Oxygenation And Oxygen Therapy
Suff cient O2 must be delivered to the tissues to support metabolism, and the tissues must be able to utilize it. Tissue hypoxia can be caused by low arterial Po2 and therefore blood O2 content (hypoxaemia); inadequate tissue blood ﬂow (ischaemia, cardiac failure, emboli); low haemoglobin concentration (anaemia); abnormal oxygen dissociation curve (haemoglobinopathies, CO poisoning); and poisoning of intracellular oxygen usage (e.g. cyanide and sepsis). Tissue hypoxia occurs within 4 minutes of failure of any of these systems because tissue and lung O2 reserves are small. Clinical features are often non-specific including altered mental state, dyspnoea, hyperventilation, arrhythmias and hypotension (see Chapter 23). Anaemia and abnormal dissociation curves are discussed in Chapter 8.
Measuring tissue hypoxia
Arterial oxygen saturation (Sao2) is measured with a pulse oximeter, and partial pressure of oxygen (Pao2) by blood gas analysis. SaO2 should be measured regularly in all breathless patients. However, both Pao2 and Sao2 can be normal when tissue hypoxia is caused by low cardiac output states, anaemia and failure of tissue O2 use. In these circumstances, mixed venous oxygen partial pressure (Pv - o2), which is measured in blood taken from a pulmonary artery catheter, approx- imates to mean tissue Po2. However, severe hypoxia in a single organ (e.g. due to an arterial embolus) may be associated with a normal Pao2, Sao2 and Pvo2.
Given correctly O2 is a lifesaving drug, but it is often used without appropriate evaluation of potential benefit and side effects. Figure 43a lists indications for initiating O2 therapy, whereas Figure 43b lists potential risks. Immediate assessment of airways, breathing and circulation is essential to confir airway patency and good circulation. Figure 43c illustrates important features of O2 delivery systems. The aims of O2 therapy depend on the risk of developing type 2 (hyper- capnic, CO2 retaining) respiratory failure (Chapter 23):
In normal patients (low risk of type 2 respiratory failure) aim for an SaO2 of 94-98% (92-98% if >70 years), i.e. the plateau of the O2-haemoglobin dissociation curve; increasing PaO2 further has no impact on O2 delivery as little O2 is dissolved in plasma (Chapter 8).
In patients at risk of type 2 respiratory failure (e.g. COPD) target SaO2 should be 88-92% pending arterial blood gas (ABG) analysis. A higher SaO2 has few advantages but results in hypoventilation, hypercapnia and respiratory acidosis in patients dependent on hypoxic respiratory drive (Chapter 11).
Initial O2 dose and delivery method depends on cause of hypoxia:
High-dose supplemental oxygen (>60%) is delivered through a non-rebreathing, reservoir mask at 10-15 L/min (Fig. 43c(iii)). Indicating conditions include cardiac or respiratory arrest, shock, major trauma, sepsis, CO poisoning and critical illness. Once the patient is stable, the O2 dose is reduced to maintain an SaO2 of 92-98%. Seriously ill patients at risk of hypercapnic respiratory failure (HCRF) are initially treated with high-dose O2 pending ABG analysis.
Moderate-dose supplemental oxygen (40–60%) is given in serious illnesses (e.g. pneumonia) through nasal cannulae (2-6 L/min) or simple face masks (5-10 L/min), aiming for an SaO2 of 92-98% (Fig. 43c(i,ii)). A reservoir mask is substituted if this is not achieved. Low-dose (controlled) supplemental oxygen (24–28%) is delivered through a f xed performance Venturi mask (Fig. 43c(iv)). It is indicated in patients at risk of CO2 retaining, type 2 respiratory failure, including COPD, neuromuscular disease, chest wall disorders and cystic fibrosis Target SaO2 is 88-92% whilst awaiting ABG results. If Paco2 is normal, the SaO2 is adjusted to 92-98% (except in patients with previous type 2 respiratory failure) and ABG rechecked at 1 hour. A raised Paco2 and bicarbonate with normal pH suggest longstanding hypercapnia and type 2 respiratory failure (Chapter 10); the target SaO2 should therefore be 88-92% with repeat ABG at 1 hour. If the patient is hypercapnic (Paco2 >6 kPa) and acidotic (pH <7.35), non-invasive ventilation (NIV, Chapter 42) should be considered. Venturi masks are replaced with nasal cannulae (1-2 L/min) when the patient is stable. An O2 alert card and Venturi mask are issued to patients with previous type 2 respiratory failure to warn future emergency staff of the potential risk.
Oxygen therapy is of little benefi in 'normoxic' patients because the haemoglobin is fully saturated. Restoration of tissue blood flow is often more important in these cases. In myocardial infarction, drug overdoses, metabolic disorders, hyperventilation or during labour in non-hypoxic pregnant women, O2 therapy is of little value. It may actually be harmful in normoxic patients with strokes, paraquat poisoning or acid inhalation, and to the fetus in normoxic obstetric emergencies. However, in CO poisoning high-dose O2 is essential, despite a normal PaO2, to reduce the half-life of carboxyhaemoglobin (Chapter 8).
Stop oxygen therapy when the patient is clinically stable on low-dose O2 (e.g. 1-2 L/min) and SaO2 is within the desired range on two consecutive occasions. Monitor SaO2 for 5 minutes after stopping O2 and recheck at 1 hour.
Other techniques to improve oxygenation
1. Anaemia: Failure of tissue O2 delivery is best corrected by blood transfusion.
2. Block of airways by mucus and retention of secretions (e.g. cystic fibrosis Chapter 34) requires physiotherapy, mucolytic agents and occasionally bronchoscopy to remove blockages and improve alveolar ventilation.
3. Fluid restriction reduces alveolar oedema when alveolar permeabil-ity is increased (e.g. ARDS, Chapter 41).
4. Alveolar recruitment improves oxygenation by reducing VA/Q mis-match and shunt (Chapters 13 and 14). Simple postural changes may improve oxygenation. Sitting upright optimizes VA/Q matching in the alert patient. Regular turning and prone positioning improve secretion drainage and oxygenation in supine patients. Techniques that increase mean alveolar pressures (e.g. PEEP, CPAP and increased in- spiratory/expiratory ratio) also improve alveolar recruitment and oxygenation (Chapters 42).
5. Ventilatory support (e.g. NIV) improves oxygenation by correcting hypoventilation and associated hypercapnia (Chapters 9 and 42).