Background/Epidemiology
Participation in athletics and recreational exercise is increasing across all age groups and genders, with the largest increase in activity seen in the elderly age group.
These active individuals are presenting to the emergency department (ED) with cardiac concerns related to exercise and with cardiac conditions that occur during athletic activity.
Unfortunately, often the initial presentation of an underlying cardiac problem is sudden cardiac death (SCD).
However, in some cases there may be prodromal symptoms for which the athlete seeks care in the ED such as chest pain, dyspnea, dizziness, palpitations, near syncope or syncope, or a history of heart disease in young family members.
For these reasons, the emergency physician should be familiar with basic concepts of sports cardiology as well as both the urgent and emergent management of these conditions.
Cardiac screening of athletes for potentially catastrophic cardiac conditions has generated much debate. To date, several protocols have been proposed but no universally accepted consensus has been reached.
Most of these protocols differ on recommendations for cardiac testing. They have several key features in common and all recommend:
Attention should be given to personal and family history, with particular focus on cardiac and pulmonary conditions.
This also features a focused review of symptoms, with particular attention given to symptoms that develop during activity.
A complete physical exam should be performed, again focusing on cardiac and pulmonary exams.
It is advised to assess the cardiac and pulmonary portions of the exam in multiple positions (supine and standing) to try to elicit murmurs and arrhythmias.
The most widely known position statements follow, with key recommendations regarding cardiac screening:
American Heart Association1
Individualized testing should be performed based on concerning findings.
EKG, echocardiography and stress testing are optional in asymptomatic athletes less than 40 years of age.
A minimum of an EKG should be performed in the asymptomatic athlete more than 40 years of age, particularly when the individual is starting a new exercise program.
European Society of Cardiology
EKGs are recommended for all athletes regardless of age and symptomatology.
Further testing (echocardiogram, stress testing, MRI, catheterization) is recommended for all athletes with any abnormal finding on physical exam or EKG. The type of testing is based on the initial abnormality detected.
National Collegiate Athletic Association (NCAA)2
There is no recommendation regarding which physician should perform the athletic screening evaluation. University-affiliated physicians perform 85 percent of these evaluations; 15 percent of exams are performed by a physician of the athlete’s choice.
Repeat cardiovascular screening and examination is required every two years regardless of whether the athlete has been asymptomatic during this time period.
Despite the NCAA Sports Medicine Handbook guidelines, a recent study found that only 21 of 257 NCAA schools met American Heart Association cardiovascular screening recommendations.3
International Olympic Committee4
EKGs are required on all athletes.
Further testing (echocardiogram, stress testing, MRI, catheterization) is recommended for all athletes with any abnormal finding on physical exam or EKG. The type of testing is based on the initial abnormality detected.
Research is currently being conducted to determine if a greater focus on family history of SCD at less than 35 years of age (compared to the currently recommended screening for family death at less than 50 years of age) may increase sensitivity of screening5 in all of the earlier-mentioned protocols.
Anatomical Considerations/Pathophysiology
Given that the heart is composed of striated muscle, it stands to reason that a series of morphologic and physiologic changes may result from regular athletic activity, just as is seen in skeletal muscle.
Several morphologic changes in the heart, particularly in the ventricles, have been linked to regular athletic activity.
Increased left ventricle cavity dimension (i.e., increased volume).
Increased left ventricle wall thickness.
The combination of these two changes typically results in increased cardiac mass.
The changes seen in the heart are a result of the type of athletic activity preferred by the individual.
Isometric activities (such as long distance running and swimming) will increase the fiber length without changing the amount of tension across fibers, thus increasing the ventricular dimension → increased preload.
Isotonic activities (such as weight lifting and other power exercises) usually increase the tension across the muscle fibers without changing fiber length, thus increasing the ventricular wall thickness→ increased afterload.
Pure examples of isolated isometric or isotonic activities are rare; most athletic activities result in a combination of these changes.
Genetics also play a role in the extent of changes seen in an individual.
Male athletes typically have greater amounts of cardiac remodeling than female athletes in the same sport, but female athletes also experience these exercise-related cardiac changes.
