(see also Swan-Ganz Pulmonary Artery Catheter; ScVO2 Monitoring; Starling's Law)
Stroke volume variation (SVV) measures the change in the volume of blood that is ejected from the left ventricle to the aorta with each contraction. It requires the use of a transducer attached to an arterial line (radial or femoral) that communicates with a bedside monitor for the most accurate measurement. The FloTrac sensor with EV1000 monitor (see Fig. 2.68) is an example of a homodynamic monitoring system that provides continuous stroke volume (SV) and/or SVV measurements.
Optimizing circulating blood volume (preload) is a first-line therapy to improve oxygen delivery (DO2) to tissues. Via technology, by monitoring the changes in SV and/or SVV, a determination of the patient's cardiac “fluid responsiveness” is made. By establishing that preload is increased with the administration of a fluid bolus, the potential harm that may occur from excessive IV fluid administration is decreased.
Differing patient populations require variations in the approach to this hemodynamic measurement. In Figure 2.69, an algorithm is shown that predicts the effectiveness of using an IV fluid bolus to increase cardiac preload by measuring SV. This algorithm is appropriate for all patients that have SV monitoring available. An increase in a patient's SV of 10% or greater would indicate that preload would improve with fluid bolus. Using Starling's law, boluses continue until an outcome of < 10% is achieved.
When SVV is used to determine preload responsiveness (see Figure 2.70), only patients who are on 100% control positive-pressure ventilation with 8 mL/kg ideal body weight are candidates. The measurement of SVV is determined by variation in the arterial waveform pattern that is influenced by positive-pressure ventilation of the patient. Positive-pressure ventilation causes a “reverse” pulsus paradoxus effect, meaning the arterial pressure will rise with inspiration and fall on expiration. With each positive-pressure breath, intrathoracic pressure is increased, causing variations in the arterial pressure waveform. This pattern in the atrial pulsation is the mechanism measured in SVV.
SVV may also be calculated by measuring the difference between maximum and minimum SV on the arterial waveform and using the following equation:
Sedation may be required to prevent distortion of values from any respiratory effort from patient. SVV can be adversely altered by arrhythmias, increased PEEP, and vasodilating drugs. The normal SVV is <10% to 15%. The goal of resuscitation therapy is to achieve an SVV of <13%.