There are clues to help you decide whether or not your patient may be prone to CO2 retention:
• Patients with chronic hypoxaemia develop compensatory responses - polycythaemia and pulmonary hypertension (or cor pulmonale). Look for these.
• Background history - what is the patient normally like and what medication is being taken? Are there any previous lung function tests?
• History of the acute episode.
• Analysis of admission arterial blood gases.
If your patient is young and normally fit and well you can be virtually certain that any rise in CO2 is due to a problem with ventilation and nothing to do with oxygen therapy. If the acute diagnosis is a drug overdose, head injury, neuromuscular weakness, or acute left ventricular failure, the high CO2 is due to a problem with ventilation. Note that patients with a background of COPD can also present with these problems. In terms of the history, a newly diagnosed patient with COPD who still goes hill-walking is less likely than a housebound patient on long-term oxygen therapy to have chronic hypoxaemia/hypercapnia. Analysis of the admission arterial blood gases can also give useful information. Both these patients have COPD:
• pH 7 36, PaCO2 9 0 kPa (65 3 mmHg), bicarbonate 35 mmol/l, BE +6, PaO2 6 0 kPa (46 mmHg)
• pH 725, PaCO2 80 kPa (653 mmHg), bicarbonate 26 mmol/l, BE - 2, PaO2 8 0 kPa (62 mmHg)
The first is from a patient who has a chronically high PaCO2 (because the pH is normal and the base excess is high). The hypoxaemia is also likely to be chronic. The second is from an acutely decompensated patient who is hypoxaemic and hypoperfused (because the base excess is low). This patient needs oxygen, assistance with ventilation and intravenous fluids. Non-invasive ventilation in COPD should be instituted early - as soon as the pH falls below 735 according to trials -because the further the degree of respiratory acidosis, the less the chances of recovery (see Chapter 4). Worsening respiratory acidosis may require intubation. In summary:
• The most common cause of hypercapnia is a problem with ventilation - this has nothing to do with oxygen therapy.
• In patients with COPD, use Venturi masks titrated to arterial blood gases and institute non-invasive ventilation early where indicated.
1. A 60-year-old lady arrives in the Emergency Department with breathlessness. She was given 12 litres per minute oxygen via a simple face mask by the paramedics. She is on inhalers for COPD, is a smoker, and a diabetic. She is clammy and has widespread crackles and wheeze in the lungs. The chest x ray film has an appearance consistent with severe left ventricular failure. Her blood gases show: pH 7-15, PaCO2 8-0 kPa (61-5 mmHg), PaO2 9-0 kPa (69-2 mmHg), bicarbonate 20 mmol/l, BE - 6. The attending doctor has taken the oxygen mask off because of "CO2 retention" by the time you arrive. The oxygen saturations were 95% and are now 85%. Blood pressure is 140/70 mmHg. Comment on her oxygen therapy.
2. A 50-year-old man arrives in the Medical Admissions Unit with breathlessness. He is an ex-miner, has COPD, and is on inhalers at home. His blood gases on 28% oxygen show: pH 7-4, PaCO2 8-5 kPa (65-3 mmHg), PaO2 8-5 kPa (65-3 mmHg), bicarbonate 38-4 mmol litre-1, BE + 7. A colleague asks you if he needs noninvasive ventilation because of his hypercapnia. What is your reply?
3. A 30-year-old patient on the chemotherapy ward becomes unwell with breathlessness. The nurses report oxygen saturations of 75%. When you go to the patient, you find the other observations are as follows: pulse 130 per minute, blood pressure 70/40 mmHg, respiratory rate 40 per minute, patient confused. Blood gases on air show: pH 7-1, PaCO2 3-0 kPa (23 mmHg), PaO2 11 kPa (115 mmHg), bicarbonate 6-8 mmol/l, BE - 20. The chest is clear. A chest x ray film is taken and is normal. Can you explain the oxygen saturations and the breathlessness?
4. A 50-year-old man is undergoing a urological procedure. As part of this, intravenous methylene blue is given. Shortly afterwards, the junior anaesthetist notices the patient's oxygen saturations drop suddenly to 70%. All the equipment seems to be working normally. Worried that the patient has had some kind of embolism, he calls his senior. What is the explanation?
5. A 45-year-old man arrives unconscious in the Emergency Department. There is no history available apart from the fact that he was found collapsed in his car by passers-by. On examination he is unresponsive, pulse 90 per minute, blood pressure 130/60 mmHg, oxygen saturations 98% on 15 litres per minute oxygen via a reservoir bag mask. His ECG shows widespread ST depression and his arterial blood gases show: pH 7-25, PaCO2 6-0 kPa (46 mmHg), PaO2 7-5 kPa (57-6 mmHg), bicarbonate 19-4 mmol/l, BE - 10. His full blood count is normal. What is the explanation for the discrepancy in the SaO2 and PaO2?
6. A 25-year-old man with no past medical history was found on the floor at home having taken a mixed overdose of benzodiazepines and tricyclic antidepressant tablets. He is drowsy (Glasgow Coma Score is 8) and he has probably aspirated, because there is right upper lobe consolidation on the chest x ray film. He arrives hypothermic (34°C) and arterial blood gases on 15 litres per minute via a reservoir bag mask show: pH 7-2, PaCO2 9.-5 kPa (73 mmHg), PaO2
12-0 kPa (92-3 mmHg), bicarbonate 27-3 mmol/l, BE + 2. His blood pressure is 80/50 mmHg and his pulse is 120 per minute. The attending doctor changes his oxygen to a 28% Venturi mask because of his high CO2 and repeat blood gases show: pH 7-2, PaCO2 9-0 kPa (69-2 mmHg), PaO2 6-0 kPa (46-1 mmHg), bicarbonate 26 mmol/l, BE +1. What would your management be?
