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  Questions

  
  
• 1.
  

  What are the etiology and pathophysiology of right ventricular failure?

  
  
• 2.
  

  What is the impact of chronic pulmonary arterial hypertension on right ventricular function?

  
  
• 3.
  

  How is right ventricular failure diagnosed?

  
  
• 4.
  

  Explain the treatment strategies for right ventricular failure.

  
  
• 5.
  

  What intraoperative monitoring is recommended for patients with right ventricular failure?

  
  
• 6.
  

  What is the prognosis of patients with right ventricular failure?

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.

Moderate tricuspid regurgitation.

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.