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PubMed1982

Cardiovascular performance and oxyhemoglobin dissociation after acetazolamide in metabolic alkalosis.

In patients with metabolic alkalosis, compensatory alveolar hypoventilation may induce hypercapnia and hypoxemia. In edematous or normally-hydrated patients without electrolyte deficiencies, acetazolamide--a carbonic anhydrase inhibitor--has been advocated to correct the primary acid-base disturbance, thereby preventing hypoxemia. The hemodynamic consequences and the effect on oxyhemoglobin dissociation of acetazolamide, were studied. Twelve critically ill patients with metabolic alkalosis were given 15 mg/kg body wt. acetazolamide intravenously. Cardiovascular performance was completely unchanged. The P50 was 26.6 mm Hg at the beginning and the end of the study, indicating that hemoglobin-oxygen affinity is unaffected by acetazolamide. In six patients, investigated after open-heart surgery, the arterial oxygen tension increased by 10-45%. This was probably related to the combined effects of slight reductions in total body oxygen consumption or shunting of venous blood through the lungs. Eight of the 12 patients were on controlled ventilation. After acetazolamide there was a mean increase in mixed venous carbon dioxide tension (PvCO2) of 4.5 mm Hg, with no increase in arterial carbon dioxide tension (PaCO2), indicating only a limited interference with carbon dioxide uptake and release of the carbonic anhydrase inhibition. No other adverse reactions were observed.

Acetazolamide↗
PubMed1976

The response of Ca-mediated action potentials and contractile activity in mammalian ventricular myocardium towards alkalosis.

Alkalosis (pH 7.8) produced by reduction of CO2 concentration augmented both upstroke velocity of Ca action potentials and isometric contractile force of mammalian heart muscle. If the increase of pH to 7.8 was achieved by a raise of HCO3 concentration (with simultaneous reduction of CO2 concentration), the positive inotropic response was not accompanied by an augmented Ca current. Obviously, the well-known positive inotropic effect of alkalosis does not only depend upon the enhancement of transmembrane Ca influx during excitation, but can be mediated alone by affecting intracellular Ca movements as well.

Action Potentials↗
PubMed1989

The effect of induced alkalosis and acidosis on plasma lactate and work output in elite oarsmen.

In order to test the effect of artificially induced alkalosis and acidosis on the appearance of plasma lactate and work production, six well-trained oarsmen (age = 23.8 +/- 2.5 years; mass = 82.0 +/- 7.5 kg) were tested on three separate occasions after ingestion of 0.3 g.kg-1. NH4Cl (acidotic), NaHCO3 (alkalotic) or a placebo (control). Blood was taken from a forearm vein immediately prior to exercise for determination of pH and bicarbonate. One hour following the ingestion period, subjects rowed on a stationary ergometer at a pre-determined sub-maximal rate for 4 min, then underwent an immediate transition to a maximal effort for 2 min. Blood samples from an indwelling catheter placed in the cephalic vein were taken at rest and every 30 s during the 6 min exercise period as well as at 1, 3, 6, 9, 12, 15, 18, 21, 25 and 30 min during the passive recovery period. Pre-exercise blood values demonstrated significant differences (p less than 0.01) in pH and bicarbonate in all three conditions. Work outputs were unchanged in the submaximal test and in the maximal test (p greater than 0.05), although a trend toward decreased production was evident in the acidotic condition. Analysis of exercise blood samples using ANOVA with repeated measures revealed that the linear increase in plasma lactate concentration during control was significantly greater than acidosis (p less than 0.01). Although plasma lactate values during alkalosis were consistently elevated above control there was no significant difference in the linear trend (p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1989

Hydrochloric acid for treating metabolic alkalosis.

