Acid-base disorders respiratory

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. 

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... 

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... 

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. 

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... 

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,... 

Arterial blood gases are the primary tools for evaluation of therapeutic outcome. They should be monitored closely to ensure resolution of simple acid-base disorders without deterioration to mixed disorders due to compensatory mechanisms. For example, arterial blood gases should be obtained every 2 to 4 hours during the acute phase of respiratory acidosis and then every 12 to 24 hours as acidosis improves. 

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. 

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. 

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. 

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... 

Kaehny WD. Pafiiogenesis and management of respiratory and mixed acid-base disorders. In Schrier RW, ed. Renal and Electrolyte Disorders, 5th ed. Philadelphia, Lippincott, Williams Wilkins, 1997 172—191. 

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. 

Respiratory acid-base disorders affect directly the PCO,. Impaired respiratory function causes a build up of CO, in blotnl. whereas, less commonly, hyperventilation can cause a decreased PCO,. 

Primary problems with CO excretion are reflected in PCO these are called respiratory acid-base disorders. 

An important consideration is, which results should be reported when ICa " "], pH, and the calculated [Ca " "] at pH 7.4 are all produced by the instrument. The algorithms used to calculate the latter variable assume normal concentrations of total protein and albumin, normal binding of Ca " " to plasma proteins, and a standard Ap[Ca ]/ApH ratio of 0.23 for all patients [23]. Use of these algorithms also assumes that in vivo and in vitro pH changes have equivalent effects on Ca and that respiratory and metabolic acid-base disorders produce equivalent changes in Ca [23]. Since these assumptions probably oversimplify the complex equilibria between species, particularly in critically ill patients, it is generally agreed that only the measured Ca and the pH values should be reported. 

For metabolic acid-base disorders, the body has two lines of defence. The first is respiratory compensation. In the case of metabolic acidosis, the fall in pH... 

In any disorder of acid-base physiology, there are liable to be two components, respiratory and metabolic, and the contribution of each must be identified. For the respiratory component, the arterial PCO2 immediately indicates any deviation from normality (Table 4.1 A). If this is within normal limits, there is no respiratory component to the acid-base disorder. 

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. 

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