A patient with known systolic heart failure (left ventricular ejection fraction ~20%) presented with shortness of breath after missing diuretics for a few days. Lung ultrasound done by the ER physician showed bilateral B-lines suggestive of pulmonary edema and right > left pleural effusion. Admitted for intravenous diuresis. One day later, urine output was ~3 liters, patient felt comfortable and documented weight was down by 6 kg from the time of presentation (different scale). Pedal edema was trace and jugular venous distension not appreciated.
Now, focused question for physician performing POCUS: can we transition to home dose of oral furosemide and discharge? Let’s see how individual components of POCUS help answer this question.
Sono-auscultation of the heart (basic echo without spectral Doppler) shows significantly reduced LV ejection fraction on PLAX view, at least moderate tricuspid regurgitation qualitatively on RV inflow view. Does this change anything? No, because these are not unexpected findings.
Next sono-auscultation of lungs was performed, which revealed predominantly A-line pattern on most anterior and upper lateral zones. Right pleural effusion noted as documented in the ER note. Representative images shown below. Does this change anything? Maybe. Its probably OK to transition to oral diuretic.
However, inferior vena cava (IVC) appears plethoric in both axes. Now this tells you that the right atrial pressure is high (estimated 15 mmHg as the diameter is >2.1 cm and collapsibility <50%). Should we continue intravenous diuretic for some more time? Maybe yes. Other argument could be that patients with severe heart failure and pulmonary hypertension have chronically dilated IVC. Moreover, this patient has tricuspid regurgitation. Should we trust IVC? Need more information.
Next obtained pulsed wave Doppler tracing of hepatic vein. Looks like S<D pattern (best guess without EKG). Change anything? S<D says the right atrial pressure is high. Tricuspid regurgitation can also make the amplitude of S wave smaller. Without knowing this patient’s baseline, it has same limitations as the IVC. Obviously, most clinics out there don’t do VExUS, so having a baseline is impossible.
Next step is to obtain portal vein Doppler. Below tracing reveals 100% pulsatility with some flow reversal (below-the-baseline blebs) suggestive of severe congestion. Does this change management? Yes, this patient would likely benefit from continued IV diuresis. OK, there is congestion, but why not oral medication? Because portal pulsatility suggests gut edema and consequent poor bioavailability of furosemide. Can this pulsatility be chronic? 100% pulsatility is less likely to be baseline for anybody (except severe chronic pre-capillary pulmonary hypertension). We can use portal vein as a tool to monitor response to decongestive therapy.
Follow up images 2 days later (7 liters net negative) are shown below. While IVC is still enlarged and suggestive of elevated right atrial pressure, appears a little less plethoric. Hepatic and portal vein waveforms have normalized. Patient discharged home.
Some points to note. It is well-known that there is a dissociation between clinical congestion and hemodynamic congestion in heart failure and bedside tools to detect hemodynamic congestion are limited. In this setting, patient symptoms, physical examination, daily weights, and serial biomarker measurements, such as BNP have been shown to have insufficient sensitivity and specificity. POCUS allows us to assess hemodynamics and observe the response to therapy in real time. For example, we found A-lines on lung POCUS compared to B-lines at presentation. Lung ultrasound is a reasonable indicator of LV end diastolic pressure. However, isolated POCUS parameters have their limitations and as such, multi-organ POCUS must be the norm paying attention both left and right heart markers. Choosing the right POCUS parameter to answer the focused question you have in mind is the key.