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Results for “BODY FLUID BALANCE”

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PubMed1996

Fluid and electrolyte management in the neurologically-impaired patient.

Maintaining a homeostatic fluid state in patients with neurological disease is a common challenge that nurses encounter when caring for the critically ill patient. The human body regulates fluid and chemical balances within precise ranges. Control mechanisms are found in both the neural and the renal systems. Disturbances within these systems are common in the neurologically-impaired patient because maintenance of homeostasis ultimately rests within the injured brain itself. Virtually any intracranial pathology can affect this precise feedback mechanism which regulates fluid volume. In addition, medications commonly administered cause profound fluid and electrolyte shifts. Proper management of all of these imbalances requires a thorough understanding of how the body maintains homeostasis, the factors that can disturb it and the various treatment modalities for each entity.

Critical Illness↗
PubMed1993

Immune consequences of burn injury.

The purpose of the immune system is to protect cells from invasion by microorganisms. The body has three equally important interactive immune defense systems, all of which are profoundly disrupted with major burn injury. The immune response to burn injury is immediate, prolonged, and severe. The end result in individuals surviving burn shock is immunosuppression, with increased susceptibility to potentially fatal systemic burn wound or pulmonary sepsis. Nursing actions to support the humoral and cell-mediated immune system of the burned patient include providing nutritional support to maintain serum protein levels at optimal levels; measures to decrease edema and promote angiogenesis in areas of partial-thickness injury; meticulous treatment of the wound to prevent infection and promote healing; monitoring of antibiotic use; conservative use of invasive techniques, including intubation and vascular access devices; maintenance of fluid and electrolyte balance and body temperature; and energy conservation measures.

Antibody Formation↗
PubMed1988

Neuronal sensitivities in preoptic tissue slices: interactions among homeostatic systems.

The preoptic area participates in many homeostatic systems, which include the regulation of body temperature, fluid and metabolite balance, and reproduction. Some preoptic neurons have been shown to be sensitive to either temperature, osmotic pressure, glucose, testosterone or estradiol. While previous studies have treated these as separate and distinct neuronal populations, this paper reviews recent experiments which show that many neurons have multiple sensitivities to these endogenous factors. Neurons in preoptic tissue slices were tested for their responses to changes in temperature, as well as various perfusion media containing 30 pg/ml testosterone or estradiol, low glucose (1.0 mM) or increased osmotic pressure (309 mosmol/kg). The steroid-sensitive, osmosensitive and glucosensitive neurons were not confined to the temperature insensitive neurons; but instead nearly half of the thermosensitive neurons responded to these nonthermal stimuli. In addition, many osmosensitive neurons showed glucosensitivity and steroid-sensitivity. This suggests that, even at the neuronal level, there is a basis for interactions between homeostatic systems.

Action Potentials↗
PubMed1979

A review of the consequences of fluid and electrolyte shifts in weightlessness.

This review describes the renal-endocrine mechanisms related to the early losses of fluid-electrolytes from the body during weightlessness as well as their contribution to longer term adaptation of fluid-electrolyte balance. The hypotheses presented were generated by a systematic analysis of body fluid and renal dynamics observed under conditions of actual and simulated spaceflight. These have increased our understanding of the effects of acute headward fluid shifts on renal excretion, the factors promoting excess sodium excretion and the regulation of extracellular fluid composition.

Adaptation, Physiological↗
PubMed1993

Osteopetrorickets. The paradox of plenty. Pathophysiology and treatment.

