Federico Villa

Effects of periodic lung recruitment maneuvers on gas exchange and respiratory mechanics in mechanically ventilated acute respiratory distress syndrome (ARDS) patients.

Objective: We wished to investigate whether volume recruitment maneuvers (VRMs) could improve alveolar recruitment and oxygenation in acute respiratory distress syndrome (ARDS) patients, ventilated at relatively low positive end-expiratory pressure (PEEP). Setting: General intensive care unit (ICU) located in a teaching hospital. Patients: 15 PEEP responder ARDS patients undergoing continuous positive pressure ventilation (CPPV) with sedation and muscle paralysis. Interventions: We identified a low (9.4 ± 3 cmH2O) and a high (16.0 ± 2 cmH2O) level of PEEP associated with target oxygenation values. Using a custom modified mechanical ventilator, we applied in random order three steps lasting 30 min: (1) CPPV at the low PEEP level (CPPVlo); (2) CPPV at the high PEEP level (CPPVhi); (3) CPPV at low PEEP with the superimposition of periodic VRMs (CPPVvrm). VRMs were performed twice a minute by increasing PEEP to the high level for two breaths. Each brace of two breaths was spaced 30 seconds from the preceding one. Measurements and results: We measured gas exchange, hemodynamics, respiratory mechanics, and the end expiratory lung volume (EELV). Compared to CPPVlo, CPPVvrm resulted in higher PaO2 (117.9 ± 40.6 vs 79.4 ± 13.6 mmHg, P < 0.01) and EELV (1.50 ± 0.62 vs 1.26 ± 0.50 l, P < 0.05), and in lower venous admixture (Qva/Qt) (0.42 ± 0.07 vs 0.48 ± 0.07, P < 0.01). During CPPVhi, we observed significantly higher PaO2 (139.3 ± 32.5 mmHg) and lower Qva/Qt (0.37 ± 0.08) compared to CPPVlo (P < 0.01) and to CPPVvrm (P < 0.05). Conclusions: VRMs can improve oxygenation and alveolar recruitment during CPPV at relatively low PEEP, but are relatively less effective than a continuous high PEEP level.

Induced abdominal compartment syndrome increases intracranial pressure in neurotrauma patients: A prospective study

pObjectiveTo evaluate the effect of a stepwise increase in intra-abdominal pressure (IAP) on intracranial pressure (ICP) and to further define the pressure transmission characteristics of different body compartments. DesignA prospective, nonrandomized study. SettingA multidisciplinary intensive care unit at a university medical center. PatientsFifteen patients with moderate-to-severe head injury. InterventionsAll patients were studied after the initial stabilization and resolution of intracranial hypertension. Measurements were carried out before and 20 mins after IAP was increased by positioning a soft, 15-L water bag on the patient’s abdomen. Measurements and Main Results Placing weights upon the abdomen generated a significant increase in IAP, which rose from 4.7 ± 2.9 to 15.5 ± 4.1 mm Hg (p < .001). The rise in IAP caused concomitant and rapid increases in central venous pressure (from 6.2 ± 2.4 to 10.4 ± 2.9 mm Hg;p < .001), internal jugular pressure (from 11.9 ± 3.2 to 14.3 ± 2.4 mm Hg;p < .001), and ICP (from 12.0 ± 4.2 to 15.5 ± 4.4 mm Hg;p < .001). Thoracic transmural pressure, calculated as the difference between central venous pressure and esophageal pressure, remained constant during the protocol. Respiratory system compliance decreased from 58.9 ± 9.8 to 44.9 ± 9.4 mL/cm H2O (p < .001) in all patients because of decreased chest wall compliance. The mean arterial pressure increased from 94 ± 11 to 100 ± 13 mm Hg (p < .01), which allowed the maintenance of a stable cerebral perfusion pressure (82.4 ± 10.3 vs. 84.7 ± 11.5 mm Hg;p = NS) despite the ICP increase. ConclusionsIncreased IAP causes a significant rise in ICP in head trauma patients. This effect seems to be the result of an increase in intrathoracic pressure, which causes a functional obstruction to cerebral venous outflow. Routine assessment of IAP may help clinicians to identify remediable causes of increased ICP. Caution should be used when applying laparoscopic techniques in neurotrauma patients.

