Up to 20% of all motor vehicle collision deaths are due to blunt cardiac injury, which can be sustained from any of the mechanisms listed in Table 262-2.16 Rapid deceleration is the most common mechanism responsible for most blunt cardiac injury followed by a direct blow to the precordium. Blunt cardiac injury results in a range of conditions from clinically silent transient dysrhythmias to cardiac wall rupture
TABLE 262-2Mechanisms for Blunt Cardiac Injury ||Download (.pdf) TABLE 262-2 Mechanisms for Blunt Cardiac Injury
Direct precordial impact
Crush injury from compression between the sternum and spine
Abrupt pressure fluctuations in the chest and abdomen
Shearing from rapid deceleration or torsion causing a tear in the heart at a point of fixation (right atrium and vena cava)
Injury from rib fracture fragments
Hydraulic effect resulting in cardiac rupture
The most common reported injury is "myocardial or cardiac contusion." These terms are nonspecific and have been used to report a wide range of injuries. Further, there is not a clear definition or a gold standard for testing, which makes the diagnosis and treatment difficult. The term blunt cardiac injury has replaced the terms cardiac contusion and myocardial contusion. Blunt cardiac injury can encompass cardiac dysfunction (diminished contractility in the absence of dysrhythmia or hemorrhage), dysrhythmias, specific injuries (septal rupture, valvular injuries, myocardial infarction), and cardiac rupture, the most devastating blunt cardiac injury.3,17,18
Blunt cardiac injury most often involves the right heart due to the anterior location of the right atrium and ventricle within the mediastinum. Injury often involves more than one chamber in over half of the reported cases.19
The pathologic changes seen in blunt cardiac injury typically include subendocardial hemorrhage and a much larger area of focal myocardial edema, interstitial hemorrhage, and myocytolysis with infiltrates of polymorphonuclear leukocytes. Additional myocardial injury may occur if there are concomitant intimal tears or compression from adjacent hemorrhage or edema. Myocardial injury may also be due to redistribution of coronary blood flow. Minor myocardial marker elevation or ECG abnormalities and dyskinesia or dysrhythmias resolve over time, usually within the first 24 hours.16 Blunt cardiac injury can lead to death from complex dysrhythmias, acute heart failure, cardiac-free wall rupture, or laceration of a coronary artery that causes extracardiac hemorrhage. Most of these lethal mechanisms result in death at the scene of the injury.20,21,22 Less severe injuries to the ventricular wall may lead to delayed necrosis and clinically manifest as delayed rupture days after admission. If a low-pressure chamber or coronary vein is injured, patients may survive until presentation to the hospital.23
Blunt cardiac injury can also result in rupture of an atrial or ventricular septum, resulting in shunting of blood and presentation similar to heart failure.24 Similarly, blunt cardiac injury can result in regurgitation of blood from a high-pressure chamber or artery into a lower-pressure chamber, such as with an acute valve dysfunction or papillary muscle injury.25,26 Valvular injury, as opposed to blunt myocardial injury, tends to worsen over time. The degeneration of the valve's function appears to depend on its location. High-pressure valves like the aorta and mitral valves tend to manifest symptoms immediately or within the first few weeks, whereas lower-pressure valves like the pulmonic and tricuspid can be asymptomatic for years.16 Coronary arteries can have occlusion, dissection, or spasm that can manifest as immediate or delayed injury patterns. Coronary artery injury presents most often in a myocardial infarction pattern.27
Nonspecific signs and concomitant injuries will affect clinical presentation. These other findings in the trauma patient may make it difficult to determine whether symptoms stem from cardiac or other injuries. Specific signs of cardiac injury (e.g., distended neck veins or specific murmurs) may not be present if the patient is hypotensive from other injuries. Symptoms of cardiac injury may occur in a delayed fashion coincident with fluid resuscitation.
Commotio cordis, meaning "disturbance of the heart" in Latin, is sudden death as a result of blunt trauma to the chest wall. It often results from an innocent-appearing chest wall blow. It is the second most common cause of death in youth athletics following hypertrophic obstructive cardiomyopathy. Usually victims are young athletes who are struck in the chest by hard projectiles that are used in the particular sport. Sports using small dense projectiles like baseball, hockey, and lacrosse have the highest incidence of commotio cordis. The hardness of the impact object, location of impact, and velocity of the object impacts the risk of development of ventricular fibrillation. Commotio cordis blows are generally low impact, most of which are insufficient to cause any significant structural damage to the ribs, sternum, or heart. Commotio cordis is a primary electrical event resulting in the induction of ventricular fibrillation; it is a result of a blow that occurs 10 to 30 ms before the peak of the T wave, a time of vulnerability to ventricular fibrillation. Autopsy findings show normal cardiac anatomy with no evidence of injury. The overall survival rate is less than 15%, but due to increasing prevalence of automated external defibrillators being placed in sporting venues, survival rates may improve.28
The exact incidence of cardiac dysfunction (decreased contractility) in blunt cardiac injury is unknown. Further, the cause of dysfunction may be difficult to determine in the hypotensive, multiply injured trauma patient. Patients almost universally present with chest pain. The pain usually results from associated thoracic trauma (Table 262-3). Associated blunt injury to the lung can lead to a rise in pulmonary vascular resistance, which can result in a reduction in preload of the left ventricle. This, coupled with the reduced cardiac output of the involved right ventricle, can lead to hypotension.18,29 The damaged myocardial tissue may be a focus for both atrial and ventricular dysrhythmias, which may further produce decreased contractility and hemodynamic deterioration.
