Overview
Spontaneous breathing starts from an illustrative I:E ratio of 1:2. Hypoxemia, congestion and low perfusion can increase respiratory drive; anaphylaxis uses a bronchospasm phenotype with a longer expiratory fraction. The ratio is not inferred from wedge pressure alone.
Thoracic pressure transmission and changes in ventricular filling are distinct effects. A breath may shift a measured pressure baseline and also change systolic pulse amplitude. The size of those responses is explicitly modeled rather than computed from a detailed thoracic anatomy.
Breath timing and drive
Spontaneous inspiration and expiration use smooth half-cosine trajectories with independently allocated durations. Congestion and shock can shorten expiratory rest; the spontaneous rate is bounded. Neurogenic injury does not automatically receive intact shock-related drive. Intubation uses the selected controlled rate when the ventilator is active.
The ventilator supplies its actual breath sequence, volumes, elastic pressure and inspiratory duration to respiration, pleth, pressure variation and imaging. Resistive peak airway pressure is not treated as if it were alveolar/pleural pressure.
Pericardial and myocardial responses
In spontaneous tamponade/constriction, RV filling increases during inspiration while LV filling and arterial pulse pressure fall; expiration reverses the pattern. The representative flow factors use larger swings than normal. Restriction uses a smaller concordant ventricular response. These are diagnostic teaching patterns, not patient-specific respiratory sensitivity measurements.
Constrictive pressure transmission differs from ordinary thoracic transmission: atrial/wedge pressure and ventricular pressure do not all move identically. Under positive-pressure ventilation, spontaneous inspiratory rules are replaced by a different volume/pressure-dependent response with a short left-sided delay.
Large atrial communication
A large ASD can redistribute flow between atria and buffer respiratory ventricular filling and pulse-pressure variation, including in the modeled tamponade example. The buffer is an explicit communication property, not inferred only from Qp/Qs. It does not remove pericardial constraint or all transmitted thoracic-pressure variation.
PAPVR alone does not automatically produce the fixed-splitting/ASD exception. Advanced pulmonary vascular disease and other concurrent states are handled by the shunt model rather than assuming all shunts behave alike.
Cycle figures versus continuous monitors
Continuous pressure traces retain ongoing breathing. The linked cardiac-cycle/PV study uses a representative end-expiratory state while live, and permits end-expiration, end-inspiration or respiratory-mean comparison when paused. This stabilizes a single-cycle educational outline without suppressing respiration in the main monitors.
References & further reading