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1.
Applied Physiology of Fluid Resuscitation in Critical Illness.
Arshed, S, Pinsky, MR
Critical care clinics. 2018;(2):267-277
Abstract
Fluids during resuscitation from shock increase mean systemic pressure and venous return. The pressure gradient for venous return must increase. Mean systemic pressure is the amount of vascular space in unstressed and stressed volume, mostly unstressed. Shock states can decrease mean systemic pressure by increasing unstressed volume, decreasing total blood volume, or decreasing the pressure gradient for venous return. Crystalloids across bodily spaces restore normal volume, whereas colloids remain in the intravascular space. Electrolyte content of fluids matters and excess chloride impairs renal blood flow. Albumin seems to be more effective at restoring blood volume in severe sepsis, but not in other conditions.
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An alternative hypothesis to the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension.
Kurtz, TW, DiCarlo, SE, Pravenec, M, Schmidlin, O, Tanaka, M, Morris, RC
Kidney international. 2016;(5):965-973
Abstract
It is widely held that in response to high salt diets, normal individuals are acutely and chronically resistant to salt-induced hypertension because they rapidly excrete salt and retain little of it so that their blood volume, and therefore blood pressure, does not increase. Conversely, it is also widely held that salt-sensitive individuals develop salt-induced hypertension because of an impaired renal capacity to excrete salt that causes greater salt retention and blood volume expansion than that which occurs in normal salt-resistant individuals. Here we review results of both acute and chronic salt-loading studies that have compared salt-induced changes in sodium retention and blood volume between normal subjects (salt-resistant normotensive control subjects) and salt-sensitive subjects. The results of properly controlled studies strongly support an alternative view: during acute or chronic increases in salt intake, normal salt-resistant subjects undergo substantial salt retention and do not excrete salt more rapidly, retain less sodium, or undergo lesser blood volume expansion than do salt-sensitive subjects. These observations: (i) directly conflict with the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension, and (ii) have implications for contemporary understanding of how various genetic, immunologic, and other factors determine acute and chronic blood pressure responses to high salt diets.
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Characteristics of fluids used for intravascular volume replacement.
De Backer, D, Cortés, DO
Best practice & research. Clinical anaesthesiology. 2012;(4):441-51
Abstract
In this review, the relative merits of the different fluid solutions used for fluid replacement will be discussed. Differences in chemical composition may have important implications on volume expansion capacities but also on organ function. Among crystalloids, differences in electrolyte composition, and in particular chloride load, alter acid base status but may also affect other aspects of organ function. Large observational cohorts suggest that chloride load may be associated with a poor outcome. Colloids provide greater expansion capacities than crystalloids. When colloids are indicated, albumin should be preferred as it is the only one that has been proved to be safe in a large randomized trial. Cumulative evidence suggests that starches, even of the new generations, are associated with development of acute kidney injury. Hypertonic solutions may represent an interesting option in some groups of patients but more research is needed in this field.
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4.
Hot and heavy volume loading in the heat-stressed, haemorrhagic male: modulating the Frank-Starling curve.
Banks, L, Lewis, E
The Journal of physiology. 2011;(Pt 4):777-8
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Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume.
Cravo, SL, Lopes, OU, Pedrino, GR
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas. 2011;(9):877-82
Abstract
Water deprivation and hypernatremia are major challenges for water and sodium homeostasis. Cellular integrity requires maintenance of water and sodium concentration within narrow limits. This regulation is obtained through engagement of multiple mechanisms and neural pathways that regulate the volume and composition of the extracellular fluid. The purpose of this short review is to summarize the literature on central neural mechanisms underlying cardiovascular, hormonal and autonomic responses to circulating volume changes, and some of the findings obtained in the last 12 years by our laboratory. We review data on neural pathways that start with afferents in the carotid body that project to medullary relays in the nucleus tractus solitarii and caudal ventrolateral medulla, which in turn project to the median preoptic nucleus in the forebrain. We also review data suggesting that noradrenergic A1 cells in the caudal ventrolateral medulla represent an essential link in neural pathways controlling extracellular fluid volume and renal sodium excretion. Finally, recent data from our laboratory suggest that these structures may also be involved in the beneficial effects of intravenous infusion of hypertonic saline on recovery from hemorrhagic shock.
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6.
Current technique of fluid status assessment.
