The clinical assessment of fluid balance.
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1. Assessment of nutrition in patients with chronic renal failure by body composition measurement techniques may be affected by variable hydration. 2. This study aimed to derive a four-component model of body composition (consisting of fat, protein, total body water and body mineral) from a combination of dual-energy X-ray absorptiometry and total body water measured by deuterium oxide dilution, allowing assessment of body protein stores without the effect of variation in hydration. Patients with chronic renal failure on haemodialysis, peritoneal dialysis and conservative treatment and a control group were studied. Patients with chronic renal failure were at an 'ideal' state of hydration on clinical assessment. 3. Hydration was defined by total body water as a percentage of fat-free mass measured by dual-energy X-ray absorptiometry, and no differences were found between chronic renal failure subgroups and control subjects (except in the female undialysed chronic renal failure subgroup). Hydration was significantly correlated with percentage total body fat in the control groups but not in patients with chronic renal failure. 4. Lean tissue measured by dual-energy X-ray absorptiometry was significantly reduced in three of the six chronic renal failure groups compared with control subjects (male and female patients on haemodialysis and female patients on peritoneal dialysis). Protein estimated from the four-component model failed to detect these abnormalities. 5. Lean tissue measured by dual-energy X-ray absorptiometry in normal subjects strongly correlated with fat-free mass measured by total body potassium in normal subjects (male r = 0.91; female r = 0.89, both P < 0.0001). The correlation of protein estimated from the four-component model with fat-free mass measured by total body potassium was far weaker in male control subjects (r = 0.51, P < 0.05) and not significant in female control subjects (r = 0.38, P not significant). In the normal subjects protein estimated from the four-component model showed a much greater variation from protein estimated by total body potassium than did protein estimated simply as 27% of dual-energy X-ray absorptiometry fat-free mass minus total body mineral. 6. Hydration in patients with chronic renal failure in whom fluid balance is believed to be normal on clinical criteria does not differ from that in normal subjects. The combined model of dual-energy X-ray absorptiometry and total body water is not a useful method for the measurement of body protein.
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In this paper I have presented two closely related themes both of which seem to be fundamental in understanding the pathophysiology of hypertension. The first theme is the dominant role of the volume-excretion function of the kidneys in setting the long-term arterial pressure level. That is, each person in general has a rather steady intake of salt, water, and those other constituents that make up extracellular fluid. When the arterial pressure is normal, the kidney excretion of these constituents is exactly the correct amount to balance the intake of each of them. When the pressure is too great, there is more loss than gain, and the body fluid volume decreases; therefore, the pressure falls until the exact balance point is reached again; it is only at this balance point that the loss and gain are equal. At any pressure below the balance point, volume gain is greater than loss, and the pressure will continue to rise until the exact balance level is again reached. This capability of the kidney mechanism to return the pressure all-the-way back to the level of balance between input and output--not merely part-way back--is called the "infinite gain" characteristic of this pressure control system, and the level to which the pressure is controlled is called the "set-point" of the system. In pathophysiological states, the set-point for pressure control can be increased to hypertensive levels as a result of (1) a pathophysiological change in renal function or (2) increased salt and volume intake; then hypertension will ensue. Other abnormalities of circulatory function that do not affect one of these two factors cannot cause chronic hypertension because of the infinite gain feature of the renal-volume mechanism for pressure control. One such condition that does not cause hypertension without some concurrent abnormality that affects renal function is a primary increase in total peripheral resistance. The second theme is that whole-body autoregulation causes the blood flow in all parts of the body to return or remain near to normal when high arterial pressure tries to increase the flow. It does this by increasing the resistance in all parts of the peripheral arterial tree. Therefore, in effect, autoregulation converts any tendency to high cardiac output hypertension into high resistance hypertension. Yet, in so far as is now known, the pressure level will be the same with or without autoregulation.(ABSTRACT TRUNCATED AT 400 WORDS)
Regulation of fluid balance is a complex subject. Sharon Edwards discusses the physiological principles involved.
