Mixed Acid-Base Disorders

Pathophysiology of Mixed Disorders

Mixed forms are characterized by concurrent shifts acting via entirely different pathological mechanisms.

• Mixed acidosis in heart failure. The respiratory component develops due to impaired alveolar perfusion and pulmonary edema. The metabolic component is twofold: a metabolic shift occurs due to circulatory hypoxia (lactate accumulation), while an excretory renal factor is added due to renal hypoperfusion.
• Mixed alkalosis in brain injury. The respiratory component is caused by central hyperventilation. The non-respiratory component is represented by excretory gastric alkalosis, which develops due to the loss of acidic contents from recurrent vomiting.

Combined Forms (Opposing Shifts)

In combined disorders, processes shifting the pH in opposite directions occur simultaneously within the body. The resulting pH depends on which factor dominates—metabolic or functional (pulmonary and renal status).

• Chronic Obstructive Pulmonary Disease (COPD). The disease itself causes hypoventilation and respiratory acidosis. However, treatment with glucocorticoids can provoke an excretory, chloride-responsive renal alkalosis.
• Severe chronic gastroenteritis. Vomiting leads to the loss of acidic gastric contents (excretory gastric alkalosis). Simultaneously, diarrhea causes the loss of alkaline intestinal secretions (excretory intestinal acidosis). This complex presentation requires continuous monitoring of acid-base status to adjust treatment.

Principles of Management for Respiratory Disorders

Respiratory Acidosis The primary goal is to reduce or completely eliminate respiratory failure. Acute forms require emergency management to restore alveolar ventilation. Chronic management is based on three principles:

1. Etiotropic: Elimination of the underlying causes of acidosis (hypoventilation, pulmonary hypoperfusion, reduced diffusion capacity of the blood-gas barrier).
2. Pathogenetic: Management of hypercapnia (elevated $CO_2$ levels) by normalizing gas exchange.
3. Symptomatic: Relief of headache, marked tachycardia or bradycardia, psychomotor agitation, and excessive sweating.

Respiratory Alkalosis The primary goal is the correction of $CO_2$ deficit.

• Etiotropic treatment aims to eliminate the underlying cause of hyperventilation.
• Pathogenetic treatment includes breathing gas mixtures enriched with $CO_2$ (e.g., carbogen) and correcting water-electrolyte balance with buffer solutions.
• Symptomatic treatment involves the use of anticonvulsants, cardioprotective agents, and vasoactive drugs.

Symptomatic Therapy for Non-Respiratory Alkalosis

Treatment focuses on managing complications of the underlying disease and the alkalosis itself, as well as alleviating debilitating symptoms.

• Correction of protein metabolism. Alkalosis causes a deficiency of potassium ($K^+$), which is a crucial cofactor for protein-synthesizing enzymes. Potassium repletion is essential to normalize protein turnover.
• Cardiovascular stabilization. Cardioprotective and vasoactive drugs are used to normalize myocardial contractility and vascular tone.
• Management of GI dysfunction. Alkalosis slows peristalsis and causes constipation as well as impaired luminal and membrane digestion. Management involves enzyme preparations, gastric and intestinal secretion components, and cholinomimetics.