Critical Cerebral Perfusion Pressure Research Articles

Dynamic Cerebrovascular and Intracranial Pressure Reactivity Assessment of Impaired Cerebrovascular Autoregulation in Intracranial Hypertension.

We previously suggested that the discrepancy between a critical cerebral perfusion pressure (CPP) of 30 mmHg, obtained by increasing intracranial pressure (ICP), and 60 mmHg, obtained by decreasing arterial pressure, was due to pathological microvascular shunting at high ICP [1], and that the determination of the critical CPP by the static cerebral blood flow (CBF) autoregulation curve is not valid with intracranial hypertension. Here, we demonstrated that induced dynamic ICP reactivity (iPRx), and cerebrovascular reactivity (CVRx) tests accurately identify the critical CPP in the hypertensive rat brain, which differs from that obtained by the static autoregulation curve. Step changes in CPP from 70 to 50 and 30 mmHg were made by increasing ICP using an artificial cerebrospinal fluid reservoir connected to the cisterna magna. At each CPP, a transient 10-mmHg increase in arterial pressure was induced by bolus intravenous dopamine. iPRx and iCVRx were calculated as ΔICP/Δ mean arterial pressure (MAP) and as ΔCBF/ΔMAP, respectively. The critical CPP at high ICP, obtained by iPRx and iCVRx, is 50 mmHg, where compromised capillary flow, transition of blood flow to nonnutritive microvascular shunts, tissue hypoxia, and brain-blood barrier leakage begin to occur, which is higher than the 30 mmHg determined by static autoregulation.

Critical cerebral perfusion pressure at high intracranial pressure measured by induced cerebrovascular and intracranial pressure reactivity.

The lower limit of cerebral blood flow autoregulation is the critical cerebral perfusion pressure at which cerebral blood flow begins to fall. It is important that cerebral perfusion pressure be maintained above this level to ensure adequate cerebral blood flow, especially in patients with high intracranial pressure. However, the critical cerebral perfusion pressure of 50 mm Hg, obtained by decreasing mean arterial pressure, differs from the value of 30 mm Hg, obtained by increasing intracranial pressure, which we previously showed was due to microvascular shunt flow maintenance of a falsely high cerebral blood flow. The present study shows that the critical cerebral perfusion pressure, measured by increasing intracranial pressure to decrease cerebral perfusion pressure, is inaccurate but accurately determined by dopamine-induced dynamic intracranial pressure reactivity and cerebrovascular reactivity. Cerebral perfusion pressure was decreased either by increasing intracranial pressure or decreasing mean arterial pressure and the critical cerebral perfusion pressure by both methods compared. Cortical Doppler flux, intracranial pressure, and mean arterial pressure were monitored throughout the study. At each cerebral perfusion pressure, we measured microvascular RBC flow velocity, blood-brain barrier integrity (transcapillary dye extravasation), and tissue oxygenation (reduced nicotinamide adenine dinucleotide) in the cerebral cortex of rats using in vivo two-photon laser scanning microscopy. University laboratory. Male Sprague-Dawley rats. At each cerebral perfusion pressure, dopamine-induced arterial pressure transients (~10 mm Hg, ~45 s duration) were used to measure induced intracranial pressure reactivity (Δ intracranial pressure/Δ mean arterial pressure) and induced cerebrovascular reactivity (Δ cerebral blood flow/Δ mean arterial pressure). At a normal cerebral perfusion pressure of 70 mm Hg, 10 mm Hg mean arterial pressure pulses had no effect on intracranial pressure or cerebral blood flow (induced intracranial pressure reactivity = -0.03 ± 0.07 and induced cerebrovascular reactivity = -0.02 ± 0.09), reflecting intact autoregulation. Decreasing cerebral perfusion pressure to 50 mm Hg by increasing intracranial pressure increased induced intracranial pressure reactivity and induced cerebrovascular reactivity to 0.24 ± 0.09 and 0.31 ± 0.13, respectively, reflecting impaired autoregulation (p < 0.05). By static cerebral blood flow, the first significant decrease in cerebral blood flow occurred at a cerebral perfusion pressure of 30 mm Hg (0.71 ± 0.08, p < 0.05). Critical cerebral perfusion pressure of 50 mm Hg was accurately determined by induced intracranial pressure reactivity and induced cerebrovascular reactivity, whereas the static method failed.

