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MRCP(UK) Part 1

15.3 Acid-Base Disorders & Blood Gas Analysis

Q: A 24-year-old woman is brought to the emergency department after ingesting an unknown quantity of an over-the-counter medication 4 hours earlier following an argument. She is tachypnoeic, agitated, diaphoretic, and complains of nausea, epigastric discomfort, and loud bilateral ringing in her ears (tinnitus). On examination, her respiratory rate is 32 breaths/minute, pulse is 108 bpm regular, and blood pressure is 114/72 mmHg. Chest auscultation reveals clear lung fields bilaterally. Arterial blood gas on room air reveals: pH 7.48, PaCO2 3.2 kPa (24 mmHg), PaO2 13.5 kPa (101 mmHg), bicarbonate 16 mmol/L, base excess -8 mmol/L. Simultaneous serum biochemistry demonstrates: sodium 140 mmol/L, potassium 4.0 mmol/L, chloride 100 mmol/L, urea 5.2 mmol/L, creatinine 78 mcmol/L, glucose 6.2 mmol/L. What is the primary acid-base disturbance pattern present in this patient?

Mixed primary respiratory alkalosis and high anion gap metabolic acidosis. Mixed primary respiratory alkalosis and high anion gap metabolic acidosis is the correct pattern. This clinical presentation—tachypnoea, diaphoresis, epigastric pain, and bilateral tinnitus following an intentional overdose—is classic for acute salicylate (aspirin) toxicity. Salicylates exert a dual toxicological effect: (1) direct stimulation of the medullary respiratory center in the brainstem, driving alveolar hyperventilation and inducing a primary respiratory alkalosis; and (2) toxic uncoupling of mitochondrial oxidative phosphorylation, impairing ATP generation and accelerating anaerobic glycolysis, lipolysis, and ketogenesis, thereby accumulating unmeasured organic acids (lactic, pyruvic, and keto acids) that produce a primary high anion gap metabolic acidosis (HAGMA). Analysis of the blood gas demonstrates: (1) pH is 7.48 (alkalaemia); (2) PaCO2 is 3.2 kPa (24 mmHg), reflecting profound hyperventilation; (3) serum bicarbonate is low at 16 mmol/L; and (4) the serum anion gap is elevated at 24 mmol/L: AG = Na - (Cl + HCO3) = 140 - (100 + 16) = 24 mmol/L (normal 10–14 mmol/L). Furthermore, applying Winter's formula to determine expected compensation for the metabolic acidosis: Expected PaCO2 = 1.5 × [HCO3-] + 8 ± 2 = 1.5 × 16 + 8 = 32 mmHg (± 2 mmHg). The patient's actual PaCO2 of 24 mmHg is significantly lower than predicted by compensation alone, unequivocally proving the coexistence of an independent primary respiratory alkalosis.

Q: A 62-year-old man with a history of hypertension managed with amlodipine presents to the medical assessment unit with a 4-day history of profuse, watery, non-bloody diarrhoea and generalised weakness following a suspected gastroenteritis outbreak. On physical examination, he appears lethargic with dry mucous membranes, collapsed peripheral veins, blood pressure 96/60 mmHg, and a heart rate of 104 bpm. Cardiorespiratory examination is normal. Laboratory investigations reveal: serum sodium 136 mmol/L, potassium 3.1 mmol/L, chloride 114 mmol/L, bicarbonate 14 mmol/L, urea 12.4 mmol/L, creatinine 138 mcmol/L. Arterial blood gas demonstrates: pH 7.28, PaCO2 3.9 kPa (29 mmHg), PaO2 12.8 kPa, bicarbonate 14 mmol/L. Simultaneous spot urine electrolytes demonstrate: urinary sodium 32 mmol/L, urinary potassium 22 mmol/L, and urinary chloride 78 mmol/L. What is the calculated urine anion gap and the corresponding pathophysiological mechanism of his acid-base disorder?

