Answer: A - Diffuse asymmetrical B-lines with spared areas; some areas of pleural irregularity

The clips reveal B-lines throughout most areas of the lungs, though there is focal sparing (with A-lines visible) in L1 and L2. There are also areas of pleural irregularity, most obvious in R3 and L1, though this is not diffuse. There are more B-lines present on the right side than the left (asymmetrical distribution).

Note there are also consolidations at the bases; these appear non-translobar with a shred sign present (especially in L4), though a more posterior probe position may have revealed translobar consolidations/hepatization. These consolidations are accompanied by small-moderate bilateral simple-appearing pleural effusions.

Answer: D - Moderate/severely depressed LV function, mildly impaired RV function, mild-moderate MR

Estimated qualitatively, the LV function appears moderate to severely depressed (EF approx 30%); myocardial thickening and contractility are both visibly reduced.

The RV does not appear dilated (size is <2/3 the size of the LV). Visually the function appears reasonable, but TAPSE is low at 1.5cm (normal is at least 1.7cm); therefore, we suspected mild RV impairment.

The PLAX view with colour doppler over the mitral valve reveals what is likely mild-to-moderate MR; though this should be corroborated in additional views.

Answer: B - Reduced VTI in keeping with reduced LV function; though CO likely preserved due to tachycardia

The measured VTI here is low, at 13.6cm (normal: 18-22cm), in keeping with the patient’s reduced LV function seen on 2D POCUS. However, cardiac output is maintained due to tachycardia – use of a 20mm estimated LVOT diameter gives a calculated cardiac output of 5.7L/min (normal: 4-8L/min). The spectral waveform is adequate for tracing.

For more on how to calculate cardiac output using LVOT VTI measurements, see the ubcimpocus screencast here.

Answer: C - IVC is non-plethoric and appears to collapse with respiration. Hepatic vein profile is normal.

In the long-axis IVC view, we see evidence of collapse with inspiration; although there is likely a small degree of lateral translation with respiration. However, the short-axis view – which also reveals collapse with respiration – corroborates this finding (which is why this second view can be so helpful).

When assessing the IVC in a patient like this, it is important to be aware that respiratory effort can impact IVC collapsibility. Significant respiratory effort (and substantial intrathoraic pressure swings with respiration) can cause IVC collapse even in the presence of elevated right atrial pressures. While this patient certainly did have elevated work of breathing, the ovoid shape (as opposed to a very circular shape seen in plethoric IVCs) in the short-axis view is another indicator that this patient did not have significant congestion.

Finally, the hepatic vein also supports the lack of venous congestion in this patient. This profile appear essentially normal, with S and D waves both below the baseline, and S slightly larger than D. Scanning the hepatic vein to look for evidence of venous congestion is part of the VEXUS protocol; for more on solid organ doppler for venous congestion, see the ubcimpocus screencast on the Venous Congestion here.

Answer: A - Suggestive of a predominant infectious/inflammatory etiology in an immunocompromised patient, such as atypical/fungal infection, aspiration, or ARDS. Cannot exclude overlying cardiogenic pulmonary edema, but a lack of systemic venous congestion makes this less likely.

The lung ultrasound clips are most in keeping with infectious/inflammatory pathology, given the areas of pleural irregularity, focal sparing, and an asymmetrical distribution of B-lines.

The pleural effusions were most likely reflective of increased capillary permeability in the context of profound systemic inflammation. Of course, bilateral pleural effusions are often cardiogenic in nature; however, the collapsible IVC makes this less likely. It is also possible that the effusions are parapneumonic in the context of infection.

Although the cardiac clips do certainly reveal depressed LVEF, the collapsible IVC and normal hepatic vein profile make a significant contribution from cardiogenic pulmonary edema less likely – however, this cannot be excluded.

Answer: C* - Vasopressors (ie norepinephrine) for vasodilatory shock

Given the patient’s history of persistent fungemia and the suspected inflammatory/infectious etiology of her hypoxemia, treatment for septic shock with vasopressors is reasonable here. The choice of an agent with some inotropic action, such as epinephrine, would also be appropriate given the depressed LV function. A pure inotrope such as dobutamine or milrinone would cause additional vasodilation that would be undesirable given her suspected pathology.

Additional fluids are risky in this situation given her lung pathology and cardiac function – even though the B-lines are not likely to be due purely to cardiogenic pulmonary edema, the presence of diffuse lung pathology increases the risk associated with fluid administration, especially given her depressed cardiac function. Likewise, the presence of bilateral pleural effusions – even though they may not be cardiogenic in origin – suggests significant potential harm with further fluids.

Treatment of tachycardia with beta-blockers would be harmful here, as the tachycardia is compensatory and is currently serving to help maintain cardiac output. Treat the underlying cause!