Female athletes of African/Caribbean ethnicity tend to have greater amounts of cardiac changes than their Caucasian counterparts in the same sports.6
The morphological adaptations seen from regular activity typically result in a slight increase in VO2 max, which may improve performance slightly, particular in more endurance-based events.
Structural changes that result from regular athletic activity tend to resolve during periods of decreased training or deconditioning.
The key clinical challenge is to determine pathologic vs. physiologic adaptations in athletes presenting to the ED.
EKG guidelines are available to help the clinician distinguish exercise-related cardiac conditions from potentially pathologic cardiac conditions.
EXERCISE-ASSOCIATED EKG CHANGES7
The previously discussed morphologic changes in the heart may result in EKG changes; the emergency physician should be aware of the resultant changes and consider the possibility of athlete’s heart when evaluating active patients.
The extent of EKG changes seen is dependent on gender, genetics, and specific sport; an athlete’s underlying medical conditions may also contribute to the EKG changes seen.
A total of 90 percent of athletes have some degree of bradycardia; the degree of bradycardia seen is sport specific.
A heart rate less than 60 is considered bradycardic.
A portion of the bradycardia is likely due to increased vagal tone.
Athletes with heart rates of 45–60 are typically asymptomatic.
If the athlete is asymptomatic and has no other EKG findings, no further workup is required.
A heart rate of less than 30 should not be attributed solely to athletic training and warrants further evaluation for pathologic etiology.
Conduction delays
As many as one-third of athletes have a conduction delay on EKG.
First-degree AV block is most common and is seen in 35 percent of athletes.
This finding is seen in athletes participating in both endurance and power sports.
A first-degree AV block is considered a benign finding; athletes with this finding do not require further evaluation.
Second-degree heart block is characterized by a conduction delay resulting in the heart skipping (dropping) a beat.
The Mobitz type 1 conduction delay is characterized by a gradual increase in the PR interval until a beat is dropped.
The Mobitz type 1 block is a common sequela of regular athletic activity; the exact mechanism for the development of this condition remains unclear.
Up to 10 percent of athletes have a Mobitz type 1 block on routine EKG testing.
Athletes with a Mobitz type 1 block are usually asymptomatic; the change in conduction is typically found on routine EKG testing.
If the athlete is asymptomatic, no further evaluation is required. If the athlete is symptomatic, admission is necessary for further testing, including standard cardiac biomarkers and electrophysiologic evaluation.
Early repolarization (J-point elevation)
J-point elevation is defined as a positive notching of the ST segment as it comes off the QRS complex or an upward sloping of the terminal portion of the QRS complex.
There are three components:8
J wave
ST elevation (often originating from the J wave).
QRS blurring.
The location of the J-point elevation is indicative of the risks associated with the condition.
J-point elevation in the lateral precordial leads is typically seen in the athletic patient.
J-point elevation in these leads is considered benign.
J-point elevation may be seen in up to 58 percent of athletes; higher rates are typically seen in endurance athletes.9
Further evaluation is not currently recommended in asymptomatic athletes with J-point elevation isolated to the lateral precordial leads.9
Increased p-wave amplitude and notched p waves are associated with regular athletic training.
Incomplete right bundle branch block (iRBBB) is characterized by a wide QRS and is associated with athletic activity.
These findings are believed to result from the increased atrial dimensions that result from the increased preload associated with regular athletic activity, particularly endurance exercise.
Up to 50 percent of athletes may have an incomplete RBBB.
Endurance athletes are more likely to be affected than power athletes.
Incomplete RBBB is significantly more common in males than in females.
Incomplete and complete RBBB may be seen in patients with atrial septal defects (ASD); attention should be paid to the cardiac exam to rule out murmurs associated with ASD.
Asymptomatic athletes with incomplete RBBB may be discharged with cardiology follow-up.
Any athlete that is symptomatic with an incomplete RBBB should be admitted for continuous cardiac monitoring, routine lab testing, and electrocardiology testing.
Premature atrial complexes (PACs) and premature ventricular contractions (PVCs) are common in athletes, particularly endurance athletes.
Athletes with frequent PACs or PVCs may be asymptomatic, or may present with palpitations, lightheadedness, or near syncope.
Asymptomatic athletes with PACs require no further evaluation.
