stroke volume variation to assess fluid responsiveness


A growing body of literature demonstrates the deleterious effects of indiscriminate administration of IV fluids to patients in the ICU, and a number of techniques have been developed to predict volume responsiveness. These include echocardiographic estimates of ejection fraction and/or stroke volume (SV), change in inferior vena cava (IVC) diameter, pulse pressure variability, and various techniques involving SV variability, SV, or SV index (SVI).

SV can be measured or estimated in a variety of ways: echocardiography, flow analysis at the aortic root via Doppler ultrasonography, chest wall electrical bioimpedance, flow-directed pulmonary artery catheter, and arterial pulse contour analysis. Most of these techniques, when combined with either a passive leg raise maneuver or a 4 mL/kg fluid bolus, demonstrate high area under the receiver operating characteristic curve (meaning high sensitivity and specificity) for predicting a response to IV fluid administration.

Two studies, one retrospective and one prospective, randomized controlled trial, evaluated whether temporarily holding fluid administration when SV increased by <10% with a passive leg raise maneuver or a rapid, small fluid bolus would affect multiple patient-centered outcomes among patients with sepsis and septic shock. The retrospective analysis demonstrated lower net fluid balance in the ICU, reduced requirement for renal replacement therapy, reduced requirement for mechanical ventilation, and shorter ICU and hospital stays. The Fluid Response Evaluation in Sepsis Hypotension and Shock (FRESH) trial had as its primary outcome net fluid balance at 72 h; it also evaluated several secondary outcomes, including need for renal replacement therapy, need for and duration of mechanical ventilation, survival to hospital discharge, and ICU length of stay. The group who received restricted fluid volumes based on SV nonresponsiveness received less fluid in the ICU and had a lower proportion requiring renal replacement therapy or mechanical ventilation. Both of the studies used noninvasive cardiac output monitoring via electrical bioimpedance; however, the principle should apply to any technique that assesses SV with precision. Because beat-to-beat SV is averaged over time, this measurement is not altered by arrhythmias (choice B is correct).

Variation in IVC diameter with inspiration is evaluated with ultrasonography at the subdiaphragmatic (intraabdominal) level and is dependent on central venous pressure, intrapleural pressure, intraabdominal pressure, and distensibility (compliance) of the IVC. During positive pressure ventilation, increases in intrapleural pressure result in resistance to intrathoracic venous blood flow. If the IVC is not distended by high right atrial and central venous pressures, venous blood will accumulate during inspiration causing an increase in the IVC diameter. Using the formula (_D_Max - _D_Min)/_D_Min, where D represents measured IVC diameter, changes >18% are deemed to predict volume responsiveness. However, the technique requires mechanical ventilation with >8 mL/kg tidal volumes and passive ventilation. Negative pleural pressures generated by spontaneous ventilatory efforts alter the relationship. Also, during spontaneous breathing without the use of a ventilator, pleural pressure swings are insufficient to cause variation in IVC diameter reliably, except in cases of upper or lower airway obstruction; such negative pleural pressure changes will result in reduced IVC diameter during inspiration. This patient is breathing spontaneously, which alters the reliability of the measurement. In addition, his tidal volume of 450 mL represents 3.6 mL/kg of actual body weight and 6.35 mL/kg of ideal body weight, too low to achieve accuracy via this IVC measurement. Finally, his BMI of 37 kg/m2 suggests the possibility of increased abdominal pressure that could alter changes in IVC diameter (choice A is incorrect). Arrhythmias do not alter the respiratory changes in IVC diameter.

In patients receiving passive mechanical ventilation, pulse pressure variability is a surrogate for the SV variability that occurs with positive pressure ventilation. Reproducibility in SV variability and pulse pressure variability requires a tidal volume of 10 mL/kg to ensure adequate intrapleural pressure swings to alter venous return; it also requires absence of arrhythmia, especially atrial fibrillation (choice C is incorrect). 1 23456

Footnotes

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