The relation between intracranial pressure,mean arterial pressure and cerebral blood flow in patients with severe head injury

In patients with severe head injuries ICP, MAP and CBF were measured continuously. In most patients there was a positive vasopressor response to increasing ICP, but the ICP/MAP ratio varied considerably in individual cases. CBF was diminished either by increasing ICP or by decreasing MAP. This effect was more marked with ICP above 40 mm Hg or MAP below 110 mm Hg. In terminal stages there was often a negative MAP/ICP ratio accompanied by massive cerebral hyperaemia. Key words: Severe head injury--intracranial pressure--mean arterial pressure--cerebral blood flow--cerebral perfusion pressure--critical limit of ICP and CBF. Abbreviations: ICP equals intracranial pressure (mm Hg); CBF, Flow equals cerebral blood flow (ml/min); MAP equals mean arterial pressure (mm Hg); CPP equals cerebral perfusion pressure (mm Hg) (difference between MAP and ICP); BP equals blood pressure.     

Cerebral blood flow at constant cerebral perfusion pressure but changing arterial and intracranial pressure: relationship to autoregulation

Therapeutic agents for reducing raised intracranial pressure (ICP) may do so at the expense of reduced mean arterial pressure (MAP). As a consequence, cerebral perfusion pressure (CPP) = (MAP - ICP) may not improve. It is unknown whether the level of MAP alters cerebral blood flow (CBF) when MAP and ICP change in parallel so that CPP remains constant. This study investigates CBF at a constant CPP but varying levels of MAP and ICP in 12 anaesthetized cats. CBF was studied at three levels of CPP: 60 (n = 4), 50 (n = 4), and 40 mm Hg (n = 4) under conditions of both intact and impaired autoregulation. At CPP levels of 50 and 60 mm Hg, when autoregulation was intact, CBF remained unchanged. With loss of autoregulation, there was a trend for CBF to increase as MAP and ICP were increased in parallel at a CPP of 50 and 60 mm Hg, although the relationship did not achieve statistical significance. Absolute CBF levels were, however, significantly different between the autoregulating and nonautoregulating groups (p <0.001). At a CPP of 40 mm Hg, CBF showed a linear correlation with blood pressure (BP) (r = 0.57, p <0.05). These results demonstrate that when autoregulation is impaired, there is a functional difference between autoregulating and nonautoregulating cerebral vessels despite similar MAP and CPP. These results also show that at a CPP of 40 mm Hg when autoregulation is impaired, CBF depends more on arterial driving pressure than on CPP.     

Effects of diaspirin cross-linked haemoglobin on post-traumatic cerebral perfusion pressure and blood flow in a rodent model of diffuse brain injury

Diaspirin cross-linked haemoglobin (DCLHb) is a new oxygen carrying blood substitute with vasoactive properties. Vasoactive properties may be mediated via high affinity binding of nitric oxide by the haem moiety. Using a rodent model of head injury combined with ischaemia, we studied the effects of DCLHb on cerebral blood flow (CBF) and intracranial pressure (ICP). Twenty anaesthetized rats were allocated randomly to receive treatment with DCLHb 400 mg kg-1 i.v. or placebo (oncotically matched plasma protein substitute 4.5% i.v.). To produce diffusely increased ICP, after a severe weight drop injury, all animals underwent a 30-min period of bilateral carotid ligation combined with a period of induced hypotension. After reperfusion, DCLHb or placebo was infused and the animals instrumented for measurement of intraventricular ICP and CBF in the region of the sensorimotor cortex using the hydrogen clearance technique. Mean arterial pressure (MAP), ICP, cerebral perfusion pressure (CPP) (CPP = MAP - ICP) and CBF were measured 4 h after injury in all animals. DCLHb significantly reduced ICP from mean 13 (SEM 2) to 3 (1) mm Hg (P < 0.001), increased CPP from 52 (8) to 95 (6) mm Hg (P < 0.001) and increased CBF from 21 (2) to 29 (2) ml 100 g-1 min-1 (P = 0.032). We conclude that DCLHb improved CPP without a reduction in CBF in a rodent model of post-traumatic brain swelling.      

