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Ann Thorac Surg 2002;73:180-189
© 2002 The Society of Thoracic Surgeons
a Department of Cardiac Surgery, Children’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
b Department of Pathology, Children’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
c Department of Neurology, Children’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
d Department of Anesthesia and Intensive Care, Children’s Hospital and Harvard Medical School, Boston, Massachusetts, USA
* Address reprint requests to Dr Jonas, Department of Cardiac Surgery, Children’s Hospital, 300 Longwood Ave, Boston, MA 02115, USA
e-mail: richard.jonas{at}tch.harvard.edu
Presented at the Poster Session of the Thirty-seventh Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 29–31, 2001.
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Abstract |
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Methods. Thirty-six piglets (9.2 ± 1.1 kg) underwent DHCA under varying conditions with continuous monitoring by NIRS (pH-stat or alpha-stat strategy, hematocrit 20% or 30%, DHCA time 60, 80, or 100 minutes). Neurological recovery was evaluated daily. The brain was fixed in situ on postoperative day 4 and a histological score (HS) for neurological injury was assessed.
Results. Oxygenated hemoglobin (HbO2) and total hemoglobin signals detected by NIRS were significantly lower with alpha-stat strategy during cooling (p < 0.001), suggesting insufficient cerebral blood supply and oxygenation. HbO2 declined to a plateau (nadir) during DHCA. Time to nadir was significantly shorter in lower hematocrit groups (p < 0.01). Significantly delayed neurologic recovery was seen with alpha-stat strategy compared with pH-stat (p < 0.05). The alpha-stat group had a worse histological score compared with those assigned to pH-stat (p < 0.001). Neurologic impairment was estimated to be over 10 times more likely for animals randomized to alpha-stat compared with pH-stat strategy (odds ratio = 10.7, 95% confidence interval = 3.8 to 25.2).
Conclusions. Combination of alpha-stat strategy and lower hematocrit exacerbates neurological injury after DHCA. The mechanism of injury is inadequate cerebral oxygenation during cooling and a longer plateau period of minimal O2 extraction during DHCA.
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Introduction |
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Cardiopulmonary bypass (CPB) strategies vary greatly between different centers [9]. The alpha-stat strategy continues to be widely employed for pediatric cardiac surgery though there are no good data to support this practice. Hemodilution also is used to a widely varying degree. In the current study, we explored the interaction of pH strategy and hematocrit. We hypothesized that a combination of alpha-stat and hemodilution would be particularly injurious because of limited oxygen delivery. We used a piglet survival model that allows determination of both behavioral as well as histological endpoints. NIRS was also used to monitor oxygen delivery.
The technique of NIRS continues to hold out the promise of becoming a real-time method for monitoring oxygen delivery to the brain during deep hypothermic bypass and circulatory arrest. In the past, we were hopeful that the cytochrome a,a3 signal would be particularly helpful because unloading of oxygen from hemoglobin is hampered by an alkaline pH as seen with alpha-stat particularly in combination with hypothermia [10]. However, a laboratory study in which cyanide was administered in a piglet bypass model has failed to validate the cytochrome signal that is overwhelmed by the changes in hematocrit that occur during cardiopulmonary bypass [11]. Nevertheless, we found in a recent study in which we manipulated temperature, hematocrit, and circulatory arrest time but not pH strategy that the Tissue Oxygenation Index (ratio of oxygenated to total hemoglobin) derived from NIRS as well as the Oxyhemoglobin Nadir Time (the time from oxyhemoglobin signal reaching its nadir during circulatory arrest until reperfusion) are useful indices for predicting neurological injury during and after circulatory arrest [12].
