Impaired Cerebral Blood Flow Autoregulation Research Articles

Hyperventilation restores cerebral blood flow autoregulation in patients with acute liver failure

Background/Aims: In patients with acute liver failure loss of cerebral blood flow autoregulation may result from cerebral vasodilation. Since arterial hypocapnia induces cerebral vasoconstriction, we investigated whether cerebral blood flow autoregulation could be reestablished by mechanical hyperventilation. Methods: Seven consecutive patients (median age 45, range 30–50 years with acute liver failure and hepatic encephalopathy stage IV entered the study. They were all maintained on mechanical ventilation. Cerebral blood flow autoregulation was evaluated by using transcranial Doppler sonography to assess mean flow velocity (V mean) in the middle cerebral artery, during a rise in mean arterial pressure by norepinephrine infusion (0.5–10 μg/h). The patients were subsequently hyperventilated for 15 min before cerebral blood flow autoregulation was re-evaluated in the same mean arterial pressure range. Results: At baseline PaCO 2 (4.0 (3.5–4.9)kPa), all patients had impaired cerebral blood flow autoregulation as V mean increased from 47 (30–78) to 68 (49–107) cm · s −1 ( p<0.05), as MAP was raised from 82 (60–88) to 106 (89–183) mmHg. During hyperventilation, five of seven patients restored cerebral autoregulation as V mean remained unchanged at 51 (45–70) cm·s −1 during a rise in MAP from 84 (65–94) to 110 (89–130) mmHg. Cerebral blood flow autoregulation was not restored in two patients, but hyperventilation reduced the slope of the mean arterial pressure-V mean correlation. These two patients had renal failure and were treated with intermittent hemodialysis. Conclusions: Cerebral blood flow autoregulation was restored by hyperventilation in five of seven patients with acute liver failure, indicating that cerebral vasodilatation is of pathophysiological importance in dys-regulation of cerebral circulation in acute liver failure.

Cerebral blood flow in the diabetic patient.

Diabetes is a major risk factor for cardiovascular disease. Coronary revascularization utilizing cardiopulmonary bypass (CPB) is frequently required for the diabetic patient. Nondiabetic individuals can autoregulate cerebral blood flow (CBF) through metabolic and perfusion pressure mechanisms during CPB. However, it has been reported that diabetic patients have impaired CBF autoregulation during CPB. It is possible, therefore, that impaired CBF autoregulation may contribute to postoperative neuropsychologic dysfunction. The mechanisms for this defect may reside in impaired endothelial-dependent responses in the diabetic that are related to morphological and functional changes linking the vascular endothelium and the vascular smooth muscle. The morphological changes occurring in the diabetic include microangiopathy and macroangiopathy which are characterized by endothelial cell (EC) hyperplasia and basement membrane thickening. Also, significant functional changes in local control of vascular tone, such as an imbalance in the synthesis and secretion of vasoactive factors by the EC and abnormal reactivity of the vascular smooth muscle, are seen in the diabetic when compared to the nondiabetic. More specifically, vascular responses to both calcium-dependent pathways of vasoconstriction and nitric oxide pathways of vasorelaxation have been shown to significantly differ between the diabetic and nondiabetic. The emphasis of this discussion is to examine the molecular mechanisms by which diabetes alters vascular function, with emphasis placed on regulation of cerebral artery blood flow during CPB.

