CO Poisoning Warning SpO₂ will read falsely normal (carboxyhaemoglobin is read as oxyhaemoglobin by standard pulse oximeters). Diagnosis requires co-oximetry on ABG sample. Treat with high-flow 100% O₂.
5-Step Systematic ABG Interpretation
Is the pH normal, acidaemic, or alkalaemic?Normal 7.35–7.45. pH <7.35 = acidaemia; pH >7.45 = alkalaemia. Even if pH is in normal range, a disorder may still be present (compensated).
Look at PaCO₂ — does it explain the pH?If pH ↓ and CO₂ ↑ = respiratory acidosis is primary. If pH ↑ and CO₂ ↓ = respiratory alkalosis is primary. CO₂ same direction as pH change = metabolic primary.
Look at HCO₃⁻ — does it explain the pH?If pH ↓ and HCO₃⁻ ↓ = metabolic acidosis is primary. If pH ↑ and HCO₃⁻ ↑ = metabolic alkalosis is primary.
Is there compensation?Lungs compensate for metabolic disorders (fast). Kidneys compensate for respiratory disorders (slow, 3–5 days). Compensation never fully corrects pH (except metabolic alkalosis sometimes).
Is there a mixed disorder?Compare expected vs actual compensation using formulas. If compensation is inappropriate (too much or too little) = mixed acid-base disorder.
Respiratory Acidosis
↓ pH
↑ CO₂
Causes
COPD exacerbation (Type 2 failure)
Opiate / sedative overdose
Neuromuscular weakness (MG, GBS)
Severe asthma (exhaustion)
Chest wall deformity / obesity hypoventilation
Central respiratory depression
Compensation (renal — takes 3–5 days)
Kidneys retain HCO₃⁻ → ↑ HCO₃⁻
Acute: HCO₃⁻ ↑ 1 mmol/L per 10 mmHg ↑ CO₂
Chronic: HCO₃⁻ ↑ 3.5 mmol/L per 10 mmHg ↑ CO₂
Respiratory Alkalosis
↑ pH
↓ CO₂
Causes
Anxiety / hyperventilation
Pain
Pulmonary embolism (early)
Early salicylate (aspirin) poisoning
Mechanical ventilation (over-ventilation)
Liver failure / pregnancy
Altitude, fever, sepsis
Compensation (renal)
Kidneys excrete HCO₃⁻ → ↓ HCO₃⁻
Acute: HCO₃⁻ ↓ 2 mmol/L per 10 mmHg ↓ CO₂
Chronic: HCO₃⁻ ↓ 5 mmol/L per 10 mmHg ↓ CO₂
Metabolic Acidosis — Anion Gap Analysis
↓ pH
↓ HCO₃⁻
Anion Gap = Na⁺ − (Cl⁻ + HCO₃⁻) | Normal: 8–12 mmol/L (up to 16 if albumin not corrected)
Discard / waste 3 mL first (dead space + diluted blood)
Collect sample into heparinised syringe
Flush line; ensure waveform returns
Clearly label sample as ARTERIAL
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NEVER inject medication via an arterial line. Intra-arterial injection of drugs (including potassium, antibiotics, anaesthetic agents) causes severe vasospasm and limb-threatening ischaemia. Label ALL arterial lines prominently with RED "ARTERIAL" tape. This is a critical patient safety issue and a common exam topic.
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Arterial vs Venous Differentiation Arterial blood is pulsatile, bright red, and flows under pressure. Venous blood is darker, non-pulsatile, and flows slowly. Always confirm placement with waveform before use. Mis-labelling arterial samples as venous (or vice versa) is a significant clinical error.
Capnography — ETCO₂ Monitoring
End-tidal CO₂ (ETCO₂) measures CO₂ at end of exhalation — approximates alveolar and (in normal lungs) arterial PaCO₂
Normal ETCO₂
3.5 – 5.0 kPa
35 – 45 mmHg
Normal Capnogram Phases
Phase I (A–B): Inspiratory baseline — dead space gas, CO₂ ≈ 0
Phase II (B–C): Upstroke — alveolar gas mixing with dead space, CO₂ rising
Phase III (C–D): Alveolar plateau — plateau of CO₂-rich alveolar gas; ETCO₂ read at peak D
Phase IV (D–E): Inspiratory downstroke — rapid fall to baseline
Elevated ETCO₂
Hypoventilation (↓ respiratory rate/depth)
↑ CO₂ production — sepsis, fever, MH
Rebreathing (exhausted soda lime, equipment fault)
Obstruction (bronchospasm — shark fin waveform)
Low ETCO₂
Hyperventilation
Poor circulation / cardiac arrest
PE (dead space ventilation — V/Q mismatch)
Oesophageal intubation (ETCO₂ ≈ 0)
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ETCO₂ During CPR ETCO₂ <1.3 kPa (10 mmHg) after 20 min CPR = poor prognosis. Sudden ↑ ETCO₂ during CPR = indicator of ROSC (return of spontaneous circulation).
