Objective: The aim of this study was to assess whether thermodilution-derived parameters of right and left ventricular cardiac function (right ventricular ejection fraction, global ejection fraction, cardiac function index) are able to track changes of cardiac contractile function and whether they are influenced by substantial preload reduction.
Design: Prospective animal study.
Setting: University-affiliated animal research laboratory.
Subjects: Domestic pigs.
Interventions: Sixteen domestic pigs were studied. Right ventricular ejection fraction, global ejection fraction, and cardiac function index were compared to direct measurement of left ventricular rate of maximum systolic pressure rise and the left ventricular rate of maximum systolic pressure rise corrected to preload. Measurements were done with normal cardiac function during normo- and hypovolemia. Thereafter, cardiac function was impaired by continuous infusion of verapamil and measurements were repeated during normo- and hypovolemia (withdrawal of blood 20 mL kg body weight).
Measurements and main results: With normal cardiac function, hypovolemia led to a significant decrease of right ventricular ejection fraction from 36.7% ± 6.6% to 29.8% ± 5.8% (p < .001), global ejection fraction from 40.5% ± 6.2% to 33.6% ± 7.6% (p < .001), and the left ventricular rate of maximum systolic pressure rise from 2104 ± 390 mm Hg sec to 1297 ± 438 mm Hg sec (p < .001). Cardiac function index (8.92 ± 2.20 min to 7.93 ± 1.54 min) and the left ventricular rate of maximum systolic pressure rise corrected to preload (18.2 ± 4.7 mm Hg sec mL to 15.2 ± 4.3 mm Hg sec mL) did not change significantly. Infusion of verapamil led to a significant reduction of right ventricular ejection fraction, global ejection fraction, cardiac function index, the left ventricular rate of maximum systolic pressure rise, and the left ventricular rate of maximum systolic pressure rise corrected to preload (p < .001). Now, hypovolemia led to a significant decrease of right ventricular ejection fraction (29.1% ± 4.6% to 24.9% ± 5.9%; p < .001), global ejection fraction (37.1% ± 4.7% to 31.9% ± 3.9%; p < .05), cardiac function index (7.58 ± 1.02 to 6.27 ± 1.19 min; p < .05), and the left ventricular rate of maximum systolic pressure rise (733 ± 141 mm Hg sec to 426 ± 108 mm Hg sec; p < .05). Only the left ventricular rate of maximum systolic pressure rise corrected to preload did not change significantly (6.7 ± 1.3 mm Hg sec mL to 4.6 ± 1 mm Hg sec mL; p > .05).
Conclusions: Right ventricular ejection fraction, global ejection fraction, and cardiac function index enable detection of changes in load-independent, intrinsic cardiac contractility. Importantly, they also reflect changes of contractile function caused by substantial decrease of preload, emphasizing the importance of assessing both cardiac contractile function in coherence with cardiac preload to differentiate between reduced intrinsic contractility and hypovolemia.