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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.
Metabolic alkalosis is usually accompanied by low blood potassium concentration, causing, e.g., muscular weakness, muscle pain, and muscle cramps (from disturbed function of the skeletal muscles), and muscle spasms (from disturbed function of smooth muscles). It may also cause low blood calcium concentration.
These are characterized by a serum pH below 7.4 (acidosis) or above 7.4 (alkalosis), and whether the cause is from a metabolic process or respiratory process. If the body experiences one of these derangements, the body will try to compensate by inducing an opposite process (e.g. induced respiratory alkalosis for a primary metabolic acidosis). [7]
When this happens the numerator is large, the denominator is small, and the result is a delta ratio which is high (>2). This means a combined high anion gap metabolic acidosis and a pre-existing either respiratory acidosis or metabolic alkalosis (causing the high bicarbonate) – i.e. a mixed acid–base metabolic acidosis. [citation needed]
In general, the cause of a hyperchloremic metabolic acidosis is a loss of base, either a gastrointestinal loss or a renal loss [citation needed]. Gastrointestinal loss of bicarbonate (HCO − 3) [citation needed] Severe diarrhea (vomiting will tend to cause hypochloraemic alkalosis) Pancreatic fistula with loss of bicarbonate rich pancreatic fluid
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.
Metabolic acidosis is compensated for in the lungs, as increased exhalation of carbon dioxide promptly shifts the buffering equation to reduce metabolic acid. This is a result of stimulation to chemoreceptors , which increases alveolar ventilation , leading to respiratory compensation, otherwise known as Kussmaul breathing (a specific type of ...
Hyperventilation due to the compensation for metabolic acidosis persists for 24 to 48 hours after correction of the acidosis, and can lead to respiratory alkalosis. [3] This compensation process can occur within minutes. [4] In metabolic alkalosis, chemoreceptors sense a deranged acid-base balance with a plasma pH of greater than normal (>7.4 ...