Preload-adjusted right ventricular maximal power: concept and validation

2004 ◽  
Vol 287 (4) ◽  
pp. H1632-H1640 ◽  
Author(s):  
Soren Schenk ◽  
Zoran B. Popović ◽  
Yoshie Ochiai ◽  
Fernando Casas ◽  
Patrick M. McCarthy ◽  
...  

Right ventricular (RV) maximal power (PWRmx) is dependent on preload. The objective of this study was to test our hypothesis that the PWRmx versus end-diastolic volume (EDV) relationship, analogous to the load-independent stroke work (SW) versus EDV relationship (preload-recruitable SW, PRSW), is linear, with the PWR x-axis intercept (V0PWR) corresponding to the PRSW intercept (V0SW). If our hypothesis is correct, the preload sensitivity of PWRmx could be eliminated by adjusting for EDV and V0PWR. Ten dogs were instrumented with a pulmonary flow probe, micromanometers, and RV conductance catheter. Data were obtained during bicaval occlusions under various conditions and fitted to PWRmx = a·(EDV − V0PWR)β, where a is the slope of the relationship. The PWRmx versus EDV relationship did not deviate from linearity (β = 1.09, P = not significant vs. 1), and V0PWR correlated with V0SW ( r = 0.93, P <0.0001). V0PRW was related to steady-state EDV and left ventricular end-diastolic pressure, allowing for estimation of V0PWR (V0Est) and single-beat PWRmx preload adjustment. Dividing PWRmx by the difference of EDV and V0PWR (PAMPV0PWR) eliminated preload dependency down to 50% of the baseline EDV. PWRmx adjustment using V0Est (PAMPV0Est) showed similar preload independency. Enhancing contractility increased PAMPV0PWR and PAMPV0Est from 176 ± 52 to 394 ± 205 W/ml × 104 and 145 ± 51 to 404 ± 261 W/ml × 104, respectively, accompanied by an increase of PRSW from 13.0 ± 4.5 to 29.7 ± 16.4 mmHg (all P <0.01). PAMPV0PWR and PAMPV0Est correlated with PRSW ( r = 0.85; r = 0.77; both P <0.001). Numerical modeling confirmed the accuracy of our experimental data. Thus preload adjustment of PWRmx should consider a linear PWRmx versus EDV relationship with distinct V0PWR. PAMPV0PWR is a preload-independent estimate of RV contractility that may eventually be determined noninvasively.

2001 ◽  
Vol 281 (6) ◽  
pp. H2385-H2391 ◽  
Author(s):  
Thomas D. Moore ◽  
Michael P. Frenneaux ◽  
Rozsa Sas ◽  
J. J. Atherton ◽  
Jayne A. Morris-Thurgood ◽  
...  

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.


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 ◽  
...  

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.


1990 ◽  
Vol 258 (4) ◽  
pp. H1079-H1086 ◽  
Author(s):  
R. J. Applegate ◽  
W. P. Santamore ◽  
H. S. Klopfenstein ◽  
W. C. Little

We evaluated the contribution of the thorax and the undisturbed pericardium to the external pressure of the euvolemic left ventricle in thirteen anesthetized dogs. Left ventricular (LV) end-diastolic pressure (EDP) in the euvolemic state was 7 +/- 2 mmHg initially and increased to 10 +/- 2 mmHg after the chest and pericardium were opened. LV end-diastolic volume (conductance catheter) was 43 +/- 20 ml initially and did not change after the chest or the pericardium was opened. Intrathoracic (PIT) and pericardial (PPER) pressures were calculated as the difference in LV chamber pressure before and after opening these spaces. Thus for the LV, PIT was -3 +/- 1 mmHg, and PPER was 0 +/- 2 mmHg. Isovolumic relaxation, early diastolic filling, and total diastolic filling were not significantly altered after the chest or pericardium was opened. Thus under euvolemic conditions in this model pericardial pressure is negligible, and the external pressure of the undisturbed left ventricle is negative and equal to intrathoracic pressure.


1987 ◽  
Vol 253 (3) ◽  
pp. H512-H518
Author(s):  
P. Schiereck ◽  
J. H. Nieuwenhuijs ◽  
E. L. de Beer ◽  
M. W. van Hessen ◽  
F. A. van Kaam ◽  
...  

