Abstract

which is always >0 and b1, can also have in vivo negative values, so it can activate “compensations”, that is, mechanisms supporting, “temporarily” or “chronically”, compartments that do not work properly. For instance, high arterial stiffness leads to a fast reflection of pressure waves so that they return to the aortic valve when it is still open. These waves “disturb” the flow, during its ejection from the ventricle during systole. This high velocity reflection implies high vascular resistance, so an adequate SV can be maintained by the left ventricle and higher blood pressures, which, in turn, lead to a further reduction in arterialwall distensibility. All these phenomena can be “summarized” in CCE values, which trend toward negative values over time. Table 1 shows the values of the means±SD of 30 heartbeats: for IABP, 15 heartbeats during assisted and 15 heartbeats not assisted; for cardioversion, 15 beats before and 15 after electrical shock; for aortic valvuloplasty, values before and after intervention. In these clinical applications we have undoubtedly a hemodynamic status modified after the intervention. CCE is objective and operator independent, its value reflects the contribution at the CVS of different organs, and because it is not related to a specific organ, is a variable indicating the systemic interaction of different organs. Moreover, the trends could be used to obtain in real time about the work dissipated due to pharmacological intervention and/or pathological conditions.

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