Potts Shunt to Be Preferred Above Atrial Septostomy in Pediatric Pulmonary Arterial Hypertension Patients: A Modeling Study.

Aims: To quantitatively evaluate the basic pathophysiological process involved in the creation of Eisenmenger syndrome in pediatric pulmonary arterial hypertension (PAH) patients by either atrial septostomy (AS) or Potts shunt (PS) as well as to predict the effects of AS or PS in future PAH patients. Methods: The multi-scale lumped parameter CircAdapt model of the cardiovascular system was used to investigate the effects of AS and PS on cardiovascular hemodynamics and mechanics, as well as on oxygen saturation in moderate to severe PAH. The reference simulation, with cardiac output set to 2.1 l/min and mean systemic pressure to 61 mmHg, was used to create a compensated moderate PAH simulation with mPAP 50 mmHg. Thereupon we created a range of decompensated PAH simulations in which mPAP was stepwise increased from 50 to 80 mmHg. Then we simulated for each level of mPAP the acute effects of either PS or AS with connection diameters ranging between 0-16 mm. Results: For any mPAP level, the effect on shunt flow size is much larger for the PS than for AS. Whereas right ventricular pump work in PS is mainly dependent on mPAP, in AS it depends on both mPAP and the size of the defect. The effects on total cardiac pump work were similar for PS and AS. As expected, PS resulted in a drastic decrease of lower body oxygen saturation, whereas in AS both the upper and lower body oxygen saturation decreased, though not as drastically as in PS. Conclusion: Our simulations support the opinion that a PS can transfer suprasystemic PAH to an Eisenmenger physiology associated with a right-to-left shunt at the arterial level. Contrary to the current opinion that PS in PAH will decompress and unload the right ventricle, we show that while a PS does lead to a decrease in mPAP toward mean systemic arterial pressure, it does not unload the right ventricle because it mainly diverts flow from the pulmonary arterial system toward the lower body systemic arteries.

Atrial septostomy benefits severe pulmonary hypertension patients by increase of left ventricular preload reserve.

At present, it is unknown why patients suffering from severe pulmonary hypertension (PH) benefit from atrial septostomy (AS). Suggested mechanisms include enhanced filling of the left ventricle, reduction of right ventricular preload, increased oxygen availability in the peripheral tissue, or a combination. A multiscale computational model of the cardiovascular system was used to assess the effects of AS in PH. Our model simulates beat-to-beat dynamics of the four cardiac chambers with valves and the systemic and pulmonary circulations, including an atrial septal defect (ASD). Oxygen saturation was computed for each model compartment. The acute effect of AS on systemic flow and oxygen delivery in PH was assessed by a series of simulations with combinations of different ASD diameters, pulmonary flows, and degrees of PH. In addition, blood pressures at rest and during exercise were compared between circulations with PH before and after AS. If PH did not result in a right atrial pressure exceeding the left one, AS caused a left-to-right shunt flow that resulted in decreased oxygenation and a further increase of right ventricular pump load. Only in the case of severe PH a right-to-left shunt flow occurred during exercise, which improved left ventricular preload reserve and maintained blood pressure but did not improve oxygenation. AS only improves symptoms of right heart failure in patients with severe PH if net right-to-left shunt flow occurs during exercise. This flow enhances left ventricular filling, allows blood pressure maintenance, but does not increase oxygen availability in the peripheral tissue.

Simulation of the Fontan circulation during rest and exercise.

The Fontan palliation was introduced as surgical repair method for tricuspid atresia, creating a univentricular serial circulation. However, it is used as treatment for other life threatening complex congenital heart diseases as well. The variation of underlying pathologies treated with this palliation makes optimization difficult. To assist the optimization process, we adjusted a lumped parameter computational model of the biventricular circulation (CircAdapt) and evaluated the univentricular circulation. The model simulates beat-to-beat dynamics of the two cardiac chambers, the valves, and the systemic and pulmonary circulations. The univentricular circulation in rest and exercise was simulated. Exercise resulted in increased stroke volume, heart rate, pulse pressure, and stressed blood volume. Central venous pressure rose as a result of the constant pulmonary resistance, reducing systemic pressure drop. Reduced systemic pressure drop implies either reduction of systemic flow or further decrease of systemic resistance. Based on our simulation results, we conclude that exercise capacity in Fontan patients is limited due to increase of central venous pressure and the impossibility to reduce systemic resistance further, restricting systemic flow.

The influence of nonlinear intra-thoracic vascular behaviour and compression characteristics on cardiac output during CPR.

Clinical observations suggest that the assumption of a linear relationship between chest compression pressure and cardiac output may be oversimplified. More complex behaviour may occur when the transmural pressure is large, changing the compliances and resistances in the intra-thoracic vasculature. A fundamental understanding of these compression induced phenomena is required for improving CPR. An extensively used, lumped element computer model (model I) of the circulation was upgraded and refined to include the intrathoracic vasculature (model II). After validation, model II was extended by adding variable compliances and resistances (model III) to the vascular structures. Successively, ranges of compression pressures, frequencies, duty cycles and compression pulse shapes were applied while controlling all other parameters. Cardiac output was then compared. The nonlinearities in compliance and resistance become important, limiting factors in cardiac output, starting in our experimental series at 70 mmHg peak compression pressure, and increasing with higher pressures. This effect is reproducible for sinusoidal and trapezoidal compression forms, resulting in lower cardiac output in all experiments at high compression pressures. Duty cycle and wait time are key parameters for cardiac output. Our data strongly indicate that vascular compliance, especially the ability of vessels to collapse (and potentially the cardiac chambers), can be a central factor in the limited output generated by chest compressions. Just pushing 'harder' or 'faster' is not always better, as an 'optimal' force and frequency may exist. Overly forceful compression can limit blood flow by restricting filling or depleting volume in the cardiac chambers and central great vessels.