Injury to the Heart and Great Vessels

The heart is a vital organ, with its arch vessels encased in the chest cavity and protected by the manubrium, sternum, and rib cage. Injury to this organ can come from blunt trauma, which includes blunt cardiac injury, more commonly referred to as cardiac contusion, coronary artery injury, atrial/ventricular/valvular rupture, and aortic or arch vessel rupture. Injury can also result from penetrating trauma, with the right ventricle being most commonly injured, and ventricular septal defect being the most common intracardiac injury.

Blunt Cardiac Injury

Historical Perspective

The first recorded cardiac chamber rupture and myocardial contusion were reported after autopsy findings as early as 1679 by Borch (as reported by Osborn ) and in 1764 by Akenside, respectively. In 1868, 76 cases reported by Fischer described 7 myocardial contusions and 69 traumatic ruptures. Experimental animal work and clinical autopsies by Bright and Beck have demonstrated that substantially severe forces are responsible for an entire range of cardiac trauma, whereas enormous force is required to rupture the heart. It is also observed that recovery is the general rule, and rupture is the exception. In 1958, a hallmark study by Parmley and colleagues of a large series of autopsy cases in the Armed Forces Institute of Pathology demonstrated that blunt traumatic heart injury had a 0.1% incidence, with the majority being isolated chamber ruptures (right then left ventricle, followed by right and left atria in decreasing order of occurrence) and some associated with combined aortic ruptures. Myocardial contusion or blunt cardiac injury, although rare, is the most common injury, whereas chamber or aortic rupture is usually fatal.

Mechanism, Pathophysiology, and Incidence

Mechanisms responsible for blunt cardiac injuries can occur from any deliverance of kinetic energy such as blast effect; direct crushing forces through the sternum or rib cage, which can also cause compression of heart against the vertebral column; and traction and torsion from deceleration forces owing to high-speed vehicular collisions and falls from great heights. A sudden rise of blood pressure from compression of the chest can injure the cardiac valves, cause a tear in the ventricular wall or septum, or result in chamber rupture.

These forces result in a continuous spectrum of cardiac injury, ranging from simple contusion to fatal cardiac chamber rupture, including comotio cordis, described as sudden cardiac arrest resultant from a sternal blow. Myocardial contusion, characterized by patchy areas of muscle necrosis and hemorrhagic infiltrate, can also impair ventricular contraction and lead to arrhythmia.

The true incidence of blunt cardiac injury remains expectedly difficult to measure, because the autopsy cases of fatal cardiac chamber rupture do not account for the majority of the blunt trauma cases, which go on to recover.

Clinical Presentation

The rupture of a cardiac chamber, coronary artery, or major intrapericardial vein or artery is usually fatal because of acute tamponade. The few patients who survive do so only because of tears in a cavity under low pressure. Myocardial contusion induces cardiac failure and arrhythmia that improve with time. Injury to a coronary artery can lead to immediate or delayed myocardial infarction with spasm or dissection of arterial wall. Valvular tears resulting in aortic or mitral insufficiency can develop into cardiac failure within a few weeks, whereas tricuspid insufficiency can appear only after several years.

Diagnosis

Paramount to an accurate diagnosis is the awareness from the history and physical findings of pain and tenderness over the anterior chest wall (which may be indistinguishable from a classic myocardial infarction), evidence of contusion, ecchymosis, anterior rib fractures, or flail chest. Many patients, however, do not exhibit characteristic symptoms. The presence of complex arrhythmias, subtle findings of a precordial thrill, or presence of a murmur may be all that is present at exam. Cardiac injury can also be reflected with hemodynamic instability marked by refractory hypotension and elevated venous pressure (external jugular vein distention may be absent in cases of severe blood loss) in the presence of cardiogenic shock.

Electrocardiography

Serial 12-lead electrocardiography has traditionally been used to screen patients to detect conduction disturbances resulting from blunt injury; however, there is no pathognomonic finding that can reliably establish the diagnosis of blunt cardiac injury. Abnormalities range from sinus tachycardia, the most commonly encountered arrhythmia, to supraventricular arrhythmias, such as atrial flutter and atrial fibrillation, ventricular tachycardia, premature ventricular contractions, ventricular fibrillation, right bundle branch block with first-degree heart block or hemiblock, third degree heart block, and T-wave or ST-segment abnormalities. The presence of a normal electrocardiography in a patient who is hemodynamically stable warrants no further investigation.

