Metabolic Alkalosis

Metabolic alkalosis is a primary increase of the bicarbonate (HCO3-) with or without a compensatory rise from Carbondioxid partial pressure (PCO2); the pH may be high or almost normal. Common causes include recurrent vomiting, hypovolemia, diuretics and hypokalemia. Renal impairment of HCO3 – excretion must be to maintain the alkalosis. Symptoms in severe cases, headache, lethargy and tetany. The diagnosis is made by clinical and ABG and measurement of serum electrolytes. The underlying condition is treated. Occasionally, the intravenous or oral administration of acetazolamide or hydrochloric acid is indicated.

(Soiehe and acid-base regulation and to acids-base disturbances).

Metabolic alkalosis is a primary increase of the bicarbonate (HCO3-) with or without a compensatory rise from Carbondioxid partial pressure (PCO2); the pH may be high or almost normal. Common causes include recurrent vomiting, hypovolemia, diuretics and hypokalemia. Renal impairment of HCO3 – excretion must be to maintain the alkalosis. Symptoms in severe cases, headache, lethargy and tetany. The diagnosis is made by clinical and ABG and measurement of serum electrolytes. The underlying condition is treated. Occasionally, the intravenous or oral administration of acetazolamide or hydrochloric acid is indicated. (Soiehe and acid-base regulation and to acids-base disturbances.) Etiology Metabolic alkalosis is bicarbonate HCO3 accumulation due to loss of acid alkali Administration The intracellular shift of hydrogen ions (H + -as occurs in hypokalemia) HCO3 retention Regardless of the initial origin means a persistent metabolic alkalosis that renal HCO3 – reabsorption rate is increased because HCO3- is freely filtered in the normal case by the kidneys and thus excreted. Volume depletion and hypokalemia are the most common stimuli increased HCO3 – reabsorption. However, any circumstance which the levels of aldosterone or mineralocorticoids (which are the sodium [Na] – reabsorption and potassium [K] – and H + excretion reinforce) increased, the HCO3 – raising mirror. So hypokalemia both a potential cause and a common consequence of metabolic alkalosis. The causes are listed. The most common are volume-depleted (especially if the loss of stomach acid chloride [Cl] by recurrent vomiting or through a nasogastric tube occur) and diuretics (see table: causes of metabolic alkalosis). Causes metabolic alkalosis cause notes Gastrointestinal acid loss * Loss of gastric acid by vomiting or a nasogastric tube loss of HCl and acid together with Kontraktionsalkalose due to aldosterone release and subsequent absorption of HCO3 Congenital Chloridorrhö Fecal Cl loss and HCO3- retention Villous adenoma Probably secondary to K depletion Renal acid loss Primary hyperaldosteronism † Congenital adrenal hyperplasia secondary hyperaldosteronism secreted † passage with volume depletion, heart failure, cirrhosis with ascites, nephrotic syndrome, Cushing’s syndrome or disease, renal artery stenosis or a tumor of the renin, on use of mixtures glycyrrhizin contained † (z. caused as liquorice, chewing tobacco, carbenoxolone, Lydia Pinkham’s Vegetable Compound) inhibiting the enzymatic conversion of cortisol to less active metabolites by glycyrrhizin Bartter syndrome † rare congenital disease that hyperaldosteronism and hypokalemic metabolic alkalosis, which in early childhood with renal salt wasting and volume depletion is manifested Gitelman syndrome † Similar to the addition Bartter syndrome characterized by hypomagnesemia and hypocalciuria manifested in young adults diuretics (thiazide and loop) ‡ M everal mechanisms: secondary hyperaldosteronism by volume depletion, Cl deficiency or Kontraktionsalkalose; can for simultaneous K depletion chlorine resistant be hypokalemia and hypomagnesemia † stimulating K- and Mg-reabsorption and excretion of H; Alkalosis unresponsive to NaCl and volume replacement until the deficiencies have been compensated; H reaches HCO3 HCO3Überschuss Posthyperkapnisch * Persistent elevation of compensatory HCO3- mirrors often Post Organic with volume, K and Cl deficiency acidosis conversion of lactic acid or keto acid due to the low K-value in the cells, the extracellular pH is increased worsens on by HCO3- therapy for acidosis NaHCO3Belastung kick at very high loads or loads of patients with hypokalemia; Serum is alkalotischer when H back into the cells milk-alkali syndrome reaches Chronic ingestion of calcium carbonate antacids ensures Ca and HCO3- oversupply; Hypercalcemia reduced PTH, increased HCO3- absorption Kontraktionsalkalose * diuretics (all types) Welding loss in cystic fibrosis NaCl loss concentrated in a specific amount of HCO3 in a smaller total volume of the body other resumption of carbohydrates after starvation decline in Hungerketose or Hungerazidose with improved cell function misuse of laxatives * unclear mechanism Some antibiotics (eg. B. carbenicillin, penicillin, Ticarzillin) Contained anion which is not reabsorbed and K and H * excretion increased chloride sensitive. † chloride resistant. be either chloride or chloride-sensitive resistant ‡ Can. Ca = calcium; Cl = chloride; H = hydrogen; HCl = hydrochloric acid; HCO3 = bicarbonate; K = potassium; Mg = magnesium; NaCl = sodium chloride; NaHCO3 = sodium bicarbonate. Metabolic alkalosis may be chloride-reactive: includes loss or excessive secretion of chloride; It can be typically produced by the i.v. better administration of sodium chloride-containing infusion solutions. Non-reactive chloride: Improves not typically shows a heavy magnesium and / or potassium deficiency or Mineralokortikoidexzess with NaCl-containing liquids, and. Both forms can coexist, for. As in patients with volume overload and hypokalemia due to high doses of diuretics. Symptoms and discomfort symptoms and discomfort of a low-grade ALKALAEMIA normally associated with the underlying condition. A heavier ALKALAEMIA increases protein binding of ionized calcium (Ca ++), leading to hypocalcemia and subsequently headache, lethargy and neuromuscular hyperexcitability (sometimes with delirium, tetany and convulsions). ALKALAEMIA also lowers the threshold for the onset of symptoms of angina pectoris and cardiac arrhythmias. An accompanying hypokalemia can cause weakness. Clinical calculator: Arterial blood gas interpretation TreeCalc diagnosis ABG and serum electrolytes The diagnosis of the cause is clinical usually Sometimes measurement of Cl- and K + in the urine The diagnostic criteria of metabolic alkalosis and the appropriate respiratory compensation are in acid-base disorders: discussed diagnosis and need ABG and measurement of serum electrolytes (including Ca and Mg). Common causes can often be identified by the history or physical examination. If the history is not clear, and the kidney function is normal, the concentrations of Cl- and K + are determined in the urine (which values ??are not suitable for patients with renal insufficiency diagnosis). Chlorine concentrations <20 mEq / l in the urine have a significant renal Cl - reabsorption and thus to a chlorine-sensitive cause (see Table: causes metabolic alkalosis). A chlorine concentration> 20 mEq / L in urine suggests chlorine-resistant causes. The potassium in the urine, and the presence or absence of hypertension may be helpful in differentiating a chlorine-resistant alkalosis. A potassium content of <30 mEq per day in urine indicates a hypokalemia or laxative abuse. A potassium content in the urine of> 30 mEq per day without hypertension suggests a diuretic abuse or Bartter- or Gitelman syndrome. A potassium content in the urine of> 30 mEq per day with hypertension requires an investigation on hyperaldosteronism, an excess of mineralocorticoid and renovascular disease. Tests typically include plasma renin activity and aldosterone and cortisol (Cushing’s syndrome: diagnosis and diagnosis). Treatment treatment of the cause I.V. isotonic saline solution (0.9%) for a chlorine-sensitive metabolic alkalosis The underlying causes are treated with special attention to the correction of hypovolemia and hypokalemia. Patients with a chlorine-sensitive metabolic alkalosis received an i.v. Infusion with a 0.9% saline solution; the infusion rate is typically 50-100 ml more per hour when the fluid losses through urine, other body fluids and the insensible perspiration together account. This is continued until the values ??for chlorine in the urine> be 25 mEq / l and returned to normal after an initial increase by the Bikarbonaturie the urine pH. Patients with a chlorine-resistant metabolic alkalosis rarely benefit from rehydration as the only measure. Patients with severe metabolic alkalosis (eg., PH> 7.6) require sometimes a faster correction of blood pH. Hemofiltration or hemodialysis is a possibility, especially if a volume overload and renal dysfunction are present. The administration of 250-375 mg po acetazolamide or iv 1 or 2 times a day increases the HCO3-excretion, but may also be the loss of K + and phosphate (PO4) in the urine promote. Patients with volume overload and diuretic-induced metabolic alkalosis and patients with metabolic alkalosis posthyperkapnischer can especially benefit from this therapy. In patients with severe metabolic alkalosis (pH> 7.6) and kidney failure, otherwise they can not undergo dialysis or should hydrochlorische acid in a 0.1 to 0.2 N solution as an i.v. Delivery is considered safe and effective, but must be administered through a central access, since the solution is hyperosmotic and can lead to sclerosis of peripheral veins. The dosage is 0.1-0.2 mmol / kg each hour. Regular monitoring of ABG and electrolytes is necessary. Summary An metabolic alkalosis is the accumulation of HCO3- due to acid losses Administration of alkaline substances, intracellular shift of hydrogen ions, or by HCO3 – retention. The most common causes are volume-depleted (especially if the loss of stomach acid and chlorine by recurrent vomiting or by gavage to come) and taking diuretics. Metabolic alkalosis with loss or excessive secretion of Cl is called chlorine-sensitive. Treat the cause and consult in patients with chlorine-sensitive metabolic alkalosis 0.9% saline i.v. at. A chlorine-resistant metabolic alkalosis occurs due to increased aldosterone effect. The treatment of chlorine-resistant metabolic alkalosis includes correction of hyperaldosteronism.

Health Life Media Team

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