RV Function

The RV remains very tricky to measure and study. Anyone who argues otherwise is either lying or should teach the rest of us and earn their Nobel Prize. Just look at the shape of the thing - the RV looks abnormal even when normal. And it possesses many different abnormal phenotypes.

TAPSE (Tricuspid Annular Plane of Systolic Excursion)

Step 1

Try to isolate the RV free wall so that the lateral annulus is moving toward the probe. This example is actually slightly tangential (free wall is moving straight up rather than up and medial). It might require rocking the probe more medially.

Step 2

M-mode through the lateral annulus. Measure between trough and peak at the same line - there may be many lines that appear stacked ontop of each other. Decrease gain to minimize noise. NEED to corroborate with S' (below).

Abnormal is < 1.6cm.

TAPSE is everyone's favorite because it's simple. But there are a few caveats. It does not have the best correlation with RV ejection fraction or stroke volume. The tricuspid annulus is also anchored against the myocardial skeleton and so it's quite affected by LV function. RV dysfunction in the setting of LV hyperdynamic function, in the example of acute PE, can cause a spuriously normal TAPSE. Contrarily, a severely reduced LV function with severely reduced MAPSE will cause the TAPSE to measure low. This may be why TAPSE measurements demonstrate the most change with inotropic therapies: because of the effect on LV rather than RV-specific effects.

RV S' (Systolic Excursion Velocity) and Myocardial Performance Index

Step 1

Same as for TAPSE but now use pulse wave tissue doppler over lateral tricuspid annulus. Angle is super important, yet again.

Step 2

Pulse wave tissue doppler through the annulus.

Abnormal S' is < 10cm/s.

Abnormal MPI (TCO - ET)/ET is > 0.55. Only valid if rhythm is regular.

RV Systolic Pressure

TR Concept

Pressure Gradient = 4 * TRVmax²

Pressure Gradient = RVSP - RAP

RVSP = 4 * TRVmax² + RAP

Step 1

Continuous wave doppler through the maximal TR jet. Sometimes it is eccentric so you may need other views (A4, PSS, RV inflow views, Subcostal) to catch it maximally.

Step 2

Trace the TR Vmax. May need to shift baseline up.

Assuming an RAP of 15 (by exam or IVC) then

RVSP = 4*4² + 15 = 64 + 15 = 79mmHg

RVSP is considered the same as sPAP if there is no pulmonic stenosis. PA pressures can change quite dramatically minute to minute. Also, PA systolic pressure are not synonymous with PA mean pressures and thus does not necessarily indicate elevated PVR. Similarly, interventions that lead to decreased PVR may not decrease the RV systolic pressures because they may be increasing the cardiac output primarily without decreasing the pressures. Hence, monitoring RVSP is not per se the best way to track pulmonary vasoreactivity to pulmonary vasodilators.

PA Mean Pressure

TR Concept

mean Pressure Gradient = 4 * TRmean²

mean Pressure Gradient ≈ mRVP - RAP

mRVP ≈ mPAP (if no pulmonic valve disease)

mPAP ≈ 4 * TRmean² + RAP

Step 1

Same thing as above

Step 2

This time trace the velocity time integral rather than the Vmax to get the Vmean.

Assuming an RAP of 15 (by exam or IVC) then

RVSP = 4*2.1² + 15 = 18 + 15 = 33mmHg

PR Concept

Pressure Gradient = 4 * PRVmax²

Pressure Gradient = mPAP - mRVEP

mRVEP ≈ RAP (if no tricuspid stenosis)

mPAP = 4 * PRVmax² + RAP

Step 1

Continuous wave doppler through maximal pulmonary regurg jet.

Step 2

Assuming a RAP (and thus RV EDP) of 15 then

mPAP = 4*2² + 15 = 16 + 15 = 31mmHg

RVOT Concept

Higher pulmonary vasculature elastance (high PVR) reflects the pressure wave backward faster. This reduces the acceleration time in the PA and correlates to higher mean PA pressures. Normal should look like a symmetric upside-down dome with a PAAT > 130ms. Abnormal is < 100ms.

Step 1

Pulse wave doppler through the RVOT.

mPAP ≈ 90 - 0.6 * PAAT

if hr < 60 or > 100 then need to index

PAATi = PAAT * 75 / HR

Step 2

Midsystolic notching also portends high mPAP.

mPAP = 90 - 0.6 * 90 = 36mmHg

Some have proposed that proximal artery obstruction (like PE) may cause disproportionate decrease in PAAT compared to the expected rise in mPAP. Consequently, they propose that PAAT < 60ms with RVSP < 60mmHg is suggestive of submassive or massive PE - I need to see more data on this.

PA Diastolic Pressure

PR Concept

Pressure Gradient = 4 * PRVed²

Pressure Gradient = dPAP - RVEDP

RVEDP ≈ RAP (if no tricuspid stenosis)

dPAP = 4 * PRVed² + RAP

Step 1

Continuous wave doppler through maximal pulmonary regurg jet.

Step 2

Assuming a RAP (and thus RV EDP) of 15 then

dPAP = 4*1² + 15 = 4 + 15 = 19mmHg

Dimensions

Acute RV Failure

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