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PubMed1982

Effect of acid-base status on the kinetics of the ventilatory response to moderate exercise.

To determine the influence of altered carotid body drive on exercise ventilatory kinetics, five subjects performed four repetitions of constant-load cycle ergometer exercise during air and O2 breathing under each of the following conditions: 1) metabolic acidosis, (NH4Cl, 0.3 g . kg-1 . day-1); 2) metabolic alkalosis (NaHCO3, 0.7 g . kg-1 . day-1); and 3) control (CaCO3, 0.1 g . kg-1 . day-1). Ventilatory and gas exchange variables were computed, breath-by-breath, and the time constant of the ventilatory response in each condition was determined by a least-squares technique. While breathing air, metabolic acidosis caused the magnitude of the ventilatory response to increase and the time constant of the ventilatory kinetics to decrease. With metabolic alkalosis the increase in ventilation caused by exercise tended to be smaller and time constant larger although these changes were not statistically significant. Hyperoxia slowed the ventilatory response in the three acid-base conditions to a similar value. Thus hyperoxia slowed the ventilatory kinetics to a greater degree during acidosis than during control or alkalosis. We conclude that ventilatory dynamics during moderate exercise can be appreciably influenced by the acid-base status with acidosis significantly speeding the response dynamics. And, as these effects are abolished by hyperoxia, they appear to be mediated via the carotid bodies, in the human.

Acid-Base Equilibrium↗
PubMed1986

Arterial blood gases and acid-base status of dogs during graded dynamic exercise.

The objective of this study was to determine whether arterial PCO2 (PaCO2) decreases or remains unchanged from resting levels during mild to moderate steady-state exercise in the dog. To accomplish this, O2 consumption (VO2) arterial blood gases and acid-base status, arterial lactate concentration ([LA-]a), and rectal temperature (Tr) were measured in 27 chronically instrumented dogs at rest, during different levels of submaximal exercise, and during maximal exercise on a motor-driven treadmill. During mild exercise [35% of maximal O2 consumption (VO2 max)], PaCO2 decreased 5.3 +/- 0.4 Torr and resulted in a respiratory alkalosis (delta pHa = +0.029 +/- 0.005). Arterial PO2 (PaO2) increased 5.9 +/- 1.5 Torr and Tr increased 0.5 +/- 0.1 degree C. As the exercise levels progressed from mild to moderate exercise (64% of VO2 max) the magnitude of the hypocapnia and the resultant respiratory alkalosis remained unchanged as PaCO2 remained 5.9 +/- 0.7 Torr below and delta pHa remained 0.029 +/- 0.008 above resting values. When the exercise work rate was increased to elicit VO2 max (96 +/- 2 ml X kg-1 X min-1) the amount of hypocapnia again remained unchanged from submaximal exercise levels and PaCO2 remained 6.0 +/- 0.6 Torr below resting values; however, this response occurred despite continued increases in Tr (delta Tr = 1.7 +/- 0.1 degree C), significant increases in [LA-]a (delta [LA-]a = 2.5 +/- 0.4), and a resultant metabolic acidosis (delta pHa = -0.031 +/- 0.011). The dog, like other nonhuman vertebrates, responded to mild and moderate steady-state exercise with a significant hyperventilation and respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1989

Effect of pH on pulmonary vascular tone, reactivity, and arachidonate metabolism.

We studied the effects of perfusate pH on pulmonary vascular tone, reactivity, and thromboxane and prostacyclin synthesis in isolated buffer-perfused rabbit lungs. Extracellular acidosis did not affect base-line vascular tone, but alkalosis had a biphasic effect. Increasing the perfusate pH from 7.40 to 7.65 caused vasodilation, whereas raising pH to 7.70-8.10 caused vasoconstriction. Removing calcium (Ca2+) from the perfusate completely prevented the vasoconstriction caused by alkalosis. Perfusate pH strikingly affected pulmonary vascular reactivity. Acidosis inhibited the vasoconstriction caused by thromboxane and potassium chloride (KCl) but did not affect the response to angiotensin II. Alkalosis, in contrast, augmented the vasoconstriction caused by thromboxane and angiotensin II but reduced the vasoconstriction caused by KCl. Changes in pH also altered thromboxane and prostacyclin synthesis after the infusion of exogenous arachidonic acid (AA) or the endogenous release of AA by the lipid peroxide tert-butyl hydroperoxide.

