The right ventricle in sepsis

Right ventricular dysfunction is common in sepsis and septic shock because of decreased myocardial contractility and elevated pulmonary vascular resistance despite a concomitant decrease in systemic vascular resistance. The mainstay of treatment for acute right heart failure includes treating the underlying cause of sepsis and reversing circulatory shock to maintain tissue perfusion and oxygen delivery. Decreasing pulmonary vascular resistance with selective pulmonary vasodilators is a reasonable approach to improving cardiac output in septic patients with right ventricular dysfunction. Treatment for right ventricular dysfunction in the setting of sepsis should concentrate on fluid repletion, monitoring for signs of RV overload, and correction of reversible causes of elevated pulmonary vascular resistance, such as hypoxia, acidosis, and lung hyperinflation.     

The right ventricle and pulmonary hypertension

In patients with pulmonary hypertension (PH), the primary cause of death is right ventricular (RV) failure. Improvement in RV function is therefore one of the most important treatment goals. In order to be able to reverse RV dysfunction and also prevent RV failure, a detailed understanding of the pathobiology of RV failure and the underlying mechanisms concerning the transition from a pressure-overloaded adapted right ventricle to a dilated and failing right ventricle is required. Here, we propose that insufficient RV contractility, myocardial fibrosis, capillary rarefaction, and a disturbed metabolism are important features of a failing right ventricle. Furthermore, an overview is provided about the potential direct RV effects of PH-targeted therapies and the effects of RV-directed medical treatments.     

The right ventricle in pulmonary hypertension

Pulmonary arterial hypertension (PAH) is a term used to classify a variety of conditions that share in common an injury to the pulmonary vasculature that produces elevations in pulmonary arterial pressure. However, it is the integrity of right ventricular function, rather than the degree of vascular injury, that is the major determinant of symptoms and survival in PAH. The article will review the normal structure and function of the right ventricle and summarize the impact of PAH and its treatments on right ventricular function.     

Double-chambered right ventricle

An asymptomatic 11-year old boy with a history of spontaneouslyregressed right ventricle (RV) rhabdomyoma was referred to ourinstitution for cardiovascular magnetic resonance (CMR),     

Double-chambered right ventricle

Between May 1974 and December 1993, 37 patients (0.75%) witha double-chambered right ventricle underwent surgical repair.The patients ranged in age from 11 months to 12 years (mean4 ± 1.1 years). Cardiac catheterization was performedin 36 patients. The proximal right chamber pressure was 118±10 mmHg and the mean ventricular gradient pressure was 75 ±10 mmHg. A ventricular septal defect was present in 36 casesand fixed subaortic stenosis in eight. Longitudinal right ventriculotomy, group I, was performed in19 patients (51.3%): 11 had a perimembranous ventricular septaldefect and eight an infundibular ventricular septal defect.Combined pulmonary arteriotomy and right atriotomy, group II,was performed in 18 patients (48.7%): 17 patients had a perimembranousventricular septal defect. The ventricular septal defect wasclosed using a double velour patch in 26 patients, continuoussuture in four and a Gore-Tex patch in six. In the ventriculotomygroup one patient died shortly after the operation (followingpulmonary complication), and ten patients required inotropicsupport. Two patients developed patch dehiscence and underwentreoperation. There were no complications in group II patientswho underwent right atriotomy. Associated cardiac anomalieswere corrected in all patients. Follow-up of 6.5 ±3.1years after operation showed that 36 patients were alive andasymptomatic. Conclusion: the transatrial approach with pulmonary arteriotomyis an appropriate and effective double-chambered right ventriclecorrection even if it is associated with a perimembranous ventricularseptal defect.     

The right ventricle in congenital heart disease

In patients with congenital heart disease the right ventricle (RV) may support the pulmonary (subpulmonary RV) or the systemic circulation (systemic RV). During the last 50 years evidence is accumulating that RV dysfunction develops in many of these patients and leads to considerable morbidity and mortality. Therefore RV function in certain groups of congenital heart disease patients needs close surveillance and timely and appropriate intervention to optimise outcomes. Despite major progress being made, assessing the RV either in the subpulmonary or the systemic circulation remains challenging, often requiring a multi-imaging approach and expertise (echocardiography, magnetic resonance imaging, nuclear and occasionally invasive assessment with angiography). This review discusses the implications of volume and pressure loading of the RV in the context of congenital heart disease and describes the most relevant imaging modalities for monitoring RV function.     

The right ventricle in pulmonary disease.

Abnormal pulmonary function that causes pulmonary artery hypertension increases right ventricular work. To compensate, the right ventricle enlarges, and cor pulmonale develops. Right ventricular failure occurs when these adaptive mechanisms cannot compensate for the hemodynamic burden. The various pulmonary diseases that are associated with right ventricular overload and the physiologic responses of the right ventricle to increased afterload are discussed in this article.     

The right ventricle in congenital heart disease.

An increasing number of children with congenital heart disease are surviving into adulthood, creating new, unusual patients with different physiologic and anatomic problems for the adult cardiologist. This article discusses those lesions affecting primarily the right ventricle.