Is cerebral perfusion pressure a major determinant of cerebral blood flow during head elevation in comatose patients with severe intracranial lesions?

OBJECT: Head elevation as a treatment for lower intracranial pressure (ICP) in patients with intracranial hypertension has been challenged in recent years. Therefore, the authors studied the effect of head position on cerebral hemodynamics in patients with severe head injury. METHODS: The effect of 0 degrees, 15 degrees, 30 degrees, and 45 degrees head elevation on ICP, cerebral blood flow (CBF), systemic arterial (PsaMonro) and jugular bulb (Pj) pressures calibrated to the level of the foramen of Monro, cerebral perfusion pressure (CPP), and the arteriovenous pressure gradient (PsaMonro - Pj) was studied in 37 patients who were comatose due to severe intracranial lesions. The CBF decreased gradually with head elevation from 0 to 45 degrees, from 46.3+/-4.8 to 28.7+/-2.3 ml x min(-1) x 100 g(-1) (mean +/- standard error, p<0.01), and the PsaMonro - Pj from 80+/-3 to 73+/-3 mm Hg (p< 0.01). The CPP remained stable between 0 degrees and 30 degrees of head elevation, at 62+/-3 mm Hg, and decreased from 62+/-3 to 57+/-4 mm Hg between 30 degrees and 45 degrees (p<0.05). A simulation showed that the 38% decrease in CBF between 0 degrees and 45 degrees resulted from PsaMonro - Pj changes for 19% of the decrease, from a diversion of the venous drainage from the internal jugular veins to vertebral venous plexus for 15%, and from CPP changes for 4%. CONCLUSIONS: During head elevation the arteriovenous pressure gradient is the major determinant of CBF. The influence of CPP on CBF decreases from 0 to 45 degrees of head elevation.     

Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients.

The traditional practice of elevating the head in order to lower intracranial pressure (ICP) in head-injured patients has been challenged in recent years. Some investigators argue that patients with intracranial hypertension should be placed in a horizontal position, the rationale being that this will increase the cerebral perfusion pressure (CPP) and thereby improve cerebral blood flow (CBF). However, ICP is generally significantly higher when the patient is in the horizontal position. This study was undertaken to clarify the issue of optimal head position in the care of head-injured patients. The effect of 0 degree and 30 degrees head elevation on ICP, CPP, CBF, mean carotid pressure, and other cerebral and systemic physiological parameters was studied in 22 head-injured patients. The mean carotid pressure was significantly lower when the patient's head was elevated at 30 degrees than at 0 degrees (84.3 +/- 14.5 mm Hg vs. 89.5 +/- 14.6 mm Hg), as was the mean ICP (14.1 +/- 6.7 mm Hg vs. 19.7 +/- 8.3 mm Hg). There was no statistically significant change in CPP, CBF, cerebral metabolic rate of oxygen, arteriovenous difference of lactate, or cerebrovascular resistance associated with the change in head position. The data indicate that head elevation to 30 degrees significantly reduced ICP in the majority of the 22 patients without reducing CPP or CBF.     

Effects of cisatracurium on cerebral and cardiovascular hemodynamics in patients with severe brain injury

Background : For neuroanesthesia and neurocritical care the use of drugs that do not increase or preferentially decrease intracranial pressure (ICP) or change cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) are preferred. The current study investigates the effects of a single rapid bolus dose of cisatracurium on cerebral blood flow velocity, ICP, CPP, mean arterial pressure (MAP) and heart rate (HR) in 24 mechanically ventilated patients with intracranial hypertension after severe brain trauma (Glasgow coma scale 6) under continuous sedation with sufentanil and midazolam.
Methods : Patients were randomly assigned to receive either 2XED95 (n=12) or 4XED95 (n=12) of cisatracurium as a rapid i.v. bolus injection. Before and after bolus administration mean cerebral blood flow velocity (BFV, cm/s) was measured in the middle cerebral artery using a 2–MHz transcranial Doppler sonography system, ICP (mm Hg) was measured using an extradural probe, and MAP (mm Hg) and HR (b/min) were measured during a study period of 20 min. Cerebral perfusion pressure (CPP=MAP–ICP) was also calculated.
Results : Our data show that a single bolus dose of up to 4 × ED95 cisatracurium caused no significant (P<0.05) changes in BFV, ICP, CPP, MAP and HR. Possible histamine-related events were not observed during the study.
Conclusions : The results from this study suggest that cisatracurium is a safe neuromuscular blocking agent for use in adult severe brain–injured patients with increased ICP under mild hyperventilation and continuous sedation.     

