Abstract 2207: Significant Impact of the Total Cavopulmonary Connection Resistance on Cardiac Output and Exercise Performance in Single Ventricles

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Kartik S Sundareswaran ◽  
Kerem Pekkan ◽  
Lakshmi Prasad Dasi ◽  
Hiroumi D Kitajima ◽  
Kevin Whitehead ◽  
...  

Introduction: The resistance of the total cavopulmonary connection (TCPC) in single ventricle (SV) circulation has long been hypothesized as a critical contributing factor to their diminished exercise capacity. We investigate this hypothesis using a lumped parameter (LP) model coupled with cardiac catheterization (cath) and computational fluid dynamics (CFD). Methods: SV pulmonary vascular resistance (1.80 ± 0.83 WU) and systemic vascular resistance (18.4 ± 7.2 WU) were obtained from cath data on 48 pts with a TCPC. TCPC resistances (0.55 ± .24 WU, min=0.24, max = 0.93) were established from CFD simulations (n=13) and in vitro experiments (n=8) conducted on anatomically accurate TCPC models from MRI. Resistance and compliance values for the normal pediatric circulation were obtained from the literature. These values were then used in a LP model developed for both the normal and SV circulation. Results: For a biventricular circulation, the cardiac output (CO) dependence on resistance is negligible, but not for the SV circulation (Fig 1a ). Capacity to increase CO with heart rate is also severely reduced for the SV. At a simulated exercise HR of 140 beats per minute, the SV patient with the highest resistance (0.93 WU) had a significantly lower increase in cardiac output (22%) when compared to an SV patient with the lowest resistance (26%) and the normal circulation (67%) (Fig 1b ). Conclusion: Hemodynamic energy cascade in a SV circulation should not be judged by stereotypes of biventricular circulation. The impact of TCPC surgical pathway resistance on cardiac output at rest and exercise was significantly higher on SVs compared to biventricular circulation. Figure 1. Impact of TCPC resistance in single ventricle vs. normal circulation, specifically (a) resting cardiac output, and (b) exercise cardiac output

2008 ◽  
Vol 295 (6) ◽  
pp. H2427-H2435 ◽  
Author(s):  
Kartik S. Sundareswaran ◽  
Kerem Pekkan ◽  
Lakshmi P. Dasi ◽  
Kevin Whitehead ◽  
Shiva Sharma ◽  
...  

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.


2002 ◽  
Vol 282 (3) ◽  
pp. H1018-H1034 ◽  
Author(s):  
Elisa Magosso ◽  
Silvio Cavalcanti ◽  
Mauro Ursino

The objective of this study was to determine the impact of a total cavopulmonary connection on the main hemodynamic quantities, both at rest and during exercise, when compared with normal biventricular circulation. The analysis was performed by means of a mathematical model of the cardiovascular system. The model incorporates the main parameters of systemic and pulmonary circulation, the pulsating heart, and the action of arterial and cardiopulmonary baroreflex mechanisms. Furthermore, the effect of changes in intrathoracic pressure on venous return is also incorporated. Finally, the response to moderate dynamic exercise is simulated, including the effect of a central command, local metabolic vasodilation, and the “muscle pump” mechanism. Simulations of resting conditions indicate that the action of baroreflex regulatory mechanisms alone can only partially compensate for the absence of the right heart. Cardiac output and mean systemic arterial pressure at rest show a large decrease compared with the normal subject. More acceptable hemodynamic quantity values are obtained by combining the action of regulatory mechanisms with a chronic change in parameters affecting mean filling pressure. With such changes assumed, simulations of the response to moderate exercise show that univentricular circulation exhibits a poor capacity to increase cardiac output and to sustain aerobic metabolism, especially when the oxygen consumption rate is increased above 1.2–1.3 l/min. The model ascribes the poor response to exercise in these patients to the incapacity to sustain venous return caused by the high resistance to venous return and/or to exhaustion of volume compensation reserve.


2011 ◽  
Vol 57 (14) ◽  
pp. E478
Author(s):  
Christopher M. Haggerty ◽  
Kartik S. Sundareswaran ◽  
Kerem Pekkan ◽  
Kirk R. Kanter ◽  
Mark A. Fogel ◽  
...  

2002 ◽  
Vol 23 (2) ◽  
pp. 171-177 ◽  
Author(s):  
C.G. DeGroff ◽  
J.D. Carlton ◽  
C.E. Weinberg ◽  
M.C. Ellison ◽  
R. Shandas ◽  
...  

2006 ◽  
Vol 101 (3) ◽  
pp. 866-872 ◽  
Author(s):  
Darija Baković ◽  
Davor Eterović ◽  
Zoran Valic ◽  
Žana Saratlija-Novaković ◽  
Ivan Palada ◽  
...  

Changes in cardiovascular parameters elicited during a maximal breath hold are well described. However, the impact of consecutive maximal breath holds on central hemodynamics in the postapneic period is unknown. Eight trained apnea divers and eight control subjects performed five successive maximal apneas, separated by a 2-min resting interval, with face immersion in cold water. Ultrasound examinations of inferior vena cava (IVC) and the heart were carried out at times 0, 10, 20, 40, and 60 min after the last apnea. The arterial oxygen saturation level and blood pressure, heart rate, and transcutaneous partial pressures of CO2and O2were monitored continuously. At 20 min after breath holds, IVC diameter increased (27.6 and 16.8% for apnea divers and controls, respectively). Subsequently, pulmonary vascular resistance increased and cardiac output decreased both in apnea divers (62.8 and 21.4%, respectively) and the control group (74.6 and 17.8%, respectively). Cardiac output decrements were due to reductions in stroke volumes in the presence of reduced end-diastolic ventricular volumes. Transcutaneous partial pressure of CO2increased in all participants during breath holding, returned to baseline between apneas, but remained slightly elevated during the postdive observation period (∼4.5%). Thus increased right ventricular afterload and decreased cardiac output were associated with CO2retention and signs of peripheralization of blood volume. These results indicate that repeated apneas may cause prolonged hemodynamic changes after resumption of normal breathing, which may suggest what happens in sleep apnea syndrome.


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