Case April 2026 Transitional Physiology at 22 weeks

Case

A 22-week infant was born vaginally following spontaneous preterm labor with PPROM, after a single dose of betamethasone administered approximately 1 hour before an expedited delivery. Delayed cord clamping was performed for 60 seconds. In the delivery room, the infant required endotracheal intubation and received surfactant within the golden hour. Umbilical central lines were subsequently placed. Birth weight was 500 g. In the early postnatal course, the infant remained on conventional mechanical ventilation with minimal settings and an FiO₂ requirement of 25%–30%, with adequate CO₂ clearance (pCO₂ ~50 mm Hg). Perfusion appeared clinically preserved, lactate was normal at 1.2 mmol/L, and urine output was 1.5 mL/kg/h. However, blood pressure values were noted to be trending downward, with a recent reading of 27/14 mm Hg, prompting a request for targeted neonatal echocardiography to assess myocardial function and ductal physiology. 

The TnECHO demonstrated findings consistent with expected transitional physiology. Biventricular systolic function was normal, with adequate cardiac output and no evidence of impaired myocardial performance. Systemic perfusion was further supported by normal Doppler profiles in the celiac artery, superior mesenteric artery, and middle cerebral artery. There were no clinical or imaging signs of intraventricular hemorrhage or bleeding, and hemoglobin remained stable. A large patent ductus arteriosus was present with bidirectional shunting, predominantly left-to-right, without evidence of left heart volume loading—specifically, no left ventricular dilation, no left atrial enlargement, and no echocardiographic markers suggestive of increased Qp:Qs. The patent foramen ovale also demonstrated bidirectional flow, predominantly left-to-right, consistent with ongoing reduction in pulmonary vascular resistance. The infant did not require significant respiratory support or supplemental oxygen beyond baseline needs. Overall, in the absence of clinical or biochemical evidence of compromised perfusion, these findings were interpreted as reflective of normal transitional adaptation rather than pathological hemodynamics. A conservative approach with careful observation and ongoing monitoring was therefore adopted.

Although this infant has a patent ductus arteriosus that is relatively unrestrictive with predominantly left-to-right shunting, our approach remains conservative. Current evidence has not consistently demonstrated that treatment with NSAIDs or acetaminophen improves major neonatal outcomes, while these therapies may expose infants to important adverse effects. NSAIDs can cause significant systemic and pulmonary vasoconstriction, with potential negative effects on renal, mesenteric, cerebral, and pulmonary perfusion. Acetaminophen, although often perceived as gentler, may also carry risks including hepatic dysfunction, cholestasis, and potential pulmonary toxicity. In addition, both strategies are often only modestly effective in achieving durable ductal constriction in extremely vulnerable infants at the cost of toxicity exposure. 

This infant evolved favorably without requiring specific hemodynamic interventions. Blood pressure progressively improved over time, while perfusion remained adequate and overall hemodynamic status remained stable. Cranial ultrasound examinations performed on day 3 and day 10 of life were both normal.

In this particular case, the Iowa PDA score would be 6, which in some centers may prompt consideration of pharmacologic treatment to accelerate ductal closure. In our approach, however, we favor conservative management and do not use these medications because of concerns regarding limited efficacy in improving meaningful clinical outcomes, modest success in achieving sustained ductal constriction, and potential medication-related toxicity. Instead, management focuses on optimizing physiology and minimizing factors that may exacerbate left-to-right shunting. We accept permissive hypercapnia and carefully monitor oxygen saturation targets to avoid excessive oxygen exposure, as both aggressive ventilation and hyperoxia can act as potent pulmonary vasodilators and increase pulmonary blood flow (Qp), thereby worsening the Qp:Qs imbalance across the PDA. We also avoid unnecessary vasopressor use in well-perfused infants, as increasing systemic vascular resistance may further augment left-to-right shunting. Ventilatory management emphasizes maintaining adequate PEEP to preserve functional residual capacity while avoiding both overinflation and underinflation of these fragile lungs. Mean airway pressure is carefully titrated to achieve appropriate lung recruitment with mild residual haziness rather than hyperexpansion, minimizing ventilator-induced lung injury during this critical phase of pulmonary development. In infants who remain mechanically ventilated beyond day 10–14 of life with ongoing significant respiratory support requirements, and in the absence of infection or contraindications, we may consider a course of postnatal corticosteroids to reduce pulmonary inflammation and facilitate successful extubation to non-invasive respiratory support (CPS recommendations). See more here on conservative management and our approaches.

