Fernando Boccalandro, MD, FACC, FSCAI

1. What is the most common cause of cardiac injury?

    Motor vehicle accidents are the most common cause of cardiac injury.

2. List the physical mechanisms of injury in cardiac trauma.

    Physical mechanisms of injury include penetrating trauma (i.e., ribs, foreign bodies, sternum); nonpenetrating trauma (or blunt cardiac injury); massive chest compression (or crush injury); deceleration, traction, or torsion of the heart or vascular structures; and sudden rise in blood pressure caused by acute abdominal compression.

3. What is myocardial contusion?

    Myocardial contusion is a common form of blunt cardiac injury; it is considered a reversible insult and is the consequence of a nonpenetrating myocardial trauma. It is detected by elevations of specific cardiac enzymes with no evidence of coronary occlusion, and by reversible wall motion abnormalities detected by echocardiography. It can manifest in the electrocardiogram (ECG) by ST-T wave changes or by arrhythmias. Myocardial contusion is pathologically characterized by areas of myocardial necrosis and hemorrhagic infiltrates that can be recognized on autopsy.

4. Which major cardiovascular structures are most commonly involved in cardiac trauma?

    Cardiac trauma most commonly involves traumatic contusion or rupture of the right ventricle (RV), aortic valve tear, left ventricle (LV) or left atrial rupture, innominate artery avulsion, aortic isthmus rupture (Fig. 61-1), left subclavian artery traumatic occlusion, and tricuspid valve tear.

5. What bedside findings can be detected in patients with suspected major cardiovascular trauma?

    Obvious clinical signs in patients with nonpenetrating trauma are rare. However, a bedside evaluation by an astute clinician to detect possible life-threatening cardiovascular and thoracic complications can reveal important signs in just a few minutes (Table 61-1).

6. Can an acute myocardial infarction complicate cardiac trauma?

    Myocardial infarction is an unusual complication in patients with chest trauma. Chest trauma can injure a coronary artery, leading to myocardial infarction due to coronary spasm, thrombosis, laceration, or dissection of the arterial wall. Patients with underlying coronary artery disease have favorable pathophysiologic conditions to suffer an acute coronary syndrome during trauma, as a result of limited coronary flow reserve, excess of circulating catecholamines, hypoxia, blood loss, and hypotension. It may be relevant in the appropriate clinical scenario to consider the possibility of cardiac syncope as the primary cause resulting in a traumatic event due to ventricular arrhythmias in a patient with an acute myocardial infarction and concomitant trauma. Chest trauma can elevate cardiac-specific enzymes without significant coronary stenosis; therefore, careful interpretation of these indicators in a trauma victim is warranted.

7. What is the most common type of myocardial infarction suffered in trauma victims?

    According to the universal definition of myocardial infarction, patients who have myocardial necrosis during trauma usually suffer a type 2 myocardial infarction. This type of myocardial necrosis is secondary to direct trauma or ischemia, and is a result of a relative imbalance of either increased myocardial oxygen demand or decreased myocardial oxygen supply (e.g., coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, anemia, or hypotension), rather than coronary occlusion caused by advanced atherosclerosis or an acute coronary thrombotic event (type 1 myocardial infarction), and is characterized by a variable increase in cardiac biomarkers with no ischemic symptoms or ECG changes.

8. What is the preferred treatment for an ST elevation acute myocardial infarction in the event of chest trauma?

    The treatment of choice is emergent coronary angiography. Thrombolytic therapy caries with it a high risk of bleeding complications. The withholding of nitrates, angiotensin-converting enzyme (ACE) inhibitors, and beta-adrenergic blocking agents (β-blockers) should be considered until it is established that the patient is hemodynamically stable. Aspirin can be used in patients with no evidence of severe bleeding. Aortic balloon counterpulsation is contraindicated in patients with acute myocardial infarction, and in patients in cardiogenic shock with acute traumatic aortic regurgitation or any suspected aortic lesions. If a coronary intervention is needed, percutaneous thrombectomy and balloon angioplasty without stenting are preferred, if the patient is not a candidate for dual antiplatelet therapy due to concomitant trauma.

