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Ann Thorac Surg 1998;66:S20-S24
© 1998 The Society of Thoracic Surgeons

Central nervous system effects of cardiopulmonary bypass

Kenneth M. Taylor, MDa

a Department of Surgery, National Heart and Lung Institute, Hammersmith Hospital, London, England, United Kingdom

Address reprint requests to Dr Taylor, Department of Surgery, National Heart & Lung Institute, Hammersmith Hospital, B Block, 2nd Floor, Du Cane Rd, London, England

Presented at "Risk Management in CABG: Significant Surgical Considerations," New Orleans, LA, Jan 24, 1998.


   Abstract
Top
 Abstract
Introduction
 Incidence and severity
 High-risk patients
 Mechanisms of cerebral injury
 Summary
 References
 
Background. The spectrum of approaches to the issue of brain injury in cardiac surgical practice ranges from refusal to acknowledge that the problem exists to an overemphasis on cerebral risks that can unduly frighten patients. An appropriate approach to therapeutic and preventive strategies requires a fitting sense of proportion and an understanding of the mechanisms of cerebral injury.

Methods. This article reviews the incidence and severity of cerebral injury during cardiopulmonary bypass, the identification of high-risk patients, and the mechanisms of injury, including hypoperfusion, microemboli, and inflammatory response. It discusses the influences of alpha-stat and pH-stat strategies on cerebral blood flow during cardiopulmonary bypass; the use of retinal angiography to image the retinal circulation, thus providing a window on the cerebral microcirculation during bypass; magnetic resonance imaging evidence of an inflammatory response in the brain during bypass; and current efforts to gain better understanding of the molecular mechanisms involved in the inflammatory response.

Results. The current incidence of stroke during cardiopulmonary bypass is somewhat lower than in the 1980s but still remains a significant problem. Levels of cognitive impairment also are unacceptably high. Recognized predictors enable us to identify patients at particularly high risk of stroke. Hypertensive patients are particularly susceptible to ischemic injury during bypass and should be perfused at mean perfusion pressures higher than those for normotensive patients. Under conditions of hypothermia, a pH-stat strategy causes loss of cerebral blood flow autoregulation, and the cerebral blood flow becomes pressure-passive. With both the pH-stat and alpha-stat strategies, cooling of the patient greatly increases the flow to metabolism ratio of the cerebral blood flow; however, this luxury perfusion brings to the brain not just an excess supply of oxygen but also an increased quantity of microemboli. Current investigative efforts are focused on the endothelial cell–leukocyte adhesion cascade, attempting to characterize ß2 and ß1 adhesion molecule expression in patients undergoing cardiac surgery. Hammersmith Hospital is about to complete a study of the effects of high-dose aprotinin on the inflammatory response pattern and on cerebral infarction.

Conclusions. Further progress in the development of therapeutic and preventive strategies with respect to cerebral injury during cardiac bypass depends on an increase in the understanding of the mechanisms involved. Current strategies should include optimizing cerebral perfusion and minimizing macroembolic and microembolic damage. The possibility of modifying the systemic inflammatory response is the most interesting challenge of the next few years.


   Introduction
Top
 Abstract
 Introduction
Incidence and severity
 High-risk patients
 Mechanisms of cerebral injury
 Summary
 References
 
My approach to the challenge posed by brain damage during cardiopulmonary bypass (CPB) is based on four principles: (1) maintain a sense of proportion; (2) identify, when possible, patients who are at high risk of experiencing cerebral dysfunction during the operation; (3) use therapeutic and preventive strategies that are based on our understanding of the mechanisms of cerebral injury; and (4) assess new developments critically.

The spectrum of approaches to the issue of brain injury in cardiac surgical practice includes, at one end, those who would emulate Admiral Horatio Nelson, who at the Battle of Copenhagen held his telescope to his blind eye because he did not wish to receive an order that he did not want to follow. This ostrichlike approach involves burying one’s head in the sand and refusing to acknowledge existence of a problem. I think we can all agree that these days this approach is unacceptable. But it is possible to go to the other end of the spectrum and become so obsessed with the cerebral issues related to cardiac surgical procedures that you forget that for the vast majority of patients the operation is required to correct potentially life-threatening cardiac anomalies. With too much emphasis on the cerebral risks associated with cardiac operation, patients can be unduly frightened and may put off consenting to the operation. Clearly, the need is to maintain a sense of proportion.