Pulse Oximetry — Principles & Limitations
How it works
Uses two wavelengths of light (660 nm red; 940 nm infrared)
Oxyhaemoglobin and deoxyhaemoglobin absorb light differently
Pulsatile component (AC) separated from non-pulsatile (DC)
SpO₂ calculated from ratio of AC/DC at each wavelength
SpO₂ Targets by Condition
Condition
Target SpO₂
Most acutely unwell patients
94 – 98%
COPD / Type 2 RF risk
88 – 92%
Post-cardiac arrest
94 – 98% (avoid hyperoxia)
Preterm neonates
91 – 95%
Palliative / comfort
Guided by symptom relief
Limitations of Pulse Oximetry
Cause
Effect on SpO₂
Motion artefact
Falsely low / erratic readings
Peripheral vasoconstriction (hypothermia, shock)
Poor signal / falsely low
Nail varnish (blue, black, green)
Falsely low
Dark skin pigmentation
May overread SpO₂ by 2–4%
CO poisoning
Falsely NORMAL (COHb read as OxyHb)
Methaemoglobinaemia
Reads approx 85% regardless of true value
Severe anaemia (Hb <5 g/dL)
May be inaccurate
Jaundice
Minimal effect with modern devices
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GCC ICU Standard Practice In ventilated patients in GCC ICUs, both continuous SpO₂ AND continuous ETCO₂ monitoring are standard of care. ETCO₂ confirms endotracheal tube position and provides early warning of haemodynamic deterioration. Waveform capnography is mandatory for intubated patients per DHA/DOH standards.
GCC-Specific Clinical Context
High Burden Conditions in GCC
COPD / Asthma: High prevalence — smoking rates (especially male), sandstorm exposure (PM2.5/PM10), occupational exposures (construction, oil/gas). COPD Type 2 failure management is a core competency.
Diabetes (Type 2): Highest prevalence globally in Gulf states. DKA is the most common ABG emergency — metabolic acidosis with high anion gap.
Obesity: High rates of obesity hypoventilation syndrome (OHS) — Type 2 respiratory failure, polycythaemia.
Heat-related illness: Hyperventilation, respiratory alkalosis; lactic acidosis in severe heatstroke.
DKA ABG Profile
Parameter
Expected change
pH
↓ Low (<7.35, often <7.1 in severe)
PaCO₂
↓ Low (Kussmaul compensation)
HCO₃⁻
↓ Very low (<15 mmol/L)
Anion gap
↑ High (>12, often >20)
K⁺
Often ↑ (but total body K⁺ ↓)
Glucose
↑ >11 mmol/L (usually >14)
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Kussmaul Breathing Deep, sighing, rapid respirations — respiratory compensation for metabolic acidosis in DKA. Not to be confused with Cheyne-Stokes (CNS/HF) or Biot's (brainstem) breathing.
⚙ Interactive ABG Interpreter
Enter blood gas values to receive a complete systematic interpretation, compensation analysis, and clinical guidance.
DHA / DOH / SCFHS Exam Practice — 10 MCQs
Click "Show Answer" after selecting your option. These question styles are representative of GCC licensing examinations.
1A patient has pH 7.28, PaCO₂ 7.8 kPa, HCO₃⁻ 28 mmol/L. What is the primary disorder?
A. Metabolic acidosis
B. Respiratory acidosis with metabolic compensation
C. Mixed respiratory and metabolic acidosis
D. Metabolic alkalosis
B. The pH is low (acidaemia). PaCO₂ is elevated — this drives the acidosis (respiratory acidosis). HCO₃⁻ is elevated at 28 mmol/L — this is renal compensation (not primary). The elevated HCO₃⁻ is consistent with chronic respiratory acidosis compensation.
2In COPD, why should supplemental oxygen be titrated to achieve SpO₂ 88–92% rather than higher?
A. To prevent pulmonary oedema from oxygen toxicity
B. High-flow O₂ abolishes hypoxic respiratory drive, causing hypoventilation and CO₂ retention
C. Higher O₂ levels cause paradoxical bronchospasm in COPD
D. To reduce the risk of oxygen-induced pneumonia
B. Chronic hypercapnia in COPD blunts the normal CO₂ drive to breathe. The hypoxic drive becomes the primary stimulus. Excessive O₂ removes this drive, leading to hypoventilation, CO₂ retention, respiratory acidosis, and CO₂ narcosis.
3A 34-year-old with poorly controlled Type 2 diabetes presents confused. ABG: pH 7.08, PaCO₂ 2.8 kPa, HCO₃⁻ 6 mmol/L, Na 138, Cl 98. What is the anion gap?