In 9 ventilated preterm infants (birth weight 810-1310 g, gestational age 26-30 weeks) we measured total body water (D2O dilution), extracellular volume (sucrose dilution) and renal function parameters at birth and when postnatal weight loss exceeded 5% of birth weight together with day to day changes of weight, fluid balance, and serum electrolytes. A significant postnatal weight loss (-89 +/- 47 g) occurred together with a reduction of total body water (-102 +/- 95 ml) and extracellular volume (-98 +/- 59 ml) in the first three days of life. The intracellular volume did not change. At the same time fluid balance was negative due to a high extrarenal water loss on day 1 and an increasing diuresis on the following days. The serum sodium concentration remained unchanged during postnatal water loss, because the negative fluid balance was accompanied by a negative sodium balance.
A 54-year-old woman had seizures and a focal neurologic deficit associated with hyponatremia induced by a thiazide diuretic. Prompt correction of hyponatremia by administration of hypertonic saline solution was followed by resolution of all neurologic defects. Metabolic balance studies and rechallenge with hydrochlorothiazide were undertaken to investigate the mechanism of the thiazide-induced hyponatremia. Abnormal vasopressin secretion was shown by a plasma vasopressin concentration of 0.5 microU/ml with a plasma osmolality of 268 mOsm/kg water after administration of a fluid challenge consisting of 45 ml/kg body weight. Rechallenge with chlorothiazide while on a sodium- and potassium-controlled balanced diet resulted in a decrease in serum sodium concentration (136 to 124 mEq/L) and plasma osmolality (283 to 261 mOsm/kg) within 18 hours. During this period, urine losses of monovalent cation were only 55 mEq and body weight was constant at 48.2 kg. A second challenge while the patient received all fluids and electrolytes intravenously again resulted in decreased serum sodium concentration (134 to 126 mEq/L) after urinary loss of only 69 mEq of cation. Thus this patient's hyponatremia cannot be accounted for solely by changes in external water and electrolyte balance; the rapidity with which changes were produced suggests that osmolar inactivation, probably intracellularly, may contribute to the severe hypotonicity seen in some patients.
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Changes in serum albumin levels and body weight are often used as indicators of the efficiency of a nutritional support regimen. Patients with moderate nutritional depletion demonstrate two distinct patterns of response during refeeding. The first is characterized by a decrease in the previously expanded extracellular fluid space with a rise in serum albumin and a loss of weight and the second by continued fluid retention with weight gain and no rise in serum albumin concentration. The second pattern has been observed in patients with ongoing stress such as infection. This study examines severely malnourished patients with no apparent inflammatory complications and demonstrates that this group responds to nutritional support in a pattern similar to that seen in the stressed patient. Eight patients with profound malnutrition were studied during the 1st week of nutritional support. Nitrogen balance was measured and the findings confirmed that all patients were anabolic. Sodium balances were used as an indicator of changes in the extracellular fluid compartment. Body weight and serum albumin were assessed daily. Body weight increased from 59 +/- 4 to 62 +/- 4% of normal (p less than 0.01) while serum albumin changed insignificantly (3.00 +/- 0.27 to 2.85 +/- 0.23 g/100 ml, NS) during the initial week of an adequate nutritional support regimen (nitrogen balance was +21.0 +/- 4.3 g, p less than 0.05). These changes were associated with a positive sodium balance (+215 +/- 20 mEq, p less than 0.05). These data confirm that some extremely malnourished patients do not experience a diuresis during the initial phase of nutritional support but rather may retain water and increase body weight.(ABSTRACT TRUNCATED AT 250 WORDS)
After exercise dehydration (3% of body weight) the restoration of water and electrolyte balance was followed in 6 male subjects. During a 2 h rest period after exercise, a drink of one of four solutions was given as 9 X 300 ml portions at 15 min intervals: control (C-drink), high potassium (K-drink), high sodium (Na-drink) or high sugar (S-drink). An exercise test (submaximal and supramaximal work) was performed before dehydration and after rehydration. Dehydration reduced plasma volume by 16%, a process reversed on resting even before fluid ingestion began, due to release of water accumulated in the muscles during exercise. After 2 h rehydration, plasma volume was above the initial resting value with all 4 drinks. The final plasma volumes after the Na-drink (+14%) and C-drink (+9%) were significantly higher than after the K- and S-drinks. The Na-drink favoured filling of the extracellular compartment, whereas the K- and S-drinks favoured intracellular rehydration. In spite of the higher than normal plasma volume after rehydration, mean heart rate during the submaximal test was 10 bpm higher after rest and rehydration than in the initial test, and was not different between the drinks. The amount of work which could be performed in the supramaximal test (105% VO2max) was 20% less after exercise dehydration and subsequent rest and rehydration than before. This reduction was similar for all drinks, and may be due to a decreased muscle glycogen content (70% of initial) at the time of the second test.
