Used almost exclusively for patients receiving positive pressure ventilation, stroke volume variation and pulse pressure gauge volume status based on a simple anatomical and physiological connection between the cardiovascular and pulmonary systems. Positive pressure ventilators periodically push air into the lungs, decreasing the preload and increasing the afterload of the right ventricle. The decrease in right ventricular preload stems from the decrease in venous return caused by the increased pleural pressure during forced inspiration. The accompanying transpulmonary increase in pressure causes the afterload in the ventricle to also increase. The combined decrease in preload and increase in afterload causes the stroke volume from the ventricle to decrease, reaching a minimum at the end of inspiration. This inspiratory reduction in right ventricular stroke volume decreases left ventricular filling after a lag of about two or three beats as blood makes it trip through the pulmonary circuit. Decreased left ventricular preload reduces left ventricular stroke volume, doing so at its minimum during the expiratory period. It follows, then, that respiratory induced variations in magnitude of ventricular stroke volume indicate should indicate preload dependence .
Extending the logic of this assumption from stroke volume to the pulse pressure, one must contend that for a given elastic artery, the amplitude of the pulse pressure is a function of stroke volume. This is true enough for the most part and as such stroke volume variation and pulse pressure variation can be considered roughly equivalent, especially in the case of their use in assessing volume responsiveness, where they are meant to estimate where along the Frank-Starling curve a patient is (see again Figure 1.5).
Stroke volume is rarely measured directly. Instead it is usually calculated from an arterial pressure waveform, if the arterial compliance and systemic vascular resistance are known or estimated . Three main systems are currently used clinically: the FloTrac system from Edwards Lifesciences, the PiCCO monitoring system from Pulsion, and LiDCO system from LiDCO. Each is invasive, requiring either a peripherally or centrally inserted arterial catheter, and each must be calibrated to make use of the pressure-volume conver- sion algorithms in their pulse contour analysis: the FloTrac requires patient information including demographics and physical characteristics and the PiCCO and LiDCO system require indicator dilution cardiac output measurements. The later two systems are also capable of measuring pulse pressure variation.
Though pulse pressure is routinely measured directly in clinic (via a blood pressure cuff), the methods to do so are often cumbersome and not suited for the longer term eval- uation needed for variation analysis. Invasive methods for measuring arterial and venous pressures are available, indeed we have mentioned many above, but are avoided for many reasons (to prevent infections, secondary injuries, etc.). Therefore what is often used for pulse pressure variation analysis is the waveform generated from pulse oximetric plethys- mography. Pulse oximetry a technique by which to measure oxygen saturation via a pho- tospectroscopic algorithm through a small portion of a patients body (such as a fingertip or an earlobe) allows for non-invasive measurement technique that reliably tracks the arterial pressure component [63, 64]. In addition to determining oxygen saturation, pulse oximetry gives some sense of the change in volume occurring at the region of interest, and is thus a plethysmographic technique. In the short term, the volume in the peripheral vasculature results from changes in pressure, and the vast majority of those pressure changes stem from the arterial components. In this way, the arterial waveform can be measured photoplethysmographically. Going still further, an envelope of the arterial pressure waveform can be fit to reveal a respiratory influence (see Figure 1.13). Defining the pulse pressure variability as the difference in the maximum and minimum values of the pulse pressure wave normalized to the maximum value ((PPMax − PPMin)/PPMax), it can now serve as a method to gauge volume status, with the mechanism of action and the logic of the approach directly analogous to the stroke volume variation case.
A meta-analysis of the literature surrounding fluid responsiveness in arterial waveform variations have shown that both stroke volume variation and pulse pressure variation to be highly predictive of fluid responsiveness (with a mean AUC of 0.84 and 0.94, respectively) . Pulse pressure variabilitys higher predictive power likely spawns from its more direct measurement as stroke volume variability relies on each manufacturer-specific algorithm for determination.
However, in cases of spontaneous breathing, stroke volume variation as a method of assessing volume status falters. This is because the amplitude and shape of the intrathoracic pressure function differs greatly for those breathing spontaneously and those receiving positive pressure ventilation. Coupled this the unpredictable nature of spontaneous breath- ing and much of the benefits of stroke volume variation are thought to become untenable [65, 66]. Unfortunately for stroke volume variation as a metric, its limited reliability under spontaneous breathing has hampered its overall adoption, especially with the rise of non-sedated, non-paralyzed patients receiving respiratory support.