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LEARNING OBJECTIVES

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LEARNING OBJECTIVES

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

  1. Compare and contrast the four 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.

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KEY CONCEPTS

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  • Image not available. Acid–base homeostasis is tightly regulated by the complex, but predictable, interactions of the kidneys, the lungs, and various buffer systems. The kidneys control serum bicarbonate (HCO3) concentration through the excretion or reabsorption of filtered HCO3, the excretion of metabolic acids, and synthesis of new HCO3. The lungs control the arterial carbon dioxide (CO2) concentration through changes in the depth and/or rate of respiration.

  • Image not available. Respiratory acidosis and alkalosis result from primary disturbances in the arterial CO2 concentration. Metabolic compensation of respiratory disturbances is a slow process, requiring days for the serum HCO3 to reach the steady state.

  • Image not available. Respiratory acidosis is caused by respiratory insufficiency resulting in an increased arterial CO2 concentration. The compensation for respiratory acidosis (if present for prolonged periods) is an increase in serum HCO3.

  • Image not available. Respiratory alkalosis is caused by hyperventilation resulting in a decreased arterial CO2 concentration. The compensation for respiratory alkalosis (if present for prolonged periods) is a decrease in serum HCO3.

  • Image not available. Metabolic acidosis and alkalosis result from primary disturbances in the serum HCO3 concentration. Respiratory compensation of metabolic disturbances begins within minutes and is complete within 12 hours.

  • Image not available. Metabolic acidosis is characterized by a decrease in serum HCO3. The anion gap is used to narrow the differential diagnosis because metabolic acidosis may be caused by addition of acids (increased anion gap) or loss of HCO3 (normal anion gap). The compensation for metabolic acidosis is an increase in ventilation with a decrease in arterial CO2.

  • Image not available. Metabolic alkalosis is characterized by an increase in serum HCO3. This disorder requires loss of fluid that is low in HCO3 from the body or addition of HCO3 to the body. The compensation for metabolic alkalosis is a decrease in ventilation with an increase in arterial CO2.

  • Image not available. Arterial blood gases, serum electrolytes, physical examination findings, the clinical history, and the patient's recent medications must be reviewed in order to establish the etiology of a given acid–base disturbance.

  • Image not available. 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 ...

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