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A breach in a wall of the heart. Free-wall rupture can allow blood to enter the pericardium, causing haemopericardium and potentially cardiac tamponade. ^[ref]

Blood within the pericardium; a sufficiently rapid collection can cause cardiac tamponade. ^[ref]

A suitable published comparison is J. B. Junor's 1858 report of cardiac rupture with a soft, fatty ventricular wall and blood in the pericardium. The comparison comes from the published clinical record.

The patient was a woman of about seventy with repeated vomiting and an initially weak pulse. She deteriorated after a severe episode of vomiting, her radial pulse becoming almost imperceptible, and died a few hours later. At examination after death, a large gallstone was found impacted in the ileum. The pericardium contained much blood. The small, atrophied heart had an extremely soft and fatty right cardiac ventricle; when it was raised, blood emerged through several small fissures, and its tissue broke under very gentle handling. ^[ref]

The comparison is anatomical and pathological: a fragile ventricular wall, escape of blood and death. There are also important differences. Morgagni's tear is in the left cardiac ventricle; J. B. Junor's reported fissures concern the right cardiac ventricle and were described during handling of a very friable heart. The latter account includes intestinal obstruction and does not reproduce Morgagni's sternal and arm pain. It supports the possibility of severe muscular degeneration in a ruptured heart, without establishing that the two patients had identical disease or that every observed fissure opened before death.

Probable muscular condition in an 1864 answer. The fibres around the tear were probably structurally weakened and softened; fatty degeneration of the heart is a strong historical pathological suggestion. This means alteration within damaged muscular fibres, rather than merely an abundance of adipose tissue outside them. In Richard Quain's account, reproduced before the examination, microscopic fatty change involved loss of the normal transverse markings and refractile fatty particles within the fibre sheath. Extensive change could accompany a pale, mottled, flabby myocardium. Those are findings one would look for, not observations supplied by the Oxford passage. ^[ref]

An appropriate investigation would compare thin preparations from the tear's margin with apparently unaffected myocardium under a microscope, looking at the cross-striation, continuity of the muscular structure and position of the fatty particles. Fat lying between bundles is different from particles lying within damaged fibres. The gross appearance, the microscopic preparation and the sampling site must be reported separately. The word “erosion” does not by itself supply these microscopic findings. ^[ref]

Modern interpretation and its limit. Rupture of a left ventricular free wall can follow myocardial infarction, where a zone of damaged myocardium becomes friable. That is a plausible modern differential for the combination of chest and arm pain, weak pulse and a tear, but the historical record does not supply coronary anatomy or histology sufficient to prove it. A sudden collection of blood in the pericardium, or haemopericardium, can impair cardiac filling and cause cardiac tamponade. This provides a mechanism compatible with the abrupt pallor and collapse; pericardial pressure was not measured in the reported case. Present-day assessment could use urgent echocardiography; that technology belongs to the later comparison. ^[ref]

The defensible conclusion is a ruptured, locally weakened myocardium, with fatty degeneration of the heart a probable nineteenth-century interpretation and infarct-related damage a modern possibility requiring additional evidence.

The treatment depends on the cause of acute pericarditis, the person's strength and the presence of pericardial effusion, myocarditis or circulatory failure. In an 1866 answer, rest, relief of pain and repeated assessment of the heart are more defensible starting points than an indiscriminate attempt to suppress every sign of inflammation by depletion.

The bedside assessment would include the history of rheumatic illness, chest pain, a pericardial friction rub, the character of the pulse, breathing, the extent of cardiac dullness on percussion and changes in the heart sounds. Serial examination matters: disappearance of a pericardial friction rub need not mean recovery if fluid is separating the inflamed surfaces. Increasing oppression of breathing, weakness or a failing pulse would require reconsidering both the disease and the treatment. Auscultation with a stethoscope and careful repeated percussion supplied information that modern imaging now refines.

