Thorac cardiovasc Surg 1981; 29(3): 168-173
DOI: 10.1055/s-2007-1023469
© Georg Thieme Verlag Stuttgart · New York

Basic Physiological Studies on Cardiac Pacing with Special Reference to the Optimal Mode and Rate after Cardiac Surgery

D. Baller, A. Hoeft, H. Korb, H. G. Wolpers, J. Zipfel, G. Hellige
  • Center of Physiology and Pathophysiology, and Department of Experimental Cardiology, Göttingen University
Further Information

Publication History

1981

Publication Date:
28 May 2008 (online)

Summary

Temporary cardiac pacing (CP) is frequently applied postoperatively in the management of low cardiac output (CO) and rhythm instability. However, uncertainty exists about the “optimal” pacing rate, range and mode due to incomplete Information on myocardial oxygen consumption (MVO2)related to its hemodynamic determinants, and on myocardial pumping efficiency (η) at CP.

In 10 intact dogs atrial pacing (AP) (90 to 210 beats/min) and ventricular pacing (VP) (70 to 330 beats/min) were investigated in normal and failing hearts. AP and VP were compared at identical rates. MVO2 (4 to 20 ml/min · 100 gr) was measured directly according to the Fick principle. Cardiac efficiency was calculated as the ratio of oxygen equivalent of external cardiac work to MvO2.

Rates with maximum CO and a maximal η occurred only in heart failure. However, maximal CO and η were obtained at different heart rates (HR). MVO2 was significantly higher (p < 0.001) under VP as compared to AP at identical rates with a mean increase of 26.5% ± 6% over AP, although hemodynamics were significantly lower under VP (p < 0.001). Myocardial pumping efficiency was markedly better under AP with a mean increase of 63% ± 4.5% over VP even in normal hearts.

Adjustment of HR at maximal response in CO may become dangerous, particularly under VP, in heart failure. AP, if applicable, may be regarded as the optimal pacing technique due to an optimal relation of improved hemodynamics to MVO2. It may be helpful in correcting an imbalance between oxygen supply and demand in cases of low output syndrome. The pathophysiologic mechanisms and further clinical implications are discussed.