REVIEW
Blunt Cardiac Trauma: A Review of the Current
Knowledge and Management
Raid Yousef, MD, and John Alfred Carr, MD
Department of Trauma Surgery, Hurley Medical and Level 1 Trauma Center, Flint, Michigan
Blunt cardiac injuries are highly lethal. A review of the
world’s English literature on the topic reveals a lack of
Level 1 Evidence and few cohesive guidelines for the
management of these patients. An online database query
was performed using the PubMed medical database.
I n 2011 the National Trauma Data Bank reported that
773,292 people in the United States required admission
to a hospital for traumatic injuries [1]. This information
was collected from their 744 participating hospitals. The
data show that cardiac trauma (blunt and penetrating) is
identified in less than 10% of all trauma admissions,
and yet cardiac trauma is associated with a much higher
mortality than other organ system injuries. Considering
the lethality of this type of injury, better guidelines
should exist to direct management.
This review will only focus on blunt cardiac injury (BCI)
and will not address penetrating injuries or blunt trauma
to the aorta. The world’s English literature on the topic of
REVIEW
BCI demonstrates a significant lack of Level 1 Evidence
and few cohesive guidelines in the management. There-
fore, this article will provide an exhaustive assessment of
the data on the topic of BCI and provide conclusions
based on the known Levels of Evidence.
Pathophysiology
Most BCIs occur due to motor vehicle crashes (approxi-
mately 50%), followed by pedestrians being struck
by motor vehicles (35%), motorcycle crashes (9%), and
the remainder are mostly secondary to falls from a sig-
nificant height [2, 3]. One autopsy study of more than
1,597 fatalities from blunt trauma identified cardiac in-
juries in 190 individuals (11.9%) [3]. Approximately
70% to 80% of those patients who sustained significant
BCI had multiple other injuries: brain (42% to 54%),
thoracic aorta (47% to 49%), lung (44% to 46%),
hemothorax (37% to 89%), rib or sternal fractures (26%
to 97%), and spinal injuries (37%) [2–7]. Patients with
severe BCI who have other associated organ injuries
often die at the scene of the accident [2–7]. Cardiac in-
juries are the only cause of death or contribute to the fatal
outcome in 45% to 76% of the individuals who die [3, 6].
Address correspondence to Dr Carr, Department of Trauma Surgery,
Hurley Medical and Level 1 Trauma Center, One Hurley Plaza, Flint,
MI 48503; e-mail: jcarr1@hurleymc.com.
Ó 2014 by The Society of Thoracic Surgeons
Published by Elsevier Inc
All relevant articles from the past 20 years were reviewed.
Conclusions are presented with their corresponding
Levels of Evidence.
(Ann Thorac Surg 2014;98:1134–40)
Ó 2014 by The Society of Thoracic Surgeons
The most common injury is transmural rupture of
a cardiac chamber, seen in 39% to 64%, or multiple
chamber ruptures in 26% [3, 7].
In contrast to motor vehicle crashes, up to 54% of
people who fall from a height exceeding 6 meters (20 feet)
have some type of BCI, from small endocardial tears
to transmural rupture [8]. The chance of cardiac injury
increases as the height increases, such that the surgeon
should be concerned about some type of possible
endocardial tear or intramural hematoma in any patient
who falls more than 6 meters (20 feet) [8]. For those
with documented cardiac injury by autopsy after death
from a fall, sternal fractures were present in 76% and
multiple sternal fractures in 16% [8]. Thus, the
combination of a fall greater than 20 feet with a sternal
fracture should prompt a thorough cardiac evaluation.
Death at the Scene
When death from blunt trauma is proven by autopsy to
be from cardiac injury, the most common lethal cardiac
injuries were transmural rupture of 1 or more cardiac
chambers (64%), tears occurring at the venous-atrial
confluence (33%), or a blunt coronary artery dissection
or tear [2, 3, 5–8]. Owing to its anterior location, the right
ventricle is the most commonly injured chamber in 40%
of the victims [3, 6–8] (Table 1). The right atrium and left
ventricle follow closely second and third, with injuries in
30% to 33% [7–9].
Tears occurring at the venous-atrial confluence are
believed to be due to rapid deceleration that results in the
freely mobile ventricles (which also have most of the mass
of the heart) continuing to move forward or laterally
while the tethered posterior veins do not move, resulting
in a distraction-avulsion injury at the venous-atrial
The full Reference Section can be viewed in the
online version of this article [http://dx.doi.org/10.1016/
j.athoracsur.2014.04.043] on http://www.annalsthoracic
surgery.org.
