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Here is a comprehensive guide to Arterial Blood Gas (ABG) — Acid-Base Disorders.
Normal ABG Values
| Parameter | Normal Value | Range |
|---|---|---|
| pH | 7.40 | 7.35–7.45 |
| PaCO₂ | 40 mmHg | 38–42 mmHg |
| PaO₂ | 100 mmHg | 75–100 mmHg |
| HCO₃⁻ | 24 mEq/L | 22–26 mEq/L |
Stepwise ABG Interpretation
Step 1 — Determine Acidemia vs. Alkalemia (pH)
- pH < 7.35 → Acidemia
- pH > 7.45 → Alkalemia
Step 2 — Identify the Primary Process
| pH | PaCO₂ | HCO₃⁻ | Disorder |
|---|---|---|---|
| ↓ | ↑ | — | Respiratory Acidosis |
| ↓ | ↓ | ↓ | Metabolic Acidosis |
| ↑ | ↓ | — | Respiratory Alkalosis |
| ↑ | ↑ | ↑ | Metabolic Alkalosis |
Key rule: In respiratory disorders, PaCO₂ moves opposite to pH. In metabolic disorders, PaCO₂ moves in the same direction as pH (as compensation).
Step 3 — Assess Compensation
Compensation never fully corrects pH (except sometimes in respiratory alkalosis).
| Primary Disorder | Compensation Formula |
|---|---|
| Metabolic acidosis | Expected PaCO₂ = 1.5 × [HCO₃⁻] + 8 ± 2 (Winter's Formula) |
| Metabolic alkalosis | Expected PaCO₂ = 0.7 × [HCO₃⁻] + 20 ± 5 |
| Acute respiratory acidosis | ↑ HCO₃⁻ = ΔPaCO₂ ÷ 10 |
| Chronic respiratory acidosis | ↑ HCO₃⁻ = 4 × (ΔPaCO₂ ÷ 10) |
| Acute respiratory alkalosis | ↓ HCO₃⁻ = 2 × (ΔPaCO₂ ÷ 10) |
| Chronic respiratory alkalosis | ↓ HCO₃⁻ = 5 × (ΔPaCO₂ ÷ 10) |
If compensation is more or less than expected → mixed disorder.
Step 4 — Calculate the Anion Gap (AG)
AG = Na⁺ − (Cl⁻ + HCO₃⁻)
Normal = 8–12 mEq/L (or up to 16 if using older norms)
Correct for albumin (hypoalbuminemia lowers AG):
Corrected AG = Measured AG + 2.5 × (4 − [albumin g/dL])
High AG metabolic acidosis causes (MUDPILES / GOLDMARK):
- Methanol, Uremia, DKA, Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates
Normal AG (hyperchloremic) metabolic acidosis — check urine anion gap:
- Urine AG positive (renal cause): RTA, renal failure
- Urine AG negative (GI cause): diarrhea, fistula
Step 5 — Delta-Delta Ratio (Δ/Δ) — if AG is elevated
Δ/Δ = (Measured AG − 12) ÷ (24 − Measured HCO₃⁻)
| Δ/Δ Ratio | Interpretation |
|---|---|
| < 1.0 | High-AG acidosis + concurrent non-AG metabolic acidosis |
| 1.0–2.0 | Pure high-AG metabolic acidosis |
| > 2.0 | High-AG acidosis + concurrent metabolic alkalosis (or chronic respiratory acidosis) |
Step 6 — Base Excess / Base Deficit
Base excess (BE): Amount of base needed to titrate 1L of blood to pH 7.4 at 37°C.
- Normal: −2 to +2
- Positive (> +4) → metabolic alkalosis
- Negative (< −4, i.e., base deficit) → metabolic acidosis
Calculating base deficit from ABG:
For every ΔPaCO₂ of 10, pH changes 0.08 in the opposite direction. Base deficit = (Expected pH − Measured pH) × 2/3 × 150.
