Cerebral Blood Flow and Autoregulation
Mannitol, albumin, and in particular dextran [Neurosurgery 11: 739, 1982; Neurology 34: 24, 1984] all help prevent RBC aggregation and can improve blood flow.
Effects of Cerebral Perfusion Pressure
CBF is maintained at a constant rate as long as MAPs range from 60 – 160 mm Hg [Doberstein in Youmans’ Neurological Surgery] – a result of this phenomena is that cerebral blood volume peaks at a CPP of 40-45 mm Hg – at normal CPP values, there is minimal vasodilation. As CPP drops towards 45, vasodilation occurs, increasing CBF and blood volume, however when CPP drops below 40-45, autoregulation fails and blood vessels begin to collapse again, lowering both blood volume and CBF [Andrews BT: Neurosurgical Intensive Care]. Furthermore, it is thought that perfusion at the upper limits of autoregulation lead to passive, irreversible dilation of arterioles – a study of induced hypertension in cats showed that for MAPs of 170-200 mm Hg, precapillary arterioles lose their function and begin to dilate, and that MAPs > 200 mm Hg lead to the formation of fusiform microaneurysms and irreversible dilatory responses which could potentially lead to blood brain barrier disruption, cerebral edema, and/or intracranial bleeding [Am J Physiol 234: H371, 1978]. Vasoresponsivity is affected by CPP, hypoxia, and hyper/hypocarbia, and may be lost secondary to ischemia. Carbon dioxide responsivity is ~ 3% change in CBF per 1 mm Hg change in pCO2. In fact, a study of acetazolamide administration in six patients revealed an increase in CBF of 53-75% without having any effect on CMRO2 [J Clin Invest 74: 1634, 1984].
Normal regional CBF is 50-60 cc/100g/min. Intact cell structure and function is maintained with rCBF down to at least 20-25 cc/100g/min, although this assumes normal metabolic rate and also may not apply due to differences in regional perfusion. Cortical potentials begin to cease at 16-18 ml/100g/min [J Neurosurg 54: 771, 1981; Acta Neuochir Suppl (Wien) 49: 2, 1990], and cell breakdown can occur anywhere between 6-23 ml/100g/min [Stroke 8: 51, 1977]. Note that the infarction threshold depends on both rCBF and duration [J Neurosurg 54: 773, 1981] – CBF of 18-23 mL/100g/min can be tolerated for two weeks, whereas 10-12 mL/100g/min can only be tolerated for 3 hours, and 8 mL/100g/min for one hour before neuronal death occurs [Acta Neurochir Suppl (Wien) 49: 2, 1990]. CMRO2 = 3.0-3.8 cc/100g/min. The coupling ratio (CBF:CMRO2) is 14-18 in the quiescent brain. CVR changes linearly with PaCO2 ranges from 20 – 80 mm Hg and CPP ranges from 60 – 160 mm Hg, i.e., these are the ranges of autoregulation.
|Key Point: Cushing’s Triad (hypertension, bradycardia, respiratory)
Cerebral Blood Flow Measurements
Transcranial Dopplers use three windows – transtemporal (MCA, ACA, PCA), transorbital (OA, ICA. Note that flow reversal in the OA is a sign of proximal ICA occlusion), and transforamental (VA, VA). Remember that vasospasm is not the only cause of increased velocity – one must also consider fever, anemia, hypoxia, dominant vessels, and vasopressors. Pulsatility index = (S – D velocity)/(mean velocity) and is an indicator of flow resistance. The Lindegaard ratio is MCA/extracranial ICA velocities – values > 3 correlate with spasm. If the angle of the insonator is 15 degrees or more, velocity will be underestimated.
AVDO2 and O2ER are inexpensive methods to assess cerebral metabolism. CMRO2 can increase 10% for every degree Celsius, and decrease 5% for every degree Celsius. Early hypothermia after traumatic brain injury has been shown in some studies to improve outcomes [NEJM 336: 540, 1997]. An AVDlactate/AVDO2 ratio > 0.8 is a reasonable indicator of increased anaerobic metabolism [J Neurosurg 70: 222, 1989; Neurosurg Clin N Am 5: 633, 1994]
There are likely two ischemic states – the first, “compensated hypoperfusion” is characterized by low CBF and increased AVDO2 as well as O2ER. Ultimately the O2ER will reach its limit, at which point the second state arises, characterized by decreasing AVDO2 (as O2ER drops) as well as increased lactate production. As long as AVDlactate/AVDO2 ratio < 0.8, AVDO2 can predict the status of cerebral blood flow [J Neurosurg 70: 222, 1989]
Several studies suggest that hyperglycemia exacerbates neuronal injury [Neurology 32: 1239, 1982; Am J Med 74: 540, 1983; Stroke 19: 764, 1988; Stroke 19: 185, 1988], although some studies of focal, permanent ischemic damage refute this [Stroke 18: 570, 1987; Stroke 20: 519, 1989]. Still, mild hypoglycemia may actually offer some neuronal protection during ischemia [Am J Med 74: 540, 1983; J Neurol Neurosurg Psychiatry 53: 847, 1990] and the idea of insulin as a neuroprotecting agent is gaining ground [J Neurol Neurosurg Psychiatry 53: 847, 1990; Neurology 51S3: S39, 1998]