Symptomatic athletes should have continuous cardiac monitoring, routine blood testing (including cardiac biomarkers), and an echocardiogram. Electrophysiology evaluation should also be considered.
CONCERNING EKG CHANGES10
Abnormal EKG changes as shown in Table 12.1 should not be attributed to regular athletic activity.
When present they should prompt further investigation.
Table 12.1 Comparison of Normal and Abnormal ECG Findings in Athletes
| Normal ECG Findings | Abnormal ECG Findings |
|---|---|
| Sinus bradycardia > 30 bpm | Profound sinus bradycardia < 30 bpm or with sinus pauses > 3 seconds |
| Sinus arrhythmia | Atrial tachyarrhythmias |
| Ectopic atrial rhythms | Premature ventricle contractions > 2 per 10-s tracing |
| Junctional escape rhythms | Ventricular arrhythmias |
| First-degree AV block | Ventricular pre-excitation with PR < 120 ms with delta wave and wide QRS > 120 ms |
| Mobitz type I second-degree AV block (Wenckebach) | Mobitz type II and complete heart block |
| Incomplete right bundle branch block | Right ventricular hypertrophy |
| Early repolarization (J-point elevation) | T-wave inversions (excludes III, aVR, V1) |
| Convex ST-segment elevation with T-wave inversions in V1-V4 in black/African males | Brugada EKG pattern |
| Isolated QRS voltage for left ventricular hypertrophy | Left axis deviation |
| Left atrial enlargement | |
| Complete left bundle branch block | |
| Pathologic Q waves | |
| ST-segment depression | |
| Long QTc (> 470 ms in males; > 480 ms in females) | |
| Short QTc (< 320 ms) | |
| Intraventricular conduction delay (QRS > 140 ms) |
bpm = beats per minute
AV = atrioventricular
ms = milliseconds
Focused History and Physical Exam
The emergency physician should rely on structured historical questions, directed family history questions, and a focused physical exam to better evaluate athletes presenting with cardiac-related concerns.
Regardless of cardiac screening recommendations, most agree that a history and physical exam screening for cardiac abnormalities in athletes should include:
Special attention given to personal and family history, with particular focus on cardiac and pulmonary conditions.
A focused review of symptoms, with particular attention given to symptoms that develop during activity.
A complete physical exam should be performed, again focusing on cardiac and pulmonary exams.
It is advised to assess the cardiac and pulmonary portions of the exam in multiple positions (e.g., supine and standing, Valsalva) to try to elicit murmurs and palpitations.
It is also important to assess symmetry of radial and femoral pulses on both the right and left sides of the body.
It is also important to discuss and consider use of (PES) in athletes presenting to the ED with athletic-associated cardiac concerns that seem age inappropriate, particularly those presenting with tachycardia, elevated blood pressure, and/or elevated temperature.
PES use is not limited to elite athletes. Multiple studies have documented the use of PES across all demographics.
Anabolic steroid use increases total cholesterol, LDL, HDL, VLDL, and triglycerides; use of these substances may lead to premature coronary artery disease in athletes.
Stimulants (caffeine, ephedrine, pseudoephedrine) are also considered PES, although caffeine in low to moderate doses is no longer banned by sports governing bodies.
Stimulant use may increase heart rate and blood pressure more than expected from regular exercise.
Stimulant use may increase an athlete’s risk for heat injury, further stressing cardiac function.
Caffeine (200 mg, or the amount in two 8-oz cups of coffee) has been shown to decrease myocardial blood flow,12 with further decreases in myocardial blood flow seen in altitude-simulated conditions.
ED EVALUATION BASICS
All athletes who present to the ED with chest pain should have an EKG and CXR performed.
It is very important to differentiate between EKG changes related to sports and exercise vs. pathologic changes.
Please see Table 12.1 and discussion in previous section.
Depending on clinical circumstances and initial diagnostic evaluation, further evaluation with cardiac biomarkers may be considered.
CK, CK MB, and troponin may all increase following prolonged athletic activity.
The patient’s creatinine level should be considered when evaluating cardiac biomarkers, as dehydration/mild rhabdomyolysis may negatively impact kidney function, thus limiting the kidney’s ability to clear cardiac biomarkers.
