#1: What are the abnormalities of the right ventricle?
#2: Name the differential diagnosis for each of the abnormalities.
#3: Does this patient have diastolic dysfunction causing one of the abnormalities?
#4: What is the most likely cause of the major abnormality?
Explanation: The abnormalities in this loop is right ventricular enlargement (RVE) and a moderator band. The moderator band is normal but is sometimes confused with a turmor, thrombus, or artifact. A moderator band is a pitfall that can be overread and misinterpreted.
The right ventricular enlargement, in this case is more interesting. The differential diagnosis for right ventricular enlargement fall into three main categories: increased afterload, increased preload, and decreased contractility. The RV is not a pressure pump, per se, but can hypertrophy in the presence of longstanding afterload conditions. Acute increases in afterload will lead to RV dilation and decreased wall motion. Chronic increased afterload leads to RV hypertrophy and normal wall motion until the afterload is so high that the RV cannot compensate and cause it to dilate and become hypokinetic. High afterload would stent the interventricular septum (IVS) (D shaped IVS) or cause it to bow towards the LV during systole as the RVSP increases.
Increased preload from chronic volume overload (ESRD, TR, PR) or a left to right shunt (ASD) would lead to RV enlargement with normal wall motion until pulmonary hypertension occurred. Then a mixed pattern would occur. ASD and TR would cause RAE as would volume overload from ESRD. The IVS would deviate towards the LV during diastole if the RVEDP exceeded the LVEDP.
In decreased contractility, the wall motion would be decreased from a RV ischemia/infarction.
A patient with diastolic dysfunction where it affects the right ventricle, causing it to dilate, would first cause left atrial dilation. Since the left atrium is not dilated, it is very unlikely that diastolic dysfunction is the underlying condition.
In this video, the IVS appears to not deviate during systole or diastole so the RVSP must be higher than normal, otherwise the normal motion for an IVS is to deviate slightly towards the RV. The wall motion of the RV is normal so contractility is normal and the pulmonary artery pressures are not so high that the RV function is affected. Since the left side of the heart appears normal - this is probably a process that is right sided only. Severe PR would cause the TV to close earlier in the diastolic period than the MV which is not the case. We suspect that there is moderate pumonary hypertension from pulmonary causes and other findings will be trivial.
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