The three primary buffering systems are the protein buffer system, the carbonic acid-bicarbonate buffer system, and the phosphate buffer system. The human body has both intracellular and extracellular fluids which must maintain a regulated pH status; this is accomplished through the three primary buffering systems independently and collectively.
The protein buffer system regulates the pH in both the extracellular fluid and ICF. The protein buffer systems depends on the ability of amino acids to respond to fluctuations in pH and responds by either accepting or releasing a hydrogen ion (H+) (Martini, 2009).
The product of the body’s disassociation of carbonic acid is a hydrogen ion and a bicarbonate ion, which together form the carbonic acid-bicarbonate buffer system (Martini, 2009). The carbonic acid–bicarbonate buffer system maintains a steady pH in the extracellular fluid given the presence of organic acids and fixed acids, but with certain limitations. The carbonic acid-bicarbonate buffer system cannot protect the EFC in pH is altered from low or high levels of CO2, it cannot function without the respiratory system and respiratory control centers function properly, and it can only buffer bicarbonate ions (Martini, 2009).
The phosphate buffer system is formed by a constant equilibrium of an. acid dihydrogen phosphate ions (H2PO4-), and a base, hydrogen phosphate ions (HPO42-). Phosphate buffers have a very low concentration within the blood, plasma, and extracellular fluids and therefore only have a supportive function in maintaining its pH. The primary function of the phosphate buffer system is the pH regulation of intracellular the pH regulation of urine (Marini, 2009)
Metabolic alkalosis is an elevation of the body’s pH due to an increase in serum bicarbonate (HCO3-) concentration. Metabolic alkalosis is usually caused by the loss of acids, the most common cause is excessive vomiting (Martini, 2009) To replace the loss of acids, the body increases the production gastric acids causing an influx of bicarbonate ions into the bloodstream, known as the alkaline tide (Martini, 2009). The compensatory mechanism of metabolic alkalosis will increase the excretion HCO3- in the urine and a decrease in ventilation as a result of alveolar hypoventilation (Martini, 2009; Pooler, 2009). Alveolar hypoventilation increases the PCO2 levels in an effort to maintain a satisfactory ratio of PCO2 and (HCO3-) within the body (Pooler, 2009).
Metabolic acidosis is the second most common acid-base imbalance characterized by a lower plasma pH due to low levels of bicarbonate (HCO3-). Metabolic acidosis results from increased acid production or decreased acid secretion. Common causes of metabolic acidosis include the overproduction of large or fixed organic acids, the kidney’s impaired ability to excrete H+ or severe bicarbonate loss (Martini, 2009). Low levels of bicarbonate (HCO3-) concentration leaves the carbonic acid–bicarbonate buffer system unable to regulate the body’s decreasing levels of pH (Martini, 2009). Metabolic acidosis involved both renal and respiratory compensatory mechanisms. The respiratory compensation will result in an increase in ventilation and a decrease in PCO2. The renal compensatory mechanism increases H+ excretion and with properly functioning kidney’s it also increases the re absorption of bicarbonate (HCO3-) (Martini, 2009; (Pooler, 2009).
Pooler, C. (2009). Disorders of Ventilation and Gas Exchange. In Hannon, R.A., Poth, C.M., & Pooler, C. (Eds.) Porth Pathophysiology: Concepts of Altered Health States. (701-790) Philadelphia, PA: Lippincott William & Wilkins.
Martini, F. (2009). Fundamentals of Anatomy & Physiology (8th ed). Pearson Learning Solutions. Retrieved from: http://digitalbookshelf.southuniversity.edu/books/0558542387/id/ch18fig10