The normal pericardium holds <50 mL and is highly compliant up to its "reserve volume" — past that it stiffens sharply. This sim uses a two-slope pericardial pressure–volume curve:
P_peri(V) = a·V for V ≤ V_reserve
P_peri(V) = a·V_r + b·(V-V_r)^1.6 for V > V_reserve (b ≫ a)
A rapid effusion (trauma, aortic dissection) hasn't stretched the sac yet, so V_reserve is small and pressure rises steeply from far less fluid than a slow, chronic effusion (malignancy, uremia), which the pericardium has had time to stretch to accommodate.
Ventricular interdependence & pulsus paradoxus: the pericardial sac is a fixed-ish total volume. During inspiration, negative intrathoracic pressure increases venous return and fills the right ventricle more — but with no room to expand outward, the interventricular septum bows left, stealing volume from the left ventricle. LV stroke volume and systolic pressure fall further on inspiration than the normal ≤10 mmHg dip, producing pulsus paradoxus:
SV_LV ≈ SV_LV0 · (1 − k·P_peri) · (1 − c·P_peri·sin(2π·t/T_resp), insp. only)
Tamponade flagged when P_peri ≳ mean venous pressure (diastolic pressures equalize)
- Effusion volume slider / Fill / Pericardiocentesis — add or drain pericardial fluid directly.
- Accumulation rate — swaps which pressure–volume curve (acute vs. chronic reserve) governs the current fluid volume.
- Heart rate / breathing rate — set the two independent clocks driving the beat-by-beat pressure trace and its respirophasic modulation.
- The bottom trace is a live arterial pressure waveform; watch its peaks sag on every inspiration once tamponade develops.
Clinically this is why tamponade calls for urgent pericardiocentesis: draining even 50–100 mL off a tense sac can restore filling because the removal drops you back down the steep part of the curve.