Oxygen-wasting effect of inotropy  in the “virtual work model”

1999 ◽  
Vol 276 (4) ◽  
pp. H1339-H1345 ◽  
Author(s):  
Christian Korvald ◽  
Odd P. Elvenes ◽  
Lars M. Ytrebø ◽  
Dag G. Sørlie ◽  
Truls Myrmel
Keyword(s):  
Virtual Work ◽  
Mechanical Energy ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Stroke Work ◽  
End Diastolic Volume ◽  
Chemomechanical Coupling ◽  
Total Mechanical Energy ◽  
Work Model ◽  
Inotropic Stimulation

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.

Effects of cardiac glycosides on myocardial function and energetics in conscious dogs

1994 ◽  
Vol 267 (5) ◽  
pp. H2042-H2049 ◽  
Author(s):  
J. C. Lucke ◽  
J. R. Elbeery ◽  
T. C. Koutlas ◽  
S. A. Gall ◽  
T. A. D'Amico ◽  
...  
Keyword(s):  
Energy Transfer ◽  
Coronary Sinus ◽  
Systolic Function ◽  
Mechanical Energy ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Stroke Work ◽  
O2 Consumption ◽  
End Diastolic Volume ◽  
Total Mechanical Energy

The physiological effects of intravenous ouabain on left ventricular (LV) systolic function and metabolic-to-mechanical energy transfer were examined in eight conscious dogs. LV pressure and volume were measured using micromanometers and ultrasonic dimension transducers during transient vena caval occlusions under control conditions and after increasing doses of ouabain. Doppler coronary flow and coronary sinus O2 saturations were used to determine arterial-to-coronary sinus O2 content difference and thereby to calculate LV O2 consumption; total mechanical energy was computed as the sum of LV stroke work and the product of end-diastolic volume and LV mean ejection pressure, neglecting LV unstressed cavitary volume. The slope (10(4) erg/ml) of the stroke work vs. end-diastolic volume relationship increased progressively with rising doses of ouabain from 7.0 +/- 1.6 at control to 9.6 +/- 1.7 after ouabain 0.75 mg (P = 0.0002). Regression analysis of LV O2 consumption (mW/cm3) vs. total mechanical energy (mW/cm3) yielded a linear relationship that did not change with 0.75 mg of ouabain (P > 0.4). These data indicate that ouabain possesses a significant positive inotropic effect on the intact left ventricle without a change in energy transfer efficiency or O2 wasting.

Mechanical determinants of myocardial oxygen consumption in conscious dogs

1995 ◽  
Vol 269 (2) ◽  
pp. H609-H620 ◽  
Author(s):  
J. R. Elbeery ◽  
J. C. Lucke ◽  
M. P. Feneley ◽  
G. W. Maier ◽  
C. H. Owen ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Myocardial Oxygen Consumption ◽  
Virtual Work ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Stroke Work ◽  
External Energy ◽  
Work Model

A new practical descriptor of metabolic to mechanical myocardial energy transfer (MET), termed the virtual work model, was evaluated in 32 conscious dogs and in 8 isolated canine hearts. An index of total mechanical energy expenditure (TME) was calculated as the sum of external energy (stroke work) and an internal energy index of heat (left ventricular end-diastolic volume times left ventricular mean ejection pressure). Physiological comparison of TME (x-axis) and myocardial oxygen consumption (MVO2; y-axis) yielded highly linear MET relationships (mean r = 0.93 +/- 0.07), with an average slope of 0.86 +/- 0.39 (SD) and a y-intercept of 9.1 +/- 6.4 mW/ml myocardium. The linear MVO2-TME relationship did not vary under steady-state vs. dynamic vena caval occlusion, increased heart rate, increased afterload, or increased inotropic state with calcium infusion. Compared with five other indexes of myocardial energetics, the virtual work model of MET was the most linear, the most practical in not requiring determination of the end-systolic pressure-volume relationship, and the most accurate predictor of MVO2 under normal and altered hemodynamic conditions.