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http://dx.doi.org/10.1016/j.athoracsur.2014.04.043
Ann Thorac Surg
2014;98:1134–40
Table 1. Autopsy Findings in 303 Blunt Cardiac Injuriesa
Finding
Pericardial tears
Transmural right atrial rupture
Right atrial hematoma
Right atrial/IVC tear with epicardial
hematoma
All right atrial injuries
Transmural left atrial rupture
Left atrial hematoma
Left atrial/pulmonary vein tear with
epicardial hematoma
All left atrial injuries
Transmural right ventricular rupture
Right ventricular intramural hematoma
All right ventricular injuries
Transmural left ventricular rupture
Left ventricular intramural hematoma
All left ventricular injuries
Ventricular septal tear
Tricuspid valve injury
Mitral valve injury
Aortic valve injury
Pulmonary valve injury
Coronary artery dissection
Coronary artery torn
Heart completely avulsed
a
Data compiled from references 3, 6, and 8. Many patients had more than
1 type of injury.
IVC ¼ inferior vena cava.
confluence. This type of injury can occur in two places: at
the junction of the inferior vena cava and the right atrium
and at the junction of the pulmonary veins and the left
atrium [3, 8, 10, 11]. One autopsy study of 190 deaths due
to BCI found almost all of the right atrial tears occurred
near the area where the inferior vena cava enters the right
atrium, and left atrial ruptures were located predomi-
nantly in the areas where the great veins lead into the
atria [3]. Unlike chamber rupture, small tears at the
confluence can be contained, and the patient may
initially be stable. Diagnosis by echocardiography
(ECHO) and repair with and without cardiopulmonary
bypass has been reported [10, 12]. No reports have
documented an isolated tear occurring at the confluence
of the superior vena cava and right atrium.
Commotio Cordis
Commotio cordis is sudden death from cardiac arrest
in a young person, often occurring during sports, after
a blunt blow to the chest in the absence of structural
cardiovascular disease [13]. Unlike motor vehicle
accidents or falls, this injury shows no anatomic
structural damage to the heart but is a pure conduction
abnormality induced by the trauma. Commotio cordis
is also a completely different phenomenon from sudden
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sports-related cardiac death from underlying congenital
heart disease or hypertrophic cardiomyopathy. This
No. (%)
traumatic injury occurs in the athlete with a normal
108 (36) heart.
64 (21) The United States Commotio Cordis Registry (224
19 (6) cases as of 2011) documented that 50% of the cases
18 (6) causing death from blunt blows to the chest occurred in
competitive sports. This most often occurs in baseball
101 (33) and is usually triggered when players are struck in the
39 (13) chest by balls that have been pitched, batted, or thrown in
5 (2) a variety of scenarios. Other than baseball, commotio
3 (1) cordis is seen mainly in softball, ice hockey, football, or
lacrosse [14]. Another 25% of commotio cordis events
47 (16) occur in recreational sports played at home, on the
83 (27) playground, or at family gatherings. The remaining 25%
38 (13) of commotio cordis happens in events unrelated to
121 (40) sports, such as kicks in the chest by animals or other
61 (20) odd events [13, 14]. Among patients in the United States
35 (12) registry, 65% of athletes with commotio cordis were
96 (32) aged between 10 and 25 years, 26% were younger than
12 (4) 10 years, and only 9% were older than 25 years. Inter-
6 (2) estingly, chest protection, in the form of a polymer foam
5 (2) pad or hard shell, appears not to be protective, because
8 (3)
athletes wearing these still died [15, 16]. Two separate
studies found that 28% and 40% of the deaths from
1 (<1)
commotio cordis occurred in athletes wearing commer-
3 (1)
cially available chest protectors [13, 15].
5 (2)
The underlying pathophysiology of the cardiac arrest
13 (4)
in these individuals has always been assumed to be
caused by the impact transmitted to the myocardium
inducing ventricular fibrillation during an electrically
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vulnerable phase of ventricular excitability, more spe-
cifically, cardiac repolarization [13, 16]. In a swine
model with a ball propelled at 30 to 40 miles per hour
striking the chest, ventricular fibrillation could only be
induced 28% of the time [17]. These chest wall strikes
were timed to occur during the narrow window of
cardiac repolarization. Multivariate analysis revealed
that the highest chance of inducing fibrillation occurred
when higher left ventricular pressures were generated
by the impact, with longer QRS duration, and QTc
variability [17].
