Total mechanical energy of a ventricle model and cardiac oxygen consumption

1979 ◽  
Vol 236 (3) ◽  
pp. H498-H505 ◽  
Author(s):  
H. Suga

Mechanical energy (ENG) required by a time-varying elastance model of the ventricle was compared with oxygen consumption per beat (VO2) of the canine left ventricle contracting under a variety of loading conditions. ENG needed for this model to increase its elastance during systole is shown to be equal to the sum of the potential energy built in the elastance during systole plus the external mechanical stroke work. This ENG is equivalent to the area (PVA) bounded by the end-systolic and end-diastolic P-V curves and the systolic limb of the P-V loop trajectory in the P-V plane. There was a high correlation (r = 0.89) between VO2s documented in the literature and PVAs assessed by the author from the accompanying P-V data from both isovolumic and ejecting contractions in 11 hearts. A linear regression analysis yielded an empirical equation: VO2 (ml O2/beat) = a . PVA (mmHg . ml/beat) + b, where a = 1.37 X 10(-5) and b = 0.027, which can be used to predict VO2 from PVA. A preliminary experimental study in my laboratory confirmed the validity of this empirical equation.

1983 ◽  
Vol 244 (2) ◽  
pp. H206-H214 ◽  
Author(s):  
H. Suga ◽  
R. Hisano ◽  
S. Hirata ◽  
T. Hayashi ◽  
O. Yamada ◽  
...  

Left ventricular (LV) systolic pressure-volume area (PVA), a new measure of total mechanical energy for the contraction, linearly correlates with its oxygen consumption per beat (VO2) regardless of contraction mode in a canine heart with stable chronotropism and inotropism. PVA is the area in the pressure-volume (PV) diagram circumscribed by the end-systolic and end-diastolic PV relation curves and the systolic segment of the PV loop and has dimensions of energy. We investigated whether primary changes in heart rate would affect the VO2-PVA relation. In the excised cross-circulated canine heart with left ventricular load controlled with a servo pump, we changed heart rate by pacing to compare the VO2-PVA relations at low [124 +/- 17 (SD) min-1] and high (193 +/- 23) heart rates. In 15 left ventricles, VO2 (ml O2 X beat-1 X 100 g LV-1) was (1.75 +/- 0.57) X 10(-5) PVA (mmHg X ml X beat-1 X 100 g LV-1) + 0.031 +/- 0.011 (ml O2 X beat-1 X 100 g LV-1). The VO2-PVA relation was virtually independent of heart rate in individual hearts. We conclude that the load-independent VO2-PVA relationship is not affected by chronotropism in a given canine left ventricle.


1990 ◽  
Vol 49 (4) ◽  
pp. 543-549 ◽  
Author(s):  
Satoshi Furukawa ◽  
Joseph E. Bavaria ◽  
Gerhard Kreiner ◽  
L.Henry Edmunds

2020 ◽  
Vol 5 (1) ◽  
pp. 15 ◽  
Author(s):  
Andrea Fusco ◽  
William Sustercich ◽  
Keegan Edgerton ◽  
Cristina Cortis ◽  
Salvador J. Jaime ◽  
...  

Rating of perceived exertion (RPE) and session RPE (sRPE) are reliable tools for predicting exercise intensity and are alternatives to more technological and physiological measurements, such as blood lactate (HLa) concentration, oxygen consumption and heart rate (HR). As sRPE may also convey some insights into accumulated fatigue, the purpose of this study was to examine the effects of progressive fatigue in response to heavier-than-normal training on sRPE, with absolute training intensity held constant, and determine its validity as marker of fatigue. Twelve young adults performed eight interval workouts over a two-week period. The percentage of maximal HR (%HRmax), HLa, RPE and sRPE were measured for each session. The HLa/RPE ratio was calculated as an index of fatigue. Multilevel regression analysis showed significant differences for %HRmax (p = 0.004), HLa concentration (p = 0.0001), RPE (p < 0.0001), HLa/RPE ratio (p = 0.0002) and sRPE (p < 0.0001) across sessions. Non-linear regression analysis revealed a very large negative relationship between HLa/RPE ratio and sRPE (r = −0.70, p < 0.0001). These results support the hypothesis that sRPE is a sensitive tool that provides information on accumulated fatigue, in addition to training intensity. Exercise scientists without access to HLa measurements may now be able to gain insights into accumulated fatigue during periods of increased training by using sRPE.


1999 ◽  
Vol 276 (4) ◽  
pp. H1339-H1345 ◽  
Author(s):  
Christian Korvald ◽  
Odd P. Elvenes ◽  
Lars M. Ytrebø ◽  
Dag G. Sørlie ◽  
Truls Myrmel

In the “virtual work model,” left ventricular total mechanical energy (TME) is linearly related to myocardial oxygen consumption (MV˙o2). This relationship (MV˙o2-TME) is supposedly independent of inotropic stimulation, vascular loading, and heart rate variations. We reexamined the effect of inotropic stimulation (dopamine) on the metabolic to mechanical energy transfer in nine open-chest anesthetized pigs. Left ventricular mechanical energy was calculated using TME (mean ejection pressure × end-diastolic volume + stroke work), TMEW(end-diastolic volume reduced by unstressed ventricular volume), and the pressure-volume area (PVA). A highly linear relationship between MV˙o2and mechanical energy was found for all three indexes during control and dopamine runs ( r = 0.87–0.99). The slopes were unaltered by dopamine. y-Axis intercepts were (control vs. dopamine) as follows (in J ⋅ beat−1⋅ 100 mg−1; means ± SD): TME, 0.36 ± 0.12 vs. 0.61 ± 0.30 ( P< 0.02); TMEW, 0.43 ± 0.16 vs. 0.72 ± 0.32 ( P < 0.02); and PVA, 0.34 ± 0.13 vs. 0.60 ± 0.30 ( P < 0.02). We conclude that the virtual work model is dependent on inotropic stimulation and that new insight into myocardial chemomechanical coupling is not added by this concept.


