Congenital Heart Disease, Start to Finish - Shunts, Cyanosis and the Fontan

Congenital heart disease is usually taught lesion by lesion, as a list of names to memorise. The physiology underneath is a much shorter list: where blood can cross, which way the resistances point it, and how completely the streams mix. Learn those and most lesions stop needing to be memorised.

One circulation engine drives all forty-one modules, and every lesion is simply a set of parameters on it. Open a defect, raise pulmonary resistance or close the duct, and the saturation, pressure and flow in every chamber respond together, with effective and recirculated pulmonary flow drawn in the vessels themselves.

Using it in a teaching session

Every lab opens with a prediction. Take a show of hands before anyone moves a slider: the wrong answers are the useful ones.

The oximetry run and the Qp:Qs modules work well together. The catheter table and the Fick working sit under each lab, so the class can watch which numbers move when the assumed oxygen consumption is wrong, and which do not.

Fallot and the spell are the clearest demonstration that cyanosis is a comparison of resistances rather than a degree of narrowing. Lower systemic resistance with the anatomy untouched and the saturation collapses.

For the sick neonate, pin the open duct in hypoplastic left heart, then close it and read the comparison: the saturation stays in the nineties while systemic flow falls away.

The Fontan modules close the course, including why a Fontan turns blue, with the branch pulmonary arteries and the two lungs drawn apart the way a catheter samples them.

What the model simplifies

It is a steady-state model of mean pressures and flows: no pulsatility, no valves and no time course, two body compartments and lumped collaterals, with phasic mixing approximated. The last module lists every simplification, and the simulator flags any state no circulation could sustain. The preset values are calibration, not patient data.