Tricuspid Regurgitation

For sportscar connaisseurs, the iconic Ferrari 512TR

Today we discussed tricuspid regurgitation at physical exam rounds. Some points:

There are generally 2 classes of TR: 1) High pressure, usually secondary to L-heart disease (high RVSP), and 2) low pressure, usually from bacterial endocarditis.

In general, only the high pressure variety is detectable on physical exam because a significant pressure gradient between the RV and RA is required to generate the findings listed below.

The JVP:
-Elevated JVP: Seen in 90% of patients. Its absence strongly argues against high pressure TR
-CV waves: a systolic impulse of the neck veins is seen in about 50-80% of patients. You normally expect to see a descent in the JVP (the X' descent) during early systole (i.e. during and right after S1). If you do not see a descent, the patient probably has a CV wave.

Precordial palpation:
-If the RV is dilated, it may occupy the space where the LV normally lies (i.e. the apex). In this situation, you may see and palpate a systolic retraction of the apex with an outward movement of the L or R lower sternal borders (where the dilated RA lies), which is described as a "rocking" motion

Murmur:
-The murmur of TR is holosystolic. In 75% of patients, it becomes louder with inspiration (called Carvallo's sign). It is usually loudest at the L lower sternal border, but if the RV is dilated enough may be loudest at the apex. The LR+ for a typical murmur is 14.6. However, the lack of a typical murmur does not rule out TR (negative LR 0.8 for mild, 0.4 for severe).

Other:
-Pulsatile liver may be palpated (wide range of sensitivities reported). It is not 100% specific for TR (constrictive pericarditis and hepatic AVMs may also cause it), but by far the most common cause. Its presence argues that the TR is moderate to severe.
-Edema, ascites: 90% of patients have edema or ascites (or both)

Reference:

There is no JAMA RCE specifically for TR; most of above is taken from
Evidence-Based Physical Diagnosis (McKee)