13.3 RV and RA Size, Pressure, Volume, and Function

Build a right-heart dataset from several views

The crescent-shaped RV wraps around the LV, so no single 2-D dimension represents its inflow, body, and outflow. Acquire parasternal long- and short-axis, RV inflow, RV-focused apical four-chamber, and subcostal views. From a conventional apical view, move laterally and rotate until the RV basal diameter is maximal, the entire free wall and apex are visible, and the LV outflow tract and coronary sinus do not falsely enter the plane. A foreshortened or oblique image can enlarge one segment while truncating another. Use 3-D RV volumes when a complete dataset with adequate temporal and spatial resolution is feasible.

Measure RV basal and mid-cavity diameters at end-diastole from the RV-focused view; measure longitudinal length from annular plane to apex. Current adult reference limits are basal diameter less than 4.1 cm, mid diameter less than 3.5 cm, and length less than 8.2 cm. Index 3-D volumes to BSA; current upper normal values are approximately 90 mL/m² for RV EDVi and 41 mL/m² for RV ESVi. Apply laboratory, sex-, age-, and method-specific references rather than mixing historical 2-D and current 3-D thresholds. RV wall thickness less than 0.5 cm is normal when measured at end-diastole from a focused subcostal or parasternal plane without including epicardial fat or trabeculation.

Acquire an RA-focused apical view by tilting superiorly and medially from the RV-focused view until the entire chamber is longest and the RA walls are not foreshortened. Measure area and volume at ventricular end-systole, just before tricuspid opening, excluding the IVC, SVC, and appendage. Current normal reference limits are RA area less than 19 cm² and disk-summation RAVI less than 30 mL/m². Linear diameter is less representative than volume. Rhythm, TR, athletic remodeling, congenital shunts, and chronic pressure or volume load affect RA size; size alone does not determine RA pressure.

Integrate complementary RV systolic measures

For FAC, trace the endocardial boundary from the lateral annulus around the free wall and apex to the septal annulus at both phases; include trabeculations and moderator band within the cavity. Do not combine a foreshortened end-diastolic frame with a different end-systolic plane. TAPSE and S′ are useful reproducible surrogates but may remain normal despite regional or nonlongitudinal dysfunction, or be reduced after cardiac surgery, pericardial disease, pacing leads, or altered translation despite a less abnormal global RVEF. Integrate FAC, 3-D RVEF, strain, visual free-wall motion, and hemodynamics. One normal metric cannot veto several valid abnormal ones.

Separate pressure overload from volume overload

Inspect septal shape in parasternal short axis. LV eccentricity index greater than 1 at end-diastole supports RV volume overload, while systolic flattening supports pressure overload; flattening in both phases suggests pressure overload with or without added volume load. Significant TR, PR, ASD, or anomalous venous return commonly produces volume loading. Pulmonary vascular disease, left-heart disease, hypoxic lung disease, RV outflow obstruction, and acute pulmonary embolic physiology can produce pressure loading. Chronic pressure load may increase RV wall thickness; acute pressure load can cause marked dilation and dysfunction without hypertrophy. Septal timing supports physiology but is not a standalone cause or pressure number.

Estimate RV systolic pressure only from a complete, dense, well-aligned TR CW envelope. Search apical, parasternal, and subcostal windows and use the highest reproducible velocity without angle correction. The equation is RVSP = 4(TR peak velocity)² + estimated RAP. In the absence of pulmonic or RVOT obstruction, RVSP approximates pulmonary artery systolic pressure. With obstruction, it describes RV pressure and must not be labeled PASP. Poor alignment, incomplete envelope, severe free TR with early pressure equalization, and uncertain RAP may underestimate or destabilize the estimate. State when RVSP cannot be calculated rather than tracing noise.

Estimate RAP from IVC diameter 0.5–3 cm from the RA junction at end-expiration and its inspiratory or sniff response in spontaneously breathing adults. An IVC 2.1 cm or smaller with at least 50% collapse supports 3 mm Hg; an IVC larger than 2.1 cm with less than 50% collapse supports 15 mm Hg. Discordant patterns are commonly assigned 8 mm Hg and refined with secondary signs such as hepatic-vein flow and RA findings. Positive-pressure ventilation, poor effort, elevated intra-abdominal pressure, athletic adaptation, and fluid shifts make standard collapse rules unreliable. Never choose RAP solely to make RVSP agree with expectation.

Reconcile size, pressure, volume, and loading

Record respiration, oxygen or ventilator state, blood pressure, rhythm, body size, and recent volume-changing treatment. TR severity can enlarge the RV and invalidate a simple pressure interpretation; afterload reduction can improve function measures without reversing chronic remodeling. Compare serial studies using the same RV-focused plane, beat selection, tracing convention, software, and reference set. Report RV and RA indexed size, hypertrophy, septal pattern, multiple systolic measures, TR-derived pressure with its assumptions, IVC/RAP confidence, and associated valve or shunt lesions. When echo metrics remain discordant, reacquire before attributing physiology; high-quality 3-D echo, CMR, CT, or invasive hemodynamics may answer the unresolved clinical question.

Do not let TAPSE stand alone

TAPSE samples basal longitudinal annular motion and is affected by angle, loading, translation, surgery, pericardial constraint, and pacing. Reconcile it with FAC, 3-D RVEF or strain when available, visual motion, RV size, and hemodynamics.