**5. Differences between atrial and ventricular unloading**

When echocardiographic monitoring discloses surrogates of low contractility, LV distention or high filling pressure (PCWP) of the left ventricle, inotropic support should be considered or up titrated to increase contractility of the myocardium, and volume load should be assessed and eventually treated. Other conditions to be considered as drivers for unloading need have been represented in (**Figure 4**).

There are different drivers for atrial or ventricular unloading (**Figure 5**).

The kind of left side's chamber decompression is strictly related to the mechanism of pulmonary congestion and left ventricular distension. The variables that need to be kept in mind are:


• Reversibility of left ventricle damage: ventricular unloading is pivotal to increase the chance of recovery.

Early IABP, or, when CPO is very low and Impella offering the adequate flow, would significantly impact the management of cardiogenic shock as it would avoid the administration of "toxic doses" of inotropes, allowing for smoother transition to VA-ECMO and routine

Even though, the combined use of IABP and VA-ECMO or Impella and VA-ECMO is well described to improve the hemodynamic facilitating and supporting conditions for recovery

Recently, a simulation published on the ASAIO Journal [63] has supported the relevance of optimal medical management, fluid removal while minimizing VA-ECMO flow, reducing blood pressure, and eventually adding inotropes to reduce PCWP and prevent pulmonary edema [64]. Recent clinical data support this notion for different clinical settings and do not advocate a routine combination of VA-ECMO and IABP. Clinical studies have shown a slight reduction in PCWP, LV dimensions, and pulmonary edema in-line with the computer simulation [65].

Patients showing PCWP above 25 mmHg or a virtually non-ejecting LV will require interventional or surgical adjunct measures, which theoretically reduce PCWP by more than 5 mmHg. It has to be kept in mind that sometimes when you think of adding an unloading is too late for the patient, a proactive management reasoning on the patient characteristics and hemo-

In a recent computer simulation, this combined approach showed only limited LV unloading, although pulsatility and increased stroke volume were noted. The CPO before VA-ECMO implantation and the native heart stroke volume after VA-ECMO implantation could be relevant determinants of the effectiveness of IABP also during VA-ECMO perfusion (**Figure 3**), while a low PAPi may push toward biventricular support with Impella or TandemHeart.

When echocardiographic monitoring discloses surrogates of low contractility, LV distention or high filling pressure (PCWP) of the left ventricle, inotropic support should be considered or up titrated to increase contractility of the myocardium, and volume load should be assessed and eventually treated. Other conditions to be considered as drivers for unloading need have

The kind of left side's chamber decompression is strictly related to the mechanism of pulmonary congestion and left ventricular distension. The variables that need to be kept in mind are:

• Adequacy of venous drainage: if the venous drainage may be considered poor, placement of pulmonary artery or left atrial drainage (comprised septostomy) may be sufficient.

• Mitral regurgitation: atrial drainage may be sufficient to unload the ventricle if a significant

**5. Differences between atrial and ventricular unloading**

There are different drivers for atrial or ventricular unloading (**Figure 5**).

mitral regurgitation impedes the distension of the left ventricle.

unloading of the LV [44–60].

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dynamics is pivotal.

been represented in (**Figure 4**).

or ventricular assist device implantation [61, 62].

• Aortic regurgitation: addressing aortic valve may be needed to avoid blood recirculation and stagnation.

**Figure 6** shows the decisional process of management of conditions that may require unloading if not properly treated, the only condition where unloading seems to be mandatory is smoking effect or slow flow through the MV. **Figure 7** shows the possible surgical invasive, minimally invasive and percutaneous approaches aiming at ventricle unloading. When atrial unloading may be sufficient, a percutaneous left atrial septostomy may be accomplished, which allows blood from the LA to drain down its pressure gradient into the right atrium (RA) to then be drained via the venous cannula. This procedure is quite common in many hemodynamic lab especially used to treat pediatric patients. A cannula may also be placed into the LA through a transseptal puncture to facilitate drainage [66]. In addition, the left atrium or left ventricle can be directly cannulated allowing blood to be vented into the venous arm of the ECMO circuit. The transition to a BiVAD (TandemHeart or Centrimag or Rotaflow) could be considered if the oxygenator is no longer needed [67]. Finally, the use of a left ventricular assist device such as the Impella (Abiomed, Danvers, MA) or BiPella (left and right Impella RP) [68] to provide left ventricular decompression as well as forward flow has been described and is gaining success due to its ease also bedside.

