In this chapter, the impact of a patent ductus arteriosus (PDA) will be discussed in the clinical setting of a neonate with an otherwise structurally normal heart (± a patent foramen ovale). Specific emphasis will be placed on preterm infants with relatively low pulmonary vascular resistance and ductal shunting that is predominantly or completely left to right.
Until recently, because the harmful effects of a PDA were thought to be self-evident, the prevailing opinion was that PDA closure was indicated in all preterm infants. The predominant question was the best method to close a PDA in such patients, and this was the subject of numerous randomized clinical trials.1,2 However, over the last decade, the rationale for the treatment of a PDA, in general, and ligation, in particular, has been increasingly challenged. The current trend is to recommend a less aggressive approach to the pharmacologic and surgical treatment of a PDA. This in turn has made the recognition of a hemodynamically significant patent ductus arteriosus (hsPDA) even more important. In this chapter, the hemodynamic effects of a PDA and its ligation will be reviewed, followed by a detailed description of the echocardiographic indices that can be helpful in identifying an hsPDA. Finally, the use of PDA flow to estimate relative pulmonary vascular resistance in the setting of pulmonary hypertension will be briefly discussed.
HEMODYNAMIC EFFECTS OF A PDA
In the presence of a PDA with left-to-right shunting, pulmonary blood flow increases, leading to an increase in pulmonary venous return to the left atrium (LA). This increase in LA volume can augment the left ventricular (LV) preload, provided no significant shunt at the patent foramen ovale (PFO) is present (see below). The increase in LV preload will increase the stroke volume according to the Starling curve.3–6 However, a PFO can significantly alter the effects of a PDA on LV stroke volume by decompressing the LA. Indeed, in the presence of a significant PFO (diameter >4 mm), right ventricular output (RVO) can even be greater than left ventricular output (LVO) despite the presence of a significant left-to-right PDA shunt.7 Despite the inherent vulnerability of the immature myocardium and the potential for decreased myocardial perfusion due to low diastolic pressure, myocardial contractility appears not to be affected by an hsPDA. With short exposure (days) to an hsPDA, both load-dependent (LV shortening fraction, or SF) and load-independent (stress-velocity index) measures of systolic function are found to be normal.8
In the presence of a PDA, the heart rate does not change; therefore, the increase in LVO is solely the result of an increase in stroke volume. As systolic blood pressure is primarily affected by changes in stroke volume and diastolic blood pressure is mainly reflective ...