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Acute pulmonary hypertension causes depression of left ventricular contractility and relaxation

Published online by Cambridge University Press:  02 March 2006

R. Amà ,
H. A. Leather ,
P. Segers ,
E. Vandermeersch  and
P. F. Wouters
R. Amà
Affiliation:
Katholieke Universiteit Leuven, Center for Experimental Surgery and Anesthesiology, Department of Anesthesiology, Belgium
H. A. Leather
Affiliation:
Katholieke Universiteit Leuven, Center for Experimental Surgery and Anesthesiology, Department of Anesthesiology, Belgium
P. Segers
Affiliation:
Ghent University, Institute Biomedical Technology, Hydraulics Laboratory, Belgium
E. Vandermeersch
Affiliation:
Katholieke Universiteit Leuven, Center for Experimental Surgery and Anesthesiology, Department of Anesthesiology, Belgium
P. F. Wouters
Affiliation:
Katholieke Universiteit Leuven, Center for Experimental Surgery and Anesthesiology, Department of Anesthesiology, Belgium
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Abstract

Summary

Background and objective: The haemodynamic effects of acute pulmonary hypertension can be largely attributed to ventricular interdependence during diastole. However, there is evidence that the two ventricles also interact during systole. The aim of the present study was to examine the effects of acute pulmonary hypertension on both components of left ventricular systole, i.e. contraction and relaxation, using load-independent indices. Methods: Ten pigs were instrumented with biventricular conductance catheters, a pulmonary artery flow probe and a high-fidelity pulmonary pressure catheter. Haemodynamic measurements were performed in baseline conditions and during stable pulmonary vasoconstriction induced by the thromboxane analogue U46619. Contractility was quantified using the end-systolic pressure–volume and preload recruitable stroke work relationships. The τ-end-systolic pressure relationship was used to assess load-dependency of relaxation. Results: Acute pulmonary hypertension caused a decrease in the slope of the left ventricular preload recruitable stroke work relationship (from 6.64 ± 1.7 to 5.19 ± 1.9, mean ± SD; P < 0.05), a rightward shift of the end-systolic pressure–volume relationship (P < 0.05), and an increase in the slope of the τ-end-systolic pressure relationship (from −0.15 ± 0.5 to 0.35 ± 0.17; P < 0.05). The diastolic chamber stiffness constant of both ventricles increased during pulmonary hypertension (P < 0.05). Conclusions: In the present model, acute pulmonary hypertension impairs left ventricular contractile function and relaxing properties. The present study provides additional evidence that, besides the well-known diastolic ventricular cross talk, systolic ventricular interaction may play a significant role in the haemodynamic consequences of acute pulmonary hypertension.

Keywords

MYOCARDIAL CONTRACTION, ventricular relaxation, ventricular interactionHYPERTENSION, PULMONARYDIASTOLEVENTRICULAR FUNCTION, LEFT, RIGHTVENTRICULAR PRESSURES
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 23 , Issue 10 , October 2006 , pp. 824 - 831
Copyright
2006 European Society of Anaesthesiology

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