Quick Summary Table
| Disorder | pH | PaCO₂ | HCO₃⁻ | Common Causes |
|---|---|---|---|---|
| Respiratory acidosis | ↓ | ↑ | ↑ (compensatory) | COPD, opioids, obesity hypoventilation, NMJ disease |
| Respiratory alkalosis | ↑ | ↓ | ↓ (compensatory) | Anxiety, PE, sepsis, altitude, pregnancy |
| Metabolic acidosis | ↓ | ↓ (compensatory) | ↓ | DKA, lactic acidosis, renal failure, diarrhea |
| Metabolic alkalosis | ↑ | ↑ (compensatory) | ↑ | Vomiting, diuretics, hyperaldosteronism, antacid overuse |
Clinical Example
84-year-old on IV morphine, rib fractures, AKI → pH 7.18, PaCO₂ 73, HCO₃⁻ 28, normal AG:
- pH < 7.35 → acidemia
- PaCO₂ ↑ → primary respiratory acidosis
- HCO₃⁻ only mildly elevated → no significant metabolic compensation → acute process
- Normal anion gap
- Diagnosis: Acute respiratory acidosis from opioid-induced respiratory depression → treat with naloxone
Sources: Current Surgical Therapy 14e, p. 1608 | Barash Clinical Anesthesia 9e, p. 1158–1161
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Here is the deep-dive on ABG acid-base disorders.
ABG Acid-Base Disorders — In Depth
The Henderson-Hasselbalch Framework
All acid-base physiology rests on:
pH = pKa + log([HCO₃⁻] / α·PCO₂)
The Kassirer-Bleich approximation is more practical at the bedside:
[H⁺] = 24 × PaCO₂ / [HCO₃⁻]
With [H⁺] in nmol/L. Key reference points: [H⁺] of 25 ≈ pH 7.6, 40 ≈ pH 7.4, 63 ≈ pH 7.2.
This equation shows the two control levers: the lungs (PaCO₂) and the kidneys (HCO₃⁻). These are independent and compensatory — each responds to disturbances in the other.
The Acid-Base Nomogram
This nomogram plots pH (x-axis) against arterial plasma [HCO₃⁻] (y-axis) with diagonal PCO₂ isobars. Each shaded region represents the expected range for a simple disorder with compensation. If an ABG plots outside the confidence band for its primary disorder → mixed disorder present.
1. Metabolic Acidosis
Pathophysiology
Three mechanisms:
- Excess endogenous acid production (lactic acid, ketoacids) — overwhelms renal excretion
- Loss of HCO₃⁻ (diarrhea, RTA) — kidneys not at fault, but bicarbonate is gone
- Impaired renal acid excretion (CKD, RTA) — ammoniagenesis fails
Respiratory compensation (hyperventilation) begins within minutes; full renal compensation takes 3–5 days. Winter's formula predicts the expected PaCO₂:
Expected PaCO₂ = 1.5 × [HCO₃⁻] + 8 ± 2
Kussmaul respiration (slow, deep breathing) is the classic sign — minimizes dead-space and maximizes CO₂ elimination.
Classification by Anion Gap
AG = Na⁺ − (Cl⁻ + HCO₃⁻) | Normal: 8–12 mEq/L
Always correct for albumin: each 1 g/dL drop in albumin below 4 g/dL → AG underestimated by ~2.5 mEq/L.
High-AG Metabolic Acidosis
Mnemonic — GOLDMARK:
- G — Glycols (ethylene glycol → oxalate; propylene glycol)
- O — 5-Oxoproline (pyroglutamic acid — chronic paracetamol users, malnourished)
- L — L-lactic acidosis (sepsis, shock, mesenteric ischaemia, metformin)
- D — D-lactic acidosis (short bowel, bacterial overgrowth)
- M — Methanol (→ formic acid; causes bilateral putaminal necrosis)
- A — Aspirin/salicylates (mixed HAGMA + respiratory alkalosis due to CNS stimulation)
- R — Renal failure (GFR <20 mL/min; sulfate, phosphate, lactate accumulate)
- K — Ketoacidosis (DKA, alcoholic, starvation)
Special points:
- Toxic alcohols: Initially raise the osmolar gap (measured − calculated osmolality >10). As the alcohol is metabolised to acid, osmolar gap falls and AG rises. So early on, both gaps may be elevated.
