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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]

The thorax is a mobile osteocartilaginous enclosure with two pleural compartments and a central mediastinum; its visceral boundaries change normally with breathing and posture. The sketch is an anterior projection, with the subject's right on the viewer's left. It distinguishes the lower margin of a lung from the lower reflection of its pleura: those are different boundaries.

The posterior wall is formed by the twelve thoracic vertebrae and adjacent parts of the ribs; laterally the ribs and intercostal muscles form a flexible wall. Anteriorly lie the sternum, costal cartilages and anterior intercostal structures. The superior aperture communicates with the neck, while the respiratory diaphragm closes the inferior aperture. The lower thoracic wall therefore overlaps upper abdominal organs: not every organ under a lower rib is inside the pleural compartment.

Each lung is covered by visceral pleura. Parietal pleura lines the chest wall, upper surface of the respiratory diaphragm and side of the mediastinum, becoming continuous with visceral pleura at the root. The potential pleural space contains a lubricating fluid film; it is not normally an air-filled gap. The right lung has three lobes, the left two, with the cardiac notch and lingula accommodating the leftward projection of the heart. Each apex projects above the first rib into the root of the neck. The roots carry the bronchi, pulmonary vessels, nerves and lymphatic connections.^[ref]

The heart and pericardium occupy chiefly the middle part of the inferior mediastinum, behind the sternum and between the lungs, with most of the cardiac bulk to the left of the median plane. The great vessels approach superiorly. The trachea divides into main bronchi behind the upper central region; the oesophagus descends behind the airway and heart. The descending thoracic aorta lies posteriorly, chiefly left of the vertebral bodies; the azygos venous route lies chiefly on the right. The thoracic duct and sympathetic chains belong to the posterior relations. A frontal projection superposes these structures and must not be mistaken for their order from front to back.

For a conventional quiet-breathing surface description, the lower lung border reaches approximately the sixth rib in the midclavicular line, eighth in the midaxillary line and tenth posteriorly near the scapular line. The pleural reflection descends approximately two ribs farther at corresponding landmarks: eighth, tenth and twelfth. These are orientation points, not immutable lines in every healthy individual. Inferiorly, the extra pleural extent forms the costodiaphragmatic recess. The right diaphragmatic dome usually stands higher, related to the underlying liver; the left is related to the stomach and other abdominal viscera.

In inspiration the respiratory diaphragm descends, the rib cage expands and lower lung margins move into the recesses; in expiration they retreat. The heart also shifts with the diaphragm and changes its surface projection as neighbouring lung expands. Deep inspiration, quiet expiration and forced expiration therefore cannot share a single normal map. The heart's own beat adds smaller cyclic movements.

Posture shifts the diaphragm and mediastinal contents: a supine position generally raises the domes compared with standing, while lateral positioning displaces mobile contents towards the dependent side. Body build, age, abdominal fullness and pregnancy change the available thoracic shape and diaphragmatic level. A distended stomach can raise the left dome and alter the cardiac projection without implying primary cardiac disease. The clinically useful comparison records posture and respiratory phase before judging an apparent difference in organ position.

There was a very distinguished knight, sixty-five years old, but with sturdy limbs and a sound balance of the humoral fluids, except that some years earlier he had suffered from long-lasting, obstinate ulcers of the legs. Weary of these, he had at last completely healed them by remedies both internal and external. More recently he had occasionally been subject to rheumatic pains, but pains so slight that they did not prevent him from leaving home, as he had indeed done on the day before his death. On 1 June these seized him more severely, at the sternum and in the arms, accompanied by disturbance of the head. After they had been treated with the measures judged most suitable, he was already largely relieved by about midday and behaved cheerfully, although his pulse was weak.

After resting following dinner, he awoke and felt the same pains as in the morning. He therefore began walking about his room, for in this way he bore them more easily. But after doing this sufficiently, he returned to bed and complained of vapours rising to his head and of tightness in his chest; in his restlessness he turned this way and that. After doing so for a considerable time, he suddenly felt that he was dying and, at the same moment, grew pale, struggled, and died immediately.

When the abdomen was opened, everything was found in its natural condition. But when the chest was opened and the lungs, which had been pushed forwards, were moved aside, the pericardium was found distended with dark, clotted blood. This had escaped from the left cardiac ventricle through a tear half an inch long, running in the direction of its length. Around it the fibres of the heart were visibly eaten away by an erosion that was not recent.

The anatomical finding is rupture of the left ventricular wall into the pericardium. This is Morgagni's account in The Seats and Causes of Diseases Investigated by Anatomy by Giovanni Battista Morgagni, Book II, Letter XXVII, article 8. The language of balanced humoral fluids, rheumatic pain, rising vapours and erosion belongs to the account's historical descriptive framework. It does not establish a modern rheumatological diagnosis or a microscopic cause of rupture. The Roman date is the fifth day before the Nones of June, counted inclusively: 1 June. The translation retains the historical half-inch measure without assigning an unjustified modern measurement to the specimen. ^[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.

Accumulation of fluid in the pericardium. Its size and effect on the circulation are distinct questions.

Inflammation of the pericardium; its cause and haemodynamic complications determine management.