Urine anion gap -24 mmol/L; gastrointestinal bicarbonate loss with intact renal ammonium excretion. Urine anion gap -24 mmol/L; gastrointestinal bicarbonate loss with intact renal ammonium excretion is the correct answer. The patient presents with acidaemia (pH 7.28) and a low bicarbonate (14 mmol/L). Calculating the serum anion gap reveals: AG = Na - (Cl + HCO3) = 136 - (114 + 14) = 8 mmol/L. Because the normal serum anion gap is 10 to 14 mmol/L, an AG of 8 mmol/L confirms a Normal Anion Gap Metabolic Acidosis (NAGMA / hyperchloraemic metabolic acidosis, with serum chloride elevated at 114 mmol/L). In NAGMA, the urine anion gap (UAG) is the definitive investigation used to differentiate gastrointestinal bicarbonate loss from renal tubular acidosis: UAG = Urine [Na+] + Urine [K+] - Urine [Cl-]. Substituting the patient's urine electrolytes yields: UAG = 32 + 22 - 78 = 54 - 78 = -24 mmol/L. Under normal physiological conditions, the kidney responds to systemic metabolic acidosis by drastically increasing renal ammoniagenesis and ammonium (NH4+) secretion. Ammonium is an unmeasured cation excreted together with chloride (NH4Cl). A negative urine anion gap (<0, typically -20 to -50 mmol/L) signifies that urinary chloride is high because it is balancing abundant unmeasured ammonium ions, confirming that the renal tubules are functioning normally and appropriately excreting acid. This establishes gastrointestinal bicarbonate loss (diarrhoea) as the cause. In distal renal tubular acidosis (Type 1 RTA), the collecting duct cannot secrete hydrogen ions to form ammonium; urinary chloride remains low, resulting in a positive urine anion gap (>0).

Key Takeaways

Systematic arterial blood gas (ABG) interpretation follows 5 steps: evaluating pH (acidaemia <7.35, alkalaemia >7.45), identifying the primary disturbance, assessing physiological compensation, calculating the serum anion gap, and performing delta-delta gap analysis.
In metabolic acidosis, respiratory compensation is predicted by Winter's formula: expected PaCO2 (mmHg) = 1.5 × [HCO3-] + 8 ± 2; an actual PaCO2 higher than predicted indicates concurrent respiratory acidosis, whereas a lower PaCO2 indicates concurrent respiratory alkalosis.
High anion gap metabolic acidosis (HAGMA; AG >14 mmol/L) is caused by unmeasured fixed acid anions recalled by GOLD MARK (Glycols, Oxoproline/paracetamol, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, Ketoacidosis); the Delta-Delta ratio (ΔAG / Δ[HCO3-]) identifies mixed disorders (<0.4–0.8 indicates concurrent NAGMA, >1.5–2.0 indicates concurrent metabolic alkalosis).
Normal anion gap metabolic acidosis (NAGMA / hyperchloraemic) is differentiated using the urine anion gap (UAG = [Na+] + [K+] - [Cl-]): negative UAG (<0) indicates appropriate renal ammonium excretion in GI bicarbonate loss (diarrhoea), whereas positive UAG (>0) confirms defective distal renal acid excretion (Type 1 distal RTA).
Metabolic alkalosis is classified by urinary chloride: saline-responsive (urinary chloride <20 mmol/L; vomiting, NG suction, past diuretics) which resolves with 0.9% saline rehydration, versus saline-resistant (urinary chloride >20 mmol/L; primary aldosteronism, Conn's, Cushing's, severe hypokalaemia, Bartter/Gitelman) which requires targeted therapy.

Last updated: September 2026

Systemic acid-base homeostasis maintains arterial pH strictly between 7.35 and 7.45 ([H+] = 35–45 nmol/L). The primary extracellular buffer is the bicarbonate-carbonic acid system, governed by the Henderson-Hasselbalch relationship:

pH = 6.1 + log([HCO3-] / (0.03 × PaCO2 [mmHg]))

Arterial blood gas (ABG) analysis is a core competency for MRCP(UK) Part 1. Mastering systematic step-by-step interpretation, compensation rules, anion gap, delta gap, and urinary electrolytes ensures diagnostic precision.

