Clinical Pearls of Venoarterial Extracorporeal Membrane Oxygenation for Cardiogenic Shock

The ratio of oxygen delivery to consumption

Bartlett and Conrad5) SA explained the ratio logically. Oxygen delivery (DO₂) is the amount of oxygen delivered to the peripheral tissues per minute, or the product of arterial oxygen content (CO₂) times the cardiac output. Oxygen is present in the blood as oxygen dissolved in the plasma and bound to hemoglobin present in the red blood cells. The following are the mathematical formulas to calculate DO₂ in a patient on ECMO.

DO₂ (cc/min)

 =Cardiac output (L/min)×arterial CO₂ (cc/dL)×10

CO₂ (cc/dL)

 =Hemoglobin bound O₂+dissolved O₂

 =(Hemoglobin [g/dL]×saturation [%]×1.36 cc/g)+(pO₂ [mmHg]×0.0031 cc/mmHg/dL)

DO₂ during VA ECMO

 =Native cardiac output×arterial CO₂+ECMO flow×perfusate CO₂

If we take a closer look at the formula, DO₂ is controlled by cardiac output, hemoglobin concentration, hemoglobin saturation, and dissolved oxygen, in that order. Therefore, if DO₂ is insufficient, it is necessary to calibrate it in the above order to efficiently increase DO₂.

Oxygen consumption (VO₂) is controlled by tissue metabolism. The normal DO₂:VO₂ ratio is 5:1. Mixed venous oxygen saturation (SvO₂) results from this ratio. If systemic DO₂ is moderately decreased and there is no change in VO₂, the amount of oxygen extracted from each deciliter of arterial blood is greater. This results in decreased SvO₂. If DO₂ is severely decreased, there is insufficient oxygen to meet metabolic demands, anaerobic metabolism occurs, and, finally, lactic acidosis and shock occur. In practice, this situation occurs when the DO₂:VO₂ ratio is less than 2:1. Therefore, the overall goal of management is to keep DO₂ at least twice the VO₂, and preferably 5 times the VO₂. Since SvO₂ reflects this ratio accurately, it is one of the most important considerations when monitoring and managing critically ill patients.

ECMO is indicated when other treatment modalities cannot sustain the DO₂:VO₂ ratio. If DO₂:VO₂ ratio decreases due to decreased DO₂ in cardiogenic shock, ECMO can increase systemic blood flow to replace the reduced cardiac output. Cardiogenic and obstructive shock reduces not only the cardiac output but also CO₂ in the blood due to ventilation-perfusion mismatch. ECMO can correct both the decreased cardiac output and CO₂. In septic shock, DO₂:VO₂ ratio decreases due to the increase in VO_2. Moreover, if the septic shock is combined with decreased cardiac contractility, DO₂ is decreased, further reducing DO₂:VO₂ ratio, hence, ECMO may be considered.

To summarize, VA ECMO can be an option for the treatment of various types of shock because it can increase CO₂ and systemic blood flow and eventually increase DO₂. Hence, the goal of VA ECMO is as follows: to restore organ blood flow and adequate tissue oxygenation while awaiting recovery, without damaging to the lungs or circulation.6)

Interaction between the native cardiovascular system and venoarterial extracorporeal membrane oxygenation

The important basic pressure-volume loop of left ventricle (LV) are shown in Figure 2A. The loop changes as cardiogenic shock occurs (Figure 2B). In the beginning, the stroke volume and the left ventricular end-systolic pressure (LVESP) decrease. Left ventricular end-diastolic pressure (LVEDP) or left ventricular end-diastolic volume (LVEDV) can be increased secondarily but not greatly in a short time. As the cardiogenic shock develops some more, LVEDP and LVEDV begin to increase, maintaining some linear correlation. If the cardiac shock persists, LVEDV increases, but LVEDP increases furthermore. Subtle increases in LVEDV can be associated with substantial increases in LVEDP due to the nonlinear end-diastolic pressure-volume relationship.7)

Figure 2 Pressure-volume loops before and after VA ECMO. (A) Normal pressure-volume loop. (B) Representative pressure-volume loop as heart failure persists and deteriorates. (C) Impact of ECMO flow during VA ECMO. (D) Impact of decreasing PVR during VA ECMO. (E) Impact of inotropic agent during VA ECMO. (F) Impact of decreasing preload during VA ECMO. Modified from Burkhoff et al.7) CGS = cardiogenic shock; ECMO = extracorporeal membrane oxygenation; LV = left ventricle; LVEDP = left ventricular end-diastolic pressure; LVSP = left ventricular systolic pressure; PVR = peripheral vascular resistance; VA = venoarterial. Click for larger imageDownload as PowerPoint slide

