A lesson from Pathophysiology of Metabolic Acidosis and Alkalosis

Acute Metabolic Acidosis

In acute metabolic acidosis, the most critical effects are seen in the cardiovascular system:

Reduced Cardiac Contractility and Cardiac Output: Acidosis can impair myocardial contractility, reducing cardiac output, particularly when the blood pH drops below 7.1. This can lead to hypotension and shock, as vasodilation of arterial vessels also contributes to lower blood pressure.

Ventricular Arrhythmias: Severe acidemia predisposes individuals to life-threatening arrhythmias due to the increased excitability of cardiac tissues.

Resistance to Catecholamines: Infused catecholamines, such as epinephrine, become less effective in severe metabolic acidosis, limiting their ability to improve cardiac function and constrict blood vessels during shock.

Alteration in Oxygen-Hemoglobin Affinity: Acidosis causes a shift in the oxygen-hemoglobin dissociation curve (Bohr effect), decreasing hemoglobin’s affinity for oxygen, thereby impairing oxygen delivery to tissues.

Neurological Effects: Mental confusion, lethargy, and even coma can occur in acute metabolic acidosis, though brain pH is only minimally affected.

Impaired Immune Function: Acidosis reduces the bactericidal activity of leukocytes and dampens the immune response, increasing susceptibility to infections.

Insulin Resistance: Acidosis interferes with insulin receptor binding, impairing glucose metabolism and leading to hyperglycemia, particularly in critically ill patients.

Impaired Cellular Energy Production: The activity of enzymes involved in glycolysis, such as 6-phosphofructokinase, is pH-dependent. Acidosis slows cellular metabolism, decreasing energy production.

Apoptosis: Metabolic acidosis promotes programmed cell death, further contributing to tissue damage and organ dysfunction.

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