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PubMed1978

Chronotropic response of isolated atria to acid base alterations.

The effect of acid-base alterations on spontaneous rate was analysed using isolated atria exposed to cumulative degrees of acidosis produced either by adding HCl or by increasing PCO2 in the incubation medium. Frequncy vs. pH curves were made to assess chronotropic response to acid-base changes. Heart rate was increased in alkalosis and decreased when the pH of the medium was lowered. Both "respiratory" and "metabolic" alterations affected the contraction rate to the same extent. Decreasing pH from normal values seemed to decrease heart rate more than the enhancement produced by the same change in pH towards the alkalotic side. When frequency was plotted as a function of hydrogen ion activity (aH+) a more linear relationship was obtained, either with pure "metabolic" or with "respiratory" acid-base alterations. Increasing (aH+) from normal values seemed to decrease heart rate to the same extent (respiratory alterations) or even less (metabolic alterations) than the enhancement produced by the same change in (aH+) towards the alkalotic side. Neither the increase in rate produced by alkalosis nor the decrease induced by acidosis were prevented by blocking the neurotransmitters by atropine or propranolol.

Acidosis↗
PubMed1965

CARCINOMA OF LUNG WITH ADRENAL HYPERFUNCTION AND HYPERCALCEMIA TREATED BY PARATHYROIDECTOMY.

A case of severe hypercalcemia secondary to carcinoma of the lung is described in which hypokalemic alkalosis, renal failure and pancreatitis were also present. The relative importance of the few bone metastases found at autopsy is considered, and a probable endocrine-like effect of the tumour in the development of the hypercalcemia is postulated. Treatment of the hypercalcemia included administration of corticosteroids and disodium EDTA, peritoneal dialysis and subtotal parathyroidectomy; the most effective of these was peritoneal dialysis. Subtotal parathyroidectomy failed to produce a further decrease in serum calcium values. The occurrence of hypokalemic alkalosis in the presence of increased adrenocortical function and its relationship to the carcinoma of the lung are discussed. The possibility that this neoplasm produced two factors which caused systemic effects ordinarily associated with the function of endocrine glands must be considered.

Adrenal Cortex Hormones↗
PubMed1978

[Acid-base metabolism in patients with hepatic cirrhosis treated with portacaval anastomosis at various intervals after the operation].

In a series of 68 cirrhotics subjected to portacaval anastomosis for digestive haemorrhage, alterations in the acid base balance, 3, 6, 12, 24 and 48 weeks after anastomosis, were examined. Following operation, an increase in the incidence of the usual acid base disturbances of liver cirrhosis is observed. Respiratory alkalosis increases with no direct relationship to teh postoperative increase in ammoniemia, the main stimulating agent of the resporatory centres. This is probably because the active fraction on the nerve cells is the non-ionized one only, freely diffusible through the haematoencephalic barrier, the plasma concentration of which is a function of blood pH. Postoperative metabolic alkalosis is secondary to the potassium and chloride depletion consequent on operative trauma, on the malnutrition syndrome and, in the case of potassium, on secondary hyperaldosteronism which, unlike what is observed in the other groups of cirrhotics, is uncorrected by anastomosis. After the shunt, metabolic acidosis may be the expression of an increase in lactates and pyruvates following on further liver function deterioration, and of a functional renal insufficiency which anastomosis makes more manifest.

Acid-Base Equilibrium↗
PubMed1993

[Disorders of the acid-base equilibrium in delirium tremens].

The objective of the present work was to assess the most frequent disorder of the acid-base equilibrium in delirium tremens. The author examined a group of 77 alcoholics with delirium tremens. In 62 (80.5%) by the Astrup method respiratory alkalosis was detected, in 7 (9%) metabolic alkalosis was recorded, in 1 (1.5%) metabolic acidosis and in 7 patients (9%) the values of the acid-base equilibrium were normal. In predominant alkalotic syndrome the mean serum potassium level was lower, 3.4 mmol/l (2.2-4.6), and the level of chlorides 97.8 mmol/l (50-144.5). The mean sodium concentration was 138.1 mmol/l (121.5 to 147). The author discusses the causes of the impaired acid-base balance in delirium tremens. It is assumed that the main cause is the rebound phenomenon of the respiratory centre which causes hyperventilation and changes of the ion metabolisms induced by alcohol abuse and its discontinuation. A negative effect is exerted by shortage of energy substrates and protein catabolism the effect of ethyl alcohol on the intermediary metabolism, the psychosis as such, insufficiency of parenchymatous organs and neurohumoral dysregulation after discontinued alcohol intake. Examination of the acid-base equilibrium in delirium tremens is essential for differential diagnosis, correct treatment and prevention of complications. The author discusses briefly treatment of delirium tremens and principles of correction of associated acid-base and ion disorders.