Discussion

At birth, pulmonary vascular resistance (PVR) falls quickly, while systemic vascular resistance (SVR) rises quickly after placental separation. The biggest change happens in the first minutes to hours after delivery, but pulmonary vascular transition continues for weeks. Expected timing PVR: there is a rapid, marked fall in the first breaths and first hours, often described as a 5–10-fold drop soon after birth, with further decline over the next 4–6 weeks. SVR rises immediately after cord clamping/placental separation, with the major increase occurring in the immediate postnatal period rather than over weeks. More complete pulmonary vascular remodeling: may continue for about 6 weeks or longer in some descriptions (see "Fetal Circulation and the Transitional Period" in Physiology Definitions section).

In a stable extremely preterm infant during the first 24–48 hours of life, “normal” TnECHO findings should be interpreted within the context of ongoing cardiopulmonary transition rather than against the expectations of an established postnatal circulation. Typical findings include a patent ductus arteriosus (PDA) and patent foramen ovale (PFO), often with bidirectional or predominantly left-to-right ductal shunting, mild early right ventricular dominance, and no evidence of significant ventricular dysfunction, pathologic right-to-left shunting, or obstructive physiology. Importantly, it is very common—and physiologically appropriate—to observe a mildly bidirectional PDA during the first 24 hours of life, often with brief right-to-left shunting in systole or early systole, reflecting transitioning PVR that is part of normal transition (and is not called "pulmonary hypertension", as it is not pathological).

In infants born at the edge of viability, postnatal transitional physiology differs profoundly from that of term newborns because the cardiopulmonary circulation remains structurally and functionally immature. Successful transition requires lung aeration, a fall in PVR, increased pulmonary blood flow, and replacement of placental venous return by pulmonary venous return as the principal source of left ventricular preload. In extremely preterm infants, this process is often delayed and unstable. The lungs are surfactant-deficient, functional residual capacity is difficult to establish, and respiratory support is frequently required early. Even relatively modest positive-pressure ventilation and mean airway pressures may increase intrathoracic pressure and impose a significant afterload burden on the immature right ventricle. As a result, the decline in PVR may be slower, less complete, and highly sensitive to oxygenation, lung recruitment, acidosis, and ventilatory strategy.

The PFO and PDA are not incidental findings, but central components of transitional circulation. The PFO functions as a dynamic flap valve, with shunting determined primarily by atrial filling patterns and ventricular compliance. Early right-to-left interatrial flow reflects preferential streaming of systemic venous return across a relatively noncompliant right ventricle and a still-restrictive pulmonary vascular bed. As pulmonary blood flow improves and left atrial filling increases, shunting progressively shifts toward left-to-right flow, eventually allowing functional closure. Similarly, ductal shunting is governed by the balance between pulmonary and systemic vascular impedance. Early after birth, when PVR remains elevated and systemic vascular resistance (SVR) rises after cord clamping, bidirectional ductal flow is expected. As PVR falls and pulmonary vasodilation progresses, the transductal gradient increasingly favors left-to-right shunting—often over more than 24 hours rather than immediately after birth.

These hemodynamic changes are particularly important at low gestational ages because both ventricles are preload-sensitive, have limited reserve, and tolerate afterload poorly. The right ventricle remains a major contributor to overall circulation early after birth, while the left ventricle must assume full systemic output despite now depending almost entirely on pulmonary venous return for preload. If pulmonary blood flow remains limited because of persistently elevated PVR, left ventricular filling and systemic output may remain reduced. Later, when a larger PDA becomes predominantly left-to-right, pulmonary blood flow may increase substantially, but some of that output is recirculated through the lungs rather than contributing to effective systemic organ perfusion. This creates the classic paradox of elevated measured left ventricular output with decreased effective systemic blood flow to the gut, kidneys, and brain.

