The induction of general anesthesia for congestive heart failure (CHF) patients undergoing VAD placement is crucial due to the risk of myocardial depression, severe hypotension, and multiorgan dysfunction, the latter potentially related to anesthetic drug metabolism. Compared with normal physiology, heart failure also results in a slow circulation and a reduced distribution volume for anesthetic drugs. As a result, when conventional doses are administered, drug concentrations are usually higher among heart failure patients. The anesthesiologist must be mindful of this fact using incremental doses of anesthetic drugs and allowing time to evaluate their effects [20]. Furthermore, in this patients high endogenous catecholamine level supports hemodynamics, and induction of general anesthesia may alter this balance; for this reason, start the induction only when operating room is available and, in critical patients (high inotropic support, very low cardiac performance), perform the induction of GA having ECLS/CPB in “stand-by” support.

Pancuronium provides hemodynamic stability due to vagolytic and indirect sympathomimetic properties and a longer duration of action. It may result in a prolonged neuromuscular blockade in patients with kidney dysfunction and CHF.

Rocuronium enables fast-track anesthesia, has a rapid onset of effect, and has an antidote.

Patients undergoing LVAD implantation are at particular risk for developing right-sided heart failure. Pulmonary hypertension may impair this situation due to increased RV afterload. Mechanical ventilation must be set in order to avoid hypoxia and hypercapnia that contribute to pulmonary vasoconstriction and subsequent pulmonary hypertension [27, 28]. VAD patients may often undergo medium- to long-term ventilation afterward. A protective ventilations strategy, as for ARDS patients, has been promoted in order to minimize the potential for ventilator-induced lung injury [29]. Positive end-expiratory pressure could be carefully used, though high PEEP has been not shown to systematically influence right-ventricular function [30]. That’s why, as a conclusion, a maximum tidal volume of 6–8 mL/kg (ideal body weight) is preferable, and a best PEEP should be set to optimize lung compliance and minimize vascular pulmonary resistance and then RV dysfunction (which can be continuously monitored via transesophageal echocardiography during ventilation setup) (◘ Table 16.4).

Perioperative fluid management during VAD surgery should aim to guarantee adequate intravascular volume and VAD flows but without overloading the right ventricle.

VAD patients usually have a preexisting volume deficiency due to diuretic therapy.

Although there has been a longstanding debate on this topic and the controversy between colloids and crystalloids is still open [31], intravascular volume optimization for VAD implantation is a crucial point. Before and during the induction of anesthesia, the volume deficiency should be replaced. After weaning from CPB, volume management should aim to provide sufficient VAD flows and avoid a collapse of the left ventricle. Transfusion of RBCs is often required to provide adequate tissue oxygenation; the trigger for that must come from a combination of mixed venous oxygen saturation, lactate plasma levels, and hemoglobin plasma levels [32–34]. Hemolysis is an important issue in VAD patients, less in the intracorporeal centrifugal VAD and axial technology LVAD and more in BVAD support; hemopexin and haptoglobin, in addition to free hemoglobin, can assess erythrocyte damage [35] (◘ Table 16.5).

Patients suffering from CHF are typically managed preoperatively with inotropes (dopamine, dobutamine, epinephrine) and phosphodiesterase-III (PDE-III) inhibitors (milrinone or enoximone). Vasopressors such as norepinephrine or vasopressin should be available to ensure a sufficient perfusion pressure, since vasoplegia occurs in up to 40% of VAD patients [36–38]. The main causes of the abovementioned vasoplegia are the lack of vasopressin and the increased production of nitric oxide by nitric oxide synthases [39, 40]. Low-dose vasopressin (defined as <0.04 U/min) started before CPB generally decreases the need of postoperative vasopressors [38–41], but not in severe cases of vasoplegia where high doses of multiple vasopressors (norepinephrine, vasopressin, or phenylephrine) are needed. Methylene blue administration can be considered in catecholamine-resistant vasoplegic shock.

