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PubMed1979

Acid-base disturbance in patients with fulminant hepatic failure.

Forty-two arterial blood pH and gas determinations were carried out on 11 patients with fulminant hepatic failure. The most common type of acid-base disturbance was that of respiratory alkalosis in 22 cases (52.4%). This was partially compensated in 13 subjects (31.0%) while an accompanying metabolic alkalosis was present in 9 (21.5%). Partially compensated metabolic acidosis was observed on 15 occasions (35.7%), all of which were in patients with laboratory evidence of impaired renal failure. The mental status of the patients was evaluated in each of the categories of acid-base disturbances. Some degree of correlation was evident between the PCO2 and the magnitude of base excess and that of the severity of the encephalopathy. The lower PCO2 and greater negative base excess values tended to be nearly always present in totally comatose subjects. By contrast, there was no clear cut relationship between pH and mental state.

Acid-Base Imbalance↗
PubMed2002

Liddle syndrome in a newborn infant.

A 10-week-old female infant developed hypertension. The elevated blood pressure was associated with metabolic alkalosis and urinary chloride wastage. The family history was unremarkable. Her urinalysis, blood urea nitrogen (BUN), and serum creatinine concentrations were all normal. A renal ultrasound was normal. A technetium-99m diethylenetriaminopentoacetic acid (DTPA) renal scan with captopril showed normal blood flow bilaterally. The head ultrasound and echocardiogram were normal. Blood epinephrine, norepinephrine, catecholamines, thyroxine, and steroid levels were also normal. Treatment with various combinations of labetalol, hydralazine, captopril, methyldopa, nifedipine, and spironolactone, all at high doses, failed to control the elevated blood pressure. Serum aldosterone level and peripheral plasma renin activity were low. The lack of therapeutic response to spironolactone, with a good response to amiloride and recurrence of hypertension and metabolic alkalosis after amiloride cessation that was subsequently treated with amiloride, established the diagnosis of Liddle syndrome. To our knowledge, this is the youngest patient with Liddle syndrome that has been reported in the literature.

Alkalosis↗
PubMed2006

Pseudo-Bartter syndrome in a pregnant mother and her fetus.

Pseudo-Bartter syndrome presents the same clinical and biological characteristics as Bartter syndrome but without primary renal tubule abnormalities. We relate the case of a premature baby presenting at birth with severe hypokalemic metabolic alkalosis associated with hyponatremia and hypochloremia. Maternal blood at the time of delivery showed the same electrolyte perturbations. The baby's mother had suffered from anorexia and vomiting during pregnancy. A few weeks after birth the baby's blood abnormalities had almost returned to normal. Chloride depletion is at the origin of both maternal and fetal hypokalemic alkalosis.

Adult↗
PubMed1975

Intracellular pH in unanesthetized dogs during panting.

Intracellular pH, arterial blood gases and several plasma enzymes were estimated in unanesthetized dogs during a 3-hour exposure to 30 degrees C/50% relative humidity, and 40 degrees C/50% relative humidity. No change occurred during mild heat stress, whereas during severe heat stress a profound respiratory alkalosis developed together with an increase in intracellular pH from 7.03 to 7.29. Most plasma enzymes increased by about 300% or more. In spite of extreme panting body temperature rose to 42.2 degrees C. Exposure to 40 degrees C/50% relative humidity with 4% CO2 in the climatic chamber inhibited the respiratory alkalosis and the increase of plasma enzymes. Though the panting frequency was lower the ventilatory heat dissipation was more efficient. Body temperature rose to only 39.8 degrees C. It is concluded that the intracellular buffering is not able to prevent marked changes of the intracellular pH during panting.

Acid-Base Equilibrium↗
PubMed1979

Effect of hypocapnia on intracellular pH during metabolic acidosis.

Separate and combined effects of acute metabolic acidosis and hypocapnia were determined in skeletal and cardiac muscles of intact rats. Normocapnic metabolic acidosis, imposed by intraperitoneal injection of hydrochloric acid (6 mEq/kg), did not change skeletal muscle intracellular acid--base parameters. Hypocapnia, induced by mechanical hyperventilation, resulted in intracellular alkalosis within skeletal muscle during both respiratory alkalosis and compensated metabolic acidosis; changes of skeletal muscle intracellular bicarbonate concentration per unit change in carbon dioxide tension were identical during these two experimental procedures. These data suggest that processes other than physicochemical buffering neutralize protons taken into skeletal muscle cells during acute metabolic acidosis. The acid--base state of the heart was quite stable during these experimental manipulations; thus, it appears that cardiac muscle has an extraordinary buffering ability. Moreover, our data suggest that processes other than physicochemical buffering maintain cardiac intracellular pH normal during hypocapnia.

