Singbartl, Kai

Abstract Peripheral veno‐arterial extracorporeal membrane oxygenation (pVA‐ECMO) has gained increasing value in the management of patients with critical cardiogenic shock (cCS), allowing time for myocardial recovery. Failure of myocardial recovery has life‐altering consequences: transition to durable mechanical circulatory support (dMCS), urgent heart transplantation, or withdrawal of support. Clinical factors controlling myocardial recovery under these circumstances remain largely unknown. Using a retrospective cohort, we developed a model for early prediction of transition to dMCS in patients undergoing pVA‐ECMO for cCS. To promote myocardial recovery, our clinical management centered around left ventricular pressure unloading, that is, targeting pulmonary capillary wedge pressures (PCWP) ≤18 mm Hg. We collected demographic data, laboratory findings, inotrope use, and two‐dimensional transthoracic echocardiography measurements, all limited to the first 72h of pVA‐ECMO (D1‐3). Out of 70 patients who were alive after pVA‐ECMO, 27 patients underwent implantation of dMCS. There was no significant difference in survival to hospital discharge between patients with or without transition to dMCS. Ejection fraction D1‐3 (per 10% increase, OR 0.37 [0.17‐0.79]) and amount of inotropic support D1‐3 (OR 4.77 [1.6‐14.18]) but neither myocardial wall tension nor PCWP emerged as significant predictors of transition to dMCS. Optimism‐corrected c‐index (0.90 [0.89‐0.90]) revealed an excellent discriminative ability of our model. In summary, our model for early prediction of transition to dMCS in patients with cCS undergoing pVA‐ECMO identifies indicators of inotropic state as relevant factors. Absence of markers for myocardial oxygen consumption or left ventricular pressure loading allows us to hypothesize sufficient cardiac unloading in our cohort with PCWP‐targeted management.

AbstractThe liver and kidney are key organs of metabolic homeostasis in the body and display complex interactions. Liver diseases often have direct and immediate effects on renal physiology and function. Conversely, acute kidney injury (AKI) is a common problem in patients with both acute and chronic liver diseases. AKI in patients with acute liver failure is usually multifactorial and involves insults similar to those seen in the general AKI population. Liver cirrhosis affects and is directly affected by aberrations in systemic and renal hemodynamics, inflammatory response, renal handling of sodium and free water excretion, and additional nonvasomotor mechanisms. Subsequent problems, for example, worsening ascites, hyponatremia, and AKI, often complicate management of patients with chronic progressive liver disease and add to their morbidity and mortality. Thus, AKI must be carefully defined and diagnosed in patients with liver disease. The kidney also plays a pivotal role in balancing acid–base disturbances resulting from advanced liver disease, making AKI in the setting of end-stage liver disease very difficult to manage clinically. While renal dysfunction in these patients often resolves following orthotopic liver transplant, dialysis may be required as a bridge to transplantation to mitigate the metabolic disarray found in these critically ill patients.

AbstractVeno‐arterial extracorporeal membrane oxygenation (VA‐ECMO) provides mechanical circulatory support for patients with advanced cardiogenic shock, facilitating myocardial recovery and limiting multi‐organ failure. In patients with severely limited left ventricular ejection, peripheral VA‐ECMO can further increase left ventricular and left atrial pressures (LAP). Failure to decompress the left heart under these circumstances can result in pulmonary edema and upper body hypoxemia, that is, myocardial and cerebral ischemia. Atrial septostomy can decrease LAP in these situations. However, the effects of atrial septostomy on upper body oxygenation remain unknown. After IRB approval, we identified 9 out of 242 adult VA‐ECMO patients between January 2011 and June 2016 who also underwent atrial septostomy for refractory pulmonary edema/upper body hypoxemia. We analyzed LAP/pulmonary capillary wedge pressure (PCWP), right atrial pressures (RAPs), PaO2/FiO2 ratios (blood samples from right radial artery), intrathoracic volume status, and resolution of pulmonary edema before and up to 48 h after septostomy. There were no procedure‐related complications. Thirty‐day survival was 44%. LAP/PCWP decreased by approximately 40% immediately following septostomy and remained so for at least 24 h. PaO2/FiO2 ratios significantly increased from 0.49 (0.38–2.12) before to 5.35 (3.01–7.69) immediately after septostomy and continued so for 24 h, 6.6 (4.49–10.93). Radiographic measurements also indicated a significant improvement in thoracic intravascular volume status after atrial septostomy. Atrial septostomy reduces LAP and improves upper body oxygenation and intrathoracic vascular volume status in patients developing severe refractory pulmonary edema while undergoing peripheral VA‐ECMO. Atrial septostomy therefore appears safe and suitable to reduce the risk of upper body ischemia under these circumstances.