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Enhanced systolic function of the right ventricle during respiratory distress syndrome in newborn lambs
M De Vroomen1, P Steendijk, R H Lopes Cardozo
1Department of Cardiology, Leiden University Medical Center, 2300 RC Leiden, The Netherlands.
Insights
Respiratory distress syndrome (RDS) increases pulmonary hypertension, raising right ventricle (RV) afterload. However, the newborn lamb heart maintains cardiac output by enhancing RV systolic function.
Area of Science:
- Neonatal physiology
- Cardiovascular research
- Pulmonary medicine
Background:
- Respiratory distress syndrome (RDS) is associated with pulmonary hypertension.
- Increased pulmonary arterial pressure may compromise right ventricular (RV) function due to elevated afterload.
Purpose of the Study:
- To investigate biventricular cardiac function in an experimental model of RDS.
- To determine the impact of increased RV afterload on cardiac output and systolic function in newborns.
Main Methods:
- RDS was induced in newborn lambs via lung lavages.
- Biventricular function was assessed using pressure-conductance catheters to derive end-systolic pressure-volume relations.
- Hemodynamic parameters, including pulmonary arterial pressure and stroke volume, were monitored over a 4-hour period.
Main Results:
- A sustained twofold increase in mean pulmonary arterial pressure was observed in lambs with RDS.
- Despite elevated RV afterload, stroke volume was maintained, and RV end-diastolic volume showed minimal increase.
- Right ventricular systolic function significantly improved, evidenced by a leftward shift and increased slope of the end-systolic pressure-volume relation.
- Left ventricular systolic function remained unchanged, and control animals showed no significant alterations.
Conclusions:
- The newborn heart effectively maintains cardiac output under increased RV afterload conditions.
- Enhanced RV systolic function, achieved through homeometric autoregulation, is the primary mechanism for maintaining cardiac output in RDS.
- This study highlights the adaptive capacity of the neonatal cardiovascular system to pulmonary hypertension.
Abstract:
Respiratory distress syndrome (RDS) causes pulmonary hypertension. It is often suggested that this increased afterload for the right ventricle (RV) might lead to cardiac dysfunction. To examine this, we studied biventricular function in an experimental model. RDS was induced by lung lavages in seven newborn lambs. Five additional lambs served as controls. Cardiac function was quantified by indexes derived from end-systolic pressure-volume relations obtained by pressure-conductance catheters. After lung lavages, a twofold increase of mean pulmonary arterial pressure (from 15 to 34 mmHg) was obtained and lasted for the full 4-h study period. Stroke volume was maintained (5.2 +/- 0.6 ml at baseline and 6.1 +/- 1.4 ml at 4 h of RDS), while RV end-diastolic volume showed only a slight increase (from 6.5 +/- 2.3 ml at baseline to 7.7 +/- 1.3 ml at 4 h RDS). RV systolic function improved significantly, as indicated by a leftward shift and increased slope of the end-systolic pressure-volume relation. Left ventricular systolic function showed no changes. In control animals, pulmonary arterial pressure did not increase and right and left ventricular systolic function remained unaffected. In the face of increased RV afterload, the newborn heart is able to maintain cardiac output, primarily by improving systolic RV function through homeometric autoregulation.
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