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Material and methods |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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All surgical procedures were performed under sterile conditions. For the intraoperative monitoring and blood sampling, arterial and venous lines were placed in the left superficial femoral artery and right femoral vein, respectively. The right femoral artery was exposed for the CPB arterial cannula, and a right anterolateral thoracotomy was performed in the third intercostal space to expose the right atrium for venous cannulation. After systemic heparinization (300 IU/kg), an 8F arterial cannula (Medtronic Bio-Medics, Minneapolis, MN) and a 28F venous cannula (Research Medical, Inc, Midvale, UT) were inserted into the right femoral artery and right atrial appendage, respectively.
All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" prepared by the Institute of Laboratory Animal Resources and published by the National Institute of Health (NIH publication No. 86-23, revised in 1985).
Experimental groups and conditions
The experimental design included these three parameters with two or three possible values resulting in 2 x 3 x 2 = 12 experimental settings. Each setting was performed in 3 piglets. In the group with hematocrit 20%, the CPB prime consisted of 400 mL heparinized blood and 800 mL crystalloid solution. The other group (hematocrit of 30%) was prepared with 1,200 mL heparinized whole-blood prime. For ease of description, 4 groups were compared according to pH strategy and hematocrit conditions (pH-stat 30%, pH-stat 20%, alpha-stat 30%, alpha-stat 20%). Operative conditions and intraoperative data including NIRS data were evaluated between the groups and the relationship between NIRS data and the neurological outcome was examined comprehensively.
CPB technique
The CPB circuit consisted of a roller-pump, membrane oxygenator (Minimax; Medtronic, Inc, Anaheim, CA) and sterile tubing, with 40 µm arterial filter (Olson Medical Sales, Inc, Ashland, MA). The prime was determined by the experimental protocol. Methylprednisolone (30 mg/kg), furosemide (0.25 mg/kg), sodium bicarbonate (10 ml), cephazolin sodium (25 mg/kg), fentanyl (50 µg/kg), and pancuronium (0.5 mg/kg) were added to the prime. Full bypass flow was set at 100 ml/kg/min. Either pH-stat or alpha-stat strategy was selected according to the experimental protocol. CPB was started and animals were perfused for 10 minutes at normothermia (37°C). Animals were then cooled to an esophageal temperature of 13°C to 14°C over 40 minutes according to the experimental protocol. Ventilation was stopped after the establishment of CPB. Each group underwent 60, 80, or 100 minutes of DHCA at 14°C to 15°C. Before reperfusion, methylprednisolone (30 mg/kg), furosemide (0.25 mg/kg), sodium bicarbonate (10 ml), and mannitol (0.5 g/kg) were administered into the pump. Reperfusion was begun at 100 ml/kg/min and animals were warmed to 37°C. Rewarming protocol including maximal perfusate temperature was identical in all groups. The heart was defibrillated as necessary at an esophageal temperature of 30°C. Fresh whole blood from a donor pig, drawn on the operative day, was transfused into the prime as required to increase hematocrit to at least 25% in all groups during rewarming. Ventilation (100% oxygen) was started 10 minutes before the weaning from CPB. After 40 minutes of rewarming, animals were weaned from CPB and the arterial and atrial cannulae were removed. Protamine (5 mg/kg) was administered intravenously after the animal was hemodynamically stable. The wound was closed in a sterile fashion. No or minimal catecholamine was used at the time of weaning from CPB.
Postoperative management
Animals remained sedated and paralyzed and were mechanically ventilated and monitored continuously for 12 hours after operation, at which time chest tubes were removed and animals were weaned from ventilation and extubated. Neurological and behavioral evaluations were performed at 24-hour intervals beginning on postoperative day 1. Neurologic scoring data was adapted from the neurologic deficit score (NDS) and overall performance category (OPC) [13]. On postoperative day 4, the brain was fixed with 4 liters of 4% formaldehyde solution and the histological outcomes were assessed [14].
Data collection
Body weight
Body weight was measured before the experiment and on postoperative days 1 and 4.
Total body water estimation by bioelectrical impedance
Percent change of total body water was measured at the baseline and repeated at the weaning from CPB, 1 hour and 3 hours after the procedure, and on postoperative day 1 [15].
