UNASSIGNED: The arterial pressure waveform reflects the interaction between the heart and the arterial system and carries potentially relevant information about circulatory status. According to the commonly accepted \'wave transmission model\', the net BP waveform results from the super-position of discrete forward and backward pressure waves, with the forward wave in systole determined mainly by the left ventricular (LV) ejection function and the backward by the wave reflection from the periphery, the timing and amplitude of which depend on arterial stiffness, the wave propagation speed and the extent of downstream admittance mismatching. However, this approach obscures the \'Windkessel function\' of the elastic arteries. Recently, a \'reservoir-excess pressure\' model has been proposed, which interprets the arterial BP waveform as a composite of a volume-related \'reservoir\' pressure and a wave-related \'excess\' pressure.
UNASSIGNED: In this study we applied the reservoir-excess pressure approach to the analysis of carotid arterial pressure waveforms (applanation tonometry) in 10 young healthy volunteers before and after a 5-week head down tilt bed rest which induced a significant reduction in stroke volume (SV), end-diastolic LV volume and LV longitudinal function without significant changes in central blood pressure, cardiac output, total peripheral resistance and aortic stiffness. Forward and backward pressure components were also determined by wave separation analysis.
UNASSIGNED: Compared to the baseline state, bed rest induced a significant reduction in LV ejection time (LVET), diastolic time (DT), backward pressure amplitude (bP) and pressure reservoir integral (INTPR). INTPR correlated directly with LVET, DT, time to the peak of backward wave (bT) and stroke volume, while excess pressure integral (INTXSP) correlated directly with central pressure. Furthermore, Δ.INTPR correlated directly with Δ.LVET, and Δ.DT, and in multivariate analysis INTPR was independently related to LVET and DT and INTXSP to central systolic BP.
UNASSIGNED: This is an hypothesis generating paper which adds support to the idea that the reservoir-wave hypothesis applied to non-invasively obtained carotid pressure waveforms is of potential clinical usefulness.

Anaesthesia-induced changes in renal perfusion are dependent on the choice of anaesthetic agent. However, the effects of varying inspired oxygen fraction (FiO2) on renal perfusion and oxygenation during TIVA (propofol + fentanyl) or volatile anaesthesia (VA; isoflurane) are unknown.
In 16 Merino ewes, we surgically implanted a renal artery flow probe and laser-Doppler and oxygen-sensing probes in the renal medulla and cortex. We compared the systemic and renal effects of graded alterations in FiO2 (0.21, 0.40, 0.60, and 1.0) during TIVA or VA and compared the changes with those in the non-anaesthetised state.
Compared with the non-anaesthetised state, TIVA and VA decreased renal blood flow (-50% vs -75%), renal oxygen delivery (-50% vs -80%), and renal cortical (-40% vs -60%) and medullary perfusion (-50% vs -75%). At an FiO2 of 0.21, both anaesthetic regimens induced similar reductions in cortical (-58 vs -65%) and medullary (-37% vs -38%) oxygenation. At higher concentrations of FiO2, renal blood flow and renal tissue perfusion were not changed, but intrarenal oxygenation improved similarly under TIVA and VA. In particular, at an FiO2 of ≥0.40 and ≤0.60, cortical and medullary oxygen tension were similar to the non-anaesthetised state.
Irrespective of FiO2, TIVA decreased renal and intrarenal perfusion less than VA, but at low FiO2 concentrations both led to equivalent reductions in renal cortical and medullary oxygenation. However, with FiO2 between 0.40 and 0.60 during TIVA or VA, both cortical and medullary oxygenation was maintained at normal physiological levels.

