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J Thorac Cardiovasc Surg 1994;108:446-454
© 1994 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Sendai, Japan
From the Department of Thoracic and Cardiovascular Surgery, Tohoku University School of Medicine, Sendai, Japan.
Presented in part at the Thirty-ninth Congress of the European Society for Cardiovascular Surgery, Budapest, Hungary, Sept. 9-12, 1990.
Received for publication July 30, 1993. Accepted for publication Feb. 22, 1994. Address for reprints: Mitsuaki Sadahiro, MD, Department of Thoracic and Cardiovascular Surgery, Tohoku University School of Medicine, 1-1 Seiryocho, Aobaku, Sendai, 980, Japan.
Abstract
Twenty-four adult mongrel dogs were divided into four equal groups according to the following method of cardiopulmonary bypass: normothermic continuous (so-called nonpulsatile) perfusion, normothermic pulsatile perfusion, hypothermic continuous perfusion, and hypothermic pulsatile perfusion. Cerebral blood flow was determined by measuring the volume of sagittal sinus venous blood outflow with a transit-time ultrasonic flowmeter. Cardiopulmonary bypass was initiated at a flow rate of 80 ml/kg per minute. Cerebral temperature was maintained at 37º C per minute. Cerebral temperature was maintained at 37º C in the normothermic groups at 25º C in the hypothermic groups. Aterial pH and carbon dioxide were maintained within the physiologic range by alpha-stat acid-base regulation. Mean cerebral perfusion pressure and blood flow were not affected during the 90 minutes of the bypass. The respective values were 67.1 mm Hg and 37.1 ml/100 gm brain per minute with normothermic continuous perfusion, 72.8 mm Hg and 39.0 ml/100 gm per minute with nonpulsatile perfusion, 98.0 mm Hg and 23.0 ml/100 gm per minute with hypotermic pulsatile perfusion. Pump flow rates were altered from 10 to 120 ml/kg per minute in a stepwise fashion to obtain graded changes of perfusion pressure. Cerebral blood fow, however, was not changed significantly by cerebral perfusion pressure so long as perfusion pressure was greater than 50 mm Hg. Conversely, cerebral blood flow changed proportionally with cerebral perfusion pressure at a pressure less than 50 mm Hg. The correlation between cerebral blood flow and perfusion pressure was described as two separate line determined by linear regression. The slope of regression lines relating cerebral blood flow to perfusion was 0.16 ± 0.08 for cerebral perfusion pressure above 50 mm Hg and 0.68 ± 0.11 below 50 mm Hg in the normothermic continuous person group; 0.14 ± 0.09 and 0.32 ± 0.09 with normothermic pulsatile perfusion; 0.10 ± 0.04 and 0.62 ± 0.18 with hypothermic continuous perfusion; 0.09 ± 0.08 and 0.39 ± 0.04 in the hypothermic pulsatile perfusion group. The slope above 50 mm Hg was significantly smaller and closer to zero in all groups than it was at a perfusion pressure below 50 mm Hg (p < 0.05). The slope and cerebral blood flow for a perfusion pressure above 50 mm Hg was significantly (p < 0.05) smaller and higher, respectively, These data suggest that cerebral autoregulation is intact at cerebral perfusion pressure greater than 50 mm Hg during either normothermic or hypothermic cardiopulmonary bypass, In addition, compared to continuous (nonpulsatile) perfusion, pulsatile bypass generated a higher cerebral blood flow at a cerebral perfusion pressure less than 50 mm Hg. (J THORAC CARDIOVASC SURG 1994;108:446-54)
The relationship between systemic pressure and the autoregulation of cerebral blood flow (CBF) appears to be dependent on metabolism and is determined locally by metabolic demand. CBF under physiologic condition is maintained by autoregulation over a wide range of arterial pressures (60 to 150 mm Hg). 
1,2 Autoregulation is important during cardiopulmonary bypass (CPB) because maintenance of an adequate perfusion pressure may protect the brain from injuries caused by cerebral ischemia or hyperperfusion. Several recent studies reported pressure-flow autoregulation and the cerebrovascular response to arterial carbon dioxide tension during moderately hypothermic CPB (26° to 28° C) and alpha-stat blood gas management (arterial carbon dioxide tension 38 to 42 mm Hg, analyzed at 37° C). 3-6 However, the effect of nonpulsatile CPB on the autoregulatory mechanism and its relationship to cerebral circulation has not been fully elucidated. Some investigators suggest that pulsatility is necessary for the maintenance of vasomotor tone to preserve autoregulation. 7,8 Pulsatile assist devices are used occasionally during cardiac operations, and several advantages of pulsatile compared with nonpulsatile perfusion during CPB have been reported. 9-12 The absence of a consensus as to the specific merits of the various perfusion modalities that are currently available led us to investigate the extent to which autoregulation of CBF occurs during normothermic as well as moderately hypothermic CPB and to determine the effect of pulsatile perfusion on the relationship between CBF and cerebral perfusion pressure (CPP) during CPB.
