Venoarterial extracorporeal membrane oxygenation (VA ECMO) is a therapeutic option for acute cardiogenic shock. Due to the ease of implantation, VA ECMO is often placed using the femoral artery and vein. Unlike traditional left heart ventricular assist device (VAD) support, VA ECMO pressurizes the systemic arterial circuit without directly unloading the left heart. As a result, the failing left ventricle (LV) may not have sufficient contractility to open the aortic valve, resulting in elevated LV cavity pressure, pulmonary venous hypertension, pulmonary vascular injury, and acute respiratory distress syndrome.1–8 Furthermore, inadequate unloading of the LV in association with stasis and in the presence of infarcted myocardium can lead to substantial thrombus formation within LV cavity (Figure 1). The combination of extensive LV or pulmonary vascular thrombosis with acute respiratory distress syndrome would limit options for recovery, heart transplant, or transition to a long-term VAD systems.9–11 Lastly, the extent of pulmonary vascular injury may be underappreciated because the pulmonary vasculature is relatively underperfused and the majority of the cardiac output is diverted away from the lungs during VA ECMO support. A chest x-ray on VA ECMO may appear fairly normal in the setting of diminished pulmonary flow only to reveal the deleterious effects of the acute pulmonary venous hypertension once pulmonary arterial flow is restored.
Current management strategies for LV unloading while on VA ECMO include intra-aortic balloon pump, percutaneous atrial septostomy, and central ECMO cannulations using the left atrium or LV.5–8 These alternative VA ECMO techniques with LV unloading increase the complexity of acute mechanical circulatory support.
Impella 2.5 (Abiomed, Danvers, MA) is a catheter-mounted microaxial rotary pump capable of displacing 2.5 L of blood per minute, draining blood from the LV, and delivering it to the aortic root using the venturi effect.12–15 It has been used to augment the cardiac output and to unload the LV in the setting of cardiogenic and postcardiotomy shock.12–15 Use of the Impella in the adult population as a short-term bridge to long-term mechanical support has also been described.15,16 We present our experience with the Impella 2.5 (Abiomed) as an adjunct for aggressive LV unloading during femoral VA ECMO support before implantation of a HeartMate II (Pleasanton, CA) long-term VAD.
Venoarterial ECMO was instituted during acute cardiogenic shock via cannulation of the femoral vein and artery using Carmeda-coated circuits (Medtronic, Minneapolis, MN) and a Quadrox D oxygenator (Maquet, Wayne, NJ). Patients were fully heparinized while on VA ECMO with hourly activated clotting times adjusted within the target range of 150–180 seconds. Central hemodynamics were monitored using an arterial and pulmonary artery catheter. Transesophageal echocardiography was used to confirm the placement of all cannulae and to adjust the support settings.
The Impella pump speed was set to optimally unload the LV as assessed by transesophageal echocardiography. The therapeutic goal of the Impella was normalization of the pulmonary capillary wedge pressure to <12 mm Hg. Suitability for cardiac transplant was ascertained while on full ECMO and Impella support, including the evaluation of neurologic function and restoration of end-organ function. Improving creatinine clearance with a creatinine <2.0 mg/dl, adequate urine output >0.5 ml/kg/hr, and reduction of liver enzymes to less than twice the normal value (aspartate aminotransferase [AST]/alanine aminotransferase <50 U/L) are essential before transition to the implantable LVAD or to myocardial recovery.
Transitioning to Permanent Mechanical Circulatory Support
Transitioning to a permanent mechanical circulatory system (HeartMate II) is performed using a median sternotomy with the pump pocket created while on combined VA ECMO and Impella support. The heparinization is adjusted to a level adequate for full cardiopulmonary bypass (CPB), which is initiated through a cannula high in the ascending aorta or through a previously placed femoral arterial ECMO cannula. In all patients, the ECMO femoral venous cannula is used for CPB. The ECMO circuit is divided and connected for CPB, while remaining on Impella support. Before the initiation of CPB, the Impella is turned off to prevent air entrainment or cavitation. The percutaneously placed Impella is removed through the transapical core by gently pulling the pump into the LV and transecting the catheter above the pump housing with Mayo scissors and withdrawing the remaining catheter through the femoral sheath. A HeartMate II LVAD is then placed in a standard fashion, and the Impella sheath is removed after reversal of heparin and correction of coagulopathy at the termination of the procedure.
Data are reported as means ± standard deviation. Baseline hemodynamic and laboratory data were collected following VA EMCO insertion and 24 hours after Impella 2.5 insertion and were compared using a two-tailed Student’s t-test.
Five patients while on VA ECMO had profound LV dysfunction (ejection fraction <20%), elevated pulmonary capillary wedge pressure >18 mm Hg, intermittent or absent opening of the aortic valve, a relatively enlarged LV, and evidence of stasis in LV with spontaneous echo smoke (Figure 2), which required the percutaneous placement of an Impella 2.5 via the femoral artery in the catheterization laboratory under fluoroscopic guidance (Figure 3). All Impella was implanted within 6 hours after ECMO initiation and after echocardiogram was obtained. The age of patients ranged from 19 to 63 years. The etiology of the shock was following a myocardial infarction in four patients and postpartum in one patient. Average Impella flow was 2.0 ± 0.5 L/min during support. Evidence of improved LV unloading using the Impell 2.5 can be seen in the echocardiographic images before and after Impella support (Figure 2). The overall LV end-diastolic diameter was reduced in all patients, and the Impella 2.5 system eliminated the smoke/swirl observed before implant. Evidence of the improved hemodynamics is shown in Figure 4. Systolic pulmonary artery pressures decreased from 48 ± 7 to 21 ± 5 mm Hg (p = 0.03), and diastolic pulmonary artery pressures decreased from 30 ± 10 to 13 ± 3 mm Hg (p = 0.04) after Impella placement. Further evidence of LV unloading is demonstrated by a decrease in the end-diastolic diameter (7.8 ± 1.4 to 6.2 ± 0.8 cm, p = 0.001).
