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Alkalosis is the result of a process reducing hydrogen ion concentration of arterial blood plasma (alkalemia). In contrast to acidemia (serum pH 7.35 or lower), alkalemia occurs when the serum pH is higher than normal (7.45 or higher).
Metabolic alkalosis is an acid-base disorder in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate (HCO − 3), or alternatively a direct result of increased bicarbonate concentrations.
Hypokalemia is a low level of potassium (K +) in the blood serum. [1] Mild low potassium does not typically cause symptoms. [3] Symptoms may include feeling tired, leg cramps, weakness, and constipation. [1] Low potassium also increases the risk of an abnormal heart rhythm, which is often too slow and can cause cardiac arrest. [1] [3]
Diagnosis of contraction alkalosis is made by correlating laboratory data with clinical history and examination. Metabolic alkalosis in the presence of decreased effective circulatory volume, loop diuretic use, or other causes of intravascular depletion such as profound diarrhea should raise suspicion for contraction alkalosis as a likely etiology in the absence of other causes.
The clinical findings characteristic of Bartter syndrome is hypokalemia, metabolic alkalosis, and normal to low blood pressure. These findings may also be caused by other conditions, which may cause confusion. When diagnosing a Bartter's syndrome, the following conditions must be ruled out as possible causes of the symptomatology: [citation needed]
In summary, hyperaldosteronism causes hypernatremia, hypokalemia, and metabolic alkalosis. [ 13 ] Finer notes on aldosterone include the fact that it stimulates sodium-potassium ATPase in muscle cells , increasing intracellular potassium and also increases sodium reabsorption all along the intestine and nephron , possibly due to widespread ...
Acute aspirin or salicylates overdose or poisoning can cause initial respiratory alkalosis though metabolic acidosis ensues thereafter. The acid-base, fluid, and electrolyte abnormalities observed in salicylate toxicity can be grouped into three broad phases:
Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).. The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, and cor pulmonale.