Cardiac biomarkers may rise to a level considered positive in a nonactive patient.13, 14, 15 The clinical challenge is to determine reactive versus pathologic elevation in these biomarkers.
Biomarker levels typically return to baseline forty-eight to seventy-two hours post event.
The amount of biomarker elevation may be related to training intensity, with those running less than 35 miles/week more likely to have significantly increased levels relative to the athlete running more than 45 miles/week.15
Female athletes are also likely to have elevated biomarkers after athletic activity,16 however the increase is typically not as significant as in active males in the same sport.
Teenagers have also been found to spill markers after a 90-minute run.17 Age of less than 20 alone is not enough to rule out true cardiac etiology in athletes presenting with exercise-associated cardiac concerns.
Research is currently underway to determine if gender-specific cardiac biomarkers may also help better evaluate active patients with cardiac concerns.
Basic ACLS protocols and guidelines should be followed for all patients whose initial presentation is SCD.18
Symptomatic athletes should be admitted for continuous cardiac monitoring and additional evaluation.
Asymptomatic athletes with incidental, benign EKG changes may safely be discharged from the ED with close follow-up, either with a PCP, a sports medicine specialist, or a cardiologist.
Depending on clinical scenario and risk factors, consider holding athlete from further sports participation until further evaluated as an outpatient by cardiology.
Differential Diagnosis – Structural and Inherited Arrhythmia Disorders
Sudden Cardiac Death
General Description
The incidence of SCD is increasing in both the general and athletic population.
The shocking nature of sports-related SCD is drawing increasing attention to these events by the popular press.
Approximately 300,000 SCDs/year occur in the general population.
A total of 3/1000 high school athletes per year suffer a SCD.1
Four cardiac related deaths/year occur among NCAA athletes.19
One in 184,000 marathoners experiences sudden cardiac arrest during a race.20
These numbers are likely an underestimation of the true incidence of sudden cardiac arrest among runners. Given the nature and layout of most road races, it is difficult to record the actual number of runners presenting to surrounding EDs, as runners may present to a variety of hospitals in the vicinity of a race.
A recent study has shown that individuals of African or Caribbean descent are much more likely to suffer an exercise-related sudden cardiac event than those of other ethnic backgrounds.21
Males are much more frequently affected by SCD during exercise than are females; the ratio is 9:1.1
Although both the general population and the active population suffer SCD, the risk factors for a cardiac event differ between the two groups (Table 12.2).
Table 12.2 Risk of Sudden Cardiac Death in the General vs. the Athletic Population
| Risk Factor | General Population | Athletic Population |
|---|---|---|
| Coronary artery disease | 80% | 2.5% |
| Hypertrophic cardiomyopathy | 5% | 80% |
| Coronary artery anomalies | 14% | |
| Mitral valve prolapse | 5% | |
| Acquired valve disease | 5% | 2.5% |
Mechanism
The mechanism of SCD during exercise is unknown.
Several theories about the etiology of sudden cardiac arrest have been proposed.
Various arrhythmias, including atrial fibrillation, ventricular fibrillation, and atrial fibrillation triggering ventricular fibrillation, have been linked to SCD in athletes. The trigger for these arrhythmias also remains the focus of current research.
Inadequate cardiac output has also been considered a trigger of SCD in athletes; it is not clear if this reduced output is a result of structural changes, genetic characteristics, or increased heart rate associated with exercise.
Current leading theory is that the true etiology of SCD during athletic activity is likely a combination of inadequate cardiac output and an arrhythmia.
Presentation
Patient may be in fulminant cardiac arrest on presentation to the ED or may have been resuscitated in the field by bystanders and/or emergency medical system (EMS) providers.
The most common presenting arrhythmia is ventricular fibrillation.
Patients may present with tachyarrhythmias, bradyarrhythmias or asystole.
Physical Exam
An exam appropriate to the clinical presentation should be performed. However, patients in cardiac arrest will not have pulses and will not be breathing spontaneously.
Essential Diagnostics
As appropriate to the urgency of the clinical situation.
If patient is stable, essential workup includes:
IV, O2, monitor
EKG, CXR
Laboratory evaluation, including CBC, CMP, and cardiac biomarkers.
