From the Guidelines
Hyperoxemia can lead to several harmful consequences, including oxygen toxicity, vasoconstriction, and absorption atelectasis, emphasizing the need for careful oxygen titration to maintain saturation at appropriate levels, such as 88-92% for COPD patients and 94-98% for others, as recommended by the BTS guideline for oxygen use in adults in healthcare and emergency settings 1. The primary effects of hyperoxemia include damage to lung tissue through the formation of reactive oxygen species, which can cause acute lung injury and present as acute respiratory distress syndrome with inflammation and alveolar damage. Hyperoxemia also causes vasoconstriction in cerebral, coronary, and systemic circulation, potentially reducing blood flow to vital organs despite high oxygen levels. Prolonged exposure to hyperoxemia can lead to absorption atelectasis as nitrogen is washed out of alveoli, causing lung collapse. Additionally, hyperoxemia can suppress respiratory drive in patients with chronic CO2 retention, potentially causing respiratory acidosis, and cellular damage extends beyond the lungs to affect the central nervous system, causing seizures and other neurological symptoms. Some specific conditions, such as myocardial infarction and acute coronary syndromes, stroke, and poisoning with paraquat or bleomycin, may be harmed by supplemental oxygen, and the benefits and harms of oxygen therapy in these cases are unknown or may cause increased infarct size, as noted in the BTS guideline 1 and the European Resuscitation Council and European Society of Intensive Care Medicine 2015 guidelines for post-resuscitation care 1. Key aspects of management include:
- Using the lowest effective FiO2
- Regular arterial blood gas monitoring to prevent complications
- Targeting saturation levels based on individual patient conditions, such as 88-92% for COPD patients and 94-98% for others, to minimize the risk of hyperoxemia and its associated harmful consequences, as supported by the European Resuscitation Council and European Society of Intensive Care Medicine 2015 guidelines for post-resuscitation care 1.
From the Research
Consequences of Hyperoxemia
- Hyperoxemia may induce harmful hemodynamic effects, including peripheral and coronary vasoconstriction, and direct cellular toxicity through the production of reactive oxygen species 2
- Emerging evidence has shown that hyperoxia is associated with adverse clinical outcomes, such as increased mortality and worse functional outcome in patients admitted to the ICU after cardiac arrest 2, 3
- Arterial hyperoxemia during the first hour after return of spontaneous circulation (ROSC) may cause increased oxidative damage, increased neuronal death, and worse neurologic function 3
- Hyperoxemia is defined as PaO2 > 125 mmHg, and the SpO2 cut-off values with the lowest risk of hyperoxemia were determined as above 96% 4
- The adverse effects of long-term oxygen therapy, such as reduced mobility and social stigma, also need to be considered 5
Management of Hyperoxemia
- A conservative approach to supplemental oxygen therapy (SOT) can reduce side effects compared with higher concentration oxygen regimens 5
- Automated oxygen administration devices might reduce dyspnea during exercise and COPD exacerbations, and may help to optimize SOT 5
- Current recommendations for SOT need to be revised to focus on patients who respond best and benefit most from this therapy 5
- The aim of oxygen therapy should be to maintain the partial arterial oxygen pressure (PaO2) in a physiological range, and the SpO2 level marking an increased risk of arterial hypoxemia is not substantially different in acutely ill versus stable patients 4
- An SpO2 target of 95% maximizes the likelihood of maintaining PaO2 in the physiological range in acutely ill patients receiving supplemental oxygen 4