Loss of cerebral blood flow autoregulation and assessment of the critical cerebral perfusion pressure at high ICP (674.14)

Objective: To study the effect of increased intracranial pressure (ICP) on the critical cerebral perfusion pressure (CPP) and its relationship to the loss of cerebral blood flow (CBF) autoregulation.Background: Earlier studies showed that the critical cerebral perfusion pressure (CPP) fell from 60 to 30 mmHg as determined by decreasing arterial pressure as opposed to increasing intracranial pressure (ICP), respectively. We hypothesized that the decrease in the critical CPP at high ICP was due to microvascular shunting resulting in a pathological higher CBF at a lower CPP.Methods: Using two‐photon laser scanning microscopy (2PLSM) we measured microvascular (3‐25 m diam) flow velocity in rat cerebral cortex by increasing ICP or decreasing arterial blood pressure. In separate studies we also increased ICP progressively while monitoring the capillary (CAP) to microvascular shunt (MVS) ratio to study the effect of increasing ICP on the development of microvascular shunts.Results: The reduction in critical CPP with increasing ICP was due to increased microvascular shunting resulting in a sustained CBF at a lower critical CPP, which therefore decreased the critical CPP from 60 to 30 mmHg and associated with increased microvascular shunting. A progressive increase in ICP resulted in a parallel increase in the ratio of MVS/CAP ratio.Conclusion: The decrease in critical CPP obtained when ICP is increased as opposed to decreasing arterial pressure is due to the opening of microvascular shunts thereby creating low resistance microvascular conduits through the brain. The progressive increase in MVS with increasing ICP leads to the loss of CBF autoregulation, which differs from that observed at high CO2.Grant Funding Source: NIH RO3 NS051639;AHA 2BGIA11730011

Role of microvascular shunts in the loss of cerebral blood flow autoregulation.

Historically, determination of the critical cerebral perfusion pressure (CPP) was done in animals by a progressive lowering of arterial pressure yielding a nominal critical CPP of 60 mmHg. Subsequently, it was shown that if the CPP was decreased by increasing intracranial pressure (ICP), critical CPP fell to 30 mmHg. This discrepancy was unexplained. We recently provided evidence that the decrease in critical CPP was due to microvascular shunting resulting in maintained cerebral blood flow (CBF) at a lower CPP. We demonstrated by a progressive increase in ICP in rats using two-photon laser scanning microscopy (2PLSM) that the transition from capillary to microvascular shunt flow is a pathological process. We surmise that the loss of CBF autoregulation revealed by decreasing arterial pressure occurs by dilation of normal cerebral blood vessels whereas that which occurs by increasing ICP is due to microvascular shunting. Our observations indicate that the loss of CBF autoregulation we observed in brain injured patients that changes on an hourly or daily basis reflects an important pathophysiological process impacting on outcome that remains to be determined.

Abstract 42: Cerebrovascular Reactivity (CVRx) and Intracranial Pressure Reactivity (PRx) Assessment of Impaired Cerebrovascular Autoregulation in Intracranial Hypertension

