RV enlargement in arrest, and how it’s not always a PE

RV enlargement in arrest, and how it's not always a PE

While preparing for a recent grand rounds lecture, I uncovered something rather interesting: The fact that the RV can enlarge during cardiac arrest independently of the presence of a pulmonary embolism. It turns out that the data showing RV enlargement as a marker of a pulmonary embolism is actually mostly extrapolated from alive patients (in which it has been shown to be a pretty good marker of submassive and massive PE).  There is very minimal data on RV enlargement in arrest in humans, but there are some animal studies that suggest that the RV enlarges in many causes of arrest, including hypoxia and arrhythmias.  
Check out the podcast, and the summary of the literature on the PDF below:


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  1. Ash Mukherjee : August 28, 2019 at 6:28 am

    Interesting that I have been scanning for 15 years and I don’t think I’d say I see RV dilatation very commonly in Cardiac arrests.
    I feel with no evidence to back me, that in prolonged arrests, there is likely RV dilatation (not sure you can use the word strain in an arrest). Maybe because the pulmonary circulation which is capacitance type of circulation and it gets congested along with as one mentioned the high Pressures from ventilation.
    I have never felt RV dilatation on its own in CA warranted thrombolysis but if the clinical context suggests a decent probability, RV dilatation becomes a data point helping in the DX.

  2. Domagoj Damjanovic : August 29, 2019 at 7:11 am

    Jacob, Mike, thank you for highlighting this. When talking resuscitation ultrasound, the evaluation of reversible causes is oftentimes reduced to simple concepts (not bad in itself), and RV dilation stands for (high likelihood of) PE. The data you are discussion simply help avoid oversimplification and traps, which is great!
    Can also add current data from clinical TEE study by Felipe Teran @FTeranMD and colleagues: https://www.ncbi.nlm.nih.gov/pubmed/30779977. They found RV dilation in 57% of the intra-arrest patients. The manuscript has a detailed discussion on this.
    And not to forget, a non-dilated RV on echo still helps in ruling out a PE as THE current underlying cause of the arrest, in case there was some cliinical suspicion, from history e.g. As with a pneumothorax, this has as a value in itself, no? While we often claim that the role of PoCUS is mainly rule in, not rule out, in arrest this is different. Supports the view, that resuscitation ultrasound is a thing of its own and needs specific considerations along intra-arrest physiology, which is not simply the end of a continuum from peri-arrest. Cheers, Do

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