AcidosisEdit

Acidosis is a medical condition defined by a fall in the blood’s pH below the normal range, typically around 7.35 to 7.45. It results from an excess of acid in the body or a loss of bicarbonate, or from impaired excretion of acid by the kidneys. In clinical practice, acidosis is understood as a disturbance of the body’s acid-base balance, which the respiratory and renal systems normally regulate in concert. When these systems cannot keep pace with acid production or loss, organ function can deteriorate, and urgent evaluation and treatment become essential. For readers looking to connect this topic with broader physiology, see acid-base balance and pH.

In medicine, acidosis is most often described in two broad categories: metabolic acidosis and respiratory acidosis. Many patients have a combination of problems, but recognizing the dominant driver helps guide urgent management. See metabolic acidosis and respiratory acidosis for the principal pathways and examples.

Pathophysiology

The body maintains a narrow pH window through a balance of two main forces: the respiratory system, which controls CO2 in the blood, and the kidneys, which regulate bicarbonate (HCO3−). The Henderson–Hasselbalch framework is a convenient way to understand this balance: pH is influenced by the ratio of bicarbonate to dissolved carbon dioxide (pCO2). When CO2 rises or bicarbonate falls, pH drops; when CO2 falls or bicarbonate rises, pH rises. See Henderson-Hasselbalch equation and carbon dioxide for more detail.

  • Metabolic processes generate fixed acids (for example from glucose metabolism, fatty acid oxidation, or ketone production) and often consume bicarbonate. If acid production exceeds buffering capacity or bicarbonate is lost (for example through the gut, urine, or dialysate), metabolic acidosis can develop. See metabolic acidosis.
  • Respiratory acidosis arises when ventilation is insufficient to remove CO2, leading to CO2 retention and an acidifying effect on the blood. See respiratory acidosis.
  • The kidneys can compensate for respiratory acidosis by retaining bicarbonate and excreting hydrogen ions, while the lungs can compensate for metabolic acidosis by increasing ventilation to blow off CO2. These compensations have limits, and when they’re overwhelmed, acidosis progresses.
  • A key diagnostic tool is the anion gap, which helps distinguish different forms of metabolic acidosis. See anion gap and lactic acidosis for common examples.

Causes and types

Metabolic acidosis

  • Anion gap metabolic acidosis (high anion gap) often reflects the accumulation of unmeasured anions. Common etiologies are summarized by the mnemonic MUDPILES and include methanol or ethylene glycol poisoning, uremia, diabetic ketoacidosis, portosystemic shunting, iron or isoniazid toxicity, lactic acidosis, ethylene glycol and salicylate poisoning, among others. See lactic acidosis, diabetic ketoacidosis, methanol poisoning, ethylene glycol poisoning, and salicylates.
  • Non-anion gap (hyperchloremic) metabolic acidosis occurs when bicarbonate is lost or not adequately reabsorbed, with a compensatory rise in chloride. Causes include gastrointestinal bicarbonate loss (for example from severe diarrhea), certain renal tubular disorders, and some medications. See non-anion gap metabolic acidosis.
  • Lactic acidosis is a particularly important subset, driven by tissue hypoperfusion or impaired cellular metabolism, and it intersects with critical illness, sepsis, and shock. See lactic acidosis.
  • Diabetic ketoacidosis and other states of excess ketone production (for example starvation or alcoholic ketoacidosis) contribute to metabolic acidosis via ketoacid accumulation. See diabetic ketoacidosis.
  • Renal failure–associated acidosis reflects reduced acid excretion and reduced bicarbonate generation. See renal failure.

Respiratory acidosis

  • Acute respiratory acidosis arises from sudden alveolar hypoventilation due to airway obstruction, chest trauma, central respiratory depression, or acute lung disease. It is characterized by elevated CO2 and a decrease in pH; the body attempts renal compensation over time.
  • Chronic respiratory acidosis occurs when the underlying lung disease persists, as in advanced COPD, with gradual but partial renal compensation. See COPD, respiratory failure.