Blood pressure during this period is therefore a poor standalone marker of cardiovascular adequacy. Mean arterial pressure is often numerically low in extremely preterm infants because vascular tone is immature, myocardial performance is limited, and the circulation is still adapting to the abrupt loss of the low-resistance placental circulation. A falling blood pressure may reflect low preload, impaired myocardial function, vasodilation, evolving left-to-right ductal shunting, infection-related vasoplegia, adrenal insufficiency, hypovolemia, or simply expected transitional physiology. For this reason, hypotension should never be interpreted in isolation, but always alongside clinical perfusion, lactate, urine output, acid–base status, and targeted echocardiographic assessment.

In the setting of a well-perfused infant with reassuring clinical examination, stable metabolic markers, and a TnECHO demonstrating normal ventricular function, no evidence of underfilling, no significant pulmonary hypertensive physiology, no ventricular hypertrophy, and no left or right ventricular outflow tract obstruction, a low or falling blood pressure alone does not mandate intervention. Likewise, the presence of a mildly bidirectional PDA with brief right-to-left shunting in the first 24 hours should not automatically trigger treatment. In this context, careful observation and watchful waiting are often the most appropriate strategy, avoiding unnecessary vasopressors, volume loading, or pharmacologic ductal closure that may expose the infant to harm without physiologic benefit.

The key question is not whether the blood pressure is numerically low or whether the ductus remains open, but whether the transitional circulation is providing effective systemic perfusion while the infant adapts from fetal to postnatal life. TnECHO is valuable precisely because it helps distinguish expected transitional physiology from true hemodynamic compromise, allowing clinicians to avoid unnecessary interventions and support physiology rather than react to isolated numbers.

Parasternal Long Axis View

PDA View and Suprasternal View

The observation of a brief right-to-left shunt through a patent ductus arteriosus (PDA) during early systole is a recognized hemodynamic phenomenon, particularly during the neonatal period or in clinical states where pulmonary and systemic pressures and/or resistances are nearly equal. This transient reversal of flow is primarily attributed to the kinetic energy and momentum of the right ventricular ejection rather than just a simple pressure gradient. The flow dynamics from the right side facilitate this early systolic shunt. During ventricular systole, the right ventricle ejects blood in a stream that is directed straight through the main pulmonary artery and toward the ductus. Because neonatal systolic resistances/pressures are often balanced, this directed kinetic force allows pulmonary arterial blood to pass into the descending aorta. This effect is further enhanced by the Bernoulli effect created by the aortic stream as it is channeled around the arch to the descending aorta, which can effectively "pull" blood from the pulmonary trunk into the aorta at the ductal orifice. The directness of the stream from the right ventricle to the ductus and the timing of ejection may participate to this early right to left shunting that can be part of normal transitional physiology when PVR are still falling. In contrast, the aortic flow must travel around the arch before reaching the ductus, supporting the concept that the right-sided output has a more immediate mechanical influence on the ductal lumen at the onset of systole. This bidirectional pattern, with a brief right-to-left early systolic flow in early systole and left-to-right flow in diastole, is a hallmark of the "transitional" PDA flow profile . As pulmonary vascular resistance falls and pulmonary artery pressure drops below systemic levels, these kinetic effects are overcome by the widening pressure gradient, and the shunt eventually becomes exclusively left-to-right throughout the cardiac cycle. This profile is expected in the first 24 to 48 hours of life.  

Unrestrictive, pulsatile left-to-right PDA shunting with a brief right-to-left component in early systole. This pattern indicates that pulmonary vascular resistance is lower than systemic vascular resistance for most of the cardiac cycle. The brief early systolic right-to-left shunt is commonly seen during the transitional period, when pulmonary vascular resistance is still falling. It reflects a short interval in very early systole during which pulmonary artery pressure transiently exceeds aortic pressure, potentially with a contribution from RVOT flow being directed across the ductus toward the aorta.

Parasternal Short Axis View

Apical Views

Subcostal View

Cranial POCUS