Assessment of systemic blood flow and myocardial function in the neonatal period using ultrasound

Introduction

Echocardiography is widely used to assess systemic blood flow and heart function in the newborn infant. This chapter gives an overview of conventional echocardiographic methods for the assessment of systemic blood flow, ventricular size, and myocardial function in newborns in the absence of congenital heart defects.

Reliable methods to monitor cardiovascular and hemodynamic function are important for assessment of circulatory disturbances and guide optimal therapy in the newborn infant. ^, Evidence of functional echocardiography improving neonatal outcome is emerging in the form of observational studies showing changes in care and reduced use of medications for patent ductus arteriosus (PDA) treatment and inotropes for borderline hypotension with normal systemic blood flow. ^, Two-dimensional (2D) and Doppler echocardiography is useful to assess hemodynamic status in routine clinical practice, as well as in clinical research. A complex integration of different echocardiographic modalities is necessary for the assessment of structure and dimension, blood flow, myocardial function, and loading conditions. Basic knowledge of physical and technical principles of the different modalities, sufficient operator skills, and experience in measuring relevant echocardiographic indices, as well as a comprehensive understanding of normal physiological and pathological processes, are essential for the optimal use of echocardiography.

Echocardiography has a central role in diagnosing and monitoring congenital heart disease, screening for PDA in preterm neonates, assessing heart function and pulmonary hemodynamics, detecting pericardial or pleural effusion and thrombosis, and verifying central line placement. The most common scenarios for functional echocardiography in neonates are circulatory assessment during the transitional circulation period in very premature infants, assessment of PDA beyond the early transitional period, exploration of the reasons for circulatory compromise and hypotension, and diagnosis and following of treatment for persistent pulmonary hypertension of the newborn.

Understanding the physiology of cardiovascular adaptation after birth and the effect of diseases and prematurity are key factors in interpretation. The complex and dramatic cardiorespiratory changes that take place during the transitional phase from fetal to neonatal circulation may be critical in both preterm and sick term infants. The onset of breathing promotes a rapid decrease in pulmonary vascular resistance, with a subsequent increase in pulmonary blood flow. The augmentation in pulmonary venous return increases the left heart preload and enables the left heart to handle the raised afterload following cord clamping and disconnection of the low-resistance placenta circuit. Chapter 6 discusses the effects of the timing of cord clamping on cardiovascular transition. While the right ventricle (RV) plays the dominant role in fetal life, the left ventricle (LV) gradually dominates after birth.

Closure of the fetal shunts normally starts with functional closure of the foramen ovale due to the altered pressure difference between the left and right atria, even though a small left-to-right shunt across the foramen ovale may be persistent over time. The changes in pulmonary and systemic vascular resistance after onset of breathing and cord clamping reverse the shunting of blood through the ductus arteriosus from right-to-left shunting to left-to-right. In term neonates the functional closure of the ductus arteriosus normally takes place within the first 2–3 days of postnatal life, while the ductus venosus may be persistent for several days after birth.

A variety of conditions in the perinatal period, such as asphyxia, respiratory distress, sepsis, and metabolic and hematological diseases, as well as positive pressure ventilation, may affect the cardiovascular system and hence disturb the transitional phase. Persistent high pulmonary vascular resistance might be due to fetal and/or perinatal hypoxia, resulting in abnormal pulmonary vascular development and/or responsiveness to local vascular mediators or to hypoxia caused by lung disease or apnea. Typical findings in pulmonary hypertension are bidirectional flow across the foramen ovale, bidirectional or right-to-left flow across the ductus arteriosus, and increased RV afterload, especially in the case of restrictive ductal flow. The latter may affect coronary blood flow and subsequently myocardial perfusion and function. The resultant decrease in left ventricular filling further affects myocardial function. Systemic circulatory failure (shock) may develop due to low systemic blood flow.

Preterm infants are especially vulnerable in the transitional circulatory phase (see Chapter 7 ). The fetal myocardium has a higher water content and a less organized structure compared to later in life. Mononucleated cardiomyocytes, fewer sarcomeres, and different isoforms of contractile proteins make the heart less compliant, with reduced cardiac functional reserves and less contractile ability. The immature heart is less tolerant to the abrupt changes in preload and afterload at birth. ^, In preterm neonates with a PDA the effect of the gradually increasing left-to-right ductal shunting on cardiac performance has opposite effects on the pulmonary and the systemic circulation. It contributes to the increased pulmonary blood flow immediately after birth, but a significant left-to-right shunt may impair systemic blood flow and cause a deterioration in cardiac performance and organ perfusion.

When the blood flow decreases, compensatory mechanisms redistribute the blood supply to vital organs by selective vasodilatation and vasoconstriction. In this compensatory phase of shock the blood pressure can remain normal, although the blood supply to the body is low. As long as the net systemic vascular resistance is higher than normal, the blood pressure can remain normal despite reduced systemic blood flow. Applying the indices discussed in this chapter can help the intensivist to identify shock in this compensatory phase, enabling intervention at an early stage.

Assessment of systemic blood flow by ultrasound

Systemic blood flow is a complex and dynamic variable with rapid fluctuations caused by the changes in activity and metabolic demand of the different organs. Doppler echocardiography offers direct and indirect measures of systemic and organ blood flow.

Blood flow by Doppler echocardiography is calculated as the product of the displacement of the velocity profile, called the velocity-time integral (VTI) of blood flow velocity, the cross-sectional area of the vessel at the site of the measurement, and the heart rate. VTI is measured by tracing the pulsed Doppler velocity signal. The cross-sectional area is found by measuring the diameter (D) and calculating the area as (π × (D/2) ² ). Assuming a circular vessel with constant cross-sectional area, blood flow (volume per time, usually mL/min) is calculated as (VTI [for one heartbeat] × cross-sectional area × heart rate). ^, A prerequisite for this calculation is a laminar parabolic flow profile representative of long, straight blood vessels under steady flow conditions, meaning that blood in the entire cross-sectional area moves at the speed drawn as the outer edge of the VTI. This prerequisite is probably met to a less extent in venous than arterial vessels, as is the assumption of a circular cross-sectional shape of the vessel. Blood flow in neonates is usually indexed by weight (mL/kg/min) and not body surface area because neonates and children have a relatively larger body surface area compared with body weight than adults. This results in non-linear-indexed hemodynamic variables. It is important to minimize the angle of insonation when obtaining the VTI and to assess the diameter with the ultrasound beam perpendicular to the vessel at the true (maximal) diameter. An inappropriate angle will underestimate the VTI and overestimate the diameter. Due to the squaring of the radius in the formula, inaccurate measures of the diameter may have considerable influence. We recommend averaging the measurements from a minimum of three cardiac cycles to minimize measurement error. Intra- and inter-observer variability significantly affects the Doppler flow measurements. Variation between measurements may be within the range of 30% in arteries and 50% in veins.