Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess) PDF

2/22/24, 2:22 PM Realizeit for Student Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess) Metabolic alkalosis is a clinical disturbance characterized by a high pH (decreased H+ concentration) and a high plasma bicarbonate concentration. It is caused by a gain of bicarbonate or a loss of...

2/22/24, 2:22 PM Realizeit for Student Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess) Metabolic alkalosis is a clinical disturbance characterized by a high pH (decreased H+ concentration) and a high plasma bicarbonate concentration. It is caused by a gain of bicarbonate or a loss of H+ (Emmett & Szerlip, 2017a; Norris, 2019). Pathophysiology A common cause of metabolic alkalosis is severe vomiting or gastric suction that causes loss of stomach HCl (hydrogen and chloride ions). The disorder also occurs in pyloric stenosis, in which only gastric fluid is lost. Gastric fluid has an acid pH (usually 1 to 3), and loss of this highly acidic fluid pulls H+ ions from the bloodstream to replenish the gastric acid. As a result, the bloodstream loses H+ ions and becomes alkalotic. Other situations predisposing to metabolic alkalosis include those associated with loss of potassium, such as diuretic therapy that promotes excretion of potassium (e.g., thiazides, furosemide), and ACTH secretion (as in hyperaldosteronism and Cushing’s syndrome) (Emmett & Szerlip, 2017a; Norris, 2019). Hypokalemia produces alkalosis in two ways: (1) when the bloodstream is low in K+, the nephrons reabsorb K+ into the bloodstream and secrete H+ into the tubule fluid which is excreted in the urine and (2) when the bloodstream is low in K+, intracellular potassium moves out of the cells into the ECF, and as potassium ions leave the cells, hydrogen ions must enter to maintain electroneutrality (Mount, 2017c). Excessive alkali ingestion from antacids containing bicarbonate or from the use of sodium bicarbonate during cardiopulmonary resuscitation can also cause metabolic alkalosis (Emmett & Szerlip, 2017b). Chronic metabolic alkalosis can occur with long-term diuretic therapy (thiazides or furosemide), villous adenoma in the GI tract, external drainage of gastric fluids, significant potassium depletion, cystic fibrosis, and the chronic ingestion of milk and calcium carbonate (Emmett & Szerlip, 2017b). Clinical Manifestations In alkalosis, H+ ions are decreased in the bloodstream, leaving negatively charged proteins attracting other positive ions. Calcium (Ca++) ions bind to these proteins. As calcium ions bind to proteins in the bloodstream, free Ca++ ions decrease in the bloodstream and hypocalcemia develops. Alkalosis is primarily manifested by symptoms related to hypocalcemia, such as tingling of the fingers and toes, dizziness, and tetany (cramping muscles). Because it is the ionized fraction of calcium that is diminished in metabolic alkalosis, neuromuscular symptoms due to hypocalcemia are often the predominant symptoms (Emmett & Szerlip, 2017c). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zRrdbUNNMKTSTb3II3pEltD4s%2fPbBdKcWtJFoZ4TUro%2b%… 1/3 2/22/24, 2:22 PM Realizeit for Student In metabolic alkalosis, the lungs attempt to compensate by slowing respiratory rate, which increases CO2 retention, and in turn increases H+ content of the blood (see carbonic acid equation). If the kidneys are functional, there is increased renal excretion of HCO3− and conservation of H+ in an attempt to reduce the alkalinity of the bloodstream. As the pH of blood increases in metabolic alkalosis, H+ ions are reabsorbed into the bloodstream to neutralize the blood. As the nephrons increase H+ ion reabsorption, they excrete K+, and hypokalemia develops (Larkin & Zimmanck, 2015). In hypokalemia a prominent U wave often develops on the ECG and ventricular rhythm disturbances, such as PVCs, may occur. Hypokalemia also can lead to decreased GI motility and paralytic ileus (Emmett & Szerlip, 2017c). Assessment and Diagnostic Findings In metabolic alkalosis, evaluation of ABGs reveals a pH greater than 7.45 and a serum bicarbonate concentration greater than 26 mEq/L. The PaCO2 increases as the lungs attempt to compensate for the excess bicarbonate by retaining CO2. This hypoventilation is more pronounced in patients who are semiconscious, unconscious, or debilitated than in patients who are alert. Because of hypoventilation the patient may develop hypoxemia (Emmett & Szerlip, 2017c). Urine chloride levels may help identify the cause of metabolic alkalosis if the patient’s history provides inadequate information. Metabolic alkalosis is the setting in which urine chloride concentration may be a more accurate estimate of fluid volume than the urine sodium concentration. Urine chloride concentrations can help to determine the source of the metabolic alkalosis. Urine chloride concentrations can be used to differentiate between vomiting, diuretic therapy, and excessive adrenocorticosteroid secretion as the cause of the metabolic alkalosis. In patients with vomiting or cystic fibrosis, those receiving nutritional repletion, and those receiving diuretic therapy, hypovolemia and hypochloremia produce urine chloride concentrations lower than 25 mEq/L. Signs of hypovolemia are not present, and the urine chloride concentration exceeds 40 mEq/L in patients with mineralocorticoid excess or alkali loading; these patients usually have expanded fluid volume (Emmett & Palmer, 2019). Medical Management Treatment of both acute and chronic metabolic alkalosis is aimed at correcting the underlying acid– base disorder. Because volume depletion is commonly present with GI losses of H+, the patient’s I&O must be monitored carefully. Treatment includes restoring normal fluid volume by administering normal saline because continued volume depletion perpetuates the alkalosis. In patients with hypokalemia, potassium is given as KCl to replace both K+ and Cl− losses. Proton pump inhibitors (e.g., omeprazole) are recommended to reduce the production of gastric hydrogen chloride (HCl). This decreased HCl will in turn decrease the loss of HCl with gastric suction in metabolic alkalosis. Carbonic anhydrase inhibitors (e.g., https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zRrdbUNNMKTSTb3II3pEltD4s%2fPbBdKcWtJFoZ4TUro%2b%… 2/3 2/22/24, 2:22 PM Realizeit for Student acetazolamide) are useful in treating metabolic alkalosis in patients who cannot tolerate rapid volume expansion (e.g., patients with heart failure). Carbonic anhydrase inhibitors act at the nephron to enhance bicarbonate excretion (Mehta & Emmett, 2018). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zRrdbUNNMKTSTb3II3pEltD4s%2fPbBdKcWtJFoZ4TUro%2b%… 3/3