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Biomedical subjects

H Benson

Publications and source records attributed to H Benson.

At least 109 records · Page 6Linked to original sources
PubMed1970

Hemodynamic effects of pneumonia. I. Normal and hypodynamic responses.

Since an excessive mortality from pneumonia persists in spite of antimicrobial therapy, the hemodynamics during and after the acute phase of pneumonia were studied in 17 patients. None of the patients had clinical heart disease and all had normal venous pressures. The arteriovenous oxygen difference was used to assess the adequacy of the circulation to meet peripheral tissue perfusion, and a spectrum of arteriovenous oxygen differences was noted. In 11 patients, tissue perfusion was considered adequate because the arteriovenous oxygen difference did not exceed 5.5 vol%. In six patients, the arteriovenous oxygen difference was greater than 5.5 vol% and these six patients differed hemodynamically from the others. In these six patients during the acute phase of pneumonia, cardiac output was decreased, and total peripheral resistance and hematocrit were increased. When five patients with varying arteriovenous oxygen difference were studied during exercise in the acute phase, cardiac output increased while venous pressure remained unchanged. Arteriovenous oxygen difference in these five exercising patients increased in all, but most markedly in those with an initially widened arteriovenous oxygen difference. The inadequate response to pneumonia is most consistent with depressed myocardial function, but the possibility of decreased intravascular volume as a contributory factor could not be excluded.

Adult↗
PubMed1970

Hemodynamic effects of pneumonia. II. Expansion of plasma volume.

Previous work has demonstrated that approximately one-third of patients with pneumonia have a hypodynamic circulatory response. This response is characterized by an abnormally wide arteriovenous oxygen difference, a low cardiac output, increased peripheral resistance, and an increased hematocrit. This state was found to abate in convalescence. In an attempt to elucidate the pathogenesis of this hypodynamic state, nine additional patients were studied hemodynamically during the acute phase of pneumonia before and during acute expansion of blood volume by low molecular weight dextran (seven patients) or normal saline (two patients). Five patients were restudied before and during acute blood volume expansion in convalescence. Three patients with pneumonia had a normal arteriovenous oxygen difference (< 5.5 vol%), and six patients were hypodynamic in that their arteriovenous oxygen differences were greater than 5.5 vol%. With expansion of blood volume in the acute phase of pneumonia, all patients showed an increase in cardiac output, a decrease in arteriovenous oxygen difference, and a decrease in peripheral vascular resistance; however, the percentage change in the hypodynamic patients was not as great as occurred in the patients with normal hemodynamics nor as great as occurred when restudied in convalescence. Likewise, all patients had a normal or near normal hemodynamic profile in convalescence. In addition, ventricular function in the acute phase of pneumonia was depressed. The findings suggest that the hypodynamic state associated with acute pneumonia is due to depressed myocardial contractility to which relative hypovolemia may contribute.

Acute Disease↗