An increase in plasma bicarbonate concentration and an increase in blood pH characterize metabolic alkalosis. A mixed disturbance of metabolic alkalosis and metabolic acidosis can be diagnosed by a significantly increased anion gap in the presence of a normal or near-normal serum pH. Metabolic alkalosis can result from ECF hydrogen ion loss, the addition of bicarbonate or bicarbonate precursors to the ECF, or ECF volume contraction. Clinically, metabolic alkalosis is often divided into chloride-responsive and chloride-resistant states (Table 4). Chloride-responsive states are usually associated with volume and chloride depletion (e.g., vomiting or nasogastric suction) and characterized by a low urinary chloride concentration, <10 mEq/L. One exception is the active use of diuretics in which instance urine chloride concentration may be >10mEq/L. The elderly are more highly predisposed to developing volume depletion. Milk alkali syndrome and diuretic use should always be considered in an older patient with metabolic alkalosis. By contrast, chloride-resistant metabolic alkalosis is usually due to a high aldosterone or aldosterone-like state, such as primary hyperaldos-teronism or Cushing’s syndrome, and associated with an increase in sodium retention, hypertension and a high urinary chloride concentration.
Table 4. Common Causes of Metabolic Alkalosis in the Elderly
|Chloride ( CI”) Responsive (Urine CI <10)||Chloride Resistant (Urine CI >10)|
|Gastric fluid loss||Mineralocorticoid excess|
|Postdiuretic therapy||Primary/secondary Cortisol excess|
|Milk alkali syndrome|
Patients may develop muscle cramps, weakness, and hypereflexia. Marked increases in serum pH can induce seizures. Associated alveolar hypoventilation can lead to a reduction in PO2 and signs of hypoxia or to CO2 retention. Hypochloremia and hypokalemia are almost invariably present, and severe hypokalemia can lead to cardiac arrhythmias. Volume contraction often leads to increased serum urea nitrogen and serum creatinine levels.
Initial treatment is directed toward correcting the underlying disease process. Specific therapy for chloride-responsive metabolic alkalosis requires administration of sodium chloride and frequently potassium chloride. In the volume-depleted older patient, 100-125 cc/hr of normal saline for 24-48 hours with reassessment of arterial blood gases is adequate in most instances. If clinical hypotension is present, more aggressive fluid administration is indicated. If hypokalemia is present 20-40 mmol of potassium chloride should be added to each liter of normal saline. In chloride-resistant states, the use of direct or indirect aldosterone antagonists, such as spironolactone or amiloride, is often effective, while a definitive diagnosis is being sought.
Respiratory acidosis is characterized by an increase in PCO2 and a reduction in pH. The increased PCO2 results in an increased carbonic acid concentration. In respiratory acidosis, carbonic acid is buffered by intracellular buffers, including hemoglobin and phosphate, resulting in a small increase in plasma bicarbonate concentration. The kidneys compensate by increasing acid secretion and replenishing the bicarbonate pool.
This renal response may take three-to-four hours to fully develop. Conditions, such as pulmonary obstruction, stroke, primary depression of the respiratory center, mechanical/structural defect, or a neuromuscular disorder, can lead to a reduction in alveolar ventilation with PCO2 retention and acidemia. Salicylate intoxication which classically presents as a mixed metabolic acidosis and respiratory alkalosis may present as a respiratory acidosis in the elderly due to the frequent association of other ingested substances, primarily central nervous system depressants.
Patients may present with respiratory distress, dyspnea, confusion, and/or lethargy. If severe, patient may show signs of increased intracranial pressure due to vasodilatory properties of PCO2 that increases cerebral blood flow.
The treatment of respiratory acidosis is correction of the underlying disorder and restoration of adequate ventilation. This may necessitate the use of mechanical ventilation. In addition to the standard clinical assessment, urine drug screening for possible overdose or intoxication is critical, particularly for salicylate toxicity and central nervous system depressants.
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Respiratory alkalosis is a common acid-base disorder encountered in the elderly. It results from increased alveolar ventilation leading to a reduced PCO2 and an elevated plasma pH. The initial response to alkalemia is buffering with intracellular protons. Renal compensation occurs over several days with a reduction in both net acid excretion and bicarbonate reclamation, reducing plasma bicarbonate concentration and lowering plasma pH towards normal. Clinical disorders which increase the central nervous system respiratory drive or stimulate chemoreceptors may lead to hyperventilation and reduce systemic PCO2. In the elderly, it is especially important to consider anxiety and associated hyperventilation, central nervous system infection/infarction, sepsis, pulmonary edema, pulmonary emboli and/or medications/drugs—especially salicylate intoxication.
The patient often presents with hyperventilation and signs of hypocapnia. These may include a sensation of light headedness, perioral and extremity paresthesias, muscle cramps, seizures and cardiac arrhythmias. In the elderly respiratory alkalosis may often be a clue to a state of a serious underlying disorder.
The only effective therapy is to treat the underlying disorder. The transient use of a rebreathing mask, bag, or similar instrument may help resolve the acute symptoms of hypocapnia. Serum salicylate levels should be checked to exclude occult salicylate toxicity.
Appropriate cultures and broad-spectrum antibiotics should be instituted if there is a suspicion of sepsis.
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In summary, the elderly—particularly acutely ill elderly—are at a greater risk for the development of marked derangements in systemic acid-base homeostasis that may delay recovery, prolong hospitalizations, and adversely affect clinical outcomes. There is unequivocal evidence that more severe acid-base disorders are associated with a greater risk for mortality. A greater understanding of the changes in renal physiology and related neurohormonal responses that occur with aging can help guide the clinician toward a more timely and appropriate response to a given disease process.