#### **Figure 4.** Factors driving unloading need in crash and burn patients. It has to be considered the possibility of unloading LV if signs of fluid overload (high pulsatility and LV distension at Echo and hemodynamic data) are not effectively treated with diuretics. Unloading is needed when there is low or absent LVEF, absent pulsatility without vasodilatation, smoking effect or slow flow through the MV.

**Figure 5.** Atrial or ventricular unloading, decision making graph. In the graph, the pathological conditions in the blue dots are drivers of ventricular unloading while that ones in the red dots are drivers for atrial decompression. In green the first step therapy according to etiology.

Left-to-right shunt can achieve effective decompression of the left ventricle in the setting of VA-ECMO at the presence of atrial communication (atrial septal defect or patent foramen ovale); atrial shunt can be, however, created also artificially with a percutaneous blade or balloon septostomy [69]. The procedure may be fruitful to induce pulmonary decongestion reducing atrial pressure and pulmonary edema but led to a suboptimal LV decompression.

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**Figure 7.** Surgical invasive, minimally invasive and percutaneous approaches to ventricle unloading.

An alternative way to perform atrial unloading, under guidance by bedside transoesophageal echocardiography, is by transseptal puncture and placement of a drain (8 Fr to 15 Fr). The percutaneous atrial transseptal cannula can then be placed and connected to the inflow part

The left ventricle can be vented directly by placing a transaortic vent through the axillary artery or by echocardiography-guided insertion of a pigtail catheter into the left ventricle through the aortic valve and connected to the inflow part of the ECMO circuit [71]. Fumagalli et al. [72] achieved the decompression with a catheter placed percutaneously through the aortic valve into the left ventricle. The blood drained from the left ventricle was pumped into the femoral artery through the VA-ECMO circuit. The normalization of left heart filling pressures led to the resolution of pulmonary edema, and the patient underwent successful heart transplantation. Barbone et al. [73] claimed LV unloading with a 7 Fr pigtail catheter inserted into the left ventricle via the femoral artery contralateral to the arterial outflow cannula. Using this approach in three different patients, the authors described resolution of LV distension and prevention of lung congestion without major complications. However, a so long and tight

of the ECMO circuit, thus, decompressing the pulmonary circulation [70].

**Figure 6.** Management of conditions that may require unloading if not properly treated.

**Figure 7.** Surgical invasive, minimally invasive and percutaneous approaches to ventricle unloading.

Left-to-right shunt can achieve effective decompression of the left ventricle in the setting of VA-ECMO at the presence of atrial communication (atrial septal defect or patent foramen ovale); atrial shunt can be, however, created also artificially with a percutaneous blade or balloon septostomy [69]. The procedure may be fruitful to induce pulmonary decongestion reducing atrial pressure and pulmonary edema but led to a suboptimal LV decompression.

An alternative way to perform atrial unloading, under guidance by bedside transoesophageal echocardiography, is by transseptal puncture and placement of a drain (8 Fr to 15 Fr). The percutaneous atrial transseptal cannula can then be placed and connected to the inflow part of the ECMO circuit, thus, decompressing the pulmonary circulation [70].

The left ventricle can be vented directly by placing a transaortic vent through the axillary artery or by echocardiography-guided insertion of a pigtail catheter into the left ventricle through the aortic valve and connected to the inflow part of the ECMO circuit [71]. Fumagalli et al. [72] achieved the decompression with a catheter placed percutaneously through the aortic valve into the left ventricle. The blood drained from the left ventricle was pumped into the femoral artery through the VA-ECMO circuit. The normalization of left heart filling pressures led to the resolution of pulmonary edema, and the patient underwent successful heart transplantation. Barbone et al. [73] claimed LV unloading with a 7 Fr pigtail catheter inserted into the left ventricle via the femoral artery contralateral to the arterial outflow cannula. Using this approach in three different patients, the authors described resolution of LV distension and prevention of lung congestion without major complications. However, a so long and tight

**Figure 6.** Management of conditions that may require unloading if not properly treated.

**Figure 5.** Atrial or ventricular unloading, decision making graph. In the graph, the pathological conditions in the blue dots are drivers of ventricular unloading while that ones in the red dots are drivers for atrial decompression. In green

the first step therapy according to etiology.

