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Ann Thorac Surg 1995;60:165-169
© 1995 The Society of Thoracic Surgeons

Cerebral Blood Flow Is Determined by Arterial Pressure and Not Cardiopulmonary Bypass Flow Rate

Departments of Anesthesiology and Surgery, College of Physicians and Surgeons, Columbia University, and Anesthesiology and Surgery Services, Presbyterian Hospital in the City of New York, New York, New York

Accepted for publication March 22, 1995.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Background. During cardiopulmonary bypass, global hypoperfusion of the brain has been shown to result in ischemic insult and subsequent neurologic injury. Furthermore, outcome after focal cerebral ischemia depends on collateral circulation, which is determined by the parameters of global perfusion. We therefore measured cerebral blood flow during independent manipulations of arterial blood pressure and pump flow rate to determine which of these hemodynamic parameters regulates cerebral perfusion during cardiopulmonary bypass.

Methods. Seven anesthesized baboons were placed on cardiopulmonary bypass and cooled to 28°C. Pump flow rate and arterial blood pressure were altered in varied sequence to each of four conditions: (1) full flow (2.23 ± 0.06 L • min^-1 • m^-2, mean ± standard deviation) at high pressure (61 ± 2 mm Hg), (2) full flow (2.23 ± 0.06 L • min^-1 • m^-2) at low pressure (24 ± 3 mm Hg), (3) low flow (0.75 L • min^-1 • m^-2) at high pressure (62 ± 2 mm Hg), and (4) low flow (0.75 L • min^-1 • m^-2 at low pressure (23 ± 3 mm Hg). During each of these hemodynamic conditions cerebral blood flow was measured by washout of intracarotid xenon¹³³.

Results. Cerebral blood flow was greater at high blood pressure than at low pressure during cardiopulmonary bypass both at low flow (34 ± 8.3 versus 14.1 ± 3.7 mL • min^-1 • 100 g^-1) and full flow (27.6 ± 9.9 versus 16.8 ± 3.7 mL • min^-1 • 100 g^-1) (p < 0.01). At comparable mean arterial blood pressures alteration of pump flow rate produced no changes in cerebral blood flow.

Conclusions. These results indicate that cerebral blood flow during moderately hypothermic cardiopulmonary bypass is regulated by arterial blood pressure and not pump flow rate.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
See also page 169.

Neurologic injury after cardiopulmonary bypass (CPB) resulting in cognitive dysfunction, stroke, or death is an important complication of cardiothoracic operations [1, 2]. Inadequate global perfusion of the brain during bypass has been implicated as an important factor in the etiology of this problem [3–5]. Furthermore, outcome from focal ischemia due to embolization or atherosclerotic cerebrovascular disease depends on the adequacy of collateral circulation, which is determined by the parameters of global perfusion. During CPB clinical manipulations of pump flow rate and systemic arterial blood pressure are employed routinely to preserve cerebral blood flow (CBF), because it is well established that low pump flow concomitant with low arterial pressure results in decreased cerebral perfusion. However, the independent effects of arterial pressure and pump flow rate on CBF during CPB are not understood clearly. Clinical studies have shown that moderate changes in pump flow rate or arterial pressure result in either moderate or no changes in CBF [6–9]. Previous studies of CPB in laboratory animals have not included independent manipulation of pressure and pump flow rate. Therefore, in a primate model we investigated the independent effects of arterial pressure and pump flow rate on CBF during CPB, both within and below the hemodynamic limits of cerebral autoregulation.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
After approval by the Institutional Animal Care and Use Committee of Columbia University, 7 adult baboons (5 to 15 kg) of either sex were studied. 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 Institutes of Health (NIH publication 85-23, revised 1985).

Anesthesia was induced with ketamine (10 mg/kg) administered intramuscularly. Thereafter the trachea was intubated and ventilation controlled with oxygen and isoflurane, 0.25% end-tidal concentration. Femoral venous and arterial catheters were inserted. Fentanyl (10 µg/kg) was administered as an intravenous bolus, followed by a continuous infusion of 2 µg • kg^-1 • h^-1. Additional boluses of fentanyl were administered when indicated. Midazolam was administered intravenously at a continuous rate of 0.03 mg • kg^-1 • h^-1. Vecuronium was administered intravenously for neuromuscular blockade. Electrocardiogram, arterial blood pressure, and tympanic, esophageal, and rectal temperature were recorded continuously. End-tidal carbon dioxide tension (pCO₂) and isoflurane concentration were measured by infrared analysis (Datex CapnoMac, Helsinki, Finland). An 18-gauge needle was inserted into a lumbar intervertebral space until cerebrospinal fluid was aspirated, after which a thin Teflon catheter was threaded into the subarachnoid space.

