Neonatal Hemodynamics: From Developmental Physiology to Comprehensive Monitoring

Sabine L Vrancken, Arno F van Heijst, Willem P de Boode, Sabine L Vrancken, Arno F van Heijst, Willem P de Boode

Abstract

Maintenance of neonatal circulatory homeostasis is a real challenge, due to the complex physiology during postnatal transition and the inherent immaturity of the cardiovascular system and other relevant organs. It is known that abnormal cardiovascular function during the neonatal period is associated with increased risk of severe morbidity and mortality. Understanding the functional and structural characteristics of the neonatal circulation is, therefore, essential, as therapeutic hemodynamic interventions should be based on the assumed underlying (patho)physiology. The clinical assessment of systemic blood flow (SBF) by indirect parameters, such as blood pressure, capillary refill time, heart rate, urine output, and central-peripheral temperature difference is inaccurate. As blood pressure is no surrogate for SBF, information on cardiac output and systemic vascular resistance should be obtained in combination with an evaluation of end organ perfusion. Accurate and reliable hemodynamic monitoring systems are required to detect inadequate tissue perfusion and oxygenation at an early stage before this result in irreversible damage. Also, the hemodynamic response to the initiated treatment should be re-evaluated regularly as changes in cardiovascular function can occur quickly. New insights in the understanding of neonatal cardiovascular physiology are reviewed and several methods for current and future neonatal hemodynamic monitoring are discussed.

Keywords: cardiac output; developmental physiology; hemodynamic monitoring; hemodynamics; neonate; preterm infant.

Figures

Figure 1
Figure 1
Relationship between oxygen delivery and oxygen consumption. VO2, oxygen consumption; DO2, oxygen delivery; SvO2, (mixed) venous oxygen saturation; OER, oxygen extraction ratio. X-axis shows the gradual decrease in DO2 with the lowest DO2 on the right side of the figure; Light gray area: VO2 = DO2 independent; Dark gray area: VO2 = DO2 dependent.
Figure 2
Figure 2
The neonatal circulation. RVO, right ventricular output; PBF pulmonary blood flow; LVO, left ventricular output; AAo, blood flow in ascending aorta; DAo, blood flow in descending aorta; DA, ductus arteriosus; VCS, vena cava superior; VCI, vena cava inferior; VR, venous return.
Figure 3
Figure 3
Schematic representation of the Frank–Starling curve. 1 = adult cardiac function; 2 = fetal/neonatal cardiac function. A similar change in preload will result in a larger increase in cardiac output/stroke volume in adults than in neonates.
Figure 4
Figure 4
Intravascular volumes and pressure in the venous compartment. Green interrupted line = Pmsf mean systemic filling pressure; dark blue box = unstressed volume = that volume which is required to fill the vasculature without increase in transmural pressure; light blue box = stressed volume = any amount of volume added to the unstressed volume that leads to an increase in transmural pressure.
Figure 5
Figure 5
Relationship between PVR and lung volume. RV residual volume; FRC, functional residual capacity; TLC, total lung capacity; PVR, pulmonary vascular resistance; blue zone lowest pulmonary vascular resistance.

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