TABLE 262-3Associated Injuries with Blunt Cardiac Trauma3 ||Download (.pdf) TABLE 262-3 Associated Injuries with Blunt Cardiac Trauma3
|Associated Injuries ||Incidence of Finding in Patients with Blunt Cardiac Injury |
|Thoracic injury || |
| Chest pain ||18%–92% |
| Rib fracture ||18%–69% |
| Aortic or great vessel injury ||20%–40% |
| Hemothorax ||7%–64% |
| Pulmonary contusion ||6%–58% |
| Pneumothorax ||7%–40% |
| Flail chest ||4%–38% |
| Sternal fracture ||0%–60% |
|Head injury ||20%–73% |
|Extremity injury ||20%–66% |
|Abdominal solid organ injury ||5%–43% |
|Spinal injury ||10%–20% |
Monitor for dysrhythmias. Persistent tachycardia, new bundle branch block, supraventricular tachycardia, atrial and ventricular fibrillation, and minor dysrhythmias (occasional premature ventricular contraction) can occur after blunt injury.
INJURY TO THE PERICARDIUM
Direct impact or increased intra-abdominal pressure can cause pericardial tears. The tears usually occur on the left side of the pericardium parallel to the phrenic nerve. Herniation can occur through the defect leading to cardiac dysfunction and dysrhythmias. These tears in the pericardium often are missed and may have little clinical impact. Physical examination (pericardial rub), point-of-care US, or CT findings (pneumopericardium, displacement of the heart, abnormal bowel gas in chest or around heart, or evidence of intra-abdominal contents inside pericardium) may lead to the diagnosis. Patients with detectable pericardial rents are usually taken to the operating room for repair unless the tear is too large so that closure would lead to tension on the pericardium and potentially produce myocardial dysfunction.
INJURY TO CARDIAC VALVES, PAPILLARY MUSCLES, CHORDAE TENDINEAE, AND SEPTUM
Injury to cardiac valves occurs in approximately 10% of blunt cardiac injury. Isolated valvular injuries appear to be rare. The aortic valve is most often involved, followed by the mitral and tricuspid valves. Injury to the aortic valve can cause severe regurgitation with development of pulmonary edema. Presentation may vary from new murmur to acute valvular insufficiency with right- or left-sided cardiac failure. A widened pulse pressure can be seen with acute aortic valvular injuries. Septal injuries are also rare with variable presentations, ranging from insignificant tears to frank rupture. They may occur in isolation or with valvular injury. The muscular portion of the septum can rupture several days after blunt trauma. Suspect patients with new-onset murmurs of having valvular, septal, or papillary muscle pathology. Any patients with clinical or echocardiographic evidence of injury require emergent surgical consultation. Treatment for septal and valvular injury is generally surgical, and timing depends on the presenting signs and acuity. Acute heart failure resulting from elevated pulmonary pressure due to structural injury warrants rapid surgical intervention, whereas small septal injuries with minimal clinical effects can be treated conservatively because many eventually close spontaneously.30
INJURY TO CORONARY VESSELS/MYOCARDIAL INFARCTION
Although blunt cardiac injury rarely leads to injury of the coronary vessels, arteriovenous fistula, coronary artery dissection, and coronary thromboses have been reported.31,32 The most common artery involved is the left anterior descending artery. Coronary artery injury presents in the same fashion as atherosclerotic heart disease, has similar treatment by percutaneous coronary intervention with stenting, and has a more favorable prognosis. Because of the possibility of other injuries, extreme caution must be taken in using anticoagulation therapy due to bleeding complications.31,32 Fibrinolytic therapy is contraindicated.
