Overview
The preset starts at HR 120/min, BP 78/54 mmHg and nominal CO 2.3 L/min, with RAP/RVEDP 18 mmHg, PA 44/23 mmHg, wedge 8 mmHg and LVEDP 7 mmHg. Derived PVR is high, but PA systolic pressure is lower than in the chronic PH example because the acute RV lacks the same pressure-generating reserve. These are synthetic reference values, not diagnostic thresholds.
Acute RV dilation, low RV ejection and reduced LV filling follow the pressure/flow state without adding new RV hypertrophy or obligatory pulmonary edema. A saddle location alone does not determine severity. Mixed LV or mitral disease can raise wedge; chronic PH can add hypertrophy and higher pulmonary load.
Rhythm and ECG presentations
The contextual selector offers sinus tachycardia, AF and flutter, plus explicitly peri-arrest sinus bradycardia, slow AF and junctional rhythms. These are chosen scenarios, not an automatic disease progression or frequency distribution. Marked slowing reduces modeled output and systemic pressure; rate and rhythm remain editable.
Auto ECG selects right bundle branch block with strain, incomplete block, S1Q3T3 or S1S2S3. Some variants add anterior/inferior T inversion. ECG changes are neither sensitive nor specific for PE. An RVH/strain morphology is also available, with auto-selection restricted to coexisting chronic pulmonary hypertension.
Ventilation, gas exchange and reperfusion
A chosen V/Q deficit lowers room-air saturation; ventilation adds dead space without assuming pulmonary edema or new stiff-lung disease. Fibrinolysis partially improves flow, resistance and the gas-exchange deficit. High positive pressure can worsen RV loading and venous return; oxygen alone does not remove the obstruction.
Manual settings, medications, ventilation, MCS and coexisting disease continue through the shared intervention model. Coronary angioplasty is not PE thrombectomy or balloon pulmonary angioplasty and does not reduce acute pulmonary obstruction.
References & further reading
