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Acid-base disorders metabolic

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. [Pg.573]

Respiratory and metabolic derangements can occur in isolation or in combination. If a patient has an isolated primary acid-base disorder that is not accompanied by another primary acid-base disorder, a simple (uncomplicated) disorder... [Pg.421]

Because C02 is a volatile acid, it can rapidly be changed by the respiratory system. If a respiratory acid-base disturbance is present for minutes to hours it is considered an acute disorder while if it is present for days or longer it is considered a chronic disorder. By definition, the metabolic machinery that regulates HC03 results in slow changes in serum bicarbonate and all metabolic disorders are chronic. This means that there are six simple acid-base disorders as outlined in Table 25-1.2... [Pg.421]

Changes that follow the primary disorder and attempt to restore the blood pH to normal are referred to as compensatory changes. It should be stressed that compensation never normalizes the pH. Because all metabolic acid-base disorders are chronic and the normal respiratory system can quickly alter the PaC02, essentially all metabolic disorders are accompanied by some degree of respiratory compensation.3 Similarly, chronic respiratory acid-base disorders are typically accompanied by attempts at metabolic compensation.4,5 However, with acute respiratory acid-base disorders there is insufficient time for the metabolic pathways to compensate significantly.6 As such, acute respiratory derangements are essentially uncompensated. [Pg.421]

The amount of compensation (metabolic or respiratory) can be reliably predicted based on the degree of derangement in the primary disorder. Table 25-1 outlines the simple acid-base disorders and provides formulas for calculating the... [Pg.421]

Metabolic acidosis An acid-base disorder caused by overproduction or accumulation of acid (often lactic acid see lactic acidosis) or a deficit of base (i.e., bicarbonate). [Pg.1571]

Mixed acid-base disorder More than one of the following disorders occurring simultaneously acidosis (metabolic or respiratory) and alkalosis (metabolic or respiratory). [Pg.1571]

Failure of compensation is responsible for mixed acid-base disorders such as respiratory acidosis and metabolic acidosis, or respiratory alkalosis and metabolic alkalosis. In contrast, excess compensation is responsible for metabolic acidosis and respiratory alkalosis, or metabolic alkalosis and respiratory acidosis. [Pg.860]

The most common mixed acid-base disorder is respiratory and metabolic alkalosis, which occurs in critically ill surgical patients with respiratory alkalosis caused by mechanical ventilation, hypoxia, sepsis, hypotension,... [Pg.860]

Because of the short duration and severity of the metabolic acidosis, together with a near-normal lactate concentration, acid ingestion was the most likely cause for his acid-base disorder. This diagnosis was confirmed once the composition of the ingested fluid was known. [Pg.593]

Metabolic Osteoporosis, fluid, electrolyte, and acid-base disorders... [Pg.392]

Acid-base disorders Initial metabolic alkalosis (resulting from decreased urea synthesis with reduced bicarbonate consumption) may be superimposed by respiratory alkalosis as an outcome of disorders in lung function. During the further course, metabolic acidosis (with renal insufficiency) and respiratory acidosis (with pulmonary insufficiency) can be expected. In advanced or severe stages of the disease, lactate acidosis may develop in some 50% of all comatose patients owing to restricted gluconeogenesis. [Pg.380]

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. [Pg.1757]

Most metabolic acid-base disorders develop slowly, within hours in diabetic ketoacidosis and months or even years in chronic renal disease. The respiratory system responds immediately to a change in acid-base status, but several hours maybe required for the response to become maximal. The maximum response is not attained until both the central and peripheral chemoreceptors are fully stimulated. For example, in the early stages of metabolic acidosis, plasma pH decreases, but because H ions equilibrate rather slowly across the blood-brain barrier, the pH in CSF remains nearly normal. However, because peripheral chemoreceptors are stimulated by the decreased plasma pH, hyperventilation occurs, and plasma PCO2 decreases. When this occurs, the PCO2 of the CSF decreases immediately because CO2 equilibrates rapidly across the blood-brain barrier, leading to a rise in the pH of the CSF. This will inhibit the central chemoreceptors. But as plasma bicarbonate gradually falls because of acidosis, bicarbonate concentration and pH in the CSF wih also fall over several hours. At this point, stimulation of respiration becomes maximal as both the central and peripheral chemoreceptors are maximally stimulated. [Pg.1763]

