Acid-base disorders alkalosis

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

Respiratory acid-base disorders are caused by altered alveolar ventilation producing changes in arterial carbon dioxide tension (PaC02). Respiratory acidosis is characterized by increased PaC02, whereas respiratory alkalosis is characterized by decreased PaC02. 

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. 

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,... 

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. 

The following clinical terms are used to describe the acid-base status. Addemia is defined as an arterial blood pH <7.35 d.nd alkalemia indicates an arterial blood pH >7.45. Acidosis and alkalosis refer to patliological states that lead to acidemia or alkalemia. For example, in common acid-base disorders... 

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. 

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. °... 

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... 

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 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. 

Acid-base disorders can be classified as acidosis or alkalosis, compensated or uncompensated, fully or partially compensated. 

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 ]. 

The need for a better measure of the metabolic component of an acid-base disorder. At first sight, w e might think that the deviation of the standard bicarbonate from the value for normal blood is all the information that we need about the non-respiratory component of an acid- base disorder. However, the change in standard bicarbonate underestimates the non-respiratory component of the acid base disorder. To illustrate this, consider uncompensated metabolic alkalosis, produced by the addition of alkali, such as sodium hydroxide, to the blood. Each of the buffer acids in the blood (protein buffer acid and CO2) buffers some of the added alkali as shown in the two chemical reactions in Table 4.2A. Protein buffer acid combines with some of the alkali to yield water and protein buffer base CO2 from metabolism combines with most of the rest of the alkali to yield bicarbonate. The result is an increase in concentration both of non-bicarbonate buffer base Pr and of bicarbonate. 

Let us now consider what happens when the effect which was secondary in the primary respiratory disorder is instead the primary disorder. This would then be a primary metabolic alkalosis, as in the vomiting of gastric contents. In the uncompensated condition, there is a positive base excess with a normal partial pressure of carbon dioxide already noted (Table 4.4C). The respiratory compensation is hypoventilation, brought about by the partial withdrawal of the normal stimulus of hydrogen ions to the peripheral chemoreceptors. The partial pressure of carbon dioxide rises, adding a respiratory component to the acid-base disorder (Table 4.4D). 

Figure 3.4 Identification of various acid-base disturbances. Acute disorders are synonymous with uncompensated disturbances, whereas chronic conditions are synonymous with partially compensated or compensated disturbances. If a specific case falls outside the shaded areas, a compound acid-base disturbance may be suspected, such as the coexistence of respiratory acidosis (partially compensated) and metabolic alkalosis. Unshaded areas may also indicate a transient state between an acute (uncompensated) state and a chronic (partially compensated) condition. (From Cogan MG, Rector FC Jr., Seldin DW. In Brenner BM, and Rector FC Jr, eds. The Kidney, 2nd ed., Vol. 1, Philadelphia WB Saunders, 1986, p. 860.)...

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... 

The unmeasured anion is commonly known as the anion gap, which is normally 12 4 mEq/L. This value is useful in assessing the acid-base status of a patient and in diagnosing metabolic acidosis. Disorders that cause a high anion gap are metabolic acidosis, dehydration, therapy with sodium salts of strong acids, therapy with certain antibiotics (e.g., carbenicillin), and alkalosis. A decrease in the normal anion gap occurs in various plasma dilution states, hypercalcemia, hypermagnesemia, hypernatremia, hypoalbuminemia, disorders associated with hyperviscosity, some paraproteinemias, and bromide toxicity. 

Acid-base disturbances frequently coexist with two or more simple disorders (Table 39-2). In these settings, blood pH is either severely depressed (e.g., a patient with metabolic acidosis and respiratory acidosis) or normal. Both plasma HCOj and pH may be within normal limits when metabolic alkalosis and metabolic ketoacidosis coexist, as in a patient with diabetic ketoacidosis who is vomiting. In this situation, an elevated anion gap may be the initial abnormality that can be detected in the underlying mixed acid-base disturbance. 

As with the metabolic acid-base disturbances, there are two cardinal respiratory acid-base disturbances respiratory acidosis and respiratory alkalosis. These disorders are generated by a primary alteration in carbon dioxide excretion, which changes the concentration of carbon dioxide, and therefore the carbonic acid concentration in body fluids. A primary reduction in PaC02 causes a rise in pH (respiratory alkalosis), and a primary increase in PaC02 causes a decrease in pH (respiratory acidosis). Unlike the metabolic disturbances, for which respiratory compensation is rapid, metabolic compensation for the respiratory disturbances is slow. Hence these disturbances can be further divided into acute disorders, with a duration of minutes to hours that is too short for metabolic compensation to have occurred, and chronic disorders, that have been present long enough for metabolic compensation to be complete. 

Acidosis and alkalosis arc clinical terms which define the primary acid-base disturbance. They can be used even when the 1H 1 is within the normal range, i.e. w hen the disorders are fully compensated. The deHnitions are ... 

Where the two acid-base conditions arc antagonistic in the way they affect the [H. one of the disorders may mimic the compensatory response. A patient may present with a metabolic acidosis and a co-existent respiratory alkalosis, as occurs commonly in salicylate overdose. The respiratory disorder may appear, at first sight, to be simply the compensatory response. 

In contrast, hypokalemia follows potassium loss in hyperemesis and diarrhea, by fistulas, or by disorders in tubular function as well as in endocrine dysregulations (hyperaldosteronism). Additional important reasons are disturbances in the acid-base equilibrium, especially alkalosis. 

Carbon dioxide is a respiratory gas and in aqueous solution is essentially an acid. Disorders of respiration therefore have serious acid-base consequences. When aeration of the blood in the pulmonary capillaries is impaired, accumulation of carbon dioxide leads directly to an acidification of the extracellular fluid this is called lespiratory acidosis. Conversely in circumstances when aeration of the blood in the pulmonary capillaries is excessive, carbon dioxide is washed out of the body, leading to the condition of respiratory alkalosis. 

In general, if the primary disturbance causes an excess of unwanted add in the body, the compensation involves addition to the body of extra alkali to neutralize the acid. A primary acidosis calls up in response a physiological alkalosis. The disorder of acid-base physiology is then a mixture of these two components which operate in opposite directions. A primary addosis is accompanied by a secondary (compensatory) alkalosis and vice versa. It is clearly important to unravel the different components of an add-base disorder from an examination of a sample of arterial blood. 

Explain that the acid-base status can be deduced from the blood biochemistry in cases of uncompensated respiratory or metabolic disorder. Demonstrate examples of compensated disorders (e.g. compensated respiratory acidosis and compensated metabolic alkalosis) in which the same abnormality of blood biochemistry may be reached by different routes. Hence explain the need, in such cases, to seek each cause and evaluate its effect. 

Mixed disorder of acid-base pbysioiogy This expression is used with two different meanings. Some authors use it to indicate the co-existence of two primary abnormalities, e.g. respiratory acidosis and metabolic acidosis. Others use it as a synonym for compensated , when a primary disorder is accompanied by a super-added physiological response, e.g. compensated respiratory acidosis, when the primary disorder is acidosis and the renal compensation adds a physiological metabolic alkalosis. 

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