Bases acids balanced with

For Further Reading J. A. Kraut and N. E. Madias, Approach to patients with acid—base disorders, Respiratory Care, vol. 46, no. 4, April 2001, pp. 392—403. J. Squires, Artificial blood, Science, vol. 295, Feb. 8, 2002, pp. 1002-1005. Lynn Taylor and Norman P. Curthoys, Glutamine metabolism Role in Acid-Base Balance, Biochemistry and Molecular Biology Education, vol. 32, no. 5, 2004, pp. 291-304. 

Rainwater and snowmelt water are primary factors determining the very nature of the terrestrial carbon cycle, with photosynthesis acting as the primary exchange mechanism from the atmosphere. Bicarbonate is the most prevalent ion in natural surface waters (rivers and lakes), which are extremely important in the carbon cycle, accoxmting for 90% of the carbon flux between the land surface and oceans (Holmen, Chapter 11). In addition, bicarbonate is a major component of soil water and a contributor to its natural acid-base balance. The carbonate equilibrium controls the pH of most natural waters, and high concentrations of bicarbonate provide a pH buffer in many systems. Other acid-base reactions (discussed in Chapter 16), particularly in the atmosphere, also influence pH (in both natural and polluted systems) but are generally less important than the carbonate system on a global basis. 

It is also often taken for granted that many of the Earth s subsystems are exposed to free oxygen (O2), leading to a range of one-way reactions of reduced materials (such as organic carbon or metal sulfides) to an oxidized form. As pointed out many times in earlier chapters, the oxidation-reduction status of the planet is the consequence of the dynamic interactions of biogeochemical cycles. As is the case with the acid-base balances, there is considerable sensitivity to perturbations of "redox" conditions, sometimes dramatically as in the case of bodies of water that suddenly become anaerobic because of eutrophication. Another extreme... 

Figure 1. Acid-base balance evaluation diagram with 13 diagnostic areas (1)...

The body s normal daily potassium requirement is 0.5 to 1 mEq/kg (0.5 to 1 mmol/kg) or 40 to 80 mEq (40 to 80 mmol) to maintain a serum potassium concentration of 3.5 to 5 mEq/L (3.5 to 5 mmol/L). Potassium is the most abundant cation in the ICF, balancing the sodium contained in the ECF and maintaining electroneutrality of bodily fluids. Because the majority of potassium is intracellular, serum potassium concentration is not a good measure of total body potassium however, clinical manifestations of potassium disorders correlate well with serum potassium. The acid-base balance of the body affects serum potassium concentrations. Hyperkalemia is routinely seen in... 

Concentration limits for chloride and acetate in PN typically are linked to limitations for sodium and potassium. The usual ratio of chloride acetate in PN is about 1 1 to 1.5 1. Chloride and acetate primarily play a role in acid-base balance. Acetate is converted to bicarbonate at a 1 1 molar ratio. This conversion appears to occur mostly outside the liver. Bicarbonate never should be added to or coinfused with PN solutions. This can lead to the release of carbon dioxide and potentially result in the formation of calcium or magnesium carbonate (very insoluble salts). 

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

Chemoreceptor response to increased arterial hydrogen ion concentration. An increase in arterial hydrogen ion concentration, or a decrease in arterial pH, stimulates the peripheral chemoreceptors and enhances ventilation. This response is important in maintaining acid-base balance. For example, under conditions of metabolic acidosis, caused by the accumulation of acids in the blood, the enhanced ventilation eliminates carbon dioxide and thus reduces the concentration of H+ ions in the blood. Metabolic acidosis may occur in patients with uncontrolled diabetes mellitus or when tissues become hypoxic and produce lactic acid. An increase in arterial hydrogen ion concentration has no effect on the central chemoreceptors. Hydrogen ions are unable to cross the blood-brain barrier. 

Along with the respiratory system, the renal system maintains acid-base balance by altering the excretion of hydrogen and bicarbonate ions in the urine. When the extracellular fluid becomes acidic and pH decreases, the... 

When considering the topic of acid-base balance, there are two key terms with which you should be familiar. These are pH and pKa. Calculations of a patient s acid-base status will utilize these terms. 

Homeostasis. The blood ensures that a balanced distribution of water is maintained between the vascular system, the cells (intracellular space), and the extracellular space. The acid-base balance is regulated by the blood in combination with the lungs, liver, and kidneys (see p. 288). The regulation of body temperature also depends on the controlled transport of heat by the blood. 

The kidneys main function is excretion of water and water-soluble substances (1). This is closely associated with their role in regulating the body s electrolyte and acid-base balance (homeostasis, 2 see pp.326 and 328). Both excretion and homeostasis are subject to hormonal control. The kidneys are also involved in synthesizing several hormones (3 see p. 315). Finally, the kidneys also play a role in the intermediary metabolism (4), particularly in amino acid degradation and gluconeo-genesis (see p. 154). 

Pharmacology Potassium participates in a number of essential physiological processes, such as maintenance of intracellular tonicity and a proper relationship with sodium across cell membranes, cellular metabolism, transmission of nerve impulses, contraction of cardiac, skeletal, and smooth muscle, acid-base balance, and maintenance of normal renal function. Normal potassium serum levels range from 3.5 to 5 mEq/L. 

Metabolic or respiratory acidosis Cautiously institute amiloride in severely ill patients in whom respiratory or metabolic acidosis may occur, such as patients with cardiopulmonary disease or poorly controlled diabetes. Monitor acid-base balance frequently. Shifts in acid-base balance alter the ratio of extracellular/intracellular potassium the development of acidosis may be associated with rapid increases in serum potassium. 

Alkalinization of urine Hematuria, renal colic, costovertebral pain, and formation of urate stones associated with use in gouty patients may be prevented by alkalization of urine and liberal fluid intake monitor acid-base balance. 

The kidney regulates the acid-base balance of the body by control over resorption of sodium ions, which may exchange for hydrogen ions in the kidney tubule. Since most dietaries are of acid-ash, the urine is usually more acid than the original plasma filtrate and much of the phosphate excreted is thus changed to the acid monosodium salt, Within the range of normal variability, with an alkaline ash diet, the urine may become alkaline, and in extreme instances, some sodium bicarbonate may be excreted. 

For adequate toxicologic evaluation, determinations should be made on lipids, hormones, acid/base balance, methemoglobin, and cholinesterase activity. In other words, additional clinical biochemistry may be resorted to wherever necessary to arrive at meaningful conclusions in association with the observed effects. Urinalysis, although not required on a routine basis, should be performed whenever there is an indication based on observed toxicity. 

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