Blood gas analyses
Arterial blood gas values, including electrocyte, glucose, and lactate concentrations, were measured at baseline, every 10 minutes during cooling and rewarming, and after the procedure as needed (NOVA 900; Nova Biomedical, Waltham, MA). Blood gas values were presented at an electrode temperature of 37°C.
Near-infrared spectroscopy
A pair of fiberoptic optodes was attached to the head of the animal with a probe holder after induction of anesthesia. The optodes spacing was 4.0 cm in a coronal plane. These two optodes, a transmitter, and a receiver of laser light of near-infrared wavelength, were connected to NIRS (NIRO300; Hamamatsu Photonics K.K., Hamamatsu City, Japan). This device calculated the relative concentration changes in oxygenated hemoglobin (HbO2), deoxygenated hemoglobin (HHb), and oxidized cytochrome a,a3 (CytO2), and the Tissue Oxygenation Index (TOI) which is calculated from the ratio of oxygenated to total hemoglobin. Data were recorded every 10 seconds after the induction of anesthesia and for 3 hours after weaning from CPB.
Biochemical analyses
Blood samples were drawn before CPB and on postoperative day 1 to measure total protein, albumin, total bilirubin, aspartate transaminase, alanine transaminase, lactate dehydrogenase, creatinine kinase, alkaline phosphatase, blood urea nitrogen, and creatinine.
Neurologic and behavioral evaluations
Details have been described elsewhere [13]. NDS (500 = brain death, 0 = normal) and OPC (5 = brain death, 4 = coma, 3 = severe impairment, 2 = moderate impairment, 1 = normal) were used for the neurologic and behavioral evaluations and were carried out by one veterinarian who was blinded to the experimental protocol.
Histologic assessment
Details have been described elsewhere [7, 14]. Histological damage was rated using the following categorical scale: (5 = cavitated lesions with necrosis, 4 = significant damage to neurons, 3 = large clusters of injured neurons, 2 = small clusters of damaged neurons, 1 = isolated neuronal damage, 0 = normal). To avoid bias, all specimens were examined by a single neuropathologist in a blinded fashion.
Statistical analysis
Continuous data including hemodynamic and perfusion variables were compared between pH-strategy and hematocrit groups using factorial analysis of variance (ANOVA) with the post-hoc Scheffé method. Since the Wilk–Shapiro test revealed significant departures from normality for NDS, OPC, and histologic scores, these outcomes were compared by the nonparametric Kruskal–Wallis and Mann–Whitney U tests with a Bonferroni criterion of p < 0.008 (0.05/6) considered statistically significant. Correlation between normalized HbO2 nadir time and neurologic outcome was assessed by the Spearman rank-order correlation coefficient (rs). Regression models were applied to determine the effects of pH, hematocrit, and duration of DHCA on brain damage as measured by neurologic and histologic scores. All data are expressed in terms of the mean ± SD unless otherwise specified. Statistical analysis was performed using the SAS software package (version 6.12, SAS Institute, Cary, NC). All reported p values are two-tailed.
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Results |
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Near-infrared spectroscopy
Near-infrared spectroscopy (NIRS) variables were analyzed by factorial ANOVA with the post-hoc Scheffé method to compare pH-strategy and hematocrit groups at selected points (Fig 1).
Five NIRS variables are presented: oxyhemoglobin (HbO2) signal, deoxyhemoglobin (HHb) signal, total hemoglobin (HbT) signal, oxidized cytochrome a,a3 (CytO2) signal, and tissue oxygenation index (TOI). Groups were compared using ANOVA and the post-hoc Scheffé method.
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The HHb signal for all 4 groups declined and reached nadir values during cooling; it then increased at the onset of DHCA and decreased subsequently during the rewarming period, returning to baseline values during the post-bypass period (Fig 1B).
