Supplemental oxygen is used excessively in cardiac patients and may expose these patients to significant periods of hyperoxia. While use of oxygen is often necessary to treat hypoxia, its excessive use could lead to worse outcomes, according to a viewpoint published in the Sept. 21 issue of the Journal of the American College of Cardiology.
“Over the past century, multiple studies lacking the precision of today’s advanced technology provided conflicting data on the effects of oxygen therapy in normoxic cardiac patients,” wrote Raman Moradkhan, MD, and Lawrence I. Sinoway, MD, of the Pennsylvania State University College of Medicine in Hershey, Pa. In addition, they said that no previous trials have confirmed the benefits of oxygen usage; however, its use has become widespread in cardiac patients.
Currently, the American College of Cardiology and American Heart Association task force recommend oxygen use for the correction of arterial oxygen desaturation (Class I) and for all patients with unstable angina and non-STEMI and uncomplicated STEMI within six hours after presentation (Class II).
According to the authors, these recommendations are based on the fact that increasing arterial oxygen tension decreases acute ischemic injury and infarct area and that some patients with uncomplicated MI have arterial hypoxemia due to fluid retention. But, Moradkhan and Sinoway said that evidence supporting these recommendations is limited.
A recent study that evaluated coronary blood velocity (CBV), along with coronary vascular resistance (CVR) in seven patients by means of ultrasound, showed that hyperoxia decreased CBV by 15 percent and increased CVR by 20 percent. The authors said that this indicated “a direct vasoconstrictor effect of hyperoxia on the coronary circulation not mediated through autonomic reflexes.”
The researchers said that multiple studies have supported the fact that hyperoxia leads to the generation of reactive oxygen species, which can decrease the bioavailability of nitric oxide and results in vasoconstriction.
Additionally, Moradkhan and Sinoway found that:
- K+ATP channels in hyperoxia-induced vasoconstriction can play an important role in regulating coronary artery blood flow at rest and during hypoxia and ischemia;
- Hyperoxia may affect the release of angiotensin II with subsequent changes in endothelin-1 levels, which can increase vascular tone; and
- Hyperoxia can increase the production of vasoconstrictor 20-HETE, which plays a role in myogenic regulation.
The authors noted that excessive oxygen use may be related to a physician's attempt to maintain oxyhemoglobin saturations that are close to 100 percent; however, because of the excessive use, patients are exposed to hyperoxia.
Moradkhan and Sinoway speculated that oxygen's increased use is because medical staff do not recognize that oxygen is a vasoactive substance. Additionally, they said that when transcutaneous blood oxyhemoglobin saturation approaches 100 percent, blood oxygen tensions have a tendency to increase and often go undetected. Lastly, oxygen tension is often not adequately monitored.
“Although the use of oxygen is clearly appropriate and advisable to treat hypoxia, we hypothesize that excessive use of supplemental oxygen in normoxic cardiac patients could potentially lead to worse outcomes in a number of patients.
“We propose that such [clinical] studies are imperative to delineate the precise role of oxygen therapy in these conditions. In the interim, the potential physiologic ramifications of such therapy should be considered," the authors concluded.