- Salicylate OD: Produces a mixed picture — primary respiratory alkalosis (direct medullary stimulation) + HAGMA (lactic acid, ketone formation). Treat with IV NaHCO₃ to alkalinise urine and trap salicylate ions.
- DKA: May present as HAGMA or normal-AG (hyperchloremic) acidosis, depending on hydration status and how fast ketones are renally excreted.
Normal-AG (Hyperchloremic) Metabolic Acidosis
HCO₃⁻ replaced by Cl⁻, so AG unchanged. Causes:
| Category | Examples |
|---|---|
| GI HCO₃⁻ loss | Diarrhea (most common), ileostomy, pancreatic/biliary fistula, cholestyramine |
| Renal HCO₃⁻ loss | Proximal RTA (Type 2), carbonic anhydrase inhibitors (acetazolamide) |
| Impaired renal H⁺ excretion | Distal RTA (Type 1), Type 4 RTA (hypoaldosteronism), early CKD (GFR 20–50) |
| Iatrogenic | Large-volume normal saline infusion (dilutional), ammonium chloride, TPN amino acids |
| Urologic diversion | Uretero-sigmoidostomy (ileum/colon Cl⁻/HCO₃⁻ exchangers absorb urine Cl⁻ → lose HCO₃⁻) |
Differentiating GI vs. renal cause → Urine Anion Gap (UAG):
UAG = Urine (Na⁺ + K⁺) − Urine Cl⁻
| UAG | Interpretation |
|---|---|
| Negative (< 0) | Renal NH₄⁺ excretion is intact → GI cause (diarrhea) |
| Positive (> +20) | Kidneys failing to excrete NH₄⁺ → RTA or renal failure |
Note: UAG is unreliable in HAGMA because unmeasured anions (lactate, ketones) are present in urine instead of NH₄⁺.
RTA Subtypes
| Type | Defect | Urine pH | K⁺ | Cause |
|---|---|---|---|---|
| 1 (Distal) | H⁺ secretion failure in collecting duct | >5.5 | ↓ (hypokalemia) | Sjögren's, amphotericin, medullary sponge kidney |
| 2 (Proximal) | HCO₃⁻ reabsorption failure | <5.5 (when acidotic) | ↓ | Fanconi syndrome, acetazolamide, multiple myeloma |
| 4 | Hypoaldosteronism → ↓ NH₄⁺ excretion | <5.5 | ↑ (hyperkalemia) | DM nephropathy, NSAIDs, ACEi/ARBs, heparin |
Treatment of Metabolic Acidosis
- Priority is treating the underlying cause (insulin for DKA, fluids/vasopressors for lactic acidosis, naloxone for opioid OD)
- NaHCO₃ is indicated for:
- Chronic hyperchloremic acidosis (RTA) — prevents bone catabolism
- pH <7.1 with severe hyperkalemia (shifts K⁺ intracellularly)
- Salicylate/tricyclic OD (urinary alkalinisation)
- Severe metabolic acidosis with concurrent respiratory acidosis (mixed)
- NaHCO₃ is NOT clearly beneficial in DKA, lactic acidosis due to sepsis/shock — risks include paradoxical intracellular acidosis (CO₂ generated crosses membranes faster than HCO₃⁻), left-shift of O₂–Hb dissociation curve, decreased ionised Ca²⁺
2. Metabolic Alkalosis
Pathophysiology
Occurs when H⁺ is lost or HCO₃⁻ is gained. The kidney normally excretes excess HCO₃⁻ easily — alkalosis is maintained only when the kidney's ability to excrete HCO₃⁻ is impaired. The key perpetuating factor is usually volume depletion (activates RAAS → Na⁺/H⁺ exchange keeps reclaiming HCO₃⁻) or hypokalemia (drives H⁺ into cells, increases renal H⁺ secretion).