Osmotherapy constitutes a first-line intervention for intracranial hypertension management. However, hyperosmolar solutes exert various systematic effects, among which their impact on systemic haemodynamics is poorly clarified. This review aims to appraise the clinical evidence of the effect of mannitol and hypertonic saline (HTS) on cardiac performance in neurosurgical and neurocritical care patients.
A database search was conducted to identify randomized clinical trials and observational studies reporting HTS or mannitol use in acute brain injury setting. The primary end-points were alterations of cardiac output (CO) and other haemodynamic variables, while the impact of osmotic agents on intracranial pressure, brain relaxation, plasma osmolality, electrolyte levels and urinary output constituted secondary outcomes.
Eight studies, enrolling 182 patients in total, were included. HTS exerted a more profound cardiac output augmentation than mannitol, but no distinct difference between groups occurred. Central venous pressure, stroke volume and stroke volume variation were favourably affected by both osmotic agents, whilst the reported changes in blood pressure were inconclusive. HTS infusion yielded a larger intracranial pressure reduction than mannitol but had an equivalent effect on brain relaxation. Mannitol presented a more potent diuretic effect than HTS. Effect on serum osmolality was alike in both osmotic agents, but contrary to HTS-promoted hypernatraemia, mannitol use induced transient hyponatraemia.
Mannitol or HTS administration seems to induce an enhancement of cardiac performance; being more prominent after HTS infusion. This effect combined with mannitol-induced enhancement of diuresis and HTS-promoted increase of plasma sodium concentration could partially explain the effects of osmotherapy on cerebral haemodynamics.

OBJECTIVE: Cirrhosis and portal hypertension are characterised by a hyperdynamic circulation, which is independently associated with variceal size. Non-invasive techniques for measurement of systemic haemodynamics are now available. The aim of the study was to prospectively assess the accuracy of systemic haemodynamics measured non-invasively for the detection of oesophageal varices in cirrhotic patients as compared to other currently available non-invasive methods.
METHODS: In a study of 29 cirrhotic patients, systemic haemodynamics were studied non-invasively using the Finometer® (mean arterial pressure (MAP), cardiac output (CO)/index, heart rate (HR), peripheral vascular resistance) and portal pressure was assessed by hepatic venous pressure gradient. Sensitivity, specificity, predictive values and area under the receiver operating characteristic (ROC) curves were assessed for predicting presence of varices and large oesophageal varices. Results were compared to child\'s classification, platelet/spleen ratio and ALT/AST ratios as predictors of the presence of large varices.
RESULTS: Using finometry large oesophageal varices were correctly predicted in 83% of patients compared to other non-invasive techniques (range 66-76%).
CONCLUSIONS: Non-invasive assessment of systemic haemodynamics using finometry could aid the identification of patients who do not immediately require variceal surveillance reducing the numbers of endoscopies and ensuring services are provided to those most likely to benefit.

Spontaneous breathing has been shown to improve global haemodynamics in patients with bidirectional cavopulmonary shunt. What has not been evaluated, however, is the effect of spontaneous breathing on the distribution of cardiac output after bidirectional cavopulmonary shunt. We investigated the effects of extubation on systemic haemodynamics and regional tissue oxygen saturation, and determined whether redistribution of cardiac output is present after extubation in these patients.
In 24 patients undergoing bidirectional cavopulmonary shunt, standard haemodynamic variables including heart rate, arterial blood pressure and central venous pressure were monitored continuously. Near-infrared spectroscopy of the brain and mesenteric circulation was monitored and recorded every hour. Cardiac index, derived from ascending aorta flow, was measured by ultrasound at three time points: 30 min before, 30 min after and 12 h after extubation.
The central venous pressure decreased significantly from 19.50 ± 3.65 mmHg before extubation to 16.17 ± 3.41 mmHg 30 min after extubation (P = 0.006) and 13.96 ± 2.49 mmHg 12 h after extubation (P = 0.001). Cardiac index increased significantly from 3.32 ± 0.43 l/min/m(2) before extubation to 3.73 ± 0.51 l/min/m(2) 30 min after extubation (P = 0.012) and 3.98 ± 0.54 l/min/m(2) 12 h after extubation (P = 0.001). Cerebral oxygen saturation increased from 50.83 ± 5.84% before extubation to 56.79 ± 8.64% 30 min after extubation (P = 0.023), then remained unchanged for the following 12 h. Mesenteric oxygen saturation remained unchanged during the early period of extubation, but increased significantly 12 h after extubation (P = 0.002).
The lower values of cerebral oxygen saturation before extubation indicated that the cerebral blood flow was less satisfactory. During the early period of extubation, despite the increase in cardiac index, the mesenteric oxygen saturation is lower than that at 12 h after extubation, suggesting that the obligatory increase in respiratory muscle perfusion and the increase in cerebral oxygen saturation have utilized most of the flow from the increased cardiac index. The increase in mesenteric oxygen saturation 12 h after extubation suggests a gradual improvement in microcirculation and macrocirculation.