MATERIALS AND METHODS
Experimental design.
Twenty-four adult mongrel dogs with an average body weight of 16.6 ± 3.8 kg were used. They were divided into the following groups: NC group, normothermic CPB with continuous (nonpulsatile) perfusion (n = 6, brain temperature 37° C); NP group, normothermic CPB with pulsatile perfusion (n = 6, brain temperature 37° C); HC group, hypothermic CPB with continuous (nonpulsatile) perfusion (n = 6, brain temperature 25° C); and HP group, hypothermic CPB with pulsatile perfusion (n = 6, brain temperature 25° C).
Anesthesia was induced with intravenous thiopental sodium (25 mg/kg) and intramuscular atropine sulfate (0.02 mg/kg). After endotracheal intubation, the animals' lungs were ventilated with a volume-constant respirator (model 480-6, Shinano, Tokyo, Japan) adjusted to a tidal volume of 20 ml/kg at a rate of 25 breaths/min. Anesthesia was maintained with 0.5% halothane in 100% oxygen. Transfemoral polyethylene catheters advanced to the level of the aortic arch were placed for hemodynamic monitoring and arterial sampling.
CPB was maintained at a flow rate of 80 ml/kg per minute for 90 minutes in all groups before flow rate was altered for subsequent studies. Brain temperature was kept at 37° C in the normothermic groups (NC, NP). Core cooling to 25° C averaged 30 minutes in the hypothermic groups (HC, HP). A pulsatile assist device was used in the pulsatile perfusion groups (NP, HP) to generate a pulse pressure throughout CPB.
Graded changes in perfusion pressure were obtained by increasing pump flow rate from 80 to 100 to 120 ml/kg per minute and then decreasing it in a stepwise fashion from 80 to 60, 40, 20, and 10 ml/kg per minute. After the preparation had stabilized at each flow rate, mean perfusion pressure and CBF were recorded to document the correlation between CPP and CBF. In addition, arterial and sagittal sinus blood were withdrawn for determination of oxygen content and calculation of cerebral oxygen consumption.
Measurement of CBF.
CBF was determined by measuring the volume of sagittal sinus venous outflow with a transit-time ultrasonic flowmeter (Transonic system T201, Transonic System Inc., Ithaca, N.Y.). The sagittal sinus was exposed about 1 cm anterior to the occipital process by a round midline craniotomy with a diameter of 3 cm. After heparin (3 mg/kg) was administered, an 8F polyethylene tube (outer diameter 2.75 mm) was inserted into the sagittal sinus and the tip of the tube was advanced anterior to the level of the coronal suture. Venous blood flow from the sagittal sinus passed into superior vena cava through the outflow tube, which was inserted from the azygos vein. The ultrasonic transit-time flow probe was placed in the circuit between the sagittal sinus and the superior vena cava. The distal tip of the outflow tube, which drained into the superior vena cava, was placed in a reservoir to maintain a constant sagittal sinus outflow pressure whenever pump flow rate was changed. The reservoir was initially primed with saline solution, and the fluid level was set at the level of the right atrium by returning the collected venous flow to the perfusion circuit via a roller pump. Sagittal sinus outflow pressure was continuously monitored distal to the flow probe and maintained at less than 4 mm Hg.
Thermistors were placed in the esophagus and brain. The brain thermistor was positioned 5 mm deep in the outer cerebral cortex of the mid-central parietal lobe through a burr hole in the skull. Intracranial pressure was measured by an epidural pressure-monitoring balloon catheter that was introduced into the epidural space through the same burr hole that was used for the brain thermistor (Fig. 1).
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CPB.
The heart was approached from a right lateral thoracotomy and CPB was initiated at a flow rate of 80 ml/min per kilogram. The ascending aorta was cannulated (Sarns 5.2 mm cannula, Sarns Inc./3M Health Care, Ann Arbor, Mich.) and venous return was accomplished with bicaval cannulas (20F, 24F) inserted via the right atrium.
The ascending aorta was crossclamped and the left atrium was vented to the extracorporeal circuit. The perfusion system consisted of a conventional roller pump, cardiotomy reservoir, and membrane oxygenator with an internal heat exchanger (HPO-25, Mera, Tokyo, Japan). The reservoir was primed with homologous heparinized blood and lactated Ringer's solution, dextran, sodium bicarbonate, and mannitol. The oxygenator was ventilated with 100% oxygen at a ventilation/perfusion ratio of 1:1 and 0.5% halothane was added.