Angiotensin II↗
PubMed1994

Relationship between intracellular pH, extracellular pH, and ventilation during dilution acidosis.

Previous experiments showed that acute hyperosmolality results in an extracellular acidosis that does not stimulate respiratory compensation (C.E. Kasserra, D. R. Jones, and M. R. Hughes. Respir. Physiol. 85: 383-393, 1991). The data suggested that development of the extracellular dilution acidosis would also result in a concomitant intracellular contraction alkalosis. The effects of acute hyperosmolality and lactacidosis on systemic intracellular pH (pHi) were studied in the conscious Pekin duck in an effort to separate the effects of pHi and extracellular pH (pHe) on ventilatory control. Brain pH was also measured during systemic hyperosmolality to determine the relationship between blood and brain pHi. Hyperosmolality caused a concurrent extracellular acidosis and intracellular alkalosis in pectoral muscle, whereas lactic acid infusion decreased both pHe and pHi. Ventilation was stimulated only during lactacidosis and did not change during hyperosmolality. Brain pHi did not show a consistent significant increase in response to systemic hyperosmolality over 1 h but did show a trend toward an alkalosis. Measurement of high-energy phosphate metabolites (phosphocreatine, ATP, and Pi) indicated an increase of metabolic rate during hyperosmolality. With the assumption that similar pHi changes were occurring in chemoreceptive cells, the results suggest that ventilation was responding to pHi changes and that much of the depressive response to acute hyperosmotic disturbance was peripherally generated.

Acidosis, Lactic↗
PubMed1975

Impairment of myocardial O2 supply due to hyperventilation.

Thirteen patients with ischemic coronary heart disease purposely hyperventilated for seven minutes in order to induce hypocapnic alkalosis. One patient experienced chest pain, and one exhibited chemical signs of myocardial hypoxia. Heart rate, blood pressure and myocardial O2 consumption did not change significantly. Coronary blood flow decreased and coronary (a-v)O2 difference widened. Since the alkalosis increased the blood O2 affinity, the fall in PO2 in coronary venous blood was proportionately even greater than the fall in O2 concentration. Thus, hypocapnic alkalosis due to hyperventilation interferes with myocardial O2 supply by 1) coronary vasoconstriction and 2) increased O2 affinity of blood.

Coronary Circulation↗
PubMed2005

Angiotensin II increases H+-ATPase B1 subunit expression in medullary collecting ducts.

Metabolic alkalosis is a common feature of hypokalemic hypertensive syndromes associated with angiotensin II excess. The alkalosis-generating effect of angiotensin II is usually ascribed to its stimulatory effect on aldosterone secretion, a hormone that upregulates collecting duct hydrogen ion secretion. We studied the effect of angiotensin II infusions on the expression of B1 and a4 protein, subunits of the renal H+-ATPase in adrenalectomized rats. Adrenalectomized rats were given either angiotensin II or vehicle for 7 days via osmotic mini-pumps. H+-ATPase B1 protein expression was evaluated by Western blot analysis in isolated medulla and cortex plasma membrane preparations from one kidney, whereas the contralateral kidney was used for immunostaining. By Western blotting, the relative abundance of B1 protein was 2-fold higher in renal medulla membranes from rats with intact adrenal glands (sham surgery) than from adrenalectomized rats (219+/-47%, n=12; P<0.05). In contrast to renal medulla, adrenalectomy did not significantly alter the relative abundance of B1 protein in renal cortex. Angiotensin II also did not significantly alter the relative levels of B1 protein in the cortex, but it increased it significantly in renal medullary membranes (231+/-56%, n=8; P<0.005). Moreover, enhanced H+-ATPase B1 subunit protein immunoreactivity was found in medullary collecting duct segments of rats infused with angiotensin II. In contrast to B1, expression of a4, another subunit of the H+-ATPase was not altered by adrenalectomy or angiotensin II. We conclude that adrenalectomy decreases whereas angiotensin II increases H+-ATPase B1 subunit expression in medullary, but not in cortical collecting ducts. By increasing the relative abundance of the B1 subunit of H+-ATPase in the collecting duct, angiotensin II excess may lead to increased hydrogen ion secretion and thus metabolic alkalosis-a common feature of hypertensive syndromes associated with angiotensin II overactivity.

Adrenalectomy↗
PubMed2005

Potassium supplementation reduces cardiac and renal hypertrophy independent of blood pressure in DOCA/salt mice.

