Transesophageal echocardiographic monitoring of preoperative acute hypervolemic hemodilution

Preoperative acute hypervolemic hemodilution is used in anesthesia to reduce the loss of blood cells during intraoperative bleeding. Indications for use of the technique might be broadened if it can be shown to be safe in older as well as younger patients. Few data are available describing heart function in humans subjected to hypervolemic hemodilution.

Nineteen anesthetized Jehovah's Witnesses (ages 22-70 yr) without evidence of heart disease had hypervolemic hemodilution before surgery in three stages, each consisting of an infusion of 500 ml dextran 40 (50 g/l) and 500 ml Ringer's lactate over a 10-min period. After each stage, the size and function of the left ventricle were recorded by transesophageal cross-sectional echocardiography in the short-axis view. Simultaneously heart rate, arterial blood pressure, pulmonary arterial and wedge pressures and cardiac output were recorded, to compare the echocardiographic and hemodynamic data.

No complications occurred. Hypervolemic hemodilution resulted in an increased cardiac output by increasing the stroke volume from 48 ml in basal conditions to 67, 71, and 72 ml over the three stages, whereas heart rate did not increase. There was an initial increase in end-diastolic volume of the left ventricle, as assessed from the cross-sectional end-diastolic area from 12.9 to 15.5, 16.6, and 16.9 cm2 followed by a decrease in the in cross-sectional end-systolic area from 6.3 to 6.8, 6.0, and 5.7 cm2. The increase in wedge pressures (from 5.9 to 12.4, 17.9, and 22.6 mmHg) did not lead to progressive cardiac dilation. There was a curvilinear relation between wedge pressure and cross-sectional end-diastolic area. Stroke volume did not decrease, nor did cross-sectional end-systolic area increase; instead, a decrease in end-systolic area was a common observation.

The described regimen of acute hypervolemic hemodilution is well tolerated during anesthesia by patients without heart disease and does not lead to cardiac failure. It leads to an increase in stroke volume that is generated initially from an increase in end-diastolic volume, followed in many patients by a decrease in end-systolic volume, the mechanism of which is as yet unclear.