Unlike hypoxic or ischemic cardiac arrest, however,
most of the time this population tends to be refractory
to cardiopulmonary resuscitation and defibrillation,
even when it is begun immediately after arrest [18, 19].
This raises the possibility that commotio cordis may
occur due to a combination of ventricular fibrillation
and coronary vasospasm or segmental changes in
myocardial contractility [18]. Although a review of the
literature from the 1990s will identify a few rare case
reports of survivors, most victims died immediately at
the scene [13]. For example, a published report in
1995 that documented the chronology in 25 patients
showed that without cardiopulmonary resuscitation and
defibrillation within 3 minutes, all died (n ¼ 6). With
cardiopulmonary resuscitation and defibrillation within
3 minutes (n ¼ 19), only 2 were restored to a normal
cardiac rhythm, but both later died from severe hypoxic
brain injury [13].
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The latest commotio cordis registry data show that
survival has increased over time and that the number of
successful resuscitations between 2006 and 2009 exceeded
the number of deaths by 20%. This improvement is
probably the result of increased public awareness, the
increased availability of automatic external defibrillators,
and earlier activation of the chain of survival, including
initiation of cardiopulmonary resuscitation, defibrillation,
and advanced life support measures [14].
More effort should be made to prevent these largely
avoidable deaths, and this can be accomplished by
providing more education, especially to coaches, better-
designed athletic equipment (eg, effective chest-wall
protectors), and wide access to automatic external de-
fibrillators at organized athletic events [14, 19, 20].
Survivors to the Hospital
Most of the blunt trauma victims with BCI who do survive
to the hospital tend to have injuries that are less severe.
Other than cardiac tamponade from bleeding, the other
potentially treatable and reversible BCIs can be divided
into two large groups: (1) structural cardiac injuries,
which include intramural hematoma (IMH), valvular
injury, ventricular septal rupture, coronary artery injury,
myocardial infarction, and (2) electrical disturbances,
such as atrial and ventricular dysrhythmias, and con-
duction disturbances.
Intramural Hematoma
IMH most commonly occurs in the right ventricle (13% of
REVIEW
all patients with BCI), followed closely by the left
ventricle (12%) [3, 6, 8]. Although diagnosis of IMH can
be made by computed tomography or magnetic reso-
nance imaging, the method of choice for noninvasive
diagnosis is by ECHO [21–24]. IMH can cause premature
ventricular contractions and transient bundle branch
block (BBB), but the clinical course tends to be benign.
Knowledge of the resolution and natural history of IMH
does not come from the trauma literature but from
complications that have occurred after surgical and
percutaneous coronary interventions resulting in an IMH
[25–29]. With conservative management, all IMHs tend to
resolve spontaneously after 4 to 12 weeks, as docu-
mented by follow-up ECHO [25–29]. A large IMH can
cause a BBB, bifascicular block, or complete heart block if
it is within the interatrial septum near the atrioventric-
ular node [30, 31]. This requires close observation, but
the treatment is supportive because the IMH will resolve
with time.
Valvular Injury
Another common injury pattern from blunt cardiac
trauma is papillary muscle rupture leading to acute
valvular regurgitation. This can occur with the tricuspid
and mitral valves. Acute aortic valve injury has also been
described; however, only one case of BCI causing acute
pulmonary valve disruption has been documented [3].
Injury to the papillary muscle, the chordae, or the
mitral valve is well documented [32, 33]. A review of the
Ann Thorac Surg
2014;98:1134–40
world’s literature on the subject from 1964 to 2010 iden-
tified 82 reported patients, and 57% required a valve
replacement [34]. The papillary muscles were most
commonly injured, followed by the chordae, and then
the mitral leaflets [34].