Introduction: We previously showed that the decrease in critical cerebral perfusion pressure (CPP) to 30 mmHg obtained by cerebral blood flow (CBF) autoregulation curve with increasing intracranial pressure (ICP), compared to 60 mmHg when CPP is reduced by decreasing arterial pressure, was due to pathological microvascular shunting at high ICP. We concluded that determination of the critical CPP by the CBF autoregulation curve is not applicable to brains at high ICP. We hypothesized that dynamic ICP (PRx) and cerebrovascular (CVRx) reactivity would better detect impaired autoregulation. Methods: In vivo 2-photon laser scanning microscopy (2PLSM) over the rat parietal cortex was used to measure microvascular (MV) flow velocity, NADH fluorescence (hypoxia) and blood brain barrier (BBB) integrity (fluorescein dye extravasation). Doppler flow, temperatures, ICP, arterial pressure and blood gases were monitored. CPP was reduced stepwise from 70 to 50 and 30 mmHg by increasing ICP. At each CPP, a transient 10 mmHg rise in mean arterial pressure (MAP) was induced by i.v. dopamine bolus. PRx is a ratio of the ICP change in response to MAP increase (PRx=ΔICP/ΔMAP). CVRx is a ratio of the change in CBF with MAP change (CVRx=ΔCBF/ΔMAP). Results: CBF autoregulation curves indicated a critical CPP of 30 mmHg at high ICP. However, our 2PLSM data show that reduction of CPP to 50 mmHg by increasing ICP caused a transition from capillary to microvascular shunt flow associated with brain edema, hypoxia and BBB opening. At a normal CPP (70 mmHg) blood pressure challenge caused no change in ICP (PRx=-0.03±0.07, n=5), i.e., intact pressure reactivity. When CPP was decreased to 50 and 30 mmHg by ICP elevation, PRx increased to 0.09±0.16 and 0.26±0.14, respectively (n=7, p&lt;0.05). Similarly at a normal CPP MAP challenge showed a CVRx of -0.02±0.05, reflecting intact cerebral autoregulation. When CPP was decreased to 50 and 30 mmHg by ICP, CVRx increased to 0.11±0.13 and 0.26±0.14, respectively, reflecting impaired autoregulation (p&lt;0.05). Conclusions: As determined by PRx and CVRx at high ICP the critical CPP is 50 mmHg where MV shunting, brain edema, hypoxia and BBB leakage begin to occur which is higher than the 30 mmHg determined by static autoregulation.

High Intracranial Pressure Effects on Cerebral Cortical Microvascular Flow in Rats

To manage patients with high intracranial pressure (ICP), clinicians need to know the critical cerebral perfusion pressure (CPP) required to maintain cerebral blood flow (CBF). Historically, the critical CPP obtained by decreasing mean arterial pressure (MAP) to lower CPP was 60 mm Hg, which fell to 30 mm Hg when CPP was reduced by increasing ICP. We examined whether this decrease in critical CPP was due to a pathological shift from capillary (CAP) to high-velocity microvessel flow or thoroughfare channel (TFC) shunt flow. Cortical microvessel red blood cell velocity and NADH fluorescence were measured by in vivo two-photon laser scanning microscopy in rats at CPP of 70, 50, and 30 mm Hg by increasing ICP or decreasing MAP. Water content was measured by wet/dry weight, and cortical perfusion by laser Doppler flux. Reduction of CPP by raising ICP increased TFC shunt flow from 30.4±2.3% to 51.2±5.2% (mean±SEM, p<0.001), NADH increased by 20.3±6.8% and 58.1±8.2% (p<0.01), and brain water content from 72.9±0.47% to 77.8±2.42% (p<0.01). Decreasing CPP by MAP decreased TFC shunt flow with a smaller rise in NADH and no edema. Doppler flux decreased less with increasing ICP than decreasing MAP. The decrease seen in the critical CPP with increased ICP is likely due to a redistribution of microvascular flow from capillary to microvascular shunt flow or TFC shunt flow, resulting in a pathologically elevated CBF associated with tissue hypoxia and brain edema, characteristic of non-nutritive shunt flow.

