The total cavopulmonary connection resistance: a significant impact on single ventricle hemodynamics at rest and exercise

Abstract

Little is known about the impact of the total cavopulmonary connection (TCPC) on resting and exercise hemodynamics in a single ventricle (SV) circulation. The aim of this study was to elucidate this mechanism using a lumped parameter model of the SV circulation. Pulmonary vascular resistance (1.96+/-0.80 WU) and systemic vascular resistances (18.4+/-7.2 WU) were obtained from catheterization data on 40 patients with a TCPC. TCPC resistances (0.39+/-0.26 WU) were established using computational fluid dynamic simulations conducted on anatomically accurate three-dimensional models reconstructed from MRI (n=16). These parameters were used in a lumped parameter model of the SV circulation to investigate the impact of TCPC resistance on SV hemodynamics under resting and exercise conditions. A biventricular model was used for comparison. For a biventricular circulation, the cardiac output (CO) dependence on TCPC resistance was negligible (sensitivity=-0.064 l.min(-1).WU(-1)) but not for the SV circulation (sensitivity=-0.88 l.min(-1).WU(-1)). The capacity to increase CO with heart rate was also severely reduced for the SV. At a simulated heart rate of 150 beats/min, the SV patient with the highest resistance (1.08 WU) had a significantly lower increase in CO (20.5%) compared with the SV patient with the lowest resistance (50%) and normal circulation (119%). This was due to the increased afterload (+35%) and decreased preload (-12%) associated with the SV circulation. In conclusion, TCPC resistance has a significant impact on resting hemodynamics and the exercise capacity of patients with a SV physiology.

Fig. 1.

Three-dimensional anatomic reconstructions of the total cavopulmonary connection (TCPC) models used in this study. In total, there were six intra-atrial models (models M01, M03, M04, M05, M14, and M15), nine extracardiac models (models M02, M06, M07, M08, M09, M10, M12, M13, M16), and one inferior vena cava-main pulmonary artery TCPC model (model M11).

Fig. 2.

Schematics describing the lumped parameter models used in the study. A: biventricular circulation; B: univentricular circulation. R, resistance; C, compliance; E, load; PVB, pulmonary venous bed; PAB, pulmonary arterial bed; RV, right ventricle; RA, right atrium; LA, left atrium; LV, left ventricle; SAB, systemic arterial bed; SVB, systemic venous bed; MV, mitral valve; AV, aortic valve.

Fig. 4.

Impact of R_TCPC on cardiac output (A), end-systolic pressure (B), central venous pressure (C), afterload (E_a; D), preload (E_es; E), and the ventricular vascular coupling ratio (F) under resting conditions.

Fig. 3.

R_TCPC plotted as a function of cardiac index representing 16 geometries used in the study. These curves were used as inputs to the lumped parameter model. The maximum resistance curve corresponds to model M16, whereas the minimum resistance curve corresponds to model M6. The mean resistance curve is the mean resistance at rest, moderate exercise, and severe exercise, respectively.

Fig. 5.

Impact of increasing heart rate on cardiac output (A), end-systolic pressure (B), central venous pressure (C), ventricular E_a (D), ventricular E_es (E), vascular-ventricular coupling (F), R_TCPC (G), and R_TCPC/pulmonary vascular resistance (PVR) (H) for the case of a normal biventricular circulation (⧫) and single ventricle scenarios with a low-resistance TCPC (▪), mean-resistance TCPC (•), or high-resistance TCPC (▴).

Fig. 6.

Cardiac index versus resistance for the 16 patients in the study. The cardiac index was evaluated using MRI, and the resistance was evaluated using computational fluid dynamics.