The same injury pattern can occur with the tricuspid
valve, although the presentation may be subtler because
wide-open tricuspid regurgitation can be well tolerated. In
fact, patients may be asymptomatic after the accident
and only be diagnosed with tricuspid regurgitation
months or years later [35]. However, this is not true in all
cases, and acute right ventricular failure has been
described in patients with complete papillary disruption
[36]. An association of traumatic tricuspid injury and
heart block has been documented, ranging from first
degree to complete heart block [37]. Thus, close
observation is necessary and may require transvenous
temporary pacing, followed by permanent pacemaker
insertion if necessary. Diagnosis of all valvular injuries is
made by ECHO, and the operation required is usually a
valve replacement, although recently more of these
injuries are being treated by repair or annuloplasty with
valve salvage [38–40].
Postinjury findings of a new holosystolic murmur
cannot always be attributed to valve pathology. A rare,
but well-described, lesion occurring after cardiac trauma
is an acute ventricular septal defect (VSD), which usually
occurs within the membranous portion [41–43]. The
defect may be single or multiple [44]. Depending on
the size of the defect, there may be little hemodynamic
change or complete hemodynamic instability [45, 46].
Diagnosis can be made promptly using ECHO.
Coronary Artery Injury
Acute coronary artery dissection can also occur from
blunt cardiac trauma. The pathophysiology in these
cases tends to be direct impact over the left anterior
descending coronary artery or the left main coronary
artery [47–49]. The area of the dissection usually origi-
nates in a previously diseased portion of the left anterior
descending artery and very rarely occurs in an elastic,
normal vessel. The dissection is likely related to plaque
rupture, which initiates the dissection as the intima over
the plaque tears, and the blood flow then propagates
the injury [50, 51]. The torn intima then creates a flap
that obstructs the blood flow and produces infarction.
The infarction will usually involve the apex, septum, or
both, as the septal branches and distal left anterior
descending artery occlude and thrombose. Acute coro-
nary occlusion and dissection from blunt trauma has been
successfully managed by percutaneous techniques [48,
51–53]. An elevated level of cardiac troponin I (cTnI)
with ST segment elevation represents coronary artery
occlusion or dissection and should prompt immediate
coronary angiography with revascularization as appro-
priate [54, 55].
Traumatic VSD also requires surgery and patch closure
in most cases with a large defect or the presence of a
significant shunt. The first successful transcatheter
closure of a traumatic VSD was described in 2004 [56] and
Ann Thorac Surg
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has been successfully performed many times since [57].
However, it is important in these cases for the clinician
to realize that unlike a congenital VSD with a fibrous
ring of tissue around the defect, a traumatic VSD will
be surrounded by necrotic and friable muscle that is
not resilient and may not hold or support an occluder
device [58].
Serum Troponin Levels After Cardiac Trauma
The literature on detecting a BCI by serum troponin
measurement is somewhat controversial. There are three
types of Tn: TnI, which binds to actin to hold the
troponin-tropomyosin complex to the myofilaments; TnT,
which binds to tropomyosin to form the troponin-
tropomyosin complex; and TnC, which binds to calcium
ions to cause a conformational change in TnI. All three
types of Tn are present in cardiac and skeletal muscle.
There is no Tn in smooth muscle.
TnI is present in skeletal muscle and cardiac muscle.
The three isoforms of Tn I are: cTnI, a slow skeletal
muscle TnI isoform (ssTnI), and a fast skeletal muscle TnI
isoform (fsTnI). They are encoded by different genes and
are specifically expressed in cardiac, slow skeletal muscle,
and fast skeletal muscle, respectively. Commercially
available testing kits purport to detect one isoform and
not the other, such that no cross-detection occurs be-
tween the cardiac and skeletal isoforms. The cardiac iso-
form (cTnI) differs from the skeletal muscle isoform
(ssTnI) by only an extended N-terminal sequence of 32
amino acid residues [59]. If there is significant cross-
reactivity, then an elevated TnI after blunt chest trauma
may represent myocardial damage (mostly cTnI) or may
represent skeletal muscle and chest wall damage (mostly
ssTnI or fsTnI).
When the initial monoclonal antibody enzyme immu-
noassays were first developed, separate studies found
cross-reactivity with both skeletal and cardiac TnI in up
to 30% of the antibodies [60, 61]. In addition, intraassay
and interassay variances within different commercially
available TnI assay kits range from 4% to 14% [62, 63].
Even recently, the “high-sensitivity” or “fourth genera-
tion” cTnT (but not the cTnI) assays have shown cross-
reactivity in patients with diseased skeletal muscle [64].
