Cardiac magnetic resonance in the study of neonatal haemodynamics

Summary

Circulatory failure plays a key role in the pathogenesis of mortality and key morbidity such as cerebral injury in the preterm infant. However awareness of the pathophysiology of circulatory failure itself is not well understood. Similarly there is significant uncertainty over optimal treatment approaches, particularly for inotropic therapies.

Current uncertainties are perpetuated by difficulties with accurately assessing circulatory function. Cardiac magnetic resonance (CMR) imaging has produced significant advances in understanding of adult circulatory function, and acts as a powerful biomarker for interventional studies. Although routine circulatory assessment by CMR in the neonatal population is not currently a realistic goal, it could provide insights into pathophysiology; and act as an outcome measure in clinical trials in small numbers of infants in specialist centres. This review focuses on available CMR techniques, scope for use in the neonatal population, and our initial experience with the technique.

Introduction

Whereas the overall care provided to sick newborn infants has improved greatly in recent decades, the most prematurely born infants remain at high risk of death and disability.¹ The impact of preterm birth on the population is vast – with an estimated annual socioeconomic burden of more than £3 billion in the UK alone.²

Circulatory failure causes significant neonatal mortality. As high quality research has improved preterm respiratory care, an increasing proportion of deaths occur due to episodes of sepsis or necrotising enterocolitis.³ In these systemic inflammatory disorders the release of pro-inflammatory cytokines may directly impair myocardial function,⁴ making circulatory failure the final mechanism of death.

Circulatory factors are also linked to key morbidity. Failing cardiac function has been shown to cause cerebral hypoperfusion,⁵ and episodes of low cerebral blood flow are central to the pathophysiology of preterm brain injury which causes long term disability.⁶

Improving circulatory management is therefore a research priority in preterm infants,⁷ although understanding of the pathophysiology and optimal treatment of circulatory failure are hampered by the limited tools available to monitor circulatory function.⁸

All circulatory function relies on the interplay of preload, contractility and afterload. The preterm transitional circulation is further complicated by the persistence of fetal shunt pathways (foramen ovale and ductus arteriosus) which may significantly alter circulatory dynamics. A robust assessment of the newborn circulation therefore needs to quantify preload, contractility, afterload and systemic perfusion.

Current methods fall short of this ideal; in particular, monitoring of circulatory status in the neonatal unit still relies heavily on arterial blood pressure. Systemic arterial blood pressure is the product of systemic blood flow and systemic vascular resistance, and cannot itself distinguish between the two. While clinicians presumably feel that monitoring systemic blood pressure is a screening tool for low systemic perfusion, in fact blood pressure is at best weakly predictive of volume of blood flow,⁹ and some studies have suggested no¹⁰ or even an inverse¹¹ relation between blood pressure and flow in newborn preterm infants. Other clinical assessments such as capillary refill time, volume of urine output, etc., also have limited value in indicating circulatory health.⁹

A number of research tools, including echocardiography and near infra-red spectroscopy (NIRS) both reviewed elsewhere in this issue of Seminars have produced important advances in understanding of circulatory physiology, and echocardiography clearly has a role in the assessment of circulatory status at the cotside. However, neither technique is without its limitations. Current echocardiographic modalities cannot reliably measure cardiac preload¹²; measures of contractility are limited by irregular ventricular contours seen in the newborn period¹³; and measures of cardiac output and systemic perfusion have limited repeatability.¹⁴ NIRS similarly has limited repeatability in its assessment of perfusion,¹⁵ and cannot assess the elements of cardiac preload and contractility which are necessary to advance understanding of circulatory failure.