Acidosis↗
PubMed1981

Electrolyte composition of cerebrospinal fluid in acute acid-base disorders.

Electrolyte composition of cisternal CSF was measured during 4 hours of respiratory and metabolic acid-base disturbance in anesthetized dogs. Three groups of dogs were studied: (1), isocapnic metabolic alkalosis; (2), acute respiratory acidosis; and (3), combined respiratory acidosis and metabolic alkalosis. Cisternal CSF [K+] remained unchanged despite significant changes in plasma [K+], PCO2 and [HCO3-]; suggesting that mechanisms involved in regulation of CSF [K+] continue to operate normally under such conditions. Cisternal [Na+] and osmolality remained unchanged with almost identical reciprocal equimolar changes in CSF concentration of Cl- and HCO3- during the acid-base disorders studied. The regulatory mechanisms involved in this Cl- -HCO3- exchange may be different in different acid-base disorders, but since CSF [Na+] is kept constant, CSF [HCO3-] in any acid-base disorder equals the difference between CSF [Na+] and CSF [Cl-].

Acid-Base Imbalance↗
PubMed1987

Skeletal muscle oxygen availability during respiratory acid-base disturbances in cats.

Respiratory acid-base disorders elicit physiological responses that alter O2 delivery to various tissues. We have used a near infrared (NIR) optical technique to monitor cytochrome a,a3 oxidation state, tissue O2 store (relative hemoglobin plus myoglobin oxygenation), and regional blood volume in intact resting skeletal muscle during respiratory acid-base disturbances in anesthetized cats. Hypercapnic acidosis and hypocapnic alkalosis were produced in separate groups of animals by ventilation with increasing concentrations of CO2 (n = 13) or hyperventilation (n = 8). Respiratory acidosis decreased oxygen availability to hindlimb muscle while respiratory alkalosis did not change tissue oxygenation. Inspired CO2 progressively decreased muscle blood volume, cytochrome a,a3 oxidation level, and muscle oxygen store. These optical responses were greatly attenuated both by pre-treatment with bretylium and by hemorrhagic hypotension, suggesting mediation through sympathetic vasoconstriction. Metabolic acidosis, produced by intravenous HCl infusion (n = 8), did not reproduce the hindlimb optical responses mediated by CO2. These experiments demonstrate that hypercapnic acidosis significantly decreases oxygen supply to resting skeletal muscle in the anesthetized cat, probably via neuroregulatory responses to CO2 which do not depend on changes in arterial [H+] in the tested pH range.

Acidosis, Respiratory↗
PubMed1988

Regulation of pH and HCO3 in brain and CSF of the developing mammalian central nervous system.

Acute (2-h) metabolic acidosis or alkalosis was induced in immature rats to ascertain the ability of their incompletely-developed CNS to regulate pH when challenged with perturbations in blood [H] and [HCO3]. Brain and cisternal CSF pH were determined from steady-state distribution of [14C]dimethadione, a weak organic acid. By 1 week post partum, there was a remarkable stability of pH in the cerebral cortex of animals subjected to arterial pH extremes of 7.1 and 7.5. However, CSF pH in 1-week-old animals rendered alkalotic remained 0.07-0.08 units above control due to lack of a compensatory increase in pCO2, and to a blood-CSF barrier apparently more permeable to HCO3. As arterial HCO3, i.e. [HCO3]art, was varied from about 10 to 30 mmol/l, the infants maintained [HCO3]csf only half as effectively as adults, i.e. delta [HCO3]art was 0.4 and 0.2 at 1 and greater than 4 weeks, respectively. Throughout postnatal ontogenesis, [HCO3]csf was more resistant to alteration by metabolic acidosis than by alkalosis. Overall, the results indicate that immature rats challenged with systemic acid-base loads are less capable than adults in regulating CSF pH, but they are able to maintain brain pH.

