| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J Thorac Cardiovasc Surg 2000;119:855-856
© 2000 The American Association for Thoracic Surgery
LETTERS TO THE EDITOR |
Research Department, Kokura Memorial Hospital, 1-1 Kifune-cho, Kokura-kitaku, Kitakyushu-shi, Fukuoka, 802-8555, Japan
Assistant Professor, II Department of Physiology, University of Ryukyus School of Medicine, Okinawa, Japan
To the Editor:
Kawahara and associates, in their article, "Balloon Pump–Induced Pulsatile Perfusion During Cardiopulmonary Bypass Does not Improve Brain Oxygenation" (J Thorac Cardiovasc Surg 1999;118:361-6), are to be applauded for their attempts at defining the role that pulsatile perfusion induced by the intra-aortic balloon pump (IABP) may have in preventing the decrease of internal jugular venous oxygen saturation (SjvO 2) and regional cerebral oxygenation during cardiopulmonary bypass (CPB), under almost normothermic, alpha-stat managed conditions. However, the explanations given for their negative results seem to us inadequate or incomplete. At least three other possibilities might be considered:
Before discussing whether pulsatility was or was not effective in improving the decreased SjvO 2, attention must be directed to what might be the more fundamental point of the problem. There appears to us to be a basic flaw in the design of the protocol: Observations were made during CPB under lower pressures than the baseline control in both groups. These differences were dismissed with the argument that they were within the autoregulated pressure ranges. The low SjvO 2 and regional cerebral oxygenation observed during CPB in both groups returned to normal as blood pressures returned to control levels after CPB in a time frame strongly suggestive of a cause-effect relationship, without the need of invoking other factors. If so, two important implications can be inferred:
1; the cerebral blood flow at a mean arterial pressure of 65 mm Hg remains similar to that at 110 mm Hg 2; therefore the lower limits of autoregulation probably lie in the range of 65 to 70 mm Hg, and not at 50 mm Hg. Thus the validity of the widely accepted concepts of autoregulation being maintained at pressures as low as 20 to 40 mm Hg 3 or even 50 mm Hg 4 during alpha-stat, pulsatile or nonpulsatile CPB is challenged. It would have been interesting to have followed the SjvO 2 at more frequent intervals to determine the time dependency of the phenomenon, which may explain the development of low SjvO 2 in both groups as a function of perfusion time. If we accept the SjvO 2 as the indicator of flow-metabolism coupling, then there is need to conceptually change the figures for the pressures currently considered as being within the autoregulation range during CPB. By contrast, if a pressure of 50 to 65 mm Hg is accepted as sufficient to maintain metabolic normalcy, then lower SjvO 2 figures during CPB (pulsatile or nonpulsatile) would have to be accepted as "normal," although nonphysiologic. Since it is widely known that low SvjO 2 correlates with cognitive dysfunction in patients after CPB, the first premise seems to be in need of revision.
If pump flows were maintained unchanged, the pulsatility per se would not ameliorate the SjvO 2. More detailed pressure-flow metabolic studies as a function of time-duration of perfusion might be required to elucidate the true nature and meaning of the decreased SjvO 2, and not only the presence or absence of pulsatility.
2. The beneficial effects of pulsatile flow seem to be mediated by the production of L -arginine and nitric oxide by the pulse-induced stretch of the vascular endothelium. 5 It is unlikely that the modest IABP–induced pulse pressure of only 24 ± 8 mm Hg would generate a dp/dt of 645 ± 64 mm Hg/s, particularly at the level of small cerebral arteries, and thus be enough to produce sufficient stretch to induce significant production of L -arginine in the small cerebral arteries. If the pulse pressure was not sufficient, then significant cerebral vasodilation would not be obtained to affect the SjvO 2, and hence the IABP-induced pulsatility would be unable to ameliorate the impaired SjvO 2. A similar study using a pulsatile system capable of producing a pulse pressure of 50 to 60 mm Hg 6 to mimic that produced by the natural heart would be needed to be able to definitely exclude or include the role played by pulsatility. The study only demonstrates that the modest IABP-induced pulsatility was not effective but by no means excludes the role pulsatility may have.
3. It is widely known that during CPB the levels of circulating endogenous catecholamines including norepinephrine are increased. During systemic infusion of norepinephrine, increased electrical brain activity (consisting of increased low-voltage high-frequency waves and decreased high-voltage slow-frequency waves) suggestive of promotion of excitatory (N -methyl-D -aspartate?) receptor activation has been noted in nonischemic rabbits (unpublished observations of electroencephalograms concurrent to brain microdialysis studies), which may lead to Na+ and Ca++ influx. To maintain the normal Na+ and Ca++ transmembrane gradient, the demand for mechanisms to extrude them, which are highly oxygen consuming, will be increased. Therefore during late CPB the decreased SjvO 2 might be a manifestation of that increased oxygen extraction not counteracted by the anesthetics, pressures, or pulsatility used by the authors. The exact effect of increased circulating catecholamines during CPB on the cerebral vasculature is not known, but if it was equivalent to increased sympathetic activity, then vasoconstriction of small cerebral vessels would result with consequent decreased flow. 7 If both effects are operating, the development of decreased SjvO 2 over the first 20 minutes of perfusion and the return to normal after CPB, also in 20 or 30 minutes, are easily explainable.
Norepinephrine determination with and without blockade in conjunction with metabolic studies across the brain in both groups might shed some light.
12/8/104877 doi:10.1067/mtc.2000.104877
References
This article has been cited by other articles:
|
|
 |
|
  T. W. Willcox and R. van Uden Best Practice for Cardiopulmonary Bypass in the High-Risk Elderly Patient Seminars in Cardiothoracic and Vascular Anesthesia, December 1, 2002; 6(4): 293 - 300. [Abstract] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