Six patients with severe metabolic alkalosis were treated with intravenous hydrochloric acid (HCl) infusion. HCl was given through a central venous catheter, at a concentration of 0.1 mEq per ml. At least two of the following criteria were considered for initiation of the therapy: An arterial pH of greater than 7.45, a base excess (BE) of greater than +7 mmol/L, a PaCO2 of greater than 50 mmHg. The HCl amount was calculated using the BE formula, however, two thirds was infused for avoiding excessive acid loading. Patients were monitored by the blood gases, serum electrolytes, hemoglobin, hematocrit, bilirubin determinations and blood smear findings. While a significant decrease was noticed in pH and BE values, moderate changes were detected in PaCO2 due to different ventilatory status of the cases. All laboratory test results remained within normal limits and no complication was encountered. The advantage of the therapy is that less volume is needed for the correction of alkalosis, particularly in the cases requiring fluid restriction. HCl therapy, moreover, is a safe and time-saving method because of having rapid response to the treatment in the critically ill surgical patients.

Acid-Base Equilibrium↗
PubMed1994

The effect of acute metabolic alkalosis on bicarbonate transport along the loop of Henle. The role of active transport processes and passive paracellular backflux.

The loop of Henle (LOH) reabsorbs approximately 15% of filtered HCO3- via a luminal Na(+)-H+ exchanger and H+ATPase. During acute metabolic alkalosis (AMA) induced by i.v. HCO3- infusion, we have observed previously inhibition of LOH net HCO3- reabsorption (JHCO3-), which contributes to urinary elimination of the HCO3- load and correction of the systemic alkalosis. To determine whether the activities of the Na(+)-H+ exchanger and/or H(+)-ATPase are reduced during AMA, two inhibitors believed to be sufficiently specific for each transporter were delivered by in vivo LOH microperfusion during AMA. AMA reduced LOH JHCO3- from 205.0 +/- 10.8 to 96.2 +/- 11.8 pmol.min-1 (P < 0.001). Luminal perfusion with bafilomycin A1 (10(-4) mol.l-1) caused a further reduction in JHCO3- by 83% and ethylisopropylamiloride (EIPA; 5.10(-4) mol.l-1) completely abolished net HCO3- reabsorption. The combination of bafilomycin A1 and EIPA in the luminal perfusate was additive, resulting in net HCO3- secretion (-66.6 +/- 20.8 pmol.min-1; P < 0.001) and abolished net fluid reabsorption (from 5.0 +/- 0.6 during AMA to 0.2 +/- 1.1 nl.min-1; P < 0.001). To establish whether HCO3- secretion via luminal stilbene-sensitive transport mechanism participates in LOH adaptation to AMA, we added diisothiocyanato-2,2'-stilbenedisulphonate (DIDS; 10(-4) mol.l-1) to the perfusate. No effect was found.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMedDate not supplied

The psychosis of metabolic alkalosis.

Metabolic alkalosis as an additional etiology for organic psychosis is presented and covered, with theoretical and clinical considerations, including treatment. Illustrative case histories are cited and certain parameters of acid-base equilibrium are described as favorable to the normal awake state, while substantial deviation towards metabolic alkalosis is seen as conducive to psychotic aberration.

Acid-Base Equilibrium↗
PubMed1999

Acute respiratory alkalosis associated with low minute ventilation in a patient with severe hypothyroidism.

PURPOSE: Patients with severe hypothyroidism present unique challenges to anesthesiologists and demonstrate much increased perioperative risks. Overall, they display increased sensitivity to anesthetics, higher incidence of perioperative cardiovascular morbidity, increased risks for postoperative ventilatory failure and other physiological derangements. The previously described physiological basis for the increased incidence of postoperative ventilatory failure in hypothyroid patients includes decreased central and peripheral ventilatory responses to hypercarbia and hypoxia, muscle weakness, depressed central respiratory drive, and resultant alveolar hypoventilation. These ventilatory failures are associated most frequently with severe hypoxia and carbon dioxide (CO2) retention. The purpose of this clinical report is to discuss an interesting and unique anesthetic presentation of a patient with severe hypothyroidism. CLINICAL FEATURES: We describe an unique presentation of ventilatory failure in a 58 yr old man with severe hypothyroidism. He had exceedingly low perioperative respiratory rate (3-4 bpm) and minute ventilation volume, and at the same time developed primary acute respiratory alkalosis and associated hypocarbia (P(ET)CO2 approximately 320-22 mmHg). CONCLUSION: Our patient's ventilatory failure was based on unacceptably low minute ventilation and respiratory rate that was unable to sustain adequate oxygenation. His profoundly lowered basal metabolic rate and decreased CO2 production, resulting probably from severe hypothyroidism, may have resulted in development of acute respiratory alkalosis in spite of concurrently diminished minute ventilation.

