A 52-year-old woman with a history of recurrent pulmonary emboli presents with jugular venous distention, ascites, and lower extremity edema. Laboratory studies reveal a mild transaminitis and an international normalized ratio of 1.3. She is referred for hemodynamic assessment.

The right ventricle (RV) has historically been ignored in the generalized assessment of cardiac function, with much of the attention being shifted to the left ventricle (LV) instead. The relative ease of imaging the LV and the known clinical consequences of LV dysfunction are likely reasons for the overshadowing of RV assessments; however, increasing recognition of RV importance in cardiac outcomes has refocused attention toward the “forgotten” ventricle.¹

Embryologically, the RV and LV do not share the same origin. Mammalian studies of cardiac development have shown that the precursor cells of RV development originate in the anterior heart field, which is separate in origin from the LV.² Morphologically, in the developed adult heart, the unique origins of the two ventricles lead to a combination of shared and separated fibers. Surface fibers of the heart are continuous between both ventricles; however, deep fibers appear to be distinct and run in different directions, thus affecting the mechanics of ventricular contraction.³ The LV contracts by the well-described “twisting” motion by shortening along the longitudinal and radial axes, but RV contraction is more complex. The RV free wall shortens along the radial access, and only the septum shortens longitudinally.⁴ Although the geometric motion of the septum can be visualized more as left ventricular, its contribution to RV contraction is significant (estimated between 20% and 80%).^4,5 This intricate interdependence between ventricles contributes to the complexity of assessing RV function.

The size and shape of the RV create difficulty in imaging the chamber, both for size estimation as well as functional assessment. Whereas the LV has a regular ellipsoid shape, the RV is semi-lunar and wraps itself around a portion of the RV. Two-dimensional imaging, such as standard echocardiography, is unable to capture the entire chamber in single or orthogonal views.⁶ Newer 3-dimensional echocardiography techniques have an improved ability to see the entire RV, but full resolution and assessment of function continue to be difficult and may be limited by the availability of technology capable of obtaining such images.⁷ Cardiac magnetic resonance imaging offers good resolution in evaluating the irregularly shaped RV⁸ but is often limited by the ability of a patient to undergo such imaging (eg, the presence of pacemakers or defibrillators). Given these challenges, noninvasive imaging is limited in its ability to assess RV function.

As an alternative to noninvasive imaging, hemodynamic assessments of the RV can be performed to better understand the function of the subpulmonic ventricle. This assessment is typically done with the insertion of a pulmonary artery catheter, a procedure often referred to as a right heart catheterization. A variety of techniques, approaches, and catheters can be used for a hemodynamic assessment, but it is most commonly done by using a Swan-Ganz catheter.^9-11 Obtaining central venous access allows passage of catheters into the right atrium via either the superior or inferior vena cava, through the tricuspid valve into the RV, and then out the RV outflow tract into the pulmonary artery (PA). Balloon-tipped catheters can then be advanced to obtain a PA occlusive pressure, also known as a pulmonary capillary wedge pressure (PCWP), which serves as surrogate for left atrial pressures. Careful attention should be paid to the measurement of the PCWP, which ideally is recorded at the end of normal expiration¹² (Figure 5-1). In addition to pressure measurements, cardiac output can be estimated by using either the Fick or thermodilution methods, described in detail elsewhere.¹³ Once these measurements and estimations are obtained, calculations can be made to better understand the performance of the RV.

Differences between the RV and LV extend beyond geometric shape. Although both ventricles have pre- and afterload sensitivity, the response to changes in these parameters are different for each. Figure 5-2 compares a typical pressure-volume loop of an RV to that of an LV and shows that each ventricle behaves uniquely during the cardiac cycle.¹⁴ Furthermore, the RV has been shown to be more sensitive to afterload changes than the LV.¹⁵ Likewise, the RV is also more responsive to preload changes than the LV, resulting in a greater increase in stroke work for the same amount of preload increase.¹⁶ True RV performance should be measured under a variety of loading conditions to create a family of pressure-volume loops.¹⁷ From these loops, the load-independent measure of end-systolic elastance can be calculated (Figure 5-3).⁴ In clinical practice, such measurements and calculations are not routinely performed due to the need for specialized equipment. Consequently, alternative forms of RV assessment from more readily obtained measurements have been explored.