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A model for cardiopulmonary bypass redesign

Maine Medical Center, Cardiac Surgery Division, Portland, ME, USA and The Northern New England Cardiovascular Disease Study Group, Lebanon, ME, USA, groomr{at}mmc.org

D S Likosky

Maine Medical Center, Cardiac Surgery Division, Portland, ME, USA and The Northern New England Cardiovascular Disease Study Group, Lebanon, ME, USA

R J Forest

Maine Medical Center, Cardiac Surgery Division, Portland, ME, USA and The Northern New England Cardiovascular Disease Study Group, Lebanon, ME, USA

G T O’Connor

Maine Medical Center, Cardiac Surgery Division, Portland, ME, USA and The Northern New England Cardiovascular Disease Study Group, Lebanon, ME, USA

J R Morton

Maine Medical Center, Cardiac Surgery Division, Portland, ME, USA and The Northern New England Cardiovascular Disease Study Group, Lebanon, ME, USA

C S Ross

Maine Medical Center, Cardiac Surgery Division, Portland, ME, USA and The Northern New England Cardiovascular Disease Study Group, Lebanon, ME, USA

C Clark

Maine Medical Center, Cardiac Surgery Division, Portland, ME, USA and The Northern New England Cardiovascular Disease Study Group, Lebanon, ME, USA

R Kramer

Maine Medical Center, Cardiac Surgery Division, Portland, ME, USA and The Northern New England Cardiovascular Disease Study Group, Lebanon, ME, USA

Introduction: A portion of patients undergoing cardiac surgery may develop focal and/or subtle brain injuries secondary to cardiac surgery. There is evidence that, in some cases, these injuries may be related to cardiopulmonary bypass (CPB). Embolism and hypoperfusion are the dominant mechanisms for focal neurologic injuries among coronary artery bypass graft (CABG) surgery patients. Recent studies suggest that these mechanisms may also produce the more prevalent subtle neurological deficits. The aim of our current work is to obtain a thorough understanding of the processes of care associated with the production of embolic activity, cerebral hypoperfusion, and hemodynamic aberrations that often occur during CPB.

Methods: We developed a system for simultaneous recording of physiologic parameters, embolic activity in the CPB circuit and in the cerebral arteries, and near infrared regional cerebral oxyhemoglobin saturation (NIRS) during cardiac surgery. All data were synchronized with a video recording of the surgical procedure. Periods of embolic activity and NIRS were subsequently related to surgical and CPB processes of care through a systematic review of the patient’s surgical case video.

Results: To date, we have enrolled 47 patients undergoing coronary and/or valvular procedures. We have observed wide variation across patients in detected cerebral embolic counts, NIRS and physiologic parameters. We have identified increased embolic counts in the CPB circuit related to specific processes and events such as the method of venous drainage, the entrainment of air in the venous line, the injection of medications into the CPB circuit and blood sampling from the CPB circuit. A portion of detected changes in NIRS were related to periods of hypotension and positioning of the heart during the construction of distal coronary artery grafts on the posterior coronary artery vessels.

Summary: Use of this model provides the surgical team with detailed information regarding the contribution of CPB to the creation of precursors of neurological injury. This system provides meaningful data to guide the surgical team in the redesign of the CPB system and associated techniques.

Perfusion, Vol. 19, No. 4, 257-261 (2004)
DOI: 10.1191/0269216304pf749oa


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