Jørgen Thorvaldson

Changes in cardiac dynamics by opening an interventricular shunt in dogs

Changes in right and left ventricular (RV, LV) dynamics caused by an interventricular shunt were examined in open-chest dogs. At a pulmonary to systemic blood flow ratio of 1.7 +/- 0.2 pulmonary flow increased by 53 +/- 13%, whereas aortic flow decreased by 9 +/- 2%. Shunt flow was continuous from the left to the right ventricle throughout the cardiac cycle, but 72 +/- 4% took place during the LV ejection phase. Peak systolic LV pressure declined by 6 +/- 3 mm Hg, LV end-diastolic segment length (SL) rose, and systolic shortening of the SL increased. Peak systolic RV pressure rose from 28 +/- 3 to 36 +/- 3 mm Hg and RV end-diastolic and end-systolic SL rose almost equally. Accordingly, RV systolic SL shortening did not rise despite the substantial augmentation in RV outflow. The transseptal end-diastolic pressure gradient did not rise, while the transseptal peak systolic gradient decreased when the shunt was opened. Similarly directed alterations were observed when the shunt was opened at different preloads and when the shunt flow was varied. Local work in the anterior wall of the right ventricle (calculated from the RV pressure SL loop) rose by 26 +/- 4%, whereas RV stroke work (product of mean systolic right ventricular pressure and pulmonary flow) rose by 57 +/- 12%; difference, P less than 0.05. LV stroke work and local work in anterior LV free wall rose in proportion when the shunt was opened.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac performance: optimal heart rate for maximal cardiac output

To determine optimal heart rate for the maximal cardiac output at various levels of inotropy and blood volume, the relationship between heart rate (HR) and stroke volume (SV) was examined in anaesthetized dogs during right atrial pacing. Myocardial inotropy was raised by intravenous infusion of isoproterenol, a stimulator of adrenergic beta-receptors, and reduced by propranolol, an inhibitor of adrenergic beta-receptors. Circulating blood volume was increased by saline infusion. Within the range of optimal heart rate, SV and HR were inversely related: SV = k (HR0-HR), where k indicates the relationship between changes in SV and HR. The intercept with the HR axis is HR0. At constant HR a rise in inotropy increased SV and a fall in inotropy reduced SV. These changes in SV were eual at every HR, and k was therefore constant. In contrast, blood volume expansion increased SV more at low than at high HR (k increased), but HR0 was not significantly changed. Calculated maximal cardiac output: k.HR02/4, and optimal heart/rate: HR0/2, agreed with observations when maximal cardiac output was raised from 1900 to 4500 ml/min by increasing blood volume and inotropy. Optimal HR was not influenced by changes in blood volume, but was increased from 160 to 200 beats/min by increasing inotropy. We conclude that the optimal heart rate and the maximal cardiac output can be predicted from the linear relationship between SV and HR during right atrial pacing.