We have demonstrated previously that deoxycorticosterone acetate (DOCA)/salt induces cardiac hypertrophy and left ventricular dysfunction independent of blood pressure (BP) in 1-renin gene mice. Because these mice also develop hypokalemia and metabolic alkalosis caused by mineralocorticoid excess, we investigated whether correcting hypokalemia by dietary potassium supplementation would prevent the DOCA/salt-induced cardiac hypertrophy, cardiac dysfunction, and electrocardiographic changes in normotensive, 1-renin gene and hypertensive, 2-renin gene mice. All mice were studied after 5 weeks of DOCA and salt administration. Potassium was given by adding 0.4 or 0.6% KCl to the drinking water. Our results show that correction of hypokalemia and metabolic alkalosis prevents cardiac hypertrophy and normalizes cardiac function without affecting BP in normotensive, 1-renin gene mice. In hypertensive, 2-renin gene mice, potassium supplementation induces a significant decrease in BP. The decrease in BP and correction of kalemia are associated with a significant but partial correction of cardiac hypertrophy. In both group of mice, electrocardiographic alterations were measured after administration of DOCA/salt, which could be corrected by potassium supplementation. Thus, these results show that correction of hypokalemia and metabolic alkalosis does prevent the development of cardiac hypertrophy and normalizes cardiac function independent of BP in normotensive, 1-renin gene mice that receive excess mineralocorticoid and salt. In 2-renin gene, hypertensive mice, potassium supplementation also prevents the development of cardiac hypertrophy, but the effect cannot be separated from the decrease in BP.

Animals↗
PubMed1994

Bicarbonate transport along the loop of Henle. II. Effects of acid-base, dietary, and neurohumoral determinants.

The loop of Henle contributes to renal acidification by reabsorbing about 15% of filtered bicarbonate. To study the effects on loop of Henle bicarbonate transport (JHCO3) of acid-base disturbances and of several factors known to modulate sodium transport, these in vivo microperfusion studies were carried out in rats during: (a) acute and chronic metabolic acidosis, (b) acute and chronic (hypokalemic) metabolic alkalosis, (c) a control sodium diet, (d) a high-sodium diet, (e) angiotensin II (AII) intravenous infusion, (f) simultaneously intravenous infusion of both AII and the AT1 receptor antagonist DuP 753, (g) acute ipsilateral mechanicochemical renal denervation. Acute and chronic metabolic acidosis increased JHCO3; acute metabolic alkalosis significantly reduced JHCO3, whereas chronic hypokalemic alkalosis did not alter JHCO3. Bicarbonate transport increased in animals on a high-sodium intake and following AII administration, and the latter was inhibited by the AII (AT1) receptor antagonist DuP 753; acute renal denervation lowered bicarbonate transport. These data indicate that bicarbonate reabsorption along the loop of Henle in vivo is closely linked to systemic acid-base status and to several factors known to modulate sodium transport.

Acid-Base Imbalance↗
PubMed1986

[A case of 21-hydroxylase deficiency and Bartter's syndrome associated with a balanced 6-9 translocation].

A 17-year-old female weighing 37 kg and 140 cm in height was referred to our hospital for evaluation of dwarfism and primary amenorrhea. She was delivered with 3350 g in weight and 50 cm in height after a ten month pregnancy without complications. No abnormal findings were revealed in physical appearance except critomegaly. Episodes of nausea, vomiting and dehydration were rare throughout her childhood, but she had a tendency to salt craving. At the age of 14, her height was 140 cm. On admission, her physical development was markedly retarded for her age, except external genitalia. Diffuse pigmentations on the trunk and extremities were observed. Her blood pressure was normal (112/62 mm Hg). Serum potassium concentration was 2.9 mEq/L. Arterial-blood gas analysis revealed metabolic alkalosis. Both of renin activity (PRA) and aldosterone concentration (PAC) in plasma at rest were markedly elevated to 15.5 ng/ml/h and 107.1 ng/dl, respectively. The plasma concentrations of pregnenolone (1449 ng/dl), progesterone (178 ng/dl), 17-OH-pregnenolone (1613 ng/dl), 17-OH-progesterone (180 ng/dl), dehydroepiandrosterone (3706 ng/dl), androstendione (824.6 ng/dl) and testosterone (900 ng/dl) were high, whereas deoxycorticosterone (15.7 ng/dl), corticosterone (0.65 microgram/dl) and cortisol (6.8 micrograms/dl) were within normal limits. Urinary 17-KS excretion showed high levels between 65.7 and 109.4 mg/day, while urinary 17-OHCS excretion was normal (5.7-7.0 mg/day). Vascular response to angiotensin II (A-II) was attenuated. Distal fractional chloride reabsorption was decreased (CH2O/CH2O+CCl = 0.62, normal: 0.92 +/- 0.04). Moderate hyperplasia of the juxtaglomerular cells was demonstrated in biopsy specimen of the kidney. Cytogenetic studies showed a 46, XX chromosome constitution with translocation of the long arm of chromosome 6 to the short arm of chromosome 9. Her mother as well as younger brother and sister, whose electrolytes and arterial-blood gas analysis showed normal values, had chromosomes with the same translocation. Treatment with dexamethasone (2 mg/day) reduced every adrenal steroids to normal range, but PRA and PAC remained high levels. Furthermore, neither hypokalemic alkalosis nor vasoreactivity to exogenous A-II was improved. Indomethacin (75 mg/day) decreased urinary excretion of prostaglandin E2 from a high level of 738.4 ng/day to 433.4 ng/day and normalized metabolic alkalosis. Vascular response to A-II was moderately improved. However, serum potassium remained low.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMedDate not supplied

