The Effect of Cardiopulmonary Lymphatic Obstruction on
Heart and Lung Function

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.

References

• 1 Cui Y, Urschel J D, Petrelli N J. The effect of cardiopulmonary lymphatic obstruction on heart and lung function.  Thorac Cardiov Surg. 2001;  49 35-40
• 2 Mehlhorn U, Davis K L, Burke E J, Adams D, Laine G A, Allen S J. Impact of cardiopulmonary bypass and cardioplegic arrest on myocardial lymphatic function.  Am J Physiol (Heart Circ Physiol). 1995;  268 (37) H178-H183
• 3 Mehlhorn U, Allen S J, Adams D L. et al . Normothermic continuous antegrade blood cardioplegia does not prevent myocardial edema and cardiac dysfunction.  Circulation. 1995;  92 1939-1946
• 4 Allen S J, Geissler H J, Davis K L. et al . Augmenting cardiac contractility hastens myocardial edema resolution after cardiopulmonary bypass and cardioplegic arrest.  Anesth Analg. 1997;  85 987-992
• 5 Schertel E R, Daye R M, McClure D E, Lai T, Miyamoto M, Myerowitz P D. Mechanical workload-myocardial water content relationship in isolated rat hearts.  Am J Physiol (Heart Circ Physiol). 1997;  273 (42) H271-H278
• 6 Taylor A E, Drake R E. Fluid and protein movement across the pulmonary circulation. In: Staub NC ed. Lung biology in health and disease: lung water and solute exchange. New York; Marcel Dekker 1978: 148
• 7 Geissler H J, Davis K L, Laine G A, Brennan M L, Mehlhorn U, Allen S J. Contamination of lymph from the major prenodal cardiac lymphatic in dogs.  Am J Physiol (Heart Circ Physiol). 1999;  276 (45) H1795-H1800