Acute Disease↗
PubMed1996

Effect of metabolic alkalosis and metabolic acidosis on urinary kallikrein excretion of anaesthetized rats: evidence for a role of blood pH as regulator of renal kallikrein secretion.

The effect of altering the acid-base status on urinary kallikrein excretion of barbiturate-anaesthetized rats was investigated. Alkalosis was induced in a group of rats by intravenous (i.v.) infusion of NaOH at 0.45 mmol x h(-1) for 30 min. Acidosis was induced in two groups of rats by i.v. infusion of HCl at 1.5 mmol x h(-1) for 30 min (uncompensated acidosis) or 0.15 mmol x h(-1) for 3 h (compensated acidosis), respectively. Time controls received 0.45 mmol x h(-1) NaCl. Rats with alkalosis excreted less kallikrein than their controls (P < 0.05). Rats with uncompensated acidosis excreted more active kallikrein (P < 0.05), whereas rats with compensated acidosis excreted similar amounts when compared with their respective controls. In rats with uncompensated acid-base derangements, the urinary kallikrein excreted per millilitre of glomerular filtrate was correlated with blood H+ activity (r = 0.99, P < 0.01). Arterial blood pressure, haematocrit, glomerular filtration rate, urine flow rate and Na+ and K+ excretions of experimental and control animals did not differ. Thus, renal kallikrein secretion into the tubular fluid appears to be regulated by blood proton activity. This, along with our previous demonstration that kallikrein inhibits HCO3- secretion into the tubular lumen (Renal Physiol 17:301-306, 1994; J Physiol (Lond) 488:163-170, 1995), indicates that this enzyme is part of a feedback loop regulating acid-base balance.

Acidosis↗
PubMed2006

A case of recurrent renal failure associated with metabolic alkalosis induced by protracted vomiting.

We describe a case of recurrent deterioration of renal function in a 54-year-old man who was found to have metabolic alkalosis, with a maximum PaCO(2) of 73.9 mmHg and a bicarbonate concentration of 55.3 mmol/l. He had a gradual exacerbation of nausea and vomiting due to atrophic gastritis, with a scarred, deformed pyloric part of the stomach and a duodenal bulb secondary to chronic peptic ulcer. His metabolic alkalosis and deteriorated renal function were corrected by intravenous saline with or without potassium chloride. However, his recovered creatinine clearance was at most 60 l/day (41.6 ml/min). A renal biopsy revealed cellular infiltration of mononuclear cells and atrophic change in the tubulointerstitium, suggesting chronic interstitial nephritis. Latent renal insufficiency and dehydration induced by protracted vomiting may easily induce a rapid and recurrent deterioration of renal function, and control of vomiting seemed to be the cardinal measure. Initially, his nausea and vomiting seemed to be successfully controlled by medication, however, they later became persistent and surgical correction of the stomach was carried out. Postoperative recovery was smooth, and the patient's vomiting and recurrent deterioration of renal function finally settled.

Acid-Base Equilibrium↗
PubMed1986

Hypoproteinemic alkalosis.

Hypoproteinemia by itself causes a nonrespiratory ("metabolic") alkalosis. On the average, a decrease in plasma albumin concentration of 1 g/dl produces an increase in "standard" bicarbonate of 3.4 mM/liter, and an apparent base excess of +3.7 meq/liter; it also reduces the value of the normal anion gap by about 3 meq/liter. Concentration of plasma protein should be measured as part of the analysis of acid-base status. Interpretation of acid-base data requires special consideration in "primary hypoproteinemic alkalosis."