Compensatory hypoventilation raises PaCO₂ by ~0.6–0.7 mmHg per 1 mEq/L rise in HCO₃⁻. Compensation rarely exceeds PaCO₂ of 55 mmHg (hypoxia drives ventilation back up).
Classification: Chloride-Responsive vs. Chloride-Resistant
| Chloride-Responsive | Chloride-Resistant | |
|---|---|---|
| Urine Cl⁻ | < 20 mEq/L | > 40 mEq/L |
| Mechanism | Volume/Cl⁻ depletion → RAAS activation | Mineralocorticoid excess or severe K⁺ depletion |
| Causes | Vomiting/NG suction, diuretics (remote), posthypercapnia, diarrhoea with Cl⁻ loss, villous adenoma | Hyperaldosteronism, Cushing's, Bartter/Gitelman syndrome, exogenous steroids, renal artery stenosis, severe hypokalemia, milk-alkali syndrome |
| Treatment | IV 0.9% saline + KCl → kidneys excrete HCO₃⁻ | Treat underlying cause; spironolactone, K⁺ repletion; acetazolamide; HCl infusion (central line) for refractory cases |
Posthypercapnia alkalosis: When chronic respiratory acidosis (↑ PaCO₂ → ↑ HCO₃⁻ compensation) is rapidly corrected (e.g., intubation of a COPD patient), PaCO₂ normalises but the HCO₃⁻ takes days to correct → metabolic alkalosis appears.
Clinical Features of Severe Alkalosis
- Neuromuscular: Tetany, muscle cramps, weakness (from ↓ ionised Ca²⁺, hypokalaemia)
- Cardiac: Arrhythmias (especially with concurrent hypokalaemia)
- Respiratory: Hypoventilation (compensation) — can worsen respiratory failure
- CNS: Confusion, obtundation
3. Respiratory Acidosis
Pathophysiology
Any cause of alveolar hypoventilation → CO₂ retention → ↑ PaCO₂ → acidaemia.
Buffering timeline:
- Acute (<24 h): Cellular buffers (proteins, phosphate) raise HCO₃⁻ by ~1 mEq/L per 10 mmHg ↑ PaCO₂
- Chronic (>24–48 h): Renal adaptation raises HCO₃⁻ by ~4 mEq/L per 10 mmHg ↑ PaCO₂ (max ~38 mEq/L)
Causes (Organised by Level)
| Level | Examples |
|---|---|
| Respiratory centre depression | Opioids, benzodiazepines, anaesthetic agents, head trauma, brainstem stroke, obesity hypoventilation, sleep apnoea |
| Neuromuscular | GBS, MG, ALS, diaphragm paralysis, hypophosphataemia, hypokalaemia, botulism |
| Airways/lungs | Severe asthma, COPD exacerbation, ARDS (late), pneumonia, pulmonary oedema |
| Mechanical ventilation | Inadequate tidal volume/rate, high PEEP causing dead space, ventilator circuit leak |
| Thoracic wall | Flail chest, kyphoscoliosis, morbid obesity |
Clinical Features
| Severity | Features |
|---|---|
| Mild/chronic | Sleep disturbance, daytime somnolence, personality change, memory loss |
| Moderate | Anxiety, confusion, asterixis, tremor, headache, papilloedema (cerebral vasodilation from CO₂) |
| Severe/acute | Psychosis, seizures, coma |
Cerebral vasodilation from hypercapnia can mimic raised ICP with papilloedema and focal signs.
Permissive Hypercapnia
Intentional strategy in ARDS/severe asthma — accept ↑ PaCO₂ to use lung-protective low tidal volumes (6 mL/kg IBW). Target: pH ≥7.20–7.25. Caution: Worsens if concurrent metabolic acidosis (lactic acidosis) is present. Short-term NaHCO₃ may be used if pH is critically low.