The HbT signal increased during the cooling phase for all groups except alpha-stat 20%. The 4 groups increased after DHCA and then leveled off slightly higher than baseline values (Fig 1C). Animals in the pH-stat group demonstrated the highest HbT values throughout the time course, and these values were significantly higher than pH-stat 20% and alpha-stat 20% at the end of cooling, all points during DHCA, during rewarming at 5 and 20 minutes (p < 0.001) and 40 minutes (p = 0.03). Similarly, HbT was higher in the alpha-stat 30% group versus alpha-stat 20% at these same times points (p < 0.001). In addition, HbT was significantly higher for pH-stat 30% versus pH-stat 20% (p = 0.007) and alpha-stat 30% versus alpha-stat 20% (p < 0.001) at the completion of DHCA (60 minutes). During the weaning period, the only group differences occurred between pH-stat 30% versus pH-stat 20% at 5 minutes (p = 0.01). HbT signal was not statistically different between the 4 groups when the animals were off pump from 30 minutes to 3 hours (all p > 0.10).
The oxidized cytochrome a,a3 signal fell during the cooling phase for animals in the pH-stat 20% group and increased slightly in the other groups. During DHCA, the CytO2 signal decreased reaching the lowest value for each group at the end of DHCA (60 minutes). Rewarming increased the levels of CytO2 to near baseline levels that continued throughout the weaning period (Fig 1D). The pH-stat 30% group had a significantly higher CytO2 signal compared with pH-stat 20% throughout the cooling phase from 5 minutes (p = 0.02) to the end of cooling (p = 0.004), at the beginning and end of DHCA (p < 0.001), and 5 minutes after rewarming (p = 0.01). Although no significant differences were detected between the groups from the end of rewarming throughout the weaning period (all p > 0.10), both the pH-stat 30% and alpha-stat 30% groups reached baseline levels whereas both pH-stat 20% and alpha-stat 20% groups did not.
TOI showed an increase during the cooling phase, a sharp decrease during DHCA, followed by another sharp increase with values superseding baseline during rewarming (Fig 1E). Although the pH-stat 30% group had a lower TOI compared with alpha-stat (p < 0.001) and both pH-stat 20% and alpha-stat 30% (p = 0.03) at the end of DHCA, its TOI rebounded sharply 5 minutes after rewarming. Throughout the 3-hour post-bypass period, all 4 groups flattened out and returned to their baseline levels.
From the onset of DHCA, there was a decline in HbO2, HbT, CytO2, and TOI, whereas the HHb signal increased reciprocally. As reported previously [12], the decrease in the HbO2 signal (HbO2 decay curve) during DHCA can be described by a logarithmic function, HbO2 = a log(t) + b, such that dHbO2/dt = a/t, where t is the length of time after the onset of DHCA and a and b are constants. We have defined that HbO2 signal reaches the plateau state (nadir value) when the slope of the fitted curve, namely the differential coefficient dHbO2/dt, exceeds -0.5. Time to reach the plateau was calculated in each case. ANOVA with post-hoc Scheffé comparisons revealed highly significant differences between hematocrit levels but not between different pH-strategies. In the pH-stat 30% and alpha-stat 30% groups, the times to reach the nadir state were 51 ± 12 and 45 ± 7 minutes, respectively (p = 0.44). In the pH-stat 20% and alpha-stat 20% groups, the times to reach the nadir state were 28 ± 7 and 26 ± 7 minutes, respectively (p = 0.93). Mean time to nadir was approximately 20 to 25 minutes shorter, longer in the pH-stat 20% and alpha-stat 20% groups (p < 0.001) compared with pH-stat 30%. Alternatively, time to nadir was approximately 20 minutes shorter in the pH-stat 20% (p = 0.006) and alpha-stat 20% (p = 0.002) groups compared with alpha-stat 30%.
