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 1,549 records · Page 86Linked to original sources
PubMed1988

Clinical signs, diagnosis, and treatment of alkalemia in dogs: 20 cases (1982-1984).

Alkalemia (pH greater than 7.50) was measured in 20 dogs admitted over a 3-year period for various clinical disorders. Alkalemia was detected in only 2.08% of all dogs in which blood pH and blood-gas estimations were made. Thirteen dogs had metabolic alkalosis (HCO3- greater than 24 mEq/L, PCO2 greater than 30 mm of Hg), of which 8 had uncompensated metabolic alkalosis, and of which 5 had partially compensated metabolic alkalosis. Seven dogs had respiratory alkalosis (PCO2 less than 30 mm of Hg, HCO3- less than 24 mEq/L); 4 of these had uncompensated respiratory alkalosis and 3 had partially compensated respiratory alkalosis. Ten dogs had double or triple acid-base abnormalities. Dogs with metabolic alkalosis had a preponderance of clinical signs associated with gastrointestinal disorders (10 dogs). Overzealous administration of sodium bicarbonate or diuretics, in addition to anorexia, polyuria, or hyperbilirubinemia may have contributed to metabolic alkalosis in 8 of the dogs. Most of the dogs in this group had low serum K+ and Cl- values. Two dogs with metabolic alkalosis had PCO2 values greater than 60 mm of Hg, and 1 of these had arterial hypoxemia (PaO2 less than 80 mm of Hg). Treatments included replacement of fluid and electrolytes (Na+, K+, and Cl-), and surgery as indicated (8 dogs). Six dogs with respiratory alkalosis had a variety of airway, pulmonary, or cardiac disorders, and 3 of these had arterial hypoxemia. Two other dogs were excessively ventilated during surgery, and 1 dog had apparent postoperative pain that may have contributed to the respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Imbalance↗
PubMed1998

Molecular mechanisms of the reversal of imipramine-induced sodium channel blockade by alkalinization in human cardiac myocytes.

BACKGROUND: Alkalinizing agents reverse cardiotoxicity of a variety of sodium channel blockers, including tricyclic antidepressants, but their mechanisms of action are poorly understood. PURPOSE: To establish the mechanisms by which alkalinization diminishes the sodium channel blocking action of imipramine. METHODS: The whole-cell voltage-clamp technique was used to measure INa during a variety of depolarizing pulse protocols in isolated human atrial myocytes, in the presence and absence of imipramine. A three-state model was used to analyze state-dependent INa block. RESULTS: Imipramine (1 and 5 microM) strongly inhibited INa. Experimental data and piecewise exponential analysis suggested significant binding to both activated and inactivated states. Alkalosis antagonized imipramine-induced INa blockade by increasing the unbinding rate, with intracellular alkalosis being more effective than extracellular alkalosis. The dissociation constant (Kd) for the inactivated state was increased from 0.55 to 1.40 microM by extracellular alkalosis and to 2.51 microM by intracellular alkalosis. Along with the reversal of drug-induced shifts in the inactivation curve, these data indicate that alkalosis on either side of the membrane antagonized drug interactions with the inactivated state. On the other hand, only intracellular alkalosis antagonized activated state block, increasing the Kd from 0.67 microM to 2.18 microM, while extracellular alkalosis left the activated state Kd unaltered at 0.67 microM. CONCLUSIONS: Alkalinization antagonizes the INa-blocking action of imipramine by promoting unbinding from the receptor. Intracellular alkalosis has a particularly important effect related to the activated-state interaction. The lipid-soluble, uncharged moiety appears to be a critical determinant of imipramine's ability to dissociate from the Na+ channel receptor.

Adrenergic Uptake Inhibitors↗
PubMed2006

[Characteristics of acid-base balance in patients with chronic severe hepatitis: analysis of 126 cases].

OBJECTIVE: To investigate the characteristics of acid-base balance in patients with chronic severe hepatitis. METHODS: Samples of venous blood and arterial blood were collected from 126 patients with chronic severe hepatitis, 106 males and 20 females, aged 44 +/- 13 (25 - 74), to undergo measurement of the potassium, sodium, and chloride ions, and urea nitrogen and creatine, blood electrolytes and blood gas analysis respectively. RESULTS: Acid-base disturbance (ABD) was found in 115 of the 126 patients (91.3%). 40 of the 115 patients with ABD (31.7%) had respiratory alkalosis combined with metabolic alkalosis, 32 of them (25.4%) had respiratory alkalosis combined with metabolic acidosis; 28 of them (22.2%) had pure respiratory alkalosis, and 8 (6.3%) had pure metabolic acidosis. Five patients had triple acid-base disturbance, 4 of which had respiratory alkalosis (combined with metabolic alkalosis and metabolic acidosis, 3.2%), and 1 of which had respiratory acidosis (combined with metabolic alkalosis and metabolic acidosis, 0.8%). There was no significantly difference in the prevalence rates of pure acid-base disturbance and multiple acid-base disturbances between the patients with cirrhosis-base chronic severe hepatitis and those with chronic hepatitis-based chronic severe hepatitis. Hypoxia symptoms were seen in 34 patients (27%). 103 patients died. All the 15 patients with their blood pH < 7.35 died. CONCLUSION: ABD in the patients with chronic severe hepatitis is mainly alkalosis with respiratory alkalosis as the basic ABD type. The appearance of ABD is not associated with the underlying illness. Patients of chronic severe hepatitis often suffer from hypoxia. Low blood pH is an important factor causing death.