Adult↗
PubMed2001

Sclerochoroidal calcification: clinical manifestations and systemic associations.

BACKGROUND: Sclerochoroidal calcification is an unusual ocular condition that is believed to be idiopathic in most cases. OBJECTIVES: To describe the clinical manifestations of sclerochoroidal calcification and to investigate its possible systemic associations. METHODS: This noncomparative consecutive case series included patients diagnosed as having sclerochoroidal calcification based on clinical characteristics and diagnostic test findings. We analyzed the demographic, systemic, and ocular features of 27 such patients. Systemic evaluation included tests for calcium-phosphorus metabolism in 19 patients and renal tubular hypokalemic metabolic alkalosis syndromes (Bartter or Gitelman syndrome) in 13. RESULTS: All the patients were asymptomatic older (mean age, 70 years) white individuals, incidentally noted as having a choroidal lesion on routine examination. Among 38 eyes, the main referral diagnoses were choroidal metastasis in 10 eyes (26%), choroidal melanoma in 8 (21%), and choroidal nevus in 4 (11%). Sixteen patients (59%) had unilateral clinical findings, while 11 (41%) had bilateral. The Snellen visual acuity was 20/50 or better in 37 eyes (97%). Cogan scleral plaque was visible anterior to the insertion of horizontal rectus muscles in 10 eyes (26%). Among 77 foci, there were a mean of 2 foci of sclerochoroidal calcification in each eye, 41 yellow (53%), 32 yellow-white (42%), 2 white (3%), and 2 orange (3%), measuring a mean 2.6 mm in diameter and 1.1 mm in thickness. The most common locations were postequatorial in 45 (58%), along the temporal vascular arcades in 30 (39%), and in the superotemporal quadrant in 43 (56%). A-scan and B-scan ultrasonography revealed dense echoes compatible with calcium, with orbital shadowing. All the lesions remained stable in size and configuration during a mean follow-up of 38 months. One patient developed a choroidal neovascular membrane over the area of sclerochoroidal calcification. Investigations for abnormal calcium-phosphorus metabolism in 19 patients revealed primary hyperparathyroidism in 1 patient (5%). Clinical and biochemical evaluation of 13 patients demonstrated hypomagnesemia in 6 (46%). Four patients (31%) met the criteria for the diagnosis of Gitelman syndrome. CONCLUSIONS: Sclerochoroidal calcification usually manifests as multiple discrete yellow placoid lesions in the midperipheral fundus of asymptomatic older white individuals. Although most cases may be idiopathic in nature, some patients may have underlying systemic disorders involving abnormal calcium-phosphorus metabolism or renal tubular hypokalemic metabolic alkalosis syndromes. All patients with sclerochoroidal calcification should be tested for these treatable systemic associations.

Adult↗
PubMed1976

Pancreatitis and severe metabolic abnormalities due to phenformin therapy.

Two elderly diabetic patients with abdominal pain were demonstrated to have complications of phenformin hydrochloride therapy. The first developed severe lactic acidosis treated with sodium bicarbonate given intravenously and followed by rebound alkalosis. The second showed severe acidosis (specimens for lactate determination were unfortunately unsatisfactory for analysis) and similar alkalotic rebound after therapy. She then developed severe pancreatitis, proved at operation, no cause for which other than phenformin was apparent. Poor renal and hepatic function predispose to these conditions by increasing serum phenformin levels and by decreasing urinary excretion of its metabolites. The acidosis should be treated judiciously with sodium bicarbonate administered intravenously. A rebound alkalosis, ensuring as the accumulated lactate is metabolized, is best treated by potassium chloride and ammonium chloride given intravenously. The mechanism by which phenformin causes pancreatitis is unknown, but termination of therapy causes cessation of the pancreatitis.

Acidosis↗
PubMed1997

Insulin-dependent diabetes mellitus presenting with ketoalkalosis in Rett syndrome.

