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Traumatic cardiac injury may be caused by either penetrating or nonpenetrating trauma. Penetrating injuries most often result from gunshot or knife wounds, and the site of entry is usually obvious. Nonpenetrating injuries most often occur during motor vehicle accidents, either from rapid deceleration or from impact of the chest against the steering wheel; the former may be associated with significant cardiac injury even in the absence of external signs of thoracic trauma.


Myocardial contusion is a nonspecific term that relates to a broad spectrum of nonpenetrating cardiac injuries. Importantly, the cardiac issues may initially be overlooked in trauma patients as the clinical focus is directed toward other, more obvious injuries. Myocardial necrosis may occur as a direct result of the blunt injury or as a result of traumatic coronary laceration, dissection, or thrombosis. The contused myocardium is pathologically similar to infarcted myocardium and may be associated with atrial or ventricular arrhythmias; conduction disturbances including bundle branch block; or abnormalities on electrocardiogram (ECG) resembling those of infarction or pericarditis. Thus, it is important to consider blunt cardiac injury as a cause of otherwise unexplained ECG changes in a trauma patient. Serum creatine kinase, myocardial band (CK-MB) isoenzyme levels are increased in ~20% of patients who experience blunt chest trauma but may be falsely elevated in the presence of massive skeletal muscle injury. Cardiac troponin levels are more specific for identifying cardiac damage; patients with normal troponin levels 4–6 h after chest trauma are very unlikely to have cardiac injury. Echocardiography is useful in detecting structural and functional sequelae of blunt cardiac injury, including regional wall motion abnormalities (most commonly involving the right ventricle, interventricular septum, or left ventricular apex), pericardial effusion, valvular dysfunction, and ventricular rupture.

Traumatic rupture of the cardiac valves or their supporting structures, most commonly of the tricuspid or mitral valve, leads to acute valvular incompetence. This complication is usually heralded by the development of a loud murmur, may be associated with rapidly progressive heart failure, and can be diagnosed by either transthoracic or transesophageal echocardiography.

The most serious consequence of nonpenetrating cardiac injury is myocardial rupture, which may result in hemopericardium and tamponade (free wall rupture) or intracardiac shunting (ventricular septal rupture). Although generally it is fatal, up to 40% of patients with cardiac rupture have been reported to survive long enough to reach a specialized trauma center. Hemopericardium also may result from traumatic rupture of a pericardial vessel or a coronary artery. Additionally, pericarditis and/or pericardial effusion may develop weeks or even months after blunt chest trauma as a manifestation of the post–cardiac injury syndrome, an inflammatory condition that resembles the postpericardiotomy syndrome (Chap. 265).

Blunt, nonpenetrating, often innocent-appearing injuries to the chest may trigger ventricular fibrillation even in the absence of structural myocardial damage. This syndrome, referred to as commotio cordis, occurs most ...

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