Self-assessment - discussion
1. This patient has COPD, but:
• the problem is severe acute left ventricular failure (LVF);
• acute hypoxaemia will aggravate cardiac ischaemia;
• other aspects of the history and examination may give clues as to whether or not she is likely to have severe COPD.
The arterial blood gases show a mixed respiratory and metabolic acidosis with relative hypoxaemia. Ventilatory failure owing to LVF is the main reason for the high PaCO2 and needs treatment as soon as possible. Initial treatment should concentrate on A, B, C. Medical treatment for left ventricular failure is required. Intubation is indicated if there is no improvement. Non-invasive continuous positive airway pressure (CPAP) may be tried first in an ICU setting. The patient should not be hypoxaemic.
2. No. His pH is normal. His PaCO2 is normally high (he has a high standard bicarbonate and BE to have fully compensated for his chronic respiratory acidosis). He should stay on a Venturi mask whilst unwell.
3. The main reason why this patient's oxygen saturations are so low is hypoperfusion. The PaO2 is normal on air - this makes pulmonary embolism (PE) unlikely in someone so unwell (cancer and chemotherapy are two independent risk factors for PE). This patient has circulatory shock as illustrated by the low blood pressure and severe metabolic acidosis seen on the arterial blood gases. Shocked patients breathe faster because of circulatory hypoxia and metabolic acidosis. The history and examination will tell you whether or not this shock is due to bleeding (Are the platelets very low?) or severe sepsis (Is the white cell count very low?). Patients with septic shock do not always have the classical warm peripheries and bounding pulses - they can be peripherally vasoconstricted. Treatment priorities are A, B (including high concentration oxygen therapy), and C - the patient needs fluid. Oxygen delivery can be optimised by correcting any fluid deficit and improving cardiac output. Severe anaemia may require blood transfusion.
4. Methylene blue in the circulation affects oxygen saturation measurement. The apparently low saturations return to normal within a few minutes. The junior anaesthetist did the right thing: he checked the airway (tube position), breathing (listened to the chest and checked the ventilator settings), and circulation (measured blood pressure and pulse) before asking for advice.
5. The arterial blood gases show a metabolic acidosis with hypoxaemia. The PaCO2 is at the upper limit of normal. It should be low in a metabolic acidosis, indicating a relative respiratory acidosis as well. Treatment priorities in this patient are as follows: securing the airway and administering the highest concentration of oxygen possible, assessing and treating breathing problems, and correcting any circulation problems. There is a discrepancy between the SaO2 of 98% and the arterial blood gas result, which shows a PaO2 of 7-5 kPa (57-6 mmHg). Tied in with the history and ischaemic-looking ECG, the explanation for this is carbon monoxide (CO) poisoning. CO poisoning produces carboxyhaemoglobin seen by the pulse oximeter as oxyhaemoglobin causing an overestimation of saturations. CO poisoning is the commonest cause of death by poisoning in the UK. Mortality is especially high in those with preexisting atherosclerosis. Toxicity is not just due to COHb formation. Free radicals, platelet activating factors and cytochrome AA3 formation also play a part. Loss of CO from the body is a slow process at normal atmospheric pressure and oxygen concentration (21%). It takes 4-5 hours for the concentration of CO to fall to half its original value (Table 2.2). CO removal is increased by increasing the oxygen concentration or by placing the victim in a hyperbaric chamber. This increases the amount of oxygen in the blood, forcing off CO.
Table 2.2 Half life of CO depending on conditions
Oxygen concentration Half life of CO (minutes)
Room air (21%) 240-300 15 litres/min reservoir bag mask (80%) 80-100
Intubated and ventilated 50-70
(with 100% oxygen)
Hyperbaric chamber 20-25 (100% oxygen at 3 atmospheres)
There is debate as to whether treatment with hyperbaric oxygen is superior to ventilation with 100% oxygen on intensive care. Five randomised trials to date disagree. Therefore a pragmatic approach is recommended:
• any history of unconsciousness
• neurological or psychiatric features at the time of examination
• pregnancy (because the fetal COHb curve is shifted to the left of the mother's)
• ECG changes are all features that lead to hyperbaric oxygen being considered -but the risks of transporting critically ill patients to a hyperbaric unit also needs to be taken into account. Ventilation with 100% oxygen is an acceptable alternative, and treatment with high concentrations of oxygen should continue for a minimum of 12 hours.
6. This is a 25-year-old man with no previous medical problems. He does not have chronic hypoxaemia. He will not "retain CO2" - he has a problem with ventilation. The arterial blood gases show an acute respiratory acidosis with a lower PaO2 than expected. He has a reduced conscious level so his airway needs to be secured. He needs a high concentration of oxygen (that is, 15 litres per minute via a reservoir bag mask) until he is intubated. He has several reasons to have a problem with ventilation - reduced conscious level, aspiration pneumonia, and respiratory depressant drugs. With regards to circulation, he needs volume expansion with warmed fluids. The combination of cardiac toxins he has taken with superimposed hypoxaemia and hypoperfusion could lead to cardiac arrest. Sodium bicarbonate infusion is indicated in severe tricyclic poisoning (see Chapter 9). Flumazenil (a benzodiazepine antidote) is not advised when significant amounts of tricyclic antidepressants have also been taken as it reduces the fit threshold. It is worth measuring creatinine kinase levels in this case as rhabdomyolysis (from lying on the floor for a long time) will affect fluid management.
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