The most severe form of blunt cardiac injury is cardiac rupture. Most patients with cardiac rupture die at the scene of the trauma. The right-sided portion of the heart is much more prone to rupture due to its more anterior location, as are the thin-walled atria compared with the thicker-walled, stronger ventricles. In patients who survive to ED arrival, the physical examination may reveal a "splashing mill wheel" sounding murmur ("bruit de Moulin"), but this finding is rare. ECG may show conduction defects or, if herniation has occurred, axis deviation. A skilled sonographer can rapidly reveal the diagnosis, and immediate thoracotomy is required for survival.22
CLINICAL FEATURES OF BLUNT CARDIAC TRAUMA
The most common symptom of cardiac trauma is chest pain. All different qualities of chest pain occur, ranging from pleuritic to pressure-like. Even the classic crushing retrosternal pain of myocardial ischemia can occur if coronary arteries are involved. Patients with injuries on the chest wall such as rib fractures, sternal fractures, or clavicular fractures may have underlying cardiac injury. Be cautious about attributing symptoms only to superficial chest wall because pericardial and myocardial structures may be damaged as well. Patients may have shortness of breath due to overlying chest and pulmonary injury or due to myocardial dysfunction from cardiac tamponade or heart failure. Other nonspecific symptoms such as lightheadedness and palpitations are also common.18 Clinical findings vary widely depending on the structures injured, the extent of the injuries, concomitant injuries, and the patient's body habitus and mental status.
Close observation of heart rate and blood pressure and their associated trends is important. Listening to breath sounds and heart sounds may assist in diagnosing cardiac injury. Clear lungs with muffled heart sounds may be indicative of cardiac tamponade, but this finding is quite rare and difficult to detect in a noisy ED. Course crackles in the lungs, extra heart sounds, and elevated jugular venous pressure may be present if myocardial dysfunction leads to heart failure. Often, the presence of unexplained tachycardia may be the only finding of cardiac injury.
Place the patient on a cardiac monitor, and obtain an ECG. The negative predictive value for cardiac injury in a patient with a normal ECG is about 80% to 90%, but using the ECG alone does not exclude cardiac injury.18,33 A clinically significant cardiac event can occur over the first 24 hours following injury.34 The ECG is more sensitive for left ventricular injury than right-sided injury and is poorly sensitive for the more common right-sided injuries. Nondiagnostic findings on ECG, such as sinus tachycardia and nonspecific ST-T wave changes, do not help diagnose blunt cardiac injury. A small subset of blunt cardiac injury patients may have symptoms and ECG findings consistent with myocardial infarction. In such patients, consider coronary artery disease or acute coronary artery dissection, which may manifest with thrombosis of a cardiac artery and typically develops 5 to 7 days after injury17,35 (Table 262-4).
TABLE 262-4Electrocardiographic Findings in Cardiac Injury36 ||Download (.pdf) TABLE 262-4 Electrocardiographic Findings in Cardiac Injury36
Right bundle branch block
Atrioventricular nodal conduction disorders (first-, second-, and third-degree atrioventricular block)
In patients in whom concern for blunt cardiac injury exists but in whom the ECG is normal, monitor for 4 to 6 hours with repeat examinations, ECGs, and cardiac monitoring. If there are no new signs or symptoms and no abnormalities occur during this time period, patients can be safely discharged in absence of any other injuries.37 If the ECG is abnormal but there is no hemodynamic instability, admit the patient to a monitored setting, with serial ECGs to monitor for disease progression.
Although cardiac markers can be used to assist in the diagnosis of myocardial trauma, the utility of cardiac biomarkers in the setting of blunt cardiac injury remains unclear.38 Creatine kinase has limited reliability in the trauma patient because it is elevated in cases of severe skeletal muscle, liver, diaphragm, or intestinal injury; the creatine kinase-MB fraction will therefore be elevated as well. Creatine kinase-MB fraction elevation has been shown to occur in this situation in the absence of clinical evidence of cardiac injury. The isolated elevation of creatine kinase-MB, with no other associated injury, is not predictive of complications and mortality.39 Thus, obtaining creatine kinase-MB measurements is of no value.
Cardiac troponins, specifically troponin I and troponin T, are very specific to myocardial injury and can detect very small amounts of myocardial necrosis. Neither cardiac troponin I nor cardiac troponin T is released with skeletal muscle injury. Elevation of troponins occurs in all myocardial trauma, including both blunt and penetrating trauma, surgery, ablation, pacing, defibrillator shocks, cardioversion, and interventional cardiac procedures. The sensitivity and specificity of troponins for blunt cardiac injury vary from 12% to 23% and 97% to 100%, respectively.33,40 Also, injuries remote from the chest from multisystem trauma and the presence of preexisting disease may result in dysrhythmia and elevated biomarkers, making their presence even less specific.41
Troponins in conjunction with a presenting ECG may increase the effectiveness of risk stratification. Patients with a normal ECG and normal serial measurements of serial cardiac troponin I had no significant blunt cardiac injury–related complications in one study.42 The sensitivity of an abnormal ECG and elevated cardiac troponin I for clinically significant blunt cardiac injury (cardiogenic shock, dysrhythmias requiring intervention, or structural cardiac abnormalities related to trauma) was 100%, with a positive predictive value of 62%.40 Clinically significant blunt cardiac injury can occur without elevation of troponins, but there is usually an abnormality of the ECG. Monitor any serum troponin elevation and follow serially. Increased troponin levels at admission or within 6 hours of arrival have correlated with increasing risk of dysrhythmia and decreased ejection fraction.43 Troponin elevations have been associated with ventricular dysrhythmias and left ventricular dysfunction.44
Ultimately, the use of cardiac biomarkers may not affect the management of blunt trauma patients with hemodynamic instability, signs of severe injury, or an abnormal ECG. Such patients generally undergo echocardiography and are admitted regardless of biomarker elevation.
