- 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. A functioning right ventricle (RV) is critical to effective loading of the left ventricle (LV). Perioperative RV failure can be quite challenging for the anesthesiologist as it often occurs in the setting of pulmonary artery hypertension, which can be difficult to treat.
The 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) occurs secondary to pathologic processes affecting the valve itself or as a consequence of RV dilatation. RV dilatation may occur in the setting of pressure or volume overload. Increased RV systolic pressure develops when the RV must work against an increased resistance. This can occur in clinical situations, which increase pulmonary artery (PA) pressure such as mitral stenosis, severe mitral regurgitation, severe left ventricular dysfunction, pulmonary embolism, primary pulmonary hypertension, or lung disease.
Endocarditis, connective tissue diseases, carcinoid syndrome, anorectic drugs (fenfluramine), Ebstein abnormality (an apically positioned tricuspid valve), pergolide, and chest radiation therapy can likewise result in TR. Ebstein anomaly is due to apical displacement of the tricuspid valve leaflets especially the septal leaflet associated with TR and RV dysfunction.
Patients with TS frequently present with other valvular diseases associated with rheumatic heart disease (eg, mitral stenosis, aortic stenosis). Consequently, their clinical features often represent the impact of these lesions. Long before the patient presents for surgery, echocardiography will have diagnosed any associated 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 readily produce TR even with normal valve structure. Transvenous pacemaker wires or catheters can both cause a mild degree of TR as well. Additionally, many patients have echocardiographically detected TR without clinical significance.
The right ventricle and the interaction between the right and left heart are critical to maintaining healthy cardiovascular function. Although patients can survive with only a single ventricle devoted to the systemic circulation (eg, 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 can develop both acutely and chronically. Acute RV failure can be seen associated with sudden increases in pulmonary vascular resistance (eg, during a protamine reaction) or secondary to myocardial ischemia and infarction. Chronic RV failure presents secondary to progressive increases in pulmonary hypertension (eg, from mitral stenosis, lung diseases, etc) or volume overload ...