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.

The TTE images clearly demonstrate a grossly abnormal mitral valve, but it’s hard to delineate exactly what’s going on. Dialysis patients (as this patient was) are often predisposed to significant mitral valve annular calcification (MAC). When initially assessing this valve, it was difficult to confidently distinguish between severe MAC and potential endocarditis (although highly suspicious for this). 

Luckily, we have ready access to a TEE probe, so we quickly made the decision to have a closer look at the valve with TEE. As you can see from those images, the MV pathology is much better delineated and we can assess the MV (and its various scallops) using different omniplane angles.  Now we can see a large, independently mobile, hyperechoic lesion primarily on the posterior mitral valve leaflet (although there also looks like there may be some smaller lesions on the AMVL as well). Finally, you might also have noticed a few lesions on the NCC of the aortic valve. Given the pathology evident on the MV, these would also be highly suspicious for AV endocarditis as well (although could also represent calcification). 

In the end this patient would grow MRSA in her blood which ultimately would have prompted the team to order an echocardiogram to look for endocarditis. But, using POCUS TEE the patient’s endocarditis was diagnosed more promptly which gave the treating team more diagnostic confidence, avoided chasing other potential diagnoses, and facilitated expedited consultation and management with the appropriate services.

If you’ve been following along the COTW series, you might have picked up on the key finding here pretty easily. This is another case of systolic anterior motion (SAM) of the mitral valve and highlights that this can be a relatively common occurrence in the ICU!

Although not fully assessed, the LV has findings consistent with concentric LV hypertrophy. This, plus the combination of her tachycardia, and relative hypovolemia created a substrate for SAM. See a still image below showing the extent of dynamic LVOT obstruction as a result of the SAM. The initial gradient of 94mmHg is quite high and could have ultimately led to hemodynamic collapse if appropriate steps were not taken.  

Luckily, however, this was picked up on, and the patient was further fluid resuscitated, and beta-blockade was initiated. A repeat POCUS two days later shows improvement in the SAM (see below), and a much lower gradient of lesser potential hemodynamic consequence. 

You can go back to previous weeks in the last few months for other cases of SAM and for more detail on its diagnosis and management! 

See everybody in 2020!

Ok – there’s a lot going on in this study.  The most shocking and obvious finding is the severely depressed LV function. From a POCUS perspective we often think about classifying LVEF into 4 categories: hyperdynamic (EF > 70%), normal (EF 50-70%), moderately depressed (EF 30-50%), and severely depressed (EF < 30%). This heart certainly falls into that last category, as we see in several views that the LV walls are hardly contracting. There is some regionality here, with the basal segments contracting slightly more than the apex, which appears almost completely akinetic. As a testament to this, we actually see spontaneous echo contrast in the LV apex (visible both in the PSAX and the modified A4C views), which is evidence of very low velocity blood flow and is a nidus for LV thrombus formation. Our LVOT VTI of 6 (recall that normal is 18-22) confirms that this is primary cardiogenic shock with an alarmingly low cardiac output.

To make matters even worse – not all of that cardiac output is going forward! In an apical 5-chamber with colour Doppler, we note a red jet during diastole that represents aortic regurgitation. Spectral Doppler is then used to generate a pressure half-time, which is a semi-quantitative measure of severity. In severe aortic regurgitation, the pressures between the aorta and the LV equalize very quickly (due to a high volume of flow through an incompetent valve), resulting in a fast PHT. In this case, the PHT falls into the moderate category (200ms-500ms) – not life-threatening, but certainly not helping her already paltry cardiac output.

There are a few other findings that the astute among you will have picked up. The right ventricle appears to have mildly reduced function with a borderline TAPSE, although S’ is normal. There is severe TR, and there appears to be a hyperechoic density on the ventricular side of the tricuspid valve. This was hypothesized to represent a ruptured chordae or pap muscle rather than a vegetation, due to the lack of independent movement and its location on the ventricular (high-pressure) side of the valve.

Finally, a pulse-wave Doppler interrogation of the RV outflow tract reveals marked respiratory variation. This is a marker of adverse heart-lung interactions and is most typically associated with one of three things: significant RV dysfunction, high pulmonary afterload (often due to ventilator settings in the ICU), or hypovolemia.  Given that this patient had only mildly impaired RV function and was on minimal ventilator settings, we hypothesized that she actually may be slightly hypovolemic (which is very counterintuitive given her profound LV failure). This is supported by her diminutive IVC (which was measured at 1.4cm).

