The Physiology of Percutaneous Right Ventricular Assist Device—Potential Effects on Ventilation-Perfusion Matching

Field: Medicine (Health Sciences)

Right ventricular failure complicates left ventricular assist device (LVAD), heart transplantation, and end-stage heart failure (ESHF). The dual lumen Protek Duo cannula (TandemLife, Pittsburgh, PA) connected to a centrifugal extracorporeal pump has been used as a percutaneous right ventricular assist device (RVAD) for right ventricular (RV) failure.1 The Protek Duo cannula is inserted via the right internal jugular vein (RIJV) with the tip positioned in the main pulmonary artery (PA) and is capable of providing about 4 L/minute of flow. In the current study, we describe the physiologic changes associated with continuous-flow RVAD using the 29-Fr Protek Duo cannula. In our institution, we have performed 11 percutaneous RVAD using the Protek Duo cannula since January 2016. All cases were performed in the catheter lab by the same operator. In brief, the RIJV was accessed under ultrasound guidance. A Swan-Ganz or multipurpose catheter was steered into the PA under fluoroscopy; with the former, the balloon was inflated during passage to the PA and with the latter, the multipurpose catheter was prolapsed across the tricuspid valve to avoid entangling the tricuspid valve chordae. The catheter was then exchanged for an Amplatz extrastiff 0.035" wire. The Protek Duo cannula was then advanced over the wire after serial dilatation to the PA. There were no insertion-related complications. The cannula was advanced further into the PA in one patient on the intensive care unit after insertion. Indications for RVAD were RV failure post LVAD (n = 7), postheart transplant (n = 2), and ESHF (n = 2, both with concomitant Impella support). The median duration of support was 10 days (minimum 1 day, maximum 29 days). There were 4 deaths at less than 90 days: ESHF (n = 2) and post LVAD (n = 2). Baseline and 3-hour postinsertion arterial blood gases, end-tidal carbon dioxide (ETCO2), and hemodynamic parameters were compared to assess the physiologic changes. Four patients were excluded for this analysis for the following reasons: converted from peripheral venoarterial extracorporeal membrane oxygenation (VA ECMO) (n = 1, post transplant), had oxygenators with the RVAD (n = 1 post LVAD and n = 1 ESHF), and conversion to VA ECMO (n = 1 ESHF). Hence, the physiologic changes were studied in seven patients (Table 1). There were no changes in ventilator parameters during this period of assessment.Table 1.: Patient Characteristics (n = 7)Percutaneous RVAD resulted in a drop in central venous pressure (CVP 16.4 ± 2.1 to 12.8 ± 2.7 mm Hg, p = 0.024) and blood pressure increase (64.5 ± 4.1 to 75.1 ± 9.9 mm Hg, p = 0.030) with no significant change in inotropic/vasopressor use. There was a rise in arterial carbon dioxide (CO2) without significant changes in ETCO2, which resulted in an increase in the arterial ETCO2 gradient (Figure 1). The modest change in arterial pH (7.35 ± 0.06 to 7.33 ± 0.05, p = 0.646) reflected the increase in arterial CO2, as there were reductions in base deficits (−4.5 ± 2.9 to −2.7 ± 1.7, p = 0.259) and lactate levels (5.0 ± 2.2 to 2.2 ± 0.5 IU, p = 0.027). There was no significant change in oxygenation ([partial pressure of arterial oxygen] PaO2 12.2 ± 2.9 to 12.6 ± 1.4 kPa, p = 0.838) (see Table 1, Supplemental Digital Content, https://links.lww.com/ASAIO/A374). None of the patients required extracorporeal CO2 removal.Figure 1.: Changes in arterial (5.151 ± 0.791 to 6.238 ± 0.688 kPa, p = 0.034), end-tidal (4.186 ± 0.607 to 4.401 ± 0.73 kPa, p = 0.605), and the arterial to end-tidal CO2 gradient (1.329 ± 0.26 to 1.838 ± 0.426 kPa, p = 0.036) at 3 hours post RVAD support. CO2, carbon dioxide; RVAD, right ventricular assist device.Several studies have described the use of different percutaneous RVADs, including dual cannula, single dual-lumen cannula, and the right-sided Impella RP.2,3 In this study, we demonstrated a similar acute drop in CVP (as reported by others), which was accompanied by modest increase in arterial pressure without any significant change in vasopressor use. In addition, we studied the acute effects of RVAD on arterial ETCO2 gradient. The effects of continuous-flow (or less pulsatile flow) with RVAD on the pulmonary circulation and ventilation-perfusion matching have received little attention. Deriving from the Bohr equation, alveolar dead space (VDalv), expressed as a fraction of alveolar tidal volume (VTalv), is directly related to the arterial-ETCO2 gradient4: VDalv/VTalv is directly related to (arterial ETCO2)/arterial CO2. Therefore, the rise in arterial ETCO2 gradient is consistent with an increased in fractional VDalv. To our knowledge, there are no previous reports on the effects of continuous-flow on ventilation-perfusion matching in the lungs. The mechanism for potential increase in VDalv/VTalv cannot be determined from this study. Positive pressure ventilation exacerbates regional ventilation-perfusion mismatch because of dorsal-ventral intra-abdominal pressure gradient and consequent preferential ventilation of the ventral regions.5 In addition, alveolar pressure under positive pressure ventilation and low-flow conditions (right heart failure) may exceed pulmonary arterial pressure to convert West zone 2 to zone 1 physiology and increase dead space ventilation. It is possible that continuous-flow RVAD may further divert blood flow away from West zone 2 regions preferentially to lower resistance West zone 3 regions resulting in more regions with zone 1 physiology. The increase in zone 1 regions and exacerbation of ventilation-perfusion mismatch may explain the increase in arterial CO2 without significant effects on oxygenation. The small number of patients in this study is a major limitation. In addition, we studied a relatively short time frame. The 3-hour time frame was selected to allow sufficient time to study the effects of RVAD support while avoiding other confounding factors, such as changes in mechanical ventilation, development of other respiratory changes, or change in CO2 production (e.g., changes in metabolic activity). Isolating the effects of RVAD would be challenging with these confounding factors over a longer period of time. Other limitations include the lack of simultaneous PA pressure monitoring to assess pulsatility (PA catheters are removed at the time of insertion) and assessment of ventilation-perfusion matching. In conclusion, we have shown that 1) acceptable outcomes can be achieved in selected patients with RV failure with the Protek Duo cannula coupled with a centrifugal pump and 2) this RVAD improves hemodynamics but worsens the arterial ETCO2 gradient (which suggests increased VDalv) without affecting oxygenation in the short-term in most patients with RV failure. Our data indicate the potential for ventilation-perfusion mismatch in some patients supported with percutaneous RVAD, which needs further study.