The RV contracts by three separate mechanisms, the first of which is an inward movement of the free wall followed by contraction of deeper longitudinal muscle fibers that draw the tricuspid annulus toward the apex and finally traction of the free wall from LV contraction generating a forward stroke volume. Normal baseline RV ejection fraction (RVEF) ranges from 40 to 76% and varies based on loading conditions [7].

RV function, like the LV, is affected by preload, afterload, and contractility. This complex relationship is best illustrated by differences in pressure-volume curves. The RV pressure-volume loop is more triangular in shape with the pulmonary valve opening early in systole once RV pressure reaches the low pulmonary pressure. As there is very little time spent in isovolumetric contraction, the loop assumes a triangular configuration in contrast to a square LV loop. This also hints to the fact that the RV performs primarily volume work [11] (Fig. 3.2).

The slope of the end-systolic pressure-volume relationship is called ventricular elastance and is a relatively load-independent measure of ventricular contractility. Dell’Italia demonstrated that the normal maximal RV elastance was 1.3 ± 0.84 mmHg/mL, four times lower than the LV. Consequently, the RV is more afterload sensitive than the LV [12]. This is demonstrated in the acute setting (i.e., massive pulmonary embolism), where RV stroke volume decreases significantly with sudden increase in pulmonary artery pressure.

Similar to the LV, in a normal RV, based on the Frank-Starling principle, an increase in preload improves contraction. However, in RV failure, the curves flatten and move down and to the right depict a drop in RV output with increase in preload (Fig. 3.3).

The pericardium encases both ventricles and under normal circumstances provides an important protective barrier from overdistention and direct pathogen invasion. In addition, it also imparts a diastolic interdependence effect on both ventricles [13, 14]. Bernheim first hypothesized the importance of the interventricular relationship [15]. Henderson and Prince later demonstrated that volume and pressure loading of one ventricle decreased the output of the other [16]. This was clinically demonstrated in 1956 by Dexter as deterioration of LV function in patients with atrial septal defects who developed RV pressure and volume overload, a phenomenon called “reverse Bernheim effect” in which he postulated that the leftward septal shift resulted in impaired LV filling [17] (Fig. 3.4).

Multiple methods have been used to measure RV function clinically. Cardiac MRI is the most accurate tool to assess RV diastolic and systolic volumes as well as the RVEF [7]. By MRI, RVEF ranges 47–76%. A technique not used frequently is radionuclide angiography by which RVEF is usually 40–45%. Echo is least accurate in assessing RVEF but the most clinically used. Two-dimensional echo assessment by Simpson’s rule can be used and correlates well with MRI; however, this is dependent on the quality of the images. RV fractional change area can be measured in four-chamber views and easily incorporated into most echo reports. Tricuspid annular plane systolic excursion (TAPSE) is another useful quantitative measurement of RV systolic performance [18, 19]. RV myocardial performance index, a ratio of isovolumic time interval to ventricular ejection time, doesn’t involve ventricular geometry and is a load-independent measure of RV function. Finally, tissue Doppler imaging also allows for quantitative RV assessment. Finally, myocardial strain and speckle-tracking analysis can also be used to define RV function [20, 21] (Table 3.2).

Invasive hemodynamic assessment is the gold standard to assess RV function and can often tease out acute RVF from chronic RV dysfunction. Direct measurement of RA, RV, and PA pressures can clarify inconclusive noninvasive data. RV stroke work index (RVSWI) , pulmonary artery pulsatility index (PAPi) , and a RA to pulmonary capillary wedge pressure ratio have all been used to measure RV function [22] and predict RV failure post-LVAD implantation. At the Texas Heart Institute, we routinely use noninvasive parameters including TAPSE, tissue Doppler imaging (TDI) , PAPi, and RA/PCWP ratio to aid in clinical decision-making (Table 3.3).

The definition of RVF remains nebulous due to the use of inconsistent criteria in different publications. Some authors have described RVF as a need for intravenous inotrope or pulmonary vasodilator therapy for 14 days postoperatively and/or need for RVAD, while others defined it as simply a requirement for RVAD. Others still have used two or more of the following hemodynamic parameters to define RVF: central venous pressure greater than 16 mmHg, mean arterial pressure lower than 55 mmHg, cardiac index less than 2.0 L/min/m², inotrope support >20 units, and mixed venous saturation lower than 55%, all in the absence of cardiac tamponade [23–28].

