Why the study?
Does increased heart rate induced by atropine affect arterial and venous oxygen saturation in patients with heart disease?
Does increased heart rate induced by atropine affect arterial and venous oxygen saturation in patients with heart disease?
In patients with heart disease, tachycardia induced by atropine does not decrease arterial oxygen saturation, suggesting that rapid heart rate alone does not cause arterial anoxemia.
Tachycardia alone warrants no change in oxygenation concerns for heart disease; single case report leaves open rhythm- and valve-specific effects.
The present study was undertaken in an attempt to contribute to the solution of the problem of the effect of rapid heart rate on the oxygen satu'ration of the arterial blood. In 1921 Barcroft, Bock and Roughton (1) reported that they had found normal saturation of the arterial blood in a patient during an attack of paroxysmal-tachycardia. Carter and Stewart (2) later reported a case in which there was a marked decrease in the oxygen saturation of the arterial blood during attacks of paroxysmal auricular tachycardia, and Dieuaide (3) had the same experience in a patient during attacks of paroxysmal. ventricular tachycardia. Meakins (4) found normal saturation of the arterial blood with oxygen during regular and irregular tachycardia artificially induced in dogs. These dogs were under paraldehyde anesthesia and since the chests were open they were kept alive by artificial respiration. The author has had occasion to repeat these experiments under the same conditions and has confirmed these obser- vations (5). More recently, Stewart, Crawford and Hastings (6) in their study of the effect of rapid heart rate on the blood flow in normal unanesthetized dogs found that the oxygen saturation of the arterial blood remained unchanged during rapid auricular fibrillation and was usually unchanged during regular tachycardia.
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Harold J. Stewart (1926) studied this question.
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