After median sternotomy, the right common carotid artery and its internal and external branches were exposed surgically. A 19-mm, 24-gauge Teflon catheter (Angiocath; Becton Dickinson, Sandy, UT) was inserted into the common carotid artery, and pressures were transduced. The ipsilateral external branches of the carotid artery were occluded temporarily during measurement of CBF. A thin catheter was inserted into the right jugular vein and advanced to the jugular bulb.

The superior vena cava, inferior vena cava, and aorta were cannulated, and cardiopulmonary bypass was initiated. The bypass circuit consisted of a Medtronic-Minimax oxygenator (Medtronic, Minneapolis, MN), a BP-50 Centrifugal Bio-Pump (Medtronic), and -inch tubing. The system was primed with 175 mL of Normosol-R and 175 mL of 6% Hespan (DuPont, Wilmington, DE). All surgical blood loss was collected and processed with a Cell Saver 1 (Haemonetics, Braintree, MA) and then added to the bypass circuit. Heparin was administered to maintain activated clotting time greater than 480 seconds.

Nonpulsatile cardiopulmonary bypass was initiated at a flow rate of 2.25 L • min^-1 • m^-2, and baboons were then cooled until tympanic membrane temperature decreased to 28°C. Tympanic membrane temperature has been shown to approximate brain temperature reliably [10]. At that point, CPB pump flow rate and arterial blood pressure were altered in varied sequence to each of four conditions: (1) full flow (2.25 L • min^-1 • m^-2) and mean arterial pressure of 60 mm Hg, (2) full flow (2.25 L • min^-1 • m^-2) at arterial pressure of 20 mm Hg, (3) low flow (0.75 L • min^-1 • m^-2) at arterial pressure of 60 mm Hg, and (4) low flow at arterial blood pressure of 20 mm Hg. Arterial pressure was measured as mean pressure transduced from the common carotid artery catheter. Reductions in arterial blood pressure were achieved by subarachnoid injection of lidocaine 2% solution. If a dose sufficient to produce spinal block did not result in the target blood pressure, nitroprusside was administered as an intravenous infusion. Elevations of arterial blood pressure were achieved by variable tension on a snare encircling the descending aorta. Changes in bypass flow rate were made by varying the speed of the centrifugal pump. Arterial blood gases were measured at 37°C, independent of body temperature (alpha-stat blood gas management).

Cerebral blood flow was measured before CPB and during each of the four hemodynamic conditions during CPB. For each determination, 700 µCi of xenon¹³³ in 0.8 mL of saline solution was injected into the common carotid artery and flushed with 2 mL of normal saline solution [11]. Single collimators directed at the superior parietal cortex detected radioactive washout with a Novo Cerebrograph 10a (Novo Diagnostics Systems, Bagsvaard, Denmark). Additional detectors were placed over the aortic cannula to confirm the absence of significant recirculation of isotope. Clearance was recorded for at least 12 minutes, and CBF was determined by the initial slope, as described by Olesen and associates [12], fitting a monoexponential decay curve to activity recorded from the scalp for 60 seconds beginning 3 seconds after attaining its peak value [13]. Spahn and colleagues [14] have validated the technique of washout of arterial ¹³³Xe during CPB by comparison with the method of Kety-Schmidt. Values for the blood-tissue partition coefficient for ¹³³Xe were corrected for hematocrit and temperature [15]. Arterial and jugular venous samples were drawn and analyzed at 37°C in a blood-gas analyzer and CO-Oximeter (Instrumentation Laboratory, Lexington, MA). Arterial and venous oxygen content were calculated by standard formulas [16]. Cerebral metabolic rate for O₂ was calculated as the product of CBF and the arterial-venous oxygen content difference. Values for cerebral blood flow, arterial venous O₂ content difference, cerebral oxygen metabolic rate, arterial blood pressure, hematocrit, arterial carbon dioxide tension and temperature were compared by repeated measures analysis of variance. Multiple comparisons were made with Fisher's protected least significant difference testing. A value of p less than 0.05 was considered significant.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
The predetermined hemodynamic conditions were achieved in all baboons. In 3 baboons nitroprusside was administered after spinal block to reduce mean arterial blood pressure to less than 30 mm Hg during full-flow bypass. In 1 animal the full-flow pump rate was set at 2.1 L • min^-1 • m^-2, which was the maximum rate achievable without volume loading that would have resulted in hemodilution compared with previous bypass conditions.

