Why is blood ph tightly regulated




















Kamal, A. Abuzenadah et al. Dudek, S. Datta, T. Franke et al. Rasgon and L. Steen, B. Terry, E. Rivera et al. Holloway, V. Bezaire, G. Heigenhauser et al. Wibom, E. Hultman, M. Johansson, K. Matherei, D. Constantin-Teodosiu, and P. View at: Google Scholar N. Bradley, L. Snook, S. Jain, G. Heigenhauser, A. Bonen, and L. Susuki, O. Ito, H. Takahashi, and K. Parkhouse, D. McKenzie, P. Hochachka, and W. View at: Google Scholar P. Arthur, M.

Hogan, D. Bebout, P. Wagner, and P. DeSouza, L. Shapiro, C. Clevenger et al. Dubouchaud, G. Butterfield, E. Wolfel, B. Bergman, and G. Baker, K. Mccullagh, and A. Bonen, K. McCullagh, C. Putman, E. Hultman, N. Jones, and G. Narumi, A. Furugen, M. Kobayashi, S. Otake, S. Itagaki, and K. Aoi, M. Tsuzuki, M. Fujie, S. Iwashita, and M. Iwashita, M. Fujie, and M. Skelton, D. Kremer, E. Smith, and L. Rassanan, K. Lampinen, and A.

View at: Google Scholar T. Nagao, S. Meguro, T. Hase et al. Squadrito, H. Marini, A. Bitto et al. Yoshida, P. Jacques, J. Meigs et al. Asemi, M. Samimi, Z. Tabassi, H. Shakeri, and A. Ramel, A. Kiely, G. Morais, N. Bandarra, and I. Vessby, M. Uusitupa, K. Hermansen et al. Bhuvaneswari and C. Takikawa, S. Inoue, F. Horio, and T.

Greene, B. Nelson, K. Robinson, and M. Lee, H. Lee, and H. Wang and M. An example of a weak basic solution is seawater, which has a pH near 8. How can organisms whose bodies require a near-neutral pH ingest acidic and basic substances a human drinking orange juice, for example and survive? Buffers are the key. When bicarbonate ions combine with free hydrogen ions and become carbonic acid, hydrogen ions are removed, moderating pH changes. Similarly, excess carbonic acid can be converted into carbon dioxide gas and exhaled through the lungs; this prevents too many free hydrogen ions from building up in the blood and dangerously reducing its pH; likewise, if too much OH — is introduced into the system, carbonic acid will combine with it to create bicarbonate, lowering the pH.

Antacids, which combat excess stomach acid, are another example of buffers. Distinguish between buffer solutions, ventilation, and renal function as buffer systems to control acid—base balance.

Acid—base homeostasis concerns the proper balance between acids and bases; it is also called body pH. The body is very sensitive to its pH level, so strong mechanisms exist to maintain it.

Outside an acceptable range of pH, proteins are denatured and digested, enzymes lose their ability to function, and death may occur. A buffer solution is an aqueous solution of a weak acid and its conjugate base, or a weak base and its conjugate acid.

Its pH changes very little when a small amount of strong acid or base is added to it. Buffer solutions are used as a means of keeping pH at a nearly constant value in a wide variety of chemical applications.

Many life forms thrive only in a relatively small pH range, so they utilize a buffer solution to maintain a constant pH. One example of a buffer solution found in nature is blood. Several buffering agents that reversibly bind hydrogen ions and impede any change in pH exist. Extracellular buffers include bicarbonate and ammonia, whereas proteins and phosphates act as intracellular buffers.

Acid—base imbalances that overcome the buffer system can be compensated in the short term by changing the rate of ventilation. The kidneys are slower to compensate, but renal physiology has several powerful mechanisms to control pH by the excretion of excess acid or base. In response to acidosis, the tubular cells reabsorb more bicarbonate from the tubular fluid, and the collecting duct cells secrete more hydrogen and generate more bicarbonate, and ammoniagenesis leads to an increase of the NH 3 buffer.

Scand J Lab Invest. Siggaard-Andersen O:. The acid—base Status of the Blood, 4th ed. Copenhagen: Munksgaard,. N Engl J Med.

PubMed Article Google Scholar. Br J Anesth. Schlichtig R: Acid—base balance quantitation. Magder S: Pathophysiology of metabolic acid—base disturbances in patients with critical illness. In: Critical Care Nephrology. Edited by Ronco C, Bellomo R. Gattinoni L, Lissoni A: Respiratory acid—base disturbances in patients with critical illness. J Lab Clin Med. J Crit Care. Kirschbaum B: Increased anion gap after liver transplantation. Am J Med Sci. J Appl Physiol. Bourke E, Haussinger D: pH homeostasis: the conceptual change.

In: The Kidney Today. Selected Topics in Renal Science. Edited by Berlin GM. Contrib Nephrol. Basel: Karger,. Oliver J, Bourke E: Adaptations in urea and ammonium excretion in metabolic acidosis in the rat: a reinterpretation. Clin Sci Mol Med. CAS Google Scholar. In: Comparative and Environmental Physiology. Edited by Heisler N. Springer: Berlin,. Moore EW: The alkaline tide.