Minor preload dependence of O2 consumption of unloaded contraction in dog heart

1989 ◽  
Vol 256 (5) ◽  
pp. H1289-H1294 ◽  
Author(s):  
Y. Yasumura ◽  
T. Nozawa ◽  
S. Futaki ◽  
N. Tanaka ◽  
H. Suga
Keyword(s):  
Mechanical Load ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Ventricular Volume ◽  
Dog Heart ◽  
End Diastolic Volume ◽  
Pressure Development ◽  
Total Mechanical Energy ◽  
Whole Heart ◽  
Length Dependent Activation

We studied whether end-diastolic volume (EDV) would affect myocardial oxygen consumption (VO2) of mechanically unloaded contraction in the cross-circulated dog heart, as expected from the concept of the myocardial length-dependent activation. We made preloaded but maximally unloaded contractions from different EDVs by quickly releasing ventricular volume to eliminate systolic pressure development and hence to minimize the VO2 for mechanical load during the contraction. We then studied the relation between VO2 and EDV. The VO2 of the almost unloaded contraction from a relatively large EDV slightly exceeded the VO2 of the isovolumic contraction at V0, where V0 is the volume at which peak isovolumic pressure was zero. However, the excess VO2 could be ascribed to the residual systolic pressure-volume area (PVA) adversely produced from the large EDV, where PVA is a measure of the total mechanical energy generated during contraction. Therefore, we considered that VO2 was practically little dependent on EDV. We interpreted this finding as an indication that an increase, if any, in VO2 due to the length-dependent activation of the excitation-contraction coupling was practically negligible in the whole heart preparation.

Beneficial influence of vasoactive intestinal peptide on ventriculovascular coupling in closed-chest dogs

1992 ◽  
Vol 263 (4) ◽  
pp. H1300-H1305
Author(s):  
J. T. Colston ◽  
G. L. Freeman
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Mechanical Energy ◽  
Left Ventricular ◽  
Arterial System ◽  
Stroke Work ◽  
Vascular Effects ◽  
Arterial Elastance ◽  
End Diastolic Volume ◽  
Before And After ◽  
Effective Arterial Elastance

The effect of vasoactive intestinal peptide (VIP) on ventriculovascular coupling in the intact cardiovascular system has not been defined. We studied seven dogs chronically instrumented with left ventricular (LV) pressure manometers and three sets of diameter gauges before and after infusions of 0.02, 0.05, and 0.10 microgram.kg-1.min-1 VIP. The dogs were studied after autonomic blockade, anesthesia, and intubation, with a fixed heart rate of 160 beats/min. Contractility was assessed using LV elastance at end systole (Ees) and the slope of the stroke work-end-diastolic volume relation. The vascular influence of VIP was quantified by determining effective arterial elastance (Ea) under steady-state conditions. The overall effect on ventriculovascular coupling was assessed using the transfer of mechanical energy from LV to the arterial system (TransPVA) quantified as the percentage of pressure-volume area (PVA) expressed as stroke work. LV relaxation was measured using the time constant of LV pressure decay. The results showed that VIP increased contractility (Ees increased to 129, 156, and 181% of control; P < 0.01 for all vs. control) and decreased effective arterial elastance (Ea fell to 84, 68, and 64% of control; P < 0.0155 vs. control for the two higher doses). VIP had no consistent effects on LV relaxation. Thus, in addition to its positive ventricular effects (increased contractility), VIP has beneficial vascular effects (reduced Ea). These properties combine to improve ventriculovascular coupling, such that VIP enhances delivery of mechanical energy from the LV to the circulatory bed.

Resizable Ventricular Patch Plasty in the Porcine Left Ventricle a Pilot Study

2010 ◽  
Vol 5 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Willemijn H. F. Huijgen ◽  
Paul F. Gründeman ◽  
Tycho van der Spoel ◽  
Maarten-Jan Cramer ◽  
Paul Steendijk ◽  
...  
Keyword(s):  
Pilot Study ◽  
Animal Experiments ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Left Ventricular Aneurysm ◽  
Patch Shape ◽  
End Diastolic Volume ◽  
Patch Plasty