   Incidence and severity
Top
 Abstract
 Introduction
 Incidence and severity
High-risk patients
 Mechanisms of cerebral injury
 Summary
 References
 
Maintaining an appropriate sense of proportion requires knowledge of both the incidence and severity of cerebral injury during CPB. Severity can range from a major stroke, which can be an absolutely disastrous result of otherwise successful cardiac operations, to cognitive defect, or a disturbance in neuropsychologic function—the significance of which many of us have some difficulty understanding.

In two large studies of cerebral injury in cardiac surgical patients done in the 1980s, Shaw and associates [1] found an incidence of stroke of 4.8% and Breuer and coworkers [2] found an incidence of 5.2%. In comparison, in three studies reported in 1997, Borger and colleagues [3] found an incidence of 1.5% in patients having coronary artery bypass graft (CABG) operations; Ahlgren and Aren [4] found an incidence of 2.5% among patients having CABG procedures and 3.0% among patients undergoing mixed surgical procedures; and Goldsborough and coworkers [5] found an incidence of 3.2% in patients having CABG operations and 3.1% among patients undergoing mixed surgical procedures. The incidence of stroke is somewhat lower now than it was more than a decade ago, but it is still far from a point at which it can be regarded as an insignificant problem in cardiac surgical practice.

Consensus conferences have been held to assess how cognitive or functional deficit in the brain can best be assessed. It has been shown that computerized neuropsychologic testing can provide an objective and fairly comprehensive assessment of intellectual function. Studies of cognitive testing have shown cognitive impairment to be a consequence of cardiac operations in a high proportion of patients. In a typical study reported by Smith [6], about 60% of patients undergoing CABG operations demonstrated significant impairment of neuropsychologic function at 8 days after the operation. The incidence of impairment fell to about 25% to 30% at 8 weeks, and remained at only slightly lower levels at 1 year. Such levels are unacceptably high in terms of the continual striving to refine our techniques.


   High-risk patients
Top
 Abstract
 Introduction
 Incidence and severity
 High-risk patients
Mechanisms of cerebral injury
 Summary
 References
 
Identifying high-risk patients is important, and the five criteria predictive of stroke risk in cardiac surgery patients identified at The Johns Hopkins Hospital have been helpful in this regard. These criteria are age older than 70 years, hypertension, diabetes, history of previous stroke, and asymptomatic carotid bruit [5]. Two 1997 assessments also found age, diabetes, and previous stroke to be predictors of risk, but interestingly, not hypertension [3, 4]. These predictors enable us to identify patients at particularly high risk and then, hopefully, to apply methods that may reduce or even prevent cerebral injury.


   Mechanisms of cerebral injury
Top
 Abstract
 Introduction
 Incidence and severity
 High-risk patients
 Mechanisms of cerebral injury
Summary
 References
 
Hypoperfusion
As noted above, I am convinced that progress in our approach to the problem of cerebral injury in cardiac surgical procedures requires that therapy and prevention strategies be directly related to the mechanisms of injury. The first culprit that comes to mind is hypoperfusion. Three questions must be addressed: Is cerebral blood flow altered during CPB? Is any reduction in cerebral blood flow that occurs sufficient to cause ischemic injury? Are there subgroups of patients with increased susceptibility to ischemic injury?

