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Systemic vascular resistance: an unreliable index of left ventricular afterload
Insights
Systemic vascular resistance (SVR) is an unreliable measure of left ventricular afterload. Left ventricular end-systolic wall stress (sigma es) provides a more accurate assessment by considering factors beyond peripheral tone.
Area of Science:
- Cardiology
- Physiology
- Biomedical Engineering
Background:
- Systemic vascular resistance (SVR) is commonly used to assess left ventricular afterload.
- However, SVR may not accurately reflect ventricular internal fiber load as it only measures peripheral vasomotor tone.
Purpose of the Study:
- To investigate the relationship between SVR and left ventricular end-systolic wall stress (sigma es).
- To determine if SVR is a reliable index of left ventricular afterload during pharmacologic interventions.
Main Methods:
- Eight dogs were instrumented with hemodynamic monitoring (aortic, right atrial, and left ventricular pressures, cardiac output).
- Left ventricular dimensions and wall thickness were assessed using echocardiography.
- SVR and sigma es were calculated under baseline conditions and during infusions of vasodilators (nitroprusside) and inotropes (methoxamine, dobutamine, norepinephrine).
Main Results:
- SVR underestimated changes in sigma es by 22% to 54% when afterload was altered.
- During norepinephrine infusion, SVR increased by 21% while sigma es decreased by 9%, demonstrating discordant changes.
- Pharmacologic interventions revealed significant discrepancies between SVR and sigma es.
Conclusions:
- Systemic vascular resistance is an unreliable index of left ventricular afterload.
- Left ventricular end-systolic wall stress (sigma es) is a more comprehensive measure, incorporating peripheral loading and myocardial factors.
- Accurate assessment of left ventricular afterload requires consideration of both internal and external myocardial factors.
Abstract:
Systemic vascular resistance (SVR) is a frequently used clinical index of left ventricular afterload. However, SVR may not adequately assess left ventricular afterload (i.e., ventricular internal fiber load during systole) since it reflects only peripheral vasomotor tone. In contrast, left ventricular end-systolic wall stress (sigma es) reflects the combined effects of peripheral loading conditions and left ventricular chamber pressure, dimension, and wall thickness. To determine the relationship between SVR and sigma es, left ventricular afterload and contractility were pharmacologically altered in eight dogs instrumented with central aortic microtip and Swan-Ganz thermodilution catheters. Left ventricular wall thicknesses and dimensions were measured from two-dimensionally targeted M mode echocardiograms. Aortic, right atrial, and left ventricular end-systolic pressures as well as cardiac output were recorded. SVR and sigma es were determined under control conditions as well as during infusions of nitroprusside, methoxamine, dobutamine, and norepinephrine. Control data acquired before each drug infusion were similar. When compared with baseline values, SVR underestimated the magnitude of change in left ventricular sigma es by 22% when afterload alone was decreased (nitroprusside), 54% when afterload alone was increased (methoxamine), and 50% when afterload was decreased and contractility was augmented (dobutamine). Most importantly, when afterload was minimally decreased in association with augmented contractility (norepinephrine), SVR increased by 21% while sigma es fell by 9%. Thus, discordant changes in left ventricular afterload (i.e., sigma es) and SVR can occur during pharmacologic interventions. SVR is an unreliable index of left ventricular afterload, reflecting only peripheral arteriolar tone rather than left ventricular systolic wall force. This emphasizes the fact that a true measure of left ventricular afterload must consider the interaction of factors internal and external to the myocardium.