Acute pulmonary hypertension causes depression of left ventricular contractility and relaxation
| Autor: | R. Ama, Patrick Wouters, Eugene Vandermeersch, H. A. Leather, Patrick Segers |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
medicine.medical_specialty
Swine Hypertension Pulmonary Diastole Blood Pressure Ventricular Dysfunction Left Heart Rate Internal medicine medicine.artery medicine Animals Systole Cardiac Output Pulmonary wedge pressure Cardiac cycle business.industry Stroke Volume medicine.disease Pulmonary hypertension Myocardial Contraction Preload Disease Models Animal Anesthesiology and Pain Medicine Blood pressure Anesthesia Pulmonary artery Acute Disease Cardiology Vascular Resistance business |
| Zdroj: | European journal of anaesthesiology. 23(10) |
| ISSN: | 0265-0215 |
| Popis: | SummaryBackground 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. |
| Databáze: | OpenAIRE |
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