Frank Peacock, W, Soto, KM
Congestive heart failure (Greenwich, Conn.). 2010;:S45-51
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Abstract
Early in the management of acute illness, it is critically important that volume status is accurately estimated. If inappropriate therapy is given because of errors in volume assessment, acute mortality rates are increased. Unfortunately, as the gold standard of radioisotopic volume measurement is costly and time-consuming, in the acute care environment clinicians are forced to rely on less accurate measures. In this manuscript, the authors review the currently available techniques of volume assessment for patients presenting with acute illness. In addition to discussing the accuracy of the history, physical examination, and radiography, acoustic cardiography and bedside ultrasonography are presented.
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Oliguria and fluid overload.
Rimmelé, T, Kellum, JA
Contributions to nephrology. 2010;:39-45
Abstract
Oliguria is a very common clinical situation that is also often difficult to interpret since it may represent either the expression of a disease or an appropriate response of the kidneys to extracellular volume depletion or decreased renal blood flow. In patients with acute kidney injury, oliguria is independently associated with mortality. Fluid overload is a complication of the impaired sodium and water excretion observed in patients with oliguric acute kidney injury. Fluid overload leads not only to cardiopulmonary complications such as congestive heart failure and pulmonary edema requiring mechanical ventilation but also to several others such as delayed wound healing, tissue breakdown, and impaired bowel function. The aim of this short review is to point out the deleterious effects of these two related clinical situations emphasizing their pathophysiology.
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Monitoring fluid status at the outpatient level: the need for more precision.
McDonald, K
Congestive heart failure (Greenwich, Conn.). 2010;:S52-5
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Abstract
Accurate determination of fluid status in patients with heart failure is a critical aspect of care of this population. Early detection of emerging fluid overload would allow for prompt intervention, potentially aborting clinical deterioration and avoiding hospitalization. While many strategies are available to determine fluid status of patients, all areas are compromised by less-than-optimal sensitivity and specificity. Recent work on the role of bioimpedance as a means of assessing a patient's fluid status indicates that this parameter may have a role in monitoring patients with heart failure. This article reviews present techniques available for assessment of fluid status and focuses on the additional information provided by bioimpedance assessment.
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Blood volume response to physical activity and inactivity.
Convertino, VA
The American journal of the medical sciences. 2007;(1):72-9
Abstract
Data from both cross-sectional and longitudinal studies provide compelling evidence that circulating blood volume can be influenced by regular physical activity or inactivity. Expansion or contraction of plasma volume can account for most of the alteration in circulating blood volume during the initial 1 to 2 weeks of changing physical activity patterns; after this time, altered blood volume may be distributed equally between plasma and red cell volumes. Alterations in circulating blood volume that accompany changes in physical activity represent a net change in total body water and solutes that are associated with increased or decreased water intake and urine volume and solute output. The mechanism of altered urine output appears to be a modified renal tubular reabsorption of sodium. The expansion of blood volume that accompanies physical activity provides advantages of greater body fluid for heat dissipation (sweating) and thermoregulatory stability as well as larger vascular volume for greater cardiac filling and stroke volume and cardiovascular stability during exercise and orthostatic challenges. The opposite is true when blood volume is reduced during periods of relative physical inactivity. The observation that underlying mechanisms for alteration in blood volume with physical activity and inactivity are similar but respond directly opposite suggests that they are intricately related. These relations have implications as to a mechanism by which physical activity and fitness may be protective against reduced blood volume and subsequent development of cardiovascular disease associated with aging.
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The sympathetic nervous system and blood volume regulation: lessons from autonomic failure patients.
Biaggioni, I
The American journal of the medical sciences. 2007;(1):61-4
Abstract
Patients with autonomic failure provide a unique opportunity to study the role of sympathetic function on the regulation of blood volume. These patients have a reversal of the normal diurnal variation in urine output and have twice as much natriuresis during the night. Autonomic failure patients are also unable to conserve sodium and fail to decrease natriuresis in response to dietary sodium restriction. Whereas normal subjects are able to maintain blood pressure within narrow values throughout a wide range of plasma volumes, blood pressure is linearly correlated to changes in plasma volume in autonomic failure patients. Fludrocortisone is often used to increase plasma volume in these patients, but this effect is only transient; its long-term effectiveness probably is due to potentiation of the pressor effects of norepinephrine. On the other hand, epoetin-alpha is effective in correcting the mild anemia that autonomic failure patients commonly have and improves their orthostatic hypotension in part by increasing intravascular volume. Autonomic failure patients, therefore, illustrate the role the sympathetic nervous system has in the regulation of sodium and volume. Conversely, a high salt diet induces sympathoinhibition in normal subjects. Paradoxically, sympathetic activity is increased in patients with salt-sensitive hypertension and contributes to their increase in blood pressure. Thus, in both these conditions the feedback mechanisms involving the sympathetic nervous system and volume homeostasis are impaired.