Dangers in using beta-blockers in patients with venovenous extracorporeal membrane oxygenation

Article information

Acute Crit Care. 2022;37(4):683-684

Publication date (electronic) : 2022 July 18

doi : https://doi.org/10.4266/acc.2022.00661

Diego Rodríguez Álvarez, Elena Pérez-Costa, Juan José Menéndez Suso

Pediatric Intensive Care Department, La Paz University Hospital, Madrid, Spain

Corresponding author: Diego Rodríguez Álvarez Pediatric Intensive Care Department, La Paz University Hospital, Paseo de la Castellana, 261, Madrid 28046, Spain Tel: +34-60-549-5869 E-mail: diegorodral@gmail.com

Received 2022 May 15; Accepted 2022 June 16.

Dear Editor:

We have read with interest the review “Awakening in extracorporeal membrane oxygenation as a bridge to lung transplantation” by Lee [1] published in your journal, explaining how the application of awake venovenous extracorporeal membrane oxygenation (VV-ECMO) performed by an appropriately trained ECMO multi-disciplinary team, can be useful as a bridging strategy, in patients waiting for lung transplantation.

We fully agree with the awake ECMO management proposed by Lee [1]. However, the section “Problems during Awake ECMO” discusses the problem of hypoxemia due to excessive patient cardiac output (CO). The proposed solution is to use beta-blockers to resolve hypoxemia in patients with high CO, as a result of increased heart rate. We would like to point out the possible inaccuracy of this recommendation for managing refractory hypoxemia in patients with VV-ECMO.

Since the work of Guarracino et al. [2], there have been numerous publications recommending the use of beta-blockers to increase oxygen saturation (SaO₂) in situations of high CO [3]. The blood propelled by the heart is a mixture of the flow coming from the VV-ECMO, with an SaO₂ in the blood exiting the oxygenator (membrane) (SmO₂) of approximately 100%, and the desaturated venous flow, with a central venous oxygen saturation (ScvO₂) of approximately 40%–70%, which returns to the heart through the vena cava. By using beta-blockers and slowing the heart rate, the total CO will be lowered. Whereas the ECMO flow will remain constant, the desaturated venous flow will decrease. Less venous flow will be needed to complete the total CO, and therefore the blood mixture will have a higher SaO₂, as derived from the following formula described by Messaï et al. [4]:

SaO2≈SpaO2=EFCOSmO2+1−EFCOScvO2+ΔSaO2, in which SpaO₂ is SaO₂ in the pulmonary artery, EF is the effective flow rate (EF=(1−recirculation)×pump flow) and ∆SaO₂ is the increase in SaO₂ due to dissolved oxygen (%).

The increase in oxygen consumption stimulates the general visceral afferent fibers (by mechanoreceptors, nociceptors, and chemoreceptors) that activate the autonomic nervous system, generating a response (in this case, tachycardia) to increase the supply of oxygen according to the formula: DO₂=CO × CaO₂, where CaO₂ is the arterial oxygen content according to the formula CaO₂=1.34×SaO₂×Hb+pO₂×0.0031, where pO₂ is the partial pressure of oxygen and Hb is the hemoglobin content. SaO₂ is only part of the equation in oxygen supply.

Following the mathematical model of Zanella et al. [5], we can confirm that increasing the CO while keeping the rest of the variables constant will lead to an increase in oxygen delivery (DO₂) despite a decrease in SaO₂. As the heart rate increases, the CO will increase. If CO is increased by a value of k, SaO₂ can be calculated using the following formula:

SaO2=EFSmO2−ScvO2+kCOScvO2+ΔSaO2 kCO obtaining a decrease in SaO₂ for any value k increase in CO. Substituting SaO₂ in the DO₂ equation results in the following formula: DO₂=EF×1.34×Hb(SmO₂-ScvO₂ )+kCO×1.34×Hb(ScvO₂+∆SaO₂ )+(kCO×pO₂×0.0031)

where for any value k increase in CO, there will be an increase in DO₂. These formulas show that by increasing the CO by a proportion k, the SaO₂ will decrease, while the total DO₂ will increase.

The study by Guarracino et al. [2 ], on which numerous review articles are based, corresponds only to a series of three patient cases that did not report their SaO₂, did not indicate how CO was calculated, and observed that DO₂ decreased when the heart rate decreased. The objective for patients with VV-ECMO assistance should be to prevent hypoxia rather than hypoxemia, and maintain adequate DO₂. We believe that more studies are necessary along these lines to be able to make a strong recommendation against the use of beta-blockers in VV-ECMO patients with high CO.