Rickets is a common and paradoxical feature of infantile malignant osteopetrosis and results from the inability of osteoclasts to maintain a normal calcium-phosphorus balance in the extracellular fluid. Despite a markedly positive total body calcium balance, rickets arises when the serum calcium x phosphorus product is insufficient to mineralize newly formed chondroid and osteoid. In five children with malignant infantile osteopetrosis, there were clinical, radiographic, biochemical, and histologic findings of rickets. Characteristic biochemical abnormalities included hypocalcemia, hypophosphatemia, and elevated levels of serum acid phosphatase, alkaline phosphatase, c-terminal parathyroid hormone, and 1,25-dihydroxyvitamin D. The urinary calcium/creatinine ratio was markedly depressed. The serum calcium x phosphorus product was below 30 in all children at the time the rickets was diagnosed, and above 40 by the time the rickets had resolved. Baseline bone density measurements were markedly elevated in all children (> 5 standard deviation above normal) and showed even significant increases (> 7 SD) when the rickets was treated with vitamin D and calcium. The children showed marked clinical improvement, decreased lethargy, increase in mobility and activity, and stimulation of appetite, without any additional adverse hematologic or neurologic effects. The rickets was reversible in all children: in one by HLA-identical sibling bone marrow transplantation and in four by physiologic doses of vitamin D and calcium. The parathyroid and renal responses to hypocalcemia were appropriate, but glucocorticoids, used in treating the hematologic complications of the disease, may have blunted the intestinal response to maximal vitamin D stimulation. This latter blockade can be overcome by increasing dietary calcium. By liberalizing rather than by restricting calcium and phosphorus intake, hypocalcemia can be minimized, phosphorus metabolism can be improved, and rickets can be cured.

Bone Marrow Transplantation↗
PubMed2004

Fluid balance.

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Blood Volume↗
PubMed1992

Hyperkalemia in very low birth weight infants.

PURPOSE: To assess the frequency and pathogenesis of hyperkalemia in the very low birth weight infant. METHODS: Infants who weighed less than 1000 gm at birth were prospectively entered into the study within 12 hours of birth. Potential risk factors for hyperkalemia were assessed. Body weight, fluid and electrolyte balance, serum levels of sodium and potassium, creatinine clearance, fractional sodium excretion, and urine sodium/potassium ratio were measured every 8 hours for 72 hours. Measurements of plasma renin, serum aldosterone, and plasma atrial natriuretic factor were made at study entry and repeated when hyperkalemia (serum potassium greater than 6.5 mmol/L) occurred or at 72 hours. Infants in whom hyperkalemia developed were compared with those in whom it did not. RESULTS: Thirty-one infants completed the study; hyperkalemia developed in 16 (51.6%). The only difference in the occurrence of perinatal complications was the more frequent occurrence of pH less than 7.20 in infants with subsequent development of hyperkalemia. Creatinine clearance, urine output, and potassium excretion were significantly lower in the hyperkalemia group during the first 24 hours. Serum potassium concentration at 24 hours was inversely related to urine output in the prior 24 hours. Fractional sodium excretion, urine sodium/potassium ratio, and levels of renin, aldosterone, and atrial natriuretic factor did not differ between groups. CONCLUSIONS: Hyperkalemia is a frequent complication in very low birth weight infants. Infants with low urinary flow rates during the first few hours after birth are at greatest risk for the development of hyperkalemia.

Aldosterone↗
PubMed1998

Presence of atrial natriuretic peptide in two desert rodents: comparison with rat.

Atrial natriuretic peptide (ANP) was characterized and assayed in plasmas, hearts, and brains of two Algerian desert rodents, Psammomys obesus and Meriones libycus along with vasopressin, which was assayed in hypophyses and hypothalami. Using reverse-phase high-performance liquid chromatography and radioimmunoassay, we showed, in plasmas and hearts of both species of desert rats, the presence of peptides similar to rat N- and C-terminal ANP but in lower amounts than in Wistar rats. Conversely, C-terminal ANP was abundantly detected in hypophyses from Meriones libycus rats. As these peptides, through their diuretic and natriuretic activities, are involved in body fluid regulation and electrolyte balance, the reduction of ANP stores in both plasmas and hearts suggests that diuresis and natriuresis are lowered in both species of mammals adapted to arid environments. This could occur because of the vasopressin-mediated adaptation, but also in response to the low ANP involvement in hydro-osmotic regulations, even in Psammomys, which has a dietary salt loading. On the other hand, the higher C-terminal ANP contents in the hypophysis of Meriones than in Psammomys and Wistar rats remain to be understood.

Acclimatization↗
PubMed2001

Expression of B-type natriuretic peptide in atrial natriuretic peptide gene disrupted mice.

Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are two hormones produced and secreted by the heart to control blood pressure, body fluid homeostasis and electrolyte balance. Each peptide binds to a common family of 3 receptors (GC-A, GC-B and C-receptor) with varying degrees of affinity. The proANP gene disrupted mouse model provides an excellent opportunity to examine the regulation and expression of BNP in the absence ofANP. A new radioimmunoassay (RIA) was developed in order to measure mouse BNP peptide levels in the plasma, atrium and ventricle of the mouse. A detection limit of 3-6 pg/tube was achieved by this assay. Results show that plasma and ventricular level of BNP were unchanged among the three genotypes of mice. However, a significant decrease in the BNP level was noted in the atrium. The homozygous mutant (ANP-/-) had undetectable levels of BNP in the atrium, while the heterozygous (ANP+/-) and wild-type (ANP+/+) mice had 430 and 910 pg/mg in the atrium, respectively. Northern Blot analysis shows the ANP-/- mice has a 40% reduction of BNP mRNA level in the atrium and a 5-fold increase in the ventricle as compared with that of the ANP+/+ mouse. Our data suggest that there is a compensatory response of BNP expression to proANP gene disruption. Despite the changes in the atrial and ventricular tissue mRNA and peptide levels, the plasma BNP level remains unaltered in the ANP-/- mice. We conclude that the inability of BNP to completely compensate for the lack of ANP eventually leads to chronic hypertension in the proANP gene disrupted mice.

Animals↗
PubMed2004

Effect of nesiritide on length of hospital stay in patients with decompensated heart failure.

We examined the effect of nesiritide, administered as initial therapy, on length of hospital stay (LOS) and renal function through a retrospective analysis of 129 consecutive admissions to the coronary care unit in 98 patients diagnosed with congestive heart failure. Nesiritide was infused during 58 admissions (nesiritide group) while other therapies, not including nesiritide, were used during 71 admissions (non-nesiritide group). Although the nesiritide group showed lower baseline left ventricular ejection fraction and systolic blood pressure, higher serum creatinine, and a longer QRS interval, the LOS of this group was significantly shorter compared to the non-nesiritide group (3.91 +/- 1.3 vs 4.77 +/- 1.7 days, P = .0023). Both groups were similar with respect to body weight change (negative fluid balance), a slight decrease in blood urea nitrogen, and unchanged serum creatinine. Nesiritide as an initial therapy for treatment of congestive heart failure results in a more rapid hospital discharge without compromising renal function.

Aged↗
PubMed2003

[Indications for continuous renal function replacement therapy].

One of the most important achievements in the contemporary intensive care management is introduction of continuous renal replacement therapy (CRRT). The most common indications for CRRT are acute renal failure complicated with heart failure, volume overload, hypercatabolism, acute or chronic liver failure, and/or brain swelling. Less common indications include systemic inflammatory response (SIRS), sepsis, multiorgan failure (MOF), adult respiratory distress syndrome, crush syndrome, tumor lysis syndrome, lactacidosis, and chronic heart failure. Methods of CRRT could be used during or after open heart operations, heart, lung or/and liver transplantation in adults and children. Modern approach to treatment of acute renal failure introduces dialysis early in the course of disease in order to avoid complications on other organs. Sepsis, SIRS and septic shock are still major therapeutic problems in intensive care units with a mortality rate over 50%. Numerous uncontrolled and several controlled clinical studies have demonstrated that CRRT could remove inflammatory substances including cytokines, activated components of the complement, and derivatives of the arachidonic acid. Hemodynamic stability and gas exchange in the lungs were significantly improved. These is due not only to removal of inflammatory substances but also to other nonspecific hemodynamic effects (control of body temperature, fluid and metabolic balance). Besides the convection, cytokines could be removed from the plasma with adsorption on the membrane of dialyzer or hemofilter. Prophylactic use of CCRT in patients with normal renal function, without disturbances in fluid excretion and with normal hemodynamics is still controversial, while the possible benefit is not higher than the risks of invasive therapeutic method, and there is no evidence that prophylactic CCRT could prevent development of acute renal failure in these patients. However, current knowledge of MOF pathophysiology justifies the use of CRRT in patients with signs of heart failure, disturbances in metabolic and fluid homeostasis and sepsis, and in patients with the risk of developing acute respiratory failure or MOF, despite the mild impairment of renal function according to laboratory results.

Humans↗