Clinical Causes of Acid-Base Disorders
From the previous discussion, it is obvious that any factor that decreases the rate of pulmonary ventilation also increases the PCO2 of extracellular fluid. This causes an increase in H2CO3 and H+concentration, thus re-sulting in acidosis. Because the acidosis is caused by an abnormality in respiration, it is called respiratoryacidosis.
Respiratory acidosis can occur from pathological conditions that damage the respiratory centers or that decrease the ability of the lungs to eliminate CO2. For example, damage to the respiratory center in the medulla oblongata can lead to respiratory acidosis. Also, obstruction of the passageways of the respiratory tract, pneumonia, emphysema, or decreased pulmonary mem-brane surface area, as well as any factor that interferes with the exchange of gases between the blood and the alveolar air, can cause respiratory acidosis.
In respiratory acidosis, the compensatory responses available are (1) the buffers of the body fluids and (2) the kidneys, which require several days to compensate for the disorder.
Respiratory alkalosis is caused by overventilation by the lungs. Rarely does this occur because of physical pathological conditions. However, a psychoneurosis can occasionally cause overbreathing to the extent that a person becomes alkalotic.
A physiologic type of respiratory alkalosis occurs when a person ascends to high altitude. The low oxygen content of the air stimulates respiration, which causes excess loss of CO2 and development of mild respiratory alkalosis. Again, the major means for compensation are the chemical buffers of the body fluids and the ability of the kidneys to increase HCO3– excretion.
The term metabolic acidosis refers to all other types of acidosis besides those caused by excess CO2 in the body fluids. Metabolic acidosis can result from several general causes: (1) failure of the kidneys to excrete metabolic acids normally formed in the body, (2) formation of excess quantities of metabolic acids in the body, (3) addition of metabolic acids to the body by ingestion or infusion of acids, and (4) loss of base from the body fluids, which has the same effect as adding an acid to the body fluids. Some specific conditions that cause meta-bolic acidosis are the following.
Renal Tubular Acidosis. This type of acidosis results froma defect in renal secretion of H+ or in reabsorption of HCO3–, or both. These disorders are generally of two types: (1) impairment of renal tubular HCO3– reab-sorption, causing loss of HCO3– in the urine, or (2) inability of the renal tubular H+ secretory mechanism to establish a normal acidic urine, causing the excretion of an alkaline urine. In these cases, inadequate amounts of titratable acid and NH4+ are excreted, so that there is net accumulation of acid in the body fluids. Some causes of renal tubular acidosis include chronic renal failure, insufficient aldosterone secretion (Addison’s disease), and several hereditary and acquired disorders that impair tubular function, such as Fanconi’s syndrome.
Diarrhea. Severe diarrhea is probably the most frequentcause of metabolic acidosis. The cause of this acidosis isthe loss of large amounts of sodium bicarbonate into the feces. The gastrointestinal secretions normally containlarge amounts of bicarbonate, and diarrhea results in the loss of HCO3– from the body, which has the same effect as losing large amounts of bicarbonate in the urine. This form of metabolic acidosis is particularly serious and can cause death, especially in young children.
Vomiting of Intestinal Contents. Vomiting of gastric con-tents alone would cause loss of acid and a tendency toward alkalosis because the stomach secretions are highly acidic. However, vomiting large amounts from deeper in the gastrointestinal tract, which sometimes occurs, causes loss of bicarbonate and results in meta-bolic acidosis in the same way that diarrhea causes acidosis.
Diabetes Mellitus. Diabetes mellitus is caused by lack ofinsulin secretion by the pancreas (type I diabetes) or by insufficient insulin secretion to compensate for decreased sensitivity to the effects of insulin (type II diabetes). In the absence of sufficient insulin, the normal use of glucose for metabolism is prevented. Instead, some of the fats are split into acetoacetic acid, and this is metabolized by the tissues for energy in place of glucose. With severe diabetes mellitus, blood acetoacetic acid levels can rise very high, causing severe metabolic acidosis. In an attempt to compensate for this acidosis, large amounts of acid are excreted in the urine, some-times as much as 500 mmol/day.
Ingestion of Acids. Rarely are large amounts of acidsingested in normal foods. However, severe metabolic acidosis occasionally results from the ingestion of certain acidic poisons. Some of these include acetylsali-cylics (aspirin) and methyl alcohol (which forms formic acid when it is metabolized).
Chronic Renal Failure. When kidney function declinesmarkedly, there is a buildup of the anions of weak acids in the body fluids that are not being excreted by the kidneys. In addition, the decreased glomerular filtration rate reduces the excretion of phosphates and NH4+, which reduces the amount of bicarbonate added back to the body fluids. Thus, chronic renal failure can be associated with severe metabolic acidosis.
When there is excess retention of HCO3– or loss of H+ from the body, this results in metabolic alkalosis. Meta-bolic alkalosis is not nearly as common as metabolic aci-dosis, but some of the causes of metabolic alkalosis are as follows.
AdministrationofDiuretics(ExcepttheCarbonicAnhydrase Inhibitors). All diuretics cause increasedflow offluidalong the tubules, usually causing increased flow in the distal and collecting tubules. This leads to increased reabsorption of Na+ from these parts of the nephrons. Because the sodium reabsorption here is coupled with H+ secretion, the enhanced sodium reabsorption also leads to an increase in H+ secretion and an increase in bicarbonate reabsorption. These changes lead to the development of alkalosis, characterized by increased extracellular fluid bicarbonate concentration.
Excess Aldosterone. When large amounts of aldosteroneare secreted by the adrenal glands, a mild metabolic alkalosis develops. As discussed previously, aldosterone promotes extensive reabsorption of Na+from the distal and collecting tubules and at the same time stimulates the secretion of H+ by the intercalated cells of the col-lecting tubules. This increased secretion of H+ leads to its increased excretion by the kidneys and, therefore, metabolic alkalosis.
Vomiting of Gastric Contents. Vomiting of the gastric con-tents alone, without vomiting of the lower gastrointesti-nal contents, causes loss of the HCl secreted by the stomach mucosa. The net result is a loss of acid from the extracellular fluid and development of metabolic alka-losis. This type of alkalosis occurs especially in neonates who have pyloric obstruction caused by hypertrophied pyloric sphincter muscles.
Ingestion of Alkaline Drugs. A common cause of metabolicalkalosis is ingestion of alkaline drugs, such as sodium bicarbonate, for the treatment of gastritis or peptic ulcer.
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