Adolescent↗
PubMed1993

Post-ischemic brain tissue alkalosis suppressed by U74006F.

We monitored chronically (for 1 week) the effect of the 21-aminosteroid U74006F, a potent lipid peroxidation inhibitor, on the pH profile of the rat brain following transient forebrain ischemia. Eight rats were treated initially with 3 mg/kg i.v. of U74006F 1 min after reperfusion. A second dose of 1.5 mg/kg i.v. was given 60 min after reperfusion. A vehicle group (n = 9) was treated in the same manner, using the same volume of the vehicle solution, 20 mM citric acid, 3 mM sodium citrate, and 8 mM NaCl. Statistically significant interaction between group and time (P = 0.003) was detected for pH. Brain pH of the vehicle treated animals were significantly higher than the U74006F treated group at 24 h (P = 0.009) and 48 h (P = 0.009) of reperfusion. Chronic post-ischemic brain tissue alkalosis at 24 h (pH 7.22 +/- 0.12) and 48 h (pH 7.25 +/- 0.11) post-ischemia, observed among the vehicle treated animals (and untreated animals), was suppressed by treatment with U74006F. These results suggest a coupling between post-ischemic brain tissue alkalosis and free radical induced lipid peroxidation.

Alkalosis↗
PubMed1982

Blood flow distribution during artificially induced respiratory hypocapnic alkalosis in the fowl.

In birds, hyperthermia is normally associated with panting and progressive respiratory alkalosis. The effect of respiratory alkalosis on capillary blood flow distribution was examined by artificially hyperventilating normothermic fowls, thereby dissociating it of the normally occurring concomitant hyperthermia. In contrast with mammals, in which hyperventilation associated with hypocapnia reduced blood flow to the brain, uterus and other organs, in the hen blood flow distribution in most organs remained unaltered. This indicates that the potential change in acid-base balance which develops in the hyperthermic birds during panting is not likely to affect the regulation of blood flow. The comb and wattles were the only affected organs, in which capillary blood flow diminished to about 45% of normal values. This reduction did not prevent a vasodilatation in those organs in hyperthermic fowls, though it probably limited its full expression.

Alkalosis, Respiratory↗
PubMed1989

Histological changes in the skin of Rana pipiens produced by metabolic alkalosis.

The frog skin has been shown to excrete various electrolytes, the rates can be altered by varying metabolic conditions. The present study was performed to determine if metabolic alkalosis results in histological changes in the skin that are characteristic of this state. Rana pipiens were loaded with NaHCO3 and skin biopsies obtained (I). These biopsies were compared with biopsies from either control, unloaded frogs (II), or from NaCl loaded (III) frogs. In blind studies of microscopic sections, 13 of 15 biopsies of a mixture of I and II were correctly diagnosed, and similarly, 18 of 20 of I and III were correctly diagnosed (P = 0.0037, and 0.0002, respectively). The changes due to NaHCO3 treatment included; (1) an abundance of large euchromatin cells on or near the surface; (2) changes in the basal cell layer with elongation and rotation of the nuclei; (3) lighter cells in the spinosal layer; and, (4) sometimes the skin became thicker. We conclude that metabolic alkalosis results in characteristic histological changes in the skin, and that this is probably related to the ability of the skin to excrete bicarbonate.

Alkalosis↗
PubMed1988

Altered drinking responses in dogs with chronic metabolic alkalosis.