Objective Endoventricular circular patch plasty is a method used to reconstruct the ventricular cavity in patients with (post) ischemic left ventricular aneurysm or global dilatation. However, late redilatation with mitral regurgitation has been reported, in which postoperative apex shape seems to play an important role. We studied the feasibility of ventricular volume downsizing with a variably shaped patch in porcine hearts. Methods In five in vitro and two acute animal experiments, a dyskinetic aneurysm was simulated with a pericardial insert. Reducing patch surface by changing patch shape diminished end-diastolic volume. In vitro, static end-diastolic volume was determined for each patch shape using volumetry and echocardiography. In the acute animal experiments, preliminary observations of patch behavior in live material were made, and pressure/time relationship, dPdTmax, was registered. Results In vitro, bringing the convex patch into a flat plane reduced LV volume from 66 ± 7 mL (aneurysm) to 49 ± 5 mL. Four of 5 patch shapes further reduced volume to a mean of 38 ± 7 mL (P = 0.03). The in vitro echocardiographic measurements correlated with volumetry findings (r = 0.81). In the acute animal experiments, dPdTmax varied with patch shape, independent of volume changes. Conclusions In this pilot study, in vitro shape configuration of the resizable ventricular patch resulted in a calibrated end-diastolic volume reduction. The data of the two in vivo pilot experiments clearly indicate that change in patch configuration in the situation of more or less unchanged end-diastolic volume had impact on cardiac performance. Future studies must substantiate the results of this observation.

Cardiac dysfunction in mice lacking cytochrome-c oxidase subunit VIaH

2002 ◽  
Vol 282 (2) ◽  
pp. H726-H733 ◽  
Author(s):  
Nina B. Radford ◽  
Bang Wan ◽  
Angela Richman ◽  
Lidia S. Szczepaniak ◽  
Jia-Ling Li ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Cardiac Dysfunction ◽  
Mechanical Performance ◽  
Left Ventricular ◽  
Mutant Mice ◽  
Stroke Work ◽  
Wild Type ◽  
Oxidase Subunit ◽  
End Diastolic Volume

Cytochrome -c oxidase subunit VIaH (COXVIaH) has been implicated in the modulation of COX activity. A gene-targeting strategy was undertaken to generate mice that lacked COXVIaH to determine its role in regulation of oxidative energy production and mechanical performance in cardiac muscle. Total COX activity was decreased in hearts from mutant mice, which appears to be a consequence of altered assembly of the holoenzyme COX. However, total myocardial ATP was not significantly different in wild-type and mutant mice. Myocardial performance was examined using the isolated working heart preparation. As left atrial filling pressure increased, hearts from mutant mice were unable to generate equivalent stroke work compared with hearts from wild-type mice. Direct measurement of left ventricular end-diastolic volume using magnetic resonance imaging revealed that cardiac dysfunction was a consequence of impaired ventricular filling or diastolic dysfunction. These findings suggest that a genetic deficiency of COXVIaH has a measurable impact on myocardial diastolic performance despite the presence of normal cellular ATP levels.

scholarly journals Ventricular interaction and external constraint account for decreased stroke work during volume loading in CHF

2001 ◽  
Vol 281 (6) ◽  
pp. H2385-H2391 ◽  
Author(s):  
Thomas D. Moore ◽  
Michael P. Frenneaux ◽  
Rozsa Sas ◽  
J. J. Atherton ◽  
Jayne A. Morris-Thurgood ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular ◽  
Negative Slope ◽  
Segment Length ◽  
Stroke Work ◽  
Volume Loading ◽  
End Diastolic Volume ◽  
Pulmonary Capillary ◽  
Apparent Decrease ◽  
Pericardial Pressure

The slope of the stroke work (SW)-pulmonary capillary wedge pressure (PCWP) relation may be negative in congestive heart failure (CHF), implying decreased contractility based on the premise that PCWP is simply related to left ventricular (LV) end-diastolic volume. We hypothesized that the negative slope is explained by decreased transmural LV end-diastolic pressure (LVEDP), despite the increased LVEDP, and that contractility remains unchanged. Rapid pacing produced CHF in six dogs. Hemodynamic and dimension changes were then measured under anesthesia during volume manipulation. Volume loading increased pericardial pressure and LVEDP but decreased transmural LVEDP and SW. Right ventricular diameter increased and septum-to-LV free wall diameter decreased. Although the slopes of the SW-LVEDP relations were negative, the SW-transmural LVEDP relations remained positive, indicating unchanged contractility. Similarly, the SW-segment length relations suggested unchanged contractility. Pressure surrounding the LV must be subtracted from LVEDP to calculate transmural LVEDP accurately. When this was done in this model, the apparent decrease in contractility was no longer evident. Despite the increased LVEDP during volume loading, transmural LVEDP and therefore SW decreased and contractility remained unchanged.

