Background. Neurologic complications, primarily resulting from ischemic ins
ults, represent the leading cause of morbidity and disability, and the seco
nd most common source of death, after cardiac operations. Previous studies
have reported that increases las occur during the rewarming phase of cardio
pulmonary bypass [CPB]) or decreases in brain temperature of a mere 0.5 deg
rees to 2 degrees C can significantly worsen or improve, respectively, post
ischemic neurologic outcome. The purpose of the present study was to evalua
te a novel approach of selectively cooling the brain during hypothermic CPB
and subsequent rewarming.
Methods. Sixteen dogs were anesthetized with either intravenous pentobarbit
al or inhaled halothane (n = 8 per group). Normocapnia (alpha stat techniqu
e) and a blood pressure near 75 mm Hg were maintained. Temperatures were mo
nitored by placing thermistors in the esophagus (ie, core), parietal epidur
al space, and brain parenchyma at depths of 1 and 2 cm beneath the dura. Du
ring CPB, core temperature was actively cycled from 38 degrees C to 28 degr
ees C, and then returned to 38 degrees C. Forced air pericranial cooling la
ir temperature of approximately 13 degrees C) was initiated simultaneous wi
th the onset of CPB, and maintained throughout the bypass period. Brain-to-
core temperature gradients were calculated by subtracting the core temperat
ure from regional brain temperatures.
Results. In halothane-anesthetized dogs, brain temperatures at all monitori
ng sites were significantly less than core during all phases of CPB, with o
ne exception (2 cm during systemic cooling). Brain cooling was most promine
nt during and after systemic rewarming. For example, during systemic rewarm
ing, average temperatures in the parietal epidural space, and 1 and 2 cm be
neath the dura, were 3.3 degrees +/- 1.3 degrees C (mean +/- standard devia
tion), 3.2 degrees +/- 1.4 degrees C, and 1.6 degrees +/- 1.0 degrees C, co
oler than the core, respectively. Similar trends, but of a greater magnitud
e, were noted in pentobarbital-anesthetized dogs. For example, during syste
mic rewarming, corresponding brain temperatures were 6.5 degrees +/- 1.7 de
grees C, 6.3 degrees +/- 1.6 degrees C, and 4.2 degrees +/- 1.3 degrees C c
ooler than the core, respectively.
Conclusions. The magnitude of selective brain cooling observed in both stud
y groups typically exceeded the 0.5 degrees to 2.0 degrees C change previou
sly reported to modulate ischemic injury, and was most prominent during the
latter phases of CPB. When compared with previous research from our labora
tory, application of cold forced air to the cranial surface resulted in bra
in temperatures that were cooler than those observed during hypothermic CPB
without pericranial cooling. On the basis of the assumption that similar b
eneficial brain temperature changes can be induced in humans, we speculate
that selective convective brain cooling may enable clinicians to improve ne
urologic outcome after hypothermic CPB. (C) 1998 by The Society of Thoracic
Surgeons.