Defined as a failure of the right ventricle (RV) to maintain adequate flow through the pulmonary circulation to allow adequate LV filling, right ventricular failure remains a significant and vexing problem after cardiac transplantation and a source of major morbidity and mortality in the perioperative period [34]. Severe RV failure is defined by ballooning of the RV with corresponding end-organ dysfunction or the need for mechanical circulatory support with a right ventricular assist device (RVAD) [35].

The most common risk factor for RV failure following OHT is ischemia-reperfusion injury, which is caused by the process of organ procurement, cold ischemic transport, and implantation/reperfusion. Other risk factors include mechanical trauma during transport and implantation, warm ischemia in the operating room, coronary air embolus, and any extrinsic factor that would raise pulmonary vascular resistance, such as mechanical ventilation with high PEEP and acute and/or chronic recipient pulmonary hypertension [35]. Common causes of posttransplant RV failure are summarized in ◘ Fig. 30.2.

The complicated geometry of the RV makes it difficult to measure its function directly. Jugular venous distention, peripheral edema, a split second heart sound, and a tricuspid regurgitation murmur are clinical data suggestive of elevated right-sided filling pressures, especially in the absence of left-sided dysfunction. A number of echocardiographic adjuncts, such as RV size, tricuspid annular plane systolic excursion (longitudinal displacement of the RV base relative to the RV apex), and estimated RV systolic pressure, are helpful in the diagnosis of RV failure, although each of these can be affected by factors extrinsic to RV function [34]. Pulmonary artery (PA) catheters are routinely left in place following OHT and data such as central venous pressure (CVP) and PA pressure are crucial in making this diagnosis.

Elements of the management of RV failure can be grouped into those modifying preload, afterload, and the intrinsic contractility of the ventricle (◘ Fig. 30.3). The RV is a thin-walled and highly compliant chamber that responds poorly to acute increases in preload. Acute distention of the RV can induce a level of wall tension beyond which it is unable to pump effectively. Furthermore, ventricular interdependence, a phenomenon in which massive RV distention can cause the ventricular septum, which forms the posterior wall of the RV, to invert its curvature and impede LV filling. Poor LV filling has a negative impact on its function, which can exacerbate right heart failure. Conversely, inadequate filling of the RV, most commonly caused by systemic hypovolemia, can also impair RV output [36]. The great sensitivity of the RV to fluid overload mandates careful management of volume status in these patients, often with the aggressive use of diuretics and, in some cases, hemofiltration [34, 36].

Decreased contractility in RV failure is considered to be due either to impaired inotropy or impaired myocardial perfusion. Impaired inotropy can be due to myocardial stunning from ischemia-reperfusion injury, mechanical trauma, and donor or recipient sepsis [35, 36]. Perfusion to the myocardium of the right ventricle can be compromised by impaired inflow to the right coronary system, which can be caused by air embolism or thromboembolism of the right coronary artery (RCA), kinking of the RCA due to extrinsic compression or problems with allograft positioning at implantation, and impaired global coronary perfusion due to LV dysfunction. Impaired RV contractility is managed primarily with inotropes, such as dobutamine, milrinone, and isoproterenol. Isoproterenol is customarily used for several days after OHT for its positive chronotropic effects, although there are no prospective studies comparing its effectiveness in this regard to other inotropes [37, 38].

Right ventricular afterload is dictated by the pulmonic valve and the resistance of the pulmonary vascular bed. Pulmonary vasoconstriction, which can elevate pulmonary vascular resistance (PVR) can be caused by hypoxia, hypercarbia , acidosis, massive transfusion, and protamine administration, all of which can be common at the time of OHT [36]. Extrinsic compression or other compromise of pulmonary inflow caused by pneumothorax, massive pleural effusion, pulmonary embolus, and elevated intrathoracic pressures caused by positive-pressure ventilation with high PEEP can also increase PVR [36]. Complications associated with the PA anastomosis, such as narrowing or kinking, can create a fixed mechanical impediment to RV unloading and must be, along with the other factors listed above, avoided or corrected at the time of implantation.

Recipient pulmonary hypertension (PH), defined as invasively measured mean pulmonary artery pressure ≥25 mmHg, is associated with high morbidity and mortality in the acute postoperative period after OHT [35]. Chronic elevation of left-sided filling pressures resulting from LV systolic dysfunction is the most common cause of pulmonary hypertension in OHT recipients [39]. Other common causes of pulmonary hypertension include chronic hypoxia (e.g., COPD, sleep apnea, and developmental/interstitial lung disease), chronic pulmonary thromboembolic disease, and secondary effects of many systemic illnesses, such as chronic kidney disease, sarcoidosis, and hemolytic anemias. Pulmonary arterial hypertension, which can be idiopathic or associated with other comorbid conditions such as scleroderma or portal hypertension, is rare in OHT recipients.

