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Updated: Jul 20, 2026

Evaluation of Right Ventricular Function in Experimental Models of Pulmonary Arterial Hypertension
Published on: June 27, 2025
Adaptation of the right ventricle to an increased afterload in the chronically volume overloaded heart
Gábor Szabó1, Pál Soós, Susanne Bährle
1Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. dzsi@hotmail.com
Insights
Chronic volume overload does not impair right ventricular contractility but limits its ability to adapt to increased afterload. The heart compensates using the Frank-Starling mechanism.
Area of Science:
- Cardiology
- Physiology
- Heart Failure Research
Background:
- Increased right ventricular afterload is a frequent complication post-cardiac surgery for heart diseases.
- Understanding the right ventricle's response to afterload is crucial for managing these patients.
Purpose of the Study:
- To investigate the effects of acute increases in right ventricular afterload.
- To compare responses in normal versus chronically volume-overloaded hearts.
Main Methods:
- Chronic volume overload was induced in dogs via arteriovenous shunts for 3 months.
- Pulmonary banding was used to acutely increase right ventricular afterload.
- Right ventricular pressures, volumes, and contractility were measured using conductance catheterization.
Main Results:
- Chronically volume-overloaded hearts showed increased baseline right ventricular pressures and volumes.
- In control hearts, increased afterload enhanced contractility without changing end-diastolic pressure/volume.
- In overloaded hearts, increased afterload led to less contractility improvement and elevated end-diastolic pressure/volume.
Conclusions:
- Chronic volume overload does not inherently reduce right ventricular contractility.
- The adaptive (inotropic) response to increased afterload is diminished in volume-overloaded hearts.
- The Frank-Starling mechanism plays a compensatory role in these conditions.
Background:
Increased right ventricular afterload is a common problem after correction of various heart diseases with chronic volume overload. We determined the effects of an acute increase of right ventricular afterload in normal and chronically volume overloaded hearts.
Methods:
In 6 dogs, volume overload was induced by chronic arteriovenous shunts for 3 months. Six sham-operated animals served as controls. After closing the shunts, right ventricular systolic and end-diastolic pressure as well as end-diastolic volume were measured by conductance catheter. In addition, pressure-volume loops were recorded. Myocardial contractility was described by the slope of the end-systolic pressure-volume relationship. Afterload was increased to right ventricular systolic pressure to 35 mm Hg and to 50 mm Hg by pulmonary banding.
Results:
Chronic volume overload resulted in a significant increase of right ventricular systolic pressure (34 +/- 2 versus 25 +/- 2 mm Hg, p < 0.05), end-diastolic pressure (10.4 +/- 1.7 versus 6.8 +/- 0.4 mm Hg, p < 0.05), and end-diastolic volume (39 +/- 2 versus 33 +/- 3 mL, p < 0.05). Baseline contractility (1.47 +/- 0.24 versus 1.53 +/- 0.32 mm Hg/mL) did not differ. While afterload increase to 35 and 50 mm Hg led to stepwise increase in contractility (2.73 +/- 0.30 mm Hg/mL and 4.15 +/- 0.30 mm Hg/mL, p < 0.05 versus baseline, respectively) at unchanged end-diastolic pressure and volume in controls, it showed only a slight increase (2.11 +/- 0.38 mm Hg/mL and 2.99 +/- 0.29 mm Hg/mL, p < 0.05 versus sham) with concomitant increase in end-diastolic pressure (12.4 +/- 2.2 mm Hg/mL and 16.3 +/- 1.9 mm Hg, p < 0.05) and volume (42 +/- 4 mL and 48 +/- 8 mL, p < 0.05) in the chronically volume overloaded group.
Conclusions:
Chronic volume overload per se does not impair right ventricular contractility. However, the inotropic adaptation (homeometric autoregulation) to an increased afterload is limited, which is partly compensated by the Frank-Starling mechanism (heterometric autoregulation).
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