Assumed oxygen consumption frequently results in large errors in the determination of cardiac output.

OBJECTIVE: We sought to investigate the differences in assumed and measured oxygen consumption values for the determination of cardiac output by using the Fick principle in a pediatric population with congenital heart disease. METHODS: The patient population consisted of 143 patients with a mean age of 11.3 years (age range, 2 days to 23.8 years) undergoing cardiac catheterization during general anesthesia and with mechanical ventilation. Oxygen consumption was measured with a standard commercial analyzing system (Deltatrac II; Datex, Engström, Helsinki, Finland). Assumed oxygen consumption values were calculated according to the formulas of Krovetz and Goldbloom and LaFarge and Miettinen. Comparisons between measurements and assumptions were performed by Bland-Altman plots. Two-sided paired t tests were used to assess a difference of the assumed and measured values. RESULTS: The range of measured oxygen consumption values was between 55.2 and 249 mL . min -1 . m -2 . The Krovetz-Goldbloom formula led to systematically larger values compared with the measured values (P = .0001; mean difference of -53.3 mL . min -1 . m -2 ; 95% confidence interval, -56.7 to -49.8 mL . min -1 . m -2 ). The use of the LaFarge-Miettinen formula tends to overestimate oxygen consumption (P = .0037; mean difference of -15.9 mL . min -1 . m -2 ; 95% confidence interval, -26.5 to -5.4 mL . min -1 . m -2 ). A similarly poor agreement was found when analyzing a subgroup of 25 patients with Fontan-type circulation. CONCLUSION: The use of assumed instead of measured oxygen consumption values introduces large errors in the determination of cardiac output.

Learning modifies subsequent induction of long-term potentiation-like and long-term depression-like plasticity in human motor cortex.

Learning may alter rapidly the output organization of adult motor cortex. It is a long-held hypothesis that modification of synaptic strength along cortical horizontal connections through long-term potentiation (LTP) and long-term depression (LTD) forms one important mechanism for learning-induced cortical plasticity. Strong evidence in favor of this hypothesis was provided for rat primary motor cortex (M1) by showing that motor learning reduced subsequent LTP but increased LTD. Whether a similar relationship exists in humans is unknown. Here, we induced LTP-like and LTD-like plasticity in the intact human M1 by an established paired associative stimulation (PAS) protocol. PAS consisted of 200 pairs of electrical stimulation of the right median nerve, followed by focal transcranial magnetic stimulation of the hand area of the left M1 at an interval equaling the individual N20 latency of the median nerve somatosensory-evoked cortical potential (PAS(N20)) or N20-5 msec (PAS(N20-5)). PAS(N20) induced reproducibly a LTP-like long-lasting (>30 min) increase in motor-evoked potentials from the left M1 to a thumb abductor muscle of the right hand, whereas PAS(N20-5) induced a LTD-like decrease. Repeated fastest possible thumb abduction movements resulted in learning, defined by an increase in maximum peak acceleration of the practiced movements, and prevented subsequent PAS(N20)-induced LTP-like plasticity but enhanced subsequent PAS(N20-5)-induced LTD-like plasticity. The same number of repeated slow thumb abduction movements did not result in learning and had no effects on PAS-induced plasticity. Findings support the view that learning in human M1 occurs through LTP-like mechanisms.