Cerebral Perfusion Pressure Based Management of Traumatic Brain Injury

Cerebral perfusion pressure (CPP) is the difference between mean arterial pressure (MAP) and intracranial pressure (ICP). Traditionally, management of traumatic brain injury (TBI) depended mainly on ICP control strategies. Based on the evidence that cerebral ischemia plays a major role in causing poor neurological outcome in traumatic brain injury (TBI) and cerebral blood flow autoregulation is shifted rightward in these patients, Rosner and colleagues suggested a treatment protocol that advocated maintaining a CPP higher than 70 mmHg, by controlling intracranial hypertension and increasing MAP by using hypervolemia and vasoactive agents, if required. Following the initial studies that showed better outcomes than other contemporary series, a number of studies tried to define the critical CPP in TBI. The threshold values suggested by these studies varied widely between 50 mmHg and higher than 70 mmHg. While there is no controversy about the adverse effects of low CPP, the major concerns in CPP-based therapy are a possible increase in brain oedema with a decrease in intracranial compliance and the systemic complications associated with the interventions used to achieve high CPP. There is no major evidence to suggest that high CPP increases ICP or decreases intracranial compliance. One major randomized trial comparing CPP-based and ICP-based strategies showed a major reduction in the incidence of cerebral ischemia with cerebral blood flow (CBF)-targeted therapy. But the same study also documented a five-fold increase in acute respiratory distress syndrome in patients managed by CPP-based strategy, and similar outcomes between the treatment groups. Following this, the brain trauma foundation (BTF) lowered the suggested CPP threshold to 60 mmHg from its original recommendation of 70 mmHg. Current research is focusing on the possibility of defining the optimal CPP for any given patient based on more objective measures of cerebral oxygenation, metabolism and CBF autoregulation. Critical thresholds of CPP in children remain ill-understood.

Determination of critical cerebral perfusion pressure in cranial hypertension

Determination of critical cerebral perfusion pressure in cranial hypertension

Adequate cerebral perfusion pressure during rewarming to prevent ischemic deterioration after therapeutic hypothermia

Ischemic deterioration during rewarming is one of the most notable clinical complications after successful therapeutic cerebral hypothermia, but the mechanism is not completely understood. Hypothermia may cause vasoconstriction and relative ischemia, especially with insufficient cerebral perfusion pressure (CPP). Various parameters were evaluated to determine the critical CPP threshold to avoid ischemia during rewarming. Cat experimental head injury was induced by inflating an epidural rubber balloon, and intracranial pressure was maintained at 30 mmHg. During rewarming after cerebral hypothermia, CPP was maintained at ≥ 120 mmHg (n = 16), 90 mmHg (n = 11), 60 mmHg (n = 11), and 40 mmHg (n = 4) by controlling the blood pressure. Cerebral blood flow, cerebral metabolic rate for oxygen, arteriovenous difference of oxygen (AVDO2), cerebral venous oxygen saturation (ScvO2), and extracellular glutamate concentrations were monitored by glutamate oxidase electrode. After rewarming, the cerebral metabolic parameters were almost restored to the pre-injury level in animals with CPP of more than 90 mmHg. However, in the animals with CPP = 60 mmHg, all parameters significantly deteriorated and indicated misery perfusion; ScvO2 was low (29.5 ± 1.1%), AVDO2 was significantly high (9.9 ± 0.8 ml 100 g-1 min-1) (one-way analysis of variance, p < 0.05), and electron microscopic features showed subcellular ischemic change. Extracellular glutamate significantly increased during the rewarming period only in the CPP = 40 mmHg group. CPP less than 60 mmHg during rewarming causes secondary ischemic insult, which might indicate continuation of cerebral vasoconstriction in hypothermia. CPP higher than 90 mmHg is required to avoid the potential risk of relative ischemia after hypothermia. [Neurol Res 2002; 24: 271-280]

Appropriate cerebral perfusion pressure during rewarming after therapeutic hypothermia.

