Acid-base balance disorders

Storage of energy thermodynamics free energy chemical equilibria and group transfer potential, acid-base balance, disorders of energy metabolism, e.g., mitochondrial myopathies, diabetic ketoacidosis 107-108, 230-268, 318, 412... 

Oh MS, Carroll HJ. Regulation of intracellular and extracellular volume. In Arieff Al, DeFronzo RA, eds. Huid, Electrolyte, and Acid-Base Balance Disorders, 2nd ed. New York, Churchill Livingstone, 1995 1-28. 

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. 

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... 

In 18 children with nalidixic acid intoxication, most of whom were aged under 1 year, the clinical effects were neurological disorders of alertness, hjrpertensive cranial syndrome, and neuronal damage some had a metabolic acidosis (30). Treatment included gastric lavage, correction of acid-base balance, and control of convulsions. 

A description of acid-base balance involves an accounting of the carbonic (H2C03, HCOh COa", and CO2) and noncar-bonic acids and conjugate bases in terms of input (intake plus metabolic production) and output (excretion plus metabolic conversion) over a given time interval. The acid-base status of the body fluids is typically assessed by measurements of total CO2 plasma pH and PCO2, because the bicarbonate/carbonic acid system is the most important buffering system of the plasma. Occasionally, measurement of total titratable acid or base, or other acid and base analytes (e.g., lactate and ammonia [NH3]) is necessary to determine the etiology of an acid-base disorder. 

These disorders are classified according to their cause and the direction of the pH change into respiratory acidosis, metabolic acidosis, respiratory alkalosis, or metabolic alkalosis. Any derangement of acid-base balance elicits... 

Acid-base disorders are common, and often serious, disturbances that may result in significant morbidity and mortality. This chapter reviews the mechanisms responsible for the maintenance of acid-base balance and the laboratory analyses that aid clinicians in their assessment of acid-base disorders. The pathophysiology of the four primary acid-base disturbances is presented, the therapeutic options are critiqued, and guidelines for the achievement of the desired therapeutic outcomes are presented. Because many drugs affect acid-base homeostasis and many acid-base abnormalities are potentially preventable, clinicians must anticipate drug-related problems in order to avoid or minimize the clinical consequences, and when necessary design appropriate treatment regimens. 

I Increased sensitivity to inhaled CO2 in panic disorder leading to panic anxiety (but paradoxically voluntary hyperventilation, causing hypocapnia, can also induce panic). I Lactate infusion (possibly by altering acid-base balance) provokes panic in attxious patients but not in controls. 

Kellum, J. A. 2007. Disorders of acid-base balance. Critical Care Medicine 35 2630-2663. 

Thomson, W. S., J. F. Adams, and R. A. Cowan. 1997. Understanding acid-base disorders. Clinical acid-base balance. Oxford Oxford University Press. 

In spite of the variety and efficiency of the body s mechanisms for maintaining a constant pH, disturbances of acid-base balance can and do occur. They may result from gross dietary imbalance, and also from respiratory, metabolic or renal disorders in which there is either too great a production or a failure of elimination of acid or base. 

Disorders of acid base balance are usually a consequence of disease such as diabetes mellitus. The main thrust of treatment is reversing the primary disease process and then the regulatory mechanisms of the body automatically reverse the acid- base abnormalities. There are, however, conditions in which the acid-base disorder must be treated directly because otherwise the patient dies of the acid base upset before the primary illness can be treated. Acidaemia in particular needs treatment. In most pathological conditions involving metabolic disorders of acid-base physiology, the result is acidaemia, alkalaemia being much less common. 

Conclusion. It is (relatively easy, difficult) from the examination of the blood alone to identify uncompensated disorders of acid-base balance but (relatively easy, difficult) to identify compensated disorders without ambiguity. From a study of the blood alone, (uncompensated, compensated) disorders of acid-base balance cannot be identified each separate factor must be sought and its effect evaluated. 

Metabolic disorder of acid-base physiology A disorder of acid-base balance not caused by a respiratory disorder. An example is the excess of acid which occurs in uncontrolled diabetes mellitus. 

Many disorders of the respiratory system, the kidneys, or the metabolic system for forming acids and bases can cause serious derangement of the acid-base balance. Some of the effects of these conditions, compared with the normal pH of the blood of 7.4, are shown in Fig. A-1 and a brief discussion of each condition follows ... 