Disposition
Admit all to the intensive care unit.
Emergent cardiology consult.
Return to sports will be determined by the etiology of the cardiac arrest, in consultation with a cardiologist.
Pearls and Pitfalls
Treat all cardiac arrest patients per current ACLS guidelines.
Current 2010 guidelines emphasize high-quality CPR and rapid defibrillation.18
Inherited Arrhythmia Disorders
Sport-Related Syncope
General Description
Sudden collapse that occurs either during or immediately after a period of exercise.
Exercise does not have to be particularly intense.
Collapse during activity is more likely to have underlying cardiac etiology than collapse immediately after exercise; this is often referred to as exercise-associated collapse (EAC) or heat syncope.
EAC is commonly the result of fatigue, mild dehydration, or orthostasis; however sport-related syncope should also be considered to rule out any underlying cardiac abnormalities.
Mechanism
Several possible mechanisms for sport-related syncope have been considered, but no definitive causative theory has been proven.
Orthostatic hypotension
Electrolyte abnormality
Structural cardiac abnormality.
Cardiac dysrhythmia
Presentation
Athletes experiencing a sport-related syncopal episode often present to the ED after prehospital care has been provided. Event physicians caring for these patients may arrive on scene when the patient is still in an altered state of consciousness.
If the collapse occurred after the athletic event it may be beneficial to keep the athlete supine and elevate the legs by flexing the hips and holding the feet in the air.
Physical Examination
The initial physical exam should ensure that no concurrent trauma was sustained during the sport-associated syncopal event. If there is any concern for a cervical spine injury or head injury, basic immobilization should be instituted.
Initial physical exam should include vital signs, blood glucose, and EKG/cardiac monitoring.
A thorough cardiopulmonary examination should be performed, with attention focused on cardiac murmurs and arrhythmias.
Essential Diagnostics
A formal EKG should be performed.
A chest x-ray may help be beneficial to evaluate for cardiomegaly or pulmonary edema.
Continuous cardiac monitoring should be performed.
Standard laboratory testing should include cardiac markers, electrolytes, and CBC. Additional tests to consider include D-dimer and thyroid studies.
If associated trauma is suspected appropriate imaging studies should be performed.
ED Treatment
Patients with exercise-associated syncope or collapse should remain on continuous cardiac monitoring while initial diagnostic studies are completed.
If an underlying cause of the syncope is identified (e.g., dehydration, electrolyte abnormality) this abnormality should be treated appropriately.
Cardiology consultation should be considered in all patients with exercise-associated syncope in whom no identifiable cause is identified.
Disposition
If no identifiable cause of the exercise-associated syncopal event is identified the patient should be admitted to cardiology to continue the evaluation.
If a noncardiac cause of the syncopal event is identified and corrected in the ED the patient may be discharged home with PCP or sports medicine follow-up. The patient should not return to athletic activity until cleared by the PCP or sports medicine physician.
If a cardiac cause of the syncopal event is identified the patient should be admitted to cardiology to continue the evaluation.
If no cause of the syncopal event is identified the patient should be admitted to cardiology to continue the evaluation.
Pediatric Considerations
Pediatric patients suffering a syncopal event during a sporting event should be admitted for further evaluation.
Pearls and Pitfalls
It is important to differentiate between whether syncope occurred during or after exercise.
Syncope that occurs during exercise is always concerning and needs further evaluation.
Causes of sports-related syncope vary from benign to life threatening, thus a high degree of suspicion should be maintained at all times.
Wolff Parkinson White syndrome (WPW)
General Description
WPW is a pre-excitation condition triggered by the presence of an accessory conduction pathway between the atria and ventricles.
The rate of WPW among athletes is similar to that of the general population, with 1 in 1000 people afflicted with this condition.11
Mechanism
The trigger(s) that leads to the development of the accessory pathway remains to be determined in both the active and in the general population.
The presence of the accessory pathway may lead to tachyarrhythmias such as supraventricular tachycardia and atrial fibrillation.
However, atrial fibrillation triggered by WPW often leads to ventricular fibrillation during exercise likely due to the further decrease in blood flow.
