Lower Limit of Cerebral Autoregulation Questioned

Robert R. Kirby, MD; David J. Cullen, MD

Letter to the Editor

To the Editor:

In the Summer 2007 issue of the
APSF Newsletter, the editors published our communication concerning catastrophic neurologic outcomes in patients having shoulder surgery in the beach chair position.1 We were gratified that the publication generated interest in some readers and several letters to the editor. While a couple of letters2,3 seemed to agree with our thesis (corrections for blood pressure should be made to account for different values in the brain compared to the usual sites of measurement in the arm: “open” model) and provided additional insights,4 others subsequently took us to task because of the authors’ hypothesis that the site of pressure measurement is irrelevant because gravity has little or no effect on blood flow to and from the brain (“closed model”).5-7

Although the original thrust of our article did not dwell on cerebral blood flow (CBF) according to the open or closed models,5 that is a topic of immense interest to us and to those who have commented on our publication.3,5,7-9

The presence or absence of a siphon effect is the key point of differentiation in closed and open systems. A vascular siphon depends on the presence of a continuous column of blood in both the arterial and venous limbs of the loop. With respect to brain perfusion, this loop includes the thoracic aorta, brain arteries and arterioles, cerebral and jugular veins, vertebral venous plexus, the superior vena cava, and the right atrium. According to the siphon concept, no work is done by gravity against blood flow to the brain, and none is performed in the return of blood from the brain, because gravitational effects are identical on the ascending and descending limbs of the vascular loop.5,8,9 The proponents of this system state that no correction is needed for blood pressure in the brain versus that in the arm, because the afferent and efferent effects of gravity cancel each other.5-9

The siphon concept is not accepted by all investigators. Opponents state that collapsible veins prevent gravitational pressure gradients from being matched on the arterial and venous sides of the vascular loop above the heart, thus preventing the siphon from operating. Fluid in the descending limb "falls" (waterfall concept) and as a result does not aid the ascending limb. If the siphon concept is invalid, the heart alone is responsible for pumping blood to the brain and overcoming viscous resistance to blood flow through the brain, and in the upright patient the descending limb does not aid ascending flow. In this case, a pressure gradient will exist from the heart to the brain, and mean arterial pressure (MAP) in the brain will be lower than that in the arm according to the difference in height of the brain above the arm (and the heart).1

Blood flow through the brain is determined by the driving pressure from the left ventricle to overcome cerebrovascular resistance, intracranial pressure, cerebral autoregulation, arterial PCO2, and venous outflow resistance. If the internal jugular veins are collapsed, a parallel route, the vertebral venous plexus, still exists and can be a conduit to maintain the descending limb of the siphon. This system is thought to be protected from collapse, because of its attachments to rigid structures. However, regardless of which outflow tract is operational, the vessels of the brain are likely to act as a "baffle" and to prevent a siphon effect from being operational at all times in upright patients.

Independent of the siphon or waterfall concepts, the lower limit of autoregulation (LLA) also is critically important. For as long as we can remember, articles and textbooks almost uniformly have quoted this value as a cerebral perfusion pressure (CPP) of 50 mm Hg, where CPP=MAP-ICP (normal ICP should be assumed to be 5-15 mm Hg). Most anesthesiologists and anesthetists have been taught this value, and many have employed it clinically, reasoning that as long as they keep the lower value for CPP at 50 mmHg, CBF will remain constant, and hypoxic ischemic encephalopathy (HIE) will not occur. However, most work over the past 35 years has demonstrated significantly higher values for the LLA, perhaps as high as 80 ± 8 mmHg.10-18 Assuming this is correct, and current evidence supports the view that it is, an anesthesiologist or nurse anesthetist who persists in adhering to the 50 mmHg value (particularly in the beach chair position) runs the risk of inducing the potentially catastrophic complication of HIE.

