9, 6, 8
Do not give beta-blockers to raise SaO2 on VV ECMO. The manoeuvre can improve the displayed saturation while reducing oxygen delivery, and it is actively harmful in recirculation — the scenario most easily mistaken for high cardiac output at the bedside. The transferable teaching point for the whole book: an intervention that raises SaO2 has not necessarily helped the patient.
No beta-blockade, within the same computational model
DOI 10.1177/02676591241262261
Beta-blockade (modelled reduction in cardiac output) for refractory hypoxaemia during VV ECMO
In-silico mathematical model, not a clinical study. No patients, no outcomes, no randomisation. Results depend entirely on the model's assumptions and on the specific parameter values chosen for each scenario. No clinical trial or observational outcome data on this practice exist.
Scenario 1 (high cardiac output, partial lung shunt): SaO2 74.2% to 79.2%, mixed venous saturation 53.5% to 44.7%. Scenario 2 (high cardiac output, complete lung shunt): SaO2 71.9% to 85%, mixed venous unchanged at 52.2%. Scenario 3 (normal cardiac output, high recirculation): SaO2 FELL 82.4% to 78.3%, mixed venous collapsed 50.8% to 25.5%. Oxygen delivery was reduced in every scenario. Authors: effects "are unpredictable and may reduce oxygen delivery"; "This study does not support the use of beta-blockers for this indication."
Simulated adult VV ECMO patients — three modelled scenarios, not real patients