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THE DETERIORATIVE EFFECT OF MYOCARDIAL INFARCTION UPON PHYSIOLOGICAL INDICES OF WORK CAPACITY
Author(s) -
Benestad Arne M.
Publication year - 1972
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.1972.tb00013.x
Subject(s) - medicine , cardiology , hyperventilation , heart rate , ventilation (architecture) , myocardial infarction , stroke volume , vo2 max , anaerobic exercise , respiratory minute volume , cardiac output , anesthesia , physical therapy , hemodynamics , blood pressure , respiratory system , mechanical engineering , engineering
The present study has been performed in order to investigate the deteriorative effect of myocardial infarction upon physiological indices of work capacity. Sixteen male patients, averaging 52 years of age, have been tested 12 weeks after the acute episode by means of bicycle ergometry in the upright position. Each patient exercised at several loads, starting at low levels and increasing the loading until the criteria of maximality were reached. All patients tolerated well the strain of heavy muscular exercise. Their maximal oxygen uptake averaged 2.05 1/min or 26.8 ml/min/kg b.wt., which is about 25% lower than average for healthy men of corresponding age. The highest recorded heart rate averaged 163 beats/min, which is lower than for healthy people. A low maximal oxygen pulse indicates reduced stroke volume. These findings suggest a reduction of the pumping capacity of the heart. The arterial systolic B.P. showed a tendency to levelling‐off at high levels of work rate, which suggests a reduced contractile power of the cardiac muscle. In 13 patients ECG changes indicating impaired oxygenation of the myocardium occurred when the work level exceeded two‐thirds of their maximal aerobic power. At lower levels of submaximal exercise the physiological response pattern of the cardiacs was similar to that of normals, except for a tendency to higher pulmonary ventilation. The cause of this hyperventilation, which was related to an increased tidal volume, is suggested to be a change of the ventilation/perfusion rate brought about by the heart infarction.