Extracorporeal membrane oxygenation (ECMO) has traditionally been used to mechanically support both the heart and lungs in patients with severe cardiorespiratory or cardiac failure.1 However, this form of mechanical support delivers blood directly into the arterial system with insufficient drainage to unload the left ventricle (LV), thereby increasing afterload and consequently, wall stress.1 In an acutely failing heart, e.g., fulminant myocarditis, this means increased oxygen demand and decreased or delayed myocardial recovery. Alternatively, left ventricular assist devices (LVAD) were designed to provide hemodynamic support in patients with severe left ventricular failure. The LVAD unload blood from the LV and propel it forward into the systemic vasculature. As a result, the heart works less, myocardial oxygen demand decreases, and myocardial recovery improves.1 The development of percutaneous LVAD devices has widened the spectrum of indications for their use; however, unlike ECMO, they do not offer respiratory support or right ventricular support. While the combined use of these devices has been rare, there have been reports suggesting that concurrent use of intra-aortic balloon pumps combined with percutaneous LVAD improve recovery of the LV.2 However, there have been no reports to this date describing the concurrent use of ECMO with percutaneous LVAD. We present the successful bridging to recovery of a patient in fulminant viral myocarditis, with severe biventricular heart failure and respiratory failure, using a combination of a percutaneous LVAD and ECMO.
A 31 year-old man with no significant medical history presented to his primary care provider after 3 days of flu-like symptoms including sore throat, fevers, and myalgia. He denied sick contacts or recent travel and after receiving more antibiotics, his symptoms worsened. He developed nausea, vomiting, diarrhea, and severe fatigue prompting him to present to an outside hospital. On physical examination, he was found to be afebrile and tachycardic with a mean arterial pressure of 60 mm Hg. He was tachypneic with bilateral crackles at the bases, jugular venous distension, tachycardia, and a gallop. Routine investigation revealed bibasilar pneumonia with leukocytosis (white blood cell 30,000 cells/µl) and acute renal failure (creatinine 5.8 mg/dl). Echocardiogram revealed a moderately reduced left ventricular systolic function (ejection fraction of 25%) with severe global hypokinesis. He required pressors and inotropic support and subsequently was transferred to our center for further evaluation and management.
On arrival, he was in cardiogenic shock with shock liver and acute renal failure. The right heart catheterization showed a reduced cardiac output and low systemic vascular resistance. Endomyocardial biopsy revealed diffuse round cell inflammation-associated inflammatory infiltrates, and fibroblastic proliferation consistent with myocarditis (Figure 1A). In the ensuing 3 days, the patient was intubated secondary to respiratory failure and worsening pulmonary edema with a metabolic and respiratory acidosis, requiring dialysis. Also, dobutamine, dopamine, epinephrine, and vasopressin were titrated to maximum doses. Unfortunately, his hemodynamic status continued to deteriorate over the course of a few hours, and 4 days after admission, he required insertion of a percutaneous LVAD (Impella 2.5; Abiomed, Danvers, MA) via the left common femoral artery. A repeat endomyocardial biopsy at the time of LVAD insertion showed florid mononuclear cell infiltrate with associated myocardial necrosis (Figure 1B). He also received antiviral therapy and intravenous immunoglobulin. Despite mechanical and pharmacological support, his respiratory and circulatory status continued to deteriorate (Figure 2). He developed biventricular cardiac failure and respiratory failure, and the patient was placed on ECMO. The right common femoral artery was cannulated distally with a 5 French cannula (Glidesheath; Terumo Medical Corporation, Somerset, NJ) for perfusion of the leg and proximally with a 22 French arterial cannula and connected to the arterial limb of the ECMO circuit. The right common femoral vein was cannulated with a 28 French cannula, directed to the right atrium and connected to the venous limb of the ECMO circuit. Extracorporeal membrane oxygenation flow was 4 L per minute and the flow on the Impella was decreased from 2.5 to 1.0 L per minute to decompress the LV. After ECMO was started, his blood pressure improved from 60 to 100 mm Hg. The patient was on high doses of vasoconstrictors (300 µg/minute of phenylephrine, 20 µg/kg/minute of dopamine, 10 µg/kg/minute of dobutamine, and 2.4 units per hour of vasopressin) before the ECMO was started and shortly after phenylephrine, dopamine, were weaned off.