According to the INTERMACS registry , RVF is present if symptoms or findings characterized by both elevation of central venous pressure (right atrial pressure > 16 mmHg on right heart catheterization, significantly dilated inferior vena cava with no inspiratory variation on echocardiography, and elevated jugular venous pressure) and manifestations of elevated CVP (peripheral edema, ascites, or hepatomegaly on exam or diagnostic imaging and laboratory evidence of worsening hepatic total bilirubin >2.0 mg/dL and renal dysfunction creatinine >2.0 mg/dL) are present [29] as illustrated in Table 3.4.

RV failure results from a number of reasons and similar to the LV can be both systolic and diastolic in nature. While the RV can accommodate increased preload, it is sensitive to increased afterload and elevations in PA pressures [29, 30]. As PA pressures increase due to worsening left-sided function, there is delayed pulmonary valve opening, leading to increased RV work and O₂ consumption. Moreover, this leads to progressive RV dilation, wall stress, and impaired coronary perfusion pressure. As the dilation progresses, geometry changes lead to tricuspid annular dilation and functional tricuspid regurgitation due to non-coaptation of leaflets. Abnormal septal activation also disrupts normal IVS function [29, 30]. Over time, if the heart failure remains untreated, cardiomyocyte stress and hypertrophy lead to irreversible apoptosis [29].

RV infarction due to obstructive coronary disease is another mechanism, which can lead to RVF although the incidence of RV infarct post-MI is low and is usually due to an isolated inferior wall MI. The likely reason for the lower incidence of ischemic RV failure compared to ischemic LV failure is probably lower RV wall stress and stroke work in addition to smaller mass requiring lower resting coronary flow and O₂ extraction [31].

RV failure after LVAD implantation results from a complex sequence of events in the setting of underlying risk factors. Multiple mechanisms have been suggested. LV decompression and increased cardiac output increase venous return to the RV. Intraoperative volume resuscitation including blood transfusions also contributes to this increase in RV preload and can aggravate a decompensated RV [32]. Abnormal interventricular septum (IVS) geometry due to excessive leftward shift at high LVAD speeds can also worsen RV function due to loss of IVS contribution to RV output [33].

Ischemic injury is another mechanism seen after prolonged bypass times, coronary ischemia, and/or loss of coronary bypass grafts or coronary embolism. Between 30 and 64% of patients with advanced HF will have associated tricuspid regurgitation, which improves after LV decompression with a LVAD [34, 35]. However, a dilated tricuspid annulus or an incompetent valve generally worsens TR after LV decompression and increased preload. Severe TR further contributes to RV failure through the development of right-sided volume overload and reduced RV ejection. Although pulmonary artery pressures improve after LV decompression, perioperative ischemia-related pulmonary endothelial injury and transfusion-related lung injury often conversely increase pulmonary vascular resistance and can result in RV failure.

Supraventricular arrhythmias are seen in more than 20% of patients after LVAD implantation and have been associated with twice the risk of RV failure [36]. More sinister rhythms like ventricular fibrillation have been associated with a 32% drop in cardiac output. Incessant postoperative VT can therefore adversely affect RV function in LVAD patients and should be avoided as far as possible [37].

Over the last three decades, many centers have worked to develop algorithms and risk scores to predict RVF after LVAD implantation . Early identification of high-risk patients remains important as it allows for the formulation of strategies to avoid RV failure. Unfortunately, most risk scores devised from retrospective, small single-center experiences provide a variable spectrum of predictors including hemodynamic, echocardiographic, biochemical, and intra- and postoperative parameters with no single model dependably forecasting RVF. Many early studies incorporated pulsatile devices in BTT cohorts and therefore did not accurately reflect outcomes in the current CF-VAD era. In addition, validation of many of these scores has demonstrated the modest real-world application [38]. In our center, we have noted that a preoperative, systemic inflammatory syndrome associated with a leukocytosis and thrombocytopenia may prime the RV for failure.