A 74-year-old woman was admitted for elective mitral valve repair. Her past medical history was significant for hypertension, diabetes, and hyperlipidemia. After an uneventful induction of general anesthesia, a pulmonary artery catheter (PAC) was placed via the right internal jugular vein. Her baseline pulmonary artery pressures were elevated (45/20 mm Hg). All other clinical and laboratory parameters were within normal limits. A transesophageal echocardiogram (TEE) obtained before cardiopulmonary bypass showed prolapse of the posterior mitral valve leaflet (P2 segment) with severe mitral regurgitation and a dilated left ventricle with normal ejection fraction. The right ventricle was mildly dilated and showed mild impairment of function. There was mild tricuspid regurgitation.
After successful surgical repair of the mitral valve, the patient was weaned off cardiopulmonary bypass on moderate inotropic support (epinephrine 0.1 μg/kg per minute). The left ventricular ejection fraction was 40%. There was now moderate right ventricular (RV) dysfunction accompanied by moderate tricuspid regurgitation ( Figure 88-1 ). The pulmonary artery pressures remained elevated (50/22 mm Hg), and central venous pressure was within normal limits (10–12 mm Hg). Cardiac index was 2.0 L/min/m 2 , and mixed venous saturation was 72%. The patient was transferred to the cardiothoracic intensive care unit (CTICU) for further postoperative management.
The patient was initially stable in the CTICU with good hemodynamic function. The epinephrine infusion was progressively weaned. However, during the first postoperative night, she received large amounts of intravenous fluids in an attempt to improve borderline systemic blood pressure. As a result, the patient’s central venous pressure increased from 10 mm Hg to 20 mm Hg, without improvement in systemic blood pressure (85/45 mm Hg). Despite increasing vasoactive support, the clinical status continued to deteriorate, showing signs of progressive low cardiac output and beginning multiorgan failure. The patient’s cardiac index and mixed venous oxygen saturation declined to 1.5 L/min/m 2 and 45%, respectively. Lactate values progressively increased reaching a maximum of 8 mmol/L. TEE performed on the morning of postoperative day 1 showed a severely depressed right ventricle and severe tricuspid regurgitation. Left ventricular ejection fraction was 50%.
The decision was made to return to the operating room for emergent implantation of a right ventricular assist device (RVAD) (Thoratec Centrimag; Thoratec, Pleasanton, CA). The procedure was uneventful, and the patient returned to the CTICU for further management. Over the course of the next 12 hours, the patient showed a dramatic improvement in hemodynamic status. The signs of early multiorgan failure (i.e., low urine output, elevated transaminases) were reversed. Over the course of the next few days, the RVAD could be progressively weaned, and the patient was taken back to the operating room on postoperative day 7 for RVAD explantation, which proceeded without difficulty. Her trachea was extubated 3 days after RVAD explantation, and she was subsequently weaned off all vasoactive support. The patient was discharged home on postoperative day 37.
What are the etiology and pathophysiology of right ventricular failure?
RV failure results from any structural or functional disorder that makes the right ventricle unable to eject blood into the pulmonary circulation. The most common etiologies of RV failure are listed in Table 88-1 . RV failure is also a prominent feature of various forms of congenital heart disease, such as tetralogy of Fallot, transposition of the great arteries, Ebstein anomaly, and Eisenmenger syndrome. Acute RV failure can also be seen in patients with sickle cell disease during acute chest syndrome.
|Left ventricular failure|
|Right ventricular ischemia|
|Intrinsic myocardial disease|
|Pressure overload |
Pulmonary valve stenosis
Chronic pulmonary hypertension from any cause
|Acute pulmonary hypertension |
Severe left ventricular dysfunction
Acute pulmonary embolism
Transfusion-related acute lung injury
|Post–cardiothoracic surgery states |
Inadequate myocardial protection
Coronary air embolism
The pathophysiology of RV failure is complex. It develops from functional impairment of the underlying free wall and interventricular septum. Myocyte fiber orientation is the key to RV performance. The septum is composed of oblique and transverse fibers. This specific orientation of fibers is essential for ventricular function and determines the ejection fraction. The concept of the septum as the “biventricular motor” is useful to understand the interdependence of both ventricles. The central role of the septum in RV function provides the basis of treatment for RV infarction and RV dysfunction after cardiac surgery.
In the case presented, the etiology of RV failure is multifactorial. On the one hand, the patient had pulmonary arterial hypertension (PAH) preoperatively. This chronic increase in afterload leads to increased wall tension, which produces increased metabolic demand. Consequently, the ischemic state of the heart during intraoperative cross-clamping is less well tolerated. On the other hand, the function of the left ventricle is frequently depressed immediately after mitral valve repair. The ischemic period and the increased afterload against which the left ventricle now has to function are the main culprits in the reduction of ejection fraction commonly encountered in this patient population.
Weaning the epinephrine, in conjunction with the large amounts of intravenous fluids administered in the CTICU, resulted in acute volume overload, tricuspid annular dilation, and severe tricuspid regurgitation. Once this spiral of RV dilation, severe tricuspid regurgitation, and RV failure was initiated, it could be broken only by rapid implementation of mechanical support.