ABSTRACT
This obituary highlights a number of contributions by Professor Jan Beneken (1934-2021) to modeling of human physiology and pharmacology and to simulation-based training.
ABSTRACT
Fetal oxygenation is sometimes compromised due to hyperstimulation of uterine contractions (UC) following labor augmentation with oxytocin. We present a model for educational simulation that incorporates the pharmacokinetic-pharmacodynamic properties of oxytocin, reproducing the effect of this drug on UC features. Six UC tracings were generated, reflecting different relevant situations. Three independent experts identified correctly the simulated situations in all tracings and attributed an average realism score of 9.4 (0-10). The model presented for simulation of the effect of oxytocin on UC provides sufficiently realistic results to be used in healthcare education and can easily be adapted to different patients and educational scenarios.
Subject(s)
Education, Medical , Models, Biological , Oxytocin/pharmacology , Uterine Contraction/drug effects , Female , Humans , Oxytocin/pharmacokinetics , Pressure , Uterus/drug effects , Uterus/physiologyABSTRACT
Simulation provides a risk free and controllable environment for training of healthcare providers. The limited realism of available simulators and training programs impedes immersive training in obstetric emergencies. In developed countries, intrapartum monitoring in high-risk cases involves continuous evaluation of foetal heart rate and uterine contractions signals. We present an essential component of a high-fidelity simulator for normal and critical situations in labour and delivery, namely an intrauterine pressure generator. The signal model behind the generator consists of a truncated Gaussian curve with the programmable features: amplitude, frequency, duration, and resting tone. Through analysis of 44h of physiological data, we demonstrate that the natural variability of these features and of the baseline pressure can be approximated by deterministic trends and stationary stochastic processes. Signal parameters can be controlled by simulation instructors, scripts, or other models to reflect different patients, pathologies, and evolving clinical situations. Twelve 40-min tracings reflecting three different patients in labour were presented to three clinical experts, who attributed similar realism scores to simulated and to real tracings.
Subject(s)
Delivery, Obstetric , Fetal Monitoring/methods , Labor, Obstetric/physiology , Obstetrics/education , Prenatal Diagnosis/methods , Pressure , Uterine Monitoring/methods , Computer Simulation , Female , Fetal Monitoring/instrumentation , Heart Rate, Fetal/physiology , Humans , Normal Distribution , Pregnancy , Prenatal Diagnosis/instrumentation , Signal Processing, Computer-Assisted , Stochastic Processes , Time Factors , Uterine Contraction/physiology , Uterine Monitoring/instrumentationABSTRACT
Birth is characterized by swift and complex transitions in hemodynamic and respiratory variables. Unrecognized pathologies or incidents may quickly become fatal or cause permanent damage. This article introduces an essential component of an acute perinatal care simulator, namely a model for educational simulation of normal hemodynamic transitions seen during and shortly after birth. We explicitly formulate educational objectives and adapt a preexisting model for the simulation of neonatal cardiovascular physiology to include essential aspects of fetal hemodynamics. From the scientific literature, we obtain model parameters that characterize these aspects quantitatively. The fetal model is controlled by a time- and event-based script of changes occurring at birth, such as onset of breathing and cord clamping, and the transitory phase up to 24 h after birth. Comparison of simulation results with published target data confirms that realistic simulated hemodynamic vital signs are achieved.
Subject(s)
Computer Simulation , Fetus/blood supply , Hemodynamics , Models, Cardiovascular , Parturition , Blood Flow Velocity , Blood Pressure , Constriction , Humans , Infant, Newborn , Perinatal Care , Regional Blood Flow , Reproducibility of Results , Respiration, Artificial , Respiratory Mechanics , Time Factors , Umbilical Cord/blood supply , Umbilical Cord/surgeryABSTRACT
We identified errors in the software implementation of the mathematical model presented in: Sá Couto CD, van Meurs WL, Goodwin JA, Andriessen P. A model for educational simulation of neonatal cardiovascular pathophysiology. Simul Healthcare 2006;1:4-12. Simulation results obtained with corrected code are presented for future reference. All but one of the simulation results do not differ by more than 9% from the previously published results. The heart rate response to acute loss of 30% of blood volume, simulated with corrected code is stronger than published target data. This modeling error was masked by errors in code implementation. We improved this response and the model by adjusting the gains and adding thresholds and saturations in the baroreflex model. General considerations on identification of model and code errors and model validity are presented.
Subject(s)
Cardiovascular Diseases/physiopathology , Cardiovascular Diseases/therapy , Computer Simulation , Education, Medical/methods , Software Design , Baroreflex/physiology , Blood Pressure/physiology , Cardiac Output/physiology , Humans , Infant, NewbornABSTRACT
Full-body patient simulators provide a technological basis for clinical education without risk to real patients. In a previous study, we described a model for educational simulation of infant cardiovascular physiology. Using essentially the same methodology, we derive a mathematical model for the cardiovascular system of a healthy 1-week-old neonate. Computer simulations of this model result in vital signs that are close to target hemodynamic variables. Simulated systemic arterial pressure waveform and left ventricular pressure-volume loop are realistic, and the system reacts appropriately to blood loss. We also adapt the model structure and change its parameters to reflect the congenital heart defects: patent ductus arteriosus, tetralogy of Fallot, complex coarctation of the aorta with patent foramen ovale, and transposition of the great arteries. Simulated vital signs are again close to target hemodynamic variables. The resulting model for neonatal cardiovascular pathophysiology is an essential step in attaining a full-body, model-driven neonatal acute care simulator.
Subject(s)
Cardiovascular Diseases , Computer Simulation , Education, Medical, Graduate/methods , Infant Welfare , Models, Educational , Cardiovascular Physiological Phenomena , Cardiovascular System , Heart Defects, Congenital , Humans , Infant, Newborn , Models, TheoreticalABSTRACT
Full-body patient simulators provide the technology and the environment necessary for excellent clinical education while eliminating risk to the patient. The extension of simulator-based training into management of basic and critical situations in complex patient populations is natural. We describe the derivation of an infant cardiovascular model through the redefinition of a complete set of parameters for an existing adult model. Specifically, we document a stepwise parameter estimation process, explicit simplifying assumptions, and sources for these parameters. The simulated vital signs are within the target hemodynamic variables, and the simulated systemic arterial pressure wave form and left ventricular pressure volume loop are realistic. The system reacts appropriately to blood loss, and incorporation of aortic stenosis is straightforward. This infant cardiovascular model can form the basis for screen-based educational simulations. The model is also an essential step in attaining a full-body, model-driven infant simulator.