Carbon dioxide was not added during CPB (nontemperature-corrected arterial carbon dioxide tension of about 40 mm Hg). Arterial blood pH was maintained at approximately 7.4 with sodium bicarbonate. Arterial carbon dioxide tension was kept between 35 and 45 mm Hg (analyzed at 37° C) by adjusting flow rate of the gas mixture. Additional drugs were not used to control perfusion pressure. Hematocrit value during CPB was kept between 20% to 25%.
An assist device (Datascope PAD system 42, Datascope Corp., Montvale, N.J.) was used to generate pulsatile flow throughout the period of CPB in the pulsatile groups (NP, HP). Pulse frequency was set at 80 per minute to maintain a pulse pressure between 25 and 30 mm Hg at a flow rate of 80 ml/kg per minute.
The brain was weighed at completion of the experiment.
Data analysis.
CBF was measured and converted to milliliters per 100 gm of brain per minute according to the method of Michenfelder, Messik, and Theye. 13 CPP was taken as the difference between perfusion pressure and intracranial pressure. Cerebral vascular resistance was calculated as the ratio between CBF and CPP.
Blood samples were drawn from the arterial and venous lines of the extracorporeal circuit and from the sagittal sinus drainage tube. The samples were analyzed at 37° C for pH, oxygen tension, and carbon dioxide tension with an IL gas analyzer (model 813, Instrumentation Laboratory, Inc., Lexington, Mass.).
Oxygen content and cerebral oxygen consumption were calculated by the following formulas:
CO2 (vol%) = (1.34 · Hb · %O2sat.)/100 + 0.003 · PO2
Cerebral oxygen consumption (ml/100 gm/min) =
(CaO2 - CSO2)/100 · CBF (ml/100 gm/min)
where CO2 is oxygen content; Hb is hemoglobin; CaO2 is arterial oxygen content, and CSO2 is sagittal sinus blood oxygen content.
The relationship between CBF and CPP was analyzed by least-squares linear regression. The slope of the regression line was used to determine the autoregulatory response and to compare the correlation of CBF to CPP between experimental groups.
Statistics.
All values are expressed as a mean ± 1 standard deviation. Differences in CBF at different flow rates were calculated by analysis of variance for repeated measures and the Scheffe test. Systemic variables, cerebral values, and the slope of regression coefficients were compared between normothermic and hypothermic conditions or between pulsatile and nonpulsatile conditions by means of analysis of variance. A p value of less than 0.05 was considered to be statistically significant.
This study was approved as a class B experiment by the Committee of Animal Experimentation, Tohoku University School of Medicine, in reference to "The Classification of Biomedical Experiments Based on Ethical Concerns for Non-human Species," Laboratory Animal Science, Special Issue, 1987:14-6.
RESULTS
The average weight of the brain and brain/body weight ratio was 81 ± 11 gm and 0.55% ± 0.09%, respectively.
Table I shows CBF, cerebral vascular resistance, cerebral oxygen consumption, and systemic variables in all groups while perfusion flow was kept at a constant rate of 80 ml/kg per minute.
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Relationship between CBF and perfusion flow rate.
CBF did not change significantly over pump flow rates ranging from 40 to 120 ml/kg per minute, but CBF decreased significantly when flow rate was less than 20 ml/kg per minute during both normothermic and hypothermic CPB with or without pulsatile perfusion (Fig. 2).
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Neither slope of the regression coefficient nor CBF and cerebral vascular resistance at a CPP between 70 and 80 mm Hg was significantly different between continuous and pulsatile perfusion groups during normothermic and hypothermic CPB (NC versus NP; HC versus HP) (Table II).
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Table III).
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The measurement of sagittal sinus venous outflow allows the continuous monitoring of hemodynamic changes in the brain and is extremely useful for the detection of cerebral autoregulatory response. However, this method cannot completely distinguish between intracranial and extracranial venous communications. 3,14 Michenfelder, Messik, and Theye 13 assumed that areas of the brain that are drained by the sagittal sinus varied little between individual preparations and averaged 43% of the total brain weight if a sagittal sinus cannulation drainage technique was used to assess flow.
CBF and cerebral oxygen consumption of this study during normothermic CPB at a perfusion flow rate of 80 ml/kg per minute were within the ranges reported by other investigators. 3,6 In addition, both CBF and cerebral oxygen consumption decreased proportionally during hypothermic (25° C) CPB, suggesting the presence of a flow–metabolic coupling in the brain. This is consistent with results reported by Michenfelder and Theye 15 that cerebral oxygen consumption decreased by an average of approximately 55% at a temperature of 10° C.