Presentation
Patients with WPW typically present to the ED with a tachydysrhythmia, near syncope, syncope, palpitations, or sudden cardiac arrest (particularly during exercise).
Physical Examination
Vital signs should be performed as soon as the patient arrives in the ED.
A thorough cardiovascular examination should be performed.
Essential Diagnostics
An EKG should be performed as soon as the patient arrives at the ED.
Several EKG findings are characteristic of WPW including:
Short PR interval
Widening of the QRS complex.
Presence of a delta wave
Routine lab testing, including cardiac markers, should be performed.
Thyroid studies should be considered.
Chest x-ray (PA and lateral) should be performed.
ED Management
If an athlete sustains a tachydysrhythmia or sudden cardiac arrest due to presumed WPW, standard ACLS resuscitation protocols should be followed.18
If circulation returns, the affected athlete should be admitted for further cardiac monitoring and evaluation, specifically electrophysiologic evaluation.
If an athlete presents to the ED with sport-related syncope, ED management is as previously described.
Disposition
All patients diagnosed with WPW in the ED should be admitted for further evaluation and testing, particularly electrophysiologic evaluation.
Cardiology should be consulted while the patient is in the ED.
Athletes found to have WPW (without associated tachydysrhythmia) on routine screening may be referred for outpatient electrophysiologic evaluation as long as the athlete remains asymptomatic.
Pediatric Considerations
WPW has been diagnosed in teenage athletes and should be considered in this patient population.
Pearls and Pitfalls
All EKGs performed in the ED should be evaluated for presence of an accessory pathway.
If an accessory pathway is suspected, the athlete needs evaluation by cardiology prior to return to sport even if asymptomatic.
All symptomatic athletes should not be allowed back to sports and need further evaluation by cardiology.
Catecholaminergic Polymorphic Ventricular Tachycardia
General Description
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a ventricular arrhythmia due to abnormalities in cardiac metabolism of calcium.
This genetically transmitted condition typically results in ventricular tachycardia (and occasionally ventricular fibrillation) and is typically triggered by exercise.
Mechanism
Significant research is being conducted to isolate the specific abnormality in calcium metabolism.
Several genetic mutations have been identified that likely contribute to this condition.
Presentation
Individuals suffering from CPVT often present to the ED after an sport-related syncopal event.
These patients may be in polymorphic ventricular tachycardia or may be in ventricular fibrillation.
Like the other channelopathies, the initial presenting symptom of CPVT may be SCD.
Physical Examination
A focused cardiopulmonary examination should be performed.
Essential Diagnostics
The patient with suspected CPVT should be immediately placed on a continuous cardiac monitor with pulse oximetry and blood pressure monitoring capacity.
A formal EKG should be performed.
The baseline EKG of patients with CPVT is typically normal (with the exception of mild bradycardia).
Patients with CPVT presenting in PVT will have the typical findings of polymorphic ventricular tachycardia.
There are no specific EKG findings unique to CPVT.
Bedside echocardiography should be considered to evaluate for other potential causes of the presenting dysrhythmia.
Routine laboratory testing should include cardiac markers, electrolytes, CBC, and thyroid studies. Additional testing may include a D-dimer.
Chest x-ray (PA and lateral) should also be performed to rule out other potential causes of the dysrhythmia.
ED Treatment
Any patient with suspected CPVT that presents with sudden cardiac arrest should have basic resuscitative measures continued until such efforts are deemed futile by the treating physician.
CPVT patients presenting with stable ventricular tachycardia should have the essential diagnostic procedures performed to attempt to elucidate the cause of the episode.
Once the essential diagnostic studies are complete, these patients should receive IV hydration during the initial evaluation process.
Possible CPVT patients with unstable ventricular tachycardia or ventricular fibrillation should be cardioverted as per ACLS protocols.
Disposition
All patients with suspected CPVT should be admitted to continue the evaluation.
Cardiology should be consulted for all suspected cases of CPVT.
Exercise testing is typically performed to try to trigger an episode of CPVT.
Cardiology will determine when (and if) a patient is able to return to sports.
If cardiology determines that CPVT is the diagnosis, patients may be started on calcium channel blockers or beta blockers. Some patients ultimately require pacemaker/defibrillator placement.