1. Systematic 5-Step ABG Interpretation Protocol

                             5-STEP ABG PROTOCOL
                                      │
             ┌────────────────────────┼────────────────────────┐
             ▼                        ▼                        ▼
      STEP 1: pH / [H+]      STEP 2: Primary Process   STEP 3: Compensation
      • <7.35 = Acidaemia    • Low HCO3 = Met Acid     • Winter's Formula
      • >7.45 = Alkalaemia   • High PaCO2 = Resp Acid  • Resp Acid/Alk Rules
      • 7.35-7.45 = Normal/  • High HCO3 = Met Alk     (Never overcompensates)
        Mixed Disorder       • Low PaCO2 = Resp Alk
                                      │
             ┌────────────────────────┴────────────────────────┐
             ▼                                                 ▼
      STEP 4: Anion Gap                                 STEP 5: Delta-Delta Ratio
      • AG = Na - (Cl + HCO3)                           • Delta AG / Delta HCO3
      • Normal: 10-14 mmol/L                            • <0.4-0.8 = Mixed HAGMA + NAGMA
      • Correct for Albumin!                            • >1.5-2.0 = Mixed HAGMA + Met Alk

Step 1: Examine the pH and [H+]

pH < 7.35 ([H+] > 45 nmol/L): Acidaemia.
pH > 7.45 ([H+] < 35 nmol/L): Alkalaemia.
Normal pH (7.35–7.45): Either completely normal physiology OR a balanced, complex mixed acid-base disorder (e.g. concurrent severe metabolic acidosis and metabolic alkalosis).

Step 2: Determine the Primary Process

Identify the parameter whose change direction matches the pH:

In acidaemia: reduced [HCO3-] (<22 mmol/L) defines a metabolic acidosis; elevated PaCO2 (>6.0 kPa / >45 mmHg) defines a respiratory acidosis.
In alkalaemia: elevated [HCO3-] (>26 mmol/L) defines a metabolic alkalosis; reduced PaCO2 (<4.7 kPa / <35 mmHg) defines a respiratory alkalosis.

Step 3: Assess Physiological Compensation

Physiological compensation never overcompensates; it brings the pH towards, but never across, the 7.40 neutral mark. If measured compensation deviates from expected values, a secondary independent acid-base disorder is present:

Metabolic Acidosis Compensation (Winter's Formula): Expected PaCO2 (mmHg) = 1.5 × [HCO3-] + 8 ± 2 (In SI units: Expected PaCO2 (kPa) = [1.5 × [HCO3-] + 8 ± 2] / 7.5).
- If measured PaCO2 > expected: Concurrent respiratory acidosis (e.g. DKA with central respiratory depression, exhaustion, or underlying COPD).
- If measured PaCO2 < expected: Concurrent respiratory alkalosis (e.g. sepsis, salicylate toxicity, pulmonary embolism).
Metabolic Alkalosis Compensation: Expected PaCO2 (mmHg) = 0.7 × [HCO3-] + 20 ± 5 (PaCO2 rises via compensatory hypoventilation, but rarely exceeds 55–60 mmHg / 7.3–8.0 kPa due to hypoxaemic respiratory drive).
Acute vs. Chronic Respiratory Acidosis:
- Acute: For every 10 mmHg (1.33 kPa) acute rise in PaCO2, [HCO3-] rises by 1 mmol/L (cellular buffering).
- Chronic (>48h): For every 10 mmHg (1.33 kPa) chronic rise in PaCO2, [HCO3-] rises by 3.5–4 mmol/L (renal H+ secretion and bicarbonate generation).
Acute vs. Chronic Respiratory Alkalosis:
- Acute: For every 10 mmHg (1.33 kPa) acute fall in PaCO2, [HCO3-] falls by 2 mmol/L.
- Chronic: For every 10 mmHg (1.33 kPa) chronic fall in PaCO2, [HCO3-] falls by 4–5 mmol/L.

Step 4: Calculate the Serum Anion Gap (AG)

Serum Anion Gap = [Na+] - ([Cl-] + [HCO3-])

Normal reference range: 10–14 mmol/L (unmeasured anions like albumin, phosphate, and sulfate exceed unmeasured cations like calcium and magnesium).
Albumin Correction: Serum albumin accounts for ~75% of the normal anion gap. For every 10 g/L reduction in serum albumin below 40 g/L, the baseline normal AG drops by 2.5 mmol/L: Corrected AG = Observed AG + 0.25 × (40 - Serum Albumin [g/L]) (In hypoalbuminaemic critically ill patients, failure to correct the anion gap masks a severe high anion gap acidosis).