A 9-year-old girl with Rett syndrome presented with typical symptoms of insulin-dependent diabetes mellitus. Upon investigation she was found to have a primary respiratory alkalosis associated with diabetes ketoacidaemia. Once non-ketotic normoglycaemia was achieved her respiratory alkalosis persisted. This was felt to be due to an abnormal breathing pattern of hyperventilation punctuated by apnoeas which is associated with Rett syndrome.

Alkalosis↗
PubMed1994

Phosphorus magnetic resonance spectroscopic imaging in patients with frontal lobe epilepsy.

Phosphorus magnetic resonance spectroscopic imaging has previously demonstrated localized metabolic abnormalities within the epileptogenic region in patients with temporal lobe epilepsy, including alkalosis, increased inorganic phosphate level, and decreased phosphomonoester levels. We studied 8 patients with frontal lobe epilepsy, finding interictal alkalosis in the epileptogenic region compared to the contralateral frontal lobe in all patients (7.10 +/- 0.05 vs 7.00 +/- 0.06, p < 0.001). Seven patients exhibited decreased phosphomonoester levels in the epileptogenic frontal lobe compared to the contralateral frontal lobe (16.0 +/- 6.0 vs 23.0 +/- 4.0, p < 0.01). In contrast to findings in temporal lobe epilepsy, inorganic phosphate level was not increased in the epileptogenic region. Based on values derived from normal control subjects, 5 patients had elevated pH in the seizure focus and 2 patients had decreased phosphomonoesters while none had abnormalities in the contralateral frontal lobe. These data suggest that magnetic resonance spectroscopy will be useful in the presurgical evaluation of patients with frontal lobe epilepsy.

Adolescent↗
PubMed1983

J10 lactate-induced polycythemia in newts.

Specimens of Triturus cristatus carnifex (Laurenti) raised for about 3 weeks in a 3 gm/liter solution of sodium lactate present a slight alkalosis and a mean increase of about 35% in the red blood cell count in comparison to control animals raised in identically oxygenated water; analogous treatment with an equal molar concentration of sodium pyruvate produces only alkalosis. Since lactate alone determines an increase in the number of erythrocytes as does hypoxia, and hypoxia always induces an increase in plasma lactate levels, it can be deduced that erythropoietin (ESF) production is stimulated by an increase in plasma lactate and not directly by a lack of oxygen. The hypothesis that ESF in newts is produced by the "lactate-sensitive cells" of the renal corpuscles, which hypertrophy after experimental anaemia or treatment with lactic acid salts, is indirectly confirmed.

Alkalosis↗
PubMed1998

Simultaneous intracellular and extracellular pH measurement in the heart by 19F NMR of 6-fluoropyridoxol.

6-Fluoropyridoxol (6-FPOL) was evaluated as a simultaneous indicator of intracellular and extracellular pH and, hence, pH gradient in perfused rat hearts. After infusion, 19F NMR spectra rapidly showed two well-resolved peaks assigned to the intracellular and extracellular compartments, and pH was calculated on the basis of chemical shift with respect to a sodium trifluoroacetate standard. To demonstrate use of this molecule, dynamic changes in myocardial pH were assessed with a time resolution of 2 min during respiratory and metabolic alkalosis or acidosis and ischemia. For a typical heart, intracellular pH (pHi) = 7.14+/-0.01 and extracellular pH (pHe) = 7.52+/-0.02. In response to metabolic alkalosis, pHi remained relatively constant and the pH gradient increased. In contrast, respiratory challenge caused a significant increase in pHi. Independent measurements using pH electrodes and 31P NMR confirmed validity of the 19F NMR results.

Alkalosis, Respiratory↗
PubMed2001

Cystic fibrosis in three children with bronchopulmonary dysplasia.

Cystic fibrosis (CF) and bronchopulmonary dysplasia (BPD) are two common causes of chronic lung disease in children. Patients with BPD or CF often have recurrent respiratory symptoms, failure to thrive, and/or metabolic alkalosis during infancy and childhood. Thus, recognizing the diagnosis of CF in an infant with BPD can be difficult. We present three infants with both BPD and CF. The infants shared a history of respiratory distress and prolonged oxygen requirements. All three also had difficulty gaining weight, even after pancreatic enzyme supplementation was instituted. Metabolic alkalosis was observed in two infants. Previous studies in children with CF suggest that early diagnosis may impact both lung health and nutritional status. A high index of suspicion is necessary for clinicians to identify these children early and intervene with appropriate therapy.