We know that in CPB we conventionally use blood flow rates lower than the normal physiologic flow of 3 to 3.2 L · min-1 · m-2. At normothermia, the blood flow rate is reduced to 2.2 to 2.4 L · min-1 · m-2. This may be further reduced to 1.6 L · min-1 · m-2 at 28°C and 1.2 L · min-1 · m-2 at 20°C. We also know that the blood supply to the brain is an autoregulated circulation, with cerebral blood flow maintained on a homeostatic plateau across a wide range of systemic arterial blood pressure ranging from about 50 to 120 mm Hg. Although homeostatic mechanisms provide this built-in protection against reduction in cerebral blood flow across this wide plateau, at either end of the plateau the cerebral blood flow becomes pressure-passive.

Normal cerebral blood flow is about 40 to 60 mL · 100 g-1 · min-1. Studies that have measured cerebral blood flow during CPB have shown it to range between 20 and 60 mL · 100 g-1 · min-1. The cerebral blood flow is influenced by the anesthetic technique, measurement method, temperature, and most important, by the arterial PCO2. Those studies that have followed up patients into the postbypass period have shown a virtual return of cerebral blood flow to normal prebypass levels.

Some years ago, Astrup and associates [7] showed that cerebral blood flow has to be reduced to less than 10 mL · 100 g-1 · min-1 before ischemic cell death occurs. This ischemic threshold in normothermia is far less than the level of cerebral blood flow during CPB recorded by most studies, and clearly, hypothermia offers additional protection. So in fact the brain is relatively resistant to reduced global perfusion, rather than being particularly susceptible, as many of us once believed. Nevertheless, we cannot be complacent about the issue of the adequacy of blood flow delivery during CPB. There are situations in which the brain does become compromised. Some areas of the brain are more susceptible to reduced global perfusion than others, representing boundary zones or watershed areas; this is particularly true of the occipitoparietal region of the brain.

Hypertensive patients are particularly susceptible to ischemic injury because although the cerebral blood flow autoregulatory curve is preserved in these patients, it is shifted to the right (Fig 1) [8]. Therefore, the normal homeostatic plateau that we comfortably maintain for normotensive patients must be reinterpreted for hypertensive patients, who should be perfused at higher mean perfusion pressures.



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  		Fig 1. Shift to the right of the cerebral blood flow autoregulatory curve in hypertensive patients. (Reprinted from [8] by permission of Edward Arnold Hodder & Stoughton.)

 
The acid-base balance strategy used under conditions of hypothermia also influences the adequacy of cerebral blood flow during CPB. With the use of the alpha-stat protocol, cerebral blood flow is well maintained in the normal range across the homeostatic plateau range of widely varying blood pressures (Fig 2) [9]. However, a pH-stat protocol artificially maintains pH, and under conditions of hypothermia, this is achieved by adding CO2 to the perfusion circuit and raising CO2 content. This causes loss of autoregulation and the cerebral blood flow becomes pressure-passive (Fig 3).



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  		Fig 2. Normal cerebral blood flow is well maintained across the homeostatic plateau range of widely varying blood pressures with use of the alpha-stat protocol. (Reprinted from [9] by permission of The Society of Thoracic Surgeons.)

 


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  		Fig 3. Autoregulation of the cerebral blood flow is lost and the cerebral blood flow becomes pressure-passive with use of the pH-stat protocol.

 
The influences of alpha-stat and pH-stat strategies on cerebral blood flow and metabolism during CPB may not be fully appreciated by many. Although physiologic cerebral blood flow is about 45 to 55 mL · 100 g-1 · min-1, the brain does not require that amount of blood flow for its oxygen requirement to be met. The cerebral metabolic rate for oxygen, or the oxygen requirement of the brain, is only 3 mL · 100 g-1 · min-1. There clearly is a built-in excess of blood supply over and above what the brain actually requires.

This flow to metabolism ratio of 15:1 in favor of flow at 37°C is altered when we cool the patient. With an alpha-stat protocol at 28°C, the ratio of flow to metabolism increases to 30:1. With pH-stat at 28°C, because of the artificial addition of CO2 that leads to cerebral vasodilation, the ratio is still further increased, to 60:1. Although this phenomenon may have been seen as positive in the past, because the brain is being supplied with blood far in excess of its need, we now are aware that this positive interpretation is rather simplistic for this excess, luxury perfusion brings to the brain not just an excess supply of oxygen, but also excesses of other components of the bypass circuit, namely microemboli.

