Effects of acute and maintained isovolemic anemia on oxygen transport was studied during rest and exercise in normal males. Following 34% reduction in hemoglobin concentration (Hb), supine and standing Q rose acutely by 56% and 20%, respectively, but returned nearly to the control value by 10-14 days, producing a decrease in PVO2. Redistribution of blood flow appeared to compensate significantly for the decrease in systemic oxygen transport. 2,3-Diphosphoglycerate rose by 18%, in vivo PO2 at half-saturation of hemoglobin (P50) rose by approximately 2 mm over 7-9 days and probably afforded some compensation. The relationship between VO2 and external work intensity was independent of Hb. During exercise, Q/VO2 and VE/VO2 were increased in acute anemia, but PVO2, for a given VO2, decreased below control levels. After 10-14 days the relative increase in VE with exercise persisted; the increase in Q was less pronounced; and PVO2 was further decreased. With both acute and extablished anemia maximal exercise capacity and maximal VO2 (VO2 max) decreased in proportion to the Hb reduction.

The hemodynamic effect of varying heart rate was studied in eight patients with aortic regurgitation. At the subjects' resting sinus rhythm and at a higher heart rate induced with right atrial pacing, left ventricular and aortic pressures and Fick cardiac outputs (FCO) were measured, and left ventricular biplane angiocardiograms were performed. Left ventricular volumes and left ventricular minute flow (LVMF) were determined from the angiograms. Regurgitant flow was quantitated by subtracting the FCO from LVMF. Increased heart rate produced highly significant reductions in the left ventricular end-diastolic pressure (LVEDP), left ventricular end-diastolic volume, and stroke volume. End-diastolic circumferential stress (EDCS) and enddiastolic load (EDL) were abnormally high at resting sinus rhythm and were markedly decreased with increased heart rate. FCO increased, but no significant changes were observed in either the LVMF or the regurgitant flow per minute.Bradyeardia in aortic regurgitation may cause pulmonary congestion secondary to high LVEDP and may accelerate left ventricular dilatation secondary to markedly elevated EDCS and EDL. The possible benefits of preventing bradyeardia in aortic regurgitation by chronic demand pacing is currently being tested.

No abstract

No abstract