Time in minutes from reaching nadir level until reperfusion was also calculated and referred to as HbO2 nadir time. Although the esophageal temperature under DHCA was the same in all groups, cerebral metabolic rate is lower with pH-stat [16, 17]. Therefore, we normalized the HbO2 nadir time by the estimated difference of cerebral metabolic rate for oxygen in the two different pH strategies [17, 18]. The following normalized HbO2 nadir times were derived: 30 ± 22 for pH-stat 30%, 51 ± 18 for pH-stat 20%, 53 ± 32 for alpha-stat 30%, and 81 ± 25 for alpha-stat 20%. ANOVA with post-hoc Scheffé comparisons indicated that the normalized HbO2 nadir time was significantly shorter in the pH-stat 30% group than the alpha-stat 20% group (p = 0.002) although no other group differences were detected (all p > 0.10).
Biochemical analyses
There were no significant differences found between the pH-strategy and hematocrit groups. Ischemic damage to the whole body as determined by enzyme changes was considered mild on the whole (data not shown).
Neurologic and behavioral evaluations
NDS and OPC showed relatively rapid recovery in all groups (Table 5). Although NDS was higher on the day of extubation (postoperative day 1) in the alpha-stat groups, differences were not significant (p = 0.18). Significant improvements were demonstrated as early as postoperative day 2 in each of the 4 groups with respect to NDS (all p < 0.01, Wilcoxon signed-ranks tests) and OPCs (all p < 0.05, Wilcoxon signed-ranks tests). On the 4th postoperative day, however, piglets in the pH-stat 30% and 20% groups all showed normal NDS and OPC scores, and these groups were significantly better compared with the alpha-stat 20% group (all p < 0.05). Four of the 9 piglets (44%) in the alpha-stat 20% group had a normal NDS on the 4th postoperative day.
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Effects of pH, hematocrit, and duration of DHCA on neurologic and histologic changes
Univariate and multivariate analyses were conducted to ascertain the effects of pH, hematocrit, and duration of DHCA on NDS and total HS. Logistic regression was utilized to determine the impact of each variable in differentiating between normal and impaired neurologic deficit on the 4th postoperative day. Results indicated that pH-strategy was a significant univariate and multivariate predictor (p < 0.001). Piglets randomized to alpha-stat strategy were estimated to be over 10 times more likely than those undergoing pH-stat to have evidence of neurologic impairment (odds ratio = 10.7, 95% confidence interval = 3.8 to 25.2). Hematocrit level and duration of DHCA did not reach statistical significance although hemodilution and longer DHCA were each associated with poorer outcome. Linear and nonlinear regression models confirmed that pH-strategy (p < 0.001) and duration of DHCA (p = 0.002) were independent predictors of total HS. Therefore, animals subjected to alpha-stat and those having a longer duration of DHCA showed more severe brain damage as determined by neurohistologic total score.
Correlation between NIRS data and neurologic outcomes
We examined the correlation between normalized HbO2 nadir time and the neurologic outcomes represented by NDS, OPC, and total HS. The Spearman rank-order correlation coefficient indicated significant positive correlations between normalized HbO2 nadir time and NDS (rs = 0.75, p < 0.001) and OPC (rs = 0.55, p = 0.002) as evaluated on the 4th postoperative day. HbO2 nadir time was also positively correlated with total HS (rs = 0.58, p < 0.001). Therefore, longer HbO2 nadir time was associated with significantly greater postoperative neurologic impairment.
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Comment |
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TopAbstractIntroductionMaterial and methodsResultsCommentAcknowledgmentsReferences |
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The piglet survival model used in this study provides reliable data that is highly relevant to clinical practice. Animals were examined daily by a veterinarian who performed the neurological assessments and was blinded to treatment assignment. To avoid bias in assessing histology, a neuropathologist with extensive experience in piglet neuropathology was blinded to experimental conditions. We believe that the method of brain fixation is important in achieving artifact-free preparations.
