PDF | Arterial pulse pressure has been widely used as surrogate of stroke volume, for example, in the guidance of fluid therapy. However. Pulse pressure/stroke volume (PP/SV) is regarded as a surrogate index of and the relation to segmental relaxation and longitudinal systolic. The goal of this study was to unveil the mechanisms underlying the relation between pulse pressure and stroke volume based on a systematic.
The insonation frequency was set at 2. Filter harmonic imaging was set as a standard for all the recordings. One sample volume region of interest ROI was placed at the basal part of each LV segment, so that there was no migration beyond the limits of the selected myocardium.
Pulse pressure - Wikipedia
An automatic ROI tracking mode was activated in order to ensure that measurements reflected the motion of a myocardial tissue segment throughout the cardiac cycle. The systolic SR parameters of basal, mid, and apical segments were analysed separately from each LV wall in the longitudinal direction, and the average of the values of three consecutive cycles was calculated for each parameter. The myocardial systolic strain parameters were calculated by integrating the SR profiles over time and compensating for drifting over the cardiac cycle.
End-systolic strain was determined. In order to define the end of systole, timing information was used from blood pool pulsed or continuous wave Doppler tracings recorded from cycles with comparable R-R interval.
The aortic valve closure click was considered as the end of the systole. Eighteen LV segments basal, mid, and apical of each wall were averaged from each patient in order to estimate the mean Global longitudinal strain S and SR values. The eighteen LV segments were also assessed for segmental diastolic dysfunction. Arterial stiffness Haemodynamic measurements were performed in a quiet laboratory. After supine rest, the patients' peripheral blood pressure was recorded over the brachial artery of the right arm using a validated semi-automated oscillometric device Omron CP; Omron Healthcare, Milton Keynes, UK.
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Three measurements were taken 2 min apart. The mean value of the last two measurements was taken as a representative of brachial blood pressure. Pulse pressure was estimated by the formula: Mean arterial pressure MAP was estimated by the formula: Stroke volume was calculated by the invasively validated method given by the formula: Arterial stiffness was then calculated using the formula: Linear regression was used to investigate the relation between two parametric variables.
- BioMed Research International
- Cardiovascular physiology
Pearson's correlation was used to evaluate bivariate linear relations. Multiple linear regression was performed, applying an enter method, in order to estimate independent predictors for diastolic dysfunction segmental DD and mean Ea and longitudinal systolic dysfunction systolic strain.
Stroke volume/pulse pressure ratio and cardiovascular risk in arterial hypertension.
Segmental DD, mean Ea, and mean strain were set as dependent variables sequentially. Bland—Altman's plot of differences 19 was used to assess intra-observer variability for S and SR in 20 randomly selected patients.Cardiovascular Events and Pulse Pressure
A P -value less than 0. Males outnumbered women, especially in the control group. Hypertensive patients had similar BSA, but were more obese and had higher blood pressure measurements compared with the control.
Hypertrophy was present in None of the control group had evidence of LVH. Patients with diastolic dysfunction had hypertension for longer periods HTN years and were taking more angiotensin-converting enzyme ACE inhibitors, Ca inhibitors, and diuretics, compared with those without diastolic dysfunction HTN-N.
Both our mathematical analysis and experimental data showed that the relative change in arterial pulse pressure due to a left ventricular blood volume perturbation was consistently smaller than the corresponding relative change in stroke volume, due to the nonlinear left ventricular pressure-volume relation during diastole that reduces the sensitivity of arterial pulse pressure to perturbations in the left ventricular blood volume.
Therefore, arterial pulse pressure must be used with care when used as surrogate of stroke volume in guiding fluid therapy. Introduction Stroke volume SV is the volume of blood pumped out by the heart to the arterial tree. It is known to be highly correlated with cardiac function in that it typically decreases in the presence of diseases such as cardiogenic shock [ 1 ], hemorrhage [ 2 ], sepsis [ 3 ], spinal cord injury [ 4 ], and hypothyroid [ 5 ].
It is also an important determinant of cardiac output, which is modulated by the demand for oxygen delivery to the tissues in the body [ 6 ] and the capacitance of the arteriovenous system [ 7 ]. Regarding its clinical applications, the interpretation of SV or correspondingly cardiac output can help caregivers to better understand the complex pathophysiological alterations in the critical illness, thereby helping to avoid deleterious effects of inotropic therapy [ 8 ], potentially harmful effects of vasopressor agents [ 9 ], and the detrimental edema in fluid administration [ 10 ].
Despite its clinical significance, SV has not been widely utilized for routine diagnostic and therapeutic purposes due to the difficulty in its measurement [ 11 ]. In fact, most state-of-the-art methods to directly measure SV e. To exploit SV in clinical applications without encountering the problems listed above, there have been numerous efforts to indirectly estimate SV from minimally invasive or noninvasive arterial circulatory measurements, which are collectively called the pulse wave analysis PWA methods [ 16 — 19 ].
In one of its simplest form, PWA is based on the assumption that SV is proportional to arterial pulse pressure hereafter called pulse pressure PP [ 16 — 19 ].
In fact, there are many existing evidences supporting this assumption [ 202126 ]. Some recent experimental investigations suggest that although SV and PP are proportionally correlated during blood volume perturbation, the relationship may not be strictly linear, and PP may underestimate SV in response to blood volume changes [ 273031 ]. It is possible that the underestimation of SV during fluid therapy may potentially require substantial correction for dosage regimen, since brute-force fluid administration based on linear SV-PP assumption is likely suboptimal.