A. 12 mmol/L (normal)
B. 34 mmol/L (high anion gap)
C. 8 mmol/L (normal)
D. 22 mmol/L (borderline)
B. Anion gap = Na − (Cl + HCO₃⁻) = 138 − (98 + 6) = 34 mmol/L. This is severely elevated, consistent with DKA (ketoacidosis). The very low pH, low HCO₃⁻, and low PaCO₂ (Kussmaul compensation) confirm severe metabolic acidosis with appropriate respiratory compensation.
4A patient's SpO₂ reads 97% but blood gas reveals PaO₂ of 8.5 kPa and the patient appears cyanosed. What is the most likely cause?
A. Calibration error in the ABG analyser
B. Venous blood was taken instead of arterial
C. Carbon monoxide poisoning (carboxyhaemoglobinaemia)
D. Methaemoglobinaemia
C. Carboxyhaemoglobin (COHb) absorbs light at similar wavelengths to oxyhaemoglobin, causing pulse oximetry to read falsely normal. ABG with co-oximetry is required. Methaemoglobinaemia would read ~85%, not 97%.
5During CPR, the ETCO₂ suddenly rises from 0.8 kPa to 4.2 kPa. What does this indicate?
A. Improved chest compression quality only
B. Return of spontaneous circulation (ROSC)
C. Oesophageal intubation
D. CO₂ accumulation from inadequate ventilation
B. A sudden, sustained rise in ETCO₂ during CPR is a strong indicator of ROSC. When the heart restarts, pulmonary blood flow returns, washing out CO₂ that has accumulated in the tissues. ETCO₂ <1.3 kPa after 20 minutes of CPR is associated with poor prognosis.
6Modified Allen's test is performed before radial artery cannulation. The hand takes 18 seconds to regain colour after releasing the ulnar artery. What is the correct action?
A. Proceed with cannulation — 18 seconds is acceptable
B. Repeat the test 3 times before deciding
C. Do not proceed — inadequate collateral circulation; choose an alternative site
D. Perform the procedure but with extra care
C. Normal reperfusion is <7 seconds, indicating adequate ulnar collateral circulation. >15 seconds indicates poor collateral supply — proceeding risks hand ischaemia if radial artery thrombosis occurs. Use femoral, brachial, or dorsalis pedis as alternatives.
7A patient has pH 7.48, PaCO₂ 3.2 kPa, HCO₃⁻ 18 mmol/L. What is the most likely diagnosis?
A. Metabolic alkalosis with respiratory compensation
B. Acute respiratory alkalosis (hyperventilation)
C. Compensated metabolic acidosis
D. Mixed alkalosis
B. pH is high (alkalaemia). PaCO₂ is very low — this is the primary driver (respiratory alkalosis). HCO₃⁻ is slightly low at 18 — this represents early/partial renal compensation. The clinical picture suggests acute hyperventilation (anxiety, pain, PE, early sepsis).
8An arterial line waveform appears dampened with a rounded, blunted systolic peak. The patient's blood pressure reads 82/60 but they appear well with good peripheral perfusion. What is the FIRST action?
A. Administer a fluid bolus for presumed hypotension
B. Check the arterial line circuit — assess for clots, kinks, air, or loose connections
C. Call the doctor immediately for urgent review
D. Remove the arterial line and replace
B. A dampened waveform is a technical problem, not necessarily a patient problem. Causes include clots in the catheter, air bubbles, kinked tubing, or loose connections. Always troubleshoot the equipment before treating the patient. Perform a fast-flush test to assess dynamic response.
9According to the Berlin definition, a patient on PEEP 8 cmH₂O with bilateral infiltrates has PaO₂/FiO₂ ratio of 150 mmHg. How is their ARDS classified?
A. Mild ARDS
B. Moderate ARDS
C. Severe ARDS
D. Does not meet Berlin criteria
B. Berlin Definition severity: Mild = PF ratio 200–300; Moderate = 100–200; Severe = <100 mmHg (all on PEEP ≥5 cmH₂O). PF ratio 150 mmHg on PEEP 8 cmH₂O = Moderate ARDS. Associated mortality approximately 32%.
10A patient with metabolic acidosis has HCO₃⁻ of 12 mmol/L. Using Winter's formula, what is the expected PaCO₂ in mmHg if compensation is appropriate?
A. 26 mmHg
B. 26 ± 2 mmHg (range 24–28)
C. 35 mmHg (normal)
D. 18 mmHg
B. Winter's formula: Expected PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2 = (1.5 × 12) + 8 ± 2 = 18 + 8 ± 2 = 26 ± 2 mmHg (24–28 mmHg). If the measured PaCO₂ is within this range, compensation is appropriate (simple metabolic acidosis). If PaCO₂ is higher than expected = concomitant respiratory acidosis; lower = respiratory alkalosis.