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The Telltale Signs of a Blunt Cardiac Injury

Fadial, Tom MD

doi: 10.1097/01.EEM.0000604596.22133.99



A 35-year-old woman with no past medical history was brought to the ED by ambulance after she was struck by fireworks, a Roman candle, that lodged in her mid-chest until the propellant was consumed. She transiently lost consciousness, but was awake upon EMS arrival.

She complained of pleuritic chest pain, and an examination revealed a circular 4x4 cm full-thickness burn to the mid-chest with surrounding deep and superficial partial-thickness burns. Her ECG showed normal sinus rhythm, and the initial serum troponin I was 32.9 (normal <0.012). CT angiography of the thorax was obtained.

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Blunt cardiac injury may be induced by multiple forces, including direct thoracic trauma, crush injury of mediastinal contents between the sternum and thoracic spine, rapid deceleration causing tears at venous-atrial confluences, abrupt pressure changes from rapid compression of abdominal contents, blast injury, or laceration from bone fracture fragments. (Crit Care Clin. 2004;20[1]:57.) The most common mechanisms of injury are motor vehicle crashes (50%), auto v. pedestrian collisions (35%), motorcycle crashes (9%), and falls from significant height (>6 m). (Ann Thorac Surg. 2014;98[3]:1134;



Blunt cardiac injury represents a spectrum of conditions. Diagnosis is challenging and critical because clinical manifestations can be absent or rapidly fatal. At one end of the spectrum is myocardial contusion. The lack of a gold standard for diagnosing this clinical entity has led to a preference for describing associated abnormalities if present (J Trauma. 1992;33[5]:649; Heart. 2003;89[5]:485;, including cardiac dysfunction (identified on echocardiography) and the next entity along the spectrum, arrhythmia. The most common arrhythmia identified in blunt cardiac injury is sinus tachycardia, followed by premature atrial or ventricular contractions, T-wave changes, and atrial fibrillation or flutter. (Mt Sinai J Med. 2006;73[2]:542.) Commotio cordis is a unique arrhythmia induced by untimely precordial impact (often in sports) during a vulnerable phase of ventricular excitability, resulting in ventricular fibrillation. (Ann Thorac Surg. 2014;98[3]:1134;

ST segment elevations after blunt cardiac injury should raise concern for myocardial infarction from coronary artery dissection, laceration, or thrombosis (often in already-diseased vessels). (Mt Sinai J Med. 2006;73[2]:542; Anesthesiology. 2004;101[6]:1262;

The remaining disease entities are increasingly rare and require careful examination or imaging for diagnosis, and patients are more unlikely to survive. Septal injury can range from small tears to rupture. Valvular injury most commonly affects the aortic valve (followed by mitral and tricuspid valves), and involves damage to leaflets or rupture of papillary muscles or chordae tendineae. The clinical presentation is of acute valvular insufficiency, including acute heart failure and murmur. (Ann Thorac Surg. 2014;98[3]:1134;; J Am Soc Echocardiogr. 2006;19[4]:469.e1;; J Trauma. 2010;68[1]:243;

A widened pulse pressure may be noted with aortic valve injury, and the manifestations of valvular injury may be delayed. (Injury. 2005;36[9]:1022.) Finally, patients are unlikely to survive myocardial wall rupture, though they may present with cardiac tamponade if the rupture is small or contained. (Ann Thorac Surg. 2014;98[3]:1134;

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The primary diagnostic modalities for blunt cardiac injury include assessment for pericardial fluid during the FAST exam, electrocardiography, and cardiac enzymes.

Electrocardiography is specific for identifying patients at risk of complications of blunt cardiac injury, but it alone is not sufficient to exclude blunt cardiac injury. One study found only 59 percent of patients with echocardiographic evidence of blunt cardiac injury (wall-motion or other chamber abnormalities) initially had abnormal ECGs. (Am Heart J. 1998;135[3]:476.) Another study found that 41 percent of patients with initially normal ECGs developed clinically significant abnormalities. (J Trauma. 1997;43[2]:304; The use of specialized electrocardiography, including right-sided ECG (to better detect right ventricular abnormalities commonly associated with blunt cardiac injury) and signal-averaged ECG, is not supported. (J Trauma. 1997;43[2]:304;; J Trauma. 2001;51[1]:60;

Several studies have supported the use of serum troponin for detecting blunt cardiac injury, particularly in combination with electrocardiography. A prospective study in 2001 evaluating patients with blunt thoracic trauma using ECG at admission and eight hours later, as well as troponin I at admission, four hours, and eight hours later, had a negative predictive value of 100% for significant blunt cardiac injury (arrhythmia requiring treatment, shock, or structural cardiac abnormalities) in patients with initially normal ECG and troponin. (J Trauma. 2001;50[2]:237.) Another prospective study included 41 patients with normal ECGs and troponin levels at admission and eight hours later who were admitted for significant mechanisms. None developed blunt cardiac injury after one to three days of observation. (J Trauma. 2003;54[1]:45; The precise timing of serum troponin analysis remains unclear.

The FAST exam may detect hemopericardium warranting immediate intervention; formal echocardiography is indicated for patients with unexplained hypotension to evaluate for valvular injury or regional wall-motion abnormalities or those with persistent arrhythmias to evaluate for arrhythmogenic intramural hematomas. (World J Surg. 2001;25[1]:108.) Sternal fractures were previously thought to increase the risk of blunt cardiac injury and mandate echocardiography, but this notion is no longer supported. (J Trauma. 1994;37[1]:59; J Trauma. 1993;35[1]:55; Eur J Surg. 2001;167[4]:243.) The role of advanced imaging, including helical CT (cardiac-gated) and MRI, remains unclear. (J Trauma Acute Care Surg. 2012;73[5 Suppl 4]:S301;

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Management of blunt cardiac injury depends on the pathologic process localized along the spectrum. (Image.) Persistent hypotension may represent myocardial contusion with cardiac dysfunction and should be evaluated with echocardiography. Similarly, echocardiography and observation with continuous telemetry monitoring are indicated for any new arrhythmia or persistent and unexplained tachycardia.

Patients with only elevation of the serum troponin without electrocardiographic abnormalities or obvious cardiac dysfunction should also be admitted for observation and serial cardiac enzymes. Traumatic myocardial infarction, valvular injury, or post-traumatic structural myocardial defects should be managed in consultation with cardiothoracic surgery. (Mt Sinai J Med. 2006;73[2]:542; J Trauma Acute Care Surg. 2012;73[5 Suppl 4]:S301;; Hockberger RS, Walls RM. Rosen's Emergency Medicine. St. Louis: Mosby, Inc.; 2002.)

The CT interpretation noted the soft-tissue defect identified on examination as well as associated pulmonary contusions and a non-displaced sternal fracture. The patient went to the operating room for washout and debridement. A transthoracic echocardiogram demonstrated trace mitral regurgitation and a small pericardial effusion. She remained hemodynamically stable, and serial troponin measures downtrended. No dysrhythmias were noted on telemetry monitoring. She was discharged on hospital day four with negative-pressure wound dressing.

Dr. Fadialis an assistant professor of emergency medicine at McGovern Medical School in Houston. As the educational technology and innovation officer there, he develops unique educational tools, including algorithms that can be found at His other medical education projects can be found at

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