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Effects of external constraint on the fetal left ventricular function curve
D A Grant1, J E Maloney, J V Tyberg
1Reproductive Medicine Research Group, University of Calgary, Alberta, Canada.
American Heart Journal
|June 1, 1992
Summary
External constraint on the fetal heart limits its stroke volume, explaining the plateau in fetal ventricular function. Reducing this constraint increased cardiac output, suggesting it
Area of Science:
- Cardiovascular Physiology
- Fetal Development
- Cardiac Mechanics
Background:
- The fetal ventricular function curve describes how the fetal heart's output changes with filling pressure.
- A plateau in this curve suggests limitations in the fetal heart's ability to increase stroke volume.
- Myocyte (heart muscle cell) immaturity has been proposed as a cause for this plateau.
Purpose of the Study:
- To investigate whether external ventricular constraint limits fetal left ventricular (LV) stroke volume.
- To determine if this constraint explains the plateau observed in the fetal ventricular function curve.
- To differentiate the effect of constraint from potential myocyte immaturity.
Main Methods:
- Studied nine fetal lambs (142-144 days' gestation) under halothane anesthesia.
- Measured LV stroke volume, LV end-diastolic pressure, and external ventricular constraint (intrapericardial pressure).
- Compared measurements under closed chest/pericardium versus open chest/pericardium conditions.
Main Results:
- Stroke volume was significantly higher with an open chest and pericardium compared to a closed chest (p < 0.01).
- Reduced external ventricular constraint increased LV transmural pressure (preload).
- Increased preload substantially elevated fetal LV stroke volume.
Conclusions:
- External ventricular constraint significantly limits fetal left ventricular stroke volume by reducing preload.
- This constraint is a primary factor responsible for the plateau in the fetal ventricular function curve.
- The plateau is likely not due to myocyte immaturity but rather mechanical limitations.