Overall, this represents a severely depressed LV (EF estimated 10-20%) with very low cardiac output, consistent with cardiogenic shock. The working clinical diagnosis is an acute-on-chronic picture: the thinning of the LV myocardium and LV dilation suggest chronicity (perhaps due to CAD), with a likely superimposed septic cardiomyopathy, as she’s now had positive cultures (and on further history was unwell at home for some time prior to her presentation).

Based on the initial POCUS findings, inotropy was uptitrated significantly, vasopressin was discontinued (pure peripheral vasoconstriction will worsen AR), and the patient received very (very!) judicious fluids. The following clips were taken the next day as a focused reassessment:

As you can see, LV function still looks severely impaired; however, with the addition of inotropy and a small increase in preload, VTI has doubled. We also no longer see signs of hypovolemia with a loss of RVOT VTI variation and a plethoric IVC (now 2.7cm). At this point, we cautioned against any further fluids and suggested continuation of inotropic support.

This case covered a lot of complex hemodynamic principles, so if you want to explore some of these topics in more depth, head on over to the screencasts at WesternSono.com. Happy scanning!

As you can see, we’ve moved beyond single measurements to determine “fluid responsiveness.” Rather, we try to deploy a whole-body approach looking at the lungs, heart and intraabdominal organs (in conjunction with integration into clinical context) to help decide whether a patient might benefit from further fluid resuscitation, diuresis or maintenance of euvolemia.

First, you can appreciate that there is an A-line pattern anteriorly with an absence of B-lines. An A-line pattern anteriorly suggests a PAOP of < 18. At the very least there is no evidence of extravascular lung water or cardiogenic pulmonary edema.

Next from a cardiac perspective, we can see a LV that has relatively normal systolic function with a normal estimated cardiac output (on 10mcg/min of NE). The LV however was quite thickened, and with an associated dilated left atrium. These 2D findings point towards diastolic dysfunction which we can further interrogate with Doppler US. Assessment of diastolic dysfunction is definitely on the more advanced side of critical care echo but there is a nice paper that I’ve attached below that summarizes an approach for the intensivist. Here, the mitral inflow pattern shows A>E, and the TDI of the lateral mitral valve annulus is low at 7.8cm/s (<10 is abnormal). The ratio of the E wave velocity to the e’ velocity can be used to estimate the LAP. Values > 14 are considered abnormal. Here the E/e’ is 11 which is borderline. Overall, this is consistent with grade I diastolic dysfunction without definite evidence of increased LAP.

Furthermore, the RV appears dilated, but with relatively normal systolic function and the interventricular septum appears normal with no paradoxical motion or septal bounce.

Finally, we interrogated the intraabdominal organs. Katie Wiskar has put together another amazing screencast (should be published on WesternSono in the next week or two) detailing the techniques and evidence to date for this.  Stayed tuned for this for more of an explanation than is provided here. We can see an IVC without much respiratory variation (although only measured in long axis in this case). The hepatic vein has normal morphology (antegrade flow S>D) and the portal vein doppler is continuous without pulsatility. However, the renal doppler show an abnormal renal resistive index of 0.84 (>0.7 is abnormal) and pulsatile renal venous flow (also abnormal). 

Putting this all together this patient has multiple markers of potential fluid intolerance. However, her LAP is not acutely elevated, she has dry lungs, and her organ doppler assessment is normal other than her abnormal renal doppler. An abnormal renal doppler assessment in this case (given no other markers of venous congestion) was likely secondary to intrinsic renal pathology such as acute tubular necrosis.  Clinically, she had a positive overall fluid balance, and had no significant peripheral edema.  Thus, overall, we thought that there was no evidence of venous congestion as the culprit of her AKI and that it would not be unreasonable to give a judicious trial of fluids, but that care should be taken to not allow the patient to become too positive in light of her markers of fluid intolerance. We also cautioned against liberal fluid use as preload augmentation would likely be of limited benefit given her already normal estimated cardiac output.