Both cTnI and cTnT have shown utility in detecting
early myocardial infarction [65, 66]. In addition, sTnI has
also become a useful marker of skeletal muscle damage in
orthopedic and soft tissue injuries [67]. In research
comparing levels of sTnI and cTnI in patients with
skeletal muscle damage secondary to trauma or intense
exercise, but no known cardiac injury, the results
consistently show elevated sTnI (8 to 17 ng/mL) with
normal cTnI (<1 ng/mL) [67–70]. Thus, both assays are
useful and specific for the detection of cardiac or skeletal
injury. However, it is an important distinction if the
elevated TnI is skeletal or cardiac in origin, because a
patient with blunt chest trauma, combined cardiac and
skeletal injury, or a multitrauma patient with many in-
juries, may have elevations of both.
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The research on this is imperfect due to poor confir-
mation of BCI in patients with an elevated cTnI level.
Some research will consider a patient to have a BCI based
on electrocardiographic (ECG) changes alone, with or
without elevated cTnI. Some research will only classify a
patient as having a cardiac injury if abnormalities are
seen on ECHO. And finally, most reports have not clari-
fied the level of cTnI considered as a positive result
(>0.4 ng/mL or 1 ng/mL). Looking at the evidence from
6 research reports that addressed this topic, where car-
diac injury was confirmed by ECHO, the results were
consistently the same. Approximately half of the patients
with a positive cTnI actually did have a cardiac injury by
ECHO [71–76]. Pooling the data, 213 patients had signif-
icant blunt chest trauma and positive serum cTnI, and
only 105 had a documented cardiac injury by ECHO
(49%) [71–76].
Further research will need to determine what level
of cTnI should be considered positive. Only 2 reports
have provided that data. Using a cutoff level of 1 ng/mL,
60% to 70% of patients with a serum cTnI level exceeding
1 ng/mL after blunt chest trauma actually had a docu-
mented cardiac injury [74, 75]. Thus, based on the data
that have been published, a cTnI level exceeding 1 ng/mL
is a “significant” finding and the individual should be
further evaluated with ECHO and close monitoring
[74, 75]. Levels between 0.4 and 1 ng/mL are likely
indicative of minor myocardial injury that will not be
appreciated by ECHO in half of the patients and have
little clinical sequelae [71–75].
These studies also provided the answer to the inter-
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esting question of what percentage of patients with a
completely normal cTnI actually did have a visible IMH
or cardiac injury by ECHO? The answer is 2 of 296, or
0.6% [71–76]. Thus, patients with a suspicion of BCI with a
normal cTnI (<0.4 ng/mL) 4 to 6 hours after injury can
be safely considered to not have BCI [77].
Electrical Disturbances
Atrial and Conduction Dysrhythmias
Sinus tachycardia is the most common ECG abnormality
among trauma victims. Results from large case series
suggest that ECG abnormalities, other than sinus tachy-
cardia, are present in 1% to 6% of patients after chest
trauma, and atrial fibrillation (AF) is the most common
[78, 79]. One series reported that 9 of 240 patients (4%)
with chest trauma showed AF on their initial ECG [80].
However, it is important to realize that the AF may not
be due necessarily to direct cardiac injury, because the
incidence of AF after chest trauma is the same as for
head and abdominal trauma [79]. Patients with rapid AF
and hemodynamic compromise should be cardioverted.
Asymptomatic hemodynamically stable patients may
benefit from a rate-control strategy using b-blockers or
calcium channel blockers with consideration of delayed
elective electrical cardioversion [81].
Paroxysmal supraventricular tachycardia after BCI
is rare but has been reported [9]. Because paroxysmal
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supraventricular tachycardia can lead to rapid
hemodynamic compromise, especially after trauma, it
is important to rapidly terminate this dysrhythmia
by administering adenosine, b-blockers, or electrical
cardioversion [81].
More common and more difficult to interpret are tran-
sient premature ventricular contractions and BBBs that
appear after traumatic blunt injury. A classic medical
teaching has been that BCI produces a right BBB. This
certainly does occur and has been reported [55, 80, 82];
however, a right BBB, even when persistent, ultimately
has almost no long-term sequelae and does not affect
a patient’s functional outcome [81]. Thus, most ECG
abnormalities after BCI tend to be transient, intermittent,
evolving, and clinically irrelevant [71–77].
