Parasternal long axis view. The Septum is significantly hypertrophied. The RV wall (anterior wall) is hypertrophied subjectively. The LV is undefilled. 

In this M-Mode, on may appreciate the significant hypertrophy and "crowding". There is some degree of systolic anterior motion of the mitral valve but no clear obstruction of the LVOT as there is still some "space" between the mitral valve and septal wall.

Flow visualized going through the RVOT (blue). 

LVOT is seen. There is opening and closing of the aortic valve, outlining that there is no direct obstruction before the valve. This view is used to measure the LVOT diameter.

Posterior sweep towards the RV inflow. One may appreciate that the RV is hypertrophied. 

Colour flow with some degree of acceleration within the LV. 

RVOT PW-Doppler enveloppe is seen here at the beginning of the TnECHO. The ejection time is very short and the VTI is low at 0.061 meter. Heart rate is 123 bpm.

Here the VTI has doubled (0.126 meter) and Heart rate is at 136 bpm. This is the VTI obtained on the PW-Doppler of the RVOT after fluid repletion. This outlines that the output has at least doubled.

PSAX. The RVOT is seen opening and closing. This is especially important in the context of RV hypertrophy to rule out RVOT / Pulmonary Valvular obstruction, stenosis, atresia. We can observe the left atrium and the left atrial appendage. The left atrial appendage (LAA) is a small, finger-like pouch on the left side of the heart, specifically the left atrium

In this PSAX, we can observe the RV and septal hypertrophy. The systolic function is vigorous for the LV (subjective). The LV walls touch each other in systole, raising concern of underfilling. 

Sweep from base of the LV to the apex. We can observe that the walls are "kissing" each other in systole. This raises concern for underfilling. 

Another sweep up to the aortic valve. The LA is appreciated and is about the size as the Aortic Valve. When there is low LA preload, this could be due to low pulmonary blood flow, which can result from low RV output. This can also be the result of low RV preload, leading to a state of underfilling. The LV attempts to compensate by accelerating heart rate to increase cardiac output in compensation.

"In this image, we observe a faint flicker of PDA flow, visualized as a small red Doppler signal. This finding is characteristic of a closing ductus arteriosus pattern, in which the lumen is nearly obliterated, permitting only minimal, brief systolic flow. The transient pressure rise during systole is sufficient to momentarily distend the residual ductal channel, allowing a brief trickle of left-to-right flow through the markedly narrowed segment.

Disappearance of Diastolic Flow is a key echocardiographic marker of imminent ductal closure. As the ductus arteriosus constricts, the diastolic pressure gradient between the aorta and pulmonary artery becomes insufficient to sustain flow, and Doppler interrogation reveals absent diastolic shunting. Residual flow may persist briefly during systole, when systemic pressure is at its peak and transiently overcomes the increased ductal resistance. In this case, a peak systolic flow velocity of 0.8 m/s (post-QRS) and nearly absent diastolic flow are consistent with a closing ductus. Based on the Bernoulli equation (ΔP = 4v²), this implies that systolic pulmonary artery pressure is at least 2.6 mmHg below systolic aortic pressure. However, Doppler-derived gradients across a closing ductus may be unreliable. As luminal narrowing progresses: 

• Underestimation may occur due to signal dropout or loss of laminar systolic flow, making the measurable velocity unrepresentative of the true peak pressure difference. 

• Overestimation may result from ductal narrowing creating a high-resistance, tunnel-like flow pattern. This leads to localized jet acceleration and turbulence, inflating the measured velocity and thus the calculated pressure gradient.

E/A velocity ratio of the RV inflow outlining A velocity higher than E velocity, often seen in patients with RV hypertrophy due to decreased compliance and filling during the early phase of diastole (passive). The underlying mechanism involves reduced RV compliance, which limits passive ventricular filling during early diastole (E-wave), thereby shifting a greater proportion of diastolic filling to the atrial contraction phase (A-wave). This pattern may be seen in neonates in early life undergoing transitional physiology as their RV was systemic during fetal life. However, this pattern typically reverses in early life as the RV remodels due to dropping PVR.

This Doppler image displays a continuous wave (CW) Doppler interrogation through the left ventricular outflow tract (LVOT) in apical four-chamber view. The tracing reveals classic features consistent with dynamic chamber acceleration, commonly seen when there is intra-cavitary acceleration due to either kissing walls (low preload) and/or some component of ventricular hypertrophy (here from the septum).

TAPSE was 9 mm - considered normal for gestational age. Indicating one marker of normal RV contractile property.

Here, we observe that the left ventricular (LV) walls are "kissing," reflecting significantly reduced LV preload. 

Here we can appreciate in the Apical 5 Chamber view that there is flow entering the LVOT anterograde. However, there is acceleration from a combination of likely decreased preload and kissing walls, as well as systolic anterior motion of the mitral valve due to septal hypertrophy. 

After fluid repletion, the LV walls are not kissing in systole and there is improved stenting of the left ventricular outflow tract (LVOT), with reduced flow acceleration observed within the left ventricular cavity. This suggests more favorable LV geometry and filling. It is worth noting that the Nyquist limit is set higher in this view compared to the previous pre-bolus images, which may partially influence the appearance of flow velocities. 

Although the interventricular septum and RV free wall remain subjectively hypertrophied in the RV-focused apical four-chamber view, there is a noticeable increase in the anechoic RV chamber size, with a larger mid-cavity diameter observed during both systole and diastole compared to the pre-bolus images. This suggests improved RV preload and diastolic filling following volume administration.

This image demonstrates a focused apical four-chamber view of the left ventricle. Compared to prior images, the myocardial walls are more clearly distinguishable from the anechoic intracavitary blood pool, reflecting improved LV filling. The left atrium also appears better filled, suggesting enhanced preload. Additionally, the left ventricle appears less hyperdynamic, consistent with improved volume status and more normalized loading conditions.

This subcostal view demonstrates an inferior vena cava (IVC) with appropriate caliber. In cases of dehydration or significantly reduced preload, the IVC would typically appear small and collapsible. However, in intubated patients on positive pressure ventilation, the IVC may appear distended due to cardiopulmonary interactions, even in the setting of true hypovolemia. Importantly, in such patients, a collapsed IVC despite positive pressure ventilation strongly suggests low preload. In this case, the view was obtained while the patient was intubated and mechanically ventilated. The imaging was performed after fluid resuscitation, and the IVC demonstrates an appropriate diameter without evidence of significant collapse, suggesting adequate volume status but with caveat that this may be influenced by the positive pressure ventilation. 

The subhepatic veins are well visualized, and color Doppler shows predominantly blue flow (away from the probe), indicating normal anterograde venous return toward the right atrium. 

Pulsed-wave Doppler of the hepatic venous flow shows more than 50% anterograde flow, consistent with normal right atrial pressures and compliant right atrial filling despite the RV hypertrophy.