Resuscitation of haemorrhagic shock with normal saline vs. lactated Ringer's: effects on oxygenation, extravascular lung water and haemodynamics.

INTRODUCTION: Pulmonary oedema and impairment of oxygenation are reported as common consequences of haemorrhagic shock and resuscitation (HSR). Surprisingly, there is little information in the literature examining differences in crystalloid type during the early phase of HSR regarding the development of pulmonary oedema, the impact on oxygenation and the haemodynamic response. These experiments were designed to determine if differences exist because of crystalloid fluid type in the development of oedema, the impact on oxygenation and the haemodynamic response to fluid administration in early HSR. METHODS: Twenty anaesthetised swine underwent a grade V liver injury and bled without resuscitation for 30 minutes. The animals were randomised to receive, in a blinded fashion, either normal saline (NS; n = 10) or lactated Ringer's solution (LR; n = 10). They were then resuscitated with study fluid to, and maintained at, the preinjury mean arterial pressure (MAP) for 90 minutes. RESULTS: Extravascular lung water index (EVLWI) began to increase immediately with resuscitation with both fluid types, increasing earlier and to a greater degree with NS. A 1 ml/kg increase in EVLWI from baseline occurred after administartion of (mean +/- standard error of the mean) 68.6 +/- 5.2 ml/kg of normal saline and 81.3 +/- 8.7 ml/kg of LR (P = 0.027). After 150 ml/kg of fluid, EVLWI increased from 9.5 +/- 0.3 ml/kg to 11.4 +/- 0.3 ml/kg NS and from 9.3 +/- 0.2 ml/kg to 10.8 +/- 0.3 ml/kg LR (P = 0.035). Despite this, oxygenation was not significantly impacted (Delta partial pressure of arterial oxygen (PaO2)/fraction of inspired oxygen (FiO2)

Assessing the prediction potential of an in silico computer model of intracranial pressure dynamics.

OBJECTIVE: Traumatic brain injury (TBI) frequently results in poor outcome, suggesting that new approaches are needed. We hypothesized that a patient-specific in silico computer model of intracranial pressure (ICP) dynamics may predict the ICP response to therapy. DESIGN: In silico model analysis of prospectively collected data. SETTING: Twenty-three and 16-bed pediatric intensive care units in two tertiary care academic hospitals. PATIENTS: Nine subjects with severe TBI undergoing ICP monitoring (7 M/2 F, age range 3-17 years). INTERVENTIONS: Random changes in head-of-bed (HOB) (0 degrees , 10 degrees , 20 degrees , 30 degrees , 40 degrees ) elevation and respiratory rate (to achieve a DeltaETco2 = +/-3-4 mm Hg) were performed daily according to a study protocol as long as an intracerebral monitoring device was in place. METHODS AND MAIN OUTCOME MEASURES: A six-compartment dynamic ICP model was developed based on published equations and parametric data (baseline model parameter values). For each of 24 physiologic challenge sessions, patient-specific model parameter values were estimated that minimized the model fitness error, the difference between model-calculated ICP and observed ICP, both for baseline parameters and patient-specific parameter. Next, model prediction error was measured using two analyses. First, a "within" session analysis estimated parameter values using data from an initial Segment A, and then used those parameter values to predict the ICP during a later Segment B. The predicted ICP for B was compared with the observed ICP for B. Second, a "between" session analysis was performed. This analysis used parameter values estimated from earlier sessions to predict the ICP in later sessions. Fitness and prediction errors were measured in terms of mean absolute error (MAE). To normalize the errors, MAE was divided by the mean absolute deviation (MAD) for the associated segment or session, yielding a measure for both model fitness error and model prediction error that is favorable when <1. RESULTS: For baseline parameter values, MAE/MAD was <1 in 2 of 24 (8%) sessions. For session-specific parameter values, MAE/MAD was <1 in 21 of 24 (88%) sessions and <0.5 in 9 of 24 (38%) sessions. Sessions with low (<12 mm Hg) (n = 8; 33%) or high (>18 mm Hg) (n = 6; 25%) ICP had lower error than moderate ICP (12-18 mm Hg) (n = 10; 42%). MAE/MAD was <1 for 6 of 22 (27%) for within-session predictions and 3 of 31 (10%) for between-session predictions. CONCLUSIONS: The protocol for collecting physiologic data in subjects with severe TBI was feasible. The in silico ICP model with session-specific parameters accurately reproduced observed ICP response to changes in head-of-bed and respiration rate. We demonstrated modest success at predicting future ICP within a session and to a lesser extent between sessions.

Cerebral blood flow heterogeneity in preterm sheep: lack of physiologic support for vascular boundary zones in fetal cerebral white matter.

Periventricular white matter (PVWM) injury is the leading cause of neurologic disability in survivors of prematurity. To address the role of ischemia in PVWM and cerebral cortical injury, we hypothesized that immaturity of spatially distal vascular 'end zones' or 'border zones' predisposes PVWM to greater decreases in cerebral blood flow (CBF) than more proximal structures. We quantified regional CBF with fluorescently labeled microspheres in 0.65 gestation fetal sheep in histopathologically defined three-dimensional regions by post hoc digital dissection and coregistration algorithms. Basal flow in PVWM was significantly lower than in gyral white matter and cortex, but was equivalent in superficial, middle, and deep PVWM. Absolute and relative CBF (expressed as percentage of basal) did not differ significantly during ischemia or reperfusion between PVWM, gyral white matter, or cortex. Moreover, CBF during ischemia-reperfusion was equivalent in three adjacent PVWM levels and was not consistent with the magnitude of severity of PVWM injury, defined by TUNEL (terminal deoxynucleotidyltransferase-mediated dUPT nick end labeling) staining. However, the magnitude of ischemia was predicted by the severity of discrete cortical lesions. Hence, unlike cerebral cortex, unique CBF disturbances did not account for the distribution of PVWM injury. Previously defined cellular maturational factors, thus, appear to have a greater influence on PVWM vulnerability to ischemic injury than the presence of immature vascular boundary zones.

Design and implementation of a portable physiologic data acquisition system.

OBJECTIVE: To describe and report the reliability of a portable, laptop-based, real-time, continuous physiologic data acquisition system (PDAS) that allows for synchronous recording of physiologic data, clinical events, and event markers at the bedside for physiologic research studies in the intensive care unit. DESIGN: Descriptive report of new research technology. SETTING: Adult and pediatric intensive care units in three tertiary care academic hospitals. PATIENTS: Sixty-four critically ill and injured patients were studied, including 34 adult (22 males and 12 females) and 30 pediatric (19 males and 11 females). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Data transmission errors during bench and field testing were measured. The PDAS was used in three separate research studies, by multiple users, and for repeated recordings of the same set of signals at various intervals for different lengths of time. Both parametric (1 Hz) and waveform (125-500 Hz) signals were recorded and analyzed. Details of the PDAS components are explained and examples are given from the three experimental physiology-based protocols. Waveform data include electrocardiogram, respiration, systemic arterial pressure (invasive and noninvasive), oxygen saturation, central venous pressure, pulmonary arterial pressure, left and right atrial pressures, intracranial pressure, and regional cerebral blood flow. Bench and field testing of the PDAS demonstrated excellent reliability with 100% accuracy and no data transmission errors. The key feature of simultaneously capturing physiologic signal data and clinical events (e.g., changes in mechanical ventilation, drug administration, clinical condition) is emphasized. CONCLUSIONS: The PDAS provides a reliable tool to record physiologic signals and associated clinical events on a second-to-second basis and may serve as an important adjunctive research tool in designing and performing clinical physiologic studies in critical illness and injury.