Chronic chloride depletion alkalosis in dogs causes a lowered osmotic threshold and increased sensitivity for vasopressin (AVP) release. Since AVP release and drinking behavior normally are closely associated over a narrow range of changes in plasma osmolality (Posm), we investigated whether alkalotic dogs would also show an altered responsiveness to the dipsogenic effects of angiotensin II (ANG II) and osmotic stimuli. Dogs made chronically alkalotic by a combination of chloride-free diet and furosemide injections developed polydipsia in the absence of any increase in solute intake and in the presence of a significant reduction in Posm. The animals were chronically hypochloremic, hyponatremic and hypokalemic, and appeared to be extracellular fluid (ECF) contracted. Plasma renin activity (PRA) was 10-fold higher in alkalotic dogs than controls. When Posm was increased by a slow 2 hr infusion of hypertonic sodium sulfate, alkalotic dogs were found to have a significantly lower osmotic threshold for inducing drinking (289.8 +/- 1.1 mOsm/kg/H2O vs. 305.1 +/- 1.3 mOsm/kg/H2O in controls), but the slope or sensitivity of the water intake/Posm relationship was not significantly different. Finally, compared to normal animals, alkalotic dogs were unresponsive to the dipsogenic effects of IV ANG II. These data indicate that the central mechanisms which mediate drinking in response to cellular and extracellular thirst stimuli are altered in chronic metabolic alkalosis.

Alkalosis↗
PubMed1995

Acid dialysate correction of metabolic alkalosis in renal failure.

Severe metabolic acidosis may occur during hemodialysis when the incorrect acid dialysis concentrate from a two-part bicarbonate dialysis system is used in an acetate dialysis machine. We deliberately applied this technique to correct severe metabolic alkalosis in a patient with chronic renal failure. Rapid correction of the metabolic alkalosis was achieved and the procedure was well tolerated.

Acetates↗
PubMed1987

Epileptiform activity induced by alkalosis in rat neocortical slices: block by antagonists of N-methyl-D-aspartate.

The effects of changing extracellular pH on epileptiform activity induced by the removal of magnesium ions from the perfusing medium were studied. The proportion of bicarbonate in the artificial cerebrospinal fluid and of CO2 in the gas mixture were altered to mimic metabolic and respiratory acid-base disturbances. Changes in pH of 0.2 unit from control produced marked effects. Epileptiform activity was enhanced by alkalosis and diminished by acidosis. In normal magnesium-containing medium metabolic alkalosis (pH greater than 7.8) induced spontaneous epileptiform activity that was blocked by selective N-methyl-D-aspartate antagonists. The relevance of these findings to acid/base changes in clinical epilepsy is discussed.

2-Amino-5-phosphonovalerate↗
PubMed1983

Metabolic alkalosis in the Yucatan miniature boar following desoxycorticosterone-acetate (DOCA) implantation.

Metabolic alkalosis was induced in adult Yucatan miniature boars by subcutaneous implantation of desoxycorticosterone-acetate impregnated silicone rubber strips. Serum pH, bicarbonate, and PaCO2 increased rapidly and consistently following implantation. As in the dog and the rat, hypokalemia was accompanied by hypochloremia. As in the rabbit, hypokalemia developed in the presence of a decreased urinary output of potassium and apparent absence of kaliuresis. The pig is resistant to the paralytic effects of hypokalemia. Implantation of DOCA is an effective means of producing chronic metabolic alkalosis in the pig which is characterized by hypokalemia and hypochloremia.

Alkalosis↗
PubMed1985

Prevention of metabolic alkalosis induced by gastric fluid loss using H2 receptor antagonist.

Gastric fluid loss is a common cause of metabolic alkalosis. We studied various acid-base parameters in 20 patients undergoing continuous nasogastric (NG) suctioning for periods ranging from 3 to 17 days. Ten patients received cimetidine 300 mg intravenously every 6 hr (cimetidine-treated group). The remaining 10 patients received an antacid compound through the NG tube (control group). The rise in plasma bicarbonate concentration was significantly greater in the control group as compared to the cimetidine-treated group. As expected, gastric acid output was considerably lower in the cimetidine-treated group than in the control group. We conclude that cimetidine administration may be used in preventing metabolic alkalosis associated with gastric fluid loss by inhibiting gastric secretion of HCl.

Adolescent↗