Cerebral Blood Flow Autoregulation in Stroke Patients

The control of blood pressure in acute stroke patients and management of hypertension in chronic stroke patients are highly important. So we attempted to clarify the clinical significance of cerebral blood flow (CBF) autoregulation in stroke patients. 1) Orthostatic hypotension in early rehabilitation: The incidence of neurological symptoms decreased when the head of the bed was elevated gradually, over days, rather than rapidly. The results indicate that a gradual elevation of the head of the bed in stepwise fashion is safer than an abrupt elevation, especially in patients with occlusions of the main cerebral artery. 2) CBF autoregulation in patients with acute brain hemorrhage: Blood pressure control is essential in managing patients with acute brain hemorrhage. Measurements of CBF autoregulation in cases wlth acute brain hemorrhage indicate that a 20% reduction in blood pressure is the maximum for maintaining cerebral circulation. 3) CBF autoregulation in patients of chronic brain infarction: The reduction of blood pressure in hypertensive patients with ischemic cerebrovascular disease should be within 20% in those without arterial occlusion, and within 10% in those with a stem occlusion of the middle cerebral artery. 4) Periventricular lucency (PVL) and CBF autoregulation: Mean cerebrovascular resistance value was elevated in chronic hypertensive patients with CT findings of severe PVL; cases of severe PVL also showed impaired CBF autoregulation. This indicates that hypertensive patients whose brain CT reveal severe PVL have an impaired CBF autoregulation. In these cases a strict regimen for lowering the blood pressure is required to prevent deterioration of the cerebral microcirculation. (Hypertens Res 1994; 17 Suppl. I: S71-S76)

Electroencephalogram, Cerebral Metabolic, and Vascular Responses to Propofol Anesthesia in Dogs

Previous studies on the cerebral effects of propofol report conflicting results regarding the cerebral metabolic rate for oxygen (CMRO2), cerebral blood flow (CBF), autoregulation of CBF, intracranial pressure, and cerebral perfusion pressure (CPP). The present studies were designed to examine these issues as well as propofol effects on the CBF responses to hypocapnia and on the electroencephalogram (EEG) in a well-known canine model that permits continuous determination of EEG activity, CMRO2, CBF, and cerebrospinal fluid (CSF) pressure. Dogs were studied at normocapnia (n = 6) and at hypocapnia (n = 6) during three doses of propofol (12, 24, and 48 mg kg(-1) h(-1)) and during a combination of propofol and elevated (20-25 mm Hg) CSF pressure. In both groups propofol caused dose-related decreases of EEG power and number of waveforms, CMRO2 (by 25-30%), and CBF (by 73-76%). The cerebral vasoconstrictor response to hypocapnia was preserved at all three doses of propofol. Autoregulation of CBF was preserved at the low and moderate doses of propofol but was impaired at the high dose of propofol (where CPP decreased significantly to approximately 41 +/- 13 mm Hg) and at the high dose of propofol combined with elevated CSF pressure (where CPP decreased significantly to approximately 32 +/- 12 mm Hg). Cerebrospinal fluid pressure decreased (by 33-42%) when the continuous infusion of propofol was begun, but returned to prepropofol values as infusion of propofol continued. The authors conclude that low and moderate doses of propofol decrease EEG activity and CMRO2, causing an associated decrease of CBF and CSF pressure. Autoregulation of CBF and cerebral vascular CO2 reactivity are preserved at these propofol doses. In contrast, high dose propofol significantly decreases CPP, resulting in impaired autoregulation of CBF.

Effects of pressure on cerebrospinal fluid formation: nonsteady-state measurements in dogs.

Effects of pressure on cerebrospinal fluid (CSF) formation were studied in dogs with a recirculatory spinal perfusion tracer clearance technique that does not require steady-state conditions. The data permit statistical analysis of the relationship between the rate of CSF formation and pressure for individual animals. Most animals showed no statistical relationship between CSF formation and intracranial pressure (ICP) and/or cerebral perfusion pressure (CPP). In this study, a disturbance of cerebral blood flow (CBF) autoregulation may have been present in five animals on the basis of CPP reductions, and four of this latter group showed formation to decrease with increasing ICP. It is suggested that CSF formation is normally pressure insensitive. With impaired autoregulation of CBF, formation may follow CBF and CPP passively.

Dynamic pressures in the pial arterial microcirculation.

Dynamic pressures in the pial arterial microcirculation.

Cerebral blood flow and oxygen consumption in man.

Cerebral blood flow and oxygen consumption in man.