Treatment
- Remove the cause (naloxone for opioids, bronchodilators for asthma/COPD, NIV/intubation)
- NIV (BiPAP) is first-line for COPD exacerbations and obesity hypoventilation
- Caution when correcting chronic respiratory acidosis rapidly — if renal HCO₃⁻ retention has occurred, normalising PaCO₂ quickly leaves behind a metabolic alkalosis (posthypercapnic alkalosis)
4. Respiratory Alkalosis
Pathophysiology
Alveolar hyperventilation → CO₂ blown off → ↓ PaCO₂ → alkalemia.
Compensation:
- Acute: HCO₃⁻ falls ~2 mEq/L per 10 mmHg ↓ PaCO₂ (cellular buffering)
- Chronic (>2–6 h → days): Kidneys reduce NH₄⁺/titratable acid excretion, decrease HCO₃⁻ reabsorption → HCO₃⁻ falls ~4–5 mEq/L per 10 mmHg ↓ PaCO₂
Chronic respiratory alkalosis is the only disorder that can be fully compensated (pH may normalise).
Causes
| Category | Examples |
|---|---|
| CNS stimulation | Anxiety/panic (hyperventilation syndrome), pain, fever, CVA, subarachnoid haemorrhage |
| Hypoxia-driven | PE, pneumonia, high altitude, severe anaemia, heart failure |
| Drugs | Salicylates (early, before HAGMA develops), progesterone (pregnancy), theophylline, catecholamines |
| Hepatic | Hepatic encephalopathy (direct CNS stimulation) |
| Sepsis | Early sepsis/SIRS — most common cause in ICU |
| Mechanical ventilation | Over-ventilation — always check settings |
Key clinical pearl: In early sepsis, the ABG typically shows a respiratory alkalosis due to the hyperdynamic phase. As sepsis progresses → lactic acidosis (HAGMA) superimposes → the pH may be falsely normalised despite two concurrent disorders.
Clinical Features
- Acute: Circumoral and peripheral paraesthesias, light-headedness, carpopedal spasm (↓ ionised Ca²⁺ from pH change), dizziness, rarely seizures
- Cardiac: Arrhythmias (coronary vasospasm from alkalosis + left-shift of O₂–Hb curve → myocardial ischaemia)
- Hypocapnia itself reduces cerebral blood flow — CNS signs even without hypoxia
Treatment
Treat the underlying cause. For panic-attack hyperventilation: paper-bag rebreathing raises PaCO₂. In mechanically ventilated patients: reduce RR or tidal volume.
5. Mixed Acid-Base Disorders
A mixed disorder is present when two or more primary disorders coexist simultaneously. Clues:
- pH and PaCO₂ move in the same direction (normally they oppose each other)
- Compensation is more or less than expected per formula
- ABG plots outside the nomogram confidence band
- Clinical history strongly suggests multiple concurrent processes
Common Mixed Disorders
| Combination | Clinical Scenario | ABG Pattern |
|---|---|---|
| Met. acidosis + Resp. alkalosis | Sepsis, salicylate OD, hepatic failure | pH may be normal; PaCO₂ lower than predicted by Winter's |
| Met. acidosis + Resp. acidosis | Cardiac arrest, severe COPD + renal failure, over-sedation in sepsis | pH very low; PaCO₂ paradoxically high |
| Met. alkalosis + Resp. acidosis | COPD on diuretics; NG suction + chronic hypoventilation | HCO₃⁻ very high; pH may be near-normal |
| Met. alkalosis + Resp. alkalosis | Liver cirrhosis + vomiting | pH very high; PaCO₂ lower than expected |
| HAGMA + Met. alkalosis | DKA + vomiting; AKI + nasogastric drainage | AG elevated but HCO₃⁻ near normal → Δ/Δ >2 |
| HAGMA + Normal-AG acidosis | DKA + diarrhoea; toluene toxicity; uremia + saline resuscitation | Δ/Δ <1; HCO₃⁻ falls more than AG rises |
| Triple disorder | Alcoholic ketoacidosis + vomiting + hepatic dysfunction | AG acidosis + met. alkalosis + resp. alkalosis |
The Delta-Delta Ratio Revisited
Δ/Δ = (AG − 12) ÷ (24 − HCO₃⁻)
This compares how much the AG has risen vs. how much HCO₃⁻ has fallen. In a pure HAGMA, every extra anion titrates exactly one HCO₃⁻, so Δ/Δ = 1.