Inotropes and PDE inhibitors support the right ventricle during weaning from CPB after LVAD placement. This must be highlighted since the performance of the right ventricle is the most crucial parameter for successful weaning from CPB post-LVAD implantation. Milrinone was preferred as the primary inotropic drug due to lack of blood pressure increase during implantation of continuous flow-generating assist devices in one study [42].

It can be used even in inhalatory manner to reduce pulmonary vascular resistance. The calcium-sensitizing agent Levosimendan and its long-lasting active metabolite OR-1896 bind to troponin C, significantly increase contractility, and reduce peripheral vascular resistances by opening adenosine triphosphate (ATP)-sensitive K channels in vascular smooth muscles [43, 44]. However, the increased myocardial contractility, which lasts at least for 7 days after a 24-h infusion is maintained, is not associated with an increase in myocardial oxygen consumption. At present, levosimendan nonresponders have been identified as high-risk candidates for right ventricular failure. Presurgery levosimendan treatment nonresponse has been identified by elevated N-terminal prohormone brain natriuretic peptide (NT-proBNP) levels and predicted postsurgery RV failure. Levosimendan however did not prevent right-sided heart failure (RHF) [45], and prospective large multicentric studies for its use in LVAD implantation are still lacking. Inotropes are usually not required in biventricular assist device placement. Vasopressors are generally required to provide adequate perfusion pressure for unsupported right ventricle and to treat also hypotension due to systemic inflammatory response coming from CPB and LVAD placement itself [46]. A number of pharmacological approaches have been promoted in order to prevent or attenuate RV dysfunction, especially inhaled nitric oxide in the contest of weaning from CPB after LVAD placement. A reduced RV contractility is revealed intraoperatively when at least three different factors increase RV preload beyond optimal filling status resulting in increased wall tension. Firstly, the increased systemic blood flow from the LVAD fills the RV more efficiently leading to RV dilatation. Too aggressive offloading of the LV with the device may cause a leftward shift in the ventricular septum increasing end diastolic volume of the RV. Thirdly, intraoperative bleeding may be quite severe, thus requiring massive transfusion. These factors may also increase PVR with devastating consequences to the dysfunctional RV. The failure of the RV to offload venous return will increase venous pressures further reducing systemic organ perfusion, which ultimately leads to multiorgan failure [47]. It’s mandatory to prevent vicious cycle of hypotension and ischemia, maintaining systolic arterial pressure, minimizing right ventricular dilation, and reducing right ventricular afterload (inhaled NO or milrinone). Indeed various case reports, observational studies, and small-scale RCTs have demonstrated beneficial effects of iNO therapy [48–51] in patients who required LVAD insertion. Nearly all of these small studies showed that iNO decreased mean PAPs and RV afterload and resulted in more stable LVAD performance. In 2005 the European expert panel concluded that it was reasonable to consider iNO during LVAD insertion because of the perceived physiological and clinical benefits and the life-threatening impact of RV failure on the overall survival [51]. A practical prospective definition of RV failure in LVAD literature includes high CVP, inotrope requirement, and LVAD flow less than 2 l/min/m², and this should guide the start of iNO therapy in theater together with high PAPs, low SvO2, and low ScVo2. However, the threshold of LVAD flows less than 2 l/min/m² seems to be too conservative. The most recent scientific statement of the American Heart Association in their recommendations for the Use of Mechanical Circulatory Support concludes that the use of selective pulmonary vasodilators (nitric oxide, prostanoids, or type 5 phosphodiesterase inhibitors) may attenuate the development of early RV failure [52]. The majority of independent consultants agree with the original European recommendations by 92% and support the use of iNO during LVAD implantation. The debate about the real effectiveness of iNO in LVADs is still open since large RCTs are still lacking and most of the small-size ones reveal the need to crossover from double-blind to open-label investigation if patients met RV failure criteria before 15 min of monitoring. This creates several bias and gets the production of systematic review and meta-analysis quite hard (◘ Table 16.6). Inhaled prostacyclin may offer an alternative to nitric oxide in the treatment of pulmonary hypertension [53].