Helen had severe Mitral Stenosis, and basically decompensated when her LV was not getting the needed volume to generate sufficient cardiac output, and when her LA pressure (and her pulmonary venous pressure) became severely elevated to lead to pulmonary edema. Patients with pulmonary edema secondary to acute heart failure can often be rescued with VA ECMO which quickly empties the LV and decompresses the pulmonary venous system. With some IV diuretics and a little time, the lungs can quickly improve and provide gas exchange. However, some patients, especially with “acute on chronic” failure need more time, and thus need more help.

Femoral VA ECMO support can provide perfusion and gas exchange, but it does not eliminate all flow into the left side of the heart. There is continued pulmonary venous return from the collateral flow from the multiple arterial branches off the aorta that feed the airway and lung parenchyma with oxygenated blood, as well as any blood that the ECMO venous cannula does not remove and is pumped from the RV into the lungs. When the patient’s lungs are also sick from edema or ARDS and inflammation, they may not be able to contribute much oxygenation, leading to highly desaturated blood for the LV to eject. Microsphere studies in animals have shown that on VA ECMO support when the LV is ejecting at all (i.e. the AV is opening and closing), that the vast majority of coronary flow comes from the LV ejection, not from the pump, even if the cannula is in the carotid artery or ascending aorta. If there is more ejection, the right arm and potentially the carotid arteries will also see desaturated blood, (which is why Femoral VA ECMO is very poor for primary respiratory support with very sick lungs). While people have referred to this situation as “Harlequin Syndrome” or “North-South Syndrome”, at the Academy we refer to this as “Proximal Hypoxemia” which better describes the actual problem and does not rely on a visual difference in patient color and cyanosis, or the differentiation of saturations between the right arm and lower extremities, which may not even be present if the LV ejection volume is small and only providing desaturated blood into the aortic root and coronaries, resulting in myocardial ischemia and EKG changes only. Learn more about the physiology of “Proximal Hypoxemia” and the configuration of VA-V ECMO in this Deep Dive.

Because of her severe hypoxemia and acute on chronic heart failure from mitral stenosis, Helen was placed on VA-V ECMO in the ICU using the femoral vessels, and the RIJ. A reperfusion catheter was also placed in her dorsalis pedis of the affected leg. With 3.5-4 L/min of arterial flow, and 500-750cc of RIJ flow, she experienced dramatic improvement with correction of her lactic acidosis, return of urine output, and recovery of consciousness. By ECMO Day #3 her lungs were completely clear and the RIJ cannula was no longer required. However, it was left in place for potential use in her planned upcoming surgery. She was extubated, and her flow maintained at about 2.5-3 L/min. On ECMO Day #7, she underwent transition from VA ECMO to CPB, and had a successful MVR, and decannulation with repair of the femoral artery. Her course was complicated by postoperative pulmonary hypertension requiring iNO and subsequently sildenafil, treatment for postoperative atrial fibrillation, brief Dialysis for AKI, as well as developing HIT and a switch to bivalirudin during coumadin initiation, but after a few weeks of recovery, she was discharged to home with her family.