| Δ/Δ | Meaning |
|---|---|
| < 1.0 | HCO₃⁻ has fallen more than AG rose → concurrent non-AG acidosis |
| 1.0–2.0 | Pure HAGMA |
| > 2.0 | HCO₃⁻ hasn't fallen as much as expected → concurrent met. alkalosis OR chronic resp. acidosis with renal HCO₃⁻ retention |
Nuance: In lactic acidosis, Δ/Δ often >1 because lactate can be redistributed intracellularly. In DKA, Δ/Δ is often <1 because excreted ketone salts represent lost potential HCO₃⁻.
6. ABG in Key Clinical Contexts
DKA
- Classic: HAGMA (AG >12), low HCO₃⁻, low pH, compensatory low PaCO₂
- Can be normo-AG if well-hydrated and excreting ketones rapidly
- Hyperkalemia at presentation despite total body K⁺ depletion (insulin deficiency + acidosis shifts K⁺ out of cells)
- During treatment: As ketones clear → watch for postherapeutic alkalosis (ketones metabolised to HCO₃⁻)
COPD Exacerbation
- Chronic resp. acidosis: ↑ PaCO₂, ↑ HCO₃⁻ (compensated), near-normal pH
- Acute-on-chronic: ↑ PaCO₂ further, pH drops — look for inadequate HCO₃⁻ rise for degree of hypercapnia
- Post-NIV/intubation: Rapid CO₂ correction → posthypercapnic metabolic alkalosis
Sepsis
- Early: Respiratory alkalosis (hyperventilation)
- Late: HAGMA from lactic acidosis (type A — impaired tissue O₂ delivery)
- Often mixed: resp. alkalosis + met. acidosis → pH deceptively near-normal
- Metformin accumulates in sepsis/AKI → can cause Type B lactic acidosis
Renal Failure
- GFR 20–50 mL/min: Hyperchloremic non-AG acidosis (impaired NH₄⁺ excretion)
- GFR <20 mL/min: HAGMA (sulfate, phosphate, organic acids accumulate)
- Chronic metabolic acidosis accelerates bone demineralisation and muscle catabolism
Pregnancy
- Chronic respiratory alkalosis (progesterone stimulates ventilation)
- Normal ABG in pregnancy: pH ~7.44, PaCO₂ ~30 mmHg, HCO₃⁻ ~20 mEq/L
- What looks like "acidosis" in a non-pregnant patient may be normal in pregnancy
7. Physiologic Effects of Severe pH Derangements
| Effect | Acidemia (pH <7.2) | Alkalemia (pH >7.6) |
|---|---|---|
| Cardiac | ↓ contractility, ↓ CO, vasodilation, ventricular arrhythmias | Arrhythmias, coronary vasospasm |
| Respiratory | Hyperventilation (met. acidosis), fatigue | Hypoventilation |
| Electrolytes | Hyperkalemia (H⁺/K⁺ exchange), ↑ ionised Ca²⁺ | Hypokalemia, ↓ ionised Ca²⁺ (tetany) |
| O₂ delivery | Right-shift O₂–Hb curve (↑ O₂ off-loading) | Left-shift O₂–Hb curve (↓ O₂ off-loading) |
| CNS | Confusion → coma | Seizures, altered consciousness |
| Enzyme function | Denaturation, impaired coagulation cascade | Reduced enzyme efficiency |
Sources:
- Brenner and Rector's The Kidney, pp. 707–715
- Murray & Nadel's Textbook of Respiratory Medicine, pp. 274–281
- Barash Clinical Anesthesia 9e, pp. 1153–1161
- Harrison's Principles of Internal Medicine 22e, pp. 1465–1471
- Fishman's Pulmonary Diseases and Disorders, pp. 3228–3236
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