Cushing H: Concerning the poisonous effect of pure sodium chloride solutions upon the nerve muscle preparation. Am J Physiol. Respir Physiol. Jabor A, Kazda A: Modeling of acid—base equilibria.

Acta Anaesth Scand. Kellum JA: Recent advances in acid—base physiology applied to critical care. Edited by Vincent JL. Heidelberg: Springer-Verlag,. Download references. You can also search for this author in PubMed Google Scholar.

Reprints and Permissions. Kellum, J. Determinants of blood pH in health and disease. Crit Care 4, 6 Download citation. Published : 24 January Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Abstract An advanced understanding of acid—base physiology is as central to the practice of critical care medicine, as are an understanding of cardiac and pulmonary physiology.

Introduction Whereas most medical and surgical subspecialists concern themselves with a specific organ eg nephrology , region of the body eg cardiothoracic surgery , or disease process eg infectious disease , practitioners of critical care are more often concerned with the interaction of various organs and disease states.

Quantification, classification, and causation In order to understand acid—base physiology, we must first agree on how to describe and measure it. Base excess In order to address the first 'shortcoming' of the Henderson-Hasselbach equation — the inability to quantify the metabolic component — several methods have been devised. Table 1 Observational acid—base patterns Full size table.

Physical-chemical properties of biologic solutions A physical—chemical analysis of acid—base physiology requires the application of two basic principles. Figure 1. Full size image. Carbon dioxide CO 2 is an independent determinant of pH and is produced by cellular metabolism or by the titration of HCO 3 - by metabolic acids. Electrolytes strong ions Blood plasma contains numerous ions.

Figure 2. Pathophysiologic mechanisms Metabolic acidoses and alkaloses are categorized according to the ions that are responsible. Conclusion Unlike many other areas in clinical medicine, the approach to acid—base physiology has not often distinguished cause from effect. References 1. Google Scholar 2. Article Google Scholar 3. Article Google Scholar 4.

Changes in the pH of CSF affect the respiratory center in the medulla oblongata, which can directly modulate breathing rate to bring the pH back into the normal range. Hypercapnia, or abnormally elevated blood levels of CO 2 , occurs in any situation that impairs respiratory functions, including pneumonia and congestive heart failure.

Hypocapnia, or abnormally low blood levels of CO 2 , occurs with any cause of hyperventilation that drives off the CO 2 , such as salicylate toxicity, elevated room temperatures, fever, or hysteria. Whereas the respiratory system together with breathing centers in the brain controls the blood levels of carbonic acid by controlling the exhalation of CO 2 , the renal system controls the blood levels of bicarbonate.

A decrease of blood bicarbonate can result from the inhibition of carbonic anhydrase by certain diuretics or from excessive bicarbonate loss due to diarrhea. Finally, low bicarbonate blood levels can result from elevated levels of ketones common in unmanaged diabetes mellitus , which bind bicarbonate in the filtrate and prevent its conservation.

Bicarbonate ions, HCO 3 — , found in the filtrate, are essential to the bicarbonate buffer system, yet the cells of the tubule are not permeable to bicarbonate ions. The steps involved in supplying bicarbonate ions to the system are seen in Figure It is also possible that salts in the filtrate, such as sulfates, phosphates, or ammonia, will capture hydrogen ions.

If this occurs, the hydrogen ions will not be available to combine with bicarbonate ions and produce CO 2. In such cases, bicarbonate ions are not conserved from the filtrate to the blood, which will also contribute to a pH imbalance and acidosis. The hydrogen ions also compete with potassium to exchange with sodium in the renal tubules. If more potassium is present than normal, potassium, rather than the hydrogen ions, will be exchanged, and increased potassium enters the filtrate.

When this occurs, fewer hydrogen ions in the filtrate participate in the conversion of bicarbonate into CO 2 and less bicarbonate is conserved. If there is less potassium, more hydrogen ions enter the filtrate to be exchanged with sodium and more bicarbonate is conserved.

Chloride ions are important in neutralizing positive ion charges in the body. If chloride is lost, the body uses bicarbonate ions in place of the lost chloride ions. Thus, lost chloride results in an increased reabsorption of bicarbonate by the renal system. Acid-Base Balance: KetoacidosisDiabetic acidosis, or ketoacidosis, occurs most frequently in people with poorly controlled diabetes mellitus.

When certain tissues in the body cannot get adequate amounts of glucose, they depend on the breakdown of fatty acids for energy. When acetyl groups break off the fatty acid chains, the acetyl groups then non-enzymatically combine to form ketone bodies, acetoacetic acid, beta-hydroxybutyric acid, and acetone, all of which increase the acidity of the blood. Ketoacidosis can be severe and, if not detected and treated properly, can lead to diabetic coma, which can be fatal. A common early symptom of ketoacidosis is deep, rapid breathing as the body attempts to drive off CO 2 and compensate for the acidosis.

Another common symptom is fruity-smelling breath, due to the exhalation of acetone. Other symptoms include dry skin and mouth, a flushed face, nausea, vomiting, and stomach pain.



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