Percutaneous Veno-arterial Extracorporeal Membrane Oxygenation: Another Tool in the Interventional-Heart Failure Armamentarium

Acute right ventricular (RV) failure is a major cause of morbidity and mortality, yet is largely ignored by clinical practice guidelines. In the setting of left-sided heart failure, inferior myocardial infarction, chronic lung disease, congenital heart disease or acute pulmonary embolus, concomitant RV dysfunction confers worse clinical outcomes.^1,2 Normal RV function is governed by pulmonary vascular resistance (PVR), systemic venous return, pericardial compliance and native contractility of both the RV free wall and interventricular septum. As compared to LV function, generating RV output requires 1/6th the energy expenditure since the majority of RV stroke work maintains forward momentum of blood flow. An impediment to pulmonary vascular flow will therefore acutely diminish RV stroke work,³ while reduced RV contractility, as in the case of isolated RV ischemia, may be well-tolerated hemodynamically until RV afterload is increased.⁴ Management of acute RV failure depends on the underlying cause. In primary RV systolic dysfunction, maintaining low PVR with or without augmenting RV contractility with inotropes often provides adequate hemodynamic support. However, when RV failure occurs in the setting of high PVR, supporting RV function with pulmonary vasodilators and inotropic therapy may be insufficient. Historically, refractory RV failure required either atrial septostomy, transplantation, or surgically-implanted mechanical RV assist devices (RVAD). In the modern era, percutaneous circulatory support devices provide an opportunity for early intervention in the cascade of RV failure. In this issue, Belohlavek et al⁵ examine four cases of RV failure with an obstructive hemodynamic pattern. In each case, emergent percutaneous veno-arterial extracorporeal membrane oxygenation (VA-ECMO) provided circulatory support via femoral-to-femoral cannulation. Two patients survived to hospital discharge, while the other two succumbed to multiorgan failure. In both cases of VA-ECMO failure, the patients presented with chronic pulmonary hypertension due to either familial disease or congenital heart defects, while in the two cases of VA-ECMO success, device support was initiated before the onset of irreversible end-organ damage. This finding highlights the need for mechanical percutaneous RV support options that can be safely implanted early in the progression of RV failure and cardiogenic shock. Each case described in this report represents a rare glimpse into the real-world application of percutaneous VA-ECMO. At present, mechanical devices for RV support include the intra-aortic balloon pump (IABP), the percutaneous RVAD (pRVAD; Figure 1A), right atrial (RA) to left atrial (LA) ECMO via transseptal puncture, and VA-ECMO (Figure 1B).⁶ The benefit of IABP therapy for RV failure is to enhance coronary perfusion and indirectly reduce RV afterload by reducing LV filling pressures.⁷ The pRVAD provides substantial hemodynamic RV support by generating centrifugal flow from the RA to pulmonary artery (PA); however, it can be limited by sensitivity to loading conditions.⁸ In the case of severe pulmonary hypertension, RA-to-PA bypass provided by the pRVAD may worsen pulmonary hypertension and increase the risk of lung injury.⁹ The widespread application of percutaneous VA-ECMO as a therapeutic option for RV failure has several advantages and disadvantages. First, VA-ECMO directly unloads the RV and pulmonary vascular circuit, thereby reducing RV and PA pressures. Second, VA-ECMO enhances systemic oxygenation, whereas pRVADs depend on native lung function. Third, percutaneous insertion of VA-ECMO cannulae into the femoral artery and vein is considerably easier than placement of a large-bore cannula into the main PA and can be performed at the bedside. This difference is critical when placing circulatory support devices under emergent conditions since bifemoral cannulation avoids risks associated with pRVAD cannulation such as: 1) mechanical injury of the RV or PA; 2) induction of ventricular arrhythmias; and 3) cannula migration into the distal PA. Furthermore, bifemoral cannulation for VA-ECMO may also be used as a means of LV or biventricular support10,11 without the need for transseptal puncture associated with percutaneous LA to femoral artery (FA) bypass. Percutaneous VA-ECMO has several potential disadvantages. First, the incidence of mechanical complications during large-bore cannulation ranges from 0.8–8%, while limb ischemia can occur in 13–25% of cases.12 Limb ischemia can be mitigated by antegrade perfusion catheters into the superficial FA. Second, circuit complications including thrombosis, oxygenator failure or pump failure occur in 3–25% of cases.¹¹ The two most catastrophic complications include systemic gas embolism and exsanguination from ruptured circuit tubing, are exceedingly rare. Third, since oxygenated blood returns to the systemic circulation via the FA, oxygenation of the superior third of the body is dependent on antegrade LV ejection, which if impaired, can result in upper-body hypoxia. Fourth, systemic inflammatory response after initiation of ECMO usually results in a period of worsening lung function prior to recovery.¹³ Finally, most intensive care units are not set up to support ECMO, which generally requires close monitoring of blood coagulation, oxygenation and perfusionist support. While percutaneous cardiac support devices have existed for over three decades, they now represent a bridge to definitive therapy or recovery as advances in coronary intervention, cardiac surgery, transplant medicine and VAD technology provide more options for patients surviving cardiogenic shock. The role of VA-ECMO in the percutaneous armamentarium of the modern catheterization laboratory will depend less on the ability to place the device, but rather on improved algorithms for patient selection, patient and device monitoring and weaning protocols.

References

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From ^*The Cardiovascular Center, Tufts Medical Center, Boston, Massachusetts; ^#Texas Heart Institute/St. Luke's Episcopal Hospital, Houston, Texas. Corresponding Author: Navin K. Kapur, MD, The Cardiovascular Center, Tufts Medical Center, 800 Washington Street, Box # 80, Boston, MA 02111. E-mail: nkapur@tuftsmedicalcenter.org