Sensitivity of left ventricular end-systolic pressure-volume relation to type of loading intervention in dogs.

Abstract

The influence of different types of loading intervention on the resulting end-systolic pressure-volume relation (ESPVR) of the left ventricle in situ was investigated in anesthetized open-chest dogs. Left ventricular volume was measured by conductance catheter and pressure was measured by tip-micromanometer. Two loading interventions were applied: a pressure intervention (INp) by gradually occluding the descending aorta and a volume intervention (INv) by rapidly infusing 180 ml blood into the vena cava. The pressure-volume loops during an intervention always showed a linear ESPVR, the slope of which, Ees, was calculated. Possible method-related artifacts were assessed and could be excluded. Results from 16 dogs show that Ees(INp) was always larger (1.37 ±0.45 kPa/ml) than Ees(INv) (0.73 ± 0.32 kPa/ml) (p<0.001). This difference was enhanced by /3-blockade through metoprolol. The same phenomenon was found for the slope (SdPV) of the relation between d P / d t^ and end-diastolic volume: SdPV(INp) = 45.17±22.63 kPa/ml/sec and SdPV(INv) = 20.55±11.13 kPa/ml/ sec. In seven dogs, a right heart bypass was performed to study the influence of stroke volume on the ESPVR by applying a pressure intervention under three conditions: with constant end-diastolic volume (decreasing stroke volume), Ees = 2.27 ±0.79 kPa/ml; with constant stroke volume, Ees = 1.59 ±0.51 kPa/ml; and with increasing stroke volume (and increasing end-diastolic volume), Ees = 1.36 ± 0.49 kPa/ml. Analysis of variance revealed a statistically significant relation between Ees and stroke volume (/X0.01). From the right heart bypass experiments, we conclude that shorteningrelated deactivation plays a role in the observed behavior of the ESPVR. However, the results from the series with intact circulation indicate that aortic occlusion has an additional effect on the slope of the ESPVR, leading to increased myocardial inotropism, perhaps mediated through a peripheral stimulus in response to decreased perfusion. (Circulation Research 1988;62:1247-1258 D iastolic cardiac muscle length, reflected by I end-diastolic ventricular volume (EDV), has a strong influence on the mechanical function of the ventricle, whether expressed as stroke volume (SV), systolic pressure, or external work. This formulation, known as Starling's law of the heart, 1 is considered rather inadequate nowadays because other variables such as aortic pressure and heart rate have an even more profound influence on cardiac mechanical performance. A reduction in total vascular resistance, for example, brought on by vasodilator therapy, reduces aortic pressure and increases SV primarily by a reduction in end-systolic volume. Rather than using ventricular function curves or graphs representing the dependence of variables such as SV or work and ejection fraction on preload (EDV) or afterload [aortic pressure, systolic left ventricular (LV) pressure], it is useful to describe ventricular performance in the pressurevolume (PV) plane. The first to propose such methods to describe the work performed by ...

Load dependency in force–length relations in isolated single cardiomyocytes

“…Strictly speaking, however, instantaneous ventricular pressure can be more or less reduced from isovolumic pressure, when the velocity of ejection is increased (Baan and Van der Velde, 1988;Leach et al, 1980;Suga et al, 1980). In papillary muscle preparation, similar force reduction has been observed in force-length (FL) relations (Hisano and Cooper, 1987).…”

A comparative study of preload‐adjusted maximal and peak power: assessment of ventricular performance in clinical practice

“…The elastance of the ventricle at that moment is influenced by ventricular resistance and the shortening deactivation that decreases the pressure generated by the ventricle. Hence the pressure-volume loop in that instant does not reflect ventricular elasticity [9][10][11][12][13]. Instead, in our opinion, ventricular power generation may be linked to the tension-velocity-length relationship of cardiac muscle, offering a different theoretical basis for the index within a physiological framework [14].…”

The step response of left ventricular pressure to ejection flow: A system oriented approach

“…A number of ejection parameters were claimed to influence the time course of elastance. Increasing stroke volume and/or ejection fraction (8,97), as well as the preload to the ventricle (8,28), were shown to result in a decrease of elastance. In contrast, after increasing afterload, the opposite occurred (8,31,84).…”

“…Increasing stroke volume and/or ejection fraction (8,97), as well as the preload to the ventricle (8,28), were shown to result in a decrease of elastance. In contrast, after increasing afterload, the opposite occurred (8,31,84). These findings were confusing since, for instance, preload, either to heart muscle (38,44), or to the intact ventricle (61,84), as well as afterload (84), were found to enhance the contractile state.…”

“…One way of dealing with deviations encountered experimentally consists of defining additional state vec- tor components and thus making the model more accurate. As to the elastance model, it was shown in isolated ventricles (97), as well as in the intact animal (8,20,28,58,91), that deviations occur for greater stroke volumes and ejection fractions. This was also shown for extreme conditions on contractile state by Burkhoff et al (19).…”