Acidosis↗
PubMed1995

Liquorice-induced hypertension--a new understanding of an old disease: case report and brief review.

The case is described of a 40-year-old female with severe hypertension and hypokalaemic metabolic alkalosis, due to prolonged liquorice ingestion. The pseudo-aldosterone-like effects of liquorice have always been attributed to glycyrrhizic acid, but its biochemical substrate has remained elusive. It is now known that glycyrrhetenic acid, the hydrolytic metabolite of glycerrhizic acid, is the active component of liquorice which causes inhibition of the peripheral metabolism of cortisol. Cortisol binds with the same affinity as aldosterone to the mineralocorticoid receptor resulting in a hypermineralocorticoid condition. Ingestion of liquorice may therefore result in retention of sodium and water, hypertension, hypokalaemia, alkalosis and suppression of the renin-aldosterone system. The literature on liquorice-induced hypertension is briefly reviewed with emphasis on the biochemical features of this mineralocorticoid excess syndrome.

Adult↗
PubMed2006

Control of rectal gland secretion by blood acid-base status in the intact dogfish shark (Squalus acanthias).

In order to address the possible role of blood acid-base status in controlling the rectal gland, dogfish were fitted with indwelling arterial catheters for blood sampling and rectal gland catheters for secretion collection. In intact, unanaesthetized animals, isosmotic volume loading with 500 mmol L-1 NaCl at a rate of 15 mL kg-1 h-1 produced a brisk, stable rectal gland secretion flow of about 4 mL kg-1 h-1. Secretion composition (500 mmol L-1 Na+ and Cl-; 5 mmol L-1 K+; <1 mmol L-1 Ca2+, Mg2+, SO(4)2-, or phosphate) was almost identical to that of the infusate with a pH of about 7.2, HCO3- mmol L-1<1 mmol L-1 and a PCO2 (1 Torr) close to PaCO2. Experimental treatments superimposed on the infusion caused the expected disturbances in systemic acid-base status: respiratory acidosis by exposure to high environmental PCO2, metabolic acidosis by infusion of HCl, and metabolic alkalosis by infusion of NaHCO3. Secretion flow decreased markedly with acidosis and increased with alkalosis, in a linear relationship with extracellular pH. Secretion composition did not change, apart from alterations in its acid-base status, and made negligible contribution to overall acid-base balance. An adaptive control of rectal gland secretion by systemic acid-base status is postulated-stimulation by the "alkaline tide" accompanying the volume load of feeding and inhibition by the metabolic acidosis accompanying the volume contraction of exercise.

Acid-Base Equilibrium↗
PubMed1984

End-tidal CO2 and tissue pH in the monitoring of acid-base changes: a composite technique for continuous, minimally invasive monitoring.

The infrared CO2 analyzer continuously monitors the CO2 tension in exhaled air at end-tidal expiration. In experimental animals, we found a consistent relationship between PaCO2 and end-tidal CO2 (ET.CO2) in the normal steady state, and in acid-base disturbances (respiratory acidosis and alkalosis, and hypoperfusion acidosis). Paired data analyses of PaCO2 (X) and ET.CO2 (Y) yielded correlation coefficients of r = 0.98 (Y = 0.96X + 4.43) during progressive hypercarbia (PaCO2: 32----110 torr), and r = 0.93 (Y = 0.89X + 0.93) during hyperventilation hypocapnia (PaCO2: 41----14 torr). The relationship between PaCO2 and ET.CO2 was seen during hypovolemic shock if pulmonary perfusion was maintained uniform in all areas of lung. The ability of the ET.CO2 sensor to predict instantaneously the PaCO2 makes it attractive enough to be used in conjunction with the subcutaneous tissue pH(pHe) sensor in the management of acid-base disturbances. After hypercarbia (FiCO2 0.15 X 40 min; PaCO2/ET.CO2: 100/101 torr), when the dogs were returned to room air, abruptly both the ET.CO2 and pHe sensors were sensitive to the changes in Fi.CO2. But the response of the ET.CO2 was swifter. The advent of transcutaneous gas monitors has shown that intermittent blood gas analyses, however frequent, are inadequate for the monitoring of the rapidly altering blood gas status in the acutely ill. The ability of the pHe sensor to identify whole-body acidosis and alkalosis combined with the speed and ease of the ET.CO2 monitor in pinpointing hypercarbic and hypocarbic states makes this two-parameter system suitable for the continuous, noninvasive monitoring of the critically ill.

