Neonatal Systemic Hypertension

Some preterm infants—particularly those with bronchopulmonary dysplasia (BPD)—may develop significant systemic hypertension, defined as blood pressure exceeding the 95th percentile for postmenstrual age (as per established references - Dionne et al.). This condition may result from a combination of elevated systemic vascular resistance (SVR), prior acute kidney injury, increased vascular stiffness, or exposure to corticosteroids. Systemic hypertension can contribute to left ventricular (LV) remodeling, increased LV stiffness, ongoing adaptation with LV hypertrophy and elevated left ventricular end-diastolic pressure (LVEDP), which may subsequently raise left atrial (LA) pressure and impair pulmonary venous drainage—thereby exacerbating pulmonary vascular disease. Indeed, Laplace's law, in the context of the heart, explains how the heart compensates for increased workload through hypertrophy. When the heart faces increased afterload (like from high blood pressure / high systemic vascular resistances) or volume overload, it responds by thickening its walls (hypertrophy). This thickening, according to Laplace's law, helps to normalize the stress on the heart muscle caused by the increased pressure or volume. However, this adaptation has limits, and excessive hypertrophy can lead to heart failure

When evaluating the right ventricular (RV)/pulmonary arterial compartment in relation to the LV/aortic compartment, whether through septal morphology or shunt directionality (e.g., across post-tricuspid defects), it is essential to interpret findings within the broader context of systemic hemodynamics. Elevated systemic blood pressure may lead to underestimation or mischaracterization of pulmonary hypertension (PH). For example, an infant may have elevated RV and pulmonary artery pressures, but the LV may appear round at peak systole—suggestive not of low RV afterload, but of concurrent systemic hypertension. Similarly, a VSD or PDA may shunt left to right because of high systemic vascular resistance relative to pulmonary vascular resistances (even if the PVR and/or PA pressures are elevated). As such, a right to left post-tricuspid shunt may not be present, despite elevated PVR and/or RV/PA pressures in the setting of high SVR and/or LV/PA pressures.

Similarly, the right ventricle (RV) may be exposed to elevated afterload with associated remodeling and reduced compliance. Concurrently, the LV may exhibit hypertrophy and diastolic dysfunction secondary to systemic hypertension, resulting in even greater impairment in LV compliance. In this setting, a left-to-right shunt at the atrial level may persist or become more prominent, despite elevated right ventricular end-diastolic pressure (RVEDP), due to the relatively higher left atrial pressures driven by impaired LV filling. As such, the expected bidirectional or right ot left shunting at the atrial level may not be present. This paradox underscores the importance of comprehensive assessment of biventricular relaxing/filling properties, shunt physiology, and systemic hemodynamics when interpreting TnECHO findings in infants with complex cardiopulmonary interactions.