Understanding PDA Spectral Doppler

Spectral Doppler interrogation is a cornerstone of echocardiographic evaluation of a patent ductus arteriosus (PDA). Beyond simply confirming ductal patency with two-dimensional and color Doppler imaging, spectral Doppler allows detailed assessment of shunt direction, velocity, and hemodynamic significance. Using pulsed-wave (PW) or continuous-wave (CW) Doppler aligned with ductal flow, clinicians can characterize shunt physiology and gain insight into the instantaneous pressure relationships between the systemic and pulmonary circulations. A restrictive PDA is one in which the effective ductal diameter is sufficiently small that flow and pressure transmission are limited by the ductal narrowing itself. In this setting, shunt magnitude is constrained by ductal resistance, and high velocities reflect a large pressure gradient across a narrow conduit. In contrast, an unrestrictive PDA is large enough that intrinsic ductal resistance is negligible, and shunt volume is determined primarily by the instantaneous systemic–pulmonary pressure gradient, as well as by the relative impedance and compliance of the two vascular beds. Importantly, the concept of ductal “restrictiveness” is not binary. Ductal shunting is governed by continuous variables—effective diameter, length, geometry, and dynamic smooth muscle tone—interacting with continuously changing systemic and pulmonary vascular resistance, impedance, and compliance. As these determinants evolve over the cardiac cycle and over postnatal time, the PDA transitions progressively from an unrestrictive to a restrictive conduit. Restrictive and unrestrictive PDAs therefore represent points along a physiologic continuum rather than discrete states. The ductus arteriosus provides a dynamic window into the interaction between the pulmonary artery and aorta throughout the cardiac cycle. During systole, when ventricular ejection raises pressures in both great arteries, ductal flow reflects the relative timing and magnitude of pressure rise, ventricular–vascular coupling, and the balance between left and right ventricular output. During diastole, differences in pressure decay dominate ductal flow behavior: pressure falls more slowly in the stiffer systemic circulation and more rapidly in the typically more compliant pulmonary vascular bed, often shaping late-diastolic and presystolic shunt velocity profiles. Because the ductus is a passive conduit, it does not generate flow but faithfully transmits moment-to-moment hydraulic relationships between the two circulations. As such, the PDA acts as a real-time integrator of ventriculo-arterial interaction, vascular compliance, impedance, and transitional physiology rather than a static anatomic lesion. The ductus itself may change caliber from beat to beat, and even within a single cardiac cycle, with a tendency toward larger diameter during systole and relative narrowing during diastole or during phases when pulmonary and systemic pressures approach equilibrium. Consequently, velocity and pressure gradients across the ductus reflect a continuously evolving balance between aortic and pulmonary arterial pressures and vascular properties, underscoring why PDA spectral Doppler patterns must be interpreted dynamically across the entire cardiac cycle rather than at a single time point.

1. Doppler Measures an Instantaneous Gradient, Not Pressure

Doppler interrogation of a patent ductus arteriosus does not measure pressure directly. Instead, it provides an instantaneous velocity that can be converted using the Bernoulli relationship into an instantaneous pressure gradient between the aorta and the pulmonary artery at that specific moment in the cardiac cycle. This gradient represents only the pressure difference between the two vascular beds at that instant and should not be equated with systolic aortic pressure, systolic pulmonary arterial pressure, or mean pressure unless strict timing assumptions are met.

2. Aortic and Pulmonary Artery Pressure Curves Are Not Synchronous

The aortic and pulmonary artery pressure waveforms have different shapes and timing characteristics. Aortic pressure rises rapidly and reaches a higher peak, while pulmonary artery pressure has a slower upstroke, a lower systolic peak, peak tend to occur relatively earlier after QRS and has a more rapid diastolic decay due to higher compliance. As a result, the maximal separation between the two curves, which determines ductal flow velocity, does not necessarily occur at peak systole. The highest PDA velocity may occur before, at, or after peak aortic or pulmonary artery pressure.

