The importance of valve alignment in determining the pressure/flow characteristics of differential pressure shunt valves with anti-gravity devices.

OBJECT: The proper functioning of shunt valves in vivo is dependent on many factors, including the valve itself, the anti-siphon device or ASD (if included), patency of inlet and outlet tubing, and location of the valve. One important, but sometimes overlooked, consideration in valve function is the valve location relative to the tip of the ventricular inlet catheter. As with any pressure measurement, the zero or reference position is an important concept. In the case of shunt valves, the position of the proximal inlet catheter tip is fixed and therefore serves as the reference point for all pressure measurements. This study was conducted to document the importance of this relationship for the pressure/flow characteristics of the shunt valve. METHODS: We bench-tested differential pressure valves (with integral anti-gravity devices; AGDs) from three manufacturers. Valves were connected to an "infinite" reservoir, and the starting head pressure for each was determined from product inserts. The inlet catheter tip was fixed at this position, and the valve body was moved in relation to the inlet catheter tip. Outflow rates were determined gravimetrically for positions varying between 4 cm above and 8 cm below the inlet catheter tip. CONCLUSIONS: All differential pressure valves utilized in this study that contained AGDs showed significant increases in outflow rate as the valve body was moved incrementally below the level of the inlet catheter tip. To allow functioning as a zero-hydrostatic pressure differential pressure valve, the AGD and the inlet catheter tip should be aligned at the same horizontal level.

The importance of shunt valve position in flow characteristics of the Medtronic PS Medical Delta valve.

This study was conducted to document the extent to which flow depends on valve position in relation to head-pressure reference. Medtronic PS Medical Delta valves (contour model, performance levels 0.5, 1.0, 1.5, and 2.0) were studied in a bench test designed to evaluate flow rates with respect to valve position in relation to the head-pressure reference postion. The valves were connected to an "infinite" reservoir by the standard inlet catheter. An initial head (proximal) pressure was selected for each valve based on package insert data. The position of the inlet catheter tip was fixed at this starting head pressure, thus making the inlet catheter tip position the reference for relative head pressures on the valve assembly. When the valve body is positioned above this level, the effective head pressure is lowered, and when the valve body is positioned below this level, the effective head pressure is raised. Flow was established with the siphon control portion of the valve body located on the same horizontal level as the inlet catheter tip (the reference head pressure or "0" position). A standard silastic catheter was attached to the outlet of the valve, and its length was fixed at 50 cm for all valves (-50 cm H(2)0). The distal end of the outlet catheter was connected to a fraction collector, and 1-minute samples (five replicates) were collected for gravimetric determination of flow rate. The valve assembly was then moved in 1-cm increments through the range of 4 cm above to 8 cm below the head-pressure reference position. Samples were collected from each position (4 cm to -8 cm) relative to the inlet catheter tip. Flow rate, in milliliters/hour, was plotted against both relative position (4 cm to -8 cm) and absolute head pressure (in centimeters of water). Each of the valves tested was shown to have a linear relationship between flow and position relative to the inlet catheter tip (or absolute head pressure). The average increase in flow per centimeter of displacement of valve from catheter tip was 16.5 ml/hr/cm (range 14.4-17.6 ml/hr/cm). Once the inlet catheter tip is fixed in position, it serves as a pressure reference. Movement of the valve above this level results in a net decrease in effective head pressure, and movement below this position results in a net increase in effective head pressure. Thus, the positioning of shunt valves in locations different from this pressure reference position should be performed only with the knowledge that significant increases in outflow rate may occur when the valve body is positioned lower than the inlet catheter tip. This increase in outflow rate is not the result of siphoning or a defect in the antisiphon device but instead the result of a net increase in effective head pressure.

ICP-CBF trauma bolt, laboratory evaluation.

Thermal diffusion flowmetry is a continuous quantitative technique of measuring regional cerebral blood flow utilizing a silastic strip probe placed through a craniotomy or craniectomy in the operating room. A new bolt like application of this technology is now available for commercial use and is especially designed for bedside placement in trauma patients. This new trauma bolt is tested in juvenile pigs who are subjected to episodes of hypercapnea to increase cerebral blood flow, and records significant changes in blood flow. Another feature of the trauma bolt is a second port for the placement of an intracranial pressure (ICP) monitor. Placement of the probe and ICP monitor were easier than with the silastic probe and had relatively little complication.

The effect of apnea on brain compliance and intracranial pressure.

The effect of 2 minutes of apnea during endotracheal intubation on intracranial pressure (ICP), compliance, and cerebral blood volume (CBV) was studied in 19 adult dogs during normo-, hypo-, and hypercapnia. The compliance was measured from the cisterna magna in response to an intrathecal bolus injection (pressure-volume index). CBV was monitored by radiolabeled red blood cell activity. These measurements were made before and after 2 minutes of apnea. At normocapnia (pCO2 of 35-40 mm Hg), a period of apnea resulted in an increase in ICP from 9.6 to 26.3 mm Hg, a decrease in compliance from 0.051 to 0.020 ml/mm Hg (60%), and an increase in CBV of 0.26 ml (9.6%). When the animals were hypocapnic (pCO2 of 24-28 mm Hg), ICP increased from 12.8 to 19.6 mm Hg, compliance fell from 0.041 to 0.029 ml/mm Hg(29%), and CBV increased 0.07 ml (3.1%). Hypercapnia (pCO2 of 50-58 mm Hg) before apnea resulted in an increase in ICP from 21.5 to 47.1 mm Hg, a decrease in compliance from 0.032 to 0.015 ml/mm Hg (52%), and an increase in CBV of 0.41 ml (13.4%). These results suggest that hyperventilation (hypocapnia) before intubation limits the adverse decrease in brain compliance and increase in ICP by reducing changes in cerebral blood volume.

