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Cardiac US

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LV dysfunction

RV DYSFUNCTION

The main acute compensatory response of the RV to volume or pressure overload is dilatation (base > 42mm, length >89mm and RVOT (PLAx) >3.3mm). As the RV dilates, it also lengthens. Eventually, the apex of the heart is formed by the RV rather than the LV. Chronic pressure overload also leads to RV hypertrophy (wall >6mm).

A4c: pulmonary HT: dilated RV and RA, septal bowing to the LV, RV forms the apex of the heart

RV VOLUME OVERLOAD

RV volume overload shifts the IV septum towards the LV in diastole, creating a D shaped LV in diastole. Usually the RV free wall remains thin.

RV PRESSURE OVERLOAD

RV pressure overload the IV septum bulges to the left in systole, creating a D shaped LV in systole.

RV hypertrophy in chronic pressure overload leads to a thick, trabeculated free wall (≥ 6mm), with a thick moderator band. 

Dilated and hypertrophied RV in PSAx - suggesting chronic changes ( Note the imaging is slightly off axis leading to exaggeration of the D shaped LV)

In comparison, acute RV pressure overload has a dilated overbearing RV, D shaped LV, but the RV free wall is thin and the moderator band is not prominent

Dilated and hypertrophied RV in PLAx

Hypertrophic RV seen in subxyphoid (soomed in to measure the free wall). >6mm in diastole is hypertrophied. 

DILATED RV (emergency causes)

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Pulmonary Embolus