Rebound intracranial hypertension in dogs after resuscitation with hypertonic solutions from hemorrhagic shock accompanied by an intracranial mass lesion

We compared intracranial pressure (ICP) and cerebral blood flow (CBF) in dogs after inflating a subdural intracranial balloon to increase ICP to 20 mm Hg, inducing hemorrhagic shock (mean arterial pressure [MAP] of 55 mm Hg), and infusing a single bolus of fluid consisting of either 54 mL/kg of 0.8% saline (SAL), 6 mL/kg of 7.2% hypertonic saline (HS), 20% hydroxyethyl starch (HES) in 0.8% SAL, or a combination fluid (HS/HES) containing 20% HES in 7.2% saline. Twenty-six dogs were ventilated with 0.5% halothane in N2O and O2 (60:40 ratio). As ICP was maintained at 20 mm Hg, rapid hemorrhage reduced MAP to 55 mm Hg (time interval of zero [T0]) which was maintained at that level for 30 minutes (until T30). Subsequently, over a 5-minute interval (T30-T35), one of the four randomly assigned resuscitation fluids was infused. Data were collected at baseline; after subdural balloon inflation; at T0, T30, T35, and 30-minute intervals thereafter for 2 hours (T65, T95, T125, and T155). CBF and ICP were compared using repeat-measure ANOVA. Cerebral blood flow was greater at T35 in the HS and HS/HES groups than in the HES group (P = .025). In the SAL group, ICP increased significantly from T0 to T35, remaining unchanged thereafter. At T35, ICP in the HS group was significantly lower than in the SAL group (P < .05) but subsequently increased. ICP in the HS/HES group exceeded that in all other groups at T95 and T125 (P < .05). After a severe reduction in cerebral perfusion pressure (CPP), HS solutions (both HS and HS/HES) were associated with a delayed rise in ICP and did not improve global forebrain CBF in comparison with conventional saline solutions.     

Phenylephrine increases cerebral perfusion pressure without increasing intracranial pressure in rabbits with balloon-elevated intracranial pressure.

Using a rabbit model of intracranial hypertension, we studied the effects of infusion of phenylephrine on intracranial pressure (ICP) and cerebral perfusion pressure (CPP). Seven New Zealand white rabbits were anesthetized with isoflurane and normocapnia was maintained. An extradural balloon was used to raise ICP to 25 +/- 1 mm Hg. Infusion of phenylephrine increased mean arterial blood pressure (MAP) (77 +/- 6 --> 95 +/- 8 mm Hg) and CPP (52 +/- 7 --> 70 +/- 7 mm Hg). ICP was unchanged during infusion of phenylephrine (25 +/- 1 vs. 25 +/- 2 mm Hg). The phenylephrine infusion was stopped after 45 minutes and MAP returned to baseline (76 +/- 8 mm Hg). We conclude that phenylephrine increased CPP because of its effect on MAP, but did not alter ICP. Phenylephrine may be used to increase CPP without raising ICP when autoregulation is intact.     

短期应用高渗盐水对重症蛛网膜下腔出血患者颅内压、脑血流量的影响

目的 探讨23.4%高渗盐水(HTS)对重症蛛网膜下腔出血(SAH)患者颅内压、脑灌注压、脑血流量(CBF)的影响.方法 16例重症SAH患者(GCS≤8分)在颅压升高时接受静脉输注23.4%HTS,监测用药前及用药后30、60、90、120、150、180 min的颅内压(ICP),平均动脉压(MAP),脑灌注压(CPP)及脑血流速度(FV).结果 用药后30 min可见ICP显著降低,同时MAP、CPP及FV显著升高(P<0.05),ICP显著降低可持续180 min,CPP和FV的改善持续约90 min(P<0.05).结论 HTS能显著降低重症SAH患者的ICP,改善脑组织灌注,可用来纠正脑缺血引起的病生理变化.     