If VA ECMO is started in this state, the pulse pressure is decreased and the mean arterial pressure (MAP) is increased. The stroke volume decreased because the amount of native cardiopulmonary circulation decreases due to the physiology of ECMO called cardiopulmonary bypass.7), 8) Increasing the ECMO flow further reduces the stroke volume, increases the LV afterload, and increases the LVEDV and especially LVEDP as shown in the Figure 2C.7)

The increased LV end-diastolic, left atrial (LA), and pulmonary capillary wedge pressures during VA ECMO can be mitigated by decreases in systemic vascular resistance or improvement in ventricular contractility. First, the peripheral vascular resistance (PVR) can be decreased as shown in Figure 2D. PVR can be reduced naturally by the baroreceptors, pharmacologically (e.g., nitroprusside) or mechanically (e.g., by intra-aortic balloon pumping).7) This increases stroke volume as well. Pharmacological enhancement of contractility is also possible, but may not be beneficial in cardiogenic shock due to their independent effects in increasing myocardial VO₂ and potential effects on heart rate and arrhythmias (Figure 2E).7) Reducing the cardiac preload through volume restriction can also reduce LVEDP or LVEDV to some extent (Figure 2F).7) Therefore, monitoring for an increase in LVEDP is important by performing serial physical examinations, chest radiographies, and echocardiographies and monitoring the pressures from Swan-Ganz catheter.9)

If the heart recovers, the pulse pressure and MAP increase. However, if it does not recover and it gets worse, the LVEDP and pulmonary capillary wedge pressure increase furthermore. These increases are detrimental to blood oxygen saturation coming from the lungs and markedly increase myocardial oxygen demand, which can worsen LV function, especially in acute myocardial ischemia or infarction.7) In such cases, the left heart venting should be considered, which will be discussed later. The typical changes of ventricular loads or coronary perfusion during VA ECMO are summarized in Table 1. Based on these physiologic interactions between the native cardiovascular system and VA ECMO, we suggest minimizing dose of vasopressors (afterload reduction), fluid removal (preload reduction), and keeping a good amount of ECMO flow (adequate tissue oxygenation). This principle will let the native heart rest while balancing tissue oxygen supply and demand.

Table 1 The changes of ventricular loads and coronary perfusion during VA ECMO Click for larger imageClick for full tableDownload as Excel file

Harlequin syndrome

During VA ECMO, perfusate blood from ECMO mixes in the aorta with the LV blood, which has traversed the lungs. Hence, the content of oxygen and carbon dioxide in the patient’s arterial blood represents a combination of blood from these 2 sources, and the total systemic blood flow is the sum of the extracorporeal flow plus the amount of blood passing through the heart and lungs.5) Fully saturated blood from the ECMO circuit will meet the blood ejected from the native ventricle. The location of this mixing point, so called the watershed point, depends upon the amount of ECMO support provided and the degree of LV ejection. If there is extremely severe myocardial dysfunction, the mixing point will typically be in the proximal ascending aorta or aortic root. As myocardial function improves, the mixing point may migrate more distally into the descending thoracic aorta. The CO₂ of blood ejected by the LV depends on the gas exchange ability of the native lungs. If significant pulmonary edema is present, hypoxic blood may perfuse the proximal aortic branches, including the coronaries and the innominate artery. The patient's upper body will appear blue, while the lower body will appear pink.10) This is the reason we call it Harlequin syndrome. The watershed point has been shown in computed tomography or fluoroscopic images in several reports.11), 12), 13), 14) Therefore, measuring saturations in the right hand or analyzing arterial blood gases from the right arm is important (Figure 3).10)

Figure 3 A simplified diagram showing the physiology of VA ECMO. Harlequin syndrome is common during VA ECMO. Patients on VA ECMO often have lung failure caused by pulmonary edema with preexisting cardiogenic shock, combined pneumonia, ventilation-perfusion mismatch, and pulmonary edema by left ventricular distension. If mixing point is distal to the aortic arch, patients are at risk of cerebral ischemia. ECMO = extracorporeal membrane oxygenation; RA = right atrium; VA = venoarterial. Click for larger imageDownload as PowerPoint slide

