LAUSR

Resuscitation with IV fluid is a ubiquitous first-line form of acute circulatory support in emergency medicine, critical care, and anesthesiology. In this edition of Anesthesiology, Kim et al. examine the ability of transcranial ultrasound of the internal carotid artery peak velocity variability to predict fluid responsiveness in mechanically ventilated children after cardiac surgery. In a cohort of 30 postoperative cardiac infants, respiratory variation of the internal carotid artery blood flow peak velocity was measured using transfontanelle ultrasound, before and after the administration of 10 ml/kg saline. Stroke volume index was measured using transesophageal echocardiography to identify fluid responders (greater than 15% increase in stroke volume index). Before fluid loading, respiratory variation of the internal carotid artery velocity was 13 ± 3% in the fluid responders (n = 17) and 8 ± 3% in the nonresponders (n = 13). Transfontanelle respiratory variation in internal carotid artery blood flow peak velocity predicted an increase in stroke volume with an area under the receiver operating characteristics curve of 0.83 (95% CI, 0.65 to 0.94). Fluid responsiveness refers to an increase in cardiac output after the rapid administration of a calibrated volume of IV fluid (a fluid bolus). This increase in cardiac output (or stroke volume), expressed as a percentage, provides an estimate of the position of the patient’s heart on the Frank–Starling curve. Varying fluid volumes (10 ml/kg or 20 ml/kg in children; 500 ml or 1,000 ml in adults; and passive leg raise), content (crystalloid or colloid), and threshold values for change in cardiac output (10% or 15%) have been used to define fluid responsiveness. In health, cardiac output increases after the administration of a fluid bolus. For this to occur, both ventricles need to be operating on the ascending portion of the Frank–Starling curve, and fluid bolus administration must increase the stressed venous blood volume, increasing the pressure gradient for venous blood flow to the right atrium. Yet, only 50% of pediatric and adult patients with acute circulatory failure are fluid responsive. The remainder receive none of the benefits of fluid bolus administration and may be harmed through tissue and end-organ edema after fluid redistribution. Fluid bolus administration itself may exacerbate this process through damage to the endothelial glycocalyx and increased venous pressure. Paradoxically, large volume fluid administration may decrease vascular tone and attenuate the cardiovascular compensatory mechanisms of hemodynamically unstable patients. This mechanism has been postulated to explain the increased mortality of patients randomized to the fluid bolus groups in the Fluid Expansion as Supportive Therapy (FEAST) trial. Large volume fluid resuscitation and a positive cumulative net fluid balance have been associated with worsening renal function, acute lung injury, prolonged intensive care unit and hospital length of stay, and mortality, when corrected for disease severity. This holds true for the patient population studied by Kim et al., highlighting the importance of fluid management in influencing patient outcome after cardiac surgery and critical illness. The ability to predict fluid responsiveness allows fluid bolus administration to be restricted to those likely to benefit, while sparing those who are not fluid responsive from potential harms.