[ Scientific Activity - Actividad Científica ] [ Brief Communications - Temas Libres ]Left Ventricle-Like Mechanical Properties of the Right
Grignola Juan Carlos; Ginés Fernando.
Facultad de Medicina. Universidad de la República. Montevideo-Uruguay.
Material and Methods
Introduction: The right ventricle (RV), unlike the left ventricle (LV), presents a triangular-shaped pressure-volume (P-V) loop, an earlier maximum elastance (Emax), and an ejection with two phases, related to the sequentially pattern of its contraction from the sinus to the conus. In addition, the RV has no isovolumic phases, and Emax, -dP/dt max and the end of ejection do not occur at the same time. These differences may depend on the particular load conditions for every ventricle.
Objective: We studied the RV mechanical properties following an acute afterload increase.
Material and methods: The ventricular, aortic and pulmonary pressures, pulmonary flow, and the ventricular volumes (sonomicrometry), were measured in five sheep between 20-30 kg, anesthetized with intravenous pentobarbital. Pulmonary arterial hypertension was induced by E.coli endotoxemia; neither preload nor contractility was modified during this period.
Results: The acute increase of the RV afterload, measured as the mean arterial pulmonary pressure (11.9 ± 1.3 to 24 ± 3.5 mmHg) produced the following changes on the RV: 1. The Emax shifted towards the end of the ejection (127.5 ± 18.5 ms) and the ejection time is shortened (57.5 ± 20.3 ms), such that, -dP/dt max occured at the end of the ejection. 2. The P-V loop became rectangular, i.e.; the systolic and diastolic phases are isovolumic. 3. The ejection showed a single phase.
Conclusions: The mechanical properties of the RV are determined by its afterload condition, mimicking the LVs ones following an acute afterload increase. This accords with the hypothesis that the normal RV contraction pattern and P-V loop depend on its loading conditions rather than reflecting a specific property of the RV myocardium.
Unlike the left ventricle (LV), the right ventricle (RV) has been largely ignored in terms of the detailed characterisation of its function. Accurate quantitative evaluation of the RV function has been limited by its complex structural geometry and contraction pattern (1). More recently, the development of tomographic imaging techniques such as computed tomography, magnetic resonance imaging and acoustic echocardiography, conductance ventriculography and sonomicrometry have allowed to estimate the RV volume and pressure-volume (P-V) loop (2-7). The cardiac cycle phases and P-V loop of the normal RV were described in an earlier study (6,7). Briefly, the RV, unlike the LV, presents a triangular-shaped P-V loop, an earlier maximum elastance (Emax), and an ejection with two phases, related to the sequential pattern of its contraction from the sinus to the conus. In addition, the RV has no isovolumic phases, and Emax, peak negative first derivative of ventricular pressure (-dP/dtmax) and the end of ejection do not occur at the same time. It was suggested that these differences may depend on the particular load conditions for every ventricle and therefore reflect the different impedance characteristics of the systemic and pulmonary vascular beds.
We studied the RV mechanical properties following an acute afterload increase.
Material and Methods:Five female merino sheep, weighting 26 ± 4,5 kg were anesthetized with intravenous injection of pentobarbital. The animals were traqueostomized and respiration was maintained with a positive pressure respirator. Arterial oxygen and carbon dioxide partial pressures were monitored. The heart was exposed through a left thoracotomy at the fifth intercostal space. The ventricular, aortic and pulmonary pressures (high fidelity microtransducers), pulmonary flow (doppler flowprobe), and the ventricular volumes (sonomicrometry) were measured (6,7). After surgical preparation, data were recorded under control conditions and after an acute increase of RV afterload. Pulmonary arterial hypertension was induced by E.coli endotoxemia (single bolus of 1mg i/v); neither preload nor contractility was modified during this period. A transient acute decrease of preload was produced by a complete inferior vena cava occlusion, in order to calculate inotropic indexes. All signals were simultaneously monitored in real time and were processed off line (6,7). In each cardiac cycle, the Emax was defined as the end-systolic point. The first derivative of LV and RV pressure (dP/dt) were calculated digitally, and were used as the reference signal to define end diastole (at the onset of its rapid upstroke). Therefore each cycle was individualized from the end of the previous diastole up to the end of the present diastole. The first derivative of ventricular volumes were also calculated digitally. Grouped data were expressed as mean ± SD. We compared grouped data by using the non-parametric Wilcoxon signal-rank test. The null hypothesis was rejected if p < 0.05. Top Results: Haemodynamic data: RV afterload, measured as the mean arterial pulmonary pressure, increased from 11.9 ± 1.3 to 24 ± 3.5 mmHg 3 to 5 minutes after i/v endotoxin infusion. Pulmonary vascular resistance increased from 444 ± 87 to 983 ± 96 (dyn.s.cm-5). There were no significant modifications in the cardiac output (CO) (1.8 ± 0.49; 1.75 ± 0.38 l/min); mean systemic arterial pressure (81.9 ± 16; 79 ± 15 mmHg); systemic vascular resistance (3480 ± 358; 3474 ± 315 dyn.s.cm-5); RV end diastolic volume (50 ± 18; 54 ± 21 ml) and RV preload recruitable work (PRSW) (9.5 ± 2.7; 11 ± 3.2 mmHg) during this period.
The aim of this study was to analyze the differences between the normal
RV P-V loop and loops obtained from the RV affected by changes in its loading conditions.
We showed that an acute and moderate RV afterload increase changes the mechanical properties of the RV, resembling LV contraction pattern. Secondly, an acute RV preload decrease does not modify the RV P-V loop morphology. These observations are in agreement with Redington et al who obtained RV rectangular shaped P-V loops in patients with raised RV systolic pressure secondary to pulmonary valvular stenosis and tetralogy of Fallot (4). Moreover, they showed that the shape of the RV P-V loop in patients with diagnosis of an ostium secundum atrial septal defect (RV volume overload) was indistinguishable from that of the normal RV (4). Schwartz et al demonstrated that RV contractile function is maintained during moderate pressure overload (RV systolic pressure 40-45 mmHg) and that the onset of RV failure coincides with severe pulmonary hypertension (³ 60 mmHg), and RV ischemia (8). The maintenance of CO and the PRSW, allow us to discard RV ischemia. Finally, Zwissler et al demonstrated that after acute pulmonary microembolisation, RV pressure-lengh loops of the inflow and outflow tract assumed a rectangular shape mimicking LV mechanical properties (9). This could explain the lost of sequentially pattern of RV contraction from the sinus to the conus (7) and the presence of a single phased ejection
Conclusions:The mechanical properties of the RV are determined by its afterload condition, mimicking the LVs ones following an acute afterload increase. This is consistent with the hypothesis that the normal RV contraction pattern and P-V loop depend on its loading conditions rather than reflecting a specific property of the RV myocardium.
Figure 1 Recordings of ventricular and arterial
pressures, ventricular volume, pulmonary flow and the first derivative
of the ventricular pressure and volume (A. Basal, B. Pulmonary hypertension). RVP: right ventricular pressure; PAP:
pulmonary arterial pressure; RVV: right ventricular volume; RV dP/dt and dV/dt: first derivative of RV pressure and
volume respectively. E and L: early and late ejection. 1: Emax, 2: -dP/dt max, 3: end of ejection.
Figure 2 Right ventricular pressure-volume loops with the end-systolic pressure-volume
relationship (ESPVR), recorded during vena cava occlusion (A. Basal conditions,
B. Pulmonary hypertension).
References:1. Redington AN, Gray HH, Hodson ME, Rigby ML, Oldershaw PJ. Br Heart J 1988; 59:23-30.
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