Thorac Cardiovasc Surg 2001; 49(6): 384
DOI: 10.1055/s-2001-19007
Letter to the Editor
© Georg Thieme Verlag Stuttgart · New York

The Effect of Cardiopulmonary Lymphatic Obstruction on
Heart and Lung Function

Y. Cui, J. D. Urschel, and N. J. Petrelli; Thorac Cardiov Surg
2001; 49 : 35-40
H. J. Geissler1 , U. Mehlhorn1 , G. A. Laine2 , S. Allen2
  • 1Department of Cardiothoracic Surgery, University of Cologne, Cologne, Germany
  • 2Center for Microvascular and Lymphatic Studies, University of Texas Medical School, Houston, Texas, USA
Further Information

Publication History

Publication Date:
17 December 2001 (online)

We would like to congratulate Cui et al. for their comprehensive and interesting review on cardiac and pulmonary lymphatic obstruction [1]. Although the deleterious effects of myocardial and pulmonary edema are widely acknowledged, the role of these organs’ lymphatic system in fluid balance is often not fully appreciated. With regard to cardiac and pulmonary lymph flow, we would like to contribute a clinically relevant aspect not mentioned in the review. As described by the authors, myocardial lymph flow depends on the heart’s contractile force during systole. However, as organized ventricular contraction is the primary determinant of myocardial lymphatic function, myocardial lymph flow almost ceases during cardioplegic arrest, resulting in substantial myocardial edema accumulation [2]. This edema contributes to the temporary cardiac dysfunction observed after cardioplegic arrest [3]. Augmenting cardiac contractility by inotropic support results in increased myocardial lymph driving pressure and hastened myocardial edema resolution after cardiopulmonary bypass and cardioplegic arrest [4]. The close relationship between mechanical workload and myocardial water content has been further investigated by Schertel et al. [5]. In isolated rat hearts, the authors found that heart rate and left ventricular pressure inversely determined the rate and degree of myocardial edema formation. Thus, impairment or absence of cardiac contractility lessens the ability of the myocardial lymphatics to remove excess interstitial fluid resulting in myocardial edema accumulation. In much the same way as myocardial lymph flow depends on ventricular contraction, pulmonary lymph flow depends on respiratory movement [6] and can be modified by ventilation parameters, such as tidal volume [7].

Among other measures in reducing myocardial or pulmonary edema formation, enhancement of these organs’ lymphatic function may improve removal of excess interstitial fluid. This may be achieved by augmenting cardiac contractility or increasing tidal volume, respectively.


Hans J. Geissler,, MD 

Department of Cardiothoracic
University of Cologne

Joseph-Stelzmann-Straße 9
50924 Köln