Abnormalities of acid-base status of the blood are always accompanied by characteristic changes in electrolyte concentrations in the plasma, especially in metabolic acid-base disorders. Hydrogen ions cannot accumulate without concomitant accumulation of anions, such as CL or lactate, or without exchange for cations, such as or NaL Consequently, electrolyte composition of blood serum or plasma is often determined along with measurements of blood gases and pH and to assess acid-base disturbances. [Pg.1767]

Metabolic acidosis is readily detected by decreased plasma bicarbonate (or a negative extracellular base excess), the primary perturbation in this acid-base disorder. Bicarbonate is lost in the buffering of excess acid. Causes include the foUowing ... [Pg.1768]

Arieff Al, DeFronzo RA. Disorders of sodium metabolism— hyponatremia. In Arieff Al, DeFronza RA, eds. Huid, Electrolyte, and Acid-Base Disorders, 2nd ed. New York, Churchill Livingstone, 1995 255-303. [Pg.964]

Metabolic alkalosis is a simple acid-base disorder that presents as al-kalemia (increased arterial pH) with an increase in plasma bicarbonate. It is an extremely common entity in hospitalized patients with acid-base disturbances. Under normal circumstances, the kidney is readily able to excrete an alkali load. Thus evaluation of patients with metabolic alkalosis must consider two separate issues (1) the initial process that generates the metabolic alkalosis and (2) alterations in renal function that maintain the alkalemic state. °... [Pg.993]

The combination of respiratory and metabolic alkalosis is the most common mixed acid-base disorder. This mixed disorder occurs frequently in critically ill surgical patients with respiratory alkalosis caused by mechanical ventilation, hypoxia, sepsis, hypotension, neurologic damage, pain, or drugs, and with metabolic alkalosis caused by vomiting or nasogastric suctioning and massive blood transfusions. It may also occur in patients with hepatic cirrhosis who hyperventilate, receive diuretics, or vomit, as well as in patients with chronic respiratory acidosis and an elevated plasma bicarbonate concentration... [Pg.1000]

Narins RG. Acid-base disorders Definitions and introductory concepts. In Narins RG, ed. Maxwell Kleeman s Clinical Disorders of Fluid and Electrolyte Metabolism, 5th ed. New York, McGraw-Hill, 1994 765—768. [Pg.1001]

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. [Pg.2649]

The dominant feature in this patient s acid-base disorder is an alkalosis as the [H" ] is low. The bicarbonate concentration is in keeping with the presence of a metabolic alkalosis, which is the dominant disorder in this case. The PCO is increased which may be partially due to a compensatory reaction to the alkalosis. However, the increase in PCO., is in excess of that associated with this degree of alkalosis. The patient had a long-standing history of respiratory disease. [Pg.69]

Metabolic acid-base disorders are those which directly cause a change in the bicarbonate concentration. Examples incluile diabetes mcliitus. where altered intemiediary metabolism in the absence of insulin cau.ses a build up of hydrogen ion from the ioni/ation of aceloacetic and P-hydroxybutyric acids, or loss of bicarbonate from the extracellular Iluid. e.g. from a duodenal fistula. [Pg.100]

Primary problems with hydrogen ion production or excretion are reflected in the IHCO,"] and these are called metabolic acid-base disorders. [Pg.100]


See other pages where Acid-base disorders metabolic is mentioned: [Pg.69]    [Pg.69]    [Pg.420]    [Pg.425]    [Pg.404]    [Pg.407]    [Pg.2895]    [Pg.252]    [Pg.259]    [Pg.1639]    [Pg.1772]    [Pg.1773]    [Pg.569]    [Pg.986]    [Pg.987]    [Pg.2608]    [Pg.101]   
See also in sourсe #XX -- [ Pg.420 ]




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