Cardiogenic shock and cardiac arrest

The best indication of VA ECMO is a cardiogenic shock. Common causes of cardiogenic shock are acute myocardial infarction, acute myocarditis, progression of cardiomyopathy, acute allograft rejection after heart transplantation, overdose of cardiotoxic drugs, refractory ventricular tachycardia, failure to wean off cardiopulmonary bypass, or cardiac failure coexistent with severe respiratory dysfunction. Although the most important step for successful VA ECMO is correct diagnosis, the timing of application is also important. Medical refractoriness is practically difficult to define. Persistent hypotension (systolic blood pressure less than 80 mmHg), increase of lactate level, worsening metabolic acidosis, frequent non-sustained ventricular tachycardia or fibrillation, and requirement of other organ support devices such as dialysis or intra-aortic balloon pump (IABP) under high-dose inotrope or vasopressor infusion suggest the timing of VA ECMO.15) It is very important to start VA ECMO before cardiac arrest. The outcome of VA ECMO before cardiac arrest is much better than that of extracorporeal cardiopulmonary resuscitation (ECPR). A common mistake in the intensive care unit is the reliance on blood pressure only in deciding the initiation of VA ECMO. The cause of cardiogenic shock, responsiveness of medical therapy, signs of organ hypoperfusion (drowsy mentality, agitation, dyspnea, cold skin, and poor urine output), and laboratory findings should be taken into consideration when making a decision to initiate VA ECMO.

ECPR is the application of rapid deployment of ECMO to provide circulatory support in patients under cardiac arrest who fail to achieve a sustained return of spontaneous circulation (ROSC).9) Two studies of propensity score matching demonstrated the neurological or survival benefits of ECPR over conventional cardiopulmonary resuscitation (CPR).16), 17) Most practitioners would agree that the goal is to minimize the duration of cardiac arrest and advocate shorter periods of CPR as being optimal. The previous reports usually suggest that the duration of CPR before ECMO should be less than 30 minutes, not greater than 60 minutes.18), 19), 20) Commonly used inclusion criteria for ECPR are as follows9): witnessed arrest,21) bystander CPR initiation within 5 minutes, high-quality and uninterrupted CPR including end-tidal CO₂ more than 10 mmHg,22) failure to achieve ROSC within 15 minutes of CPR, initial rhythm of ventricular fibrillation or ventricular tachycardia, and age less than 70 years. Nevertheless, age greater than 70 years is not an exclusion criterion.23) The 2015 American Heart Association guidelines recommended that in settings where it can be rapidly implemented, ECPR may be considered for selected patients with cardiac arrest for whom the suspected etiology of the cardiac arrest is potentially reversible during a limited period of mechanical cardiorespiratory support.22)

Pulmonary thromboembolism

Treatment of acute pulmonary thromboembolism (PTE) varies considerably depending on the amount of thrombus and vital signs. VA ECMO is useful in rapidly deteriorating vital signs such as cardiac arrest or refractory shock because of acute PTE, that is, massive PTE.24), 25), 26), 27), 28) Moreover, if we consider the ECMO's physiology of partial cardiopulmonary bypass, VA ECMO is the most suitable device for the pathophysiology of right heart failure from PTE. After the patient becomes stable, the treatment for the thrombus should be selected among the following options: anticoagulation,25), 29) systemic thrombolysis,30) catheter-directed thrombectomy or thrombolysis,31) or surgical embolectomy.24), 26) The European Society of Cardiology 2014 acute PTE guidelines briefly mention that ECMO can be used to treat massive PTE as a method for hemodynamic support and as an adjunct to surgical thrombectomy.32) Because VA ECMO itself requires systemic anticoagulation, VA ECMO with or without catheter-directed thrombectomy may cure acute PTE.31) Thrombolysis, especially systemic thrombolysis, would to be dangerous under VA ECMO. Authors have experienced severe uncontrollable cannulation site bleeding after thrombolysis.

