Ch 28 (s28.13); Ch 22 (s22.3); Ch 19 (s19.5); Ch 27
Chapter 22 s22.3 of this book instructs titration toward about 40 mmHg; in a patient starting at 100 mmHg that is a 60 percent fall and the two instructions cannot both be followed. This book adopts the percentage ceiling as binding, with 40 mmHg as the destination rather than the first stop.
Record the pre-cannulation PaCO2 so the 50 percent ceiling has a denominator, and chart the floor as a number. The blender is the hyperoxaemia knob even though Chapter 27 showed it is not the hypoxaemia knob — turning it down always works, turning it up usually does not.
Carbon dioxide is a potent cerebral vasodilator; prolonged pre-ECMO hypercapnia may impair cerebral autoregulation and produce a narrow regulatory pressure window, and rapid correction may cause cerebral vasoconstriction and cerebral ischaemia, with full-dose anticoagulation then permitting haemorrhagic conversion. Avoiding a large change in PaCO2 of over 50 percent in the peri-cannulation period for both venoarterial and venovenous ECMO is reasonable. For oxygen: hyperoxaemia is defined as mild over 100 or 120 mmHg and severe over 300 mmHg, hypoxaemia as under 60 or 70 mmHg; it is reasonable to avoid early severe hyperoxaemia and hypoxaemia within 24 hours by manipulating the fraction of delivered oxygen from the ECMO sweep gas. Low pulse pressure under 20 mmHg in the first 24 hours of venoarterial support was associated with acute brain injury. No data exist on early and optimal blood pressure goals for preventing brain injury.
Post-cannulation early physiological targets and acute brain injury