Effects of alterations in arterial CO2 tension on cerebral blood flow during acute intracranial hypertension in rats.

Cerebrovascular reactivity to CO2 in clinical and experimental studies has been found to be impaired during increased intracranial pressure (ICP). However, from previous study results it has not been possible to estimate whether the impairment was caused by elevated ICP, or caused by decreased cerebral perfusion pressure (CPP). The current study was carried out in a group of unmanipulated control rats and in six investigation groups of six rats each: two groups with elevated ICP (30 and 50 mm Hg) and spontaneous arterial blood pressure (MABP), two groups with spontaneous ICP and arterial hypotension (77 and 64 mm Hg), and two groups with elevated ICP (30 and 50 mm Hg) and arterial hypertension (124 mm Hg). Intracranial hypertension was induced by continuous infusion of lactated Ringer's solution into the cisterna magna, arterial hypotension by controlled bleeding, and arterial hypertension by continuous administration of norepinephrine intravenously. Cerebral blood flow (CBF) was measured repetitively by the intraarterial 133Xe method at different levels of arterial PCO2. In each individual animal, CO2 reactivity was calculated from an exponential regression line obtained from the corresponding CBF/PaCO2 values. By plotting each individual value of CO2 reactivity against the corresponding CPP value from the seven investigation groups, CPP was significantly and directly related to CO2 reactivity of CBF (P < .001). No correlation was found by plotting CO2 reactivity values against the corresponding MABP values or the corresponding ICP values. Thus, the results show that CO2 reactivity is at least partially determined by CPP and that the impaired CO2 reactivity observed at intracranial hypertension and arterial hypotension may be caused by reduced CPP.     

Desflurane increases intracranial pressure more and sevoflurane less than isoflurane in pigs subjected to intracranial hypertension

Desflurane and sevoflurane may have advantages over isoflurane in neuroanesthesia, but this is still under debate. A porcine model with experimental intracranial hypertension was used for paired comparison of desflurane, sevoflurane, and isoflurane with respect to the effects on cerebral blood flow (CBF), cerebrovascular resistance (CVR), and intracranial pressure (ICP). The agents, given in sequence to each of six pigs, were compared at 0.5 and 1.0 minimal alveolar concentrations (MAC) and three mean arterial blood pressure (MAP) levels (50, 70, and 90 mm Hg) at normocapnia and one MAP level (70 mm Hg) at hypocapnia. MAC for each agent had been previously determined in a standardized manner for comparison reliability. CBF was measured with Xe. MAP was lowered by inflation of a balloon catheter in the inferior caval vein and raised by inflation of a balloon catheter in the descending aorta. ICP was measured intraparenchymally. Two Fogarty catheters positioned extradurally were inflated to a baseline ICP of 20 to 22 mm Hg at 0.2 MAC of each agent. CBF and ICP with the three agents at normocapnia and MAP 70 and 90 mm Hg at both 0.5 and 1.0 MAC were as follows (P < 0.05): desflurane > isoflurane > sevoflurane. None of the agents abolished CO2 reactivity. High-dose desflurane resulted in a higher CBF at hypocapnia than corresponding doses of sevoflurane or isoflurane, but there were no significant differences between the agents in ICP at hypocapnia. The present study showed that desflurane increased ICP more and sevoflurane less than isoflurane during normoventilation, but the differences disappeared with hyperventilation.     

Effects of dihydroergotamine on intracranial pressure, cerebral blood flow, and cerebral metabolism in patients undergoing craniotomy for brain tumors.

