Oxygen for a CO2 Retainer
Mr K, aged 64, has a 45 pack-year smoking history, a chronic productive cough and worsening breathlessness. Spirometry gives FEV1/FVC = 0.51 and FEV1 = 38% of predicted. He has become drowsy and complains of morning headache. Arterial blood taken on room air: pH 7.34, PaCO2 8.1 kPa, PaO2 7.4 kPa, HCO3⁻ 31 mmol dm⁻³, Hb 172 g L⁻¹, haematocrit 0.54. Reference ranges: pH 7.35-7.45; PaCO2 4.7-6.0 kPa; PaO2 10.6-13.3 kPa; HCO3⁻ 22-26 mmol dm⁻³. A junior colleague suggests applying a 100% oxygen mask to correct the PaO2 rapidly. The district hospital has no blood gas analyser, and transfer to the regional hospital takes two hours by ambulance.
1. Interpret the blood gases and classify the disturbance. Is it acute or chronic, and what is the evidence?
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Step 1: the pH. 7.34 is below 7.35, so the patient is acidaemic; the primary problem is an acidosis.
Step 2: which acid. PaCO2 is 8.1 kPa, well above 6.0, so the acid is carbon dioxide: this is a respiratory acidosis. PaO2 of 7.4 kPa is well below 10.6, so there is also hypoxaemia, and because the CO2 is raised this is type II (hypercapnic) respiratory failure.
Step 3: compensation. HCO3⁻ is 31, above 26. The kidney has reabsorbed bicarbonate and excreted hydrogen ions, a process that takes days, so the raised bicarbonate is the compensatory response rather than a second, independent problem. The result is a chronic, partially compensated respiratory acidosis.
Step 4: why chronic? In an acute rise of PaCO2 of this size, bicarbonate would be near normal and pH would be far lower (around 7.15-7.20). A near-normal pH with a strikingly high bicarbonate can only be produced by renal compensation, so the hypercapnia has been present for a long time and is now decompensating, as the drowsiness and morning headache suggest.
Step 5: link to the spirometry. An FEV1/FVC ratio of 0.51 confirms airflow obstruction, and FEV1 at 38% of predicted makes it severe. The chronic sputum and smoking history are consistent with chronic obstructive pulmonary disease, with CO2 retention from alveolar hypoventilation and ventilation-perfusion mismatch. The drowsiness is a warning sign of CO2 narcosis, not a reason to sedate him.
2. Explain why a 100% oxygen mask may harm this patient, and state what should be done instead.
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The normal drive to breathe. Ventilation is driven mainly by central chemoreceptors in the medulla that respond to hydrogen ions in the cerebrospinal fluid, which reflect arterial CO2, with a smaller contribution from peripheral carotid and aortic chemoreceptors that respond to a fall in PaO2.
What happens in chronic CO2 retention. Bicarbonate is retained, including in the cerebrospinal fluid, so the central chemoreceptors are buffered and their response to CO2 is blunted. Ventilation in such patients depends unusually heavily on the peripheral chemoreceptors, that is, on a degree of hypoxaemia to drive breathing. Abolishing the hypoxaemia with 100% oxygen can remove that stimulus, hypoventilation follows, and PaCO2 rises further, driving the pH down and deepening the narcosis.
Two further mechanisms. First, hypoxic pulmonary vasoconstriction normally diverts blood away from poorly ventilated alveoli; a high inspired oxygen concentration reverses this, so blood is perfused through poorly ventilated units, worsening the shunt and the CO2 retention. Second, the Haldane effect: well-oxygenated haemoglobin carries less CO2, so oxygenating the blood releases CO2 into plasma and raises PaCO2. Absorption atelectasis and, over hours, oxygen toxicity are additional risks.
What to do. Oxygen is still needed, because hypoxaemia kills faster than hypercapnia, but it must be titrated: a fixed-performance Venturi mask at 24-28% aiming for a saturation of 88-92%, with blood gases (or at least oximetry and clinical review) after 30-60 minutes. Treat the exacerbation with bronchodilators, corticosteroids and antibiotics as indicated, consider non-invasive ventilation if the acidosis worsens, and arrange transfer once the patient is stabilised on controlled oxygen rather than sending him with an uncontrolled high-flow mask.
3. Explain why the haemoglobin and haematocrit are raised, calculate the effect on oxygen-carrying capacity, and judge whether the increase is beneficial.
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Why it is raised. Chronic hypoxaemia of the kidney is sensed by the peritubular interstitial cells, which release erythropoietin; this stimulates the bone marrow to increase red cell production, so Hb rises to 172 g L⁻¹ and haematocrit to 0.54. This is secondary polycythaemia, a response to the disease rather than an independent disorder.
The arithmetic. Oxygen-carrying capacity is about 1.34 mL O2 per gram of haemoglobin. At 172 g L⁻¹: 172 × 1.34 ≈ 230 mL O2 per litre of blood. At a typical 150 g L⁻¹: 150 × 1.34 ≈ 201 mL L⁻¹. That is an increase of about 29 mL L⁻¹, roughly 14%.
Why that gain is largely illusory. The gain only applies to the haemoglobin present; the limiting factor here is saturation. At PaO2 7.4 kPa, haemoglobin is only about 88-90% saturated, so much of the extra haemoglobin is not carrying oxygen anyway, and arterial oxygen content rises far less than 14%.
The cost. Blood viscosity rises steeply and non-linearly above a haematocrit of about 0.50. That increases resistance to flow, cardiac work and pulmonary vascular resistance, worsening the right heart strain that this man is already at risk of, and increases the risk of thrombosis and stroke. The extra red cells also increase the diffusing distance within the lung.
Judgement. The polycythaemia is a marker of how long and how severely he has been hypoxaemic, not a treatment. The intervention that improves survival is long-term oxygen therapy for at least 15 hours per day, which raises PaO2, suppresses erythropoietin and allows the haematocrit to fall. Routine venesection is not appropriate because it reduces oxygen delivery; a haematocrit of 0.54 in a smoker should also prompt consideration of an independent myeloproliferative cause if the hypoxaemia is corrected and the count does not fall.