Overview
A pressure trace is a function of simulation time, scenario, channel, rhythm, rate and respiratory state. Atrial and pulmonary reference contours use piecewise smooth interpolation; ventricular and arterial functions add their own systolic, relaxation and runoff behavior.
The waveforms are designed to make physiological relationships readable. Their exact shape, frequency content and transient response are not recorded catheter data or a complete fluid-filled catheter/vascular impedance simulation.
Atrial contours
RA and wedge contours combine a, c and v waves with x and y descents. The engine removes coordinated atrial contraction when appropriate and adjusts atrial timing for dissociation or conduction block. Wedge has a modeled transport delay of 0.12 cardiac cycles.
MR increases the wedge v wave; TR enlarges the RA systolic wave and alters the x descent. MS/TS amplify atrial contraction when present and slow emptying. Tamponade blunts the y descent in both RA and wedge while preserving the x descent; constriction/restriction retain prominent early emptying. Contours are recentered around their intended reference mean before later respiratory/treatment modifications.
Ventricular contours
RV pressure has a rapid systolic rise, low-pressure relaxation and an end-diastolic level distinct from its minimum. Constriction/restriction introduce a rapid early diastolic dip followed by a plateau. LV pressure follows the pullback model, including filling pressure, outflow gradients, rate and contractility.
Beat strength, ectopy, pauses, pacing and respiratory loading change the actual pressure function. Ventricular systolic pressure must be compatible with the corresponding arterial pressure during ejection; low-flow or supported states are not merely rescaled normal loops.
Arterial and PA contours
PA systolic/diastolic endpoints are solved from the desired mean and pulse contour. The mean is based on contour integration, not universally (systolic + 2 × diastolic)/3. Pulmonic regurgitation uses faster diastolic runoff and a different contour.
Every PA contour feature scales with pulse pressure. A constant-pressure input stays flat, and a common transmitted-pressure offset shifts the contour without changing its transpulmonary gradient. If the requested pulse would require a negative modeled diastolic pressure, the pulse narrows while preserving the solved mean. The contour proportions are synthetic teaching choices.
Aortic/arterial pressure includes systolic ejection, diastolic runoff and valve-specific features: a slow upstroke in AS, widened runoff in chronic AR, and spike-and-dome behavior in HOCM. Low flow narrows pulse amplitude. Treatment, PEEP and dynamic prolapse calculations preserve the solved systemic mean as pulse pressure approaches zero; a display floor must not invent additional perfusion. During continuous support, dedicated arterial reservoir functions replace the ordinary ejection contour.
Pressure rise, relaxation and optical slope
Pressure dP/dt depends on pulse amplitude, timing, preload, afterload and contractility. The model slows the rise in the selected LV pump-failure phenotypes and in the failing RV/acute PE phenotype, and makes the chosen hyperdynamic phenotype brisker. Isolated low preload, tamponade, MS or TR does not automatically imply impaired myocardial contractility; lower perfusion is expressed through the solved pulse amplitude.
The existing treatment contractility multiplier also changes the pressure-rise timing. Contraction is bounded to 0.55–1.5 times the reference rate of rise. Arterial opening/peak timing stays coupled to LV pressure so reducing inotropy cannot paradoxically steepen the pre-ejection limb to meet a fixed arterial upstroke. AS retains its delayed obstructed contour; pulmonic stenosis broadens the high-pressure RV systolic contour with severity; AR retains rapid runoff and HOCM its spike-and-dome.
Relaxation is slower in the selected pump-failure, restrictive and LV pressure-loading phenotypes. The 1.28 timing multiplier is an illustrative assumption, not a measured relaxation constant. The model does not equate every positive inotrope with improved relaxation. Respiratory/PEEP pressure shifts, regurgitation, rhythm and continuous support remain separately applied.
The pleth is a delayed, smoothed optical-volume proxy of arterial pulsatility, not a pressure measurement. Its derivative is not pressure dP/dt. It retains valve shape, AF/ectopic strength and perfusion changes without stretching a weak pulse to full height. The 180 ms transit and three-tap tissue filter are teaching assumptions; saturation is calculated separately.
Which number is which
Mean pressure is a time average. A v-wave peak is not mean LA pressure; ventricular minimum is not EDP; aortic peak and LV peak need not occur together. Mouseover explanations use channel and event timing, so an annotation is an explanation of this synthetic segment rather than an independent diagnosis.
References & further reading
