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Recently intermittent negative pressure has emerged as a potential treatment in vascular disease and has similarities with established experimental interventions such as lower body negative pressure. The direct, local influences of either method upon intravascular pressure still require some clarification however, particularly in the immediate moments following onset. We investigated the acute intravascular pressure responses to intermittent cycles of negative pressure in the supine and sitting postures. Fifteen participants (6 female) received intermittent negative pressure cycles (-37 mmHg; 9.5-sec on, 7.5-sec off) upon the lower leg in both postures. Saphenous venous (n = 15), and dorsalis pedis artery pressure (n = 3) were recorded via pressure catheter, alongside beat-by-beat systemic cardiovascular parameters (heart rate and blood pressure; n = 15), from which the arteriovenous pressure gradient was ultimately derived. Negative pressure induced a transient reduction in local intravenous pressure (Supine: 14±3 mmHg to -18±6 mmHg, p<0.001; Sitting: 58±10 mmHg to 41±10 mmHg, p<0.001). Rate of venous pressure recovery during the negative pressure plateau phase was faster during sitting, than supine (1.94±0.72 vs. 1.06±0.69 mmHg·sec-1; p = 0.002). Local intraarterial pressure did not change. External negative pressure readily transmits to the superficial intravenous environment of the leg and transiently augments the arteriovenous pressure gradient. The greatest and most sustained effect was during the supine position. The augmented arteriovenous gradient might briefly produce Poiseuille-dependent haemodynamics before local autoregulatory mechanisms engage. These findings benefit understanding of the immediate in-vivo effects of negative pressure upon the local vasculature, and may partly account for the positive clinical effects of intermittent negative pressure treatments in vascular disease. [ABSTRACT FROM AUTHOR]

Background: Changes in cardiac power parameters incorporate changes in both aortic flow and blood pressure. We hypothesized that dynamic and non-dynamic cardiac power parameters would track hypovolemia better than equivalent flow- and pressure parameters, both during spontaneous breathing and non-invasive positive pressure ventilation (NPPV). Methods: Fourteen healthy volunteers underwent lower body negative pressure (LBNP) of 0, -20, -40, -60 and -80 mmHg to simulate hypovolemia, both during spontaneous breathing and during NPPV. We recorded aortic flow using suprasternal ultrasound Doppler and blood pressure using Finometer, and calculated dynamic and non-dynamic parameters of cardiac power, flow and blood pressure. These were assessed on their association with LBNP-levels. Results: Respiratory variation in peak aortic flow was the dynamic parameter most affected during spontaneous breathing increasing 103 % (p <0.001) from baseline to LBNP-80 mmHg. Respiratory variation in pulse pressure was the most affected dynamic parameter during NPPV, increasing 119 % (p <0.001) from baseline to LBNP -80 mmHg. The cardiac power integral was the most affected non-dynamic parameter falling 59 % (p <0.001) from baseline to LBNP -80 mmHg during spontaneous breathing, and 68 % (p <0.001) during NPPV. Conclusions: Dynamic cardiac power parameters were not better than dynamic flow- and pressure parameters at tracking hypovolemia, seemingly due to previously unknown variation in peripheral vascular resistance matching respiratory changes in hemodynamics. Of non-dynamic parameters, the power parameters track hypovolemia slightly better than equivalent flow parameters, and far better than equivalent pressure parameters. [ABSTRACT FROM AUTHOR]

Reductions in cerebral oxygen saturation (ScO2) measured by near infra-red spectroscopy have been found during compensated hypovolemia in the lower body negative pressure (LBNP)-model, which may reflect reduced cerebral blood flow. However, ScO2 may also be contaminated from extracranial (scalp) tissues, mainly supplied by the external carotid artery (ECA), and it is possible that a ScO2 reduction during hypovolemia is caused by reduced scalp, and not cerebral, blood flow. The aim of the present study was to explore the associations between blood flow in precerebral arteries and ScO2 during LBNP-induced hypovolemia. Twenty healthy volunteers were exposed to LBNP 20, 40, 60 and 80 mmHg. Blood flow in the internal carotid artery (ICA), ECA and vertebral artery (VA) was measured by Doppler ultrasound. Stroke volume for calculating cardiac output was measured by suprasternal Doppler. Associations of changes within subjects were examined using linear mixed-effects regression models. LBNP reduced cardiac output, ScO2 and ICA and ECA blood flow. Changes in flow in both ICA and ECA were associated with changes in ScO2 and cardiac output. Flow in the VA did not change during LBNP and changes in VA flow were not associated with changes in ScO2 or cardiac output. During experimental compensated hypovolemia in healthy, conscious subjects, a reduced ScO2 may thus reflect a reduction in both cerebral and extracranial blood flow., Competing Interests: The authors have declared that no competing interests exist.

Background: Jehovah's Witnesses refuse transfusions of the main blood components. This challenges the safety of performing major surgical procedures. At the Norwegian Radium Hospital, we have taken the views of Jehovah's Witnesses regarding blood transfusions into account when planning major surgical procedures and perform these without such transfusions. We present a case and our experiences and routines when performing major cancer surgery on Jehovah's Witness patients., Material and Methods: The medical records of Jehovah's Witnesses, who underwent major surgery at the Norwegian Radium Hospital from April 1992 to February 2006, were surveyed retrospectively. Based on relevant literature, our routines and methods are discussed along with some legal and ethical aspects., Results and Interpretation: Major transfusion-free surgery can be performed successfully on Jehovah's Witnesses. This requires advanced planning, good routines and close collaborative team efforts. The most relevant techniques to make major surgery feasible are preoperative optimalisation of the haemoglobin levels and acute normovolemic haemodilution and the use of cell saver under surgery.