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European Heart Journal 1993 14(5):705-711;
Copyright © 1993 by the European Society of Cardiology.
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© 1993 The Europen Society of Cardiology

Effective pulmonary capillary pressure in experimental myocardial ischaemia

T. HACHENBERG*, J. MEYER*, T. BRÜSSEL*, A. GOEDDE*, N. GOEDDE*, B. VOGT{dagger}, G. BREITHARDT{dagger} and P. LAWIN*

*Department of Anaesthesiology and Intensive Care Medicine, Division of Coronary Artery Disease, Westfälische Wilhelms-Universität Münster Albert-Schweitzer-Str. 33, D-4400, Munster, Germany
{dagger}Department of Cardiology, Angiology and Institute for Research in Arteriosclerosis, Division of Coronary Artery Disease, Westfälische Wilhelms-Universität Münster Albert-Schweitzer-Str. 33, D-4400, Munster, Germany

Received 16 December 1992; .

Correspondence T. Hachenberg, Department of Anaeslhesiology and Intensive Care Medicine, Westfälische Wilhelms-Universität Münster. 33, D-4400, Munster, Germany

Abstract

Effective pulmonary capillary pressure and extravascular lung water were investigated in dogs (n=9) with normal heart function and after development of acute myocardial ischaemia. During control, no impairment of cardiopulmonary performance was observed. Extravascular lung water was in the normal range (8.1±2.8 ml. kg–1) and the effective pulmonary capillary pressure accounted for 1.36 ± 0.53 kPa (10.2±4 mmHg). No correlation between extravascular lung water and effective pulmonary capillary pressure was observed (r2=0.347, P=0.06). Arterial (RPA) and venous pulmonary resistance (RPV) were 70± 15% and 30±6%, respectively. Acute myocardial ischaemia was induced by one stage occlusion of the left anterior descending (LAD) coronary artery; measurements during the ischaemia phase were performed 60 min following LAD occlusion. Myocardial ischaemia resulted in moderate changes of cardiac output, heart rate and left ventricular end-diastolic pressure. Oxygenation deteriorated, but no hypoxaemia occurred in any animal and CO2 elimination remained unchanged. Extravascular lung water was elevated (16.5±7.9ml.kg–1, P≤0.01), and effective pulmonary capillary pressure was higher when compared with the control state (2.32±1.05 kPa (17.4±7.9mmHg), P≤0.01). There was a significant correlation between both parameters (r2=0.528, P<0.05). Longitudinal distribution of pulmonary vascular resistance was altered, and RPA decreased to 60±13% (P<0.05), while RPV increased to 40±8% (P≤0.05). It is concluded that development of lung oedema is related to elevated effective pulmonary capillary pressure in dogs with acute myocardial ischaemia. This is partially a consequence of higher pulmonary artery pressure, but also due to a vasoconstriction of the pulmonary venous compartment leading to a shift of the longitudinal distribution of pulmonary vascular resistance. In addition, release of vasoactive substances may induce leakage of the alveolocapillary membrane, favouring accumulation of extravascular lung water. The non-invasive estimation of Pceffcan be used for differentiation of factors promoting lung oedema development in acute myocardial ischaemia.

Key Words: Effective pulmonary capillary pressure • myocardial ischaemia • haemodynamics • gas exchange • extravascular lung water


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