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Acid–base pathophysiology often creates a mindset of frustration among not only student pharmacists, but many other health care providers as well, who have difficulty grasping the concepts.1 While the complexity of the concepts is certainly quite daunting, having a basic understanding will allow you to optimize the care of many critically ill patients.
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When discussing any complicated process, it is best to start from a reference point, one that can be referred to whenever confusion arises. For acid–base disturbances, that reference point is the bicarbonate–carbon dioxide buffer system, shown in Equation 31-1.2
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This simple buffering equation holds the foundation for all acid–base physiology within the human body. The processes that occur in the body drive this equation either to the left or the right in order to maintain a neutral pH. Think in terms of the left side of the equation occurring in the lungs and the right side occurring in the kidneys. Anytime the body loses hydrogen ions, the equation shifts to the right. That is to say, the lungs retain more CO2 in order to convert it into carbonic acid, which is then converted to hydrogen ions and bicarbonate, thereby replacing the lost hydrogen ions. Likewise, anytime an extra hydrogen ion is gained, the equation shifts to the left and the respiratory center is activated to increase ventilation in an effort to get rid of excess acid (CO2). However, an important point needs to be made here; CO2 and HCO3− are excreted independent of one another. If excess CO2 exists in the body, it cannot be excreted in the kidneys; rather it must be exhaled by the lungs. Similarly, if there is an increase in H+, the body cannot convert it to CO2 for excretion in the lungs; it must be excreted by the kidneys.
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From this equation all acid–base disturbances can be explained. Metabolic acidosis results from either an excess in H+ or a deficiency in HCO3−. On the other hand, metabolic alkalosis results from an excess in HCO3− or a deficiency in H+. Respiratory acidosis results from an excess in arterial carbon dioxide (Paco2), whereas respiratory alkalosis results from a deficiency in Paco2. The determination of all acid–base disturbances can be done through evaluation of electrolyte panels, arterial blood gasses (ABG), and patient assessment.
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Two final concepts that need to be discussed are the compensatory response that occurs in response to the primary acid–base disorder, as well as mixed acid–base disorders. Primary metabolic disorders can be seen as disturbances in the serum bicarbonate level, with compensation occurring via the respiratory route and reflected in the Paco2. Likewise, all respiratory disturbances will be reflected in the Paco2 level, with compensation occurring metabolically as reflected in the serum bicarbonate level. Sometimes it may ...