Ico

another that impairs renal 1 3 excretion (hypovolemia, hypokalemia, or miner-alocorticoid excess). The etiologies of metabolic alkalosis are listed in Table 28-5.

Patients with metabolic alkalosis rarely have symptoms attributable to alkalemia. Rather, complaints are usually related to volume depletion (muscle cramps, positional dizziness, weakness) or to hypokalemia (muscle weakness, polyuria, polydipsia).

In order to effectively treat metabolic alkalosis, the causative process must be identified and treated. The major causes of metabolic alkalosis are often readily apparent after carefully reviewing the patient's history and medication list. In hospitalized patients always look for administration of compounds such as citrate in blood products and acetate in parenteral nutrition that can raise the HCO3 concentration. If the etiology of the metabolic alkalosis is still unclear, measurement of the urinary chloride may be useful. Some processes leading to metabolic alkalosis (vomiting, nasogastric suction losses, factitious diarrhea) will have low urinary Cl concentrations (less than 25 mEq/L or mmol/L), while others (diuretics, hypokalemia, and mineralocorticoid excess) will have higher urinary Cl concentrations (greater than 40 mEq/L or mmol/ L).

Table 28-5 Common Causes of Metabolic Alkalosis

Urine CI" less than 10 mEq/L (less than 10 mmol/L}

Urine CI- greater than 10 mEq/L (greater than 10 mmol/L)

Alkali administration IV bicarbonate therapy Oral alkali Uterapy Parenteral nutrition with acetate "Contraction alkalosis"

postdiuretic use Decreased chloride intake Loss of gastric acid Vomiting

Nasogastric suction Posthypercapnia Villous adenomas (some)

Drugs0 Corticosteroid therapy Diuretics Hypokalemia iViineratocorttcoid excess I lyperaldosteronism ├ča rtter's syndrome Gjshing's syndrome aVlay be observed with Lherapeutic doses or overdoses.

In general, contributing factors such as diuretics, nasogastric suction, and corticos-teroids should be discontinued if possible. Any fluid deficits should be treated with IV normal saline. Recognize that patients with varieties of metabolic alkalosis with high urine Cl- (though rather uncommon) will be resistant to saline loading. Potassium supplementation should always be given if it is also deficient.

In patients with mild or moderate alkalosis who require ongoing diuresis but have

rising

3 concentrations, the carbonic anhydrase inhibitor acetazolamide can

Fl CO

' concentration. Acetazolamide is typically dosed at be used to reduce the 250 mg every 6 to 12 hours as needed to maintain the pH in a clinically acceptable i irn-

range. This agent results in gradual changes in the serum 1 1 - - 3 and is not used to acutely correct a patient's acid-base status. If alkalosis is profound and potentially life-threatening (due to seizures or ventricular tachyarrhythmias), consideration can be given to hemodialysis or transient HCl infusion. The hydrogen ion deficit (in mil-liequivalents or millimoles) can be estimated from the current bicarbonate concen-

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