Temperature, arterial pCO₂, arterial oxygen tension, pH, and hematocrit were similar for all four hemodynamic conditions during CPB (Table 1). Cerebral blood flow was greater at high blood pressure during both low-flow and full-flow CPB when compared with low blood pressure at low-flow or full-flow CPB (34.0 ± 8.3 and 27.6 ± 9.9 versus 14.1 ± 3.7 and 16.8 ± 3.7 mL • min^-1 • 100 g^-1, respectively; p < 0.01) (Fig 1). Changes in pump flow rate alone without changes in mean arterial blood pressure resulted in no change in CBF. Cerebral arterial-venous oxygen content differences and cerebral metabolic rates for oxygen were similar for all four hemodynamic conditions of CPB.

View larger version (20K): [in this window] [in a new window]   Fig 1. . Cerebral blood flow at low and high blood pressure during low-flow (open bars) and full-flow (solid bars) cardiopulmonary bypass. (*Significantly different than at low blood pressure, p < 0.01.)

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Our results indicate that arterial blood pressure and not pump flow rate determines CBF during hypothermic CPB. Cerebral blood flow at higher pressure was greater than CBF at the lower pressure, regardless of pump flow rate. Furthermore, when mean arterial pressure was maintained constant, changes in pump flow rate did not alter CBF. The hypothesis that CBF is not determined by CPB pump flow rate was supported by measurements made both within and beyond the presumed range of pressure autoregulation.

Previous studies of the determinants of CBF during CPB have yielded conflicting results. In a clinical study of 67 patients undergoing coronary bypass procedures, Govier and associates [17] measured CBF by washout of arterial ¹³³Xe. Cerebral blood flow did not correlate with mean arterial blood pressure, which ranged from 30 to 110 mm Hg. Nor did CBF correlate with bypass flow rate, which varied from 1.0 to 2.2 L • min^-1 • m^-2. In contrast, Soma and associates [18] studied 21 adult patients undergoing cardiac operations and reported that cerebral perfusion was directly dependent on pump flow rate. In that study, CPB pump flow rate was varied randomly to 70, 60, 50, and 40 mL • kg^-1 • min^-1. As a result, CBF values, measured by a modified Kety-Schmidt method employing argon, declined from 43 to 35, 33, and 25 mL • min^-1 • 100 g^-1, respectively. Although blood pressures measured at each of these pump flow rates were not significantly different, blood pressures were not controlled at constant values.

Van der Linden and colleagues [19] also supported the conclusion that pump flow rate and not perfusion pressure determines cerebral blood flow. They reported that middle cerebral artery blood flow velocity, measured by transcranial Doppler echography, in children during deep hypothermic low-flow CPB correlated with pump flow rate (r = 0.73) but not cerebral perfusion pressure (r = 0.14).

In another clinical study, Murkin and co-workers [20] measured CBF by ¹³³Xe clearance in 38 cardiac surgery patients. During CPB, in which total flow rate was maintained between 2.0 and 2.5 L • min^-1 • m^-2, mean cerebral perfusion pressures varying between 20 and 100 mm Hg did not correlate with CBF in the patient group for whom arterial pCO₂ was controlled by alpha-stat management (temperature-corrected pCO₂ kept at 27 mm Hg). However, in the pH-stat–managed patients (temperature-corrected pCO₂ kept at 40 mm Hg) CBF was correlated with cerebral perfusion pressures between 15 and 95 mm Hg. Although Murkin and co-workers did maintain pump flow rate at values between 2.0 and 2.5 L • min^-1 • m^-2, they did not control or independently manipulate arterial blood pressure as part of the study design.

