Reference phenotypes & baseline numbers

Current reference catalogue

Pressures are mmHg; forward output is L/min. LVEDP and mean wedge are separate inputs. Values are rounded here only for readability.

Deliberate phenotype choices

The tamponade example represents significant unsupported constraint, with reference output and systolic-pressure limits; compensated tamponade is possible clinically but is not this preset. The right-heart-failure example includes pulmonary vascular loading. The acute mitral-regurgitation example uses right-predominant bilateral edema. The tension-pneumothorax example is right-sided.

Sepsis starts hyperdynamic and vasodilated; additional pump or valve disease can reduce output. The preserved-output congestion phenotype does not assert a preserved ejection fraction. The high-output failure phenotype does not identify a specific cause.

Severe LVH with preserved EF and elevated filling pressure

Select Severe LVH · Preserved EF under Hemodynamic state, or search LVH, concentric hypertrophy, diastolic dysfunction or S4. This is a separate nonobstructive concentric-hypertrophy example. At its untreated sinus reference, HR is 75 bpm, BP 145/80 mmHg and CO 5.25 L/min. Mean PAWP is 22 mmHg and LVEDP is 26 mmHg; elevated filling pressure can coexist with preserved EF and adequate resting forward flow.

The isolated reference LV has EDV 112 mL and ESV 42 mL. Its 70 mL stroke volume gives EF = 100 × 70/112 = 62.5%, shared by the PV loop, Wiggers volume and PV-linked echo motion. This preserved EF is a starting phenotype, not a constraint that overrides subsequent rhythm, loading, intervention or mixed-disease effects. The separate preserved-output heart-failure preset still leaves EF unspecified.

The volume model uses a nondilated reference cavity and a lower compliance-like coefficient of 18 in the existing logarithmic filling response. Its late-filling share is 24% with organized atrial activity rather than the ordinary 14%; without organized atrial activity it retains the existing 4% passive smoothing share. LV relaxation uses the existing 1.28 timing multiplier. These are original teaching coefficients, not measured compliance, tau, transmitral Doppler or a fitted pressure–volume relationship.

The schematic echo thickens the LV wall concentrically and modestly enlarges the LA without assuming LV dilation, systolic anterior mitral motion or an obstructive outflow jet. The wall stroke width is a drawing parameter, not a calibrated millimetre measurement. Clinical LVH assessment uses indexed LV mass, relative wall thickness and the distribution of thickening; wall thickness alone does not determine cause. Severe LVH alone adds neither a dynamic LVOT pressure gradient nor a stenotic valve murmur.

A low-pitched presystolic S4 is illustrated when effective organized atrial contraction is supported, including sinus rhythm and sinus arrhythmia. AF removes S4 and the organized wedge a wave. The existing atrial-loss response lowers flow and raises filling pressure; faster rates also use the stiff-LV response. Selectable ECG examples include LVH voltage/strain, LA enlargement and nonspecific changes; none is mandatory or diagnostic in an individual patient.

This preset does not label every person with LVH as having HFpEF or hypertrophic cardiomyopathy. The cause, symptoms, clinical HF diagnosis, myocardial tissue properties, exercise reserve and prognosis are not inferred. Pressures, chamber geometry, responses and sounds are synthetic educational choices, not patient measurements or validated predictions.

How to interpret these values

Preset numbers establish an internally useful starting example. They are not measured patient data, prevalence-weighted averages, diagnostic thresholds or prognosis estimates. Select additional pathologies only when you intend to teach their combined assumptions.