Hemodynamics, or the movement of blood, is necessary to delivery oxygen to the tissues of the body. Oxygen delivery is determined by several factors, and failure of any these can lead to organ injury and/or death. Oxygen delivery is determined by (1) the oxygen level and carrying capacity of the blood, both of which are easy to measure and monitor and (2) the flow rate of blood around the systemic and pulmonary circulations. Both the circulations are driven by the heart, and the flow is measured by the output of each of the ventricles. In a mature circulation, the right ventricular output (RVO) drives the pulmonary blood flow and the left ventricular output (LVO) drives the systemic blood flow. The efficiency with which each ventricle does this is determined by the volume of blood entering the ventricle (the preload), the health (or maturity) of the myocardium (contractility), and the resistance against which the ventricle is pumping (afterload).
In preterm infants, many of the morbidities, particularly the cerebral morbidities, are thought to have an ischemic origin, and the goal of circulatory support has always been prevention of neurological morbidity. It can be seen that there are many levels at which the delivery of oxygen to tissues can fail, and sorting out this complexity in a clinical scenario is an unresolved challenge. This chapter will focus specifically on the “movement of blood” component of this physiological cascade.
THE TRANSITIONAL CIRCULATION
An understanding of neonatal circulatory pathology is intrinsically linked to an understanding of circulatory adaptation to extrauterine life. The right-sided dominance of the fetal circulation, with blood shunting right to left through the ductus arteriosus and foramen ovale to bypass the lungs, has to change rapidly to the left-sided dominance of the extrauterine circulation, with the whole cardiac output flowing through the lungs (see also Chapter 45).
At birth, this sequence must change in a very short timeframe. The lungs expand with the first breaths, the pulmonary arterioles dilate, right heart pressures fall, and blood pours into the pulmonary circulation to collect oxygen from the inhaled air. The removal of the low-resistance placenta from the systemic circulation increases resistance and pressure on the left side of the circulation, while the pulmonary blood flow increases the left heart preload. The result is a dramatic increase in the workload of the left heart. The muscle in the wall of the ductus arteriosus constricts powerfully in response to rising oxygen levels, closing functionally within the first 24 hours after birth and structurally after several days, to leave the ligamentum arteriosum, the fibrous ductal remnant that we all have.
During the last trimester of pregnancy, much of the fetal cardiopulmonary development is preparing for the major changes that accompany birth, so babies born prematurely have exquisite circulatory vulnerability during this period of the transitional circulation. More mature babies ...