Step 5: Delta Gap / Delta-Delta Analysis

In High Anion Gap Metabolic Acidosis (HAGMA), delta analysis detects occult coexisting metabolic disorders:

ΔAG = Observed AG - 12
Δ[HCO3-] = 24 - Observed [HCO3-]
Delta-Delta Ratio = ΔAG / Δ[HCO3-]
Ratio 0.8–1.2: Pure uncomplicated HAGMA (one molecule of organic acid consumes exactly one molecule of bicarbonate).
Ratio <0.4–0.8: Δ[HCO3-] is disproportionately greater than ΔAG. Bicarbonate is lower than predicted. Confirms a concurrent Normal Anion Gap (Hyperchloraemic) Metabolic Acidosis (e.g. DKA with severe diarrhoea, or DKA resuscitated with excessive 0.9% saline).
Ratio >1.5–2.0: ΔAG is disproportionately greater than Δ[HCO3-]. Bicarbonate is higher than predicted. Confirms a concurrent Metabolic Alkalosis (e.g. DKA or alcoholic ketoacidosis complicated by severe vomiting) or pre-existing compensated chronic hypercapnia.

2. High Anion Gap Metabolic Acidosis (HAGMA): The GOLD MARK Mnemonic

HAGMA (>14 mmol/L) is generated by the accumulation of unmeasured organic or inorganic fixed acids:

G — Glycols (Ethylene Glycol, Propylene Glycol): Ethylene glycol (antifreeze) is metabolized by alcohol dehydrogenase to glycolate and oxalate, causing severe HAGMA, high osmolar gap, acute kidney injury with calcium oxalate monohydrate envelope- or needle-shaped crystals in urine, and cranial neuropathies. Treatment: Fomepizole or IV ethanol, and urgent haemodialysis.
O — 5-Oxoproline (Pyroglutamic Acid): Occurs in malnourished, elderly females taking chronic therapeutic paracetamol (acetaminophen) in the setting of critical illness or hepatic/renal impairment. Glutathione depletion uncouples the gamma-glutamyl cycle, producing massive 5-oxoproline accumulation. Treatment: Discontinue paracetamol; administer intravenous N-acetylcysteine.
L — L-Lactate:
- Type A (Tissue Hypoperfusion / Hypoxia): Septic shock, cardiogenic shock, hypovolaemia, mesenteric ischaemia, carbon monoxide poisoning, severe asphyxia.
- Type B (Cellular / Toxin / Metabolic): Metformin toxicity (especially with acute renal impairment), severe liver failure, haematological malignancy (Warburg effect), phaeochromocytoma, propofol infusion syndrome, linezolid, and thiamine deficiency (wet beriberi).
D — D-Lactate: Produced by intestinal bacterial fermentation of unabsorbed carbohydrates in patients with short bowel syndrome, jejunoileal bypass, or severe malabsorption. Standard laboratory lactate assays detect only L-lactate and are entirely negative. Presents with episodic HAGMA, ataxia, slurred speech, confusion, and encephalopathy.
M — Methanol: Ingestion of methylated spirits or adulterated alcohol. Metabolized by alcohol dehydrogenase to formic acid. Produces severe HAGMA, elevated osmolar gap, visual loss with optic disc hyperaemia ('snowstorm vision'), and bilateral basal ganglia (putaminal) necrosis. Treatment: Fomepizole or ethanol, intravenous folinic acid, and emergent haemodialysis.
A — Aspirin / Salicylates: In overdose, salicylates uncouple oxidative phosphorylation, driving accumulation of pyruvic, lactic, and keto acids. Classically presents as a mixed disorder: primary respiratory alkalosis (direct stimulation of the medullary respiratory center) combined with primary HAGMA. Treatment: Urinary alkalinisation with intravenous 8.4% sodium bicarbonate, dextrose, and urgent haemodialysis if salicylate >700 mg/L (>5 mmol/L) or severe neurotoxicity.
R — Renal Failure / Uraemia: Advanced AKI or CKD (eGFR <15–20 mL/min). Decreased glomerular filtration and tubular excretion of inorganic sulfates, phosphates, and urate.
K — Ketoacidosis:
- Diabetic Ketoacidosis (DKA): Insulin deficiency driving lipolysis and ketogenesis (β-hydroxybutyrate and acetoacetate).
- Alcoholic Ketoacidosis (AKA): Chronic alcoholism with recent heavy binging followed by abrupt cessation and vomiting/starvation. Characterized by profound ketonaemia with normal or low blood glucose.
- Starvation Ketoacidosis: Mild ketonaemia after prolonged fasting; bicarbonate rarely drops below 16–18 mmol/L.

