First, you can see at least a single large hyperechoic lesion primarily localized to the left coronary cusp of the aortic valve. This is consistent with her known infective endocarditis. However, now you can also see significant flail of that cusp. With just the 2D images you would expect severe aortic regurgitation (AR). It’s always a good practice to predict what the regurgitation jet will look like before putting colour doppler on the valve! Application of colour doppler then confirms an extremely large anteriorly directed AR jet. 

From both the 2D morphology and function of the valve, and from the qualitative interpretation of the AR colour jet, we can appreciate that this is severe AR. One of the easier ways to then more quantitatively grade the severity is the measurement of the pressure half-time (PHT) which is demonstrated.  The more rapidly the flow velocities of the AR slow the faster the pressure equalization between the aorta and the LV which is indicative of the severity of the AR. A PHT of < 200ms is consistent with severe AR, between 200-500ms moderate and > 500ms is mild. In this case the PHT of 113ms is concordant with our qualitative assessment of classifying this as severe AR. The subsequent spectral tracing also includes the flow out of the AV and shows increased velocities showing that the lesion is also causing aortic stenosis (AS). When we trace the spectral envelope, we get a Vmax of 3.2m/s, and a mean gradient of 26mmHg. This is consistent with at least moderate AS as well! 

Thus, this patient developed severe AR (and moderate AS) as a complication of her infective endocarditis. This is likely the basis of her worsening dyspnea and meets indications for urgent intervention with cardiac surgery. 

These clips show significant multivalvular pathology. The most obvious striking abnormality is the significant hyperechoic structure mostly localized on the posterior mitral valve leaflet (PMVL). Although this has a differential, this was favoured to be severe mitral annular calcification (MAC). Given the size and significance of the MAC there was further concern that this may be have provided substrate for an embolic basilar artery stroke as the cause of his decreased LOC.  He was taken back for an immediate CTA which again was normal. However, the next day, an MRI was performed which unfortunately showed catastrophic multifocal, bilateral infarcts involving cortical, subcortical and brainstem structures consistent with an extensive cardioembolic etiology. Although this was an unfortunate outcome, this case still captures the power of POCUS to shed light on what was very much an undifferentiated patient with altered mental status. The study prompted further consideration of a cardioembolic stroke and expeditated the necessary investigations. Furthermore, hemodynamically significant valvular lesions (see below) were also recognized which allowed the team the alter their management to keep the patient stable while further investigations were completed. 

As a result of the PMVL pathology there is at least moderate mitral regurgitation which is only partially captured in the above clips. Furthermore, you can also notice flow acceleration through the MV suggestive of mitral stenosis. Interrogation with CW (PW was aliased in this case) shows the very high (~2m/s) mitral inflow E-wave velocities. We can then trace the mitral inflow to get a mean gradient which in this case was approximately 7 indicating moderate mitral stenosis.  

The aortic valve is also heavily calcified with very limited opening highly suggestive of significant stenosis. Thus, this was also interrogated with Doppler to further quantify its severity. First, PW Doppler was used to measure the LVOT VTI which was around 18cm. Next, CW was placed through the AV, which when traced, gave an AV VTI of 87cm, a peak velocity of 4.2m/s, and a mean gradient of 34mmHg. The dimensionless index (LVOT VTI/AV VTI) was therefore 0.21. Although the mean gradient of 34mmHg is in the moderate category the rest of the parameters converge on this being severe AS. Thus, POCUS was able to quickly discover severe multivalvular pathology that was not previously documented. 

This case again highlights how the deployment of POCUS can uncover significant pathology which can dramatically alter the hemodynamic management of patients, and simultaneously aid in determining the ultimate diagnosis of the patient. 

Thanks for reading! 

Matt 

This is an example of severe RV dilation (and RA) and dysfunction. The RV is completely overriding the LV on the apical 4-chamber and in the parasternal short axis you can appreciate the D-shaped septum during both systole and diastole suggestive of both pressure and volume overload.

The TR has been interrogated from both the RV inflow window and the A4C window. You can see a large, severe appearing jet, directed towards the septal TR leaflet. There are a variety of parameters that can be used to quantify TR, however, there are several immediate features that suggest this is severe TR without having to resort to some of these more advanced methods. First, using a qualitative analysis of the continuous wave (CW) spectral doppler tracing (from both the RV inflow and A4C windows) shows a highly dense, and at times quite triangular signal. These aspects are both consistent with severe TR. More mild forms of TR are usually less dense and more parabolic in shape. Furthermore, pulse-wave (PW) doppler of the hepatic vein shows systolic reversal of flow which is also suggestive of severe TR.

In this case the importance of recognizing that this is severe TR is that in this setting, the usual way of estimating RVSP can’t be relied upon. Usually, we apply the modified Bernoulli equation () to get the pressure gradient between the RV and RA and then add on the estimated RAP. However, in the setting of severe TR, the right atrial pressure (RAP) will increase rapidly during systole which will result in an underestimation of the RVSP. This is likely the case here as the highest-pressure gradient was only 26. There are also some other, more physics-based reasons, why in the setting of severe TR the simplifications implied in Bernoulli equation itself may break down contributing its inaccuracy.

We also interrogated the RVOT with pulse-wave doppler and measured the pulmonary artery acceleration time (PAT). Using this we can also get an estimate of the mean pulmonary artery pressure (mPAP). There are a variety of formulas but a simple one to remember is mPAP = 80 – 0.5(PAT). In this case, the PAT of 57 would yield a mPAP of ~52mmHg. This value is more in keeping with his known severe CTEPH.

Although estimating the RVSP is a great way to quantify the severity of RV pressure overload this case illustrates a potential pitfall of this method and highlights another Doppler technique that can be deployed for this purpose.