Abstract
Arterial pulse pressure has been widely used as surrogate of stroke volume, for example, in the guidance of fluid therapy. However, recent experimental investigations suggest that arterial pulse pressure is not linearly proportional to stroke volume. However, mechanisms underlying the relation between the two have not been clearly understood. The goal of this study was to elucidate how arterial pulse pressure and stroke volume respond to a perturbation in the left ventricular blood volume based on a systematic mathematical analysis. 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.
Highlights
Stroke volume (SV) is the volume of blood pumped out by the heart to the arterial tree
We made the following assumptions: during changes in end-diastolic volume due to volume perturbation, (i) the time instant corresponding to DP relative to the heart period is constant (A1); (ii) end-systolic pressure is close in value to mean arterial pressure (MAP) (A2); and (iii) left ventricular (LV) and arterial elastances remain
We elucidated the mechanisms underlying the nonlinear dependence between SV and PP
Summary
Stroke volume (SV) is the volume of blood pumped out by the heart to the arterial tree. There are many existing evidences supporting this assumption [20, 21, 26] Due to this reason, PP has been widely used as a convenient surrogate of SV during diagnostic and therapeutic procedures, such as fluid therapy [27], ventricular resynchronization therapy [28], and vasopressor/inotrope therapy [29]. In order for PP to be used as a reliable surrogate of SV during fluid therapy, the relationship between SV and PP in response to blood volume changes must be clearly understood.
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