Oxygenation And Oxygen Therapy

pediagenosis    October 09, 2019    Organ , Respiratory , science    Comment   

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 (S_ao₂) is measured with a pulse oximeter, and partial pressure of oxygen (P_ao₂) by blood gas analysis. SaO₂ should be measured regularly in all breathless patients. However, both P_ao₂ and S_ao₂ 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 (P_v - 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 P_ao₂, S_ao₂ and P_vo₂.

Oxygen therapy

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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 P_aco₂ 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 P_aco₂ 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 (P_aco₂ >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 V_A/Q mis-match and shunt (Chapters 13 and 14). Simple postural changes may improve oxygenation. Sitting upright optimizes V_A/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).