Acid-base disorders and treatment approaches

Acid Base Disorder

Regulation of normal pH is critical in Acid-Base balance. Normal pH is 7.35-7.45 and is dependent on both the function of the lungs and kidneys, and pH isa function of the ratio of HCO3- which is regulated by the kidney to Pco2 which is regulated by the lungs. This is called the Henderson-Hasselbalch equation. The classification therefore of acid-base disorder uses the HCO3/Pco2 relationship. Classification is generally divided into acidosis and alkalosis. Acidosis is due to gain of acid or loss of alkali which may be caused by metabolic factors, which is a fall in serum HCO3- or due to respiratory disorders, which increases Pco2. Alkalosis on the other hand, is due to the loss of acid or addition of base. This is caused either by metabolic or respiratory factors, or the increase in serum HCO3- or a decrease in Pco2.

There are mainly 4 different kinds of acid-base disorder: metabolic alkalosis, metabolic acidosis, respiratory alkalosis and respiratory acidosis. Mixed disorders, on the other hand, is when there is more than one acid-base disturbance that exists.

First to be discussed in metabolic acidosis, this is a clinical disturbance which is characterized by a relative increase in total body acid. This is considered as a sign of an underlying disease process which should be identified for appropriate therapy. This disorder is induced by 2 basic mechanisms: an inability of the kidneys to excrete dietary hydrogen load and an increase in the generation of hydrogen ion that is due to the addition of hydrogen or to the loss of bicarbonate due to inappropriate wasting by the kidney or the gastrointestinal tract. The body then responds to this change in several processes. The first process which is readily available is extracellular buffering, with carbonic acid (H2CO3) and is considered an open buffering system because compensatory mechanisms in respiratory carbon dioxide and renal HCO3- serve to maintain balance. Metabolic acidosis stimulated the central and peripheral chemoreceptors which control respiration and eventually results in an increase in alveolar ventilation, which results in a compensatory respiratory alkalosis. Besides extracelluar buffering by the lungs and kidneys, there is intracellular and bone buffering where hydrogen ions enter cells and be taken up by the cell and the bone buffers.

The goal in the treatment of metabolic acidosis is for patients with severe acidemia to raise the systemic pH above 7.1-7.2. This condition can be reversed by treating the underlying condition or by replacing the bicarbonate. But bicarbonate is unnecessary except in extreme cases of acidosis when the pH is

Second disorder is metabolic alkalosis. This is a primary increase in serum bicarbonate concentration which occurs as a consequence of a loss of hydrogen ion from the body or a gain in HCO3-. And metabolic alkalosis leads to a compensatory mechanism of alveolar hypoventilation with an increase in arterial carbon dioxide tension and in turn diminishes the change in pH. Metabolic alkalosis is caused by the following mechanisms: loss of hydrogen ions; shift of hydrogen ions into the intracellular space; alkali administration contraction alkalosis. And in the patient's history there are either: Vomiting or diarrhea; renal failure; or use of drugs such as loop or thiazide diuretics, licorice, tobacco chewing, carbenoxolone, fludrocortisones, glucocorticoids, antacids (eg, magnesium hydroxide) and calcium carbonate.

Metabolic alkalosis is treated with Carbonic anhydrase inhibitors and HCl. If left untreated it may lead to tetany, seizures and decreased mental status. It also decreases coronary blood flow and predisposes persons to refractory arrhythmias. This condition may also cause hypoventilation, leading to hypoxemia and impair weaning from mechanical ventilation. This is also associated with hypokalemia and may precipitate hepatic encephalopathy in susceptible patients.

Third simple acid-base disorder is respiratory acidosis. This is a clinical disturbance due to alveolar hypoventilation. The production of carbon dioxide increases and there is a failure of ventilation, which increases the partial arterial pressure of carbon dioxide. This in turn decreases the HCO3-/PaCO2 and decreases pH. This condition can either be acute or chronic. Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs, whereas, chronic respiratory acidosis may be secondary to many disorders, including COPD. This disorder can be manifested depending on the severity and on the rate of development of hypercapnia. Patients either present with anxiety and dyspnea or sleep and daytime hypersomnolence. anxiety may progress to delirium, and patients become progressively more confused, somnolent, and obtunded or sometimes called as CO2 narcosis. Respiratory acidosis may be caused by chronic obstructive pulmonary disease, neuromuscular diseases, obesity hypoventilation syndrome or CNS depression due to drugs, neurologic disorders or primary alveolar hypoventilation.

This disorder is treated primarily by correcting the underlying disorder, like the other acid-base disorders. But caution is exercised because rapid correction of the hypercapnia can cause alkalanization of the CSF which can cause seizures and metabolic alkalemia. Other forms of treatment include infusion of sodium bicarbonate, but this is rarely indicated. Some give bronchdilators, but treatment is aimed at assisting or increasing ventilation or drugs aimed at reversing the effects of certain sedative drugs also may be helpful in the event of an overdosage. Oxygen therapy and respiratory stimulants have been used but have limited efficacy in respiratory acidosis.

Lastly, respiratory alkalosis is a clinical disturbance due to alveolar hyperventilation which then leads to a decreased PaCO2 level (hypocapnia) and a decrease in PaCO2 level which increases the ratio of bicarbonate concentration (HCO3-) to PaCO2 and increases the pH level. This acid-base disorder is the most common among critically ill patients and is associated with numerous diseases and is commonly seen with patients in mechanical ventilation. On physical examination this condition can present nonspecifically and is related to the underlying illness or cause of the disorder. Many patients are anxious, tachycardic and tachypneic. There may also be positive Chvostek and Trousseau signs.