9. List the causes of shock in patients with cardiac trauma.

    The first cause to address is always hypovolemic shock caused by acute blood loss, usually from an abdominal source. If the shock persists despite fluid resuscitation or the degree of hemodynamic compromise is not in proportion to the degree of blood loss, consider cardiogenic causes or tension pneumothorax. The three main cardiac causes of cardiogenic shock are cardiac tamponade, acute valvular dysfunction, and ventricular akinesia or hypokinesia. Rupture of any intrapericardial vessel or cardiac structure (e.g., coronary arteries, proximal aorta, great veins, ventricle) can produce a rapid state of shock because of cardiac tamponade, unless there is a concomitant pericardial tear. Acute valvular dysfunction due to mechanical disruption of the valvular apparatus can lead to acute valvular regurgitation leading to shock, and is usually associated with the presence of a new murmur in physical examination. Cardiac akinesia or severe hypokinesia with temporary myocardial stunning could be a consequence of cardiac trauma and could lead to cardiogenic shock or acute heart failure. Cardiac akinesia or severe hypokinesia requires volume resuscitation to increase the cardiac preload and inotropic support until contractile recovery is achieved.

10. What workup should be considered in a patient with suspected cardiac trauma?

If the patient is stable from the cardiovascular standpoint, no further workup may be required. Routine use of cardiac biomarkers does not appear to improve the management of patients with blunt chest trauma. However, in patients older than 60 years, with ischemic symptoms or new ECG ischemic changes, cardiac biomarkers and serial ECGs may be appropriate. If more complex heart lesions are suspected, complete echocardiography with color and spectral Doppler imaging is the test of choice. This test is fast, inexpensive, and readily available to provide information regarding the pericardial space, wall motion, valvular function, myocardium, and proximal aorta. Special attention to the RV is warranted, because its anterior location close to the sternum makes it prone to myocardial contusion and to the development of RV thrombus. Transthoracic echocardiography may have important limitations in patients with complicated trauma (e.g., unstable chest, ventilated patients, chest tube drainages) because of limited echocardiographic windows. Echocardiography contrast agents and transesophageal echocardiography (TEE) could play an important role in this group of patients. TEE may not be possible in those with an unstable neck or facial trauma. In suspected aortic involvement, and in patients who are not candidates for TEE, contrast computed tomography (CT) is the test of choice.

11. What are the signs of cardiac tamponade?

    Classical signs for cardiac tamponade include three signs, known as the Beck triad: hypotension caused by decreased stroke volume, jugular-venous distension as a result of impaired venous return to the heart, and muffled heart sounds caused by fluid inside the pericardial sac. Other signs of tamponade include pulsus paradoxus and general signs of shock, such as tachycardia, tachypnea, and decreasing level of consciousness.

12. Can a patient suffering from traumatic cardiac tamponade have a normal jugular venous pulse?

    In hypovolemic patients, the jugular-venous distension may be difficult to interpret even in the presence of cardiac tamponade. Thus, attention to the volume status is important while examining the venous pulse in trauma victims.

13. How can one confirm the diagnosis in a patient with suspected pericardial tamponade?

    A large cardiac silhouette by chest radiograph and low-voltage QRS complexes or electrical alternans in the ECG can suggest the presence of cardiac tamponade. CT can identify the size of an effusion, but cannot confirm the diagnosis. Echocardiography can confirm the diagnosis of tamponade and is the test of choice. If cardiac tamponade is suspected, an echocardiogram (with respirometry) should be ordered promptly. Echocardiography can assess the amount and localization of the pericardial effusion, and identify signs of elevated intrapericardial pressure suggesting a tamponade physiology (i.e., right atrial and RV collapse, left atrial collapse). Respirometry is a very simple technique that can be performed during the echocardiographic examination, allowing timing of the respiratory cycle with the mitral and tricuspid inflow. It is used to assess the hemodynamic effect of the pericardial effusion in the ventricular filling (using spectral Doppler analysis) and can confirm the presence of cardiac tamponade.

14. How can one treat a patient with pericardial tamponade?

    Pericardial tamponade requires immediate treatment with either a surgical subxiphoid approach (pericardial window) or with a percutaneous approach using bedside echocardiography or fluoroscopic guidance.

15. What interventions during resuscitation and management of an unstable trauma patient can precipitate cardiac tamponade in a patient with a pericardial effusion?

