Background and objectives:  Our study aimed to develop an experimental animal model of acute right heart failure.  We sought to evaluate a pulsatile right-ventricular assist device (pRVAD) in this model.  The right ventricular stroke work index (RVSWI) is an excellent indicator of right ventricular dysfunction in acute and chronic right heart failure.  Recent studies demonstrated that an impaired RVSWI was associated with deterioration of heart failure and death.

RVSWI [Right Ventricular Stroke Work Index, (g*m/m²/beat)] =
SI [Stroke Volume Index (mL/beat/m²)] * (MPAP [Mean Pulmonary Arterial Pressure (mmHg)] – CVP [Central Venous Pressure (mmHg)] * 0.0136 [conversion term to equalize units]

Methods:  We induced acute pulmonary embolism by repetitive injection of 100 µm micro-spheres solution through a pigtail catheter in the pulmonary artery trunk in 28 sheep (70,2 +/- 8,58 kg) under general anesthesia.  Preoperative bullae of microspheres were given until the cardiac index (CI) decreased to < 50% of baseline and the mean pulmonary artery pressure (mPAP) doubled.  The pRVAD (PERKAT RV, Novapump GmbH, Jena, Germany) was implanted through an 18 French sheath in the right femoral vein after drop of mean arterial pressure to < 60 mmHg indicating profound shock situation.  The self-expanding pRVAD pumps blood from the vena cava inferior to the pulmonary artery at flow rates of 2 to 3 l/min.  CI was measured with thermodilution technique using an internal jugular catheter and a PiCCO2 device in the left femoral artery (Pulsion Medical Systems, Munich, Germany).  Hemodynamic parameters were recorded continuously on a digital monitoring system of the hybrid catheter laboratory.

Results:  Induction of acute pulmonary embolism resulted in a decrease in CI from 4,8 +/- 1,18 l/min. to 1,9 +/- 0,74 l/min.  MPAP increased from 17,5 +/- 4,72 mmHg to 36,4 +/- 11,94 mmHg, respectively.  It remained high under pRVAD at 33,5 +/- 11,94 mmHg.  Circulatory support improved CI to 4,1 +/- 1,11 l/min.  However, we observed an increase in RVSWI from 3,6 +/- 2,69 g*m/m²/beat in the shock situation to RVSWI for 6,6 +/- 3,37 g*m/m²/beat under pRVAD support.

Conclusion:  The presented animal model of acute right heart failure provides a good option for experimental evaluation of right-sided circulatory support devices.  The increase in RVSWI reflects the beneficial effect of pRVAD.  It closely correlates with the acute right ventricular dysfunction in this animal model.  RVSWI may be an option to monitor the effect of right ventricular circulatory support in complex cardiogenic shock patients with acute pulmonary embolism.