**6. Arterial pressure management during ECMO**

While maintenance of flows is crucial to the care of the patient on VA-ECMO, attention must also be paid to the mean arterial pressure, as the end organs require both a cardiac output and a perfusion pressure for optimal function and a low venous pressure. A goal MAP >65 mmHg may be used as a starting point but can be adjusted either lower or higher given individual circumstances keeping in mind that the differential pressure between MAP and LAP is the driving force of organ perfusion and function. On the other side, MAP should never exceed 90 mmHg to limit afterload and to promote forward flow, especially when peripheral 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 ECMO and evidences in support of every practice are still weak.

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

While maintenance of flows is crucial to the care of the patient on VA-ECMO, attention must also be paid to the mean arterial pressure, as the end organs require both a cardiac output and a perfusion pressure for optimal function and a low venous pressure. A goal MAP >65 mmHg may be used as a starting point but can be adjusted either lower or higher given individual circumstances keeping in mind that the differential pressure between MAP and LAP is the driving force of organ perfusion and function. On the other side, MAP should never exceed 90 mmHg to limit afterload and to promote forward flow, especially when peripheral

this therapeutical strategy is described in **Figure 10**.

**6. Arterial pressure management during ECMO**

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

200 Advances in Extra-corporeal Perfusion Therapies

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 ventricle. A recent study from Sakir Akin and the Erasmus group has shown how the peripheral recovery of pulsatility is a predictor of recovery that should push to weaning of ECMO [84].

VA-ECMO has to be deemed as temporary short-term support, and the risks related to the permanence of an oxygenator must focus on a rapid transition to further MCS systems. The assessment of left atrial pressure (direct or indirect) should be a mandatory tool in patients with VA-ECMO to increase the chance of recovery or transition to next support or treatment. When left atrial pressure is deemed increased in surgical unloading, or percutaneous unloading has to be considered preferring whenever possible ventricular unloading especially when

Flow Optimization, Management, and Prevention of LV Distention during VA-ECMO

http://dx.doi.org/10.5772/intechopen.80265

203

Randomized trials and registries will have to answer some of the open questions the clinician

• Which clinical and hemodynamic profiles favor upfront VA-ECMO with LV venting?

• Should we transition to durable LVAD or BiVAD as soon as the end organs recovers?

• What are the granular aspects of management that should be included in trial design for

Cristiano Amarelli acknowledges the Abiomed for the figures freely provided on the associa-

This section of your manuscript may also include funding information.

Thanks to IntechOpen for trusting and awaiting for the work to be finished.

mitral regurgitation is absent.

• To vent or not to vent?

• When is vent mandatory?

• How vent without harm the patient?

VA-ECMO and LV venting?

tion between ECMO and Impella.

No conflict of interest to declare.

**Notes/thanks/other declarations**

**Acknowledgements**

**Conflict of interest**

has to solve daily, dealing with the patient on VA-ECMO:

• When unload before and when after VA-ECMO institution?

• Which goal directs the "dose" of VA-ECMO?

• Does one VA-ECMO configuration fit all?

Reduced pulsatility may also reflect a decrease in intravascular volume or a mechanical cause of decreased venous return (i.e., atrial tamponade) that may cause a decrease in LV preload leading decreased stroke volume and pulse pressure.

VA-ECMO reduces the volume work of the right ventricle through the decreased RV preload, while pulmonary edema may cause hypoxic pulmonary vasoconstriction worsening pulmonary hypertension and increasing RV pressure work. If this setting, the right ventricle may be unable to pump to the left side of the heart, flattening arterial pressure waveform and decreasing the stroke volume. Nitric oxide with inodilators such as milrinone and dobutamine (which will also provide inotropic assistance) are needed. If systemic pressures allow, nitroglycerin or nitroprusside may also be utilized.