    In a patient with a moderate to large effusion, cardiac tamponade can be precipitated by hypovolemia or positive-pressure ventilation during trauma management. Therefore, meticulous attention to the patient’s hemodynamics is needed in these circumstances to avoid hemodynamic collapse.

16. What are the mechanisms of injury of the thoracic great vessels?

    Deceleration and traction are the most common mechanisms of injury of the thoracic arteries. Sudden horizontal deceleration creates marked shearing stress at the aortic isthmus (i.e., the junction between the mobile aortic arch and the fixed descending aorta), whereas vertical deceleration displaces the heart caudally and pulls the ascending aorta and the innominate artery. Rapid extension of the neck or traction on the shoulder can also overstretch the arch vessels and produce tears of the intima, disruption of the media, or complete rupture of the vessel wall, leading to bleeding, dissection, thrombosis, or pseudoaneurysm formation. Aortic rupture leads to immediate hypovolemic shock and death in the vast majority of cases.

17. Describe the management of thoracic arterial lesions.

    Usually, all arterial lesions require surgical repair, except benign ones like wall hematomas and limited dissections. An effort should be made to control the blood pressure with β-blockers in all arterial lesions if the patient is hemodynamically stable. Venous lesions usually do not lead to a rapid hemodynamic compromise unless the implicated vessel drains to the pericardium, possibly leading to cardiac tamponade. Thoracic aortic lesions such as limited traumatic dissections are increasingly being managed using thoracic endovascular aortic repair (TEVAR), with thoracic stent graft placement because of reduced perioperative mortality and morbidity in comparison with open surgical repair.

18. What are potential late complications of heart trauma?

    Late complications can include fistulas between different structures, constrictive pericarditis as a late consequence of hemopericardium, embolization from a mural thrombus, ventricular aneurysm formation, valvular insufficiency, and postpericardiotomy syndrome.

19. What is commotio cordis?

    Sudden death after a blunt chest trauma is a rare phenomenon known as commotio cordis. It is theorized that commotio cordis is caused by ventricular fibrillation secondary to an impact-induced energy transmission via the chest wall to the myocardium during the vulnerable repolarization period. This can cause lethal arrhythmias resulting in sudden death.

20. Describe the cardiac complications of electrical or lightning injuries.

    Patients in whom an electric current has a vertical pathway are at high risk for cardiac injury. Arrhythmias are frequently seen. Damage to the myocardium is uncommon and occurs mainly because of heat injury or coronary spasm causing myocardial ischemia. Direct current (DC) and high-tension alternate current (AC) are more likely to cause ventricular asystole, whereas low-tension AC produces ventricular fibrillation. The most common ECG abnormalities are sinus tachycardia and nonspecific ST-T wave changes.

    The effect of lightning on the heart has been called cosmic cardioversion and results in ventricular standstill and, in some reports, ventricular fibrillation. Standstill usually returns to sinus rhythm, but often the patient has a persistent respiratory arrest that causes deterioration of the rhythm. If initial ECG changes are not seen, it is unlikely that significant arrhythmias will occur later.

21. Can a patient develop a trauma-related cardiomyopathy?

    Tako-tsubo cardiomyopathy, also known as transient apical ballooning, stress-induced cardiomyopathy, and simply stress cardiomyopathy, is a nonischemic cardiomyopathy in which there is sudden temporary LV systolic dysfunction. The cause is debated and appears to involve high circulating levels of catecholamines and is not specific for mechanical trauma, but can be seen in patients after both emotional and physical trauma. Because this finding is associated with emotional stress, this condition is also known as broken heart syndrome. The typical presentation of someone with tako-tsubo cardiomyopathy is a sudden onset of congestive heart failure or chest pain associated with ECG changes suggestive of an anterior wall myocardial ischemia (which may be indistinguishable initially from an acute coronary syndrome) after a major trauma. During the course of evaluation, dilation of the LV apex with a hypercontractile base of the LV is often noted by echocardiography or angiography (Fig. 61-2). It is this finding that earned the syndrome its name tako-tsubo, or “octopus trap,” in Japan, where it was first described. Evaluation of individuals with tako-tsubo cardiomyopathy may include coronary angiography, which generally does not reveal any significant coronary artery disease. Provided that the individual survives the initial presentation, the LV function usually improves within several months with medical therapy.

Bibliography, Suggested Readings, and Websites