Hyperacute rejection, though now rare, is mediated by preformed antibodies to the allograft in the recipient. It typically presents following surgical engraftment and restoration of native circulation as an almost immediate, aggressive and potentially lethal immune attack on the organ mediated by preformed antibodies to predominantly HLA antigens. This phenomenon is covered in more detail in Chap. 12. The development of the modern prospective cytotoxic crossmatch, and subsequently the virtual cross-match (mentioned in Chap. 6) has greatly reduced the occurrence of this feared complication.

Treatment for hyperacute rejection should be initiated as soon as diagnosis is made, preferably when the recipient is still in the operating room [2]. In addition to aggressive inotropic and mechanical support for the ailing graft if necessary, aggressive treatment consisting of high dose intravenous corticosteroids, plasmapheresis, intravenous immunoglobulin, anti-thymocytye globulin as well as immediate initiation of immunosuppression maintenance therapy (calcineurin inhibitor, anti-proliferative) should also be administered. The role of complement blockade in hyperacute rejection has not yet been established.

The sudden appearance of right or left ventricular dysfunction during the first few days post-transplant may indicate the accumulation of blood or other fluid in the mediastinum. Cardiac tamponade should be excluded as a possible cause by direct surgical exploration in the event of persistent hemodynamic instability, and if present, evacuated appropriately.

Primary Graft Dysfunction is defined as left, right or biventricular dysfunction developed within 24 h after completion of cardiac surgery with no identifiable etiology. It is the most frequent cause of death in the first 30 days after transplant, occurring on average in 7% of patients [1]. The cause is thought to be multifactorial, and has been speculated to include trauma from brain death in the donor, insufficient preservation, hypothermic ischemia during transport, reperfusion injury and adverse systemic factors in the recipient such as persistent hypotension [1]. Until recently, there was no official definition for this phenomenon; however, a consensus conference in 2014 led to universal parameters for PGD with official classifications of mild, moderate and severe left ventricular PGD, as well as right ventricular PGD (see Table 9.4.). Classification is determined by the level of pharmacologic or mechanical support required in the patient. The severe category requires the presence of circulatory support such as ECMO or other mechanical assist devices. Recent data demonstrate 80% survival at 30 days among patients requiring ECMO, compared to previous rates of 50% [1]. It is hoped that a universal definition will enable more consistent recognition of this phenomenon and that treatment modalities for PGD will be more comparable. In turn, this should lead to better understanding of PGD and prevention/minimization of its adverse outcomes.

Elevated recipient pre-transplant pulmonary vascular resistance (PVR) is known to be a significant risk factor for early post-transplant right ventricular dysfunction and subsequent mortality [2, 5, 6]. Relevant literature demonstrates an RV failure risk up to 75% with a 15% mortality risk among patients with pre-transplant PVRi (indexed to body surface area) >6 Wood units × m2. In contrast, patients without increased pre-transplant PVR only demonstrate a 20% risk of RV failure [7, 8].