Overview
Acute pericarditis is a distinct condition under Pericardial disease. Its manual phase selector compares Acute inflammation, Transient constrictive physiology and Resolved inflammation. These are separate authored teaching states, not stages every patient must pass through. The cardiac playback clock does not advance inflammation or healing.
Inflammatory constriction can reverse in selected patients, but acute pericarditis does not invariably cause constriction. Chronic constrictive disease and tamponade remain separate examples. Neither a disappearing rub nor normalized ECG alone establishes clinical recovery.
What the phase selector changes
Acute inflammation does not by itself impose tamponade, a low-output shock state or chronic constrictive filling pressures. The selected transient-constrictive state adds impaired filling and the existing constriction-like atrial and respiratory ventricular-interdependence pattern. Resolved inflammation removes this selected inflammatory component while coexisting diseases and loading controls remain active.
Phase changes are explicit endpoint comparisons before downstream rhythm, loading and intervention effects. Their reference pressures and output are original synthetic choices, not values fitted to a natural-history cohort. There is no inflammatory biomarker, effusion-volume trajectory, automatic treatment response, recurrence probability or clock-based recovery model.
The baseline helper recomposes the selected pericarditis component before the existing compensation modifier. Acute inflammation uses preserved reference hemodynamics; transient constriction reuses the existing constrictive reference phenotype; resolved inflammation contributes the preserved reference without an inflammatory flag. Other selected diseases continue through the normal composition rules. A separately selected chronic constrictive or tamponade condition is not removed by resolving this component.
Changing phase retains manual output, filling and vascular targets, interventions and coexisting disease. Untouched reference BP and sinus-rate defaults may follow the newly selected phase; an explicitly changed BP or rate remains selected. Thus holding chosen controls is distinct from forcing identical final hemodynamics across different phases.
Selected inflammatory ECG
The acute Auto example adds diffuse concave ST elevation and PR depression with reciprocal aVR and selected V1 changes, preserving the underlying rhythm and QRS activation. Transient-constrictive and resolved Auto states do not obligatorily retain this acute pattern; a manual inflammatory ECG choice remains an illustrative overlay.
Clinical ECG findings vary, and the classic pattern may be absent. In the conventional evolving pattern, diffuse T inversion follows normalization of the ST segment rather than proving a simultaneous ischemic territory. The manual phase selector does not simulate that full serial ECG course. ECG appearance alone cannot distinguish every cause of chest pain or establish isolated pericardial rather than myocardial inflammation.
Representative friction rub
The acute and transient-constrictive examples include a selected scratchy friction rub. It is separate from valve murmurs and from an early-diastolic constrictive knock. The representative components follow atrial contraction, ventricular systole and early diastolic filling; the organized atrial component is omitted in AF. Pause, VF and absent native flow do not receive a new organized rub cycle.
A real rub can be intermittent and have one, two or three components; it is not obligatory in pericarditis. Its absence does not prove resolution, and more effusion can also obscure it. The synthesized sound and its coefficients are original teaching audio, without patient recordings, chest transmission, diagnostic sensitivity or calibrated loudness.
Interpretation limits
The model does not determine cause, diagnose myocarditis, quantify pericardial inflammation or decide whether a constrictive state will resolve. Imaging, clinical examination and laboratory findings are separate clinical evidence. Moving directly between endpoints is a teaching control, not a patient-specific prognosis or treatment recommendation.
References & further reading
