Acid-base disorders

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. 

Determine the appropriate management for patients with acid-base disorders. 

It is critical to treat the underlying causative process to effectively resolve most observed acid-base disorders. However, supportive treatment of the pH and electrolytes is often needed until the underlying disease state is improved. 

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... 

Acid-base disturbances are always manifestations of underlying clinical disorders. It is useful to specifically define the primary acid-base abnormality, as each disorder is caused by a limited number of disease processes. Establishing the specific disease process responsible for the observed acid-base disorder is clinically important because treatment of a given acid-base disorder will only be accomplished by correcting the underlying disease process. 

It is important to realize that the serum HCO, concentration may be affected by the presence of unmeasured endogenous acids (lactic acidosis or ketoacidosis). Bicarbonate will attempt to buffer these acids, resulting in a 1 mEq loss of serum HCO, for each 1 mEq of acid titrated. Because the cation side of the equation is not affected by this transaction, the loss of serum HC03 results in an increase in the calculated anion gap. Identification of an increased anion gap is very important for identifying the etiology of the acid-base disorder. The concept of the increased anion gap will be applied later in the case studies section. 

The excess gap represents the amount of HC03 that has been lost due to buffering unmeasured cations. The excess gap can be added back to the measured HC03 to determine what the patient s bicarbonate would be if these endogenous acids were not present. This is a very valuable tool that can be used in narrowing the differential diagnosis of certain acid-base disorders as well as in uncovering occult or mixed acid-base disorders. 

After an acid-base disorder has been completely characterized, the patient s medical history, physical exam, and medications should be reviewed in order to establish the etiology of the given disorder. Tables 25-3 through 25-7 outline the most commonly encountered causes of the primary acid-base disorders. The therapeutic approach to each of these acid-base derangements should emphasize a search for the cause, as opposed to immediate attempts to normalize the pH. Although supportive measures to prevent the sequelae of marked acid-base abnormalities is often required, these therapies will be required indefinitely if the causative process is not also identified and corrected.7,8... 

Is the anion gap excessively large If so, does calculation of the excess gap identify another acid-base disorder ... 

Continuous cardiovascular and hemodynamic monitoring should be used for significant pH disturbances, as the most serious sequelae of acid-base disorders include electrolyte abnormalities, cardiac dysrhythmias, and systemic hypotension. 

Review each patient s history, physical exam, and current medication list for potential causes of the observed acid-base disorder. 

The anion gap is the concentration of plasma anions not routinely measured by laboratory screening. It is useful in the evaluation of acid-base disorders. The anion gap is greater with increased plasma concentrations of endogenous species (e.g., phosphate, sulfate, lactate, and ketoacids) or exogenous species (e.g., salicylate, penicillin, ethylene glycol, ethanol, and methanol). The formulas for calculating the anion gap are as follows ... 

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). 

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

Acid-base disorders are caused by disturbances in hydrogen ion (H+) homeostasis, which is ordinarily maintained by extracellular buffering, renal regulation of hydrogen ion and bicarbonate, and ventilatory regulation of carbon dioxide (C02) elimination. 

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. 

Blood gases (Table 74-1), serum electrolytes, medical history, and clinical condition are the primary tools for determining the cause of acid-base disorders and for designing therapy. 

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,... 

Patients should be monitored closely because acid-base disorders can be serious and even life threatening. 

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. 

See Chap. 55, Acid-Base Disorders, authored hy John W. Devlin, Gary R. Matzke, and Paul M. Palevsky, for a more detailed discussion of this topic. 

For more information on acid-base disorders, see Chap. 74. 

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. 

In practical terms, it is often difficult to establish exactly which form of acid-base disorder is present in a patient, especially in view of the existence of compound (mixed) disorders. A nomogram presented in Figure 3.4 provides a rapid method for assessing uncomplicated disorders of this sort within a 95% confidence limit. Anything falling outside the shaded areas can be viewed as an acid-base disorder of compound nature. 

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