Parameters such as transpulmonary gradient (TPG, mean PA pressure-mean pulmonary capillary wedge pressure, mmHg) and pulmonary vascular resistance (PVR, , ), which is frequently described in Wood units (), are generally obtained with the use of a PA catheter and are useful in characterizing the severity of pulmonary hypertension [40]. At the time of measurement, patients are treated with short-acting pulmonary vasodilators to determine the reversibility of their PH. Nonreversible PH is predictive of early and late mortality after OHT because of the attendant risk of RV failure. It is generally agreed upon that a resting PVR > 5 Wood units is a contraindication to OHT, although, while mortality in this setting is strongly linked to increasing severity of PH, no threshold level of PVR is absolutely predictive of RV failure [40, 41]. Patients with PH in whom PVR can be reduced to ≤2–3 Wood units with the use of inhaled or intravenous pulmonary vasodilators prior to OHT demonstrate a mortality risk essentially equivalent to heart recipients without preexisting PH [42–45]. There may, however, be an elevated risk of post-op RV failure, and patients who have residual PH after transplant may have decreased long-term survival [42, 43].

Implantable long-term left ventricular assist device (LVAD) therapy has been used to ameliorate fixed pulmonary hypertension in patients with end-stage heart failure being considered for OHT [46–48]. Maximum benefit appears to be reached by 6 months of therapy, with decreases in TPG and PVR predicting the greatest mortality benefit after OHT compared to patients who did not receive pretransplant MCS [46, 47].

Postimplantation RV failure is commonly recognized in the operating room based on the presence of a distended and hypokinetic RV, underfilling of the LV , and/or elevated PA pressures; these can be detected by transesophageal echocardiography, direct visualization, and data from the PA catheter [49]. A low threshold should be held for the initiation of pulmonary vasodilator therapy, either with the use of either inhaled nitric oxide or prostacyclin, which are equally efficacious in this setting [50]. Both of these medications require gradual weaning because of the potential for rebound PH with rapid withdrawal of therapy. Sildenafil, commonly started either before or in the days following transplant, is also effective in combating recipient PH [51]. Slow (days to weeks) weaning of inotropic medications such as milrinone and/or dobutamine and efforts to minimize PEEP in the postoperative period can also be important adjuncts following transplantation in patients with pulmonary hypertension and/or any evidence of RV failure [36].

Frequently, mechanical circulatory support (MCS) is required in the management of posttransplant RV failure that is refractory to maximal medical therapy. IABP can be useful in the setting, with one series demonstrating near-immediate improvement in systemic and right-sided hemodynamics following IABP insertion with durable response and pump removal after an average of ~44 h of therapy [52]. More severe cases of posttransplant RV failure have required the use of right ventricular assist devices (RVADs) or biventricular assist devices (BiVADs).

Multiple case reports and series from the late 1980s through 2000 report the use of extracorporeal RVAD support immediately following OHT in a total of 20 patients [53–59]. The most common indication for MCS in this aggregate cohort was recipient pulmonary hypertension. Outcomes in these studies were almost universally poor; only three studies reported a total of four patients who survived to discharge [53–55]. Of the patients that died, nine were able to be weaned from RVAD support (56 %) before death. The most common causes of death among all non-survivors were sepsis, multisystem organ failure, and hemorrhagic complications [53, 54, 56–59].

In 2003 Kavarana et al. described a series of 20 heart recipients who received postoperative MCS , of whom 14 required either RVAD or BiVADs. Consistent with prior studies, the most common indication for support was recipient pulmonary hypertension. Of all RVAD/BiVAD recipients in this study, only six (43 %) could be weaned from support, and two of those patients went on to die of multisystem organ failure. Of those who did not wean, the most common causes of death were intraoperative arrest, refractory heart failure, and sepsis [9]. More recently, Klima et al. reported in 2005 a series of 35 patients who met criteria for severe RV failure following OHT and 15 of these patients received some combination of RVAD, ECMO, and IABP; no mortality benefit was realized from the use of MCS in this cohort [35].

Overall, the need for MCS for RV failure following heart transplantation portends extremely high mortality. Although recovery to discharge is possible, including after as long as 80 days of RVAD therapy in one case report, the incidence of fatal complications is extremely high in this cohort, and a frank and thoughtful discussion should occur between all involved providers and loved ones before this level of support is initiated [60].