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162<br />

Cardiac chest pain<br />

KALANI OLMSTED AND DEBORAH B. DIERCKS<br />

n Agents<br />

n Oxygen<br />

n Beta-blockers<br />

n Nitrates<br />

n Opioids<br />

n Benzodiazepines<br />

n Evidence<br />

Though oxygen has long been used for patients with acute coronary syn-<br />

drome (ACS), its use for ACS has become somewhat controversial.<br />

<strong>Int</strong>uitively, it seems that increasing blood oxygenation would decrease both<br />

ischemia and pain. However, studies are contradictory, and some suggest<br />

supplemental oxygen may exacerbate ischemia by decreasing coronary perfusion.<br />

1 Coronary perfusion decrease could be a result of oxygen’s hemodynamic<br />

effects of decreased stroke volume and cardiac output (accompanied<br />

by increased vascular resistance). 1<br />

The American College of Cardiology/American Heart Association (ACC/<br />

AHA) guidelines recommend supplemental oxygen for peripheral SpO2 less<br />

than 90%. 2,3 <strong>This</strong> may be a reasonable strategy but acute care clinicians are<br />

(appropriately) uncomfortable with values in the low 90s SpO2 in patients with<br />

ACS. The extensive use of short-term oxygen therapy in ACS, with rarely<br />

reported adverse effects and frequent cases of anecdotal benefit, supports oxygen<br />

administration as a benign intervention for cardiac patients with pain and<br />

subnormalperipheralpulseoximetry(SpO2). 4 Oxygen administration may, in<br />

fact, be associated with a significant “placebo” effect in reducing anginal pain. 1<br />

<strong>Int</strong>uitively, the short-term use of oxygen in the highest-risk ACS group –<br />

those with refractory pain and the need for thrombolysis or cardiac catheterization<br />

– is an indicated intervention. Accordingly, the ACC/AHA guidelines

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