Effects of pH strategy on cerebral oxygenation and metabolism
The pH-stat strategy provides greater cerebral blood flow and shifts the oxyhemoglobin dissociation curve to the right thereby potentially increasing oxygen delivery relative to the alpha-stat strategy. This is confirmed by the NIRS data in the current study. Given the same hematocrit level, lower HbO2 and HbT levels were found using alpha-stat, suggesting that this pH-strategy is associated with less oxygenation and cerebral blood volume and flow.
Reports from other laboratories have demonstrated that during deep hypothermia, pH-stat strategy reduces the cerebral metabolic rate of oxygen (CMRO2) compared with alpha-stat strategy [18, 19]. Hindman and colleagues [18] estimated that at 17°C, CMRO2 with pH-stat is 35% to 40% less than with alpha-stat. Skaryak and colleagues [19] calculated the difference of CMRO2 and found it to be 1.2 to 1.4 times greater with alpha-stat relative to pH-stat management at 18° and 14°C, respectively. In their studies, Hindman and colleagues [18] used longer duration of cooling prior to measurement (65 minutes), whereas Skaryak and colleagues [19] used 23 minutes. We previously reported that shorter cooling periods of less than 20 minutes are associated with lower cognitive development scores [20]. A shorter duration of cooling prior to circulatory arrest may increase the risk of brain damage because cerebral metabolic suppression is determined in part by the duration of cooling as seen in the above two studies. Since the cooling duration in our current study was 40 minutes, we estimated that CRMO2 with alpha-stat in our study was approximately 1.5 times greater than that with pH-stat at 15°C and used this factor to normalize the HbO2 nadir time. Normalized HbO2 nadir time was closely associated with postoperative neurological behavioral score and histopathology and may prove to be a useful predictor of ischemic injury after DHCA in clinical practice.
Effect of hematocrit on brain during hypothermic CPB
We have accumulated considerable evidence in previous laboratory studies that outcome after deep hypothermic bypass with circulatory arrest is improved with 30% hematocrit compared with 20% hematocrit. Recently, we explored the interaction of hematocrit, temperature, and duration of circulatory arrest and confirmed that a hematocrit of 20% increases vulnerability to brain injury with higher temperature and longer duration of arrest [12]. In that study, as well as this one, the time to reach a nadir level for HbO2 was significantly longer with a higher hematocrit. For animals that had the pH-stat strategy, the time to reach nadir was 51 minutes with hematocrit 30%, and 28 minutes with hematocrit 20%. On the other hand, among the animals that had 30% hematocrit, mean time to nadir was only 6 minutes less in the alpha-stat group. This suggests that a hematocrit difference of 10% may have a greater influence than the choice of pH strategy. However, it is important to remember that pH strategy influences metabolic rate. When the nadir time is "normalized" to account for this, we found that pH strategy and hematocrit both have an important influence.
Additive effects of pH strategy and hematocrit on cerebral outcome
The gold standard endpoint of this study was histological assessment of the brain. Animals with alpha-stat and lower hematocrit had a worse outcome than animals in either of the pH-stat groups. NIRS data suggest that the mechanism is an earlier cessation of aerobic metabolism due to less oxygen availability from the beginning of the arrest period.
Relevance to continuous cardiopulmonary bypass
The relevance of this work to the majority of cardiac surgical patients who do not undergo circulatory arrest remains to be determined. However, it is interesting to note that a study of patients undergoing atrial septal defect closure using continuous full-flow bypass and mild hypothermia but with severe hemodilution and alpha-stat revealed a significantly worse developmental outcome relative to matched patients who had device closure of their atrial septal defect without bypass [21]. Other evidence that transient hypoxia, without loss of consciousness or indications of global or focal neurologic injury, can result in profound memory and neurologic complications exists in literature describing studies in high-altitude mountaineers [22–24]. Perhaps there may be factors other than microembolization that could explain the cognitive deficits that are consistently seen in adults after cardiopulmonary bypass.
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