Page 29 - ANZCP Gazette May 2023

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Perfusion
defense against hypoperfusion is “autoregulation” of flow, in which blood vessels may dilate when pressure is reduced or constrict when pressure is increased. This phenomenon is classically depicted as capable of main- taining constant flows over4 mean arterial pressures between 50 and 150 mmHg though the typical flow “plateau” is likely much narrower and potentially upwardly sloping.5
Despite uncertainty about the boundaries of autoreg- ulation and its potential perturbation by aspects of patient management (such as non-pulsatile CPB and administration of anesthetic drugs), there is evidence that it remains operant in many patients during cardiac surgery while in others it is impaired.6 Moreover, patients in whom autoregulation is significantly impaired or who experience longer periods of mean arterial pressures below the lower limit of autoregulation seem at greater risk of stroke and other major morbidities.7,8 Understanding the causes of impaired autoregulation during cardiac surgery is therefore important.
One plausible but previously unexamined contribu- tor is exposure to arterial emboli. During CPB, most of these emboli are bubbles small enough to redistribute through the cerebral circulation,9,10 but large enough to contact the endothelium, a key transducer and effector in the autoregulation process. Bubble-endothelium con- tact can cause endothelial damage,11,12 and this interac- tion was the likely cause of altered vasoreactivity in experiments in both animal models12,13 and human sub- jects.14 Similarly, exposure to arterial latex microspheres resulted in impaired regional autoregulation during CPB in dogs.15 These findings suggest that cerebral embolization may contribute to impairment of autoreg- ulation and thereby increase the risk of stroke in cardiac surgery. This is also of relevance to those interested in the pathophysiology of bubble-induced disorders like decompression sickness and arterial gas embolism.16
Autoregulation can be examined in humans using recently developed software to continuously correlate mean arterial pressure (MAP) with the cerebral blood flow velocity (CBFv). Open chamber surgery (OCS) is associated with much greater emboli exposure than closed chamber surgery (CCS), especially after removal of the aortic cross-clamp.17 We utilized this opportunity for a natural experiment to address the hypothesis that when compared to patients undergoing CCS, patients undergoing OCS would exhibit a greater increase in correlation of MAP and CBFv (implying greater impair- ment of autoregulation) after removal of the aortic cross-clamp due to greater emboli exposure. To be clear, there was no intent to associate our findings with clini- cal outcomes, a goal that would require a much larger study. This was a pathophysiological study with the intent of investigating impaired cerebral autoregulation in response to emboli exposure.
Material and methods
Approval from the Southern Health and Disability Ethics Committee (16/STH/157/AM02) and the Auckland District Health Board Research Committee (A+7371) was obtained. All patients provided written consent to participate in this study.
Twenty patients undergoing OCS (valve replacement or repair ± coronary bypass grafting [CABG]) and 20 undergoing CCS (CABG only) were enrolled. These groups constituted a sample of convenience contingent on the availability of both eligible patients and the pri- mary investigator (GJ). Patients were excluded if: preg- nant; undergoing emergency or redo surgery; or if known to have cerebrovascular or carotid disease, previ- ous stroke or transient ischemic attack. Patients were also excluded if the middle cerebral arteries (MCAs) could not be easily insonated using transcranial Doppler (TCD) in a pre-operative assessment.
Cardiopulmonary bypass was undertaken using a Stöckert S5 heart-lung machine (Sorin Group, Munich, Germany) with SMAR × TTM polyvinyl chloride tubing (COBE Cardiovascular, Arvada, CO), a Sorin Inspire 6m hard-shell venous reservoir and oxygenator (Sorin Group, Mirandola, Italy), and a Pall AL20 arterial line filter (Pall Corp, Portsmouth, UK) with crystalloid prime. Target CPB parameters included MAP ⩾ 50 mmHg, PaO2 20–30 kPa, venous oxygen saturations >70%, flow (non- pulsatile) at 2.0–3.0 L/m2/minute), hematocrit of >0.22, oxygen delivery index >270 mL/minute/m2, active or passive cooling to 34–32°C, and activated clotting time >480 s. Acid/base management followed the α–stat approach. Various cardiac de-airing techniques were used according to each surgeon’s preferences. Anesthetic man- agement was based around a volatile agent or propofol total intravenous anesthesia according to anesthetists’ preferences and institutional norms.
Measures
Cerebral blood flow velocity (bilateral MCAs) was monitored with TCD (DWL/Compumedics, Singen, Germany). After the patient was anesthetized, continu- ous emboli counts and bilateral MCA flow velocities were recorded using 2.25 MHz transducers fitted on a DiaMon head brace (DWL/Compumedics Singen, Germany). Signals representing emboli were defined as short-duration (<0.01–0.03 s) high-intensity signals (⩾4 dB above background noise) and were automati- cally counted by the Doppler device. MAP was continu- ously monitored by transducing a radial artery cannula.
Cerebral autoregulation was monitored using a con- tinuous moving correlation between CBFv and MAP calculated by ICM+ software (Cambridge University, Cambridge, UK) to produce a “mean velocity index”
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