Bicarbonate metabolic alkalosis

Metabolic alkalosis (citrate hepatically metabolized to bicarbonate)... 

These goals may minimize an overshoot metabolic alkalosis = Remember that ketoacids and lactic acid are metabolized to bicarbonate... 

Low serum chloride and elevated serum bicarbonate levels indicate metabolic alkalosis. 

This isotonic volume expander contains sodium, potassium, chloride, and lactate that approximates the fluid and electrolyte composition of the blood. Ringer s lactate (also known as lactated Ringer s or LR) provides ECF replacement and is most often used in the perioperative setting, and for patients with lower GI fluid losses, burns, or dehydration. The lactate component of LR works as a buffer to increase the pH. Large volumes of LR may cause metabolic alkalosis. Because patients with significant liver disease are unable to metabolize lactate sufficiently, Ringer s lactate administration in this population may lead to accumulation of lactate with iatrogenic lactic acidosis. The lactate is not metabolized to bicarbonate in the presence of liver disease and lactic acid can result. 

Acid-base disturbances associated with PN usually are related to the patient s underlying condition(s). However, acid-base abnormalities may develop as a result of changes in chloride or acetate concentrations in PN admixtures. Because acetate is converted to bicarbonate in the body, excessive acetate salts in PN can lead to metabolic alkalosis excessive chloride salts in PN can lead to metabolic acidosis. PN should not be used to... 

Metabolic alkalosis Increased alkalinity of body fluids caused by excessive alkali (usually bicarbonate) intake or excessive acid loss (e.g., from vomiting). 

Metabolic acidosis is characterized by decreased plasma bicarbonate concentrations (HC03 ), whereas metabolic alkalosis is characterized by increased HC03T... 

Metabolic alkalosis is initiated by increased pH and I ICC)3, which can result from loss of H+ via the GI tract (e.g., nasogastric suctioning, vomiting) or kidneys (e.g., diuretics, Cushing s syndrome), or from gain of bicarbonate (e.g., administration of bicarbonate, acetate, lactate, or citrate). 

Metabolic alkalosis is maintained by abnormal renal function that prevents the kidneys from excreting excess bicarbonate. 

In metabolic alkalosis and respiratory acidosis, pH does not usually deviate significantly from normal, but treatment can be required to maintain Pao2 and PaC02 at acceptable levels. Treatment should be aimed at decreasing plasma bicarbonate with sodium and potassium chloride therapy, allowing renal excretion of retained bicarbonate from diuretic-induced metabolic alkalosis. 

The normal levels of carbon dioxide tension (pC02) are between 36-44 mm Hg and the normal bicarbonate levels, in adults, are between 21-30 milliequivalents/liter. Metabolic alkalosis may result when pC02 goes below 36 mm Hg or bicarbonate level goes over 30 mEq/L, causing a pH greater than 7.45. 

Acidosis and alkalosis are infrequent. Metabolic acidosis is a side effect of acetazolamide therapy and is due to bicarbonate loss in the PCT. All the K+-sparing diuretics can cause metabolic acidosis by H+ retention in the cells of the collecting duct. Metabolic alkalosis is associated with the loop and thiazide drugs. Reflex responses to volume depletion cause reabsorption of HCO-3 in the PCT and H+ secretion in the collecting tubule. 

Acetazolamide can cause a metabolic acidosis in 50% of elderly patients (SEDA-11,199) occasionally (particularly if salicylates are being given or renal function is poor) the acidosis can be severe. It does this by inhibiting renal bicarbonate reabsorption. This effect is of particular use in treating patients with chronic respiratory acidosis with superimposed metabolic alkalosis. Life-threatening metabolic acidosis is rarely observed in the absence of renal insufficiency and/or diabetes mellitus. In three patients with central nervous system pathology alone conventional doses of acetazolamide resulted in severe metabolic acidosis (34). After withdrawal it took up to 48 hours for the metabolic acidosis and accompanying hyperventilation to resolve. 

Sodium bicarbonate (eg, baking soda, Alka Seltzer) reacts rapidly with HC1 to produce carbon dioxide and NaCl. Formation of carbon dioxide results in gastric distention and belching. Unreacted alkali is readily absorbed, potentially causing metabolic alkalosis when given in high doses or to patients with renal insufficiency. Sodium chloride absorption may exacerbate fluid retention in patients with heart failure, hypertension, and renal insufficiency. 

Calcium carbonate(eg, Turns, Os-Cal) is less soluble and reacts more slowly than sodium bicarbonate with HC1 to form carbon dioxide and CaCl2. Like sodium bicarbonate, calcium carbonate may cause belching or metabolic alkalosis. Calcium carbonate is used for a number of other indications apart from its antacid properties (see Chapter 42 Agents That Affect Bone Mineral Homeostasis). Excessive doses of either sodium bicarbonate or calcium carbonate with calcium-containing dairy products can lead to hypercalcemia, renal insufficiency, and metabolic alkalosis (milk-alkali syndrome). 

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. 

Caution in hypocalcemia, hypokalemia, metabolic alkalosis, respiratory alkalosis, Bartter s syndrome (powder for oral suspension contains 1,680 mg or 20 mEq of sodium bicarbonate)... 

ANTACIDS - MAGNESIUM- CONTAINING SODIUM POLYSTYRENE SULPHONATE Cases of metabolic alkalosis Uncertain possibly absorption of bicarbonate due to its abnormal neutralization in the stomach Consider an alternative antacid or administer sodium polystyrene sulphonate as an enema. If both need to be co administered orally, monitor U Es and blood gases closely... 

Acid-base disorders Initial metabolic alkalosis (resulting from decreased urea synthesis with reduced bicarbonate consumption) may be superimposed by respiratory alkalosis as an outcome of disorders in lung function. During the further course, metabolic acidosis (with renal insufficiency) and respiratory acidosis (with pulmonary insufficiency) can be expected. In advanced or severe stages of the disease, lactate acidosis may develop in some 50% of all comatose patients owing to restricted gluconeogenesis. 

Hjq)onatremia is rare, and persistent hyponatremia very rare in patients taking cisplatin (162). In a detailed description of the biochemical abnormalities that can result from renal tubular dysfunction after cisplatin therapy, it was noted that hypocalciuria is more common than hypomagnesemia, and that there tends to be a state of reduced serum bicarbonate. The most severe renal tubular damage caused by cisplatin is characterized by hypocalciuria, total body magnesium deficiency, and hypokalemic metabolic alkalosis (163). 

Sodium bicarbonate is metabolized to the sodium cation, which is eliminated from the body by renal excretion, and the bicarbonate anion, which becomes part of the body s bicarbonate store. Any carbon dioxide formed is eliminated via the lungs. Administration of excessive amounts of sodium bicarbonate may thus disturb the body s electrolyte balance, leading to metabolic alkalosis or possibly sodium overload with potentially serious consequences. The amount of sodium present in antacids and effervescent formulations has been sufficient to exacerbate chronic heart failure, especially in elderly patients. ... 

Around 60-70% of the filtered sodium is usually reabsorbed in the proximal tubule therefore, acetazolamide could be expected to have a rather potent diuretic effect. However, it produces rather modest diuresis because most of the excess sodium leaving the proximal tubule can be reabsorbed in the more distal segments of the nephron. Furthermore, its diuretic action is progressively diminished by the development of hyperchloremic metabolic acidosis caused by the loss of bicarbonate ions into the urine (Martinez-Maldonado Cordova 1990, Rose 1989, 1991, Wilcox 1991). In humans, the primary indication for acetazolamide (as a diuretic agent) is the treatment of edema with metabolic alkalosis. 

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