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Foundation Sciences · Physiology
Acid-Base Balance
Acid-base balance is the physiological process of maintaining the arterial blood pH between 7.35 and 7.45. This is essential for optimal enzyme function and cellular metabolism. The body utilizes chemical buffers (bicarbonate), the respiratory system (CO2 excretion), and the renal system (H+ excretion and HCO3- regeneration). Disturbance of this balance leads to acidosis or alkalosis, often indicating severe underlying pathology.
📌 Learning Objectives
- Describe the physiological mechanisms involved in maintaining acid-base homeostasis.
- Explain the roles of chemical buffers, the respiratory system, and the renal system in pH regulation.
- Identify the primary acid-base disorders (respiratory acidosis/alkalosis, metabolic acidosis/alkalosis) from Arterial Blood Gas (ABG) results.
- Apply the principles of compensation to interpret complex acid-base disturbances.
- Correlate common clinical conditions with their expected acid-base derangements.
📋 Overview
Interpreting Arterial Blood Gases (ABGs) is a cornerstone skill for finals and a common OSCE station. Acid-base balance is about maintaining a tight pH range (7.35-7.45) crucial for enzyme function and cellular processes. The body has three main lines of defence: immediate chemical buffers (e.g., bicarbonate), rapid respiratory compensation (altering CO2 excretion), and slower, but powerful, renal compensation (adjusting H+ and HCO3- excretion/reabsorption). Understanding how these systems interact is key to diagnosing and managing critical conditions like DKA, sepsis, and respiratory failure. You'll be expected to identify primary disorders (metabolic or respiratory acidosis/alkalosis) and assess the degree of compensation.
🔬 Basic Science
The bicarbonate buffer system (CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-) is central. Carbonic anhydrase rapidly interconverts CO2 and H2CO3. The lungs regulate CO2 (acid), and the kidneys regulate HCO3- (base) and H+. In metabolic acidosis, excess H+ consumes HCO3-. If the H+ comes from unmeasured acids (e.g., lactate, ketoacids), the anion gap widens. If it's due to HCO3- loss (e.g., diarrhoea, renal tubular acidosis), Cl- increases to maintain electroneutrality, resulting in a normal anion gap (hyperchloraemic) metabolic acidosis. Respiratory acidosis is CO2 retention (hypoventilation), while respiratory alkalosis is CO2 washout (hyperventilation). Compensation is the body's attempt to normalise pH; the system not primarily affected tries to correct the imbalance. For example, in metabolic acidosis, the lungs increase ventilation to reduce PaCO2.
🏥 Clinical Relevance
ABG interpretation is vital in acute medicine. Recognising a life-threatening metabolic acidosis (e.g., DKA, severe sepsis with lactic acidosis) or acute respiratory failure (e.g., severe asthma, COPD exacerbation) from ABGs is a common finals scenario. Salicylate overdose is a classic mixed disorder, causing both respiratory alkalosis (direct stimulation of respiratory centre) and high anion gap metabolic acidosis. Chronic respiratory conditions like COPD often lead to compensated respiratory acidosis (high PaCO2, high HCO3-), which is different from acute respiratory failure. Always consider the patient's clinical picture alongside the ABG results.
🧪 Investigations
Arterial Blood Gas (ABG) is the definitive investigation. You must be able to interpret the pH, PaCO2, HCO3-, and often the PaO2 and base excess/deficit. A venous blood gas (VBG) can give a good estimate of pH and HCO3- but is unreliable for PaO2 and PaCO2. When interpreting, follow a systematic approach: 1. Is the pH acidotic or alkalotic? 2. Is the primary problem respiratory (PaCO2) or metabolic (HCO3-)? 3. Is there appropriate compensation? 4. If metabolic acidosis, calculate the anion gap. Base excess/deficit indicates the metabolic component: negative base excess means metabolic acidosis, positive means metabolic alkalosis.
💊 Management
Management is always directed at the underlying cause. For DKA, it's insulin, fluids, and electrolytes. For sepsis, it's antibiotics, fluids, and source control. Sodium bicarbonate is rarely indicated for metabolic acidosis and only in severe cases (pH <7.1) under specialist guidance, as it can worsen intracellular acidosis and cause fluid overload. In chronic compensated conditions, the aim is to manage the disease, not necessarily to 'correct' the ABG values to normal, as the compensation is physiological.
Revision Resources – expand the sections below for high-yield notes, exam pearls, key facts and further reading.
MLA High-Yield Notes & Quick Revision ⌄
Master the step-by-step ABG interpretation. It's a guaranteed question in SBAs and often an OSCE station.
1. **pH:** Is it <7.35 (acidosis) or >7.45 (alkalosis)?
2. **PaCO2:** Is it moving in the *opposite* direction to pH (respiratory problem)? High PaCO2 = acidosis, low PaCO2 = alkalosis.
3. **HCO3-:** Is it moving in the *same* direction as pH (metabolic problem)? Low HCO3- = acidosis, high HCO3- = alkalosis.
4. **Compensation:** If the primary problem is respiratory, is the HCO3- trying to normalise the pH? If metabolic, is the PaCO2 trying to normalise the pH? If the pH is normal but PaCO2 and HCO3- are abnormal, it's fully compensated. If pH is abnormal but the 'compensatory' value is also abnormal, it's partially compensated.
