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Objective: The pressure-volume index (PVI) can be used to assess the cerebrospinal fluid dynamics and intracranial elastance in critically ill brain injured patients. The dependency of PVI on the state of cerebral autoregulation within the physiologic range of cerebral perfusion pressure (CPP) can be described by mathematical models that account for changes in cerebral blood volume during PVI testing. This relationship has never been verified clinically using direct PVI measurement and independent cerebral autoregulation assessment.Design, Setting, and Patients: PVI and cerebral autoregulation were prospectively assessed in a cohort of 19 comatose patients admitted to an academic intensive care unit in Brescia, Italy.Intervention: None.Methods: PVI was measured injecting a fixed volume of 2 ml of 0.9% sodium chloride solution into the cerebral ventricles through an intraventricular catheter. Cerebral autoregulation was assessed using transcranial Doppler transient hyperaemic response (THR) test.Measurements and Results: Fifty-nine PVI assessments and 59 THR tests were performed. Mean PVI was 20.0 (SD 10.2) millilitres in sessions when autoregulation was intact (THR test >or=1.1) and 31.6 (8.8) millilitres in sessions with defective autoregulation (THR test <1.1) (DeltaPVI = 11.7 ml, 95% CI = 4.7-19.3 ml; P = 0.002). Intracranial pressure, CPP and brain CT findings were not significantly different between the measurements with intact and disturbed autoregulation.Conclusions: Cerebral autoregulation status can affect PVI estimation despite a normal CPP. PVI measurement may overestimate the tolerance of the intracranial system to volume loads in patients with disturbed cerebral autoregulation. [ABSTRACT FROM AUTHOR]

The pressure–volume index (PVI) can be used to assess the cerebrospinal fluid dynamics and intracranial elastance in critically ill brain injured patients. The dependency of PVI on the state of cerebral autoregulation within the physiologic range of cerebral perfusion pressure (CPP) can be described by mathematical models that account for changes in cerebral blood volume during PVI testing. This relationship has never been verified clinically using direct PVI measurement and independent cerebral autoregulation assessment. PVI and cerebral autoregulation were prospectively assessed in a cohort of 19 comatose patients admitted to an academic intensive care unit in Brescia, Italy. None. PVI was measured injecting a fixed volume of 2 ml of 0.9% sodium chloride solution into the cerebral ventricles through an intraventricular catheter. Cerebral autoregulation was assessed using transcranial Doppler transient hyperaemic response (THR) test. Fifty-nine PVI assessments and 59 THR tests were performed. Mean PVI was 20.0 (SD 10.2) millilitres in sessions when autoregulation was intact (THR test ≥1.1) and 31.6 (8.8) millilitres in sessions with defective autoregulation (THR test <1.1) (ΔPVI = 11.7 ml, 95% CI = 4.7–19.3 ml; P = 0.002). Intracranial pressure, CPP and brain CT findings were not significantly different between the measurements with intact and disturbed autoregulation. Cerebral autoregulation status can affect PVI estimation despite a normal CPP. PVI measurement may overestimate the tolerance of the intracranial system to volume loads in patients with disturbed cerebral autoregulation. [ABSTRACT FROM AUTHOR]

Recent studies have demonstrated that bedside cranial burr hole and insertion of intraparenchymal catheters for intracranial pressure monitoring performed by intensive care physicians is a safe procedure, with a complication rate comparable to other series published by neurosurgeons. The overall morbidity rate is comparable to, or even lower than, that caused by central vein catheterization. The procedure is also quite simple and modern disposable intracranial procedural kits are available. After the skin is prepped the land- mark for skin incision, called the 'Kocher's point', located about 2-A cm lateral to the midline (mid-pupillary line) and 2-3 cm anterior to the coronal suture, is found. Then the surgical field is prepared with the sterile drapes and the skin infiltrated with local anaesthetic (0.5% lidocaine with 1: 200 000 epinephrine). After skin incision and retraction of the skin and subcutaneous tissue, the periosteum should be scraped off in order expose the skull. The skin is then divaricated, exposing the underlying bone. The hole is drilled with either an electric drill or a twist drill (the drilling procedure must be performed with the drill held within 100 of the perpendicular position to the incision site). The hole is then irrigated with sterile saline and an 18-G spinal needle may be used to open the dura (exercise caution when perforating the dura so as to avoid damage to the underlying structures). Following opening of the dura, the Bolt, containing a stylet, is screwed manually into the skull at approximately 5 mm to 1 cm for adults. The stylet is then removed after the bolt has been screwed in, after which the bolt should be filled with saline. Finally, the zeroing of the transducer is performed by simply holding the tip in air while zeroing on the monitor. The transducer is inserted inside the bolt and the screw tightened. The intracranial pressure value can then be read. [ABSTRACT FROM AUTHOR]