In contrast, Rogers and colleagues [6] independently manipulated blood pressure by infusing phenylephrine in patients during CPB to elevate blood pressure deliberately while maintaining a constant pump flow rate of 2.0 L • min^-1 • m^-2. In patients for whom arterial pCO₂ was alpha-stat managed (temperature-uncorrected pCO₂ = 40 mm Hg) deliberate elevation of mean arterial pressure from 56 ± 7 to 84 ± 8 mm Hg did not change CBF, as measured by ¹³³Xe clearance. In the pH-stat–managed group (temperature-uncorrected pCO₂ = 57 mm Hg), raising mean arterial blood pressure from 53 ± 8 to 77 ± 9 mm Hg increased CBF by 41%. In a subsequent study of parallel design using sodium nitroprusside to reduce arterial blood pressure deliberately, Rogers and colleagues [7] reported that a reduction in mean arterial pressure from 75 ± 5 to 54 ± 5 mm Hg did not reduce CBF in patients for whom pCO₂ was alpha-stat managed (temperature-uncorrected pCO₂ = 42 mm Hg). However, in pH-stat–managed patients (temperature-uncorrected pCO₂ = 60 mm Hg), CBF decreased when mean arterial pressure was reduced deliberately from 76 ± 9 to 50 ± 6 mm Hg. In both studies pump flow rate was held constant while blood pressure was altered independently. In a subsequent clinical study, Rogers and colleagues [8] randomly varied pump flow rate to 1.75 and 2.25 L • min^-1 • m^-2 and noted no associated spontaneous changes in systemic blood pressure. Cerebral blood flows at these two pump flow rates were similar. In all the work of this group these deliberate changes in blood pressure and pump flow were relatively moderate and did not transcend the limits of cerebral autoregulation where risk of neurologic injury is presumed greatest.

Most recently, in a large clinical study, moderate increases or decreases in mean arterial blood pressure (between 51 and 75 mm Hg) during alpha-stat–managed CPB were shown to result in small proportional changes in CBF (0.86 mL • min^-1 • 100 g^-1 for every 10 mm Hg change in pressure) when bypass pump flow rate was kept constant [9]. The much greater proportional changes in CBF with changes in blood pressure reported in our study indicates that autoregulation of cerebral blood flow is impaired substantially at blood pressures near 20 mm Hg.

In multiple studies involving animal models of CPB, reductions in pump flow rate producing decreases in systemic arterial blood pressure have resulted in decreases in cerebral perfusion. Fox and associates [21] varied CPB pump flow rate to four different values between 0.25 and 1.75 L • min^-1 • m^-2 in cynomolgus monkeys and measured CBF by injection of radioactive microspheres. As pump flow declined from 1.5 to 1.0 to 0.5 L • min^-1 • m^-2 mean arterial pressure declined from 32.8 to 24.5 to 16.3 mm Hg, and CBF declined from 45 to 41 to 23 mL • min^-1 • 100 g^-1, respectively. Similarly, Tanaka and colleagues [22], in a dog model of CPB where CBF was determined by venous outflow from the isolated sagittal sinus, sequentially lowered pump flow rate to obtain perfusion pressures ranging from 90 to 20 mm Hg. When pump flow rate declined so as to produce perfusion pressures less than 40 mm Hg, decreases in arterial pressure produced marked decreases in CBF. In rabbits, Hindman and co-workers [23] varied CPB pump flow rate to 50, 70, and 100 mL • kg^-1 • min^-1. Each decrease in pump flow rate produced a decrease in mean arterial pressure resulting in decreased CBF, as measured by microspheres.

Our study design is unusual for its independent manipulation, over wide ranges, of bypass pump flow and systemic arterial pressure. Spinal blockade and variable constriction of the descending aorta were employed to limit pharmacologic agents that might affect cerebral vascular tone directly. Although sodium nitroprusside, employed in 3 animals, may have caused some dilation of cerebral resistance vessels [24], CBF values in these animals were no different than in animals whose blood pressure was decreased with spinal blockade alone. Furthermore, CBF during full flow at low pressure, when 3 animals received nitroprusside, was not higher than CBF during low flow at low pressure when no nitroprusside was administered. Although elevation of blood pressure by constriction of the aorta may divert blood flow preferentially to the brain, this is exactly what is accomplished with any alternate technique (mechanical, pharmacologic, or physiologic) that increases systemic vascular resistance. Aortic constriction raises arterial pressure without a direct effect on cerebral vascular tone. Phenylephrine, for example, would increase systemic vascular resistance, divert blood preferentially to the brain, and perhaps alter cerebrovascular tone directly.

In conclusion, cerebral blood flow during hypothermic CPB is regulated by arterial blood pressure and not pump flow rate. In clinical practice, management of CPB should be directed at maintaining arterial blood pressure at both high and low pump flow rates to preserve perfusion of the brain.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Supported in part by National Institutes of Health grant RO1-NS 27713.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Presented in part at the Ninth European Congress of Anaesthesiology, Jerusalem, Israel, October 2–7, 1994.

Address reprint requests to Dr Schwartz, Neuroanesthesia, Columbia University, Rm 901, 161 Fort Washington Ave, New York, NY 10032.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

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