3. Normal Anion Gap Metabolic Acidosis (NAGMA) & Urine Anion Gap

In NAGMA, the loss of bicarbonate is matched by an equimolar retention of chloride by the kidneys to preserve electroneutrality, resulting in hyperchloraemic metabolic acidosis with a normal anion gap (10–14 mmol/L).

Feature	High Anion Gap Metabolic Acidosis (HAGMA)	Normal Anion Gap Metabolic Acidosis (NAGMA)
Serum Anion Gap	Elevated (>14 mmol/L, often >20–30)	Normal (10–14 mmol/L)
Serum Chloride	Normal	Elevated (Hyperchloraemia, typically >108–112 mmol/L)
Primary Mechanism	Addition of unmeasured fixed acids (A-); H+ titrates HCO3-, leaving A- unmeasured	Direct physical loss of HCO3- or failure of renal H+ excretion with compensatory renal Cl- retention
Etiologies	GOLD MARK (Glycols, Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, Ketoacidosis)	Gastrointestinal losses (diarrhoea, enterostomy, fistula), Renal Tubular Acidosis (Types 1, 2, 4), Acetazolamide, Iatrogenic 0.9% saline resuscitation
Urine Anion Gap (UAG)	Not applicable	Critical discriminator: Differentiates GI bicarbonate loss (negative UAG) from Distal RTA (positive UAG)

The Urine Anion Gap (UAG)

Urine Anion Gap (UAG) = [Urine Na+] + [Urine K+] - [Urine Cl-]

The healthy kidney excretes excess fixed acid primarily in the form of ammonium (NH4+) paired with chloride (NH4Cl). Because ammonium is an unmeasured cation, high renal excretion of NH4Cl causes urinary chloride to substantially exceed the sum of urinary sodium and potassium.
Negative UAG (<0, typically -20 to -50 mmol/L): Indicates intact renal ammoniagenesis and distal hydrogen ion secretion. Diagnoses: Gastrointestinal bicarbonate loss (severe diarrhoea, laxative abuse, enterocutaneous fistula).
Positive UAG (>0, typically +10 to +40 mmol/L): Indicates impaired distal renal ammonium excretion. Diagnoses: Type 1 (Distal) Renal Tubular Acidosis.

Summary of Renal Tubular Acidosis (RTA)

Type 1 (Distal RTA): Inability of collecting duct α-intercalated cells to secrete H+ via H+-ATPase. Urine pH persistently >5.5 despite severe systemic acidaemia, positive UAG, hypokalaemia, hypercalciuria, hypocitraturia, and recurrent medullary nephrocalcinosis. Associated with autoimmune diseases (Sjögren's, SLE), amphotericin B, and lithium. Treatment: Oral sodium bicarbonate or potassium citrate.
Type 2 (Proximal RTA): Defective proximal tubular bicarbonate reabsorption. Variable urine pH (<5.5 once serum bicarbonate falls below the reduced tubular threshold). Hypokalaemia, absence of nephrocalcinosis. Frequently associated with generalized proximal dysfunction (Fanconi syndrome: renal glycosuria with normal blood sugar, aminoaciduria, phosphaturia with rickets/osteomalacia). Associated with multiple myeloma, Wilson's disease, and tenofovir. Treatment: High-dose oral bicarbonate.
Type 4 (Hyperkalaemic RTA): Aldosterone deficiency or resistance. Decreased aldosterone reduces ENaC activity, impairing luminal electronegativity and blunting both K+ and H+ secretion. Hyperkalaemia, hyperchloraemic metabolic acidosis, urine pH <5.5. Causes: Diabetic nephropathy (hyporeninaemic hypoaldosteronism), Addison's disease, ACE inhibitors, ARBs, spironolactone, amiloride, trimethoprim, calcineurin inhibitors. Treatment: Fludrocortisone, loop diuretics, potassium restriction.

