We talk the nitty-gritty of assessing the right heart using echocardiography, with our friend Matt Siuba (@msiuba), intensivist at the Cleveland Clinic and master of zentensivism. Learn more at the Intensive Care Academy! Find us on Patreon here! Buy your merch here! Takeaway lessons * RV echo starts with evaluating three things: size, squeeze, and septal kinetics. * Size should be 2/3 the LV * Squeeze can be assessed in a variety of ways * The septum should not be bowing into the LV. * Dilation is an early and somewhat compensatory finding, and can be used as a screening test (the “D-dimer of RV dysfunction”). Septal changes are probably later and more of a sign of dysfunction (i.e. not compensatory). * Evaluating the RV’s ejection fraction is impractical due to its complex shape (without 3D echo or cardiac MRI or other advanced tools). So methods like TAPSE that reduce it to its longitudinal function become a more practical surrogate. * TAPSE is not an isolated marker of RV contractility, but a marker of the overall RV-PA unit. However, this is probably a feature, not a failure. You don’t really want to know how the RV is contracting in the abstract, but how it’s contracting in its current loading conditions. So TAPSE will vary by afterload and preload, but not artifactually—i.e. if the loading conditions change and TAPSE improves, then contractility is better in the current conditions. * s’ is similar to TAPSE, and similarly limited (mainly evaluating longitudinal function). It assesses velocity, not movement, which theoretically may represent something different (maybe a better marker of function?), although that difference is not very well studied; some studies do suggest that s’ may be more sensitive to changes after adding an inotrope, but who knows if that means anything. The most common cause for a big discrepancy between TAPSE and s’ is probably technical error, not a clinical distinction. * RVSP can be useful as a marker of afterload, but says nothing about the cause of RVSP—high left sided pressures vs high PVR—and also incorporates the RV function, so separating all this out can be difficult. * TAPSE/PASP (or TAPSE/RVSP) ratio might be a somewhat more accurate marker of RV/PA coupling, but not really clear if it’s clinically better than using the TAPSE alone, which is already a fair marker of RV/PA coupling. By measuring more things, it also introduces more room for technical error (usually underestimating RVSP), such as the need to estimate the TV gradient and the CVP. More tricuspid regurgitation will also tend to reduce the ratio, without necessarily indicating better RV function. * CVP estimates derived from the IVC are very unreliable in the critically ill. Many chronic PH patients have chronically distended IVCs regardless of their RAP. Using a transduced CVP is probably better. You can also just trend the TV gradient as a marker of its own and ignore the CVP component. * Shortening of the PA acceleration time (PAAT or PVAT) is a useful marker of pulmonary afterload. Notching of the waveform usually indicates a very high afterload, much more likely to be caused by pulmonary factors than high left heart pressures.