What is the difference between Alkalosis and Acidosis?

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Acidosis vs. Alkalosis: Key Differences

Acidosis and alkalosis represent opposite ends of the pH spectrum: acidosis occurs when blood pH falls below 7.35 due to excess acid or CO2 accumulation, while alkalosis occurs when pH rises above 7.45 due to excess bicarbonate or loss of acid.

Fundamental Definitions

Acidosis

  • Metabolic acidosis is characterized by decreased blood pH (<7.35), reduced serum bicarbonate (<22 mmol/L), and may present with elevated lactate levels and increased base deficit 1
  • Respiratory acidosis occurs when carbon dioxide accumulates due to inadequate ventilation, resulting in elevated PaCO2 levels above 46 mmHg and decreased blood pH below 7.35 2
  • Metabolic acidosis results from either failure to excrete acids produced by normal metabolism (e.g., renal failure) or increased acid production from abnormal metabolic conditions (e.g., diabetic ketoacidosis) 3
  • Respiratory acidosis develops when CO2 combines with water to form carbonic acid, which dissociates into bicarbonate and hydrogen ions, leading to increased blood acidity 2

Alkalosis

  • Metabolic alkalosis is characterized by elevated pH and elevated plasma bicarbonate levels above normal 4
  • When bicarbonate is elevated, PaCO2 must also be elevated to maintain pH in the normal range through compensatory hypoventilation 4
  • Metabolic alkalosis is due to loss of hydrogen ions (usually from stomach or kidneys) or ingestion of alkali 5
  • Severe metabolic alkalosis in critically ill patients (arterial blood pH of 7.55 or higher) is associated with significantly increased mortality 6

Pathophysiological Mechanisms

How Acidosis Develops

  • Metabolic causes: Excessive acid load (endogenous or exogenous), impaired renal excretion of hydrogen ions, or bicarbonate loss 5
  • Respiratory causes: Hypoventilation leading to CO2 retention, with approximately 20% of patients with acute COPD exacerbations developing respiratory acidosis 3
  • Lactic acidosis in shock results from inadequate oxygen delivery to tissues, producing lactate as a byproduct 1
  • The "anion gap" (unmeasured anions) helps establish the mechanism: normal anion gap indicates bicarbonate loss or chloride salt ingestion, while elevated gap indicates presence of other acids 5

How Alkalosis Develops

  • Metabolic alkalosis requires both generation and maintenance of high bicarbonate levels to persist 4
  • Generation occurs through gastrointestinal hydrogen and chloride loss or renal causes 4
  • In congestive heart failure, diuretic therapy causes activation of the renin-angiotensin system, chloride depletion, increased distal sodium delivery, hypokalemia, and increased urine acidification, all contributing to bicarbonate retention 7
  • Factors that impair renal bicarbonate elimination include volume contraction, low GFR, potassium deficiency, hypochloremia, aldosterone excess, and elevated arterial CO2 6

Compensatory Responses

Acidosis Compensation

  • Metabolic acidosis: Compensation consists of hyperventilation (respiratory compensation) and enhanced renal excretion of hydrogen ions, chiefly as ammonium 5
  • Respiratory acidosis: In chronic situations, a compensatory rise in serum bicarbonate concentration occurs through renal bicarbonate retention 2
  • Chronic respiratory acidosis is often associated with compensatory metabolic alkalosis due to renal bicarbonate retention 2

Alkalosis Compensation

  • Metabolic alkalosis: Compensation is mainly through decreased alveolar ventilation to increase PaCO2 and renal excretion of bicarbonate 5, 4
  • The kidney normally prevents metabolic alkalosis by enhancing bicarbonate excretion through increased filtration, decreased absorption, and enhanced secretion 6

Clinical Presentations

Acidosis Manifestations

  • In acute respiratory acidosis, pH falls below 7.35 with elevated CO2 levels, while chronic respiratory acidosis may show normal pH due to renal compensation 2
  • Brain injuries, strokes, or tumors affecting respiratory centers in the medulla can impair central respiratory drive, causing respiratory acidosis 2
  • Metabolic acidosis in alcoholics presents as a mixed acid-base disturbance with lactic acidosis, ketoacidosis, and acetic acidosis 8

Alkalosis Manifestations

  • Severe alkalosis may be accompanied by hyperirritability or tetany 9
  • Metabolic alkalosis, isolated or in combination with another abnormality, is the most common acid-base disorder in patients with congestive heart failure 7

Treatment Approaches

Treating Acidosis

  • Metabolic acidosis: Treatment focuses on addressing the underlying cause and may require bicarbonate supplementation when severe (pH < 7.2) 3
  • In chronic kidney disease, pharmacological treatment may be considered when bicarbonate levels are less than 18 mmol/L 3
  • Respiratory acidosis: Treatment primarily targets improving ventilation to reduce CO2 levels, with mechanical ventilation required in acute cases 3
  • For lactic acidosis due to tissue hypoxia, the primary focus is on improving oxygen delivery 3
  • Careful oxygen therapy is essential in chronic respiratory acidosis, as excessive oxygen can worsen hypercapnia in conditions like COPD 3
  • The best method of reversing acidosis associated with cardiac arrest is to restore spontaneous circulation 10

Treating Alkalosis

  • Treatment is based on eliminating generation and maintenance factors, chloride and potassium repletion, enhancement of renal bicarbonate excretion (such as acetazolamide), direct titration of base excess (hydrochloric acid), or low-bicarbonate dialysis if accompanied by kidney failure 7
  • Measurement of urinary chloride helps establish the mechanism: very low urinary chloride indicates saline-responsive alkalosis (usually gastric H+ loss), which responds to saline administration 5
  • Moderately low urinary chloride indicates saline-resistant alkalosis, which requires potassium in treatment 5
  • Should alkalosis result from bicarbonate overdose, the bicarbonate should be stopped and 0.9% sodium chloride injection may be given; potassium chloride may be indicated if there is hypokalemia 9
  • In severe alkalosis with hyperirritability or tetany, calcium gluconate may control symptoms, and an acidifying agent such as ammonium chloride may be indicated 9

Critical Pitfalls

  • Avoid excessive bicarbonate supplementation in acidosis to prevent rebound alkalosis 3
  • In metabolic alkalosis, do not overlook accompanying reduction in ECF volume, which may play an important role in pathogenesis 8
  • Arterial blood-gas analysis alone may be misleading; even co-terminous arterial and mixed central venous samples may be of little value in estimating myocardial and cerebral intracellular acid-base status 10
  • In alcohol-induced acidosis, metabolic alkalosis may be present but overlooked due to indirect loss of sodium bicarbonate as sodium β-hydroxybutyrate in urine 8

References

Guideline

Acidosis in Shock: Pathophysiological Mechanisms and Clinical Implications

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Respiratory Acidosis: Pathophysiology and Clinical Implications

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Acidosis Treatment Guidelines

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Diagnosis and management of metabolic alkalosis.

Journal of the Indian Medical Association, 2006

Research

Metabolic Alkalosis Pathogenesis, Diagnosis, and Treatment: Core Curriculum 2022.

American journal of kidney diseases : the official journal of the National Kidney Foundation, 2022

Research

Treatment of severe metabolic alkalosis in a patient with congestive heart failure.

American journal of kidney diseases : the official journal of the National Kidney Foundation, 2013

Research

Metabolic acidosis in the alcoholic: a pathophysiologic approach.

Metabolism: clinical and experimental, 1983

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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