4. Metabolic Alkalosis: Saline-Responsive vs Saline-Resistant

Metabolic alkalosis (arterial pH > 7.45, [HCO3-] > 26 mmol/L) is classified by measuring spot urinary chloride, which guides definitive therapy:

                               Metabolic Alkalosis
                              (pH > 7.45, HCO3 > 26)
                                         │
                           Measure Spot Urinary Chloride
                         ┌───────────────┴───────────────┐
                         ▼                               ▼
               Urinary Chloride <20             Urinary Chloride >20
                SALINE-RESPONSIVE                SALINE-RESISTANT
                         │                               │
               • Vomiting / NG suction          • Primary Hyperaldosteronism
               • Prior diuretic therapy           (Conn's Syndrome)
               • Volume/Chloride depletion      • Cushing's Syndrome
               • Paradoxical aciduria           • Severe hypokalaemia (<2.0)
                         │                      • Bartter / Gitelman
               RESUSPENSION WITH 0.9% NaCl               │
                                                DOES NOT RESPOND TO SALINE
                                                (Treat underlying endocrinopathy)

Saline-Responsive Metabolic Alkalosis (Urinary Chloride <20 mmol/L)

Etiology: Prolonged vomiting, nasogastric suction, prior loop or thiazide diuretic therapy (after diuretic effect has waned), villous adenoma of the rectum, congenital chloridorrhoea.
Pathophysiology: Loss of gastric HCl produces volume contraction, hypochloraemia, and hypokalaemia. Hypochloraemia limits chloride delivery to the cortical collecting duct, impairing apical pendrin (Cl- / HCO3- exchanger) activity, preventing bicarbonate excretion. Concurrent hypovolaemia stimulates aldosterone, which drives Na+ reabsorption and forces intercalated cells to excrete H+ and K+ into urine, generating paradoxical aciduria.
Management: Rapidly corrects with intravenous 0.9% Sodium Chloride and potassium chloride supplementation. Saline expands intravascular volume (suppressing aldosterone) and replenishes chloride, permitting pendrin to excrete bicarbonate.

Saline-Resistant Metabolic Alkalosis (Urinary Chloride >20 mmol/L)

Etiology: Primary aldosteronism (Conn's syndrome, bilateral adrenal hyperplasia), Cushing's syndrome, renovascular hypertension, excessive licorice ingestion (glycyrrhizic acid), renin-secreting tumors, Liddle syndrome, Bartter syndrome, Gitelman syndrome, and profound hypokalaemia ([K+] < 2.0 mmol/L).
Pathophysiology: Autonomous mineralocorticoid activity drives continuous ENaC sodium reabsorption, lumen-negative voltage, and intercalated cell H+-ATPase secretion, independent of volume or chloride status.
Management: Does NOT correct with 0.9% saline. Requires specific therapy directed at the underlying endocrinopathy (unilateral adrenalectomy in Conn's adenoma, spironolactone/eplerenone in bilateral hyperplasia, amiloride in Liddle syndrome).