Transcranial Doppler is an innovative, flexible, accessible tool for the bedside monitoring of static and dynamic cerebral flow and treatment response. Introduced by Rune Aaslid in 1982, it has become indispensable in clinical practice. The main obstacle to ultrasound penetration of the skull is bone. Low frequencies, 1-2 MHz, reduce the attenuation of the ultrasound wave caused by bone. Transcranial Doppler also provides the advantage of acoustic windows representing specific points of the skull where the bone is thin enough to allow ultrasounds to penetrate. There are four acoustic windows: transtemporal, transorbital, suboccipital and retromandibular. The identification of each intracranial vessel is based on the following elements: (a) velocity and direction; (b) depth of signal capture; (c) possibility of following the vessel its whole length; (d) spatial relationship with other vessels; and (e) response to homolateral and contralateral carotid compression. The main fields of clinical application of transcranial Doppler are assessment of vasospasm, detection of stenosis of the intracranial arteries, evaluation of cerebrovascular autoregulation, non-invasive estimation of intracranial pressure, measure of effective downstream pressure and assessment of brain death. Mean flow velocity is directly proportional to flow and inversely proportional to the section of the vessel. Any circumstance that leads to a variation of one of these factors can thus affect mean velocity. The main pathological condition affecting flow velocity is the vasospasm. Vasospasm is a frequent complication of subarachnoid haemorrhage, it often remains clinically silent and the factors that make it symptomatic are largely unknown. Threshold velocities above which vasospasm comes into place are well defined as regards the median cerebral artery, while there is no consensus for the other vessels. Nevertheless, an increase in velocity alone is not sufficient to arrive at a diagnosis of vasospasm; a condition of hyperaemia also presents with an increase in flow velocity. The Lindegaard Index has therefore been introduced, which is defined by the ratio between the mean flow velocity in the median cerebral artery and the mean flow velocity in the internal carotid artery. Criteria for diagnosis of a stenosis >50% of an intracranial vessel with transcranial Doppler include: (a) segmentary acceleration of flow velocity; (b) drop in velocity below the stenotic segment; (c) asymmetry; and (d) circumscribed flow disturbances (turbulence and musical murmur). The transcranial Doppler enables us to assess both components of self-regulation. The static component is measured by observing changes in flow velocity caused by pharmacologically induced episodes of hypertension and hypotension. The dynamic component of autoregulation can be measured using a method devised by Aaslid known as the 'cuff test'. A very effective and safe device for measuring cerebral autoregulation is the transient hyperaemic response test. This test is based on the compensatory vasodilatation of the arterioles, which occurs after brief compression of the common carotid. Csonyka proposed the following formula based on clinical observation for the calculation of cerebral perfusion pressure: CPP = MAP X FVd/FVm + 14. Brain death is defined as the irreversible cessation of all functions of the whole brain. The clinical criteria are usually considered sufficient to establish a diagnosis of brain death; however, they might not be sufficient in patients who have been on sedatives or when there are ethical or legal controversies. Many authors have demonstrated the existence of a transcranial Doppler pattern, which is typical of brain death. [ABSTRACT FROM AUTHOR]

Objective: Work of breathing (WoB) is currently employed to assess the afterload on the respiratory muscles and to estimate the energy expenditure for breathing. Since WoB depends on the ventilated tidal volume (TV), WoB*L(-1), the indicized form of WoB has been employed as a measure of WoB which is independent of TV. Actually, the independence of WoB*L(-1) from the ventilated TV has never been demonstrated. The aim of this study was to verify the predicted TV-independence of WoB*L(-1) on an in vitro model.Methods: Our experimental model was constituted as follows: two endotracheal tubes, with internal diameter measuring respectively 6.5 and 8.5 mm, were alternatively connected with two rubber balloons whose compliance was respectively 0.02 and 0.06 L/hPa; the system was mechanically ventilated at ten different tidal volumes, ranging from 0.3-1 l. Flow rate was kept constant (35 l/m) during the whole experiment.Results: Both elastic components of the model showed a static volume-pressure relationship which was linear in the experimental range of TV. In all combinations of resistance and compliance WoB increased quadratically whereas WoB*L(-1) increased linearly with the growing TV (p < 0.001).Conclusions: These results demonstrate the TV-dependence of WoB*L(-1) and suggest that WoB*L(-1), if TV changes, cannot be considered as an index of respiratory muscle afterload and should not be used as a guide for weaning patients from the mechanical ventilation. Finally, we introduced a new parameter (WoB1L) which seems to be a more TV-independent measure of respiratory work. [ABSTRACT FROM AUTHOR]