Experiments were performed on isolated rabbit left ventricles. Controlled ejections during otherwise isovolumic contractions were studied. The time constant of relaxation was defined as the slope of the linear approximation of the ln(P)-t relation over a 40-ms period starting 20 ms after the minimum of the first time derivative of left ventricular pressure (dP/dt) of the isovolumic contraction. Variations in time of ejection, its amplitude, and velocity are applied independently. No direct effect of the variations in time and velocity of the ejection on the time constant of relaxation was found. This is in conflict with the findings of Hori et al. (Circ. Res. 55: 31-38, 1984). The difference is due to the influence of the recovery of pressure directly after the end of ejection in their study. This effect is present especially when ejection was timed to take place late in the contraction phase. The effect of the variation of the amplitude of the ejection on the time constant was similar to the effect of the end-diastolic pressure on the end-diastolic volume. It is concluded that the time constant of relaxation depends linearly on the same processes that are responsible for the height of the end-diastolic pressure.


Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Rajat Kalra ◽  
Tamas Alexy ◽  
Jason Bartos ◽  
Andrea M Elliott ◽  
Anthony Prisco ◽  
...  

Introduction: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a frequently used hemodynamic support strategy, but considerable debate exists about its hemodynamic effects. We evaluated changes in left ventricular (LV) function, volumes, and work in patients treated with VA-ECMO using invasive LV catheterization and three-dimensional echocardiographic volumes. Methods: In this case series, patients underwent evaluation due to persistent vasoplegia or poor LV function despite treatment with VA-ECMO. Hemodynamic parameters were reported as medians with interquartile ranges. Paired comparisons were done to evaluate hemodynamics at the baseline (highest) and lowest tolerated levels of VA-ECMO support. Results: Six patients aged 53.5 (41.8, 57.8) years were included. Three patients received VA-ECMO for refractory cardiogenic shock and three patients for extracorporeal cardiopulmonary resuscitation. The baseline LV ejection fraction was 22.1% (19.0%, 24.7%). The baseline and lowest VA-ECMO flows were 4.0 (4.0, 4.0) L/min and 1.0 (1.0, 1.5) L/min, respectively. Compared to the lowest flow, full VA-ECMO support reduced LV end-diastolic volume [116 (90, 153) versus 94 (58, 119) mL, p=0.03], LV end-diastolic pressure [16 (12, 24) versus 14 (9,15) mmHg, p=0.03], LV stroke work [2640 (1800, 4275) versus 1953 (759, 2179) mL*mmHg, p=0.03], and pressure-volume area [6864 (4038, 7715) versus 4575 (3142, 5888) mL*mmHg; p=0.046], respectively. The pressure-volume curves at the highest and lowest VA-ECMO flows are represented in blue and red, respectively ( Figure ). Mean arterial pressure and heart rate were similar at the lowest and highest flows (p=0.17 and p=0.60, respectively). All patients were decannulated from VA-ECMO. Four survived the index hospitalization. Conclusion: High flow VA-ECMO support significantly reduced LV end-diastolic volume, end-diastolic pressure, stroke work, and pressure-volume area compared to low flow.


2012 ◽  
Vol 302 (11) ◽  
pp. H2363-H2371 ◽  
Author(s):  
Rodrigo V. Wainstein ◽  
Zion Sasson ◽  
Susanna Mak

We aimed to determine whether sex differences in humans extend to the dynamic response of the left ventricular (LV) chamber to changes in heart rate (HR). Several observations suggest sex influences LV structure and function in health; moreover, this physiology is also affected in a sex-specific manner by aging. Eight postmenopausal women and eight similarly aged men underwent a cardiac catheterization-based study for force-interval relationships of the LV. HR was controlled by right atrial (RA) pacing, and LV +dP/d tmax and volume were assessed by micromanometer-tipped catheter and Doppler echocardiography, respectively. Analysis of approximated LV pressure-volume relationships was performed using a time-varying model of elastance. External stroke work was also calculated. The relationship between HR and LV +dP/d tmax was expressed as LV +dP/d tmax = b + mHR. The slope ( m) of the relationship was steeper in women compared with men (11.8 ± 4.0 vs. 6.1 ± 4.1 mmHg·s−1·beats−1·min−1, P = 0.01). The greater increase in contractility in women was reproducibly observed after normalizing LV +dP/d tmax to LV end-diastolic volume (LVVed) or by measuring end-systolic elastance. LVVed and stroke volume decreased more in women. Thus, despite greater increases in contractility, HR was associated with a lesser rise in cardiac output and a steeper fall in external stroke work in women. Compared with men, women exhibit greater inotropic responses to incremental RA pacing, which occurs at the same time as a steeper decline in external stroke work. In older adults, we observed sexual dimorphism in determinants of LV mechanical performance.


2004 ◽  
Vol 287 (5) ◽  
pp. H2132-H2137 ◽  
Author(s):  
Pál Pacher ◽  
Jon G. Mabley ◽  
Lucas Liaudet ◽  
Oleg V. Evgenov ◽  
Anita Marton ◽  
...  