Effect on intracranial pressure of furosemide combined with varying doses and administration rates of mannitol.

The first part of this study investigated the combined use of furosemide and mannitol in the treatment of elevated intracranial pressure (ICP). Two groups of dogs were studied to determine if renal excretion of mannitol was altered in the presence of furosemide. No significant difference in excretion was noted between the two groups. Fifteen animals were used in other studies to identify the most advantageous sequence of administration of furosemide and mannitol. Infusion of mannitol followed by furosemide 15 minutes later resulted in the most profound and sustained ICP reduction. The effect on ICP reduction of varying the mannitol dose was observed in studies using single doses of 0.5 gm/kg, 0.75 gm/kg, and 1 gm/kg. The larger mannitol dose, resulting in a greater blood-brain osmotic gradient, proved to be the most efficacious in ICP reduction. A further 15 animals were used in investigations to determine whether changing the rate of delivery of the most effective mannitol dose (1 gm/kg) influenced resultant ICP reduction. The results indicated that rapid administration (2 ml/kg/min) produced higher peak serum concentrations of mannitol and more profound lowering of ICP than the same dose delivered at slower rates.

Choroid plexus Na+/K+-activated adenosine triphosphatase and cerebrospinal fluid formation.

The quantitative relationship between intraventricular fluid formation and choroid plexus Na+/K+-activated (transport) adenosine triphosphatase (ATPase) was studied in rabbit and dog by perfusing the ventricular system with a solution containing ouabain (10(-8) to 10(-3) M). The effect of ouabain in the same range of concentrations on ATPase activity was also measured by the release of inorganic orthophosphate from in vitro choroid plexus tissue. Normally, about 20 to 25% of ATPase activity in lateral ventricle plexus is Na+/K+-activated, and this component is almost completely inhibited by ouabain in a concentration of 10(-4) M. At this concentration, the rate of intraventricular cerebrospinal fluid (CSF) formation is decreased some 70 to 80% in dog and rabbit. The results of this study suggest that a portion of the intraventricular fluid formation is insensitive to cardiac glycoside inhibition and that either there are two different mechanisms responsible for choroid plexus fluid formation or there is a significant non-ATPase dependent extrachoroidal source of CSF.

Effect of mannitol and furosemide on blood-brain osmotic gradient and intracranial pressure.

The effect of mannitol (1.0 gm/kg) and furosemide (0.7 mg/kg), alone and in combination, on the blood-brain extracellular fluid and cerebrospinal fluid (CSF) osmotic gradient, elevated intracranial pressure (ICP), CSF and serum osmolality, and urine output was studied in 26 mongrel dogs. Mannitol and furosemide, when used together, produced a greater (62.4% versus 56.6%) and more sustained (5 hours versus 2 hours) fall in ICP than mannitol alone. This correlated with a prolongation of the reversal of the blood-brain osmotic gradient (-3.4 to + 38.5 mOsm/kg) and a rate of urine formation 15 times control values. There was a transient but not significant fall in serum Na+ with the combined treatment, but the arterial pressure did not vary from pretreatment levels. The results from this present study suggest that the distal loop diuretics in a dose of less than 1.0 mg/kg act synergistically with mannitol by causing preferential excretion of water over solute in the renal distal tubule, and thereby sustaining the osmotic gradient initially established by the mannitol infusion. It is possible, but unlikely in the doses used, that the additive effect of furosemide on reducing ICP in the presence of mannitol is due to interference with CSF formation or Na+ and H2O movement across the blood-brain barrier.

Starvation-induced changes in transport of ketone bodies across the blood-brain barrier.

The permeability of the blood brain barrier (BBB) to beta-hydroxybutyrate (beta-HB) was computed in fed and starved (five days) rats by the simultaneous measurement of cerebral blood flow (diffusible indicator method-123I-iodoantipyrine) and brain uptake of 14C-beta-HB (relative to a 3H2O reference). The results from the present study demonstrate that the movement of beta-HB across the BBB in rat is by a carrier-mediated process. During starvation, total movement (carrier-mediated and diffusionary) of this ketone body into brain was observed to be enhanced because of an increase in the diffusionary loss across the cerebral capillary. The calculated transport kinetics also suggest that the beta-HB molecule has a greater affinity for the transport (mediator) protein during starvation, although the maximal rate of uptake by brain due to a carrier processes mediated Vmax is decreased either because there is a smaller quantity of the mediating molecule or because there is trans inhibition by a high cellular concentration of beta-HB or some analog.

Blood-brain barrier restoration following cold injury.

Cerebral blood flow (CBF), 113mIndium-DPTA, and 14C-glucose extraction were measured simultaneously in rat brain from 2 to 58 days following a thermal insult. In the early stage of a cold induced lesion (2 days), the blood-brain barrier (BBB) was disrupted with resulting leakage and diffusionary loss of both glucose and indium-DPTA. The adjacent, nonnecrotic brain showed similar but more subtle changes. In both areas, CBF was markedly reduced. CBF and augmented loss of glucose and Indium-DPTA continued in the epicenter of the lesion for up to 58 days postinjury while the BBB function in the brain areas surrounding the lesion returned toward normal. These findings were consistent with observation of disruption of BBB activity and of immature brain capillaries during the reparative period.