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J Thorac Cardiovasc Surg 2004;127:223-233
© 2004 The American Association for Thoracic Surgery
Surgery for congenital heart disease |
a Department of Pediatric Anesthesiology, Children's Hospital of Wisconsin and Medical College of Wisconsin, Milwaukee, Wis, USA
b Department of Critical Care Medicine, Children's Hospital of Wisconsin and Medical College of Wisconsin, Milwaukee, Wis, USA
c Department of Cardiovascular Surgery, Children's Hospital of Wisconsin and Medical College of Wisconsin, Milwaukee, Wis, USA
Read at the Eighty-third Annual Meeting of The American Association for Thoracic Surgery, Boston, Mass, May 4-7, 2003.
Received for publication May 1, 2003; revisions received August 11, 2003; accepted for publication August 13, 2003.
* Address for reprints: George M. Hoffman, MD, Anesthesiology 735, Children's Hospital of Wisconsin, 9000 West Wisconsin Avenue, Milwaukee, WI 53226, USA
ghoffman{at}mcw.edu
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METHODS: Nine neonates undergoing stage 1 palliation for hypoplastic left heart syndrome had regional tissue oxygenation continuously measured by frontal cerebral and thoraco-lumbar (T10-L2) somatic (renal) reflectance oximetry probes (rSO2, INVOS; Somanetics, Troy, Mich). Surgery was accomplished using cardiopulmonary bypass with whole-body cooling (18°C-20°C) and regional cerebral perfusion through the innominate artery at flow rates guided by estimated minimum flow requirements and measured rSO2 during reconstruction of the aortic arch. Data were logged at 1-minute intervals and analyzed using repeated measures analysis of variance.
RESULTS: A total of 3176 minutes of data were analyzed. Prebypass cerebral rSO2 was 65.4 ± 8.9, and somatic rSO2 was 58.9 ± 12.4 (P < .001, cerebral vs somatic). During regional cerebral perfusion, cerebral rSO2 was 80.7 ± 8.6, and somatic rSO2 was 41.4 ± 7.1 (P < .001). Postbypass cerebral rSO2 was 53.2 ± 14.9, and somatic rSO2 was 76.4 ± 7.7 (P < .001). The risk of cerebral desaturation was significantly increased after cardiopulmonary bypass.
CONCLUSIONS: Cerebral oxygenation was maintained during regional cerebral perfusion at prebypass levels with deep hypothermia. However, after rewarming and separation from cardiopulmonary bypass, cerebral oxygenation was lower compared with prebypass or somatic values. These results indicate that cerebrovascular resistance is increased after deep hypothermic cardiopulmonary bypass, even with continuous perfusion techniques, placing the cerebral circulation at risk postoperatively.
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Monitoring and data acquisition
In all patients, blood pressure was invasively monitored with an existing umbilical artery catheter, and atrial pressure was monitored with an umbilical vein catheter if present or an atrial line placed at the time of surgery. Arterial oxygen saturation was monitored continuously in the lower extremity (Nellcor N200; Pleasanton, Calif). Systemic venous oxygenation (SvO2) was monitored continuously during CPB from the venous drainage (Terumo CDI-500; Ann Arbor, Mich) and post-CPB using a 4FR optical catheter (Abbott Oxycath; Abbott Laboratories, Abbott Park, Ill) placed in the superior vena cava before separation from CPB. Airway gas tensions were monitored using Raman spectroscopy (Ohmeda Rascal-2, Louisville, Colo). Data from these sources were captured on a clinical information system (GE/Marquette Solar; Milwaukee, Wis) and trended at 5-minute intervals. NIRS probes were placed on the patient's midline forehead (cerebral) and slightly to the right of midline on the T10-L2 posterior flank (somatic) after entry into the operating room. The probes were monitored by a dual-detector device (Somanetics INVOS 5100A, Troy, Mich) and trended at 1-minute intervals. CPB flows, temperatures, and pressures were captured at 5-minute intervals. Arterial and venous blood gases were obtained at clinically appropriate intervals, with tensions reported at 37°C (Radiometer ABL, Copenhagen, Denmark).