Microemboli
We and others have demonstrated during the years that microembolism, both gaseous and particulate, is a feature of the cerebral microcirculation during CPB. Developmentally, the eye is an outgrowth from the brain and takes its blood supply from the cerebral circulation. We have used the technique of retinal angiography to image the retinal circulation; this provides a unique window on the cerebral microcirculation. With retinal photography and a vertically mounted retinal camera focused on the macula of the eye, a very high-quality definition of the retinal microcirculation can be obtained during cardiac surgery. Figure 4 [10] shows a fluorescein angiogram of the retina around the macula, the site of entry into the retina of the optic nerve. This is the typical appearance seen at the end of CPB. There is evidence of truncation of a vessel and loss of retinal capillary perfusion, as well as other defects of other areas in the retina both centrally around the macula and more peripherally. We also have developed these techniques using computer image analysis, which enables the definition of the areas of loss of capillary circulation and their quantification by planimetry, providing a quantitative basis for comparative studies. Another technique not only produces a computerized image from the photograph of the retinal angiogram but also uses color to indicate the velocity of blood flow in the retina.



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  		Fig 4. Fluorescein retinal angiograms of the perimacular region of the retina in a patient immediately before (A) and after 80 minutes (B) of conventional cardiopulmonary bypass. (Reprinted from [10] by permission of The Lancet, Ltd.)

 
Inflammatory response
Once our retinal arteriogram studies had progressed to a certain point, we began to use magnetic resonance imaging (MRI) to look at the brain itself. Our institution, Hammersmith Hospital, has a very well-developed MRI unit; it was the first one installed in the UK. The unit is set up to receive patients who are ventilated, with patients coming to the unit directly from the intensive care unit or the operating theater. We began to compare MRI images of the brain taken in patients 24 hours before they underwent a cardiac surgical procedure with images of their brain taken immediately after the operation. Thus, patients were transferred to the MRI unit directly from the operating theater at the end of CABG operation, imaged, and then returned to the intensive care unit. Figure 5 [11] shows the MRI picture of a patient’s brain imaged 24 hours preoperatively and then within 60 minutes of the end of an uneventful CPB procedure. The postoperative image shows the brain to be acutely swollen, and the normal anatomic sulci and gyri are completely lost. In our pilot study of 6 patients, every patient showed this acute swelling of the brain at 1 hour after CPB [11]. This clearly suggested the possibility that we were seeing the effects of an inflammatory response in the brain, and led us to consider how we might continue to develop our understanding of this response in cardiac procedures.



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  		Fig 5. Magnetic resonance imaging image of a patient’s brain 24 hours before (A) and within 1 hour after uneventful cardiopulmonary bypass procedure (B). Postoperative image shows acute swelling, with normal anatomic sulci and gyri completely lost. (Reprinted from [11] by permission of The Lancet, Ltd.)

 
Our current efforts are focused on the endothelial cell–leukocyte adhesion cascade (Fig 6). Normally, white blood cells float in the bloodstream in a nonactivated state. At the initiation of an inflammatory response, selectins change that free movement of the white blood cells into a movement onto endothelial cell surfaces, where the white blood cells then begin to roll along the endothelial cells. Another group of adhesion molecules, known as integrins, change that rolling into a firm adhesion, so that the white blood cells become firmly adherent to the endothelial cells. Integrins also are involved in the final important step, which is the transmigration, or movement, of the activated and adherent white blood cells from the endothelial surface into the underlying tissue.



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  		Fig 6. Steps in the endothelial cell–leukocyte adhesion cascade.

 
Our current strategy is to characterize ß2 and ß1 adhesion molecule expression in patients undergoing cardiac surgery. We want to map the time course of this expression in neutrophils and monocytes and, on the basis of our understanding of these mechanisms, develop therapeutic and preventive strategies. We are looking not just at the increased expression of selectins and integrins but also at the increased expression by the endothelial cell of the corresponding ligands (Fig 7).