Septic shock

Sepsis was historically regarded as a contraindication to ECMO.1) A number of studies demonstrated that it could be lifesaving in neonatal and pediatric septic shock.33) Therefore in neonates and children, ECMO has been established as a valid salvage therapy. However, the evidence of its benefits in adult patients is weak, particularly in cases of refractory septic shock.34) Controversies surrounding the benefits of ECMO in septic shock with a predominantly vasoplegic phenotype persist.35) Favorable outcomes of VA ECMO in patients with septic shock combined with heart failures have been reported for recent years.36), 37), 38), 39)

When applying VA ECMO for septic shock, the central ECMO is often performed because vasoplegia requires a significant amount of ECMO flow. Central ECMO can insert the largest available cannulae directly into the right atrium and ascending aorta. MacLaren et al.33) reported that the central ECMO has been used in adult patients to achieve flows of up to 10 L/min with good outcomes. If the central ECMO is hesitant due to the bleeding risk, bilateral femoral cannulation can be considered.40) However, high-flow VA ECMO for septic shock does not seem to produce consistently favorable outcomes. We suggest using ECMO only when there are significant signs of combined cardiogenic shock such as high central venous pressure or pulmonary artery occlusion pressure.9) A sepsis patient with low LV ejection fraction and multi-organ failure already in progress is inadequate to perform VA ECMO because cardiac failure may be a sign of imminent death.

Cannulation strategies

There are 2 principles in VA ECMO configurations. One is central and another is peripheral. Although there is no clear definition of central ECMO, it generally means that at least one of the venous or arterial cannulation sites is in the central vessels (vena cava, pulmonary artery, or aorta) or cardiac chambers. Peripheral ECMO is inserted only through the peripheral vessels. Most of the VA ECMO is cannulated peripherally. The Seldinger technique is usually used for cannulation. Cannulae can be inserted blindly. However, the vast majority of patients who require VA ECMO for cardiovascular reasons have weak pulsatility.41) Therefore, ultrasound-guided cannulation or surgical exposure of the vessels is useful. Fluoroscopic-guided cannulation is also helpful in advancing the guidewire or cannula without vascular complications.21)

Peripheral cannulation entails drainage of the venous blood from the right atrium through a cannula that exits the femoral vein. Multistage cannula is usually inserted with its tip in the inferior vena cava, right atrium or superior vena cava. Less commonly, the right internal jugular vein may also be used. Typically, the arterial cannula is a short cannula inserted in the femoral artery with the tip in the common iliac artery. Alternatively, arterial blood can also be returned into the axillary or subclavian artery through a side graft or directly.42), 43)

The main advantage of peripheral cannulation is its ease of cannulation. The cannulation is often performed bedside and can even be performed in patients undergoing CPR. Disadvantages include the occurrence of Harlequin syndrome, aortic root thrombus formation, LV distension, and lower extremity ischemia. Furthermore, femoral cannulation may not be feasible in patients with significant peripheral vascular disease.44)

In some peripheral VA ECMO cases, an additional cannula can be inserted to make two kinds of triple cannulations. One is venoveno-arterial ECMO which refers to the insertion of an additional venous drainage cannula typically into the right internal jugular vein. This intends to improve drainage and unloading.44), 45) Another is veno-venoarterial or veno-arteriovenous ECMO which provides respiratory and circulatory support simultaneously. Part of the outflow is directed toward the right atrium. The relative flows of the 2 outflow limbs (arterial and oxygenated venous) are modulated using the adjustable clamps and flow sensors and must be carefully regulated as each change will impact preload, afterload, oxygenation, and location of the watershed.45)

The configuration of the central ECMO was originated from the classical cannulation during cardiac surgery. However, recently, it is performed when obtaining higher ECMO flow is necessary or peripheral cannulation is impossible. The short, large-bore venous cannulae are used for greater cardiac decompression than in peripheral cannulation. Additionally, as oxygenated blood is returned to the ascending aorta, there is less concern for retrograde flow and Harlequin syndrome.44) In most ECMO centers, chest is kept closed after central VA ECMO. After recovery from the surgery, the patient may be able to move more liberally than peripheral cannulation. This can be a significant benefit to the patients who have to wait for recovery or transplantation for longer period such as several weeks. A key disadvantage of central cannulation is that it requires entering the chest for cannulation and decannulation. As such, central cannulation results in the increased risk of bleeding, surgical reexploration, and mediastinitis.44)