5. Respiratory Acidosis vs. Respiratory Alkalosis

Respiratory Acidosis (PaCO2 > 6.0 kPa / >45 mmHg):
- Acute: Uncompensated or minimally compensated ([HCO3-] rises 1 mmol/L per 10 mmHg PaCO2 rise). Central respiratory depression (opioid overdose, benzodiazepine toxicity, severe stroke), acute airway obstruction, cardiac arrest, flail chest, acute neuromuscular failure (myasthenia gravis crisis, Guillain-Barré syndrome).
- Chronic: Fully compensated ([HCO3-] rises 3.5–4 mmol/L per 10 mmHg PaCO2 rise). Severe COPD, obesity hypoventilation syndrome (Pickwickian syndrome), severe kyphoscoliosis, motor neurone disease (ALS).
Respiratory Alkalosis (PaCO2 < 4.7 kPa / <35 mmHg):
- Acute: Minimal compensation ([HCO3-] falls 2 mmol/L per 10 mmHg PaCO2 drop). Psychogenic hyperventilation / panic attack, acute pulmonary embolism (tachypnoea and hypoxaemia), early salicylate toxicity, acute asthma (prior to exhaustion), high altitude.
- Chronic: Fully compensated ([HCO3-] falls 4–5 mmol/L per 10 mmHg PaCO2 drop). Chronic liver failure / hepatic cirrhosis, pregnancy (progesterone-mediated respiratory stimulation), prolonged mechanical hyperventilation.

Test Your Knowledge

A 24-year-old woman is brought to the emergency department after ingesting an unknown quantity of an over-the-counter medication 4 hours earlier following an argument. She is tachypnoeic, agitated, diaphoretic, and complains of nausea, epigastric discomfort, and loud bilateral ringing in her ears (tinnitus). On examination, her respiratory rate is 32 breaths/minute, pulse is 108 bpm regular, and blood pressure is 114/72 mmHg. Chest auscultation reveals clear lung fields bilaterally. Arterial blood gas on room air reveals: pH 7.48, PaCO2 3.2 kPa (24 mmHg), PaO2 13.5 kPa (101 mmHg), bicarbonate 16 mmol/L, base excess -8 mmol/L. Simultaneous serum biochemistry demonstrates: sodium 140 mmol/L, potassium 4.0 mmol/L, chloride 100 mmol/L, urea 5.2 mmol/L, creatinine 78 mcmol/L, glucose 6.2 mmol/L. What is the primary acid-base disturbance pattern present in this patient?

Pure acute respiratory alkalosis with physiological renal compensation

Pure normal anion gap metabolic acidosis with respiratory compensation

Compensated primary metabolic acidosis

Mixed primary respiratory alkalosis and high anion gap metabolic acidosis

Mixed primary respiratory acidosis and metabolic alkalosis

Test Your Knowledge

A 62-year-old man with a history of hypertension managed with amlodipine presents to the medical assessment unit with a 4-day history of profuse, watery, non-bloody diarrhoea and generalised weakness following a suspected gastroenteritis outbreak. On physical examination, he appears lethargic with dry mucous membranes, collapsed peripheral veins, blood pressure 96/60 mmHg, and a heart rate of 104 bpm. Cardiorespiratory examination is normal. Laboratory investigations reveal: serum sodium 136 mmol/L, potassium 3.1 mmol/L, chloride 114 mmol/L, bicarbonate 14 mmol/L, urea 12.4 mmol/L, creatinine 138 mcmol/L. Arterial blood gas demonstrates: pH 7.28, PaCO2 3.9 kPa (29 mmHg), PaO2 12.8 kPa, bicarbonate 14 mmol/L. Simultaneous spot urine electrolytes demonstrate: urinary sodium 32 mmol/L, urinary potassium 22 mmol/L, and urinary chloride 78 mmol/L. What is the calculated urine anion gap and the corresponding pathophysiological mechanism of his acid-base disorder?

Urine anion gap -24 mmol/L; gastrointestinal bicarbonate loss with intact renal ammonium excretion

Urine anion gap +24 mmol/L; defective distal renal tubular hydrogen ion secretion

Urine anion gap -24 mmol/L; impaired proximal renal tubular bicarbonate reabsorption

Urine anion gap +10 mmol/L; accumulation of unmeasured ketoacids in the renal collecting duct

Urine anion gap 0 mmol/L; dilutional hyperchloraemic acidosis secondary to fluid shift

