Hyperventilation tests have been mainly used in clinical practice as a provocative test for coronary artery vasospasm in patients with suspected or documented vasospastic angina [1–4]. The rationale for the use of hyperventilation tests for this purpose is based upon the demonstration that, in susceptible patients, hyperventilation may trigger a vasospasm of a major epicardial coronary artery associated with chest pain and ischemic electrocardiographic changes similar to those observed during spontaneous anginal attacks . Different pathophysiological mechanisms can be operative in the induction of coronary artery spasm by hyperventilation. Decreased plasma hydrogen ion concentration leading to metabolic alkalosis produced by prolonged, vigorous overbreathing has been considered the most important mechanism by which hyperventilation can trigger coronary artery spasm [I]. The increase in arterial blood pH reaches the peak at the end of hyperventilation, while ST segment elevation usually develops during the recovery phase early after the end of the test, when arterial pH is already decreasing toward baseline but is still significantly elevated compared to basal values .
KeywordsDioxide Depression Ischemia Cardiol Ergonovine
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