5. **Anion Gap:** Only for metabolic acidosis. Calculate Na - (Cl + HCO3). High gap suggests MUDPILES. Normal gap suggests HCO3- loss (e.g., diarrhoea, RTA).
**OSCE Tip:** Be ready to explain your ABG interpretation clearly and concisely, and suggest initial management based on the clinical scenario.
1. **pH:** Is it <7.35 (acidosis) or >7.45 (alkalosis)?
2. **PaCO2:** Is it moving in the *opposite* direction to pH (respiratory problem)? High PaCO2 = acidosis, low PaCO2 = alkalosis.
3. **HCO3-:** Is it moving in the *same* direction as pH (metabolic problem)? Low HCO3- = acidosis, high HCO3- = alkalosis.
4. **Compensation:** If the primary problem is respiratory, is the HCO3- trying to normalise the pH? If metabolic, is the PaCO2 trying to normalise the pH? If the pH is normal but PaCO2 and HCO3- are abnormal, it's fully compensated. If pH is abnormal but the 'compensatory' value is also abnormal, it's partially compensated.
5. **Anion Gap:** Only for metabolic acidosis. Calculate Na - (Cl + HCO3). High gap suggests MUDPILES. Normal gap suggests HCO3- loss (e.g., diarrhoea, RTA).
**OSCE Tip:** Be ready to explain your ABG interpretation clearly and concisely, and suggest initial management based on the clinical scenario.
Diabetic ketoacidosis
Sepsis
Chronic obstructive pulmonary disease
Acute kidney injury
Poisoning (e.g., salicylate)
Cardiac arrest
Shock
- pH 7.35-7.45 is normal.
- pCO2 is respiratory, HCO3- is metabolic.
- Acidosis = pH < 7.35; Alkalosis = pH > 7.45.
- Respiratory acidosis: high pCO2; Respiratory alkalosis: low pCO2.
- Metabolic acidosis: low HCO3-; Metabolic alkalosis: high HCO3-.
- Compensation tries to bring pH back to normal.
Exam Pearls ⌄
⭐ High Yield
Normal arterial pH is 7.35-7.45, maintained by buffer systems, lungs, and kidneys.
The bicarbonate buffer system (HCO3-/H2CO3) is the most important extracellular buffer.
Respiratory compensation for metabolic disorders involves altering pCO2 via ventilation.
Renal compensation for respiratory disorders involves adjusting H+ excretion and HCO3- reabsorption/synthesis.
Metabolic acidosis is often characterised by a low HCO3- and a compensatory drop in pCO2.
Respiratory acidosis is characterised by a high pCO2 and a compensatory rise in HCO3- (if chronic).
Anion gap calculation helps differentiate causes of metabolic acidosis.
The Henderson-Hasselbalch equation describes the relationship between pH, HCO3-, and pCO2.
💡 Clinical Pearl
Diabetic Ketoacidosis (DKA): A common cause of high anion gap metabolic acidosis due to ketone body production.
Chronic Obstructive Pulmonary Disease (COPD): Can lead to chronic respiratory acidosis due to impaired CO2 excretion.
Sepsis: Often causes lactic acidosis (a type of high anion gap metabolic acidosis) due to tissue hypoperfusion.
Renal Failure: Can result in metabolic acidosis due to impaired acid excretion and bicarbonate regeneration.
Hyperventilation Syndrome: Causes respiratory alkalosis due to excessive CO2 exhalation.
⚠️ Exam Tip — Common Mistakes
Confusing primary disorder with compensatory response (e.g., low pCO2 in metabolic acidosis is compensation, not primary respiratory alkalosis).
Failing to assess for appropriate compensation, especially in mixed disorders.
Not calculating the anion gap in metabolic acidosis.
Misinterpreting a normal pH in the presence of abnormal pCO2 and HCO3- as 'normal' rather than compensated.
Forgetting that renal compensation is slower (hours to days) than respiratory compensation (minutes to hours).
Assuming all metabolic acidosis is high anion gap.
Key Facts ⌄
Normal arterial pH: 7.35-7.45.
Normal PaCO2: 4.7-6.0 kPa (35-45 mmHg).
Normal HCO3-: 22-28 mmol/L.
Anion Gap = Na+ - (Cl- + HCO3-); normal is 8-12 mmol/L (some labs include K+, but Na+ only is common for exams).
High Anion Gap Metabolic Acidosis (HAGMA) causes (MUDPILES mnemonic): Methanol, Uraemia, DKA, Paraldehyde/Propylene glycol, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates.
Respiratory compensation for metabolic acidosis: Hyperventilation (Kussmaul breathing) to blow off CO2.
Renal compensation for respiratory acidosis: Increased H+ excretion and HCO3- reabsorption/generation.
Related Topics ⌄
References ⌄
- TeachMePhysiology - Acid-Base Balance
- GMC MLA Content Map - Physiology
- NICE CKS: Diabetes - DKA
- British Thoracic Society (BTS) Guideline: Oxygen Use
Further Resources
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