Lactic acid is the cause of one of many possible disorders in human acid-base metabolism. Lactic acidosis represents an accumulation of lactic acid in the blood and tissues. This condition gradually depletes the natural buffers in the body and there is a consequent lowering of pH. As described in the entry on Glycolysis, lactic acid is the end product til (hat pmcess. Lactic acid blood levels are determined by at least Tour factors. The rate of generation of lactic acid the rate of transport from tissues to plasma and from plasma to the liver (point of utilization of lactic acid) the rate uf utilization and excretion of lactic acid by the kidneys. Normally, all of these funclions are maintained in balance to give a normal blood lactate concentration of about I niFq/l. 

The causes of acid-base disorders, resulting laboratory values, and compensatory responses are discussed here in the traditional categorization of these disorders. However, it is often difficult to remember which disorders fall into which categories, so it is common for mnemonic devices or tables to be used to facilitate description of these disorders. A useful and more logical approach is to reaUze tliat an acidosis can only occur as a result of one (or a combination) of three mechanisms (1) increased addition of acid, (2) decreased elimination of acid, and (3) increased loss of base. Similariy, alkalosis occurs only by (1) increased addition of base, (2) decreased ehmination of base, and (3) increased loss of acid. Dufour has illustrated this simple concept by depicting the body as a two-tank vat, one of acid and one of base, with inputs and outputs for each vat (Figure 46-13). In the normal setting, these inputs and outputs are balanced an acid-base disorder then involves a perturbation in the input or output of these body reservoirs, as discussed in the next section. 

Fluid, Electrolyte, and Acid-Base Disorders The volume status of patients with ARF depends primarily on residual urine output and the type of dialysis received, if any. The patient with oliguric ARF will have impaired excretion of sodium and water. In nonoliguric ARF, considerable sodium may be lost in the urine, necessitating replacement to maintain sodium balance. This also applies to the patient who is losing considerable gastric fluids. Patients on CRRT will lose sodium via hemofiltration or dialysis and should be given sodium as part of their CRRT replacement fluid regimen. 

Patients with a jejunostomy are at risk of hypokalemia as weU, so potassium levels must be monitored closely for supplementation. Other patients at risk for potassium depletion include individuals with long-term sodium depletion, magnesium deficiency, or excessive loss from diarrhea. Metabolic alkalosis, which may occur when a patient becomes dehydrated, accelerates the renal excretion of potassium, as all hydrogen ions are conserved in an attempt to correct the acid-base disorder. As bicarbonate ions are excreted renaUy, potassium is taken with them to maintain osmotic balance. 

The observed [H ] in any acid-base disorder reflects the balance between the primary disturbance and the amount of compensation. 

Very early studies in infants and children on free amino acid-based diets reported 20-25 % additional nonprotein energy was reqnired to support nitrogen balance [22, 23]. However, in patients with metabolic disorders who have limited mobility or are nonambulatory, fewer total calories often suffice in maintaining growth and weight maintenance [24],... 

If cells are to survive and function normally, the fluid medium in which they live must be in equilibrium. Fluid and electrolyte balance, therefore, implies constancy, or homeostasis. This means that the amount and distribution of body fluids and electrolytes are normal and constant. For homeostasis to be maintained, the water and electrolytes that enter (input) the body must be relatively equal to the amount that leaves (output). An imbalance of osmolality, the amount of force of solute per volume of solvent (measured in miliosmoles per kilogram—mOsm/kg or mmol/ kg), of this medium can lead to serious disorders or even death. Fortunately, the body maintains homeostasis through a number of self-regulating systems, which include hormones, the nervous system, fluid-electrolyte balance, and acid-base systems. Els... 

Electrolyte balance Aminoglycosides cause fluid, electrolyte, and acid-base disorders by altering renal tubular function in several ways, leading to hypokalemia and acidosis or alkalosis. Stimulation of the calcium-sensing receptor has been reported to cause a Bartter-like syndrome (hypokalemic metabolic alkalosis, hypomagnesemia, hypocalcemia, and normal serum creatinine concentrations). More rarely, a proximal renal tubular acidosis (Fanconi syndrome non-anion gap metabolic acidosis) can develop. The mechanisms have been summarized [4 ]. 

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