Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ALKALOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,513 records · Page 84Linked to original sources

[Metabolic alkalosis on the surface but metabolic acidosis in depth].

Our purpose in writing this article is to emphasize the acid-base consequences and total body imbalances which follow the selective depletion of HCl. The initial body balance is an equimolar deficit of chloride and gain of bicarbonate. Within a short period of time, body balance changes; the net deficits are closer to equimolar losses of potassium and chloride. Since the loss of potassium occurred without the simultaneous loss of existing body anions (chloride or phosphate), this negative balance of potassium is accompanied by an equimolar gain of hydrogen ions. Thus when the negative balance is that of KCl, acid-base balance is present but there is a surplus of bicarbonate in the extracellular fluid (ECF) together with an equal surplus of hydrogen ions in another compartment (the intra-cellular fluid (ICF)). Moreover, if the ECF volume is contracted, a more severe degree of acidosis of the ICF may occur due to a higher PCO2 in venous blood. Given the acid-base balance and a deficit of KCl, one should not view this disorder as being "corrected" by saline at any time other than in the acute phase before a large potassium deficit occurs. Sodium chloride should be restricted to repair a deficit of sodium chloride. The emphasis on therapy is obviously to replace the deficit of KCl.

Acidosis↗

Metabolic alkalosis induced by pre-exercise ingestion of NaHCO3 does not modulate the slow component of VO2 kinetics in humans.

Seven healthy physically active nonsmoking men, aged 22.4 +/- (SD) 1.8 years performed two 6 min bouts of cycling at 40% VO2max (sub-lactate threshold/low power output exercise) and 87% VO2max (supra-lactate threshold/high power output exercise) at 70 rev.min-1, separated by 20 minutes rest, on two occasions: once as a control experiment (test C) and on a different day at approximately 1.5 h after ingestion of 250 mg (3 mmol).(kg body weight)-1 of NaHCO3 (test A). At the onset of low and high power output exercise performed after ingestion of NaHCO3, antecubital venous blood pH and HCO3- were significantly elevated (p < 0.05). Moreover, blood pH and HCO3-, tested at every minute of low and high power output exercise, was significantly higher (p < 0.05) in test A than in test C. No difference was found in plasma lactate concentration [La]pl during low power output exercise between A and C tests. In the terminal phase of the high power output exercise (87% VO2max) the level of [La]pl rose more rapidly in test A than in test C, reaching in the sixth minute of cycling 8.27 +/- 1.11 and 6.76 +/- 0.68 mmol.l-1 (p < 0.01) in test A and C, respectively. No significant differences were found in the rate of VO2 measured breath-by-breath between A and C tests, both during low and high power output exercise. The slow component of VO2 kinetics (expressed by difference between VO2 measured at the 6th minute of exercise minus the VO2 reached at the 3rd minute), occurring only during exercise corresponding to 87% VO2, was not significantly different in C and A tests (0.373 +/- 0.050 and 0.339 +/- 0.078 1 O2, respectively). The total VO2 consumed throughout the six minute cycling at power output of 40 and 87% VO2max performed in control conditions and after ingestion of NaHCO3 was not significantly different. We have demonstrated that significantly reduced exercise acidemia accompanied by a significantly elevated level of [La]pl accumulation, did not affect the slow component of the VO2 kinetics and the magnitude of oxygen uptake during exercise corresponding to 40 and 87% of VO2max.

Acid-Base Equilibrium↗