Ultrasound Case #5 – The Pulmonary Embolism?

Clips 1 and 2 are a parasternal long and then a parasternal short view. They each show a severely reduced ejection fraction and no obvious signs of RV dilation or intraventricular septal bowing. Overall both of these clips suggest a diagnosis of CHF over PE.
Clips 3 through 6 show bilateral lung POCUS findings. In the clips labeled anterior lung on both the right and the left you can see diffuse B-lines. The clips labeled lateral both show pleural effusions with some visible portions of lung in each.

Overall this series of clips paints a picture of acute CHF exacerbation and the patient should be treated as such. The management of acute heart failure varies depending on the exact etiology, however in the ED the answer is generally to reduce the patients pre-load and optimize their position on the Frank Starling curve. Since this patient is hypertensive generally the first line treatment for pre-load/afterload reduction would be sublingual or IV nitrates. Another key step in the management of CHF is respiratory support with CPAP/BiPAP, which will provide higher concentrations of inspired O2 vs room air and also serve to increase intrathoracic pressure therefore further reducing pre-load and afterload.

• As we covered in a previous post (Case 4) B-lines do not always represent pulmonary edema. However given the patient’s vital signs (hypertensive, tachycardia, hypoxic, afebrile) and echo findings of a severely reduced ejection fraction, CHF is the most likely diagnosis.
• Estimating ejection fraction comes with time as you do more ultrasounds. If you are struggling with estimating EF you can use things like e point septal separation (EPSS) or fractional shortening to help you for now. We will create some posts on how do do each of these in the future.
• I am a huge fan of the Internet Book of Critical Care (IBCC) and the chapter on CHF can be found here. Overall the goal should be to optimize the patient’s position on the Frank Starling curve. Here we see that our patient is hypertensive and will likely tolerate significant blood pressure reduction. My go to agent is generally IV nitro, low dose nitro does not work well and will leave your patient uncomfortable for longer and possibly lead to unnecessary intubations. Generally in severe cases of CHF associated edema, I start with a 400 mcg bolus over 2 minutes followed by 100 mcg/min infusion titrating to effect. See more on this from EMcrit here.
• Nitro acts as both a pre-load and afterload reducer, however it is likely that in cases of reduced LV function or excessive atrial elastance nitro acts predominantly as an afterload reducer. (1)
• BiPAP is another key step in treating acute CHF and important in reducing intubations. It serves as additional preload and afterload reduction. A key thing to remember when using BiPAP to treat CHF is that you are trying to achieve and maintain a high MEAN airway pressure. This means that unlike normal BiPAP titration where ePAP may stay at 5 or only go up a small amount as you increase your iPAP. In cases of CHF, ePAP should be increased much more aggressively along with the iPAP. By increasing them together this will achieve a higher mean airway pressure, rather than having such a significant drop during the expiratory phase. If the patient is not tolerating BiPAP you can attempt CPAP somewhere between 5-15 to achieve the same mean airway pressure, however I typically find patients like BiPAP more than CPAP.
  
  (1) Haber, H. L., Simek, C. L., Bergin, J. D., Sadun, A., Gimple, L. W., Powers, E. R., & Feldman, M. D. (1993). Bolus intravenous nitroglycerin predominantly reduces afterload in patients with excessive arterial elastance. Journal of the American College of Cardiology, 22(1), 251–257. https://doi.org/10.1016/0735-1097(93)90841-N