This study evaluated the cerebral ischemic parameters during the rewarming period after therapeutic hypothermia to determine the critical cerebral perfusion pressure (CPP) threshold to avoid ischemic deterioration. Cat experimental head injury was induced by inflation of an epidural rubber balloon to maintain intracranial pressure at 30 mmHg under hypothermia. During the rewarming period, CPP was maintained at > or = 120 mmHg, 90 mmHg, and 60 mmHg by controlling the blood pressure. CBF, CMRO2, AVDO2, and cerebral venous oxygen saturation (ScvO2) were measured. Brain extracellular glutamate concentrations were also measured by a dialysis electrode. Histological preparations of all brains were examined under an electron microscope. The cerebral metabolic parameters in animals with CPP of more than 90 mmHg returned to the base values after rewarming. However, ScvO2 was significantly lower (27 +/- 6%) and AVDO2 was significantly higher (9.4 +/- 1.8 ml/100 g/min) after rewarming in the animals with CPP = 60 mmHg, which indicated misery perfusion. Animals with CPP = 60 mmHg also showed increased extracellular glutamate concentration and histological ischemic damage (mitochondrial swelling). CPP of 60 mmHg during the rewarming period is associated with irreversible ischemia, which indicates continuation of cerebral vasoconstriction. Therefore, a CPP of greater than 90 mmHg is required to avoid cerebral ischemia.

Neurochemical changes in ventilated head-injured patients with cerebral perfusion pressure treatment failure.

The goal of intensive care management of patients with head injury is to provide them with a favourable physiological and metabolic environment for recovery of injury-compromised cells, and to prevent secondary brain insults. Clinical intracerebral microdialysis has enabled documentation of the metabolic derangement after head injury. Treatment targeted at this derangement has emphasized maintenance of optimal cerebral perfusion pressure (CPP). To determine the relationships between CPP and five clinically relevant intracerebral extracellular metabolites (glucose, lactate, glycerol, glutamate and pyruvate) in relation to different therapy intensities, 23 moderate to severe head-injury patients with hourly microdialysis samples were studied. These five metabolites were correlated with CPP and showed a biphasic relation at CPP of 65 to 67 mmHg, which was believed to be the critical CPP indicating irreversible brain damage. Relationship between intracerebral metabolites and CPP in relation to different therapy intensities was studied and suggests the critical CPP threshold in head-injured patients with high ICP and maximum therapy is elevated and should be maintained above 70 mmHg to prevent irreversible brain damage.

Advanced neuromonitoring including cerebral tissue oxygenation and outcome after traumatic brain injury

For 51 patients suffering from traumatic brain injury (GCS < 9), we compared the prognostic value of critical parameters derived from neuromonitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP) and brain tissue oxygenation (PtiO2 ) during different time periods after trauma (≤12, ≤24, ≤ 48, ≤72 and ≤96 h). For patients with good outcome (GOS = 4–5, n = 30) the proportion of critical ICP values (> 40 mmHg) was about 0.2% during all time periods. The corresponding proportions for patients with bad outcome (GOS = 1–3, n = 21) rose from 0.2% to 4.7% during increasing time periods. The frequency of critical ICP values was significantly related to outcome (p < 0.001) for time periods > 48 h after trauma. Differences of critical CPP (≤ 50 mmHg) and hypoxic PtiO2 (≤ 5 mmHg) between both outcome groups were less pronounced and for both parameters significant relations to outcome were only obtained for the longest time period (≤ 96 h, p ≤ 0.05). Higher thresholds for CPP (≤ 60 mmHg, ≤ 70 mmHg) did not reveal any relation to outcome. For all neuromonitoring parameters significant relations between the frequency of critical values and outcome could be determined. Critical ICP values provide the earliest and highest prognostic power, while critical CPP and hypoxic PtiO2 only showed prognostic power in later time periods.

