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Rapid dextran infusion in essential hypertension
Insights
Hypertensive patients show a steeper increase in cardiac output with fluid volume expansion compared to controls. This is due to reduced vascular compliance in hypertension, impacting hemodynamic responses.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
Background:
- Sustained essential hypertension is a significant cardiovascular risk factor.
- Understanding hemodynamic responses to volume expansion is crucial for managing hypertensive patients.
Purpose of the Study:
- To investigate hemodynamic parameter changes after rapid dextran infusion in hypertensive and normotensive men.
- To compare the volume expansion response between patients with sustained essential hypertension and healthy controls.
Main Methods:
- Studied 34 men (17 hypertensive, 17 normotensive controls) before and after rapid dextran infusion.
- Measured central venous pressure (CVP), cardiac output (CO), and stroke volume.
- Calculated indices of volume expansion, including ratios of changes in CO, CVP, and volume.
Main Results:
- Dextran infusion significantly increased CVP, CO, and stroke volume in both groups (p < 0.001).
- Hypertensives exhibited a significantly greater percent change in stroke volume (p < 0.001) and a higher CO/volume change ratio (p < 0.025).
- Hypertensives showed a significantly reduced volume/CVP change ratio (p < 0.001), negatively correlated with CO/stroke volume changes (r = -0.75).
Conclusions:
- The relationship between cardiac output and blood volume is steeper in hypertensive individuals.
- This steeper slope is attributed to reduced effective vascular compliance in hypertension, leading to greater CO elevation per unit volume increase.
Abstract:
Hemodynamic parameters were studied before and after rapid dextran infusion in 34 men including 17 patients with sustained essential hypertension and 17 normotensive controls. In both groups of patients, dextran infusion induced a significant increase (p less than 0.001) in central venous pressure (CVP), cardiac output (CO), and stroke volume. The percent change in stroke volume was significantly higher in hypertensives (p less than 0.001) than in controls. Three indices of volume expansion were calculated: 1) the ratio between the change in CO and the change in volume, which was significantly higher in hypertensives (p less than 0.025), 2) the ratio between the change in CO and the change in CVP, which was similar in both groups, and 3) the ratio between the change in volume and the change in CVP, which was significantly reduced in hypertensives (p less than 0.001). In the overall population, the latter ratio was negatively correlated with the change in CO (or in stroke volume) induced by expansion ( r = -0.75). The results provided evidence that: 1) the slope of the relationship between CO and blood volume was steeper in hypertensives than in normotensives, and 2) the steeper slope was due to a reduction in the effective compliance of the vascular bed, causing a greater elevation in CO per unit rise in volume.