Mixed disorders are common in complex patients, especially those with multi-organ illness, sepsis, or critical care needs. Recognition of mixed acid-base disorders requires careful interpretation of arterial blood gas results alongside the clinical picture and laboratory data. See arterial blood gas.

Clinical presentation and diagnosis

  • Presentation depends on the underlying cause and the speed with which acidosis develops. Symptoms may include malaise, weakness, confusion, shortness of breath, abdominal symptoms, or signs of dehydration and shock in severe cases.
  • Diagnostic workup centers on arterial or venous blood gas analysis, including pH, partial pressure of CO2 (pCO2), and bicarbonate (HCO3−). Clinicians also calculate the anion gap and review serum electrolytes, lactate, glucose (to assess for ketoacidosis), renal function, and possible toxin exposures. See arterial blood gas, lactic acidosis, and anion gap.
  • Imaging and targeted testing may be used to identify the underlying cause, such as ultrasound or CT to assess for organ involvement, or toxicology screens in suspected poisonings.

Treatment and management

  • The cornerstone of acidosis management is addressing the underlying cause, with supportive care as needed. This can include fluid resuscitation, optimization of hemodynamics, antibiotic therapy for septic sources, insulin therapy for diabetic ketoacidosis, or antidotes for poisoning, depending on the etiology. See sepsis and diabetic ketoacidosis.
  • Bicarbonate therapy is a debated intervention. In metabolic acidosis, bicarbonate administration is considered in select situations—most notably when pH falls very low (for example, pH ≤ 6.9) or when acidosis is associated with life-threatening hemodynamic compromise. In less severe cases, bicarbonate is used cautiously because it can cause volume overload, hypernatremia, reduced intracellular acidosis within tissues, or shifts in potassium. See bicarbonate therapy.
  • In lactic acidosis or any form of shock, correcting tissue perfusion and oxygen delivery is paramount; routine bicarbonate use is not universally recommended and is reserved for specific scenarios. See lactic acidosis.
  • For renal failure–related acidosis, renal replacement therapy (dialysis) can be necessary to restore acid-base balance and remove accumulated toxins. See dialysis.
  • Respiratory causes are addressed by improving ventilation and gas exchange, including noninvasive or invasive ventilation as indicated, while treating the underlying pulmonary or neuromuscular disease. See ventilation and respiratory failure.

Controversies and debates

  • Therapeutic thresholds for bicarbonate in metabolic acidosis remain debated among clinicians. Some emphasize aggressive correction in the most severe acidoses to stabilize hemodynamics, while others advocate restraint and reliance on the body’s compensatory mechanisms and targeted treatment of the underlying condition. The balance between potential benefit and risks such as fluid overload or electrolyte disturbances is a central discussion in critical care guidelines. See bicarbonate therapy and metabolic acidosis.
  • In the broader health-policy sphere, debates about access to emergency and critical care resources influence how acidosis management is practiced in different health systems. Proponents of market-based, transparent pricing argue that rapid, evidence-based protocols should be implemented to maximize outcomes while controlling costs. Critics worry about disparities in access to timely care and the effects of policy on the availability of essential supplies and staffing. These debates touch on questions of cost, quality, and patient responsibility, and they shape how clinicians and institutions plan for surge conditions and resource allocation. See healthcare policy and emergency medicine.
  • Some commentators on public health argue that addressing social determinants of health can reduce the incidence of conditions that predispose to acidosis (for example, diabetes and chronic kidney disease). Others maintain that while social factors matter, the immediate priority in acute care is rapid, evidence-based treatment regardless of broader social debates. In practice, clinicians aim to balance timely, protocol-driven care with attention to the patient’s overall context and safety, without allowing policy debates to delay critical interventions. See social determinants of health and acute care.
  • The ethics of aggressive intervention at the end of life in the setting of profound acidosis or multi-organ failure remains disputed in some circles, with differing views on when to shift goals of care. Clinicians weigh the likelihood of recovery, patient preferences, and resource considerations in conversations with patients and families. See end-of-life care.

See also