Acid-base and electrolyte abnormalities in dogs with gastrointestinal foreign bodies.

Gastrointestinal foreign bodies occur commonly in dogs. The objective of the study was to describe the acid-base and electrolyte abnormalities identified in dogs with gastrointestinal foreign bodies and determine if these abnormalities are related to the site or type of foreign body present. Medical records of 138 dogs were reviewed, and information on signalment, initial venous electrolyte and acid-base values, surgical findings, relevant historical information, imaging modalities used, cost of hospital visit, intra- or postoperative complications, and survival was obtained. The site of the foreign body was recorded in 94.9% of cases and the most common site was the stomach (50%), followed by the jejunum (27.5%). The foreign bodies were linear in 36.2% of cases. The most common electrolyte and acid-base abnormalities regardless of the site or type of foreign body were hypochloremia (51.2%), metabolic alkalosis (45.2%), hypokalemia (25%), and hyponatremia (20.5%). No significant association was found between electrolyte or acid-base abnormalities and the site of foreign body. Linear, as opposed to discrete, foreign bodies were more likely to be associated with a low serum sodium concentration (odds ratio, 0.85; 95% confidence interval, 0.75-0.95). Hyperlactatemia (> 2.4 mmol/L) was seen in 40.5% of dogs. A wide variety of electrolyte and acid-base derangements are found in dogs with gastrointestinal foreign bodies. Hypochloremia and metabolic alkalosis are common in these dogs. Hypochloremic, hypokalemic metabolic alkalosis is seen with both proximal and distal gastrointestinal foreign bodies.

Acid-Base Imbalance↗
PubMed1988

Effect of hydrogen ion concentration on in vitro pulmonary vascular reactivity.

The present investigation studied the effects of hydrogen ion concentration on pulmonary vascular reactivity to the biogenic amines in vitro. Pulmonary arterial segments from cats were dissected free of surrounding tissue and endothelium and isometrically suspended in tissue baths. Cumulative dose-response curves were constructed to norepinephrine, histamine, serotonin, and potassium chloride, and the protocol was designed such that only one agent and hydrogen ion concentration was studied in each vessel segment. Alkalosis ([H+] less than or equal to 28 nmol/l) produced enhanced maximum responses to all of the agents used in this study. Acidosis [( H+] greater than or equal to 52 nmol/l), in contrast, was without effect on the maximum responses to histamine, serotonin, and potassium chloride, but did produce increased maximum responses to norepinephrine. No alterations in the ED50 of the dose-response curves were observed for any of the agents tested. In general, increases in sloped of the dose response curves were correlated with hydrogen ion concentrations that demonstrated increased maximum responses, suggesting that the present observations may have resulted from hydrogen ion-induced changes in amine receptor efficacy. The present data demonstrate that (1) as in the in vivo model, pulmonary vascular amine receptor activity is related to the hydrogen ion concentration; (2) there are two hydrogen ion concentration ranges where adrenergic receptor activity was observed to be enhanced; (3) the effects of acidosis where specific for the adrenergic receptor system, since the reactivity to only norepinephrine was significantly altered by acidosis; and (4) the effects of alkalosis may have resulted from increased overall contractility of the pulmonary vascular smooth muscle cells, since the force developed to all the agents tested was enhanced by alkalosis.