In rare blunt trauma patients with ECG findings of myocardial infarction, obtain cardiac biomarkers and immediately consult with cardiology and cardiac surgery.
The FAST examination includes a cardiac window using either the subxiphoid (Figure 262-3) or parasternal long-axis approach. This allows detection of free pericardial fluid and can give an estimation of general cardiac function. Point-of-care US has been shown to have a sensitivity of 100% and a specificity of 99% for detecting pericardial effusion.45
Traumatic pericardial effusion. Large pericardial effusion (arrow) after stab wound to chest visualized by subxiphoid approach of a FAST scan. The effusion can be seen outside the right ventricular (RV) and left ventricular (LV) walls.
Point-of-care US is an invaluable tool for blunt trauma patients with unexplained, persistent shock out of proportion to apparent injuries and in any patients with signs consistent with blunt cardiac injury. Echocardiography provides information about global cardiac function, individual chamber function and wall motion, valvular function, and ejection fraction. It can also assist in alternative diagnoses for conditions such as aortic disruption/dissection, pericardial effusion, pleural effusion, and intracardiac thrombus.46 Transesophageal echocardiography has been shown to be up to three times more sensitive in diagnosing blunt cardiac injury than transthoracic echocardiography.47 Transthoracic echocardiography and transesophageal echocardiography, however, are not helpful in identifying patients at risk for developing blunt cardiac injury–related complications.16 Order echocardiography for patients demonstrating elevated cardiac markers, dysrhythmias, or myocardial dysfunction.48
TREATMENT OF BLUNT CARDIAC INJURY
Treat hypotension with boluses of crystalloid to optimize intravascular blood volume, which will also optimize preload. Trauma patients often have multiple injuries, especially in blunt injury, so the most common reason for hypotension is due to hypovolemia, not myocardial dysfunction.
Otherwise, the management of blunt cardiac injury (myocardial or cardiac contusion) is not standardized. The only universally accepted practice pattern is to observe patients with hemodynamic and continuous cardiac monitoring.18 It is generally agreed that low-risk patients (minor injuries, no dysrhythmias, and normal ECG) usually will not develop complications so that further workup is not warranted. Moderate- to high-risk patients (evidence of associated injuries, dysrhythmias, abnormal ECG) should have an evaluation that includes myocardial markers and echocardiogram. Admission to ward telemetry is appropriate for the patient with minor ECG abnormalities (premature ventricular or atrial contractions), no significant concomitant injuries, and normal hemodynamics.49,50 Telemetry monitoring criteria do not exist, but 24 to 48 hours of monitoring are reasonable for minor abnormalities.
Subsequent management depends on complications. After ruling out hypovolemia as the source of hypotension, inotropic support may be required to maintain cardiac output and blood pressure. Dysrhythmias that result in hemodynamic instability or are ventricular in origin are treated according to advanced cardiac life support algorithms. Evaluate patients who present in cardiogenic shock for a structural injury. Patients with cardiac rupture, valvular injury, papillary muscle or chordae tendineae rupture, or coronary thromboses or dissection require emergent surgery or percutaneous coronary intervention.
PERICARDIAL INFLAMMATION SYNDROME
The cause of pericardial inflammation may be a delayed hypersensitivity reaction to the presence of damaged myocardium in the pericardial cavity. Consider this syndrome in individuals who develop chest pain, fever, and pleural or pericardial effusions 2 to 4 weeks after cardiac trauma (or surgery). Patients may also have friction rubs, arthralgia, and pulmonary infiltrates. The ECG will often show ST-T wave changes consistent with pericarditis. Treatment is primarily symptomatic. Nonsteroidal anti-inflammatory drugs and rest can often reduce symptoms dramatically within 12 to 24 hours, and glucocorticoids are occasionally required. Rarely, drainage of pleural or pericardial fluid may be required to relieve symptoms or to exclude other problems.