Alkalosis↗
PubMedDate not supplied

Normocarbic hyperventilation fails to induce pulmonary vasodilation.

The pulmonary vasodilator effect of increased rate of mechanical ventilation, with and without respiratory alkalosis, was studied in chronically instrumented newborn lambs. Pulmonary hypertension was first induced by ventilating with a hypoxic gas mixture. Subsequent respiratory alkalosis caused significant decreases in pulmonary arterial pressure and pulmonary vascular resistance. When normocarbia was re-established by adding carbon dioxide to the inspired gas, with the ventilator rate being held constant, the pressure and resistance returned to the baseline hypertensive state. Therefore, mechanical factors, either direct or indirect, appear to be of minor importance in the mechanism of pulmonary vasodilation secondary to frequency-induced hyperventilation.

Alkalosis, Respiratory↗
PubMed1980

Acid-base balance and plasma glutamine concentration in man.

Plasma glutamine concentrations were measured in chronic metabolic acidosis and alkalosis in healthy male volunteers. Metabolic acidosis resulted in a significant drop in glutamine concentration while metabolic alkalosis significantly elevated glutamine levels. These changes in glutamine concentration correlated with both the bicarbonate and PCO2 levels. To determine whether bicarbonate or PCO2 levels influence the glutamine concentrations, respectively acidosis was induced by respiring 5% CO2. This resulted in a significant elevation in both PCO2 and glutamine while bicarbonate levels remained unchanged. The results demonstrate an effect of acid-base alterations upon plasma glutamine concentration mediated by PCO2.

Acidosis↗
PubMed1993

The effect of normocapnic hypoxia and the duration of exposure to hypoxia on supramaximal exercise performance.

Two investigations were designed that (a) evaluated the effect of the respiratory alkalosis that accompanies breathing an hypoxic (H) gas mixture and (b) examined the influence of the duration of breathing this H mixture on the subsequent performance of 45 s supramaximal dynamic exercise. In experiment 1, 12 men performed a 45-s Wingate Test (WT) on three occasions breathing a normoxic (N; 20.9% O2), H (11.3% O2), or normocapnic hypoxic (H+CO2; 11.5% O2, 2.25% CO2) gas mixture for 20 min prior to performing the WT. For experiment 2, nine men performed a 20-min normoxic (N20) and three hypoxic WT trials which consisted of breathing an 11% O2 balance N2 gas mixture for 10 min (H10), 20 min (H20) or 30 min (H30) prior to the WT. For experiment 1, VO2 was significantly reduced during the 45-s H [mean (SD); 1.22 (0.23) l] and H+CO2 [1.12 (0.18) l] trials compared with the N trial [1.78 (0.18) l] Peak power output (Wpeak) during WT was similar across trials. However, a small (less than 3%) but significant reduction in the mean power output (W) was observed in both the H and H+CO2 trials [6.8 (0.6) W.kg-1] compared with the N trial [7.0 (0.6) W.kg-1]. Prior to performing the WT, blood pH and PCO2 were similar [7.40 (0.02) and 5.3 (0.3) kPa, respectively] for the N and H+CO2 trials. A respiratory alkalosis accompanied the H condition [7.46 (0.02) for pH and 4.6 (0.3) kPa for PCO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effect of acute sodium bicarbonate ingestion on excess CO2 output during incremental exercise.

The effect of bicarbonate ingestion on total excess volume of CO2 output (CO2 excess), due to bicarbonate buffering of lactic acid in exercise, was studied in eight healthy male volunteers during incremental exercise on a cycle ergometer performed after ingestion (0.3 g.kg-1 body mass) of CaCO3 (control) and NaHCO3 (alkalosis). The resting arterialized venous blood pH (P < 0.05) and bicarbonate concentration ([HCO3-]b; P < 0.01) were significantly higher in acute metabolic alkalosis [AMA; pH, 7.44 (SD 0.03); [HCO3-]b, 29.4 (SD 1.5) mmol.l-1] than in the control [pH, 7.39 (SD 0.03); [HCO3-]b, 25.5 (SD 1.0) mmol.l-1]. The blood lactate concentrations ([la-]b) during exercise below the anaerobic threshold (AT) were not affected by AMA, while significantly higher [la-]b at exhaustion [12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol.l-1, P < 0.05] and at 3 min after exercise [14.41 (SD 1.75) vs 12.26 (SD 1.40) mmol.l-1, P < 0.05] were found in AMA compared with the control. The CO2 excess increased significantly from the control [3177 (SD 506) ml] to AMA [3897 (SD 381) ml; P < 0.05]. The CO2 excess per body mass was found to be significantly correlated with both the increase of [la-]b from rest to 3 min after exercise (delta[la-]b; r = 0.926, P < 0.001) and with the decrease of [HCO3-]b from rest to 3 min after exercise (delta [HCO3-]b; r = 0.872, P < 0.001), indicating that CO2 excess per body mass increased linearly with both delta [la-]b and delta [HCO3-]b.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Aldosterone-secreting adrenal cortical adenoma in an 11-year-old child and collective review of the literature.

