Fluid responsiveness in the pediatric population

Abstract

It is challenging to predict fluid responsiveness, that is, whether the cardiac index or stroke volume index would be increased by fluid administration, in the pediatric population. Previous studies on fluid responsiveness have assessed several variables derived from pressure wave measurements, plethysmography (pulse oximeter plethysmograph amplitude variation), ultrasonography, bioreactance data, and various combined methods. However, only the respiratory variation of aortic blood flow peak velocity has consistently shown a predictive ability in pediatric patients. For the prediction of fluid responsiveness in children, flow- or volume-dependent, noninvasive variables are more promising than pressure-dependent, invasive variables. This article reviews various potential variables for the prediction of fluid responsiveness in the pediatric population. Differences in anatomic and physiologic characteristics between the pediatric and adult populations are covered. In addition, some important considerations are discussed for future studies on fluid responsiveness in the pediatric population.

Keywords: Blood pressure; Cardiac output; Children; Doppler ultrasonography; Fluid therapy; Hemodynamic monitoring; Oximetry.

Fig. 1.

Frank-Starling curve. This graph represents the relationship between stroke volume and preload. The stroke volume of the heart increases in response to an increase in the volume of blood the ventricle. If preload continues to increase, the point of myocyte overstretch is reached and eventually passed. Cardiac output plateaus and then begins to fall. The pulse wave Doppler images demonstrate aortic blood peak velocity in a fluid responder (A) and a nonresponder (B). Notice that the respiratory variation in aortic blood peak flow velocity is augmented in the fluid responder compared with that in the nonresponder.

Fig. 2.

Arterial waveform. Arterial pressure wave changes according to airway pressure. ΔUp: maximal systolic blood pressure during inspiration minus apneic systolic blood pressure, ΔDown: apneic systolic blood pressure minus minimal systolic blood pressure during expiration, SPmax: maximum systolic pressure during inspiration, SPmin: minimum systolic pressure during expiration, PPmax: maximum pulse pressure, PPmin: minimum pulse pressure, SPV: systolic pressure variation, PPV: pulse pressure variation.

Fig. 3.

Respiratory variation of aortic blood flow peak velocity. Respiratory variation of aortic blood flow peak velocity is measured using transesophageal echocardiography. Sample volume of pulsed wave Doppler is located at just below the aortic annulus. Respiratory variation of aortic blood flow peak velocity (ΔVpeak) before (A) and after (B) volume loading in a fluid responder. ΔVpeak is calculated as 100 × (Vmax − Vmin) / [(Vmax + Vmin) / 2].

Fig. 4.

Measurement of transcranial Doppler via the transfontanelle approach. Respiratory variation carotid blood flow peak velocity is measured using a sector probe via the anterior fontanelle. (A) Probe application on the anterior fontanelle, (B) Coronal view of the brain and the internal carotid artery, (C) Respiratory variation carotid blood flow peak velocity in a fluid nonresponder, (D) Respiratory variation carotid blood flow peak velocity in a fluid responder.

Fig. 5.

Changes in the inferior vena cava (IVC) diameter during mechanical ventilation. The M-mode of IVC shows no significant change induced by the respiratory phase during mechanical ventilation in a 5-month-old infant. RA: right atrium.

Fig. 6.

Abdominal compression-induced blood pressure change. Arterial blood pressure waveforms are displayed in the Frank-Starling curve. The arrow indicates the start of liver compression. Notice the difference of blood pressure change during liver compression between a fluid responder (left bottom of the curve) and a nonresponder (right top of the curve).

Fig. 7.

Measurement of cardiac output using transesophageal echocardiography. Cardiac output is measured using transesophageal echocardiography in a 5-month-old infant after tetralogy of Fallot correction. Stroke volume = velocity time integral × (aortic annulus diameter / 2)² × 3.14. (A) Velocity time integral measured in the deep transgastric view using pulsed wave Doppler, (B) Aortic valve annulus measured in the mid-esophageal aortic valve long-axis view (arrow indicates the diameter of the aortic annulus).