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Upon completion of the chapter, the reader will be able to:

  1. Compare and contrast the six primary acid–base disturbances within the human body.

  2. Apply simple formulas in a systematic manner to determine the etiology of simple acid–base disturbances and the adequacy of compensation.

  3. Integrate the supplemental concepts of the anion gap and the excess gap to further assess for complex acid–base disturbances.

  4. Discuss the most common clinical causes for each primary acid–base abnormality.

  5. Describe the potential clinical complications of altered acid–base homeostasis.

  6. Propose an appropriate treatment plan for patients with deranged acid–base physiology.


Given its reputation for complexity and the need to memorize innumerable formulas, acid–base analysis intimidates many health-care providers. In reality, acid–base disorders always obey well-defined biochemical and physiological principles. The pH determines a patient’s acid–base status and an assessment of the serum bicarbonate (HCO3) and arterial blood carbon dioxide (PaCO2) values identifies the underlying process. Rigorous use of a systematic approach to arterial blood gases increases the likelihood that derangements in acid–base physiology are recognized and correctly interpreted. This chapter outlines a clinically useful approach to acid–base abnormalities and applies it in a series of increasingly complex clinical scenarios.

Disturbances of acid–base equilibrium occur in a wide variety of illnesses and are among the most frequently encountered disorders in critical care medicine. The importance of a thorough command of this content cannot be overstated given that acid–base disorders are remarkably common and may result in significant morbidity and mortality. Although severe derangements may affect virtually any organ system, the most serious clinical effects are cardiovascular (arrhythmias, impaired contractility), neurologic (coma, seizures), pulmonary (dyspnea, impaired oxygen delivery, respiratory fatigue, respiratory failure), and/or renal (hypokalemia). Changes in acid–base status also affect multiple aspects of drug disposition (clearance, protein binding) and pharmacodynamics.


Acid–base homeostasis is responsible for maintaining blood hydrogen ion concentration [H+] near normal despite the daily acidic and/or alkaline loads derived from the intake and metabolism of foods. Acid–base status is traditionally represented in terms of pH, the negative logarithm of [H+]. Because [H+] is equal to 24 times the ratio of PaCO2 to HCO3 (for PaCO2 expressed in units of mm Hg), the pH can be altered by a change in either the bicarbonate concentration or the dissolved carbon dioxide. A critically important concept is that [H+] depends only on the ratio of PaCO2 to HCO3 and not the absolute amount of either. As such, a normal PaCO2 or HCO3 alone does not guarantee that the pH will be normal. Conversely, a normal pH does not imply that either the PaCO2 or HCO3 will be normal.1

image Acid–base homeostasis is tightly regulated ...

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