Statistical analysis
Prospective, electronically captured, and manually recorded data were inserted into a common statistical database. In addition to measured variables, derived variables were calculated as follows: organ perfusion pressure (PP) = mean arterial blood pressure - central venous pressure; cerebral Da-rO2 = SaO2 - cerebral rSO2; somatic Da-rO2 = SaO2 - somatic rSO2; DrSO2 (cerebral-somatic) = cerebral rSO2 - somatic rSO2; oxygen content PP index (CaO2 · PPI) = 1.34 · hemoglobin · PP. Each patient's clinical data were divided into 5 major time periods consisting of 11 intervals, demarcated by preinduction baseline, anesthesia induction, surgical incision, initiation of CPB, initiation of myocardial ischemia with aortic crossclamp, initiation of RCP, resumption of CPB, removal of aortic crossclamp, separation from CPB, completion of modified ultrafiltration, and surgical closure. Within each interval for each patient, data were collapsed into 5 epochs of equal duration to create 55 distinct epochs for subsequent statistical analysis. Data were summarized within intervals and periods, and presented as mean ± SD if continuous and number and percent if discrete, with 95% confidence intervals (CIs) calculated as appropriate. Generalized least squares regression and analysis of variance (ANOVA) techniques were used to account for repeated measurements within patients and time intervals. Data were compared across time periods or intervals by 2-sided t tests on regression coefficients or by 2-way analysis of variance for repeated measures for comparisons of means and by the likelihood-ratio test for risk comparisons, with significance cutoff at P < .05 after correction for multiple comparisons by the Bonferroni method. All calculations were performed with a standard statistical package (STATA version 8; Stata Corp, College Station, Tex).
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Interventions to increase cerebral rSO2 may reduce neurologic morbidity in children undergoing CPB.27,28 Although absolute thresholds of rSO2 for neurologic injury are not known in human neonates, evidence from adult humans29 and neonatal piglets30 indicates that aerobic metabolism is impaired when cerebral rSO2 decreases below 44% to 47%. Critically low values for cerebral rSO2 have been reported preoperatively in neonates with a variety of congenital lesions31 and were observed with substantial frequency in our patients in the post-CPB period.
The pre-CPB rSO2 data revealed a normal cerebral arterial-regional saturation difference31 but an increased somatic arterial-regional difference, typical of a "stressed" patient with increased resistance in vascular beds subject to regional sympathetic control, with resultant redistribution of systemic perfusion from splanchnic to cerebral circulations. The baseline hemodynamic data in these infants revealed high SaO2 and high pulmonary and systemic flow ratios despite preoperative management with hypercapnia and low FIO2; thus, compromised splanchnic and somatic flow were expected.
Before CPB, SvO2 was slightly lower than cerebral rSO2, reflecting the contribution of relatively desaturated somatic blood to SvO2. After CPB, the converse was true; SvO2 was higher than cerebral rSO2, reflecting the contribution of more well-saturated somatic blood to SvO2. These findings emphasize the differences between regional and global measures of oxygen supply and demand relationships.18,32
The observed divergence of cerebral from somatic rSO2 post-CPB was expected,33 although the decrease in cerebral rSO2 from the pre-CPB baseline indicates that cerebral oxygenation may be vulnerable despite palliation of the circulation through S1P. The reasons for the reduction in cerebral rSO2 from baseline include (1) reduced global oxygen delivery, (2) reduced somatic and splanchnic resistance, (3) increased cerebral resistance, and (4) changes in the venous blood compartment.
Although global oxygen delivery (SvO2) was not routinely assessed preoperatively, SvO2 was maintained after separation from CPB until closure. Similarly, the CaO2 · PPI, a measure of regional oxygen availability, was maintained post-CPB. Thus the decrease in cerebral rSO2 post-CPB was not likely explained by a reduction in global oxygen delivery. However, because previous data have described the occurrence of decreasing SvO2 in the first 6 to 12 hours postoperatively,34 a reduction in global oxygen delivery may increase the risk of cerebral desaturation in the later postoperative period.
A reduction in splanchnic and somatic resistance by reactive hyperemia, phenoxybenzamine, milrinone, and isoflurane likely contributed to the low risk of somatic desaturation in the immediate post-CPB period. Alpha-adrenergic mechanisms of vasoconstriction are more active in splanchnic, muscle, and skin beds than in organs with intense autoregulation such as brain and heart.35-37 Therefore, alpha-adrenergic blockade would be expected to reduce the sympathetically mediated increase in somatic resistance that occurs in the patient post-CPB with reduced oxygen delivery. Our findings provide direct evidence for an effect of phenoxybenzamine to preserve perfusion in somatic beds. However, the cerebral circulation may be more vulnerable if splanchnic vasoconstriction is pharmacologically limited. Further study is necessary to quantify the potential effect of phenoxybenzamine to redistribute blood flow away from the cerebral circulation.