Monitoring of adequate oxygen delivery

Complications

Left ventricle distension and pulmonary edema

ECMO does not directly decompress the LV. Some venous blood continues to enter the right ventricle and thus is delivered through the pulmonary circulation into the LV. Additionally, bronchial circulation and Thebesian veins will also deliver blood into the LV. This blood must be ejected through the aortic valve and into the arterial circulation.10) Without satisfactory ejection, blood will accumulate under pressure, until it eventually equalizes with systemic arterial pressure. The LV will not eject if its systolic function is too poor to overcome the afterload. Without urgent correction, severe pulmonary edema will occur, followed by fatal pulmonary hemorrhage. The LV must be encouraged to eject, by maintaining inotropes and decreasing afterload or blood pressure. Liberal use of echocardiography can be helpful in demonstrating routine opening of the aortic valve and in allowing the measurement of LV dimensions.10) A pulmonary artery catheter can also be helpful by noting a progressive increase in left-sided filling pressures. Dyspnea, low SaO2 of the right hand, increased tracheal secretion, and bloody and watery sputum are classic signs of LV distension. Aggravation of bilateral pulmonary congestion after VA ECMO also suggests pulmonary edema by VA ECMO. Generally, pulmonary artery occlusion pressure or pulmonary capillary wedge pressure, diastolic pulmonary artery pressure, and mean right atrial pressure reflect directly or indirectly LVEDP. High LVEDP will affect the pulmonary artery pressure and right atrial pressure. If there is no pulmonary artery catheter, monitoring the right atrial pressure may be helpful to detect LV distension. In echocardiography, decreased LV ejection fraction with increased LV end-diastolic dimension may suggest LV distension. Echocardiography will reveal many signs of increased LVEDP. Increased amount of valve regurgitation after VA ECMO is also helpful in diagnosing LV distension. There is no single diagnostic finding of LV distension. There should be a combination of symptoms or signs and available data from invasive lines or echocardiography. If the LV is distended despite the infusion of inotropes or vasodilators, left heart must be physically decompressed.10) Kapur and Esposito56) summarized the relationship between pressure and volume of the LV during VA ECMO with or without LV venting. VA ECMO reduces biventricular volumes with a concomitant increase in MAP and both LV systolic and diastolic pressures as we explained earlier in Figure 2B. This increase in LV afterload or wall stress occurs because there is no direct venting of the left heart with VA ECMO. Venting of the left heart with an IABP, Impella device, transaortic catheter, or transseptal LA cannula during VA ECMO support reduces LVESP and LVEDV. Left heart venting not only improves left heart distension but also improves Harlequin syndrome.57) ECMO with left heart decompression is known to improve survival in severe cardiogenic shock.58)

A number of methods have been suggested for left heart venting. Venting with other mechanical circulatory support such as IABP and Impella will be discussed in detail later.

1) Percutaneous transseptal LA venting

Percutaneous transseptal LA venting is performed with transseptal cannula insertion over the wire after transseptal atrial puncture. 59), 60), 61), 62) If multistage venous cannula is available, we prefer inserting a single multistage venous cannula over the interatrial septum. This approach is referred to as LA-VA ECMO. LA-VA ECMO generally offers a sufficient biventricular decompression (Figure 4). 63)

Figure 4 LAVA ECMO. (A) In LAVA ECMO, the multistage cannula drains both in the left atrium (via end hole) and right atrium (via side holes). (B) A chest radiograph in which the cannula tip (red arrow) is placed in the left atrium through the atrial septum. ECMO = extracorporeal membrane oxygenation; LAVA = left atrial venoarterial. Click for larger imageDownload as PowerPoint slide

2) Balloon atrial septostomy

Balloon atrial septostomy or atrial septal stenting, which induces left-to-right shunt during LV dysfunction, has been introduced as a less invasive technique than LA drainage through the transseptal puncture.61), 64), 65), 66), 67) However, if the hole of septostomy is not large enough, left-to-right shunt may be ineffective.62)

3) Surgical left heart venting

Left heart vent cannula can be inserted through the right upper pulmonary vein.68) The cannulation can be performed with the right mini-thoracotomy as a less invasive technique. It can later be used as a drainage cannula for paracorporeal LV assist device if necessary.69), 70) Transapical LV cannulation through full sternotomy, lower median sternotomy,71) or left mini-thoracotomy72) is also known to be useful, which has the advantage of subsequent bridging the LV assist device later.72)

4) Transaortic catheter left ventricle venting

In LV venting catheterization, the catheter is inserted retrogradely through the aortic valve.73) Moreover, this technique is considered to be less invasive technique, but as of today, the amount of drainage collected in this technique seems to be insufficient.74), 75)

5) Percutaneous pulmonary artery venting

Percutaneous pulmonary artery venting with a 15-Fr drainage cannula via the jugular vein is considered a less invasive technique, which is inserted under fluoroscopy.76), 77)

Venting with other mechanical circulatory support such as IABP and Impella will be discussed in detail later.