Aging is associated with profound changes in the structure and function of the heart. A fundamental understanding of these processes, using relevant animal models, is required for effective prevention and treatment of cardiovascular disease in the elderly. Here, we studied cardiac performance in 4- to 5-mo-old (young) and 24- to 26-mo-old (old) Fischer 344 male rats using the Millar pressure-volume (P-V) conductance catheter system. We evaluated systolic and diastolic function in vivo at different preloads, including preload recruitable stroke work (PRSW), maximal slope of the systolic pressure increment (+dP/d t), and its relation to end-diastolic volume (+dP/d t-EDV) as well as the time constant of left ventricular pressure decay, as an index of relaxation. The slope of the end-diastolic P-V relation (EDPVR), an index of left ventricular stiffness, was also calculated. Aging was associated with decrease in left ventricular systolic pressure, +dP/d t, maximal slope of the diastolic pressure decrement, +dP/d t-EDV, PRSW, ejection fraction, stroke volume, cardiac and stroke work indexes, and efficiency. In contrast, total peripheral resistance, left ventricular end-diastolic volume, left ventricular end-diastolic pressure, and EDPVR were greater in aging than in young animals. Taken together, these data suggest that advanced aging is characterized by decreased systolic performance accompanied by delayed relaxation and increased diastolic stiffness of the heart in male Fischer 344 rats. P-V analysis is a sensitive method to determine cardiac function in rats.


1984 ◽  
Vol 57 (5) ◽  
pp. 1520-1527 ◽  
Author(s):  
W. P. Santamore ◽  
J. L. Heckman ◽  
A. A. Bove

With respiration, right ventricular end-diastolic volume fluctuates. We examined the importance of these right ventricular volume changes on left ventricular function. In six mongrel dogs, right and left ventricular volumes and pressures and esophageal pressure were simultaneously measured during normal respiration, Valsalva maneuver, and Mueller maneuver. The right and left ventricular volumes were calculated from cineradiographic positions of endocardial radiopaque markers. Increases in right ventricular volume were associated with changes in the left ventricular (LV) pressure-volume relationship. With normal respiration, right ventricular end-diastolic volume increased 2.3 +/- 0.7 ml during inspiration, LV transmural diastolic pressure was unchanged, and LV diastolic volume decreased slightly. This effect was accentuated by the Mueller maneuver; right ventricular end-diastolic volume increased 10.4 +/- 2.3 ml (P less than 0.05), while left ventricular end-diastolic pressure increased 3.6 mmHg (P less than 0.05) without a significant change in left ventricular end-diastolic volume. Conversely, with a Valsalva maneuver, right ventricular volume decreased 6.5 +/- 1.2 ml (P less than 0.05), and left ventricular end-diastolic pressure decreased 2.2 +/- 0.5 mmHg (P less than 0.05) despite an unchanged left ventricular end-diastolic volume. These changes in the left ventricular pressure-volume relationship, secondary to changes in right ventricular volumes, are probably due to ventricular interdependence. Ventricular interdependence may also be an additional factor for the decrease in left ventricular stroke volume during inspiration.


1990 ◽  
Vol 258 (2) ◽  
pp. H424-H430
Author(s):  
G. L. Freeman ◽  
J. T. Colston ◽  
J. Hultman

Adenosine, a potent vasodilator of both the peripheral and coronary vasculature, is increasingly used to produce controlled hypotension in the clinical and experimental setting. To define the influence of adenosine on left ventricular (LV) performance in conscious closed-chest dogs were studied six chronically instrumented autonomically blocked animals before and after the administration of 0.3, 0.6, and 1.2 microM.kg-1.min-1 infusions of adenosine. Systolic performance was quantified by the end-systolic pressure-volume (Pes-Ves) and stroke work end-diastolic volume (SW-EDV) relations. Active diastolic performance was quantified by the time constant of LV relaxation (T), whereas passive diastolic properties were assessed by comparing LV pressures at a common LV volume. Despite a decrease of mean arterial pressure of 51 mmHg, adenosine did not change the slope of the Pes-Ves relation or the end-systolic volume at a pressure of 100 mmHg. The slope of the SW-EDV relation was also unchanged, and its volume axis intercept was slightly reduced. There were no differences in T or in the diastolic pressure at a common LV volume. Thus adenosine appears to have little influence on systolic or diastolic LV performance aside from its marked affect on afterload, indicating it is a useful agent for producing controlled hypotension.


2012 ◽  
Vol 109 (3) ◽  
pp. 417-422 ◽  
Author(s):  
Matthew C. Schwartz ◽  
Jonathan J. Rome ◽  
Matthew J. Gillespie ◽  
Kevin Whitehead ◽  
Matthew A. Harris ◽  
...  

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