In our study, 29.9% of aortic arch surgical patients developed new-onset impaired CA after CPB with MHCA and with a worse outcomes. The occurrence of impaired CA in adult patients undergoing CPB with MHCA was consistent with children in previous reports [24, 25]. Impairment of CA was more likely to be associated with a prolonged low rScO2 (rScO2 < 55%), in which the critical threshold of rScO2 < 55% duration was 40 min.
It is known that the mechanisms for impaired CA have not yet been elucidated. Notably, there was no association between age, body mass index, gender, diabetes, hypertension, preoperative hemoglobin level and impaired CA. During CPB particularly during HCA and selective cerebral perfusion, factors might influence CA include temperature, PaO2, PaCO2, perfusion pressure, flow rate, and hematocrit [24–27]. Temperature reduction exponentially decreases cerebral metabolism and preserves cellular stores of high-energy adenosine triphosphate . Carbon dioxide is a potent cerebrovasodilator, and elevated PaCO2 can obviously increase CBF volume in both awake and anesthetized states . In our cohort, the patients with impaired or normal CA did not differ significantly in the above factors (Table 2). High PaCO2 might be detrimental to preserve the function of CA. And this variable was independently asscociated with impaired CA . In our study, the PaCO2 was higher than normal range. However, there was no significant difference between patients with impaired and normal CA. The high PaCO2 might be related to that we used pH-stat for blood gas management to ensure sufficient cerebral perfusion during MHCA. Although the seletive cerebral perfusion time showed an obviously difference between impaired CA and normal patients in our study, this variable did not reach a significant association with impaired CA consistent with the result in a literature .
We found that impaired CA seems to associate with intraoperative low rScO2. The period of rScO2 < 55% in impaired CA patients was longer than in normal CA patients. In addition, intraoperative rScO2 less than 55% for more than 40 min was independently associated with the onset of impaired CA. This result was consistent with previous studies that the period of rScO2 less than 55% during aortic surgery was closely related to the occurrence of postoperative neurological events [20, 21]. These results indicated that by regulating cerebral perfusion blood flow rate and pressure alone might not avoid the events of rScO2 lower than 55%. Other methods also should be considered, including raising hematocrit to improve oxygen delivery, maintaining deep hypothermia during the circulatory arrest to suppress cerebral metabolism, and minimizing the duration of HCA. Whereas using α-stat management during moderate hypothermia produces better neurologic outcomes than observed with pH-stat management, it is unclear which strategy is superior in adults when MHCA is used . However, given the nature of our study, we cannot confirm a causative relationship between the prolonged low rScO2 and impaired CA. In other words, improving cerebral oxygen delivery by the strategies above to reduce occurrence of impaired CA should be tested in randomized controlled trials.
Our results suggested that patients with impaired CA had a higher rate of postoperative delirium, consistent with previous studies in coronary artery bypass grafting or valve surgery under CPB [29, 30]. Patients with impaired CA were also at increased risks of in-hospital mortality, AKI, mechanical ventilation > 24 h, respiratory infection, and length of ICU stay. Like the present study, other work reported that impaired CA was associated with longer mechanical ventilation and hospital stay . The onsets of AKI, respiratory infection, and postoperative death were affected by many factors, including the cardiac function, bleeding, and the duration of mechnical ventilation. Although the events of low cardiac output and reoperation due to bleeding showed no significant difference between patients with impaired CA and those with normal CA, the causal relationship between impaired CA and postoperative death, AKI and respiratory infection was uncertain from our study which merits prospective studies. Our findings might indicate that impaired CA was one of the manifestations of systemic organ injury in patients who underwent CPB with MHCA. These observations suggested the need to comprehensively monitor patients who undergo CPB and MHCA to ensure sufficient oxygen delivery to key organs. In particular, patients with impaired CA may require early interventions before postoperative complications onset, such as increasing systemic oxygen delivery, providing renal replacement therapy, and/or giving mild hypothermia therapy.
Our study presents several limitations. First, we were able to enroll only 158 cases because of the relatively small number of total aortic arch replacement surgeries for acute type A aortic dissection at our institution. Second, COx > 0.3 was tested in the animal study as a threshold of impaired CA. Thus, perspective studies were ongoing to explore an absolute value or a certain percentage increase of COx as a measurement tool for impaired CA in adult patients. Third, because rScO2 monitoring was not routinely performed after surgery in our center, we could not further calculate postoperative COx to track the duration of impaired CA. Fourth, not all patients received a rigorous assessment by a neurologist or psychiatrist to identify the postoperative neurological complications. This may lead to an underestimation of the occurrence of postoperative neurological complications. In addition, only the temporary rather than permanent neurological complications were evaluated. Fifth, we did not analyze the potential impact of vasoconstrictors or inotropics on CA because the accuracy of the dosage and usage time could not be ensured. Finally, there is no control group without MHCA in our study. But the occurrence of new-onset impaired CA in patients who underwent CPB and HCA was higher than those who underwent CPB alone in literature. This might reveal that CPB with MHCA increased the risk of new-onset impaired CA. Large prospective studies are needed to understand more about the association between COx value and changes of CA over time during all parts of the aortic arch surgery, and the association between COx and patient outcomes.