INTRACRANIAL PRESSURE (ICP) AND VENOUS CANNULATION FOR CARDIOPULMONARY BYPASS (CPB) IN DOGS

Introduction. At the onset of CPB, the position of the aortic and venous cannulas is assessed. Classically described signs of compromised venous drainage are rare, but partial impedance to superior vena caval (SVC) flow has the potential to elevate ICP and decrease cerebral perfusion pressure. In this abstract we describe the influence of venous cannula position on ICP during cardiopulmonary bypass. Methods. Following IACUC approval, we observed ICP changes on transition to CPB in 15 dogs anesthetized with halothane, fentanyl, and midazolam. For continuous ICP monitoring, an epidural sensor was placed through burr hole. A left-sided thoracotomy was performed and venous drainage was by a 10 mm ID right atrial cannula. The blood was circulated by a centrifugal pump through an oxygenator and returned via a cannula into the root of the aorta. CPB temperature was 34-35[degree sign]C. ICP and MAP were recorded prior to and then each minute following the onset of CPB. CPB flows were adjusted to target a MAP of 50-65 mmHg. If an acute increase in ICP to >or=to 15 mmHg was identified, the surgeon was asked to reposition the venous cannula. Results. In all animals, the intracranial pressure was less than 15 mmHg prior to the onset of bypass. In 5 animals, ICP increased to >or=to 15 mmHg within the first 3 minutes of CPB. Repositioning of the venous cannula quickly returned the ICP to normal in every animal and improved venous return to the reservoir. (Figure 1)Figure 1Discussion. The initiation of CPB is a dynamic period. If MAP is decreased and superior vena caval or ICP pressure is high, then cerebral perfusion may be compromised. We found a third of animals demonstrated elevations in ICP sufficient to reduce cerebral perfusion pressure to below what has been described as the critical cerebral perfusion pressure during tepid CPB in dogs. [1] Observation of internal jugular pressure may be advantageous during the initiation of CPB or during any periods when the perfusionist detects reduced return. If the cannula or heart cannot be promptly repositioned, increasing MAP with a vasoconstrictor may be indicated to maintain cerebral perfusion pressure.

EFFECT OF TEMPERATURE ON CRITICAL CEREBRAL PERFUSION PRESSURE IN DOGS DURING CARDIOPULMONARY BYPASS (CPB)

Introduction. The purpose of this study was to determine the effect of temperature on critical cerebral perfusion pressure during CPB in dogs. The critical perfusion pressure is that mean arterial pressure (MAP) at which cerebral metabolic rate for oxygen (CMRO2) becomes O2 delivery dependent. [1] Methods. Following IACUC approval 27 dogs underwent CPB (thoracic approach) using a fentanyl-midazolam anesthetic and alpha-stat pH management. Cerebral blood flow (CBF), O2 delivery (CDO2), and CMRO2 were determined by the sagittal sinus outflow method. MAP was varied in a random order between 40 and 80 mmHg and the MAP at which cerebral variables became MAP dependent were determined at 38[degree sign]C (n=9), 28[degree sign]C (n=9), and 18[degree sign]C (n=9). Results. CDO2 was reduced in all 3 groups when the MAP < 50mmHg. At 38[degree sign]C and 28[degree sign]C, CMRO2 was reduced when MAP was < 50 mmHg and < 45 mmHg respectively. At 18[degree sign] C, CMRO2 remained unchanged to a MAP as low as 40 mmHg. Intracranial pressure remained stable and was less than 10 mmHg in all groups during all of the study periods. (Table 1)Table 1Discussion. The autoregulatory curve showed a trivial leftward shift between 38[degree sign] and 28[degree sign]C. The mean arterial pressure at which cerebral oxygen consumption becomes pressure dependent only shows a 5 mmHg leftward shift between 38[degree sign] and 28[degree sign]C where most CPB is performed. With profound hypothermia, a MAP of 40 mmHg is tolerated. These data provide some physiologic basis for management of MAP at varying CPB temperatures.

Intracranial pressure and venous cannulation for cardiopulmonary bypass.

The onset of cardiopulmonary bypass (CPB) is a period of changing hemodynamics, and during this transition, the position of the aortic and venous cannulas is assessed. Increased arterial line pressures may indicate a malposition of the aortic cannula, whereas reduced venous return to the reservoir of the CPB circuit suggests suboptimal position of a venous cannula. Classically described signs of compromised venous drainage, such as engorgement of the head and neck, are rare, and incomplete obstruction of the superior vena cavae may be difficult to detect clinically but can significantly alter cerebral physiology. Impedance to superior vena caval (SVC) flow may increase intracranial pressure (ICP) and decrease cerebral perfusion pressure (CPP) (CPP 5 mean arterial pressure [MAP] 2 [ICP] (1). In the experimental setting, we have incidentally, but repeatedly, observed this effect. The same physiologic phenomenon is of relevance in the operating suite and may bear on practice. The purpose of this article is to briefly describe the influence of venous cannula position on ICP during CPB.