Autoregulation of CBF refers to alternations in cerebral vascular resistance that occur so that CBF does not change whether CPP increases or decreases. It is generally considered that vasomotor tone is responsible for CBF autoregulation and is based in part on adenosine release, 16 as well as myogenic reflexes. 17 The presence of autoregulatory response during CPB has been of interest because of nonphysiologic conditions imposed by CBF such as nonpulsatile flow, hypothermia, and hemodilution. 7,8 Several studies indicate that cerebral pressure-flow autoregulation is preserved under most bypass conditions except for those in which pH-stat blood gas management, 18 deep hypothermia (<22° C), and circulatory arrest 19 are used.
CBF in our study did not change significantly between flow rates of 40 and 120 ml/kg per minute. The autoregulatory mechanism appeared to be intact until perfusion pressure decreased to about 50 mm Hg under normothermic and moderately hypothermic conditions regardless of continuous or pulsatile perfusion. The presence of an autoregulatory response was based on the following: (1) continuous measurement of CBF and CPP demonstrated a rapid recovery of CBF to its prior level within 30 to 60 seconds after an initial change in CBF. This occurred concomitantly with an alternation of CPP, which suggests a myogenic response; (2) CBF was not significantly changed when CPP was greater than 50 mm Hg; (3) CBF-CPP plots were divided into two parts and were analyzed by means of individual fitting lines by least squares linear regression. The slope of the representative line for a CPP above 50 mm Hg was significantly different from the slope of the steeper line for a CPP below 50 mm Hg.
Halothane is a potent vasodilator that increases CBF in normal and in ischemic brain tissue. However, Morita and associates 20 demonstrated that autoregulation was intact during 0.5% halothane anesthesia, an observation that is also consistent with our results.
We applied alpha-stat acid-base regulation during hypothermic CPB. Two different strategies, alpha-stat (nontemperature-corrected arterial carbon dioxide tension of about 40 mm Hg) and pH-stat management (temperature-corrected arterial carbon dioxide tension at about 40 mm Hg at the actual temperature) have been used. 21 pH-stat management may increase CBF because arterial carbon dioxide tension is higher than it is when alpha-stat management is used. However, this is associated with vasodilatation, which may compromise cerebral autoregulation. Johnsson, 6 Murkin, 18 and their associates have reported that alpha-stat blood gas management prevents cerebral hyperemia and preserves a physiologic coupling of CBF and cerebral metabolic rate of oxygen and an intact autoregulatory mechanism. These findings are consistent with results from the present study.
The benefits of pulsatile flow are widely known and are prominent in the CPB literature. Pulsatile perfusion better preserved renal function, 22 maintained outer cortical flow, 23 and prevented ischemic changes 24 in kidneys. Pulsatile perfusion improved subendocardial coronary flow and myocardial metabolism in the fibrillating heart during CPB. 25 Also, Dernevik, Arvidson, and William-Olsson 10 reported that CBF to the gray matter of the brain during normothermic CPB was significantly higher with pulsatile perfusion.
Pulsatile perfusion in this study of the CBF-CPP relationship in the presence of an autoregulatory response was not significantly different from nonpulsatile perfusion when CPP was greater than 50 mm Hg. Conversely, when CPP was out of the autoregulatory range (<50 mm Hg), pulsatile flow resulted in a significant improvement in the correlation between CPP and CBF. Pulsatile perfusion under normothermic or moderate hypothermic conditions resulted in a consistently higher CBF at any CPP and was also associated with a smaller decrease in CBF as CPP decreased.
These results confirm the advantageous effects of pulsatile perfusion at an extremely low flow rate as reported by Watanabe and associates 9 and appears to support the efficacy of pulsatile perfusion as a modality for achieving a significantly higher recovery ratio after profound hypothermic circulatory arrest 11 or acute local ischemia. 12
Pulsatile flow has been said to preserve the microcirculation, 26,27 improve tissue metabolism and blood flow, 26 and inhibit sludging and edema formation. 27 The mechanism by which pulsatile perfusion improves the microcirculation is not clear. Shepard, Simpson, and Sharp 28 determined that the energy needed to deliver pulsatile flow is 2.3 times that needed to produce nonpulsatile flow at the same mean perfusion pressure. It is believed that this extrahydraulic energy of each systolic thrust is distributed into the microcirculation and this helps to maintain peripheral perfusion by keeping capillary beds patent and simultaneously encourage lymphatic flow. 29 This study indicates that pulsatile perfusion was more effective at a lower perfusion pressure, below the lower limit of autoregulation, in which the cerebral vasculature was maximally dilated and a myogenic response was lost. We speculate that pulsatile energy is more hemodynamically efficient in a situation in which the cerebral vasculatures is dilated and myotonic vascular response is absent and in which the forward thrust of the mean perfusion pressure is not high enough to adequately maintain the peripheral circulation.
CONCLUSION
References
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