Anticoagulation-related complications: thromboembolism and bleeding

The primary purpose of systemic anticoagulation is to protect the major organs from thromboembolism. The secondary reason of anticoagulation is to keep ECMO circuit patent. There may be 2 sources of thrombi including native cardiopulmonary system and extracorporeal circuit. The more dangerous site of thrombi is the native cardiopulmonary system, since it is close to the coronary arteries and cerebral vessels. Currently available ECMO circuits are generally resistant to thrombus formation and sudden malfunction. It is highly important that good anticoagulation status is maintained during high-flow VA ECMO because native cardiopulmonary blood flow is slow or static (Figure 5). In adult patients, ECMO blood flow 1 L/min is enough to keep the circuit patent. At this low flow, it is almost impossible for the thrombi from ECMO to reach to the cerebral vessels.

Figure 5 Simplified diagrams are showing interaction between a patient's native cardiovascular system and VA ECMO flow. Embolic stroke is usually caused by thrombi in the native cardiac chambers rather than extracorporeal circuit. Anticoagulation is more crucial at high-flow than low-flow ECMO. ECMO = extracorporeal membrane oxygenation; VA = venoarterial. Click for larger imageDownload as PowerPoint slide

Hemolysis is also an important complication of ECMO. There are many potential causes of hemolysis including pump thrombosis, increased resistance of the membrane lung, and kinking of tube or cannulae and so on. The most common cause of hemolysis is pump thrombosis. If a thrombus is formed in the centrifugal pump, there will be excessive friction that will damage the blood cells. Massive intravascular hemolysis results in multiorgan failure and anemia.78) Plasma lactate dehydrogenase is a useful maker of hemolysis. Although it is nonspecific for hemolysis, it rapidly increases during hemolysis and normalizes after the resolution of hemolysis. Dark red-colored urine and acute renal failure are also signs of hemolysis. Significant increase of plasma-free hemoglobin (>50 mg/dL) confirms massive intravascular hemolysis.

Heparin-induced thrombocytopenia (HIT) is a rare complication reported in up to 5% of patients, and screening tests have an unacceptably high false-positive rate, while confirmation tests, that is, HIT antibody assay and serotonin release assay, are very costly.79) As the latter tests are not available in most centers including our own, we take action on a positive HIT screening test only if there is clinical evidence of HIT.80) Management of HIT includes prompt cessation of heparin and transition to a direct thrombin inhibitor, for example, argatroban. This novel drug selectively binds to circulating and clot-bound thrombin. This direct mechanism of action renders antithrombin levels irrelevant, resulting in more predictable pharmacokinetics and better efficacy. Argatroban may have a more significant platelet-preserving effect than unfractionated heparin, regardless of whether HIT is present.81) Argatroban administered during ECMO is reported to be administered significantly less (0.1–0.2 mcg/kg/min) than the recommended dose for HIT (2 mcg/kg/min).81), 82)

Intraaortic balloon pump

An IABP can be instrumental in reducing afterload 10). There are still some conflicts over the effect of IABP under VA ECMO.85), 86) However, neither report had any disclosures about the LV function or LA pressure before or after IABP. Tay et al.87) presented a hypothesis that the LV afterload may paradoxically increase during systole due to balloon deflation or “de-clamping” effect of the descending thoracic aorta. In diastole, balloon occlusion of the aorta may reduce ECMO-driven blood flow to the aortic root and arch and attenuate myocardial and cerebral perfusion (Figure 6). We believe IABP may be useful in a patient who only needs low-flow of VA ECMO than high-flow of ECMO. It also may facilitate weaning from VA ECMO. Further research on the degree of left heart decompression via IABP is deemed necessary.

Figure 6 The blood flow in a patient with pulmonary edema on VA ECMO is shown. If a patient has extremely poor left ventricular systolic function, IABP may increase cardiac afterload by systolic deflation and decrease cerebral perfusion by diastolic inflation. ECMO = extracorporeal membrane oxygenation; IABP = intra-aortic balloon pump. Click for larger imageDownload as PowerPoint slide

Impella

The Impella devices (Abiomed Inc., Danvers, MA, USA) are microaxial flow blood pumps designed to be positioned across the aortic valve, actively pumping blood from the LV into the ascending aorta. The Impella pumps are approved by the US Food and Drug Administration for only 6 hours of support but are often used for longer duration of support.10) Impella during VA ECMO has been demonstrated to be feasible and effective.88), 89), 90) Three devices for the left sided support and one for the right sided support are available.