Cardiac Enzymes and Troponins

The measurement of creatine phosphokinase with myocardial band has been shown to be unreliable, except for more specific muscle proteins including troponin (cTnT and cTnI). Combined abnormalities in electrocardiography and serial cTnI levels have been promising in showing increased sensitivity (62% if both positive) and specificity (100% if both negative), although another study has shown otherwise.

Admission electrocardiography and serial troponin levels should be obtained in patients suspected of blunt cardiac injury and followed by transthoracic echocardiography if clinically significant arrhythmias arise.

Two-Dimensional Transthoracic and Transesophageal Echocardiography

Bedside echocardiography has become an important diagnostic tool in trauma patients, detecting abnormalities in the heart (ventricular dyskinesia and valvular dysfunction), thoracic aorta, and presence of pericardial fluid. Patients are selected for this modality of examination after demonstration of abnormal electrocardiography and cardiac troponins.

Transthoracic echocardiography cannot be performed in 25% to 30% patients limited by chest wall edema, fractured ribs, and flail chest, whereas transesophageal echocardiography—a more useful adjunct in elucidating periaortic hematoma and other cardiac injuries—is limited by expertise and frequent requirement of intubation, and it cannot be performed in patients with facial or cervical trauma.

Radionuclide Scans

Technetium-99m pyrophosphate, thallium 201, single photon emission computed tomography (SPECT), and multiple gated acquisition scans (MUGA), all use the concept of radioactive substances binding to injured or infarcted sites in the myocardium. However, all have been abandoned secondary to low sensitivity and specificity in the detection of blunt cardiac injury.

Spectrum of Blunt Cardiac Injury: Assessment and Management

Pericardial Injury

Blunt rupture of the pericardium can occur from a direct forceful impact to transmitted force from sudden increased intra-abdominal pressure. Left pericardial tears parallel to the phrenic nerve are most common, followed by diaphragmatic, and right and mediastinal tears. The heart might eviscerate into the abdominal cavity or herniate through the pericardial sac with torsion of the great vessels. Patients who are stable are worked up and diagnosed with chest radiography, sonography, or computed tomography. Patients who are hemodynamically compromised clinically are treated with immediate surgical intervention (ER thoracotomy), at which time diagnosis is made and the heart is placed back into the pericardial sac, with closure of pericardium, with or without a Gore-Tex patch, to achieve a tension-free repair.

Valvular, Papillary Muscle, Chordae Tendinea, and Septal Injury

Rarely, valvular injuries occur, with the aortic valve being most commonly affected, followed by the mitral valve. Rapid displacement of blood secondary to crushing or compressive forces applied to the thoracic cage during ventricular diastole can lacerate cardiac valve leaflets (most common in the left coronary cusp, followed by the noncoronary cusp), papillary muscles, or chordae tendinea leading to valvular insufficiency. The classic signs of valvular insufficiency (new murmur, thrill or left ventricular dysfunction with cardiogenic shock, and associated pulmonary edema) may not be immediately recognized, secondary to other concomitant life-threatening injuries. In patients in stable condition, such findings should prompt further diagnostic studies, depending on the clinical status of the patient and prompt repair or replacement as necessary. Septal rupture is also uncommon, and prompt repair is necessary if the patient is symptomatic from significant left-to-right shunt resulting in pulmonary over circulation and right heart dysfunction.

Blunt Coronary Artery Injury

Injuries of the coronary arteries are extremely rare. The proximal right coronary and, more commonly, the left anterior descending artery (because of the location relative to the sternum) become injured with direct compression of sternum to coronary vessel or stretching of the vessel secondary to cardiac torsion, leading to thrombosis or intimal disruption. The result is no different than an acute myocardial infarction. Long-term sequelae of these injuries can also lead to ventricular aneurysm and eventual rupture, ventricular failure, production of emboli, or malignant arrhythmia.

Cardiac Chamber Rupture

Cardiac chamber rupture is relatively uncommon, and only a small percentage of patients survive to reach the hospital. Several mechanisms for blunt cardiac rupture have been postulated, including direct precordial impacts, compression of heart between sternum and vertebral body, transmission of pressure via abdomen into the venous return rupturing particularly the atria, acceleration/deceleration injuries leading to tears of the heart at the attachment sites to the great vessels, blast effects, and concussive blows thought to be fatal secondary to the production of malignant arrhythmias. Patients usually have persistent hypotension with evidence of pericardial tamponade. Diagnosis of widened mediastinum on chest radiograph or evidence of pericardial fluid from sonographic examination requires prompt intervention in the form of a subxyphoid window. For patients with cardiopulmonary arrest, emergency department (ED) thoracotomy may be the only chance, although the survival rate is dismal.

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