Unfortunately, as a complication to the Impella LVAD placement and high doses of vasopressors, the patient developed left leg compartment syndrome requiring fasciotomy. His hemodynamic status subsequently improved significantly. Extracorporeal membrane oxygenation was discontinued on day 8 (3 days of ECMO support), and Impella on day 9 of admission. Inotropes were completely weaned off on day 13. The remainder of his hospital course was complicated by critical illness neuropathy and myopathy requiring aggressive physical therapy and nose bleeds secondary to anticoagulation. He was eventually weaned off dialysis and extubated. He improved with supportive care and was transferred to rehabilitation and eventually discharged home.
Myocarditis is an inflammatory condition of the myocardium that may result in decreased cardiac function and the inability to maintain sufficient systemic pressures. This often results in a systemic inflammatory reaction involving activation of complement pathways, release of cytokines, and increased production of nitric oxide, which is responsible for vasodilatation and further myocardial depression.3
The initial therapy for patients in cardiogenic shock includes medications that augment the hemodynamic profile by increasing myocardial contractility and increasing systemic vascular resistance. However, when medical therapy is unable to maintain adequate cardiac output, mechanical circulatory support is indicated. Left ventricular assist devices can be lifesaving in such circumstances by improving the cardiac output and maintaining sufficient perfusion pressures to vital organs. Studies have suggested that patients presenting with fulminant myocarditis, who are successfully supported to recovery, have a 93% chance of transplantation-free survival at 11 years.4 Developments have rendered newer devices such as the Food and Drug Administration-approved Impella LVADs that aspirate blood from the LV and propel it forward into the ascending aorta.5 These devices can provide a maximum output of 2.5 (Impella 2.5) to 5.0 L/minute (Impella 5.0). In addition to providing circulatory support, the LVAD also helps in unloading the LV or decreasing preload allowing time for left ventricular recovery.6 These LVAD (Impella 2.5 and Impella LD 5.0) have been used successfully in patients with cardiogenic shock to allow time for LV recovery after fulminant myocarditis and ischemic injury.3,7,8 We initially placed the Impella in our patient to offer circulatory support and to help unload the LV. However, despite the additional support our patient continued to deteriorate because of severe biventricular failure.
In contrast, ECMO, which has been used as a bridge to LVAD, offers mechanical support via a single venoarterial circuit with oxygenation.5 Hence, it can be used to provide support for patients with respiratory failure and biventricular failure. In cases of severe LV failure, the ECMO circuit may not be able to decompress the LV, resulting in LV distension,6 thereby delaying ventricular recovery.1 It is not uncommon to insert a catheter into the pulmonary artery or into the left atrium and connect it to the venous limb of the ECMO circuit to decompress the LV in patients with severe biventricular failure on ECMO.
In patients who already have an Impella LVAD and develop biventricular failure that requires ECMO support, it is possible to keep the Impella device in place to decompress the LV while on ECMO. Also, the LVAD allows weaning the patients from ECMO earlier, because it can provide partial LV support when ECMO is removed. When used in combination with ECMO, the speed of the Impella should be reduced to a minimum that enables adequate decompression of the LV to decrease hemolysis. Furthermore, we do not advocate to use the Impella as a way to decompress the LV a priori but as an alternative way when other methods are not readily available, such as a cannula inserted to the left atrium (via transeptal approach) and connected to the venous limb of the ECMO circuit. To our knowledge, this is the first reported case of Impella LVAD and ECMO being used synergistically and successfully as a bridge to recovery.
We are thankful to Azorides R. Morales, MD, for providing the pathology images shown in the manuscript and Juan C. Infante, MD, for providing the X-ray images.
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Copyright © 2012 by the American Society for Artificial Internal Organs
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