The effects of constant infusions of small doses of adrenal steroid hormones on sodium, potassium and water metabolism were studied in male adrenalectomized rats. An infusion of 1 microgram aldosterone/day was sufficient to restore normal sodium and potassium balance in a group of rats fed an unsupplemented diet. Log doses of aldosterone (0.1-10 micrograms/day for 4 days) administered some days after adrenalectomy caused linear increases in the body weight of rats fed a sodium-supplemented diet (0.05 M-NaCl as drinking fluid) during 4 days of treatment. Increases in body weight correlated with renal sodium and water balance. When steroid treatment was started at the time of adrenalectomy, sodium balance was not significantly affected although rats treated with 1 microgram aldosterone/day ate more, drank less saline, produced a smaller volume of urine of greater osmolarity and gained more weight than controls. A dose of 100 micrograms 18-hydroxy-deoxycorticosterone/day had no significant effects. Fluid intake and urine volume were not significantly affected by 1 mg corticosterone/day but food intake, water balance and weight gain were greater than controls. Rats treated with both aldosterone and corticosterone showed a decrease in free water clearance. Aldosterone and corticosterone, both singly and in combination, reduced plasma potassium levels. Plasma sodium levels were only increased when aldosterone was administered on its own. Long-term steroid infusions have revealed more about the physiology of aldosterone action than could acute measurements of renal function.(ABSTRACT TRUNCATED AT 250 WORDS)
Riftia pachyptila is one of the most specialized invertebrate hosts of chemoautotrophic symbionts. Crucial to the functioning of this symbiosis is how these worms cope with fluctuating ion concentrations. Internal sulfate levels in R. pachyptila appear comparable with other benthic marine invertebrates, despite the production of sulfate internally by means of the bacterial oxidation of hydrogen sulfide, suggesting that these worms are able to eliminate sulfate effectively. Internal chloride levels appear comparable; however, coelomic fluid chloride levels decrease significantly as the amount of coelomic fluid bicarbonate increases, demonstrating a 1:1 stoichiometry. We believe this shift in chloride, out of the body fluids, is needed to compensate for changes in electrochemical balance caused by the large increase (up to and greater than 60 mmol L-1) in negatively charged bicarbonate. Riftia pachyptila fits the general pattern of monovalent ion concentrations that is seen in other benthic marine invertebrates, with a high [Na+] : [K+] ratio extracellularly and low [Na+] : [K+] ratio intracellularly. Extracellular pH values of 7.38+/-0.03 and 7.37+/-0. 04 for coelomic fluid and vascular blood, respectively, as well as intracellular pH values of 7.37+/-0.04 and 7.04+/-0.05 for plume and trophosome tissue, respectively, were measured. On the basis of significant decreases in extracellular pH and, in some cases, Na+ and K+, in worms exposed to carbonyl cyanide m-chlorophenylhydrazone, sodium vanadate, and N-ethylmaleimide, we suggest that high concentrations of H+-ATPases, perhaps Na+/H+- or K+/H+-ATPases, are involved in H+ elimination in these animals.