The importance of referencing osteopathic medical literature.
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Biomedical subjects
Publications and source records attributed to D A DeBias.
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Sixty two patients were randomised to be seen by osteopathic physicians for palpation of the thoracic paravertebral soft tissue, T1-T8. Twenty five patients had clinically confirmed acute myocardial infarction. Of the remainder, 22 without known cardiovascular disease served as controls and 15 were placed in an excluded group because of diagnosed cardiovascular disease other than myocardial infarction. Observations were described in predetermined standard terminology. The control group was found to have a low incidence of palpable changes throughout the thoracic dorsum, and these changes were uniformly distributed from T1 to T8. Examination of the group with myocardial infarction disclosed a significantly higher incidence of soft tissue changes (increased firmness, warmth, ropiness, oedematous changes, heavy musculature), confined almost entirely to the upper four thoracic levels. The 15 patients who were excluded from the experimental group because they had various cardiovascular diseases other than myocardial infarction also showed significantly different changes on palpation compared with the group with myocardial infarction. These findings suggest that myocardial infarction is accompanied by characteristic paravertebral soft tissue changes which are readily detected by palpation.
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Since, in a previous study, inhalation of carbon monoxide resulted in demonstrable electrocardiographic effects on the myocardium, it was of interest to determine the effects of reduced hemoglobin oxygen content following carbon monoxide inhalation on the vulnerability of the heart to fibrillation. Normal monkeys and monkeys subjected to myocardial infarction were exposed to 100 ppm (115 mg/cu m) carbon monoxide for six hours, and the vulnerability of the heart to induced fibrillation was evaluated. The mean carboxyhemoglobin (COHb) concentration attained was 9.3%. The voltage required to induce fibrillation was highest for normal, air-breathing animals and lowest for infarcted animals inhaling carbon monoxide. Infarction alone and carbon monoxide alone each required significantly less voltage for fibrillation, and when the two were combined, the effects were additive.
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