricular dP/dt. 3. Saralasin infusion increased mean aortic blood pressure slightly in normal dogs; other systemic haemodynamic parameters did not change significantly. 4. Saralasin decreased hepatic arterial flow in both normal and salt-depleted dogs, but increased blood flow to left ventricle and kidneys only in salt-depleted dogs. 5. These results suggest that saralasin exerts a partial agonist effect in normal dogs to increase arterial blood pressure, but causes a depressor response during salt depletion because it reverses the vasoconstrictor effect of angiotensin II, particularly on the renal and coronary circulations.


1991 ◽  
Vol 260 (4) ◽  
pp. R811-R816
Author(s):  
D. F. Anderson ◽  
N. D. Binder

Upper body arterial hypertension developed in 12 fetal lambs after chronic suprarenal aortic blood flow reduction. Sixty minutes after blood flow reduction, intravenous saralasin infusion was able to reduce upper body mean arterial blood pressure to control levels. Although saralasin infusion was able to decrease upper body arterial blood pressure after 1 day of hypertension, it was not able to return blood pressure to control levels. Three or more days later, saralasin was unable to cause a significant reduction in upper body arterial blood pressure. We conclude that, although the renin-angiotensin system has a role in maintaining the elevated blood pressure after greater than or equal to 1 day of suprarenal aortic blood flow reduction, some other mechanism also participates. We have ruled out a role for changing blood volume, and our results suggest that an elevation of plasma catecholamines is not responsible. Some other pathway for fluid regulation available to the fetus may be responsible.


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