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line may be argued ineffective to warrant a large amount of drainage as it is generally needed. Indeed, a recent paper indicates an algorithm to select the right dimension of the pig aiming

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An alternative approach to LV decompression is the percutaneous insertion of a venous cannula into the pulmonary artery and connection of this cannula to the inflow part of the ECMO circuit [75]. A small (15 Fr) venous cannula may be placed percutaneously to the pulmonary artery and connected to the ECMO circuit to decompress the left heart and to facilitate LV function. Surgical minimal invasive access to directly drain the pulmonary artery has been

Impella (Abiomed Inc., USA) is a catheter-based transaortic axial flow pump that can be introduced through a percutaneous femoral approach. The device is placed across the aortic valve and pumps up (2.5–5 L/min) of blood on the basis of the model (2.5, CP or 5 L) from the left ventricle to the ascending aorta. The 2.5 and the CP are placed in the groin percutaneously while the 5.0 is generally placed surgically in the right axillary artery to warrant to the patient

Koeckert et al. [75] reported the use of Impella LP 2.5 for left ventricle decompression in a 70-year-old man with acutely decompensated heart failure who was placed on VA-ECMO for cardiogenic shock with severe pulmonary edema and respiratory failure. Both devices were successfully weaned on day 5 after myocardial recovery. Narain et al. [76] described a case involving 31-year-old man with fulminant myocarditis treated with the Impella device and

to reach the right unloading flow [74].

**Figure 9.** Optimal Arterial Pressure on VA-ECMO (Copyright from ASAIO).

the possibility to be extubated and ambulatory.

also suggested.

**Figure 8.** Techniques to unload the heart during ECMO. (1) Pathophysiology of LV distension during ECMO and (2) Impella on top of ECMO (ECPELLA): pathophysiology.

**Figure 9.** Optimal Arterial Pressure on VA-ECMO (Copyright from ASAIO).

**Figure 8.** Techniques to unload the heart during ECMO. (1) Pathophysiology of LV distension during ECMO and (2)

Impella on top of ECMO (ECPELLA): pathophysiology.

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line may be argued ineffective to warrant a large amount of drainage as it is generally needed. Indeed, a recent paper indicates an algorithm to select the right dimension of the pig aiming to reach the right unloading flow [74].

An alternative approach to LV decompression is the percutaneous insertion of a venous cannula into the pulmonary artery and connection of this cannula to the inflow part of the ECMO circuit [75]. A small (15 Fr) venous cannula may be placed percutaneously to the pulmonary artery and connected to the ECMO circuit to decompress the left heart and to facilitate LV function. Surgical minimal invasive access to directly drain the pulmonary artery has been also suggested.

Impella (Abiomed Inc., USA) is a catheter-based transaortic axial flow pump that can be introduced through a percutaneous femoral approach. The device is placed across the aortic valve and pumps up (2.5–5 L/min) of blood on the basis of the model (2.5, CP or 5 L) from the left ventricle to the ascending aorta. The 2.5 and the CP are placed in the groin percutaneously while the 5.0 is generally placed surgically in the right axillary artery to warrant to the patient the possibility to be extubated and ambulatory.

