Ultrasound Case 022

Image 1: Subcostal cardiac view angled anteriorly to see the aortic valve; There is a small pericardial effusion anteriorly which seems to be exerting some pressure effect on the right ventricle with minor atrial and ventricular collapse. Both right and left sided chambers appear small and in this view the LV cavity appears almost obliterated. Although off axis the LV walls appear thickened.

Image 2: Subcostal cardiac view; The same view with the axis improved showing slightly better filling of the ventricles.

Image 3: Longitudinal IVC view; The pericardial effusion is seen measuring a maximum of 1cm in depth. The IVC is seen to fully collapse on inspiration, measuring up to 10mm in AP diameter on expiration.

Image 4: Parasternal long axis view; Marked septal basal hypertrophy also known as a sigmoid shaped septum is seen. There is also concentric LV hypertrophy. The sigmoid shaped septum results in dynamic left ventricular outflow tract obstruction (LVOTO) and systolic anterior motion of the mitral valve (SAM) is evident.

Image 5: Parasternal long axis view with colour Doppler; Aliasing due to rapid, turbulent flow through the partially obstructed LVOT is seen.

Image 6: Apical 4 chamber view: The septal hypertrophy is seen again.

Sigmoid septum with hypovolaemia and LVOTO.

This patient has longstanding hypertension and ventricular hypertrophy. In addition he has particularly marked basal septal hypertrophy (the sigmoid septum), and a small pericardial effusion. Both these had been asymptomatic until he became hypovolaemic. Hypovolaemia and tachycardia have both worsened the left ventricular outflow tract obstruction (LVOTO). This is because even at end diastole the LV is underfilled, and the sigmoid septal bulge lies even more closely to the mitral valve. As the LVOT is even smaller than usual his dynamic outflow tract obstruction becomes symptomatic.

The small pericardial effusion which would usually have no impact exerts some effect on the right sided chambers because of their hypovolaemic low pressure state.

Inotropes should be avoided in cases such as this. The resultant increased ventricular contraction will worsen the LVOTO. Tachycardia reduces ventricular filling time, again increasing the LVOTO.

In this case IV fluid administration is the first, second and third line of treatment. Negatively inotropic agents such as B-blockers may be cautiously considered if optimizing fluid status alone does not correct the problem. B-blockers minimise LVOTO by slowing the heart rate and decreasing inotropy. A well filled left ventricle without hyperdynamic contraction will ensure the LVOT stays open as long as possible.