Animals↗
PubMed1975

Effect of PCO2 on epinephrine-induced lipolysis in isolated fat cells.

The effect of different pHs obtained by changing the PCO2 and the effect of PCO2 at constant pH on the lipolysis induced by epinephrine in isolated fat cells have been investigated. An inhibition of activated lipolysis was found in acidosis while in alkalosis no significant change was detected. When the experiments were performed at different PCO2s but at constant pH, the results showed an inhibition of lipolysis by high PCO2 whereas low PCO2 did not affect it. It is concluded that either acidosis or high PCO2 lead to an inhibition of the lipolysis induced by epinephrine in isolated fat cells. As regards alkalosis and low PCO2 it seems likely that the intracellular pH is not affected to the same extent as in alkalosis by high [HCO(-3)] or under the conditions of the present experiments the [H+] needed to alterate lipolysis was not reached.

Acid-Base Equilibrium↗
PubMed2004

Effects of pH on vascular tone in rabbit basilar arteries.

Effects of pH on vascular tone and L-type Ca2+ channels were investigated using Mulvany myograph and voltage-clamp technique in rabbit basilar arteries. In rabbit basilar arteries, high K+ produced tonic contractions by 11+/-0.6 mN (mean+/-S.E.,n=19). When extracellular pH (pHo) was changed from control 7.4 to 7.9 ([alkalosis]o), K+-induced contraction was increased to 128+/-2.1% of the control (n=13). However, K+-induced contraction was decreased to 73+/-1.3% of the control at pHo 6.8 ([acidosis] o, n=4). Histamine (10 microM) also produced tonic contraction by 11+/-0.6 mN (n=17), which was blocked by post-application of nicardipine (1 microM). [alkalosis]o and [acidosis]o increased or decreased histamine-induced contraction to 134+/-5.7% and 27+/-7.6% of the control (n=4, 6). Since high K+- and histamine-induced tonic contractions were affected by nicardipine and pHo, the effect of pHo on voltage-dependent L-type Ca2+ channel (VDCCL) was studied. VDCCL was modulated by pHo: the peak value of Ca2+ channel current (IBa) at a holding of 0 mV decreased in [acidosis]o by 41+/-8.8%, whereas that increased in [alkalosis]o by 35+/-2.1% (n=3). These results suggested that the external pH regulates vascular tone partly via the modulation of VDCC in rabbit basilar arteries.

Animals↗
PubMed1999

[An assessment of acid-base imbalance in body tissues and fluids].

Ions hydrogene concentration in fluids and tissues is one of the strict regulated physiological organism variables. Most common man and animal diseases are accompanied with compensated acid-base balance shift development. But diagnosis of metabolic acidosis and alkalosis with blood indices (pH, pCO2, HCO3) doesn't reflect true tissue condition that is connected not only with respiratory and excretion system functioning but with hypercompensation of metabolic processes. Excess organic acid formation in case of metabolic alkalosis formation in tissues directed to support pH leads to acidification, what brings an essential mistake in pathogenesis understanding of such diseases as cardiomyopathy, ischemic cardiac disease, myocardial infarction, hepatitis, collagenosis, caries, peptic ulcer, macula dystrophy, atherosclerosis, virus diseases, radiation damages. Ignorance primary tissue damages doesn't allow to conduct necessary preventive measures and to cure disease. It is suggested to assess development of metabolic acidosis and alkalosis by compensated changes of regulation acid-base homeostasis system, which is the basis of all future damages and development of different diseases against this background.

Acid-Base Imbalance↗
PubMedDate not supplied

Bicarbonate transport along the loop of Henle: molecular mechanisms and regulation.