Drummond18 noted that values lower than the LLA do not necessarily mean that patients will develop HIE, but some of them do. Unfortunately, which of these individuals will is unknown preoperatively. Since publication of the initial article by Pohl and Cullen,19 several additional cases of severe brain damage occurring in healthy patients undergoing shoulder surgery in the beach chair position have come to our attention. Why then should we assume that the closed concept of CBF is always correct and, therefore, not bother to correct for MAP at the brain level? If, in the future, this concept is validated as absolute and always true, so be it, and such corrections will be unnecessary. However, because we are dealing with hypotheses rather than established facts regarding open versus closed (siphon) concepts for CBF, our feeling is that we shouldn’t bet on patients’ well-being by adhering to an unproven hypothesis and an antiquated value of the LLA that should have been retired years ago.

If we have to undergo shoulder surgery in the beach chair position, we’ll make every effort to ensure that our anesthesiologist maintains a safe and appropriate CPP well above 50 mm Hg. In so doing, we would rather be safe than sorry. Other patients deserve no less.

Robert R. Kirby, MD
David J. Cullen, MD


References

  1. Cullen DJ, Kirby RR. Beach chair position may decrease cerebral perfusion; catastrophic outcomes have occurred. APSF Newsletter 2007;22(2):25,27.
  2. Lofsky AS. Labetalol may decrease cerebral perfusion in beach chair position. APSF Newsletter 2007;22(3):52.
  3. Cucchiara RF. Hazards of beach chair position explored. APSF Newsletter 2007-08;22(4):81.
  4. Budnyk S. Hazards of beach chair position explored. APSF Newsletter 2007-08;22(4):81.
  5. Munis J. The problems of posture, pressure, and perfusion. APSF Newsletter 2008;22(4):82,83.
  6. Kleinman B. Reader calls attention to change from baseline pressure. APSF Newsletter 2008;22(1):19.
  7. Pranevicius M, Pranevicius O. Modified calculation of the cerebral perfusion pressure in a sitting position: jugular Starling resistor and related clinical implications. APSF Newsletter 2008;23(2):32,33.
  8. Gisolf J, Gisolf A, van Lieshout JJ, Karemaker JM. The siphon controversy: an integration of concepts and the brain as baffle. Am J Physiol Regul Integr Comp Physiol 2005;289:R627-9.
  9. Badeer HS. Is the water-tower analogy justified? Adv Physiol Educ 2001;25:187-8.
  10. Strandgaard S. Autoregulation of brain circulation in severe arterial hypertension. Br Med J 1973;1:507-10.
  11. Strandgaard S. Autoregulation of cerebral blood flow in hypertensive patients. The modifying influence of prolonged antihypertensive treatment on the tolerance to acute drug-induced hypertension. Circulation 1976; 53:720-7.
  12. Ohsumi H, Furuya H, Kishi Y, et al. Preoperative estimation of cerebral blood flow autoregulation curve for control of cerebral circulation after cerebral revascularization. Resuscitation 1985; 13:41-5.
  13. Waldemar G, Schmidt JF, Andersen AR, et al. Angiotensin converting enzyme inhibition and cerebral blood flow autoregulation in normotensive and hypertensive man. J Hypertens 1989; 7:229-35.
  14. Schmidt JF, Waldemar G, Vorstrup S, et al. Computerized analysis of cerebral blood flow autoregulation in humans: validation of a method for pharmacologic studies. J Cardiovasc Pharmacol 1990; 15:983-8.
  15. Larsen FS, Olsen KS, Hansen BA, et al. Transcranial Doppler is valid for determination of the lower limit of cerebral blood flow autoregulation. Stroke 1994;25:1985-8.
  16. Olsen KS, Svendsen LB, Larsen FS, et al. Effect of labetalol on cerebral blood flow, oxygen metabolism and autoregulation in healthy humans. Br J Anaesth 1995; 75:51-4.
  17. Olsen KS, Svendsen LB, Larsen FS. Validation of transcranial near-infrared spectroscopy for evaluation of cerebral blood flow autoregulation. J Neurosurg Anesth 1996; 8:280-5.
  18. Drummond JC. The lower limit of autoregulation: time to revise our thinking? Anesthesiology 1997; 86:1431-3.
  19. Pohl A, Cullen DJ. Cerebral ischemia during shoulder surgery in the upright position: a case series. J Clin Anesth 2005;17:463-9.