3. Electrical Systole Does Not Define Mechanical Systole

Mechanical ventricular systole does not extend to the end of the T wave. Peak ventricular pressure and peak arterial pressure typically occur during the early phase of ventricular repolarization, rather than at the apex of the T wave. Because PDA Doppler velocities are often referenced to the ECG, there is a risk of mislabeling velocities as “systolic” when they do not coincide with true peak mechanical systole or maximal arterial pressures.

4. Ductal Flow Is Impedance-Driven, Not Valve-Driven

Flow through the ductus arteriosus is governed by impedance rather than by valvular mechanics. The PDA is not a fixed orifice and does not fully satisfy the assumptions required for strict Bernoulli application. Ductal flow reflects the interaction of instantaneous pressure differences, ductal size and geometry, pulmonary vascular impedance, and the compliance of both arterial systems. The estimation of Right Ventricular Systolic Pressure (RVSP) via a PDA-derived gradient can result in both underestimation and overestimation. 

5. PDA-Based sPAP Estimates Tend to Underestimate True RVSP,  but can also Overestimate

When PDA peak velocity is used to estimate systolic pulmonary artery pressure by subtracting the Doppler-derived gradient from systolic blood pressure, the result often underestimates true right ventricular systolic pressure. This occurs because the peak PDA velocity is frequently measured at a time when aortic pressure has not yet reached its maximum or when pulmonary artery pressure has already begun to fall. The gradient therefore reflects a submaximal pressure difference rather than true peak systolic separation. Overestimation of RVSP occurs if the PDA gradient is underestimated. The most common cause is Doppler beam misalignment; if the ultrasound beam is not perfectly parallel to the blood flow, the recorded velocity will be lower than reality. A lower velocity produces a smaller gradient, which, when subtracted from the SBP, leaves a falsely high (overestimated) RVSP. Similarly, if the systemic blood pressure used in the calculation is measured at a different time than the echocardiogram and is falsely elevated, the resulting RVSP will be overestimated.

6. Directional Flow Changes Reflect Instantaneous Dominance

Bidirectional or transient right-to-left components of PDA flow reflect instantaneous pressure dominance rather than mean or sustained pressure relationships. Early systolic right-to-left flow may occur when pulmonary vascular resistance briefly exceeds systemic resistance, even without suprasystemic pulmonary pressures at peak systole. As systole and diastole progress, left-to-right flow typically dominates as aortic pressure remains higher while pulmonary artery pressure decays more rapidly. Net shunt direction over the cardiac cycle does not capture these instantaneous dynamics.

7. Peak Velocity Does Not Equal Peak Pressure Difference

The maximal Doppler velocity across the ductus does not necessarily correspond to the maximal physiologic pressure difference between the aorta and pulmonary artery (as the peak pressure difference may occur at different moment of the cardiac cycle). Indeed, the peak pulmonar Larger gradients may occur early in systole when pressure curves diverge rapidly, while smaller gradients may be present at the time of true peak arterial pressures. End-diastolic gradients reflect diastolic pressure separation and should not be interpreted as systolic load. Timing, rather than magnitude alone, determines physiologic meaning.

8. Limitations of Bernoulli-Based Pressure Reconstruction

Attempts to reconstruct pressure curves from PDA Doppler velocities assume stable geometry, negligible energy loss, and complete applicability of Bernoulli principles, assumptions that are rarely satisfied in neonatal ductal physiology. Turbulence, changing ductal caliber, pulsatile impedance, and compliance effects all introduce error. As a result, pressure curves extrapolated from PDA velocities should be considered conceptual aids rather than precise physiologic measurements.

9. Clinical Integration and the Role of Complementary Measures

These concepts emphasize that PDA Doppler is best interpreted as a dynamic physiologic signal rather than a static pressure estimator. While it provides valuable insight into timing, impedance, and shunt behavior, it should not be used in isolation to quantify systolic pulmonary artery pressure. Integration with tricuspid regurgitation velocity, systemic blood pressure, septal configuration, ventricular performance, and the overall clinical context remains essential for accurate hemodynamic interpretation.