The decreased cerebral rSO2 corresponded in time to a decrease in isoflurane concentration; isoflurane decreases both cerebral oxygen consumption and cerebrovascular resistance, with a resultant increase in cerebral oxygenation.38 Although isoflurane similarly alters autoregulation in all systemic beds by its vasodilatory effects, additional somatic vasodilation may not have occurred in the presence of phenoxybenzamine and milrinone. Thus, the effect of isoflurane to increase cerebral blood flow may be enhanced in the presence of additional pharmacologic reduction in somatic resistance.
Cerebral resistance is increased after hypothermic circulatory arrest and hypothermic CPB.1,5,15 This may occur as result of altered dynamic autoregulation from changes in PCO2 and pH as a result of impaired autoregulation,15,16 endothelial dysfunction,3,6,8,9 tissue edema, microvascular occlusion, cerebral edema, or other mechanical factors. Perfusion at excessive pressure has been implicated in the cerebrovascular lesion induced by hypothermic CPB.12,16,39 Although we targeted a cerebral rSO2 greater than 75% during RCP, we did not systematically reduce flow rates in patients with cerebral rSO2 greater than 90%. Although the RCP flows in our patients were in the same range (25-75 mL · kg · min) as reported by others,12-14,39,40 excessive flow during RCP may also contribute to the increased cerebrovascular resistance seen after hypothermic CPB. A target of cerebral rSO2 or jugular bulb saturation greater than 90% during CPB cooling, as in preparation for DHCA,5 thus may not be advisable if RCP will be used.
The use of a pH-stat perfusion strategy, although enhancing recovery of cerebral energetics41 if post-CPB PP is controlled, may contribute to this overperfusion lesion through alteration of cerebral autoregulation.16,42 Our results indicate that hypercapnia during pre-CPB management and pH-stat CPB management may reset cerebrovascular autoregulation for CO2 to a higher level. The enhanced sensitivity of rSO2 to changes in PP and CO2 post-CPB (Table 4) is consistent with altered autoregulation.16 The increased dependency of the cerebral circulation on PP constitutes a physiologic risk in the patient with parallel circulation, because increases in systemic blood pressure and SVR will reduce systemic blood flow.43 On the other hand, CO2 responsiveness was enhanced post-CPB in our patients, indicating that more aggressive use of hypercapnia may improve cerebral rSO2 even in the face of adequate global oxygen delivery measures.
Our findings emphasize the direct effect of hypothermic CPB and RCP on cerebrovascular resistance11,16,41 despite efforts to optimize regional oxygen delivery,44 including adjuncts to minimize the endothelial dysfunction from CPB.6,8,9 Modifications in perfusion strategy to limit changes in rSO2 may provide a means to avoid both supply-dependent oxygen conditions40 and overperfusion during hypothermia.12 Use of more moderate hypothermia during CPB and RCP may be justifiable under regional rSO2 guidance to reduce the alterations in cerebral resistance that result from deep hypothermia. However, the relationship between the effects of DHCA and hypothermic RCP on cerebral blood flow and metabolism, and any subsequent neurologic injury, is still unclear.
The cerebral circulation remains at risk post-CPB despite continuous cerebral perfusion, and neurologic dysfunction may result from postoperative cerebral ischemia independently of CPB techniques. Our results indicate that extended monitoring of brain oxygenation in the immediate postoperative period, when reduced global oxygen delivery is likely to be superimposed on increased cerebrovascular resistance, may reveal further opportunities for hemodynamic interventions to reduce the risk of cerebral ischemia.
Discussion
Dr Gil Wernovsky (Philadelphia, Pa). I found this study to be quite innovative, well designed, and thoughtfully presented. It adds to the growing body of information on the complexities of single ventricle physiology, both before and after CPB.
In the past 15 years, there have been consistent and incremental improvements in the outcomes for children undergoing stage 1 reconstruction, and many things have changed because of our clinical experience and laboratory findings.
These include changes in the methods of preoperative stabilization, the timing of surgery (as you have described in regard to the institution of CPB, including a shift to RCP to avoid DHCA), and the medical management of these patients, with increasing use of postoperative, long-acting vasodilators (such as phenoxybenzamine) and frequent postoperative monitoring. Many of these advances have been pioneered by your group in Milwaukee and others in this room.
On the basis of these studies, there has been a shift at many centers to embrace these new practices. However, before this report, there has been little information presented on the potential neurologic morbidities of two of these changes—RCP and the routine use of phenoxybenzamine.
This article contains a substantial amount of data, but I want to comment on two points and then ask Dr Hoffman three questions.
