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Hemodynamics of hypertension and of hypertensive heart disease
Insights
Essential hypertension involves progressive vasoconstriction. Early stages may show normal cardiac output due to mild constriction and volume changes, but advanced disease reduces cardiac output via increased resistance and plasma volume reduction.
Area of Science:
- Cardiovascular Physiology
- Hypertension Pathophysiology
Background:
- Essential hypertension is a complex condition.
- Hemodynamic alterations are central to its progression.
Purpose of the Study:
- To elucidate the continuum of hemodynamic changes in essential hypertension.
- To correlate vasoconstriction patterns with cardiac output and vascular resistance.
Main Methods:
- Conceptual framework based on existing physiological understanding.
- Analysis of proposed hemodynamic shifts across hypertension stages.
Main Results:
- Labile hypertension involves mild arteriolar and venoconstriction, potentially maintaining normal cardiac output.
- Advancing hypertension increases arteriolar constriction, raising total peripheral resistance and cardiac workload.
- Venular constriction in advanced stages decreases plasma volume, venous return, and cardiac output.
Conclusions:
- Hemodynamic changes in essential hypertension represent a spectrum of peripheral vasoconstriction.
- The interplay between arteriolar and venular constriction dictates changes in vascular resistance and cardiac output throughout disease progression.
Abstract:
Therefore, one may look on the hemodynamic changes in essential hypertension as a continuum of greater degrees of peripheral vasoconstriction. In labile hypertension, the mild arteriolar constriction only slightly increases vascular resistance (the "inappropriately" normal level), and the mild venoconstriction serves to redistribute blood to the heart and lungs, thereby augmenting or increasing cardiac output to its increased level. Thus, in this schema it is possible to find mildly hypertensive patients, or even some subjects with labile hypertension, with a normal cardiac output, especially if their circulating volume is already reduced. With advancing disease, arteriolar constriction increases, providing further increases in total peripheral resistance and stress upon the heart, and the coincident venular constriction reduces circulating plasma volume, venous return, and cardiac output.