Acute changes in cardiopulmonary blood volume during upright exercise stress testing in patients with coronary heart disease.

SUMMARY The effect of exercise-induced myocardial ischemia on cardiopulmonary blood volume was evaluated in patients with coronary artery disease during upright exercise stress testing. Regional pulmonary and cardiac blood volumes were monitored with a multicrystal positron camera positioned over the chest during maximal exercise on a bicycle ergometer. Inhaled carbon monoxide (< 10 ppm) labeled with cyclotron-produced carbon-il ("C) (half-life 20.3 minutes) was used to label the blood with "IC-carboxyhemoglobin. Regional "'C activity was measured over the heart and lungs during rest, exercise and recovery periods, and blood volume was calculated from regional "IC activity compared with the specific activity of a reference venous blood specimen. For patients developing angina pectoris and electrocardiographic ST-segment depression (ischemic group, n = 9), blood volume increased 18.7 ± 6.3% (SEM) (p < 0.01) over the upper lung fields and 15.4 ± 6.8% (p < 0.05) over the lower lung fields at peak exercise. Conversely, for patients without angina or ST-segment depression at peak exercise (nonischemic group, n = 7), the regional pulmonary blood volume was unchanged over both upper and lower lung fields. The cardiac blood volume rose 6.1 ± 2.6% (p < 0.05) for the former group of patients and declined 10.6 ± 5.7% (p < 0.05) for the latter group at peak exercise. Coronary arteriography revealed double-or triple-vessel coronary disease in all patients in the ischemic group and normal coronary arteries or single-vessel disease in the nonischemic group. These data indicate that an ischemic response to exercise stress testing is associated with a transient rise in pulmonary and cardiac blood volume, which may be due to ischemia-induced left ventricular dysfunction. DECREASED MYOCARDIAL perfusion causes reduced contraction of the left ventricle within seconds after the onset of ischemia.1 2 Exercise-and pacing induced angina pectoris are associated with the prompt development of regional left ventricular asyn-ergy,3, 4reduced left ventricular ejection fraction,' elevated left ventricular end-diastolic pressure,68 reduced left ventricular compliance9' 10 and a fall in cardiac output." The sudden rise in left ventricular end-diastolic and pulmonary venous pressures is reflected as a rise in pulmonary capillary wedge pressure.12 13 This elevation should result in a corresponding pressure increase in pulmonary blood volume. Previous attempts to determine the effect of angina pectoris on pulmonary blood volume have been limited by the lack of noninvasive techniques for continuously monitoring this parameter. The most widely applied technique for measuring pulmonary blood volume is the indicator-520 dilution …