Acidemia and Acidosis

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Acidemia is a state in which the arterial blood pH falls below 7.35, meaning the blood has become abnormally acidic. In contrast, acidosis describes any underlying physiological process that drives the body toward an acidic pH. Therefore, acidemia is known as the result, while acidosis is the cause, but not every acidosis process necessarily produces acidemia because compensatory mechanisms may temporarily maintain a normal pH.

Under normal conditions, the body maintains a very narrow pH range between 7.35 and 7.45, regulated primarily by the respiratory system, which controls carbon dioxide (CO₂), and the kidneys, which regulate bicarbonate (HCO₃⁻). Any disturbance in these systems has the potential to shift the acid–base balance toward acidosis.

• Normal HCO₃⁻: 22–26 mmol/L
• Normal PaCO₂: 35–45 mmHg

There are two major categories: metabolic acidosis and respiratory acidosis.

Metabolic Acidosis

Metabolic acidosis occurs when the body experiences a primary reduction in bicarbonate, which serves as one of its main physiological buffers. When bicarbonate levels fall, hydrogen ions accumulate, and the pH decreases. pH decreases because the body:

• Produces too much acid (lactic acid, ketoacids, formic acid from methanol, oxalic acid from ethylene glycol)
• Loses too much bicarbonate (GI loss by diarrhea, renal tubular acidosis by inability of kidneys to reabsorb HCO₃⁻)
• Fails to eliminate the acids it normally generates (reduced renal acid excretion especially in renal failure)

One important way of classifying metabolic acidosis is by calculating the anion gap, which helps determine whether unmeasured acids are present. A high anion gap metabolic acidosis occurs when metabolic acids such as lactate, ketones, or toxins accumulate and consume bicarbonate. Examples include:

• Diabetic ketoacidosis - ketone bodies build up in uncontrolled diabetes
• Lactic acidosis - develops during severe hypoxia, shock, or sepsis
• Uremic acidosis - caused by kidney failure in which phosphates and sulfates accumulate
• Toxic ingestions - such as methanol or ethylene glycol, where their metabolic products are strongly acidic

In contrast, a normal anion gap (hyperchloremic) metabolic acidosis appears when bicarbonate is lost but replaced by chloride, keeping the anion gap unchanged. Examples include:

• GI carbonate lost (severe diarrhea)
• Renal tubular acidosis (kidneys fail to either reabsorb bicarbonate (proximal RTA) or secrete hydrogen ions (distal RTA)
• Medications like acetazolamide by blocking bicarbonate reabsorption

The body’s natural response (compensation) to metabolic acidosis is to increase ventilation, usually seen as deep, rapid breathing known as Kussmaul respirations (occurs in minutes). This pattern helps eliminate CO₂ and partially corrects the drop in pH. Renal compensation is slower but eventually increases acid excretion and generates new bicarbonate (within hours to days).

Respiratory Acidosis

Respiratory acidosis develops when the lungs fail to adequately remove carbon dioxide, leading to its accumulation in the blood. As CO₂ combines with water to form carbonic acid, elevated CO₂ directly increases hydrogen ion concentration and reduces blood pH.

CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻

↑CO₂ → ↑H⁺ → ↓pH

Acute respiratory acidosis occurs rapidly and does not allow time for the kidneys to compensate. This situation can be caused by:

• Acute airway obstruction
• Severe asthma attacks
• Drug-induced respiratory depression (opioids or benzodiazepines)
• Neuromuscular weakness - can suddenly reduce ventilation

In these cases, the pH often drops significantly because the kidneys have not yet increased bicarbonate levels.

Chronic respiratory acidosis develops slowly in conditions such as long-standing COPD, obesity hypoventilation syndrome, or chronic neuromuscular disorders. Over time, the kidneys retain more bicarbonate to counteract the elevated CO₂, so the pH is usually closer to normal compared to the acute form, even though CO₂ levels remain high.

Unlike metabolic acidosis, respiratory acidosis cannot be compensated by the lungs themselves because the lungs are the origin of the problem. Only the kidneys can restore balance with enough time (takes days - retain HCO₃⁻ and excrete more H⁺).

Clinical Consequences

Cellular & Metabolic Effects

• Enzyme dysfunction
• Impaired ATP production
• Protein denaturation
• Decreased cardiac contractility
• Increased arrhythmia risk

Neurological Effects

• Confusion
• Lethargy
• Coma (especially with CO₂ narcosis)

Respiratory Effects

• Kussmaul breathing in metabolic acidosis
• CO₂ retention headaches in respiratory acidosis

Cardiovascular Effects

• Vasodilation → hypotension
• Reduced responsiveness to catecholamines

Quick summary

• Acidosis = process lowering pH
• Acidemia = actual pH < 7.35
• Metabolic acidosis = ↓HCO₃⁻
• Respiratory acidosis = ↑PaCO₂
• High AG metabolic acidosis = production of organic acids
• Normal AG metabolic acidosis = bicarbonate loss (diarrhea, RTA)
• Compensation: lungs for metabolic, kidneys for respiratory

References

Johnson, R. L. (2003). Robbins Basic Pathology. *Archives of Pathology & Laboratory Medicine*, 127(11), 1532. https://doi.org/10.5858/2003 127 1532 rbp

Hall, J. E. (2015). *Guyton and Hall Textbook of Medical Physiology* (13th ed.). Elsevier.