In a search for a nonsurgical intervention to control intracranial hypertension during craniotomy, the authors studied the effects of dihydroergotamine on mean arterial blood pressure (MABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and cerebral metabolism in patients who underwent craniotomy for supratentorial brain tumors. Twenty patients were randomized to receive either dihydroergotamine 0.25 mg intravenously or placebo as a bolus dose during craniotomy. Anesthesia was induced with thiopental/fentanyl/atracurium, and maintained with isoflurane/N2O/fentanyl at normocapnia. After removal of the bone flap and exposure of intact dura, ICP was measured subdurally and dihydroergotamine/placebo was administered. Intracranial pressure and MABP were measured continuously. Cerebral blood flow (after intravenous administration of 133Xe) and arteriojugular venous difference of oxygen (AVDO2) were measured before, and 30 minutes after, dihydroergotamine/placebo administration. Cerebral metabolic rate of oxygen (CMRO2) was calculated. After administration of dihydroergotamine, a significant increase in MABP from 74 to 87 mm Hg (median) and CPP from 65 to 72 mm Hg (median) were found. Simultaneously to the increase in MABP, a significant increase in ICP from 9.5 to 11.5 mm Hg (median) was disclosed, whereas no significant differences in CBF, AVDO2, or CMRO2 were found. Intracranial pressure was significantly higher after dihydroergotamine than after placebo. In conclusion, no ICP decreasing effect of a bolus dose of dihydroergotamine was found when administered to patients with brain tumors during isoflurane/N2O anesthesia. Corresponding increases in MABP and ICP suggest that abolished cerebral autoregulation might explain why dihydroergotamine was associated with an ICP increase.     

Cerebral effects of nitrous oxide during isoflurane-induced hypotension in the pig

We have studied the effects of nitrous oxide on cerebral bloodflow (CBF), cerebral blood flow velocity (CBFV) and intracranialpressure (ICP) during isoflurane-induced hypotension in 10 pigs.CBF was measured using laser Doppler flowmetry, CBFV in theright middle cerebral artery was calculated using Doppler ultrasoundand ICP was measured using an extradural ICP monitor. Each animalwas studied under four conditions, examined sequentially: (i)mean intra-arterial pressure (MAP) 85 mm Hg, maintained withisoflurane, (ii) MAP 50–55 mm Hg, induced by isofluraneonly, (iii) MAP 85 mm Hg, maintained with isoflurane and 50%nitrous oxide, and (iv) MAP 50–55 mm Hg, induced by isofluraneand 50% nitrous oxide. No significant differences were notedbetween conditions with respect to ICP. There was a significantdifference in CBF during condition (ii) compared with (i) (mean75(SD 21) vs 100(0) %) and during condition (iv) compared with(iii) (90(26) vs 109(13)%). Animals under condition (iv) exhibiteda 20% reduction in CBFV compared with those under condition(iii) (57 vs 69 cm s^–1). For animals under normotensiveconditions, addition of nitrous oxide to isoflurane resultedin a 16% increase in CBFV (69 vs 60 cm s^–1). Comparingisoflurane-induced hypotension ((ii) vs (iv)), there was nostatistical difference in either CBF or CBFV on addition of50% nitrous oxide. The correlation between changes in CBF andCBFV was not significant. We conclude that the use of nitrousoxide during isoflurane-induced hypotension has no significanteffect on CBF, CBFV or ICP compared with the use of isofluranealone.     

Effects of hyperventilation, CO2, and CSF pressure on internal carotid blood flow in the baboon.

The combined effect upon cerebral blood flow (CBF) of an elevation of cerebrospinal fluid pressure (CSFP) and changes in respiratory CO2 was studied in nine baboons under chloralose anesthesia. The animals were mildly hyperventilated and provided with increasing amounts of CO2 in O2-air. Arterial CO2 tensions (PaCO2) increased from 17 to 58 mm Hg. Internal carotid blood flow (ICBF) was measured at normal CSFP and at hydrostatically maintained 50 mm Hg CSFP. It was found that: 1) end-tidal CO2 may be used as a substitute for arterial PaCO2 determinations; 2) this elevation of CSFP has little effect on ICBF during hypercapnia and normocapnia; however, 3) during hypocapnia the ICBF is reduced an additional 20% when CSFP is elevated; that is, ICBF is reduced 50% from normal when end-tidal CO2 is reduced to 2% at this elevated level of CSFP. Caution should be exercised during hyperventilation therapy particularly if the elevated CSFP or intracranial pressure (ICP) is not reduced to approach normal levels; in these conditions, the combination of decreasing PaCO2 and elevated ICP may reduce CBF below critical levels and thus lead to cerebral hypoxia.     