On the basis of clinical laboratory data from a decade ago, many in our field have moved to avoid circulatory arrest whenever possible. However, a similar detailed assessment of this alternative, RCP in the human, is lacking.
The strategy of RCP for an average of approximately 1 hour in this study, which was preceded by bypass of approximately 45 minutes, and another period of 20 minutes or so after the period of RCP, was associated with estimates of adequate cerebral oxygen delivery by NIRS during the procedure, but significantly lower values after the procedure. As the authors state, this was not solely the result of a postoperative decrease in arterial oxygen saturation, but most likely the result of the increased postoperative cerebral vascular resistance caused by impaired autoregulation.
In addition, the patients received a potent systemic vasodilator (phenoxybenzamine) to minimize ventricular afterload.
Thus, following these combined strategies, a situation has been created that conspires to maximally shunt blood away from the central nervous system, high cerebrovascular resistance and low splanchnic resistance.
Now, this may or may not have clinical implications, and we just do not know yet. It is important to emphasize that NIRS is a surrogate variable for CNS oxygenation, and these observations must be followed up with clinical studies to determine the clinical relevance in the long term.
So I would like to ask the following three questions. First, the authors state that the rate of RCP was titrated during the procedure over a wide range (I believe it was 30-70 mL · kg · min) to achieve a target cerebral saturation of 75% or greater during the procedure.
Did you look at whether the decrease in postoperative cerebral oxygenation was related at all to the absolute rate or pressure of the cerebral blood flow that you used? One could hypothesize that higher flow rates or pressure during profound hypothermia could cause more endothelial damage and impaired autoregulation.
Second, the model that related regional cerebral saturation to the hemodynamic and bypass parameters was elegant and very interesting. The authors found that RCP, treatment with phenoxybenzamine, and a number of potentially modifiable parameters were related to lower cerebral oxygen saturations, including mean arterial pressure, lower hematocrit, and, I think, higher temperature.
Earlier in the session, Dr Gaynor presented data showing in a more heterogenous group of children that low diastolic pressure in the coronary intensive care unit was related to an increased incidence of periventricular leukomalacia.
Have you looked at the cerebral oxygenation data in the postbypass period in terms of diastolic pressure in addition to mean arterial pressure, because this could be particularly low in patients with a diastolic runoff through the shunt?
Finally, if you brought this methodology into the intensive care unit, because, as your group has shown, the real vulnerable period is 6 to 12 hours later, would the cerebral somatic difference persist into the postoperative period?
You and your group are really to be commended for continuing to investigate the implications of the changes in our strategies and to provide us with real data rather than dogma as we move forward.
Dr Hoffman. I agree that spectroscopy measurements are surrogate outcome indicators. I anticipate that with collaboration from colleagues we will be able to answer your most important question: What does this have to do with the relationship between NIRS measures and subsequent neurologic outcome?
With regard to the potential conspiracy of afterload reduction and posthypothermic CPB-increased cerebrovascular resistance, I agree that this is a major caveat and find these data compelling indication for regional saturation monitoring in this population.
The controversial question that we didn't answer, because we have largely abandoned the use of total circulatory arrest, is whether the increase in cerebrovascular resistance after DHCA is greater or less than that observed with the continuous RCP techniques.
Your first question related to the effect of perfusion flow rates on changes in cerebrovascular resistance.
I could not do the analysis that you suggested. In actuality, the perfusion flow rates vary somewhat in response to surgical manipulations on a minute-to-minute basis; our data collection technique did not allow the degree of bypass flow tracking to enable the data analysis required to answer your question, so I would have to think about the methodology.
However, there are good data showing that overperfusion, either by pressure or flow, increases the cerebrovascular lesion seen after deep hypothermic CPB.
We typically, as I think other centers do, try to overflow with a pH-stat cooling strategy to achieve a jugular venous saturation or regional NIRS saturation greater than 90% in anticipation of a potential period of cerebral circulatory arrest. I'm not sure that overperfusion is routinely necessary anymore if NIRS monitoring and continuous cerebral perfusion are used, and it may be that overperfusion is contributing to things.
You wondered about the effects of postoperative diastolic blood pressure and global hemodynamic vulnerability on cerebral perfusion. I certainly agree that the first 6 to 24 postoperative hours is the most vulnerable, critical period for these patients. We have some NIRS data for this time period, but it has not been analyzed.
Because of the anticipated postoperative vulnerability, we hope to use this technology in most postoperative patients. We're currently limited by the number of available devices, as most investigators are.