Left ventricular-arterial coupling in conscious dogs

1991 ◽  
Vol 261 (1) ◽  
pp. H70-H76 ◽  
Author(s):  
W. C. Little ◽  
C. P. Cheng
Keyword(s):  
Stroke Volume ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Conscious Dogs ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Inotropic State ◽  
End Diastolic Volume ◽  
Wide Range

We investigated the criteria for the coupling of the left ventricle (LV) and the arterial system to maximize LV stroke work (SW) and the transformation of LV pressure-volume area (PVA) to SW. We studied eight conscious dogs that were instrumented to measure LV pressure and determine LV volume from three ultrasonically determined dimensions. The LV end-systolic pressure (PES)-volume (VES) relation was determined by caval occlusion. Its slope (EES) was compared with the arterial elastance (EA) and determined as PES per stroke volume. At rest, with intact reflexes, EES/EA was 0.96 +/- 0.20 EES/EA was varied over a wide range (0.18-2.59) by the infusion of graded doses of phenylephrine and nitroprusside before and during administration of dobutamine. Maximum LV SW, at constant inotropic state and end-diastolic volume (VED), occurred when EES/EA equaled 0.99 +/- 0.15. At constant VED and contractile state, SW was within 20% of its maximum value when EES/EA was between 0.56 and 2.29. The conversion of LV PVA to SW increased as EES/EA increased. The shape of the observed relations of the SW to EES/EA and SW/PVA to EES/EA was similar to that predicted by the theoretical consideration of LV PES-VES and arterial PES-stroke volume relations. We conclude that the LV and arterial system produce maximum SW at constant VED when EES and EA are equal; however, the relation of SW to EES/EA has a broad plateau. Only when EA greatly exceeds EES does the SW fall substantially. However, the conversion of PVA to SW increases as EES/EA increases. These observations support the utility of analyzing LV-arterial coupling in the pressure-volume plane.

Ventricular performance and myocardial water content during hemodilution in dogs

1978 ◽  
Vol 235 (6) ◽  
pp. H767-H775 ◽  
Author(s):  
G. A. Geffin ◽  
M. A. Vasu ◽  
D. D. O'Keefe ◽  
D. G. Pennington ◽  
A. J. Erdmann ◽  
...  
Keyword(s):  
Water Content ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Ventricular Performance ◽  
End Diastolic Volume ◽  
Lv Mass ◽  
Right Heart Bypass ◽  
Water Gain

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.

Hypercapnic acidosis increases oxygen cost of contractility in the dog left ventricle

1994 ◽  
Vol 266 (2) ◽  
pp. H730-H740 ◽  
Author(s):  
K. Hata ◽  
Y. Goto ◽  
O. Kawaguchi ◽  
T. Takasago ◽  
A. Saeki ◽  
...  
Keyword(s):  
Mechanical Energy ◽  
Left Ventricular ◽  
Oxygen Cost ◽  
Membrane Oxygenator ◽  
Arterial Perfusion ◽  
Control Value ◽  
Arterial Blood ◽  
Total Mechanical Energy ◽  
Lv Volume ◽  
The Relationship

The effect of acidosis on left ventricular (LV) mechanoenergetics was assessed in seven excised, cross-circulated dog hearts with the use of the frameworks of the contractility index (Emax) and the relationship between myocardial oxygen consumption (VO2) and pressure-volume area (PVA; a measure of the LV total mechanical energy). Acidosis was stably maintained without hypoxia by appropriately mixing CO2 and air in a membrane oxygenator in the coronary arterial perfusion circuit. Acidosis [pH: 6.98 +/- 0.09 (SD), PCO2: 91 +/- 25 mmHg in the coronary arterial blood] decreased Emax by 45 +/- 12% (P < 0.01) and PVA by 47 +/- 12% (P < 0.01) at a fixed LV volume. When the preacidosis Emax level was restored by Ca2+ infusion during acidosis, unloaded VO2 (the VO2 intercept of the VO2-PVA relation) exceeded the control value by 19 +/- 17% (P < 0.05), indicating that acidosis required higher VO2 for nonmechanical activities at a matched Emax. Moreover, the oxygen cost of enhanced contractility (the incremental ratio of unloaded VO2 to Emax) was 1.53 +/- 0.40 times higher (P < 0.01) during acidosis than preacidosis. We conclude that acidosis results in LV contractile dysfunction accompanied by an increased oxygen cost of contractility. This increased energy cost of the excitation-contraction coupling can be accounted for by a decreased Ca2+ sensitivity of the contractile proteins during acidosis.

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