Ventricular Dysrhythmias
Ventricular dysrhythmias after chest trauma are less
common than atrial and conduction disturbances but
are much more lethal and were likely present in most of
the individuals who died at the scene. Because these
trauma victims never arrive in the trauma bay, the true
incidence of ventricular dysrhythmias is impossible to
determine. These dysrhythmias can lead to rapid deteri-
oration, so early and complete evaluation with ECHO is
warranted [81].
Initial ECG and Clinical Significance
When the Eastern Association for the Surgery of Trauma
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(EAST) published its practice guidelines for the man-
agement of BCIs in 2012, the only recommendation
that was supported by Level 1 Evidence was to obtain
an admission ECG on all patients in whom BCI was
suspected [83]. This is mostly because Level 1 Evidence is
hard to find on this topic. They also recommended (Level
2 Evidence) that if the admission ECG does show a new
abnormality, that the patient should be admitted for
continuous monitoring [83]. These recommendations
were based on 5 published studies [71, 72, 84–86];
however, many more publications have addressed the
issue of ECG in diagnosing BCI [71–77, 84–87]. One
report suggested that ECG alone can be used to rule
out a BCI [85]. Most studies, however, do not conclude
that ECG by itself can make that determination. [71–76,
84, 86, 87] because a significant number of patients who
have a normal admission ECG will be found to later
(within 24 hours) have a clinically significant cardiac
injury [71, 72, 84]. Depending upon the severity of
injury, this number may be as high as 41%, although
these data were determined by using serum cTnT and
not cTnI [83, 84]. Regardless, based on most of the
information, most experts agree that ECG alone is not
sufficient to exclude a BCI. However, the combination of
a normal ECG and a normal cTnI (<0.4 ng/mL) almost
completely excludes a clinically significant BCI, with
negative predictive values ranging from 98% to 100%
[71–77]. Thus, patients with a suspicion of cardiac injury
with a normal (<0.4 ng/mL) serum cTnI and a normal
Ann Thorac Surg
2014;98:1134–40
ECG may be safely discharged home from the emergency
department.
Late Complications After Cardiac Trauma
Most patients recover from blunt cardiac trauma without
any long-term sequelae [74]. However, a few patients with
rare and bizarre late complications have been reported,
including the late onset of complete atrioventricular
block, delayed cardiac rupture, heart failure, coronary-
to-pulmonary artery fistula, pericardial effusion, coro-
nary artery occlusion, and constrictive pericarditis [88–94].
One study that reevaluated patients with BCI 12 months
after injury with 24-hour Holter monitoring and nuclear
flow studies found that 33% had cardiac abnormalities
that had persisted since the injury [95]. For this reason, it is
recommended that any patient who sustains documented
cardiac trauma be reevaluated within 3 to 6 months of
injury, particularly if there are any symptoms of heart
failure [32, 94, 95].
Conclusions
The following Levels of Evidence are based on the Uni-
versity of Oxford Centre for Evidence Based Medicine
published guidelines [96].
1. Obtain an initial ECG on all patients in whom BCI is
suspected. Level of Evidence: 1b.
2. If the admission ECG does show a new abnormality,
the patient should be admitted for continuous moni-
toring. Level of Evidence: 2b.
3. The combination of a fall greater than 20 feet
and a sternal fracture should prompt a thorough
cardiac evaluation because the incidence of cardiac
injury in these patients is very high. Level of Evi-
dence: 2b.
4. Even a large IMH should be treated conservatively
because most will resolve over time, and usually within
3 months (see number 7). Level of Evidence: 2b.
5. After blunt chest trauma, a serum cTnI level
exceeding 1 ng/mL is abnormal and is associated with
a true cardiac injury in 60% to 70% of the patients.
These patients will require a formal ECHO and close
monitoring. Level of Evidence: 2b.
6. Patients with a suspicion of cardiac injury with a
normal (<0.4 ng/mL) serum cTnI and a normal ECG
may be safely discharged home from the emergency
department. Level of Evidence: 2b.
7. An interatrial septal hematoma and/or a traumatic
tricuspid valve injury can both produce complete
heart block, and these patients require close moni-
toring and insertion of a transvenous pacemaker if
heart block develops. Level of Evidence: 4.
8. Small tears at the venous-atrial confluence may be
contained and the patient initially stable. Diagnosis
by ECHO should prompt rapid surgical consultation
because continued or late bleeding is likely. Level of
Evidence: 4.
Ann Thorac Surg
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