No description available.

No description available.

No description available.

Obstructive sleep apnea (OSA) severity is strongly associated with the degree of overnight peripharyngeal fluid accumulation. We hypothesized that intravenous fluid loading would cause upper airway (UA) narrowing or increase the frequency of apneas and hypopneas per hour of sleep (apnea-hypopnea index; AHI). We employed a controlled, randomized double-crossover experiment in 9 healthy men aged 23-46 years. In the control, subjects were administered approximately 80 ml of normal saline intravenously during sleep. In the intervention, subjects were administered approximately 1850 ml of saline during sleep while wearing compression stockings to localize fluid rostrally. The intervention induced nuchal fluid accumulation, resulting in an increase in neck circumference (+0.1 cm during control, +0.6 cm during intervention, P< 0.01 ) and a decrease in UA cross-sectional area (-0.08 cm2 during control, -0.43 cm2 during intervention, P = 0.023). Although the intervention did not increase the AHI (control AHI = 19.5, intervention AHI = 30.3, P = 0.249), the AHI during the intervention correlated with age (r = 0.8, P < 0.01). Thus, intravenous saline loading during sleep can narrow the UA, which in older men may induce or worsen OSA. Further studies are needed to test this hypothesis.

Obstructive sleep apnea (OSA) severity is strongly associated with the degree of overnight peripharyngeal fluid accumulation. We hypothesized that intravenous fluid loading would cause upper airway (UA) narrowing or increase the frequency of apneas and hypopneas per hour of sleep (apnea-hypopnea index; AHI). We employed a controlled, randomized double-crossover experiment in 9 healthy men aged 23-46 years. In the control, subjects were administered approximately 80 ml of normal saline intravenously during sleep. In the intervention, subjects were administered approximately 1850 ml of saline during sleep while wearing compression stockings to localize fluid rostrally. The intervention induced nuchal fluid accumulation, resulting in an increase in neck circumference (+0.1 cm during control, +0.6 cm during intervention, P< 0.01 ) and a decrease in UA cross-sectional area (-0.08 cm2 during control, -0.43 cm2 during intervention, P = 0.023). Although the intervention did not increase the AHI (control AHI = 19.5, intervention AHI = 30.3, P = 0.249), the AHI during the intervention correlated with age (r = 0.8, P < 0.01). Thus, intravenous saline loading during sleep can narrow the UA, which in older men may induce or worsen OSA. Further studies are needed to test this hypothesis.

Despite years of research, the role that hypovolemia plays in orthostatic intolerance after head down bed rest (BR) and spaceflight remains unclear. Additionally, the efficacy of oral saline countermeasures, employed in an attempt to restore plasma volume (PV) after BR is questionable. Several previous studies have suggested that a new homeostatic set point is achieved in space or during BR, making attempts to restore PV temporary at best. We tested the hypotheses that one day of BR would induce a transient increase in PV followed by hypovolemia and new hormonal balance; that a salt tablet and water fluid loading (FL) countermeasure would be ineffective in restoring PV; and also that the FL would not attenuate the exaggerated hormonal responses to orthostatic stress that are expected after 28hr of BR. Plasma volume, serum sodium and osmolarity, and plasma ANP, AVP, renin, angiotensin II, aldosterone, and catecholamines were measured in nine male subjects undergoing 5 different protocols (28hr Bed Rest without Fluid Loading = 28NFL, 28hr Bed Rest with Fluid Loading = 28FL, 4hr Seated Control = 4NFLS, 4hr Seated Control with Fluid Loading = 4FLS, and 4hr Bed Rest = 4BR) in a randomized repeated measures design. The FL countermeasure was 15 ml/kg of body weight of water with 1g of NaCl per 125ml of water. Orthostatic testing by lower body negative pressure (LBNP) was performed before and after all protocols. In agreement with our first hypothesis, we observed transient reductions in renin, angiotensin II, and aldosterone, which after 25.5hr were restored to baseline, slightly augmented, and suppressed, respectively. Also after 25.5hr, PV was reduced in the 28hr BR protocols and was not restored in 28FL; however, the FL protocol increased PV during 4FLS. We additionally observed augmented renin and aldosterone responses, as well as generally elevated angiotensin II after 28NFL, but not after 28FL or any of the 4hr protocols. Furthermore, no changes in plasma norepinephrine responses to LBNP were documented from Pre-Post test in any protocol. Our results indicate that: 1) PV is reduced after short term BR and is not restored by an oral FL; 2) renin-angiotensin-aldosterone system (RAAS) responses to orthostatic stress are augmented after 28hr of BR and the amplified response can be abrogated by FL; and 3) plasma norepinephrine responses during orthostatic stress are not affected by BR or FL, suggesting that RAAS activity may be modulated by FL independently of sympathetic activity and PV during orthostasis after bed rest.

