Vasoplegic syndrome (VS) is a common complication following cardiovascular surgery with cardiopulmonary bypass (CPB), and its incidence varies from 5 to 44%. It is defined as a distributive form of shock due to a significant drop in vascular resistance after CPB. Risk factors of VS include heart failure with low ejection fraction, renal failure, pre-operative use of angiotensin-converting enzyme inhibitors, prolonged aortic cross-clamp and left ventricular assist device surgery. The pathophysiology of VS after CPB is multi-factorial. Surgical trauma, exposure to the elements of the CPB circuit and ischemia-reperfusion promote a systemic inflammatory response with the release of cytokines (IL-1β, IL-6, IL-8, and TNF-α) with vasodilating properties, both direct and indirect through the expression of inducible nitric oxide (NO) synthase. The resulting increase in NO production fosters a decrease in vascular resistance and a reduced responsiveness to vasopressor agents. Further mechanisms of vasodilation include the lowering of plasma vasopressin, the desensitization of adrenergic receptors, and the activation of ATP-dependent potassium (K_ATP) channels. Patients developing VS experience more complications and have increased mortality. Management includes primarily fluid resuscitation and conventional vasopressors (catecholamines and vasopressin), while alternative vasopressors (angiotensin 2, methylene blue, hydroxocobalamin) and anti-inflammatory strategies (corticosteroids) may be used as a rescue therapy in deteriorating patients, albeit with insufficient evidence to provide any strong recommendation. In this review, we present an update of the pathophysiological mechanisms of vasoplegic syndrome complicating CPB and discuss available therapeutic options.

Right ventricular failure (RVF) is often caused by increased afterload and disrupted coupling between the right ventricle (RV) and the pulmonary arteries (PAs). After a phase of adaptive hypertrophy, pressure-overloaded RVs evolve towards maladaptive hypertrophy and finally ventricular dilatation, with reduced stroke volume and systemic congestion. In this article, we review the concept of RV-PA coupling, which depicts the interaction between RV contractility and afterload, as well as the invasive and non-invasive techniques for its assessment. The current principles of RVF management based on pathophysiology and underlying etiology are subsequently discussed. Treatment strategies remain a challenge and range from fluid management and afterload reduction in moderate RVF to vasopressor therapy, inotropic support and, occasionally, mechanical circulatory support in severe RVF.

Infection with the novel severe acute respiratory coronavirus-2 (SARS-CoV2) results in COVID-19, a disease primarily affecting the respiratory system to provoke a spectrum of clinical manifestations, the most severe being acute respiratory distress syndrome (ARDS). A significant proportion of COVID-19 patients also develop various cardiac complications, among which dysfunction of the right ventricle (RV) appears particularly common, especially in severe forms of the disease, and which is associated with a dismal prognosis. Echocardiographic studies indeed reveal right ventricular dysfunction in up to 40% of patients, a proportion even greater when the RV is explored with strain imaging echocardiography. The pathophysiological mechanisms of RV dysfunction in COVID-19 include processes increasing the pulmonary vascular hydraulic load and others reducing RV contractility, which precipitate the acute uncoupling of the RV with the pulmonary circulation. Understanding these mechanisms provides the fundamental basis for the adequate therapeutic management of RV dysfunction, which incorporates protective mechanical ventilation, the prevention and treatment of pulmonary vasoconstriction and thrombotic complications, as well as the appropriate management of RV preload and contractility. This comprehensive review provides a detailed update of the evidence of RV dysfunction in COVID-19, its pathophysiological mechanisms, and its therapy.

Pulmonary hypertension (PH) associated with left heart diseases (PH-LHD), also termed group 2 PH, represents the most common form of PH. It develops through the passive backward transmission of elevated left heart pressures in the setting of heart failure, either with preserved (HFpEF) or reduced (HFrEF) ejection fraction, which increases the pulsatile afterload of the right ventricle (RV) by reducing pulmonary artery (PA) compliance. In a subset of patients, progressive remodeling of the pulmonary circulation resulted in a pre-capillary phenotype of PH, with elevated pulmonary vascular resistance (PVR) further increasing the RV afterload, eventually leading to RV-PA uncoupling and RV failure. The primary therapeutic objective in PH-LHD is to reduce left-sided pressures through the appropriate use of diuretics and guideline-directed medical therapies for heart failure. When pulmonary vascular remodeling is established, targeted therapies aiming to reduce PVR are theoretically appealing. So far, such targeted therapies have mostly failed to show significant positive effects in patients with PH-LHD, in contrast to their proven efficacy in other forms of pre-capillary PH. Whether such therapies may benefit some specific subgroups of patients (HFrEF, HFpEF) with specific hemodynamic phenotypes (post- or pre-capillary PH) and various degrees of RV dysfunction still needs to be addressed.

About 15 years ago, Patient Blood Management (PBM) emerged as a new paradigm in perioperative medicine and rapidly found support of all major medical societies and government bodies. Blood products are precious, scarce and expensive and their use is frequently associated with adverse short- and long-term outcomes. Recommendations and guidelines on the topic are published in an increasing rate. The concept aims at using an evidence-based approach to rationalize transfusion practices by optimizing the patient’s red blood cell mass in the pre-, intra- and postoperative periods. However, elegant as a concept, the implementation of a PBM program on an institutional level or even in a single surgical discipline like cardiac surgery, can be easier said than done. Many barriers, such as dogmatic ideas, logistics and lack of support from the medical and administrative departments need to be overcome and each center must find solutions to their specific problems. In this paper we present a narrative overview of the challenges and updated recommendations for the implementation of a PBM program in cardiac surgery.

Background: Enhanced Recovery After Surgery (ERAS) protocols have been implemented in various surgical specialties to improve patient outcomes and reduce opioid consumption. In cardiac surgery, the traditionally high-dose opioid use is associated with prolonged ventilation, intensive care unit (ICU) stays, and opioid-related adverse drug events (ORADEs). This study evaluates the impact of an ERAS^® Society-certified program on opioid consumption in patients undergoing elective cardiac surgery at Lausanne University Hospital. Methods: A retrospective, monocentric observational study was conducted comparing two patient cohorts: one treated with ERAS protocols (2023–2024) and a retrospective control group from 2019. Data were collected from the hospital’s electronic medical records and the ERAS program database. The primary outcome was total opioid consumption, measured intraoperatively and postoperatively (postoperative day (POD) 0–3). Secondary outcomes included pain control, length of stay, complications, and recovery parameters. Statistical analyses included multivariate logistic regression to identify factors associated with reduced opioid consumption. Results: Patients in the ERAS group demonstrated significantly lower total opioid consumption, whether intraoperatively (median sufentanil: 40 mcg vs. 51 mcg, p < 0.0001) or postoperatively (POD 0–3: p < 0.001). The ERAS group had faster extubation times, earlier mobilization and pain control with non-opioid analgesics, fewer complications, and shorter hospital stays (9 vs. 12 days, p < 0.001). Logistic regression identified fast-track extubation and absence of complications as strong predictors of reduced opioid use. Conclusions: The implementation of an ERAS protocol in cardiac surgery significantly reduces opioid consumption while enhancing recovery.