**5.2 Treatment of right ventricular failure**

A proposed algorithm for the treatment of RV failure used at the Montreal Heart Instituteis summarised in Fig. **10**. Assessment of RV function is performed visually when the chest is opened, by analysing RV pressure waveforms and using transesophageal echocardiography. Once RVOTO is ruled out, the etiology of RV systolic dysfunction is divided in two categories, either ischemic or not and with or without LV failure. If ischemia is suspected of causing either RV failure or bi-ventricular failure, treatments (medical and surgical) will be oriented towards the promotion of RV perfusion by means of thrombolysis, percutaneous transluminal coronary angioplasty, or CABG. Finally, pulmonary artery balloon pump, RV assist device or cavopulmonary diversion have also been described as potential treatments for severe RV dysfunction (Kaul & Fields, 2000). Otherwise, if a non-ischemic etiology is more likely or if no LV failure is present, treatments will rather be oriented towards an increase in contractility (inotropes) and a reduction in RV afterload (iNO, iPGI2, inhaled milrinone, oral sildenafil).

In a retrospective study involving patients undergoing mitral and mitral-aortic valvular surgery, Pinzani *et al*. (Pinzani et al., 1993) showed that preoperative RV failure was associated with increased perioperative mortality. Furthermore, in that study, postoperative

In a small prospective study of 14 patients with severe non-ischemic mitral regurgitation presenting high risk descriptors (LV ejection fraction (LVEF) 45% or RVEF 20%), Wencker *et al*. (Wencker et al., 2000) found that preoperative RVEF 20% predicted late

In a retrospective study of 41 patients undergoing non-emergent coronary artery bypass surgery, Maslow *et al.* (Maslow et al., 2002) have shown than RV dysfunction (right ventricular fractional area change (RVFAC)< 35%) in presence of severe LV dysfunction (LVEF ≤ 25%) was associated with an increased risk of postoperative morbidity and mortality. Furthermore, patients with RV dysfunction presented a higher prevalence of diabetes mellitus and renal disease, a higher incidence of postoperative support (inotropic or mechanical), longer ICU and hospital stays, as well as a decrease in short and long term

Haddad *et al.* (Haddad et al., 2007) further assessed the value of RV function relative to other validated risk factors in open valvular heart surgery on 50 patients undergoing valvular surgery. Patients with RV myocardial performance index (RVMPI) < 50% (*n*=20) presented a significantly higher occurrence of circulatory failure (16/20 (80%) *vs* 6/30 (20%), p<0.0001) as well as a higher postoperative heart failure mortality (14/20 (74%) *vs* 3/30 (10%), p<0.0001). In addition, multivariate analysis revealed RVMPI as the only independent predictor of heart failure and mortality among all other demographic,

Right ventricular failure after CPB is associated with a mortality rate ranging from 44% to 86% (Davila-Roman et al., 1995). The incidence of acute refractory RV failure ranges from 0.04 to 0.1% after cardiac surgery. Acute refractory RV failure has also been reported in 2-3% patients after heart trasplantationand in 20-30% patients receiving support from a LV assist

A proposed algorithm for the treatment of RV failure used at the Montreal Heart Instituteis summarised in Fig. **10**. Assessment of RV function is performed visually when the chest is opened, by analysing RV pressure waveforms and using transesophageal echocardiography. Once RVOTO is ruled out, the etiology of RV systolic dysfunction is divided in two categories, either ischemic or not and with or without LV failure. If ischemia is suspected of causing either RV failure or bi-ventricular failure, treatments (medical and surgical) will be oriented towards the promotion of RV perfusion by means of thrombolysis, percutaneous transluminal coronary angioplasty, or CABG. Finally, pulmonary artery balloon pump, RV assist device or cavopulmonary diversion have also been described as potential treatments for severe RV dysfunction (Kaul & Fields, 2000). Otherwise, if a non-ischemic etiology is more likely or if no LV failure is present, treatments will rather be oriented towards an increase in contractility (inotropes) and a reduction in RV afterload (iNO, iPGI2, inhaled milrinone, oral sildenafil).

device with a reported initial salvage rate as low as 25-30% (Kaul & Fields, 2000).

RV failure was the most important independent predictor of late survival.

postoperative death.

**Experience at the Montreal Heart Institute** 

**5.2 Treatment of right ventricular failure** 

**5.1.2 After the procedure** 

hemodynamic and echocardiographic variables (p<0.0001).

survival.

Fig. 10. Proposed approach in the treatment of right ventricular (RV) dysfunction. (LVOTO: left ventricular outflow tract obstruction; RCA: right coronary artery; RVOTO: right ventricular outflow tract obstruction; TEE: transesophageal echocardiography; TTE: transthoracic echocardiography). Presented at the 2011 Canadian Anesthesiologist Society Annual Meeting in Toronto, ON, Canada.

Optimizing oxygenation and ventilation and ruling out other reversible causes of reduction in venous return such as reduction in MAP, increase in Pra and increase in resistance to venous return will also be important in managing these patients.