Cerebral blood flow and metabolism in severely head-injured children. Part 2: Autoregulation

Autoregulation of cerebral blood flow ("CBF15") was tested in a series of 26 pediatric patients (mean age 13.2 years) with severe head injury (average Glasgow Coma Scale (GCS) score 5.5) in the acute stage. A baseline 133Xe CBF measurement was performed and then repeated, after blood pressure was increased by 29% with intravenous phenylephrine or decreased by 26% with intravenous trimethaphan camsylate. Correlations were made between CBF and clinical condition, outcome, time after injury, intracranial pressure (ICP), and pressure-volume index (PVI) changes, and the site of injury (hemispheres, diencephalon, or brain stem). The site of injury was determined with multimodality evoked potential measurements. Autoregulation was intact in 22 (59%) of 37 measurements. There was no correlation with GCS score, outcome, time after injury, site of injury, or way of testing (decreasing or increasing blood pressure). Autoregulation was statistically significantly more often impaired when CBF was either below normal -2 standard deviations (SD) (reduced flow) or above normal +2 SD (absolute hyperemia). In cases with intact autoregulation, mean ICP decreased from 17.5 to 15.0 mm Hg with higher blood pressure and increased from 19.0 to 21.3 mm Hg with lower blood pressure. When PVI was measured during the blood pressure manipulations, it was found to change in a direction opposite to the ICP change. The consequences of these findings in the management of ICP problems with blood pressure control are discussed.     

Relationship between intracranial pressure and critical closing pressure in patients with neurotrauma

BACKGROUND: The driving pressure gradient for cerebral perfusion is the difference between mean arterial pressure (MAP) and critical closing pressure (CCP = zero flow pressure). Therefore, determination of the difference between MAP and CCP should provide an appropriate monitoring of the effective cerebral perfusion pressure (CPP(eff)). Based on this concept, the authors compared conventional measurements of cerebral perfusion pressure by MAP and intracranial pressure (CPP(ICP)) with CPP(eff). METHODS: Simultaneous synchronized recordings of pressure waveforms of the radial artery and blood flow velocities of the middle cerebral artery were performed in 70 head trauma patients. CCP was calculated from pressure-flow velocity plots by linear extrapolation to zero flow. RESULTS: Intracranial pressure measured by intraventricular probes and CCP ranged from 3 to 71 and 4 to 70 mmHg, respectively. Linear correlation between ICP and CCP was r = 0.91. CPP(ICP) was 77 +/- 20 mmHg and did not differ from CPP(eff); linear correlation was r = 0.92. However, limits of agreement were only +/- 16.2 mmHg. Therefore, in 51.4% of the patients, CPP(ICP) overestimated CPP(eff) by 19.8 mmHg at most. CONCLUSION: Assuming that CPP(eff) (MAP - CCP) takes into account more determinants of cerebral downstream pressure, in individual cases, the actual gold standard of CPP determination (MAP - ICP) might overestimate the CPP(eff) of therapeutic significance.     

Cerebral hemodynamic responses to blood pressure manipulation in severely head-injured patients in the presence or absence of intracranial hypertension