Evidence of improving end-organ perfusion was observed after Impella implantation (creatinine: 1.39 ± 0.34 vs. 1.06 ± 0.21, p = 0.02; urine output: 0.3 ± 0.1 ml/kg/hr vs. 0.8 ± 0.4 ml/kg/hr, p = 0.03; AST: 710 ± 150 vs. 150 ± 52 U/L, p = 0.01; lactate: 3.0 ± 0.4 vs. 1.3 ± 0.3 mmol/L, p = 0.001). However, this improvement is likely more reflective of the improved perfusion following VA ECMO insertion. Lactate dehydrogenase was observed to be higher after Impella implantation when compared with ECMO alone (372 ± 52 vs. 246 ± 42 U/L; p = 0.05).
In spite of VA ECMO support along with LV unloading with the Impella 2.5, one patient developed progression of multisystem organ failure and care was withdrawn on post-ECMO and Impella on day 3. The Impella system functioned appropriately in achieving improved LV unloading that was, however, initiated in the presence of terminal end-organ dysfunction. No patient developed a complication related to the Impella 2.5. For patients meeting criteria for transition to long-term LVAD placement, coring of the LV for HeartMate II implantation revealed no evidence of thrombus within the ventricular cavity. Four patients were successfully bridged to HeartMate II after Impella 2.5 placement. All HeartMate II was implanted within 72 hours after Impella implantation and when the patient met criteria for long-term LVAD placement. All four patients were discharged between 23 and 30 days after HeartMate II placement.
Venoarterial extracorporeal membrane oxygenation is commonly used for temporary support during shock. Although it can be implanted via the femoral vessels to quickly reestablish normal oxygen delivery and perfusion, VA ECMO has limitations in patients with profound heart failure and acute cardiogenic shock. Venoarterial ECMO pressurizes the arterial system, increasing the afterload upon the failing heart. The increased afterload, particularly in a heart which is severely dysfunctional, will prevent the aortic valve from opening. The result is an increase in LV volume leading to distension and increased wall stress compromising myocardial recovery. Further sequelae of the increased LV volume include pulmonary venous hypertension resulting in pulmonary vascular injury, acute respiratory distress syndrome, and stasis resulting in thrombus formation within the LV cavity. In our experience, thrombosis of the LV with extension into the pulmonary vein and lung vasculature preclude recovery or transitioning to a long-term VAD.
Current management of LV distension during VA ECMO includes intra-aortic balloon pump, percutaneous atrial septostomy with a catheter placed into the left atrium, and central ECMO cannulation with direct inflow cannulae placement in the left atrium or LV. These techniques either experience ineffectiveness or technical risk and challenge.5–8 In our experience during VA ECMO, the intra-aortic balloon pump is often unable to adequately unload the LV during severe dysfunction and is the least effective technique. Although a left atrial septostomy will decrease LV distension, flow is diverted away from the LV and therefore does not fully prevent stasis and thrombus formation within the LV cavity. Furthermore, during transition to a LVAD, the atrial septum would need to be repaired. Central ECMO cannulation of the LV is effective, however, requires sternotomy or thoracotomy for placement.
Impella 2.5 has been used for LV unloading and hemodynamic support in the setting of cardiogenic shock. Due to percutaneous implantation, the Impella is an attractive option to decompress the LV without surgical intervention.17-20 Furthermore, due to the fact that the Impella not only decompresses the LV but also augments forward flow, the Impella 2.5 may be the optimal strategy to prevent LV stasis and thrombus formation.
Our experience suggests that the Impella 2.5 can sufficiently decompress the LV in combination with VA ECMO. With Impella during ECMO support, the LV end-diastolic diameter and pulmonary wedge pressure (PWP) decreased and indications of LV stasis, that is, echocardiographic smoke/swirl patterns, resolved. Not all patients require placement of the Impella during ECMO support. Evidence of pulsatility within the arterial line tracing, a PWP <18 mm Hg, and an absence of LV smoke during echocardiography demonstrate that the aortic valve is opening with every contraction. Therefore, the risk of LV distension, thrombosis, and acute respiratory distress syndrome is low. The Impella 2.5 is contraindicated in patients with established LV thrombus or significant aortic insufficiency. In patients with the presence of LV thrombus at the initial echocardiogram, we avoid implantation of the Impella 2.5 and proceed to direct LV cannulations with LV thrombectomy.
The Impella 2.5 can effectively unload the LV during peripheral VA ECMO support. Sufficient unloading not only allows for optimal hemodynamics but also prevents LV thrombus formation and pulmonary damage allowing for early placement of a long-term LVAD.
We appreciate the advice and superb technical assistance provided by Karl Q. Schwarz, MD, Ronald E. Angona, CCP, and William Hallinan, RN.
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