The loop of Henle (LOH) is an important site of renal tubule acidification. A combination of several techniques, including in vivo microperfusion, perfusion in vitro of the S3 segment of the proximal tubule and of the thick ascending limb (TAL) of Henle's loop, as well as quantitative PCR performed on isolated TAL, has permitted the definition of key transporters and their role in modulating bicarbonate reabsorption in physiological and pathophysiological conditions. Na(+)-H+ exchange is the most important transport mechanism responsible for bicarbonate reabsorption, although a small but significant contribution of H(+)-ATPase-mediated bicarbonate reabsorption can also be identified. NHE3 is the main of several NHE isoforms expressed in the TAL and in the S3 segment of the proximal tubule. Special properties of the Na(+)-H+ exchanger in the TAL are its relative insensitivity to changes in cell pH (pHi) and the tight coupling between apical and basolateral Na(+)-H+ exchange. Several hormones, including anti-diuretic hormone (ADH), angiotensin II (AII), and gluco- and mineralocorticoids regulate Na(+)-H+ exchange. Loop diuretics such as furosemide stimulate bicarbonate transport along the LOH. Systemic acid-base disturbances also modulate bicarbonate transport: acidosis increases bicarbonate reabsorption, while metabolic alkalosis has the opposite effect. Neither hypokalemic alkalosis nor respiratory alkalosis or respiratory acidosis alter bicarbonate transport along the LOH. A significant role of HCO3 backflux, most likely through the paracellular pathway of the TAL, can also be observed. Changes in extracellular osmolality also affect bicarbonate reabsorption: hypertonicity inhibits, whereas hypotonicity stimulates transport. Transport activation is also observed as an adaptive response to glomerular hyperfiltration.

Absorption↗
PubMed1992

[Effects of pH on the endocrine system and metabolism].

Changes in extra- and intracellular pH affect metabolic states and hormone responses. In general, alkalosis stimulates and acidosis inhibits glycolysis although the relationship is not a simple one. 6-phosphofructo-1-kinase, a rate limiting enzyme in glycolysis, seems to be activated directly by a rise in pH. Alkalosis stimulates the production of pyruvic acid and lactic acid. Citric acid cycle is stimulated in alkalosis and hexose monophosphate shunt pathway is facilitated in acidosis. Acid-base disorders affect the insulin secretion and insulin action. In acidosis, insulin action in the target tissues is reduced. Other hormones, including parathormone, renin-angiotensin-aldosterone system, and adrenocorticotropine, respond to the changes in pH.

Acid-Base Imbalance↗
PubMed1992

[Acid-base disturbances in surgical operation].

Metabolic acidosis immediately after surgical operation is followed by metabolic alkalosis. Hormonal change by surgical stress and anaerobic glucolysis due to tissue ischemia cause initial lactic acidosis. Later alkalosis may be caused by secondary aldosteronism and bicarbonate production from lactate and citrate supplied by massive infusion and transfusion. Postoperative complications, such as respiratory insufficiency, renal failure and hypovolemic or septic shock, cause acidosis. In the gastrointestinal surgery, acidosis can be caused by starvation and loss of bicarbonate contained in bile, pancreatic juice or intestinal fluid, and alkalosis can be caused by loss of HCl in gastric juice. Severe acidosis can be caused by extracorporeal circulation, hypothermia, low output syndrome or declamping shock in cardioaortic surgery.

Acid-Base Imbalance↗
PubMed2003

Designing 'balanced' crystalloids.

OBJECTIVE: To present a rationale for the design of balanced resuscitation and renal replacement crystalloids based on Stewart's physical chemical approach to acid-base. DATA SOURCES: Articles and published abstracts on acid-base physiology, crystalloid infusions and renal replacement therapy. SUMMARY OF REVIEW: Although it is uncertain that crystalloid-induced metabolic acidosis causes significant harm, Stewart's approach assists in designing balanced fluids without this side effect. In his analysis, the three independent variables determining acid-base balance are PCO2, the total concentration of non-volatile weak acid (A(TOT)) and the strong ion difference (SID). Raising and lowering A(TOT) while holding SID constant cause a metabolic acidosis and alkalosis respectively. Lowering and raising plasma SID while clamping A(TOT) cause a metabolic acidosis and alkalosis respectively. The SID of a crystalloid is its [HCO3-], or that part of an organic bicarbonate surrogate which is metabolised on infusion. Rapid infusion alters plasma SID towards crystalloid SID, but also lowers A(TOT) by haemodilution. We have shown that the SID of a balanced infusion crystalloid is 24 mEq/L. This generates a fall in plasma SID precisely counteracting the A(TOT) dilutional alkalosis. In contrast, a balanced renal replacement crystalloid must generate a higher plasma SID appropriate for the existing A(TOT), since there is no dilution. If A(TOT) is low, as in hypoalbuminaemia, the balanced dialysis SID falls correspondingly. A further SID reduction is needed to counteract Donnan effects within the filter. CONCLUSIONS: A crystalloid SID of 24 mEq/L is 'balanced' for rapid intravenous administration. The 'balanced' SID of renal replacement fluids is likely to be significantly higher, although less than the normal plasma SID of 42 mEq/L.

Journal Article↗