The management of cerebral perfusion pressure (CPP) remains a controversial issue in the critical care of severely head-injured patients. Recently, it has been proposed that the state of cerebrovascular autoregulation should determine individual CPP targets. To find optimal perfusion pressure, we pharmacologically manipulated CPP in a range of 51 mm Hg (median; 25th-75th percentile, 48-53 mm Hg) to 108 mm Hg (102-112 mm Hg) on Days 0, 1, and 2 after severe head injury in 13 patients and studied the effects on intracranial pressure (ICP), autoregulation capacity, and brain tissue partial pressure of oxygen. Autoregulation was expressed as a static rate of regulation for 5-mm Hg CPP intervals based on middle cerebral artery flow velocity. When ICP was normal (26 occasions), there were no major changes in the measured variables when CPP was altered from a baseline level of 78 mm Hg (74-83 mm Hg), indicating that the brain was within autoregulation limits. Conversely, when intracranial hypertension was present (11 occasions), CPP reduction to less than 77 mm Hg (73-82 mm Hg) further increased ICP, decreased the static rate of regulation, and decreased brain tissue partial pressure of oxygen, whereas a CPP increase improved these variables, indicating that the brain was operating at the lower limit of autoregulation. We conclude that daily trial manipulation of arterial blood pressure over a wide range can provide information that may be used to optimize CPP management.     

Short-term moderate hypocapnia augments detection of optimal cerebral perfusion pressure

An autoregulation-oriented strategy has been proposed to guide neurocritical therapy toward the optimal cerebral perfusion pressure (CPPOPT). The influence of ventilation changes is, however, unclear. We sought to find out whether short-term moderate hypocapnia (HC) shifts the CPPOPT or affects its detection. Thirty patients with traumatic brain injury (TBI), who required sedation and mechanical ventilation, were studied during 20?min of normocapnia (5.1±0.4?kPa) and 30 min of moderate HC (4.4±3.0?kPa). Monitoring included bilateral transcranial Doppler of the middle cerebral arteries (MCA), invasive arterial blood pressure (ABP), and intracranial pressure (ICP). Mx -autoregulatory index provided a measure for the CPP responsiveness of MCA flow velocity. CPPOPT was assessed as the CPP at which autoregulation (Mx) was working with the maximal efficiency. During normocapnia, CPPOPT (left: 80.65±6.18; right: 79.11±5.84?mm Hg) was detectable in 12 of 30 patients. Moderate HC did not shift this CPPOPT but enabled its detection in another 17 patients (CPPOPT left: 83.94±14.82; right: 85.28±14.73?mm Hg). The detection of CPPOPT was achieved via significantly improved Mx-autoregulatory index and an increase of CPP mean. It appeared that short-term moderate HC augmented the detection of an optimum CPP, and may therefore usefully support CPP-guided therapy in patients with TBI.     

The effects of aortic crossclamping and resuscitation on intracranial pressure, cerebral blood flow, and cerebral water content in a model of focal brain injury and hemorrhagic shock

Aortic crossclamping (AOXC) is performed frequently in hypotensive trauma patients who may have had a head injury. The effect of AOXC on the injured brain is unknown. We studied the effect of AOXC on mean arterial pressure (MAP), intracranial pressure (ICP), cerebral blood flow (CBF), cerebral perfusion pressure (CPP), and cerebral water content in a porcine model of focal cryogenic brain injury. Four groups of animals were studied: Group I--brain injury only; Group II--brain injury and AOXC; Group III--brain injury with hemorrhage and AOXC; and Group IV--AOXC only. Focal cryogenic grain injury increased the ICP in Groups I-III. Aortic crossclamping increased MAP, CBF, ICP, and CPP after hemorrhage in Group III. Following declamping and resuscitation there were no differences between the groups in any studied variable. Cerebral water content at the site of the focal brain injury was greater than in nonlesioned cortex but there was no significant difference between groups despite a greater positive fluid balance in hemorrhaged animals. AOXC improved perfusion to the injured brain without a significant increase in ICP. Increased MAP induced by AOXC and large fluid resuscitation appeared to have no detrimental effect on ICP, CBF, cerebral water content, or CPP in this model of brain injury.     

Efficacy of hyperventilation,blood pressure elevation,and metabolic suppression therapy in controlling intracranial pressure after head injury

OBJECT: Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP. METHODS: Thirty-three patients with a mean age of 33 +/- 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 +/- 5 to 27 +/- 5 mm Hg and in ICP from 20 +/- 11 to 13 +/- 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 +/- 5 mm Hg and ICP increased from 16 +/- 9 to 19 +/- 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 +/- 10 to 16 +/- 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression. CONCLUSIONS: Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.