Test Your Knowledge

A 49-year-old woman with a history of peptic ulcer disease presents to the acute medical unit with persistent, intractable non-bilious vomiting for 5 days secondary to suspected gastric outlet obstruction. On examination, she is moderately dehydrated with poor skin turgor, a dry furrowed tongue, blood pressure 102/64 mmHg, and heart rate 98 bpm. Abdominal examination reveals upper abdominal distension with a prominent succession splash. An arterial blood gas on room air demonstrates: pH 7.54, PaCO2 6.4 kPa (48 mmHg), PaO2 11.2 kPa, bicarbonate 38 mmol/L, base excess +13 mmol/L. Simultaneous serum biochemistry shows: sodium 137 mmol/L, potassium 2.8 mmol/L, chloride 86 mmol/L, urea 11.2 mmol/L, creatinine 118 mcmol/L. Spot urinary electrolytes reveal: urinary sodium 28 mmol/L, urinary potassium 36 mmol/L, and urinary chloride 8 mmol/L. What is the definitive initial therapeutic intervention to correct this patient's acid-base and electrolyte disturbance?

Intravenous infusion of 5% dextrose in water (D5W) at 125 mL/hour

Oral acetazolamide 250 mg twice daily

Intravenous sodium bicarbonate 8.4% infusion

Intravenous infusion of 0.1 M hydrochloric acid via a central venous catheter

Intravenous 0.9% sodium chloride infusion with potassium chloride supplementation

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16.1 Stroke Classification, Brainstem Syndromes & Hyperacute Reperfusion

Neurology: Cerebrovascular, Headache & Demyelinating Disease

MRCP

1MRCP(UK) Part 1: Exam Overview, Blueprint & Strategy

2Clinical Sciences: Cellular, Genetic & Molecular Medicine

3Clinical Sciences: Anatomy, Physiology & Immunology

4Clinical Sciences: Statistics, Epidemiology & Trial Design

5Clinical Pharmacology, Therapeutics & Toxicology

6Cardiology: Coronary Artery Disease & Heart Failure

7Cardiology: Arrhythmias, Valvular & Pericardial Disease

8Respiratory Medicine: Airway & Parenchymal Lung Disease

9Respiratory Medicine: Vascular, Pleural & Sleep Disorders

10Gastroenterology: Luminal Gastrointestinal Disease

11Gastroenterology: Liver, Biliary & Pancreatic Disease

12Endocrinology & Diabetes: Diabetes & Thyroid

13Endocrinology & Diabetes: Adrenal, Pituitary & Calcium

14Renal Medicine: AKI, Glomerular & Tubulointerstitial Disease

15Renal Medicine: Fluid, Electrolytes & Acid-Base Balance

16Neurology: Cerebrovascular, Headache & Demyelinating Disease

17Neurology: Epilepsy, Movement Disorders & Neuromuscular Disease

18Rheumatology: Inflammatory Arthritis & Connective Tissue Disease

19Rheumatology: Systemic Vasculitis & Crystal Arthropathy

20Infectious Diseases & Tropical Medicine

21Haematology: Anaemias & Red Cell Disorders

22Haematology: Malignancy, Coagulation & Transfusion Medicine

23Psychiatry in General Medicine

24Geriatric Medicine

25Dermatology

26Oncology & Palliative Medicine

27Medical Ophthalmology

MRCP(UK) Part 1

15.3 Acid-Base Disorders & Blood Gas Analysis

Key Takeaways

1. Systematic 5-Step ABG Interpretation Protocol

Step 1: Examine the pH and [H+]

Step 2: Determine the Primary Process

Step 3: Assess Physiological Compensation

Step 4: Calculate the Serum Anion Gap (AG)

Step 5: Delta Gap / Delta-Delta Analysis

2. High Anion Gap Metabolic Acidosis (HAGMA): The GOLD MARK Mnemonic

3. Normal Anion Gap Metabolic Acidosis (NAGMA) & Urine Anion Gap

The Urine Anion Gap (UAG)

Summary of Renal Tubular Acidosis (RTA)

4. Metabolic Alkalosis: Saline-Responsive vs Saline-Resistant

Saline-Responsive Metabolic Alkalosis (Urinary Chloride <20 mmol/L)

Saline-Resistant Metabolic Alkalosis (Urinary Chloride >20 mmol/L)

5. Respiratory Acidosis vs. Respiratory Alkalosis