Disorders that cause metabolic acidosis can harm patients through a variety of mechanisms (Table 8). We shall consider 4 maj or categories:
Very Fast Rate of Production of H+
In essence, the only condition associated with extremely rapid net production of acid is L-lactic aridosis due to hypoxia (Table 2). The threat here is that ATP may not be regenerated quickly enough. Quantitatively, the rate of acid addition can be approximated by
Table 9. Causes of metabolic acidosis associated with hyperkalemia. Specific disorders causing hyperkalemia in patients with metabolic acidosis are described. In addition, if tissue necrosis has occurred in a patient with metabolic acidosis, hyperkalemia may also be present.
Cause Pathophysiology Total K+ content
Renal failure Low renal excretion of K+ (and NH4+) High
Low aldosterone Low renal excretion of K+ (and NH4+) High bioactivity
DKA Insulin deficiency leads to shift Low of K+ out of the ICF
noting the rate of increase in the plasma anion gap and the rate of excretion of anions in the urine.
H+ Binding to Intracellular Proteins
The important factors here are not only the magnitude of H+ load, but also the tistue PCO2 as this determines the distribution of buffering of H+ load between the BBS and intracellular proteins. A high venous PCO2 implies that the tissue PCO2 is also high and that more H+ are buffered by intracellular proteins. Hence it follows that in the setting of metabolic acidosis associated with a low cardiac output, a very important measure to correct the intracellular acido tis is aggres sive restoration of the cardiac output (Figure 7). In addition, if the arterial PCO2 is not low enough, mechanical ventilation is essential.
Coexisting Problems of K+ Balance
Many of the risks associated with metabolic ac ido sis may come about through as so ci ated disturbances of K+ balance. Both hyperkalemia and hypokalemia may occur (Table 9). We shall be succinct here because issues con cerning K+ are discussed in the accompanying Chapter on K+.
Hyperkalemia may be involved in the etiology of metabolic acidosis, because hyperkalemia impairs NH4 excretion . In contrast, if metabolic acidosis is seen in the setting of renal failure, a low excretion of K+ and hyperkalemia may be present. Hyperkalemia is commonly seen in the setting of DKA despite the total body K+ deficit, because K+ tend to shift out of cells during insulin deficiency . Finally, tissue necrosis or ischemia can lead to both L-lactic actdosis and release of K+ from cells. Regardless of the pathophysiology, hyperkalemia can be life-threatening due to cardiac arrhythmias, and must be aggressively treated. Fortunately, one of the measures employed in the therapy of DKA, insulin, enhances K+ entry into cells, and there fore reduces the degree of hyper-kalemia.
Hypokalemia may occur either in association with the chronic metabolic actdosis of distal RTA, diarrhea, or metabolic acidosis caused by toluene (e.g., glue sniffing). Hypo-kalemia may also occur as a complication of insulin therapy in patients with DKA. Because insulin causes K+ to enter cells (Figure 9), it may unmask the total body K deficit and lead to the life-threatening complications
Table 10. Factors to consider in the use of NaHCO3.
A. Factors favoring the use of NaHCO3
- Absence of an ani on that can be metabo i ized into HCO3- (longer term consideration).
- Low like l ihood that kidneys will be able to excrete NH4+ at a high rate (longer term issue).
- Independent benefit likely to arise (e.g., in salicylate overdose to limit entry of salicylate into brain cells and to favor its urinary excretion).
- High net rate of H+ production (e.g., inability to rapidly reverse hypoxic L-lactic acidosis).
B. Factors that suggest a danger for the use of NaHCO3
- Co i ncident use of insui in in a patient with a large K+ deficit.
- Elevated ECF volume.
- Hypernatremia (minor).
of acute hypokalemia, particularly cardiac arrhythmias.
Specific problems related to the cause of the acidosis: In fact, in some ofthe causes of metabolic acidosis, the acidosis serves as a marker or a "symptom" of a serious underlying disease (e.g., methanol or ethylene glycol toxicity, Table 8). Clearly, these underlying processes must be addressed with specific therapy to avoid the adverse consequences that are independent of the acidosis.
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