EFFECTS OF INTRAVENTRICULAR PATHOLOGIES

Primo Congresso Nazionale

di Bioingegneria DESCRIBED BY A LUMPED PARAMETER
Pisa 3-5 luglio 2008 COMPUTER MODEL
Fragomeni G. A, Colacino FM A, Piedimonte F. B, Danieli G. C, Arabia M. C
A Magna Graecia University (Catanzaro), B University of Rome “Tor Vergata” (Rome) , C Calabria University (Rende)

INTRODUCTION & AIM

METHODS
Various manifestations of mechanical dysfunction
in the ischemic myocardium, as a result of In order to investigate how a ventricle affected by RD and/or reduced contractility modifies its flow rate,
coronary arterial blood flow reduction, have been pressure and volume curves, a computer model of the LV has been developed which allows different
observed in many studies. Ventricles affected by working conditions to different ventricular portions.
ischemia (IS) causing regional dyssynchrony (RD) LV is represented by a non linear time-varying elastance (NTVE) model [4, 5] (Eq. 1). It allows relating
and reduced contractility are characterized by wall instantaneous blood pressure and volume inside the ventricle during the whole cardiac cycle.
portions’ non uniform electrical and/or mechanical dV t  (Eq. 1)
behavior. Among intraventricular pathologies, RD P(t )  P0   V (t ), t   R
dt
alone causes contraction delay in different
ventricular regions, while IS causes a decrease of where t = time, V(t) = instantaneous blood volume inside the ventricle, P(t) = instantaneous blood
their contractility. A worsening of the ventricular pressure inside the ventricle, R = Inner Resistance. The instantaneous value of the elastance is given by the
end-systolic pressure-volume relationship (ESPVR) slope of the time-varying curve ϕ[V(t),t] at time t and volume V(t). Similar relations, but different
is observed in vivo in both the cases. parameters, are used to represent the atrium (see [5] for details).
The aim of the present work is the investigation The LV has been connected to an open loop vascular circuit. The venous circuit is represented by the
and the analysis of these pathologies in humans by Guyton’s model [6], while the output of the ventricle is loaded by a 5-component Noordergraaf model of the
computer simulation. arterial systemic circuit. Both LV’s valves are represented by a direct and an inverse resistance in series
A computer model of a left ventricle (LV) divided in connection with an inductor.
two regions has been developed. They are likely to The divided LV has been represented by two NTVE models [5] and its total ventricular
have variable sizes and different working contractility has been split up. Pressure has been always assumed equal in each ventricular
conditions: one of them works physiologically, the portion. The total volume V(t) has been divided in two portions V1(t) and V2(t), and all the
other can be affected by ischemia, dyssynchrony, model parameters have been divided accordingly. The LV model of each portion can be written as follows:
dV1 t 
or both (RD+IS). Results have been validated by Pt   P0  1 V1 t , t   R1 Eq.2;
literature data [1-3]. dt
dV2 t 
The information given by this computer model can Pt   P0   2 V2 t , t   R2 Eq.3.
be used: dt
• to infer the worsened global end-systolic Parameters Cases Description
pressure-volume relationship (ESPVR), as Symbol Units Physio LV RD IS RD+IS
observed in presence of IS, RD, or both;  0,76 0,53 0,62 0,43 Efficiency
• to better understand the behaviour of a dp/dtmax mmHg/s 1609,01 2355,06 971,40 2666,32 Maximum value of dp/dt
pathological left ventricle, and of its relationship PAo-ave mmHg 99,51 86,64 83,53 96,25 Average aortic pressure (mmHg)
with preload and afterload; PAt-ave mmHg 6,50 5,81 6,53 5,97 Average left atrial pressure (mmHg)
• for diagnostic purposes. QA-ave l/min 5,51 4,11 4,38 3,33 Average flow rate in Aorta (l/min)
rmax cm 3.03 3.32 3.28 3.42 End diastolic radius
SV cm3 71,59 58,69 57,72 51,50 Stroke Volume
VAED cm3 59,22 45,70 59,33 59,01 Maximum left atrial volume (cm3)
VAES cm3 27,62 15,61 32,96 21,64 Minimum left atrial volume (cm3)
Vmean cm3 79,41 116,16 109,34 142,05 LV’s mean volume
VVED cm3 115,20 145,50 138,20 167,80 Left end-diastolic Volume (cm3)

a VVES
wmin
cm3
cm
43,61
1.25
86,81
1.22
80,48
1.16
116,30
1.06
Left end-systolic Volume (cm3)
End diastolic wall thickness
s mmHg 94,39 109,20 106,21 124,70 Systolic ventricular wall stress
tIC s 0.11 0.13 0.15 0.10 Duration of the isometric contraction

Table 1 – Simulation results

RESULTS AND DISCUSSION

All the simulations carried out with the model described above allow to get information about the behaviour of
a ventricle affected by IS and/or RD (see Table 1).
Particularly, the presence of this kind of pathologies modifies pressure and flow rate curves, causing a
variation in systolic and diastolic times. An increase of mean ventricular volume can be observed.
Therefore, under the hypothesis of constant wall volume, there is a ventricular wall stress increase due
b to wall’s thickness reduction. In relation to the physiological conditions, pathological cases show changes also
from an energetic point of view: PV loops shift rightward, mean ventricular volume increases, stroke
volume decreases, and the ventricular efficiency worsens as a consequence.
Figure 1 shows a physiological LV PV loop compared with PV loops in presence of RD (a), IS (b), RD+IS (c).
The depressed ventricular function caused by regional IS and RD may be manifest as a reduction in the
slope of the ESPVR, a parallel rightward shift of the ESPVR, or both [1]. As a consequence, the LV
PV loops shift rightward.
This computer model can be translated into the clinical practice for diagnosis of intraventricular myocardial
dysfunction. It is possible to get information like the percentage of ischemic myocardium or conduction delay
and the global corresponding contractility of the LV, thus allowing the optimization of the therapeutic phase in
order to improve its impact on peripheral perfusion and haemodynamics.

c REFERENCES
[1].Sunagawa, K., et al. Circ Res, 1983. 52(2): p. 170-8.
[2].Arts, T., et al. Biophys J, 1991. 59(1): p. 93-102.
[3].Suga, H. Physiol. Rev., 1990. 70: p. 247-277.
[4].Burkhoff, D., et al. Am J Physiol Heart Circ Physiol, 2005. 289(2): p. H501-12.
Figure 1 – PV loop for the three pathological cases: RD (a), [5].Colacino, F.M., et al. Asaio J, 2007. 53(3): p. 263-77.
IS (b), and RD+IS (c). [6].Guyton, A.C., et al., Circulatory Physiology: Cardiac Output and its Regulation. II ed. 1973: W.B. Saunders.