Acidosis, Respiratory↗
PubMed1986

Spironolactone-reversible rickets associated with 11 beta-hydroxysteroid dehydrogenase deficiency syndrome.

A 7-year-old girl had growth retardation, hypertension, and hypokalemic alkalosis. Baseline serum aldosterone concentration and plasma renin activity were low and unresponsive to sodium deprivation and to orthostatic changes. Baseline serum progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, and cortisol levels were normal and adequately responsive to ACTH stimulation. No steroid was found abnormally elevated. A diagnosis of 11 beta-hydroxysteroid dehydrogenase deficiency was established on the basis of elevated urinary tetrahydrocortisol plus allotetrahydrocortisol/tetrahydrocortisone ratio, determined by gas chromatography-mass spectrometry. Evaluation of bone mineral metabolism and parathyroid function, and skeletal radiographs, revealed the presence of rickets and secondary hyperparathyroidism. Treatment with spironolactone alone for 2 months corrected hypertension, hypokalemic alkalosis, and all laboratory and radiologic evidence of rickets and hyperparathyroidism, resulting in acceleration of growth rate. The response to spironolactone suggests that a hypermineralocorticoid state is responsible for the hypertensive syndrome and that rickets and hyperparathyroidism could be a consequence of excess mineralocorticoid activity.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1984

Resuscitation and arterial blood gas abnormalities during prolonged cardiopulmonary resuscitation.

A study was undertaken to determine the pattern of arterial blood gas (ABG) concentration in the canine model undergoing prolonged cardiopulmonary resuscitation (CPR) from fibrillatory arrest, and to determine the importance of acid base abnormalities in predicting resuscitation. Ventricular fibrillation was induced electrically in 12 dogs. CPR was begun at 3 minutes and continued for 27 minutes, at which time the dogs were defibrillated. ABG samples were taken at 0, 8, 18, and 28 minutes of ventricular fibrillation. Seven of the 12 dogs were resuscitated successfully. There was no difference in pH, PCO2, or PO2 between the survivors and nonsurvivors at any of the points measured. A pattern of pH and PCO2 abnormalities was noted in each dog over 30 minutes. Each developed a respiratory alkalosis that peaked at 8 minutes. During the next 22 minutes the pH gradually declined. This combination of respiratory alkalosis and metabolic acidosis resulted in normalization of the pH at about 18 minutes of fibrillation. We concluded that when adequate ventilation is provided in the canine model undergoing CPR, significant arterial acidemia does not occur for at least 18 minutes. Further, acid base abnormalities did not correlate with successful resuscitation.

Acidosis↗
PubMed1983

Urinary sodium and chloride during renal salt retention.

One hundred ten episodes of renal salt retention (urinary sodium and/or chloride less than 10 mEq/L) were studied retrospectively to determine the significance of discordance of urinary sodium from chloride. In 16 episodes the urinary sodium exceeded chloride by at least 15 mEq/L. This disparity was associated with the necessity for urinary excretion of substantial quantities of poorly reabsorbed anions (penicillin, ketones, or diatrizoate), a rapidly falling serum bicarbonate level (due to resolving metabolic or developing respiratory alkalosis), or substantial renal insufficiency (serum creatinine greater than 3 mg/dL). In 14 of 110 episodes, urinary chloride exceeded urinary sodium by at least 15 mEq/L. These patients were more often oliguric and had a higher mean serum chloride than patients without this dissociation. In patients with oliguria, hyponatremia, or metabolic alkalosis, measurement of urinary sodium or chloride alone will, in a substantial number of cases, fail to detect renal salt retention. When evidence is sought for renal salt retention, both urinary sodium and chloride should be determined.

Aged↗
PubMed1976

Approach to acid-base problems in the critically ill and injured.

The use of the Henderson-Hasselbalch equation and the relationships between bicarbonate levels and the pCO2 or carbonic acid concentration in evaluating acid-base abnormalities are explained. The etiology, pathophysiology, diagnosis and treatment of respiratory alkalosis and acidosis and metabolic alkalosis and acidosis are discussed. The results of laboratory tests should be examined in relation to the patient's condition and consistency with other laboratory tests. Therapy is directed at correcting the underlying problems and, secondarily, at correcting the numbers. Patients respond primarily to rate of change and not absolute numbers. Therefore, problems should be corrected at approximately the rate they develop. Treatment should be guided by continued patient observation and serial laboratory studies.

