Traumatic injuries to the chest wall can arise from blunt or penetrating forces. Blunt cardiac injury occurs commonly in thoracic injury approximately 20–76% of the time and is often overlooked.¹ The range of presentations from an asymptomatic cardiac bruise to a severe cardiac rupture necessitates early recognition. Furthermore, the consequences can be quite serious and potentially fatal for unrecognized cardiac injuries; hence, early assessment and aggressive management can lead to improved outcomes. Ultrasound provides a useful method of evaluating cardiac trauma because it is readily available at the bedside, provides good image quality, and can be used serially to monitor the effects of interventions.

The patient history, including an understanding of the mechanism of injury, and the physical examination remain primary methods of gathering objective information for the trauma victim. Although there are limited data to support the use of ultrasound in blunt cardiac injury, cardiac ultrasound complements the history and physical examination particularly if there is concern for anatomical irregularities, pericardial effusion, apical thrombi, or structural damage, such as cardiac contusions, concussion, muscle rupture, or valvular disruption, that would be difficult to identify through physical examination alone. Cardiac ultrasound can also help to assess hemodynamic profiles, volume status, and the cardiac index. Transthoracic echocardiogram (TTE) is warranted as a component of the focused assessment with sonography in trauma (FAST) examination and when questionable signs are encountered on the physical examination or when symptoms manifest after a traumatic injury. Table 16-1 provides a summary of the indications for echocardiography in trauma patients.²

One of the important contributions of cardiac ultrasound is that it has portability and is noninvasive. It can be used serially to monitor a patient over time. This is highly relevant for the hemodynamic assessment of trauma patients. In a study by Gunst et al., transthoracic ultrasonographic measures were well correlated with cardiac index and central venous pressure measurements obtained by a pulmonary artery catheter.³

Blunt cardiac trauma can lead to myocardial injury and manifest as wall motion abnormality on echocardiogram without evidence of transmural myocardial infarction on electrocardiogram. The most common form of this condition is a cardiac contusion. The mechanism of injury results from direct pressure to the heart as it makes contact between the sternum and the spine. This results in an acceleration/deceleration type of injury with the heart hitting the internal sternum. Upward pressure transmitted from increased intraabdominal pressure may also worsen the effect.⁴ While there is currently no gold standard for diagnosis, there are some common features of the condition, including an impact on the right ventricle, tricuspid valve, and the left ascending coronary artery, most due to their location in proximity to the chest wall.

Patients with blunt cardiac injury may have a wide variety of manifestations. First, minor electrocardiogram changes or mild cardiac enzyme elevation may occur. Therefore, it is important to start surveillance by obtaining a baseline electrocardiogram and trending cardiac enzyme levels prior to obtaining an echocardiogram. Second, complex arrhythmias that can range from ST segment changes, heart blocks, or ventricular arrhythmias. Third, pump failure may arise either from direct injury to the myocardium or conduction abnormalities. In addition to these common manifestations, several important complications need to be kept in mind including:

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  Coronary artery laceration, which can lead to hemopericardium or cardiac tamponade

  
  
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  Septal rupture, which can present as valvular dysfunction with or without concomitant heart failure

  
  
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  Ventricular dilatation

  
  
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  Intracardiac shunt and thrombosis

  
  
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  Free wall rupture, which often leads to instantaneous death

In stable asymptomatic patients with a normal electrocardiogram after blunt cardiac injury, cardiac ultrasonography may not be helpful. However, echocardiogram may demonstrate wall motion abnormalities after trauma to the chest even if the patient is asymptomatic. Since many patients may not have a prior echocardiogram, the difficulty rests in determining whether the abnormalities were preexistent or a result of the injury.

An electrocardiogram has mixed results in terms of its diagnostic value in trauma patients. In a study by Weiss et al., an electrocardiogram was nondiagnostic in 73% of patients with a cardiac contusion.⁵ If the electrocardiogram changes are new, evolving, or result from the trauma event, this may be suggestive of a cardiac contusion.⁶ Despite these findings, an electrocardiogram is recommended as a primary surveillance in patients with suspected blunt cardiac trauma.

The use of cardiac enzymes in blunt cardiac trauma is of questionable value. Ferjani et al. have demonstrated that, in general, troponin levels, particularly troponin I or troponin T, have more diagnostic value than creatine kinase MB fraction; nonetheless, their clinical value in myocardial contusion is limited.⁷ It has been suggested that when troponin I and T levels are normal, blunt cardiac trauma is quite rare. One important caveat to this statement is that the optimal timing of these markers is important in realizing their diagnostic value. Troponin levels can peak in 4–6 hours and last for 4–6 days after cardiac trauma. Echocardiogram may be a helpful adjunct if performed within the 4–6 hours of trauma but may have less utility if the cardiac enzymes are normal after the 4–6 hours.

Other potential causes of hemodynamic compromise may occur after chest trauma and have similar manifestations to blunt cardiac trauma, such as hemothorax, pneumothorax, massive active hemorrhage, and pericardial effusion. A shock state that is unresponsive to blood or fluid resuscitation with a finding of hemothorax, could possibly be due to myocardial rupture. Therefore, hemodynamically unstable patients require immediate cardiac ultrasound to help rule out these other causes of instability.

Myocardial perfusion scintigraphy still has limited diagnostic value in blunt cardiac trauma. Large transmural defects are necessary to visualize evidence of cardiac injury using this test. In addition, the right ventricle is also poorly visualized and right ventricular injury can be missed.

Septal and valvular injury can also occur either individually or together after traumatic injury to the chest wall but they are rare occurrences. The cardiac septum can experience a small tear or a significant rupture depending on the force of the injury. The most commonly injured cardiac valve is the aortic valve followed by the mitral and then the tricuspid valve. The patient may present with a new murmur, widened pulse pressure, flash pulmonary edema, or heart failure often due to a disruption of a valvular leaflet, chordae tendineae, or papillary muscle tear.

A septal tear can also lead to an intracardiac shunt. There are also reports of right to left shunt through the patent foramen ovale after a tricuspid valve regurgitation. The most common site of a septal tear is at the apex of the intraventricular septum (Figure 16-1). Color Doppler in a four-chamber view can be performed with TTE. A bedside bubble study can also help to identify an intracardiac shunt when “air bubbles” can be seen moving within 1–2 cardiac cycles between parallel chambers. However, there are instances where TTE images are suboptimal and TEE images may be required for better visualization of the cardiac valves (Figure 16-2).