Dr Carlos Troconis (Caracas, Venezuela). Dr Hoffman, are we looking at the tip of an iceberg? Is the problem more profound? Should we look back into the cerebral fetal circulation in hypoplastic left heart syndrome? We will probably find many reports about the incidence of microcephaly with this syndrome and undeveloped microcirculation or high resistance in cerebral flow. Can you make comments on that?
Dr Hoffman. I don't know about confounding anomalies of cerebrovascular anatomy in these patients. We have to deal with what we get. We can't change who comes to us. Preoperative management is important and has obvious implications for regional perfusion, and for most people in the room, there is probably less control over that than the immediate perioperative management.
Certainly the Philadelphia group has detected profound cerebral desaturation in a diverse group of cardiac neonates preoperatively. We didn't see that here. We observed relatively normal arterial-to-brain saturation differences in these patients preoperatively, indicating adequate cerebrovascular development but the potential for wide ranges of cerebral flow related to differences in preoperative management. So the potential certainly exists.
We have the advantage of extensive monitoring during a very intense period of operative intervention, but, as you pointed out, the horse could leave the barn before we get to the operating room, or, as Dr Wernovsky anticipated, sometime afterward.
Dr Richard A. Jonas (Boston, Mass). I have a question about the positioning of your oximetrics catheter and wonder if it was truly in the jugular bulb. If it was in the superior vena cava, then you were looking at a mix of jugular venous blood and somatic venous blood. And I very much doubt your speculation that the decrease in saturation is not likely to be caused by reduced cerebral oxygen delivery.
You have proposed that there is an increase in cerebrovascular resistance, which presumably reduces cerebral blood flow and cerebral oxygen delivery.
In fact, what I would suggest is that it is very likely that cerebral blood flow, and therefore oxygen delivery, is decreased related to the position of the shunt. I believe you have created a steal from the cerebral circulation. I am going to be fascinated to see you repeat the study, which I'm sure you will, when you perform the right ventricle to pulmonary artery shunt. I believe this will show quite a different result relative to what you presented today.
I think cerebral blood flow might also be decreased because of increased cerebrovascular resistance related to edema, secondary to your use of regional perfusion.
And incidentally, if I could make a plea, RCP has been the abbreviation for retrograde cerebral perfusion, and we are really going to have to come up a different acronym for RCP, otherwise the literature is going to get very confusing.
In conclusion, until we have some mechanism for monitoring the adequacy of cerebral flow or excessive flow, you run a real risk of causing cerebral edema with regional perfusion. So that might be an additional cause for reduced cerebral blood flow. But I'm interested in the catheter position you used.
Dr Hoffman. The superior vena cava catheters are placed approximately 1 cm above the superior vena cava-right atrial junction, and we attempted to thread this up to the jugular bulb in only 1 patient.
So yes, the superior vena cava saturation is not the same as cerebral NIRS saturation. We do have data relating those two, which will be presented subsequently.
I think your point about the innominate take-off and potential cerebral steal is true, and it will be interesting to compare this cerebral NIRS data with patients who derive pulmonary blood flow from a right ventricular shunt.
The point I was trying to make about oxygen delivery was that whole-body oxygen delivery was not decreased. Therefore I agree completely that this decreased cerebral saturation we observed post-CPB is likely caused by decreased cerebral oxygen delivery related to regional resistance changes.
Dr Ross M. Ungerleider (Portland, Ore). On this basis, have you changed your postoperative strategy at all?
I mean, it seems that the most simple and straightforward thing you could do would be to keep PCO2 higher as you come off bypass, and PCO2 is related to cerebral blood flow. And in the face of the runoffs you are talking about (that you can't really do very much about it), it would seem that it might modify this. Have you tried that?
Dr Hoffman. We have used this device in a number of patients, and the effect of CO2 is immediate and apparent to anybody who bothers to look.
So yes, we have used more hypercapnia, as others have suggested, with the advantage of regional oxygenation data to guide this strategy.
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 R. E. Willoughby, K. S. Tieves, G. M. Hoffman, N. S. Ghanayem, C. M. Amlie-Lefond, M. J. Schwabe, M. J. Chusid, and C. E. Rupprecht Survival after Treatment of Rabies with Induction of Coma N. Engl. J. Med., June 16, 2005; 352(24): 2508 - 2514. [Abstract] [Full Text] [PDF]
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D. B. Andropoulos, S. A. Stayer, L. K. Diaz, and C. Ramamoorthy Neurological Monitoring for Congenital Heart Surgery Anesth. Analg., November 1, 2004; 99(5): 1365 - 1375. [Abstract] [Full Text] [PDF]
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