2000 ◽  
Vol 279 (6) ◽  
pp. H2855-H2864 ◽  
Author(s):  
Akio Saeki ◽  
Yoichi Goto ◽  
Katsuya Hata ◽  
Toshiyuki Takasago ◽  
Takehiko Nishioka ◽  
...  

Heart temperature affects left ventricular (LV) function and myocardial metabolism. However, how and whether increasing heart temperature affects LV mechanoenergetics remain unclear. We designed the present study to investigate effects of increased temperature by 5°C from 36°C on LV contractility and energetics. We analyzed the LV contractility index ( Emax) and the relation between the myocardial oxygen consumption (MV˙o2) and the pressure-volume area (PVA; a measure of LV total mechanical energy) in isovolumically contracting isolated canine hearts during normothermia (NT) and hyperthermia (HT). HT reduced Emaxby 38% ( P < 0.01) and shortened time to Emaxby 20% ( P < 0.05). HT, however, altered neither the slope nor the unloaded MV˙o2of the MV˙o2-PVA relation. HT increased the oxygen cost of contractility (the incremental ratio of unloaded MV˙o2to Emax) by 49%. When Ca2+infusion restored the reduced LV contractility during HT to the NT baseline level, the unloaded MV˙o2in HT exceeded the NT value by 36%. We conclude that HT-induced negative inotropism accompanies an increase in the oxygen cost of contractility.


2012 ◽  
Vol 182-183 ◽  
pp. 8-11
Author(s):  
Yue Feng Yuan ◽  
Wen Ying Zhang ◽  
Xing Chang

Cutting force experiments in turning aluminum-silicon alloy were carried out with cement carbide tool YG8. Experimental formulae of cutting force, back force and feed force were determined based on multi-variable linear regression analysis, and they were verified by analysis of variance, the results showed that the regressed models could be used to predict cutting force under certain conditions.


1997 ◽  
Vol 87 (3) ◽  
pp. 658-666 ◽  
Author(s):  
Kunihisa Kohno ◽  
Miyako Takaki ◽  
Kazunari Ishioka ◽  
Yasunori Nakayama ◽  
Shunsuke Suzuki ◽  
...  

Background It is still unclear whether fentanyl directly alters left ventricular (LV) contractility and oxygen consumption. This is because of the difficulty in defining and evaluating contractility and energy use independently of ventricular loading conditions and heart rate in beating whole hearts. Methods This study was conducted to clarify the mechanoenergetic effects of intracoronary fentanyl in six excised cross-circulated canine hearts. The authors used the framework of the Emax (a contractility index)-PVA (systolic pressure-volume area, a measure of total mechanical energy)-VO2 (myocardial oxygen consumption per beat) relationship practically independent of ventricular loading conditions. The authors measured LV pressure, volume, coronary flow, and arteriovenous oxygen content difference to calculate Emax, PVA, and VO2. They first obtained the VO2-PVA relationship for varied LV volumes at control Emax. The authors then obtained the VO2-PVA relationship at a constant LV volume, whereas coronary blood fentanyl concentration was increased in steps up to 240 ng/ml. Finally, they obtained the VO2-PVA relationship for varied LV volumes at the final dose of fentanyl. Results Fentanyl at any concentrations did not significantly change Emax, PVA, and VO2 from the control. The linear end-systolic pressure-volume relations and their slopes were virtually the same between the control and fentanyl volume loading in each heart. Further, either the slope (oxygen cost of PVA) or the VO2 intercept (unloaded VO2) of the linear VO2-PVA relationship remained unchanged by fentanyl. Conclusions These results indicate that intracoronary fentanyl produces virtually no effects on LV mechanoenergetics for a wide range of its blood concentration.


1987 ◽  
Vol 252 (5) ◽  
pp. H998-H1004 ◽  
Author(s):  
Y. Igarashi ◽  
Y. Goto ◽  
O. Yamada ◽  
T. Ishii ◽  
H. Suga

We compared transient slope of end-systolic pressure-volume line (T-Emax) with steady Emax (S-Emax) in isolated cross-circulated canine left ventricles. T-Emax is the slope of the end-systolic pressure-volume line (ESPVL) determined from the last steady-state ejecting contraction (SEC) and the first transient isovolumic contraction produced by end-diastolic volume clamp. S-Emax is the slope of ESPVL determined from five steady-state contractions by linear regression analysis. We obtained three T-Emax values in the same contractile state by changing ejection fraction (EF) of SEC to three levels (range 14-58%) from the same end-diastolic volume. T-Emax variably increased with EF in any contractile state. The ratios of the three T-Emax values to the same S-Emax value was 1.08 +/- 0.04 (11 ventricles, means +/- SE) for high EF, 0.87 +/- 0.06 for middle EF, and 0.69 +/- 0.07 for low EF in control contractile state. These ratios decreased under epinephrine and increased under propranolol. We conclude that T-Emax depends not only on EF but also on contractile state in isolated dog left ventricles.


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