Period practice included local bloodletting with medicinal leeches, counterirritation with a blistering agent, opium for pain and rest, and disputed Mercury treatment intended to alter inflammatory exudation. A robust adult early in an apparently vigorous inflammatory attack was treated differently by depletion advocates from an exhausted person with anaemia, previous blood loss or advanced kidney disease. Even in that framework, a rapid weak pulse was not a command to remove more blood. Nor was Mercury an uncontested standard: a medical address published in December 1866 specifically listed its use in pericarditis among unresolved therapeutic questions.^[ref]

Modern correction: establish the diagnosis, identify complications and use cause-directed treatment rather than bloodletting or mercurialization. Electrocardiography, inflammatory markers, troponin where myocardial injury is suspected and echocardiography help distinguish uncomplicated pericarditis from important associated disease. A typical uncomplicated inflammatory episode is treated with aspirin or a suitable nonsteroidal anti-inflammatory drug, usually with colchicine and appropriate gastroprotection. Renal impairment, gastrointestinal bleeding, interactions and a specific infectious or systemic cause can modify this plan. Corticosteroids have selected indications and are not the routine first choice. Activity is restricted during active disease and return to exertion follows reassessment.^[ref]

A large pericardial effusion requires attention to its haemodynamic effect, not merely its size. Cardiac tamponade requires urgent specialist drainage and stabilization. Purulent disease requires treatment of the infection and drainage; associated myocarditis or a systemic cause changes management further.^[ref] These distinctions explain why treatment cannot be fixed solely by the label “acute”.

The chief physiological routes are abrupt failure of blood circulation, failure of pulmonary ventilation or gas exchange, or catastrophic failure of the central control of those functions. Historical clinical accounts used labels such as syncope, asphyxia and medical coma in explaining deaths; these terms describe broad physiological failures rather than identifying the underlying diseases.^[ref] A brief faint or ordinary medical coma is not itself necessarily fatal.

In primary circulatory failure, effective delivery of blood to the brain stops. Modern examples include ventricular fibrillation, pulseless ventricular tachycardia, severe bradyarrhythmia and asystole. They may arise in coronary artery disease, after myocardial infarction, in cardiomyopathy, or from inherited cardiac ion channel disorders. An electrical cause may leave little distinctive gross evidence at autopsy. These modern mechanisms refine the broad historical description of cardiac syncope.^[ref]

Mechanical interruption of blood circulation gives another group: massive haemorrhage, rupture of an aortic aneurysm, cardiac tamponade, and large pulmonary embolism. The immediate deficit differs in each. Haemorrhage removes circulating volume; cardiac tamponade prevents adequate filling; pulmonary embolism obstructs flow through the pulmonary circulation. All can end with critically low cardiac output even if some electrical activity persists.^[ref]

Respiratory failure includes obstruction of the airway by a foreign body, laryngeal oedema or aspiration; drowning; and depression of breathing by drugs or major brainstem injury. Oxygen delivery then fails and secondary cardiac arrest follows. Carbon monoxide poisoning and cyanide poisoning illustrate related failure of oxygen transport or use: not every hypoxic death is caused by physical obstruction of an airway.^{[ref][ref][ref]}

A major intracranial haemorrhage or rapidly developing brain herniation can destroy or compress the pathways maintaining consciousness and breathing. A severe disturbance of electrolytes, especially potassium, may instead act directly on the heart's electrical function. A fatal seizure can involve respiratory and circulatory mechanisms; sudden unexpected death in epilepsy remains a diagnosis requiring exclusion of other causes, not merely recognition of a history of epilepsy.^[ref]

The practical distinction is between mode, immediate mechanism and underlying cause. For example, rupture of an aneurysm can cause haemorrhage, then circulatory failure, then irreversible hypoxic-ischaemic brain injury. A complete explanation identifies that chain. Inspection, histology, examination of the airway and heart, and appropriately interpreted toxicology may establish it; an unexplained sudden death cannot be assigned a precise cause from its suddenness alone.