Traditional approach

Traditional approach

In health, blood pH (which is taken as the same as ECF pH) is maintained within a narrow range of approximately 7.4 to 7.5. Traditional interpretation of acid-base status involves the Henderson-Hasselbach equation, where pH is determined by the ratio of bicarbonate to carbon dioxide. Blood pH is normal when the ratio of HCO3- to pCO2 is 20:1. Respiratory factors affect pCO2, whereas non-respiratory, or metabolic factors, affect the HCO3-. The major extracellular buffer of acids in the body is bicarbonate followed by plasma proteins and bone. Intracellular buffers include proteins, organic phosphate, inorganic phosphate and hemoglobin (in erythrocytes). Regulation of acid-base involves chemical buffering with intra- and extra-cellular buffers, control of partial pressure of carbon dioxide by altering respiration and control of bicarbonate and hydrogen excretion by the kidneys. In general, rapid changes in acid-base can be achieved by changing respiration, whereas the kidney is involved in slower, more long-term regulation of acid-base status. The kidney is central to acid-base regulation. Filtered bicarbonate is absorbed in the PCT of the kidney and regenerates the bicarbonate lost in buffering acids produced by normal body metabolism. Hydrogen is excreted by the PCT and DCT of the kidney. Excretion of H+ by the PCT is dependent on filtered phosphates and urea generated by the tubular epithelial cells. Excretion of H+ by the DCT is dependent on sodium resorption and exchanges for K+. There are four primary types of acid-base disorders: metabolic acidosis, respiratory acidosis, metabolic alkalosis, and respiratory alkalosis. The majority of patients with acid-base imbalance have either metabolic acidosis or metabolic alkalosis or a mixed disorder of both. Acidosis Acidosis can be primary metabolic (decreased HC03) or respiratory (hypercapnea) or secondary in compensation for a primary alkalosis. Acidosis has profound effects on the body, resulting in arrythmias, decreased cardiac output, depression, and bone demineralization. Primary metabolic acidosis: This can be due to loss of bicarbonate (hyperchloremic metabolic acidosis) or titration of bicarbonate (high anion gap metabolic acidosis). Primary respiratory acidosis: This is due to increased pCO2 from decreased effective alveolar hypoventilation. Any disorder interfering with normal alveolar ventilation can produce a respiratory acidosis. The most common causes are primary pulmonary disease, ranging from upper airway obstruction to pneumonia. Diseases or drugs that inhibit the medullary respiratory center also produce a profound respiratory acidosis, e.g. general anesthesia. Alkalosis Alkalosis can be primary metabolic (increased HCO3) or respiratory (hypocapnea) or secondary in compensation for a primary acidosis. Usually respiratory alkalosis is the compensatory mechanism for a primary metabolic acidosis. Alkalosis results in tetany and convulsions, weakness, polydipsia and polyuria. Primary metabolic alkalosis: This is due to loss of hydrogen (usually with chloride) from the gastrointestinal or urinary tracts. Hypochloremia is a consistent feature and indicator of metabolic alkalosis. HCO3 is generated on an equimolar basis to the amount of hydrogen lost. Primary respiratory alkalosis: This is due to hyperventilation and is associated with decreased pCO2. Hyperventilation is usually stimulated by hypoxia associated with pulmonary disease, congestive heart failure, or severe anemia. Psychogenic disturbances, neurologic disorders, or drugs that stimulate the medullary respiratory center, will also stimulate hyperventilation.

In health, blood pH (which is taken as the same as ECF pH) is maintained within a narrow range of approximately 7.4 to 7.5. Traditional interpretation of acid-base status involves the Henderson-Hasselbach equation, where pH is determined by the ratio of bicarbonate to carbon dioxide. Blood pH is normal when the ratio of HCO3- to pCO2 is 20:1. Respiratory factors affect pCO2, whereas non-respiratory, or metabolic factors, affect the HCO3-.

The major extracellular buffer of acids in the body is bicarbonate followed by plasma proteins and bone. Intracellular buffers include proteins, organic phosphate, inorganic phosphate and hemoglobin (in erythrocytes). Regulation of acid-base involves chemical buffering with intra- and extra-cellular buffers, control of partial pressure of carbon dioxide by altering respiration and control of bicarbonate and hydrogen excretion by the kidneys. In general, rapid changes in acid-base can be achieved by changing respiration, whereas the kidney is involved in slower, more long-term regulation of acid-base status.

The kidney is central to acid-base regulation. Filtered bicarbonate is absorbed in the PCT of the kidney and regenerates the bicarbonate lost in buffering acids produced by normal body metabolism. Hydrogen is excreted by the PCT and DCT of the kidney. Excretion of H+ by the PCT is dependent on filtered phosphates and urea generated by the tubular epithelial cells. Excretion of H+ by the DCT is dependent on sodium resorption and exchanges for K+.

There are four primary types of acid-base disorders: metabolic acidosis, respiratory acidosis, metabolic alkalosis, and respiratory alkalosis. The majority of patients with acid-base imbalance have either metabolic acidosis or metabolic alkalosis or a mixed disorder of both.

Acidosis

Acidosis can be primary metabolic (decreased HC03) or respiratory (hypercapnea) or secondary in compensation for a primary alkalosis. Acidosis has profound effects on the body, resulting in arrythmias, decreased cardiac output, depression, and bone demineralization.

Primary metabolic acidosis: This can be due to loss of bicarbonate (hyperchloremic metabolic acidosis) or titration of bicarbonate (high anion gap metabolic acidosis).
Primary respiratory acidosis: This is due to increased pCO2 from decreased effective alveolar hypoventilation. Any disorder interfering with normal alveolar ventilation can produce a respiratory acidosis. The most common causes are primary pulmonary disease, ranging from upper airway obstruction to pneumonia. Diseases or drugs that inhibit the medullary respiratory center also produce a profound respiratory acidosis, e.g. general anesthesia.

Alkalosis

Alkalosis can be primary metabolic (increased HCO3) or respiratory (hypocapnea) or secondary in compensation for a primary acidosis. Usually respiratory alkalosis is the compensatory mechanism for a primary metabolic acidosis. Alkalosis results in tetany and convulsions, weakness, polydipsia and polyuria.

Primary metabolic alkalosis: This is due to loss of hydrogen (usually with chloride) from the gastrointestinal or urinary tracts. Hypochloremia is a consistent feature and indicator of metabolic alkalosis. HCO3 is generated on an equimolar basis to the amount of hydrogen lost.
Primary respiratory alkalosis: This is due to hyperventilation and is associated with decreased pCO2. Hyperventilation is usually stimulated by hypoxia associated with pulmonary disease, congestive heart failure, or severe anemia. Psychogenic disturbances, neurologic disorders, or drugs that stimulate the medullary respiratory center, will also stimulate hyperventilation.