Acid-Base Imbalance↗
PubMed1976

Acute acid-base disorders. 2. Specific disturbances.

Evaluation of the acid-base status of the body requires measurement of bicarbonate (total carbon dioxide) concentration, pH, and partial pressure of CO2 in arterial blood. Calculation of standard bicarbonate and base excess or deficit is not necessary. The normal concentration of free hydrogen ions (H+) is approximately 40 millimoles/liter, which is equivalent to a pH of 7.4. The normal load of fixed acids is 50 to 80 millimoles in 24 hours. A steady state is maintained by excretion of an equal amount of H+ by the kidneys, which at the same time regenerate bicarbonate to replenish buffer stores. Renal excretion of H+ is in the form of titratable acid and ammonium. Synthesis of ammonia can increase severalfold under the stimulus of acidosis. This is the chief mechanism of long-term compensation. Metabolic acidosis can be due to an excessive acid load (endogenous or exogenous), impaired renal excretion of H+, or bicarbonate loss. Determination of the "anion gap" (unmeasured anions) helps to establish the mechanism of acidosis. Acidosis with a normal anion gap is due to either bicarbonate loss or ingestion of certain chloride salts. A gap larger than normal indicates the presence in the body of acids other than acidfying chloride salts. Management of metabolic acidosis requires accurate diagnosis, clear understanding of the mechansim, and individualized treatment. Metabloic alkalosis is due to loss of H+ (usually from stomach or kidneys) or ingestion of alkali. Measurement of urinary chloride helps establish the mechanism of alkalosis. In saline-responsive alkalosis, the urinary chloride level is very low. This is usually due to gastric loss of H+, and the condition responds to administration of saline solution. When the urinary chloride level is only moderately low, the alkalosis is probably not due to gastric loss of H+. This form of alkalosis (saline-resistant) does not respond well to administration of saline solution and requires use of potassium in treatment. Apprpriate compensatory responses to acidosis or alkalosis are critical to survival. Compensation for metabloic acidosis consists of hyperventilation and enhanced renal excretion of H+, chiefly as ammonium. In metabolic alkalosis, compensation is mainly renal excretion of bicarbonate. Respiratory acidosis is due to alveolar hypoventilation. In chronic situations, a compensatory rise in serum bicarbonate concentration is expected. Management consists of treatment of the cause of hypoventilation. Respiratory alkalosis is due to hyperventilation. Treatment requires identification and correction of the cause of hyperventilation.

Acid-Base Imbalance↗
PubMed1985

[Mechanisms of compensation of disorders of acid-base status of the blood in patients with chronic anemia].

Altogether 228 patients with hereditary microspherocytic anemia (HMA), autoimmune hemolytic anemia (AIHA) and hypoplastic anemia (HA) were examined over time for the acid-base state of the arterial blood with the use of the pCO2-buffer bases coordinate system (BE/pCO2 and pCO2/BE diagrams). Prior to surgery the respiratory alkalosis was diagnosed in 60% of HMA patients (of these, 41.7% of patients had a decompensated alkalosis), in 61.7% of AIHA patients (73%), and in 69.7% of HA patients (82.1%). It is shown that the development in the patients of chronic respiratory alkalosis should be regarded as a compensatory mechanisms associated with hemic hypoxia complicated by arterial hypoxemia. During splenectomy, there was an increase in the incidence of decompensated respiratory alkalosis. Mixed respiratory and metabolic alkalosis occurred in 8.3% of AIHA patients and in 19.6% of HA patients because of artificial ventilation of the lungs. Two hours after operation compensated metabolic acytosis was identified in 72% of HMA patients, in 33.3% of AIHA patients, and in 33.9% of HA patients. Twenty-four hours following operation the patients of all the groups had arterial hypoxemia and hypocapnia. In view of this fact the blood acid-base state was determined by the presence of respiratory alkalosis: in 47.5% of patients with HMA, in 60% of patients with AIHA, and in 54% of patients with HA. Analysis of the BE/pCO2 diagram demonstrated that in 2/3 of the patients with HMA and AIHA and in all the patients with HA, respiratory alkalosis was decompensated. It was established that electrolyte imbalance detected in the patients interfered with metabolic compensation for chronic respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