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  		Fig 7. Expression of selectins, integrins, and ligands in the process of endothelial-leukocyte adhesion. (ICAM = intracellular adhesion molecule; VCAM = vascular cell adhesion molecule.)

 
In this context, we are about to complete a sizable prospective, randomized, double-blind study of aprotinin in high dosage in relation to its effect both on the inflammatory response pattern and on cerebral MRI. The potential effects of high-dose aprotinin are considerable. It has an effect on the intrinsic clotting pathway and is a very powerful antifibrinolytic. It is a kallikrein inhibitor in the Hammersmith dosage regimen, because that was the basis on which the dosage regimen was calculated: The dosage was designed to inhibit kallikrein totally during CPB. It also has an effect on complement activation.

We look forward with interest to completing this study, breaking the code, and identifying whether this first approach to influencing the molecular basis of the inflammatory response is effective or not and what its effect might be on one particular target organ.

It is important to recognize that there are approaches other than protease inhibition that should be investigated as a means to modify the systemic inflammatory response. We also are working to develop monoclonal antibodies to the selectins, particularly L-selectin and P-selectin, and consider these possible inhibitors of cell adhesion. The use of anti–tumor necrosis factor may be somewhat controversial, given that its track record in critical care has not been particularly impressive. But it might be worth studying in the context of CPB, during which we can get the agents into patients before the insult begins.


   Summary
Top
 Abstract
 Introduction
 Incidence and severity
 High-risk patients
 Mechanisms of cerebral injury
 Summary
References
 
Further progress in the development of therapeutic and preventive strategies with respect to cerebral injury during cardiac operation depends on an increased understanding of the mechanisms involved. Currently, our strategies should include optimizing cerebral perfusion to the maximum possible and minimizing macroembolic and microembolic damage. The most interesting challenge that confronts us in the next few years is the possibility of modifying the systemic inflammatory response.


   References
Top
 Abstract
 Introduction
 Incidence and severity
 High-risk patients
 Mechanisms of cerebral injury
 Summary
 References
 

  1. Shaw P.J., Bates D., Cartlidge N.E.F., et al. Early neurological complications of coronary artery bypass surgery. Br Med J 1985;291:1384-1387.
  2. Breuer A.C., Furlan A.J., Hanson M.R., et al. Neurologic complications of open heart surgery. Cleve Clin Q 1981;48:205-206.[Medline]
  3. Borger M.A., Peniston C.M., Weisel R.D., Rao V., Cohen G., Ivanov J. Perioperative predictors of stroke following coronary bypass surgery. Perfusion 1997;12:36.
  4. Ahlgren E., Aren C. Cerebral dysfunction—a feared complication of cardiac surgery. Perfusion 1997;12:32.
  5. Goldsborough M.A., Boronicz L.M., McKhann G.M., Baumgartner W.A. Variation in stroke occurrence by cardiac procedures. Perfusion 1997;12:47.
  6. Smith P.L.C. The cerebral consequences of coronary artery bypass surgery. Ann R Coll Surg Engl 1988;70:212-216.[Medline]
  7. Astrup J., Symon L., Branston N.M., Lassen N.A. Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia. Stroke 1977;8:51-57.[Abstract/Free Full Text]
  8. Taylor K.M. Cardiac surgery and the brain. In: Smith P., Taylor K.M., eds. Cardiac surgery and the brain. London: Edward Arnold, 1993:1-14.
  9. Taylor K.M. Brain damage during cardiopulmonary bypass. Ann Thorac Surg 1998;65:S20-S26.
  10. Blauth C., Arnold J., Kohner E.M., Taylor K.M. Retinal microembolism during cardiopulmonary bypass demonstrated by fluorescein angiography. Lancet 1986;2:837-839.[Medline]
  11. Harris D.N.F., Bailey S.M., Smith P.L.C., Taylor K.M., Oatridge A., Bydder G.M. Brain swelling in the first hour after coronary artery bypass surgery. Lancet 1993;342:586-587.[Medline]



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