Koeckert et al. [75] reported the use of Impella LP 2.5 for left ventricle decompression in a 70-year-old man with acutely decompensated heart failure who was placed on VA-ECMO for cardiogenic shock with severe pulmonary edema and respiratory failure. Both devices were successfully weaned on day 5 after myocardial recovery. Narain et al. [76] described a case involving 31-year-old man with fulminant myocarditis treated with the Impella device and

cannulation limits the adequacy of drainage and leaves a remarkable amount of blood stagnating in the lung bed. A recent paper on the ASAIO Journal showed an inverse relationship between mortality and MAP in VA-ECMO but not in VV-ECMO (**Figure 10**) [79]. In the hypotensive patient, MAP may be increased by manipulating either CO or SVR. The total cardiac output of the body is composed of native cardiac output and VA-ECMO flows. Thus, hypotension may potentially be corrected by increasing VA-ECMO flows and its contribution to total CO. Assuming a centrifugal pump, this may be achieved by administering volume or by increasing the RPMs of the pump. If the problem is related to SVR, such as with septic shock, a vasoconstrictor may be needed to increase MAP, although this must be weighed against the effect of increased afterload and the increase in pressure work of the left ventricle. Many different policies exist on the management of arterial pressure during VA-ECMO: one concern is about the equivalence of MAP in patients with or without pulsatility. Physiologic autoregulation is pivotal for end-organ perfusion and particularly for the brain and kidney. Many studies dealt with ideal MAP value in the ICU patient, the most identify a cutoff of 65 mmHg, as a value usually sufficient also if the study [80] suggested a MAP of 75–85 as protective for acute kidney injury in patients with a previous history of hypertension. To our knowledge, however, there has been only few studies examining optimal MAP for patients on

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Clearly, the physiology of VA-ECMO patients is considerably different from other critically ill patients. Several studies identified to determine the optimal pressure on cardiopulmonary bypass (CPB) during cardiac surgery [81–83] and the majority supports a MAP higher than 70 mm Hg on CPB. VA-ECMO is quite different from CPB: CPB is usually initiated electively for patients on stable patients, while VA-ECMO intervenes on an unstable circulatory condition. Moreover, the circuit is not open as in the CPB, the heart is not arrested, and there is not a reservoir to avoid pulmonary fluid overload. The heart is in a dynamic parallel circulation with ECMO aiming to reach an equilibrium to eject against incoming blood flow from the ECMO circuit. The amount of workload may often be incompatible with the failing heart performance of most VA-ECMO patients. VA-ECMO could induce increased afterload and further worsen myocardial dysfunction. If a lower MAP could have the rationale to permit the heart to eject against a lower resistance decreasing the myocardial oxygen demand, the clinical impact of hypotension on the patient in cardiogenic shock has to be carefully judged. Furthermore, it may not be suitable to compare the MAP of patients with and without pulsatility because patients without pulsatility may require a higher MAP for end-organ perfusion. It may not be suitable to compare the MAP of patients with and without pulsatility because patients without pulsatility may require a higher MAP for end-organ perfusion. Pulsatility is a dynamic property due to the interaction between the two concurrent parallel circulations; indeed a loss of pulsatility may signal worsening myocardial function, while the appearance of pulsatility or an improvement in pulse pressure may signal recovery. However, the loss of pulsatility may also suggest that VA-ECMO flows are too high, so reducing the amount of blood managed from the impaired native circulation. The higher the ECMO flows, the more blood that drains into the circuit causing a more significant decrease in LV preload, stroke volume, and pulse pressure. Total bypass, where the ECMO circuit takes over 100% of the cardiac output, creates a flat, non-pulsatile arterial tracing and signifies the lack of ejection of blood from the left

ECMO and evidences in support of every practice are still weak.

**Figure 10.** Patient survival from end-organ function to myocardial recovery.

VA-ECMO. On full mechanical circulatory support, the hemodynamic status improved, and both systems were explanted after 48 h. Many centers are now moving toward the adoption of Impella as bailout for weaning and to unload the ventricle during VA-ECMO even if many warnings have been expressed regarding the risks to add more complexity to the management of an already complex patient [77, 78]. **Figure 8** shows the pathophisiology of Left Ventricle distention due to ECMO (**Figure 8-1**) and the effects of adding Impella during ECMO (**Figure 8-2**).

**Figure 9** shows all the possible surgical and percutaneous solutions to unload the left circulation, preventing pulmonary edema and, possibly, facilitating the myocardial recovery when the underlying disease is potentially reversible. According to what said before, to reach patient survival, from end-organ function to myocardial recovery, we should balance arterial pressure, flow rate and unloading passing through IABP if necessary. The delicate balance of this therapeutical strategy is described in **Figure 10**.