Pediatric Considerations
The diagnosis of CPVT should be considered in children with a family history of presenting with sport-related syncope or SCD.
Pearls and Pitfalls
A high degree of suspicion should be maintained for any symptomatic athletes.
Athletes should always be counseled against further sports participation when there is concern for CPVT or another cardiac abnormality.
Symptomatic athletes and/or athletes with abnormalities on their EKGs need either admission for further workup or close outpatient follow-up with cardiology.
Brugada Syndrome
General Description
This syndrome is a sodium channelopathy known for its characteristic EKG changes and often leads to ventricular dysrhythmias and SCD.
The condition is inherited via an autosomal-dominant transmission.
Males are much more commonly affected than females.
Young patients are much more commonly affected than those over 50.
Mechanism
Many theories exist regarding the mechanism of Brugada syndrome, with the leading theory that the condition is an autosomal-dominant inherited sodium channelopathy.
Arrhythmias may also occur due to an imbalance in sympathetic and parasympathetic tone.
Presentation
Patients with Brugada syndrome typically present with SCD.
Patients may also present after a syncopal episode.
Up to 20 percent of patients with Brugada syndrome may be asymptomatic.
Physical Examination
A focused cardiopulmonary examination should be performed.
The physical examination, however, is usually unremarkable.
Essential Diagnostics
The patient with suspected Brugada syndrome should be placed on continuous cardiac monitoring, including blood pressure and pulse oximetry.
An EKG should be performed immediately.
Characteristic EKG changes are often but not always present and include:
Pseudo–RBBB
ST/T-wave changes in V1-V3.
Basic laboratory studies include cardiac markers, basic electrolytes, point of care glucose testing, and a D-dimer (based on clinical suspicion for pulmonary embolism).
Chest x-ray (PA and lateral) should be performed to detect other possible causes of the presentation.
An echocardiogram should be performed to evaluate for other potential causes of the presentation.
ED Treatment
Patients presenting in sudden cardiac arrest should have ACLS resuscitative protocols18 followed until the treating physician determines the effort to be futile.
Patients with syncopal episodes associated with Brugada syndrome or those successfully resuscitated should have cardiac pacing (preferably transvenous) until a permanent pacemaker/defibrillator can be placed.
Disposition
All patients with suspected Brugada syndrome (previously undiagnosed) should have emergent cardiology consultation and be admitted to cardiology (preferably the cardiac care unit) to facilitate further evaluation and management.
Decisions regarding return to activities is to be made by cardiology.
These patients are not typically allowed to return to sports.
Pediatric Considerations
The diagnosis of Brugada syndrome should be considered in children, particularly males, with a family history of presenting with sport-related syncope or SCD.
Pearls and Pitfalls
Most often patients are not diagnosed with this condition until they are symptomatic and present with syncope or sudden cardiac arrest.
All family members of patients suspected of having this condition should be notified and screened.
Treatment is placement of an implantable defibrillator to prevent sudden cardiac arrest from ventricular arrhythmia.
Commotio Cordis
General Description
Sudden cardiac arrest triggered by direct, blunt chest wall trauma.
Multiple sports have had deaths related to commotio cordis, including baseball, lacrosse, and the martial arts.
Protective gear (i.e., chest protectors for baseball) has not been shown to reduce the incidence of commotio cordis.
Mechanism
Forces are transmitted directly from the chest wall to the precordium, altering the normal electrical conduction of the heart.
EKG studies have demonstrated that the transmission of forces generates an R wave prior to completion of the previously initiated T wave (R on T phenomenon) resulting in ventricular fibrillation.
Chest wall impact 30–15 milliseconds before T-wave peak is most likely to generate ventricular tachycardia.22
Chest wall impact at 40 mph is most likely to generate ventricular tachycardia.23
Presentation
If a patient is successfully resuscitated in the field, presentation to the ED will be as a standard post-arrest patient.
There may be obvious signs of chest wall trauma resulting from the blunt force that triggered commotio cordis.
Physical Examination
The treating physician should carefully examine the chest wall for signs of trauma (rib fracture, sternal fracture, contusion) in addition to the commotio cordis.
A thorough cardiopulmonary examination should be performed.
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