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Much as the mitral valve (MV) and aortic valve (AV) direct blood flow into the systemic circulation, the tricuspid valve (TV) and the pulmonic valve (PV) direct flow into the pulmonary circulation. The right ventricle (RV) ensures loading of the left ventricle (LV) by pumping blood through the normally low pressure pulmonary vasculature. Perioperative RV failure is frequently associated with pulmonary artery hypertension and systemic hypoperfusion. Treatment is directed at reducing pulmonary arterial resistance to promote the forward flow of blood into the pulmonary vasculature. Inotropes and ventricular assist devices are also used to support right heart function perioperatively.


The tricuspid valve (TV) can develop both stenotic and regurgitant lesions. Tricuspid stenosis (TS) is most often secondary to rheumatic heart disease. Less encountered causes are carcinoid and endomyocardial fibrosis. Obstructing cardiac masses can also occlude the TV.1

Tricuspid regurgitation (TR) can be primary or secondary. Primary TR is rare (approximately 15% of TR cases) and results from endocarditis, connective tissue diseases, carcinoid syndrome, anorectic drugs (fenfluramine), Ebstein anomaly, pergolide, or chest radiation. Ebstein anomaly is due to apical displacement of the tricuspid valve leaflets, especially the septal leaflet, and is associated with TR and RV dysfunction. Secondary TR is the result of left heart disease or intrinsic lung disease, which increase pulmonary artery pressures and pulmonary vascular resistance (PVR). Examples of disease processes that produce secondary TR are mitral stenosis, severe mitral regurgitation, severe left ventricular dysfunction, pulmonary embolism, primary pulmonary hypertension, or lung disease.

Patients with TS frequently present with other valvular diseases associated with rheumatic heart disease (e.g., mitral stenosis, aortic stenosis) or carcinoid disease (e.g., pulmonary valve stenosis). Consequently, their clinical features often represent the combined impact of these lesions.

The patient with TR secondary to pulmonary hypertension is likely to present with signs of right heart failure and systemic venous engorgement. Peripheral edema, hepatic dysfunction, and ascites frequently occur. Systolic pulmonary pressures greater than 55 mm Hg1 will likely result in TR even with normal valve structure. Transvenous pacemaker wires or catheters can both cause a mild degree of TR. Additionally, many patients have echocardiographically detected mild TR without clinical significance.


The interaction between the right and left heart is critical to maintaining healthy cardiovascular function. Although patients can survive with only a single ventricle devoted to the systemic circulation (e.g., Fontan circulation—Chapter 12), a functioning right heart effectively loads the LV so that the stroke volume (SV) is ejected systemically. When the RV fails, the LV may be inadequately loaded reducing SV.

RV failure develops both acutely and chronically. Acute RV failure can occur with sudden increases in PVR (e.g., during a protamine reaction) or secondary to myocardial ischemia and infarction. Chronic RV failure ...

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