Brain multimodality monitoring: an update.

Purpose of reviewAn important goal of neurocritical care is the management of secondary brain injury (SBI), that is pathological events occurring after primary insult that add further burden to outcome. Brain oedema, cerebral ischemia, energy dysfunction, seizures and systemic insults are the main components of SBI. We here review recent data showing the clinical utility of brain multimodality monitoring (BMM) for the management of SBI. Recent findingsDespite being recommended by international guidelines, standard intracranial pressure (ICP) monitoring may be insufficient to detect all episodes of SBI. ICP monitoring, combined with brain oxygen (PbtO2), cerebral microdialysis and regional cerebral blood flow, might help to target therapy (e.g. management of cerebral perfusion pressure, blood transfusion, glucose control) to patient-specific pathophysiology. Physiological parameters derived from BMM, including PbtO2 and microdialysis lactate/pyruvate ratio, correlate with outcome and have recently been incorporated into neurocritical care guidelines. Advanced intracranial devices can be complemented by quantitative electroencephalography to monitor changes of brain function and nonconvulsive seizures. SummaryBMM offers an on-line comprehensive scrutiny of the injured brain and is increasingly used for the management of SBI. Integration of monitored data using new informatics tools may help optimize therapy of brain-injured patients and quality of care.

inhalation versus endovenous sedation in subarachnoid hemorrhage patients: effects on regional cerebral blood flow*

Objective: Isoflurane is a volatile anesthetic that has a vasodilating effect on cerebral vessels producing a cerebral blood flow increase. Furthermore, it has been shown in animal studies that isoflurane, when used as a preconditioning agent, has neuroprotective properties, inducing tolerance to ischemia. However, it is not routinely used in neurointensive care because of the potential increase in intracranial pressure caused by the rise in cerebral blood flow. Nevertheless, subarachnoid hemorrhage patients who are at risk for vasospasm may benefit from an increase in cerebral blood flow. We measured regional cerebral blood flow during intravenous sedation with propofol and during sedation with isoflurane in patients with severe subarachnoid hemorrhage not having intracranial hypertension. Design: The study is a crossover, open clinical trial (NCT00830843). Setting: Neurointensive care unit of an academic hospital. Patients: Thirteen patients with severe subarachnoid hemorrhage, (median Fisher scale 4), monitored on clinical indication with intracranial pressure device and a thermal diffusion probe for the assessment of regional cerebral blood flow. An intracranial pressure >18 mm Hg was an exclusion criterion. Interventions: Cerebral and hemodynamic variables were assessed at three steps. Step 1: sedation with propofol 3–4 mg/kg/hr; step 2: after 1hr of propofol discontinuation and isoflurane 0.8%; step 3: after 1hr of propofol at the same previous infusion rate. Cerebral perfusion pressure and arterial PCO2 were maintained constant. Mean cerebral artery flow velocity and jugular vein oxygen saturation were measured at the end of each step. Measurements and Main Results: Regional cerebral blood flow increased significantly during step 2 (39.3±29mL/100 hg/min) compared to step 1 (20.8±10.7) and step 3 (24.7±8). There was no difference in regional cerebral blood flow comparing step 1 vs. step 3. No significant difference in intracranial pressure, mean cerebral artery transcranial Doppler velocity, PaCO2, cerebral perfusion pressure between the different steps. Conclusions: Isoflurane increases regional cerebral blood flow in comparison to propofol. Intracranial pressure did not change significantly in the population not affected by intracranial hypertension.

Sedation and Analgesia in Neurointensive Care

In the neurointensive care setting, specific considerations of sedation are required; sedation may act as a therapeutic agent itself, when causing a reduction in cerebral metabolic rate of oxygen, cerebral blood flow, and intracranial pressure and in the incidence of seizures. However, the physician must be aware of the effects of every sedative agent on cerebral physiology, in order to obtain beneficial effects and avoid side effects. In this chapter, the effects of sedative agents on cerebral physiology are described in order to provide knowledge for an adequate sedative strategy.