We report a rare case of primary hyperaldosteronism due to a unilateral adrenal cortical adenoma in an 11-year-old female patient. The patient presented with hypertension, hypokalaemia and metabolic alkalosis, associated with inappropriate kaliuresis. The diagnosis was supported by the following laboratory findings: elevated plasma aldosterone, suppressed plasma renin activity, nonsuppressible aldosterone secretion following saline infusion and absent plasma aldosterone response to ambulation. MRI revealed a 1 cm-diameter adrenal tumour on the left side. Even though the NP-59 scintigraphy showed the negative result, laparotomy with left adrenalectomy was performed. Pathological examination confirmed an adenoma in the adrenal cortex. The patient's blood pressure and biochemical laboratory data normalized postoperatively within 2 days. We recommend that in hypertensive children with hypokalaemia and metabolic alkalosis, primary aldosteronism should be considered.

Adrenocortical Adenoma↗
PubMed1995

Sodium citrate supplementation in inborn argininosuccinate lyase deficiency: a study in a 5-year-old patient under total parenteral nutrition.

The effects of sodium citrate supplementation to improve aspartic acid supply in a 5-year-old girl with argininosuccinate lyase deficiency were studied over a period of 5 years under constant and total parenteral nutrition. Daily increasing doses of sodium citrate (0-8 mmol/kg) were continuously infused i.v.. Her standard therapy with arginine hydrochloride (4 mmol/kg/day) and sodium benzoate (200 mg/kg/day) was continued. Serum citrulline concentrations were reduced by citrate supplementation (161.8-41.7 mumol/l). Correspondingly serum concentrations of argininosuccinate and its anhydrides rose (270-458 mumol/l), positively correlated with the doses of sodium citrate. Renal elimination of argininosuccinate did not change measurably. There was no improvement in plasma ammonia concentration, which remained between 88 and 136 mumol/l. A long-standing hepatomegaly did not improve. The patient developed a significant alkalosis with blood pH-values increasing up to 7.55. The alkalosis lead to a reduction in renal ammonium elimination by at least 5.3 mmol/kg per day; the portion of ammonium-nitrogen decreased from 54.2% to finally 9% of total urinary nitrogen. Nevertheless total urinary nitrogen elimination, as measured by pyrochemiluminescence, improved by 24.5% during the 5 days and rose from 2065 mg nitrogen/day to 2570 mg/day. This improvement could not be explained by the metabolites determined and corresponded with an increase in chemically undefined nitrogen excretion, which rose from 0% to 65.9% of total urinary nitrogen. Further investigations are necessary to elucidate the nature of these unexplained nitrogen-containing compounds. CONCLUSION. Sodium citrate supplementation improved renal nitrogen elimination in a patient with argininosuccinate lyase deficiency in the observation period of 5 days by up to 24.5%.

Alkalosis↗
PubMed1994

Chloride deficiency as a presentation or complication of cystic fibrosis.

Thirteen children with cystic fibrosis (CF), aged 1.5 months-15 years, had 18 episodes of hypochloraemia and metabolic alkalosis over the period 1983-1991. Five patients were not known to have CF prior to developing these electrolyte disturbances. There were two distinct clinical presentations: 5 patients had an acute isolated picture of heat exhaustion while 8 patients (all infants) had a more chronic course associated with failure to thrive. Many episodes were not associated with particularly high environmental temperatures, although most occurred during the summer and early autumn months. Serum electrolytes should be assessed regularly in children with CF, and this diagnosis should be considered in any infant presenting with unexplained hypochloraemic metabolic alkalosis.

Acute Disease↗