Acid-Base Imbalance↗
PubMed1982

Effects of two models of hypercalcemia on renal acid base metabolism.

The effects of two models of chronic hypercalcemia on renal acid-base metabolism were studied in rats. In the first series of experiments, rats were rendered hyperparathyroid by the autologous grafting of 20 to 24 parathyroid glands into a single recipient. Hypercalcemia (5.48 +/- 0.03 mEq/liter in high PTH animals, 4.96 +/- 0.06 mEq/liter in pair-fed controls, P less than 0.001) occurred as did metabolic alkalosis (plasma total carbon dioxide 25.44 +/- 0.47 mEq/liter vs. 23.84 +/- 0.57 in controls, P less than 0.05). The rise in total carbon dioxide was in part a renal tubular effect since urine pH was lower (6.77 +/- 0.04 vs. 6.95 +/- 0.04, day 5, P less than 0.01) bicarbonaturia less (165 +/- 26 vs. 283 +/- 28 mumoles/24 hr, day 5, P less than 0.01) and titratable acid (TA) excretion increased (164 +/- 43.4 vs. 48.2 +/- 2.53 mEq/24 hr, day 5, P less than 0.01) in hyperparathyroid animals vs. pair-fed controls. To test the specific role of hypercalcemia versus PTH in this effect, normoparathyroid animals were treated with 1.25 (OH)2 vitamin D3 or SHAM injected, Urinary cAMP was reduced in these animals (0.030 +/- 0.004 mumoles/8 hr) compared to hyperparathyroid rats (0.055 +/- 0.01 mumoles/8 hr P less than 0.05) suggesting differences i PTH levels. Hypercalcemia occurred in 1,25(OH)2 vitamin D treated animals as did increased plasma total carbon dioxide and urinary TA while urinary bicarbonate excretion and urinary pH were reduced. Because hypercalcemia was associated with elevated total carbon dioxide in both models, it is proposed that chronic hypercalcemia stimulated renal acid excretion and in a sustained manner results in metabolic alkalosis, at least in part, on a renal basis.

Acid-Base Equilibrium↗
PubMed1985

Selective dietary potassium depletion and acid-base equilibrium in the rat.

K+ depletion of two kinds was induced in two groups of rats by selective dietary restriction for up to 5 weeks. Complete metabolic studies for H+, K+, Na+ and Cl- were carried out daily during weeks 1, 3 and 5. In control rats of group A (receiving K+ with sodium chloride), plasma pH (7.47) and HCO3- (25 mmol/l), as well TA (titratable acid)--HCO3- and NH+4 urinary excretion rates, were stable, while balances were nil for K+ and slightly positive for Cl-. In K+-deprived rats of group A receiving sodium chloride, a progressive metabolic alkalosis developed (plasma pH reached 7.57 and HCO3- 35.8 mmol/l by 5 weeks), and TA--HCO3- and NH+4 urinary excretion rates were not different from controls. Plasma K+ fell progressively from 4.20 to 2.20 mmol/l, with negative K+ balance. Balances for Na+ and H2O were highly positive and plasma renin activity and aldosterone decreased by week 5. Hypochloraemia developed with positive Cl- balance. In control rats of group B (receiving K+ with neutral sodium phosphate), a slight metabolic alkalosis developed, and TA--HCO3- excretion rate was increased compared with control rats of group A.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1986

Effects of acid-base disturbances on renal handling of magnesium in the dog.

Clearance and micropuncture studies were performed in four groups of acutely thyroparathyroidectomized animals to study the effects of alkalosis and acidosis on the renal handling of magnesium. Our results indicate that chronic metabolic acidosis reduces, whereas acute metabolic alkalosis enhances, magnesium reabsorption. The site within the nephron where absorption of magnesium increases or decreases during acid-base disturbances was beyond the late proximal tubule. Tubular fluid bicarbonate was also measured in these experiments, and the results indicated that magnesium reabsorption in the distal tubule correlated to bicarbonate delivery. However, whether this was a direct or an indirect effect of bicarbonate on magnesium transport could not be delineated.

Absorption↗