Despite years of research, the role that hypovolemia plays in orthostatic intolerance after head down bed rest (BR) and spaceflight remains unclear. Additionally, the efficacy of oral saline countermeasures, employed in an attempt to restore plasma volume (PV) after BR is questionable. Several previous studies have suggested that a new homeostatic set point is achieved in space or during BR, making attempts to restore PV temporary at best. We tested the hypotheses that one day of BR would induce a transient increase in PV followed by hypovolemia and new hormonal balance; that a salt tablet and water fluid loading (FL) countermeasure would be ineffective in restoring PV; and also that the FL would not attenuate the exaggerated hormonal responses to orthostatic stress that are expected after 28hr of BR. Plasma volume, serum sodium and osmolarity, and plasma ANP, AVP, renin, angiotensin II, aldosterone, and catecholamines were measured in nine male subjects undergoing 5 different protocols (28hr Bed Rest without Fluid Loading = 28NFL, 28hr Bed Rest with Fluid Loading = 28FL, 4hr Seated Control = 4NFLS, 4hr Seated Control with Fluid Loading = 4FLS, and 4hr Bed Rest = 4BR) in a randomized repeated measures design. The FL countermeasure was 15 ml/kg of body weight of water with 1g of NaCl per 125ml of water. Orthostatic testing by lower body negative pressure (LBNP) was performed before and after all protocols. In agreement with our first hypothesis, we observed transient reductions in renin, angiotensin II, and aldosterone, which after 25.5hr were restored to baseline, slightly augmented, and suppressed, respectively. Also after 25.5hr, PV was reduced in the 28hr BR protocols and was not restored in 28FL; however, the FL protocol increased PV during 4FLS. We additionally observed augmented renin and aldosterone responses, as well as generally elevated angiotensin II after 28NFL, but not after 28FL or any of the 4hr protocols. Furthermore, no changes in plasma norepinephrine responses to LBNP were documented from Pre-Post test in any protocol. Our results indicate that: 1) PV is reduced after short term BR and is not restored by an oral FL; 2) renin-angiotensin-aldosterone system (RAAS) responses to orthostatic stress are augmented after 28hr of BR and the amplified response can be abrogated by FL; and 3) plasma norepinephrine responses during orthostatic stress are not affected by BR or FL, suggesting that RAAS activity may be modulated by FL independently of sympathetic activity and PV during orthostasis after bed rest.

Beneš J.: HEMODYNAMIKA V ČASNÉ FÁZI KRITICKÝCH STAVŮ A PERIOPERAČNÍ MEDICÍNĚ - Využití méně invazivních monitorovacích prostředků k cílené hemodynamické péči ABSTRACT Hemodynamic instability occurs very often in critically ill patients and during the perioperative period. Insufficiency in the preload, contractility and afterload contribute in major part to this phenomenon. Hemodynamic monitoring allows clinicians to recognize and to intervene early the underlying cause. Due to new technologies development in recent years it is possible to provide continuous monitoring of hemodynamic parameters with diminished invasivity. Hemodynamic optimization and goal directed therapy show treatment benefit in some groups of critically ill patients and mainly during the perioperative period. Aim of hemodynamic optimizations is to attain the best obtainable hemodynamic conditions with use of fluid loading and inotropic support. In many studies in recent years goal-directed therapy was associated with morbidity and mortality reduction. According to the results of our clinical research hemodynamic optimization using stroke volume variation and minimally invasive device based on the pressure wave analysis is feasible and show the same results as other works with more invasive devices. Key words Hemodynamic monitoring,...