There is a lot more that could be expanded on and explained further, and this is definitely on the very advanced side of critical care ultrasound. But this is meant to give the flavour for the detail and whole-body approach we have been taking at Western when approaching the very common question of whether to give fluids or not. Finally, what could have also been done, is a dynamic test (such as a passive leg raise, coupled with serial measurement of the LVOT VTI) to see if the patient was indeed fluid responsive. The absence of a 10% change in VTI would argue against fluid responsiveness and that fluid would be likely of no benefit.  A > 10% positive change would represent a normal physiologic state and we would use that in conjunction with all of the other parameters described above to decide whether fluids should be given.

Evaluation of Diastolic Dysfunction

First, the abdominal images. In the absence of pathology, normal ultrasound images of the abdomen should be unremarkable – because of the presence of air in bowel loops, we typically simply see artifact and can’t visualize the bowel itself. When the bowel becomes filled with fluid, however, we get beautiful pictures like the ones above where we can clearly see dilated loops of bowel (these were measured at 3.2cm; normal for small bowel is < 2.5cm). We also note free fluid surrounding the bowel loops in the first clip, which, in the context of dilated loops and bowel obstruction, is called the Tanga sign. In our second clip, we see a textbook demonstration of “to-and-fro” movement of bowel contents, which is highly specific for bowel obstruction. 

Next, his hypotension – his A4C clip is challenging; we get a sense of a dilated R heart, as well as marked biatrial enlargement and hyperechoic shadowing from his two mechanical valves. Particularly in the context of pulmonary hypertension, Echo images like this can be very hard to interpret to determine the cause of shock. The key here lies in the spectral doppler tracing, which swiftly answers our clinical question. We have used PW Doppler to interrogate blood flowing out of the LVOT, and tracing the resultant waveform reveals a velocity-time integral (VTI) of 24.7cm. This is supra-normal; the normal range for LVOT VTI is 18-22. (For more on how to calculate stroke volume and cardiac output using LVOT VTI measurements, see the WesternSono tutorial here: https://westernsono.ca/screencasts/echo/stroke-volume-determination/). 

This elevated VTI essentially excludes R heart failure as the cause of his hypotension. In RV failure and other causes of obstructive shock, the hemodynamic problem is a failure of the RV to deliver blood to the LV, leading to a low LVOT VTI and low cardiac output. In contrast, here we have a high LVOT VTI and high cardiac output, which is consistent with vasodilatory shock from sepsis. 

In our gentleman’s case, he was found to have C. difficile colitis complicated by ileus (accounting for his abdominal images). General surgery was consulted but he was managed conservatively with antibiotics and bowel rest. His hypotension was a result of his sepsis, rather than worsened RV failure, and was treated with vasopressors. 

That’s all for this week. Thanks for reading, and happy scanning! 

The above images show pulse wave doppler interrogation of the left MCA artery. This produced the typical spectral Doppler velocity waveform with a steep systolic upstroke and the gradual step-down diastolic flow. This is the expected appearance of flow in the absence of raised intracranial pressure. 

In the setting of raised ICP the diastolic flow becomes blunted, and can even progress to diastolic flow reversal followed by the gradual reduction of systolic flow as the ICP progressively increases towards cerebral circulatory arrest (see Figure below from Lau’s paper attached below). 

Furthermore, the actual ICP can be estimated using the Gosling pulsatility index (PI). First, the PI can be calculated from the following formula. 

Pulsatility index (PI) = (Peak systolic velocity – End diastolic velocity) / (Mean velocity) 

From the PI (which machines with the TCD software package will give you automatically from tracing the spectral waveform) you can get the ICP through the following formula:

ICP = (10.93 x PI) – 1.28 

In this case the PI was found to be 1.09. Therefore, using the above formula:

ICP = (10.93 x 1.09) – 1.28 

=10.6 – essentially a normal ICP 

Given the normal waveform and estimated ICP the parenchymal ICP monitor was thought to be non-functional. Neurosurgery was re-consulted and the ICP monitor was exchanged for an external ventricular drain (EVD) which showed a normal ICP of 10, corroborating our TCD results. 

This case illustrates the utility of point-of-care TCD to help guide the management of the neurocritical care patient. See the attached article below by Lau & Arntfield detailing the use of point-of-care TCD by intensivists. 

Click here: TCD