الفهرس 
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Abstract
Acute right ventricular failure (RVF) is a frequent and serious clinical challenge in the intensive care unit. The presence of acute RVF not only carries substantial morbidity and mortality, but also complicates the use of commonly used treatment strategies in critically ill patients.
Acute RVF is a complex clinical syndrome that can result from any structural or functional cardiac and noncardiac disorder that impairs the ability of the right heart to fill or eject appropriately and is characterized by new onset or gradually or rapidly worsening RV signs and symptoms requiring urgent therapy irrespective of the underlying cause. It is estimated to account for 3% of all acute heart failure admissions and confers worse mortality rates than acutely decompensated LVF.
The most common etiologies of RVF in the ICU are left ventricular (LV) failure, RV ischemia, acute pulmonary embolism (PE), pulmonary hypertension (PH), sepsis, acute lung injury, cardiac tamponade, and post-cardiothoracic surgery states. Arrhythmias and pericardial, congenital, and/or valvular heart disease may also contribute RV dysfunction occurs directly due to cardiodepressant effects of proinflammatory cytokines, cardiac microthrombi, and ischemia and/or arrhythmias or indirectly due to LV dysfunction, afterload increases from endothelial dysfunction, HPV, pulmonary emboli, and/or pulmonary microthrombi, as well as pre-load decreases (induced or aggravated by capillary leak syndrome). Mechanical ventilation contributes to RV dysfunction by negatively affecting pre-load and/or afterload.
LV dysfunction induces RV dysfunction via afterload increase, and/or displacement of the interventricular septum toward the RV with subsequent impairment of RV filling (known as ventricular interdependence). Important interactions between inflammation, sepsis, pulmonary endothelial dysfunction with associated PH, and RV and LV dysfunction have recently been reviewed. Heightened oxygen demands from increased heart rate, afterload, and wall tension, combined with decreased coronary perfusion from hypotension, result in subendocardial and myocardial RV ischemia.
After assessment of the underlying cause with the initial history and physical, laboratory studies, including serum cardiac biomarkers, should be obtained along with an ECG and chest radiograph, Pulmonary artery catheters (PACs) and transthoracic or transesophageal echocardiography remain the most reliable methods to diagnose RVF and evaluate the treatment response in the ICU. they provide crucial hemodynamic information in acute RVF, particularly when used in combination with echocardiographic parameters of RV function and indexes of tissue oxygenation. The critical role of bedside echocardiography, especially when combined with specific markers of RV dysfunction, such as tricuspid annular plane systolic excursion index, tissue Doppler, and Tei index, cannot be overemphasized. Cardiac magnetic resonance imaging is the most sensitive method to assess RV function; however, due to logistical issues, it is rarely used for critically ill patients.
In addition to specific therapies directed against the underlying cause of RVF, supportive measures and judicious volume management, and the use of selective pulmonary vasodilators in conjunction with inotropes seem most promising. The combination of iNO with dobutamine is best supported by current evidence, with evolving data supporting the use of inhaled prostacyclins. PDE-5 inhibitors seem to have selective actions on the RV. Levosimendan is a promising new inotrope for the treatment of RV failure, although its role in comparison to older agents such as dobutamine, adrenaline and milrinone has yet to be determined. Mechanical or surgical interventions are used as primary treatment for distinct conditions or as rescue therapy.
Future directions should include therapies specifically targeting the diseased RV. Examples include metabolic modulators aimed at reversing mitochondrial dysfunction. Stem cells are being investigated in ischemic and PAH-related RVF. Tyrosine kinase inhibitors show promise in severe PAH with RVF. Future research should consider sex-based differences in RV function. Multiple studies demonstrate female protection in acute and chronic forms of left ventricular injury. Recent data indicate a similar pattern with regard to right ventricular function. This is of interest as healthy, cardiovascular disease–free women have a higher RVEF than their male counterparts. A better understanding of the molecular mechanisms protecting the female RV in health and disease may therefore allow future therapeutic interventions that ultimately benefit patients from either sex.