Cardiac Output Requirements and Maximum Dimensions for a Neonate Total Artificial Heart

1991 ◽  
Vol 14 (11) ◽  
pp. 707-715 ◽  
Author(s):  
E. Koppert ◽  
G.M. Pantalos ◽  
R. Tieleman ◽  
P. Swier ◽  
G.L. Burns
Keyword(s):  
Cardiac Output ◽  
Artificial Heart ◽  
Total Artificial Heart ◽  
Limiting Factors ◽  
Valvular Regurgitation ◽  
Left Heart ◽  
Hypoplastic Left Heart ◽  
Term Neonates ◽  
Left Heart Syndrome ◽  
First Time

Two equally important issues need to be addressed during the early stages of the design of an implantable total artificial heart (TAH): proper anatomical fit and cardiac output capacity. As part of a first-time feasibility study to develop a neonate-size TAH, two studies were conducted to establish useful anatomical and physiological standards. The first (Study A) was conducted to determine the maximum dimensions of a neonate-size TAH. Twelve preserved hearts from full-term neonates with the hypoplastic left heart syndrome were examined. A second study (Study B) was designed to determine the acceptable minimum stroke volume compatible with minimum neonate cardiac output requirements. This study was based on a combination of: a) reported cardiac output studies in healthy term neonates, and term neonates with heart failure, b) body weight range, and c) limiting factors of TAH technology, e.g., valvular regurgitation and leveling off of the maximum cardiac output value at a specific heart rate and filling pressure. The proposed neonatal standards for TAH technology are presented.

Computational Modeling of Hypoplastic Left Heart Syndrome (HLHS) in Newborn Babies

2011 ◽  
Author(s):  
Ali Jalali ◽  
C. Nataraj ◽  
Gerard F. Jones ◽  
Daniel J. Licht
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Hypoplastic Left Heart Syndrome ◽  
Ductus Arteriosus ◽  
Compartmental Analysis ◽  
Electrical Circuit ◽  
Lumped Parameter Model ◽  
Left Heart ◽  
Hypoplastic Left Heart ◽  
Left Heart Syndrome

Hypoplastic left heart syndrome (HLHS) is a congenital heart defect (CHD) in which left side of the heart is severely underdeveloped. To better understand this unique physiology, a computational model of the hypoplastic heart was constructed on the basis of compartmental analysis. Lumped parameter model of HLHS is developed based on the electrical circuit analogy. Model is made up of three parts: hypoplastic heart, pulmonary circulation and systemic circulation. Plots of blood pressure and flow for various parts of body show great match between predicted values and what we expected for the case of HLHS babies. Influence of patent ductus arteriosus (PDA) and ASD resistances on cardiac output and pulmonary to systemic flow was also studied. Results show that by increasing the PDA resistance causes more flow to pulmonary compartments and so the ratio increases. Blood flow increases by decreasing of pulmonary artery resistant. Increasing the PDA resistance causes decrease the cardiac output because of more resistance against blood occurs. Saturation increases by decreasing of pulmonary artery resistant.

Noninvasive Cardiac Output Monitoring in Newborn with Hypoplastic Left Heart Syndrome

2020 ◽  
Vol 37 (S 02) ◽  
pp. S54-S56
Author(s):  
Italo Francesco Gatelli ◽  
Ottavio Vitelli ◽  
Gaia Chiesa ◽  
Francesca De Rienzo ◽  
Stefano Martinelli
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Oxygen Saturation ◽  
Hypoplastic Left Heart Syndrome ◽  
Clinical Condition ◽  
Prostaglandin E1 ◽  
Left Heart ◽  
Hypoplastic Left Heart ◽  
Electrical Cardiometry ◽  
Left Heart Syndrome

Objective This study aimed to describe the first two cases of electrical cardiometry applied to newborn with hypoplastic left heart syndrome for hemodynamical assessment in the first days of life before surgical correction and see if this can help decision making process in these patients. Study Design We describe two case series of two full-term newborn with hypoplastic left heart syndrome in the Neonatal Intensive Care Unit, ASST Grande Ospedale Metropolitano Niguarda, between December 2019 and January 2020. Results Case 1 was persistently hemodynamically stable with prostaglandin E1 infusion at 0.01 mcg/kg/min, showing good capillary refill time, good diuresis, no difference between pre- and postductal values of oxygen saturation or blood pressure. Electrical cardiometry monitoring constantly showed cardiac output values higher than 300 mL/kg/min. Case 2 showed poor clinical condition needing prostaglandin E1 infusion up to 0.05 mcg/kg/min, intubation and septostomy associated with low cardiac output around 190 mL/kg/min. Once cardiac output has begun to rise and reached values constantly over 300 mL/kg/min, clinical condition improved with amelioration in oxygen saturation, diuresis, blood pressure, and blood gas analysis values. She was then extubated and finally clinically stable until surgery with minimal infusion of prostaglandin E1 at 0.01 mcg/kg/min. Conclusion This case highlights how hemodynamic information provided by electrical cardiometry can be used to supplement the combined data from all monitors and the clinical situation to guide therapy in these newborns waiting surgery. Key Points

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