By the nature of their underlying disease, patients who undergo LVAD placement are uniformly high risk with regard to major cardiac surgery. Thus, they are particularly susceptible to intraoperative complications such as air embolus into the right coronary artery, aggressive transfusion of blood products, and ischemia and vasoplegia associated with prolonged cardiopulmonary bypass. Expeditious procedural times and paying scrupulous attention to intraoperative bleeding while limiting transfusion are imperative. Intraoperative transesophageal echocardiography (TEE ) is invaluable for optimizing cannula placement and initial pump speed.

On returning to the recovery unit, patients must be hemodynamically optimized. Acid-base status and electrolytes should be monitored and corrected as needed. Volume status should be assessed with invasive hemodynamic monitoring. We strive to maintain a CVP as low as can be hemodynamically tolerated through the aforementioned use of diuretics and, if needed, ultrafiltration.

Postoperative arrhythmia, while tolerated by the left ventricle, is a potential source of RV dysfunction. Patients who develop supraventricular or ventricular tachyarrhythmia should be aggressively treated with intravenous antiarrhythmics and, if necessary, synchronized cardioversion. A search should be undertaken for the underlying cause of the postoperative arrhythmia, such as high pump speeds with septal interference, suboptimal cannula positioning, electrolyte abnormalities, postoperative pericardial bleeding, or RV ischemia. Vasopressor administration should be minimized. The best time to resume tachytherapy in patients with defibrillators is not clear. We typically resume tachytherapy immediately; however, if a patient requires multiple defibrillations, adjustments may be required, including increasing the defibrillation threshold or turning off shocks altogether.

Echocardiographic guidance is necessary to optimize pump settings and, thus, hemodynamic conditions. We use intraoperative TEE to select initial device settings, and we obtain serial transthoracic echocardiograms in the early postoperative period to ensure that increases in pump speed are well tolerated. Although we frequently use ramp or “speed-change” studies to evaluate cardiac response to various pump speeds in patients with an LVAD, caution should be taken in performing such a study during the early postoperative period because high speeds may induce unnecessary RV strain. Consequently, we prefer to evaluate only one or two incrementally higher speeds, paying close attention to echocardiographic and invasive indicators of RV function.

The prophylactic use of pulmonary vasodilators after LVAD implantation in high-risk patients is appealing. The effects of inhaled nitric oxide in LVAD patients with elevated pulmonary vascular resistance (PVR) were explored in 2011 by Potapov et al. [25], who randomly assigned 150 patients with preoperative PVR greater than 200 dyn*s/cm⁻⁵ to receive either inhaled nitric oxide or placebo. Patients who received inhaled nitric oxide had less RV dysfunction, time on mechanical ventilation, and need for an RVAD than the placebo-treated patients, but these differences did not reach statistical significance. Whether prophylactic use of inhaled prostacyclins, such as epoprostenol and iloprost, may be protective has not been investigated in a placebo-controlled trial. One group that administered epoprostenol to 37 consecutive LVAD recipients found that it reduced pulmonary pressures whether it was initiated before or during weaning from cardiopulmonary bypass [26]. Whether this strategy improved clinical outcomes has yet to be determined. Despite the lack of high-quality evidence to support their use, we have a low threshold for initiating either inhaled nitric oxide or epoprostenol administration in patients who are perceived to be at high risk for RV dysfunction after LVAD placement.

In addition to targeted pulmonary vasodilators, cardiac inotropes are frequently used in the perioperative period to enhance RV support. Milrinone, a phosphodiesterase III inhibitor that increases cardiac inotropy and causes pulmonary and systemic vasodilation by increasing tissue levels of cAMP, has a particularly appealing hemodynamic profile. However, when not used selectively, intravenous milrinone can cause systemic hypotension. Inhaled milrinone has recently been explored as an alternative formulation that may not have this adverse effect. Haglund et al. [27] have described their experience with using inhaled milrinone in ten consecutive patients who underwent HeartMate II LVAD implantation. The authors note a reduction in pulmonary pressures and no episodes of sustained hypotension. In addition, institutional costs were significantly lower with the use of inhaled milrinone than with the use of inhaled nitric oxide. At our institution, LVAD patients frequently begin receiving intravenous milrinone, usually in conjunction with low-dose epinephrine, dobutamine, or both, on weaning from cardiopulmonary bypass. The adverse effects of these medications, including their proarrhythmic properties, are well-known; thus, the risks and benefits of their use in an individual patient should be continuously reassessed by using all available hemodynamic information.