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replacement) and closed-chamber surgery (CCS) such as coronary artery bypass grafting (CABG). OCS has previously been shown to be associated with greater exposure to cerebral arterial bubbles, almost certainly because gas remains in the heart chambers and pulmo- nary veins after attempts to ‘de-air’ the heart.3 Perhaps not surprisingly, there is some evidence that OCS is associated with a higher risk of adverse neurological outcomes than CCS.4 However, this comparison is com- plicated by other characteristics of the respective groups, such as differing demographics and prevalence of other relevant risk factors for such outcomes.4
Another possible approach in evaluating the signifi- cance of differing exposure to small cerebral arterial bubbles is to look for evidence that they contribute to pathophysiological events strongly associated with poor outcome. Recent work has demonstrated an association between cerebral dysautoregulation during cardiac sur- gery and post-operative stroke risk.5 The reasons why dysautoregulation arises during surgery in some patients but not others are unknown. However, there is abundant evidence from parallel fields (such as diving medicine) that the passage of small intravascular bubbles can dis- rupt vasomotor activity,6,7 and it is therefore plausible that bubble exposure is a contributor to cerebral dysau- toregulation in cardiac surgery.
Our group is undertaking a study examining cerebral autoregulation during OCS versus CCS to investigate whether greater exposure to cerebral arterial bubbles in OCS will increase the risk of dysautoregulation. This approach is predicated on older reports that open-cham- ber patients were exposed to substantially greater num- bers of bubbles,3 an issue that has received little recent attention. Here we report an evaluation of cerebral arte- rial bubble exposure during contemporary open- versus closed-chamber surgery. We hypothesized that, com- pared to CCS, OCS would result in similar exposure to bubbles during stable cardiopulmonary bypass, but to larger numbers of bubbles after the aortic cross-clamp has been removed and the heart begins to eject.
Material and methods
This study was approved by the Southern Health and Disability Ethics Committee (16/STH/157/AM02) and the Auckland District Health Board Research Committee (A+7371). Written consent was obtained from all par- ticipants.
Two groups undergoing elective heart surgery were studied, twenty patients undergoing CCS (CABG), and 20 undergoing OCS (valve repair or replacement ± CABG). Patients scheduled for surgery were enrolled as a sample of convenience based primarily on author GJ’s availability to conduct monitoring in the allo- cated research time.
Enrolled patients had pre-operative transcranial Doppler (TCD) evaluations to assess the quality of the temporal window (bilaterally) for insonation of the middle cerebral arteries (MCAs). Patients without an adequate temporal window were excluded. Other exclu- sion criteria were: patient refusal; emergency surgery; pregnancy; redo procedures; abnormal pre-operative neurological examination; ejection fraction less than 40%; existing cerebrovascular disease; a history of tran- sient ischaemic attack or stroke; and pre-existing carotid disease.
In accordance with routine practice at our institu- tion, CPB circuit components were deployed on a Stöckert S5 heart-lung machine (Sorin Group, Munich, Germany) using SMAR × TTM polyvinyl chloride tubing (COBE Cardiovascular, Arvada, CO), a Sorin Inspire 6M hard-shell venous reservoir and oxygenator (Sorin Group, Mirandola, Italy), Pall AL20 arterial line filter (Pall Corp, Portsmouth, UK), silicone replacement pump raceway tubing (Natvar, City of Industry, Los Angeles, CA) and a CSC14 cardioplegia delivery system (Sorin Group, Munich, Germany).
All circuits were flushed with CO2 through the arte- rial line filter for approximately 5 minutes at 1 L/minute before priming with Plasma-Lyte 148 (Baxter International Corporation, NSW, Australia). Cephazolin (1 g), heparin (100 IU/kg) and tranexamic acid (500 mg) were added and circulated before initiation of bypass.
Institutional clinical practice guidelines for the con- duct of CPB were followed. These include mean arte- rial pressure (MAP) ⩾ 50 mmHg, PaO2 20–30 kPa, venous oxygen saturations >70%, non-pulsatile flow (2.0–3.0 L/m2/minute), a target haematocrit of >0.22 during CPB and oxygen delivery index (DO2i) > 270 mL/ minute/m2, active or passive cooling to mild hypother- mia (34°C–32°C), –stat acid/base management, and activated clotting time (ACT) > 480 seconds. The arte- rial line filter was continuously purged during CPB via a connection to the venous inlet port. The minimum volume sensor level on the hard shell venous reservoir was set at 150–200mL as per manufacturers recom- mended guidelines for minimum volume. Ascending aortic and two-stage venous cannulation was used in all patients except for mitral valve operations, where bi-caval cannulation was used. Anaesthetic manage- ment similarly followed institutional norms without the use of nitrous oxide.
Various cardiac de-airing techniques were used according to each surgeon’s preferences. Patients in the closed-chamber group had aortic root venting through a combined “Y” antegrade cardioplegia and venting needle. After completing the proximal anastomoses, the evacuation of aortic root air was through the anastomotic site before the release of the aortic side- clamp. De-airing techniques in the open-chamber sur- gical group included left ventricular (apical), left atrial
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