Intracranial Pressure and Venous Cannulation for Cardiopulmonary Bypass

Intracranial Pressure and Venous Cannulation for Cardiopulmonary Bypass

Critical cerebral perfusion pressure during tepid heart operations in dogs

Background. The management of blood pressure during cardiopulmonary bypass varies widely. This may be particularly relevant with the trend to warmer bypass temperatures and an older patient population. Therefore, we examined the minimal perfusion pressure that maintains cerebral oxygen delivery during cardiopulmonary bypass at 33°C. Methods. Ten dogs were placed on bypass and body temperature was reduced to 33°C (α-stat pH management). At six randomly ordered mean arterial blood pressures (35, 40, 45, 50, 60, and 70 mm Hg), cerebral blood flow, oxygen delivery, and metabolic rate were determined. Results. Cerebral oxygen delivery was stable if the mean arterial pressure was greater than or equal to 60 mm Hg. If mean arterial pressure was less than or equal to 50 mm Hg, cerebral oxygen delivery decreased, and at less than 45 mm Hg cerebral ischemia was seen. Conclusions. In a dog without vascular disease, the brain becomes perfusion pressure-dependent at a mean arterial pressure of approximately 50 mm Hg. There is no leftward shift of the cerebral autoregulatory curve during bypass at 33°C. Greater support of mean arterial pressure during “tepid” cardiopulmonary bypass is indicated in the current adult surgical population that is older and has vascular comorbidity.

Mechanical conditions of rebound of the intracranial pressure after a period of cerebral compression.

Brain compression of precisely defined degree and duration was produced by means of expansion of a supratentorial epidural balloon in anaesthetized and mechanically ventilated dogs. After deflation of the balloon there was a rebound of the intracranial pressure (ICP) to values in the range 30-89 mm Hg when critical thresholds of time and compression had been exceeded during the period of compression. A time versus cerebral perfusion pressure (CPP) graph indicated a CPP threshold of about 50 mm Hg and time threshold of about 6 min. Within these limits the critical CPP varied as a function of time. The ICP rebound had an approximately exponential time course with an initial rapid rise levelling off towards a final plateau in about 30 min. The final value was dependent on the time of compression but independent of the CPP. A transtentorial pressure gradient was induced during the compression phase and reestablished after the decompression when a rebound of ICP developed. Hydrostatic compression by means of infusion of fluid into the subarachnoid space was followed by a rebound of ICP in only 2/21 of the experiments in spite of time and CPP parameters which crossed the critical thresholds defined in the balloon compression experiments. These results support the hypothesis that the rebound phenomenon is related to an ischaemic mechanism. The difference in incidence of rebound in balloon compression and hydrostatic compression can probably be accounted for by a greater depth of ischaemia in the former case because of a direct compressive effect on the vascular bed by the balloon.

Relationships between dopamine infusions and intracranial hemodynamics in patients with raised intracranial pressure

Dopamine, 1–10 μg/kg body weight/min was infused in 6 patients suffering from cerebrovascular diseases with elevated intracranial pressure and a critical cerebral perfusion pressure. Dopamine decreased intracranial pressure in 3 and increased it moderately in the other 3 patients. In all patients, the dopamine-induced rise of mean arterial pressure led to an increase of cerebral perfusion pressure. Transcranial Doppler ultrasonographic recordings of the middle cerebral artery in patients whose intracranial pressure declined revealed a decrease of the pathologically elevated cerebrovascular resistance, and an augmentation of cerebral blood supply. In conclusion, dopamine infusions may improve cerebral hemodynamics in some patients with severe brain edema. Such patients can be identified by intracranial pressure and Doppler monitoring.