Arrhythmias and Sudden Cardiac Arrest in Athletes

Upper to lower extremity ratio
<0.85
Wing span: height ration > 1.05
Thumb-index finger overlap around wrist
Scoliosis >200
Hind foot collapseHypermobile joints
High palate
Marfan facies
Minor to moderate pectus excavatum
OcularLens dislocationFlat cornea
MyopiaCardiovascularAscending aorta dilation
Ascending aorta dissectionDescending aortic dissection or dilation
Mitral valve calcification
MVP
Pulmonary artery dilation
PulmonaryNoneBlebs (typically apical)
Spontaneous pneumothoraxSkinDural ectasia (lumbosacral)Recurrent hernia
Striae


Abstracted from Sonh GH et al.27




Treatment




  • ED treatment should be tailored to the patient’s presentation.



  • The emergency physician should focus on blood pressure control in patients with aortic root dilation or aortic dissection.



Disposition




  • Previously undiagnosed but asymptomatic Marfan’s patients should be urgently evaluated as an outpatient. If this rapid outpatient evaluation cannot be arranged the patient should be admitted. Symptomatic patients should be admitted for evaluation.



  • Patients with aortic root or aortic pathology should be emergently evaluated by both cardiology and cardiovascular surgery.



  • Athletes need close monitoring but may perform low-level activities depending on amount of aortic root dilation or mitral regurgitation and family history.25



  • The decision regarding return to sports should be made by cardiology.



Complications




  • Aortic root and descending aorta dilatation may lead to aortic dissection and rupture.




    • May also cause left ventricular dysfunction and mitral valve prolapse.



Pediatric Considerations




  • Pediatric patients may display several of the characteristic findings of Marfan syndrome. Presence of these sequelae should prompt the emergency physician to inquire about family history and to initiate the evaluation regardless of whether the patient is symptomatic.



Pearls and Pitfalls




  • Patients without a known family history of Marfan syndrome may not be aware of the diagnosis. Physicians should initiate the evaluation for the syndrome if the physical features are present.




Mitral Valve Prolapse



General Description and Mechanism




  • Mitral valve prolapse (MVP) is the incomplete closure of the mitral valve typically due to structural abnormalities (congenital or acquired).




    • This incomplete closure of the valve may result in the valve intruding into the atrium during cardiac contraction.



  • Despite this abnormal valvular motion, the majority of patients with MVP are asymptomatic.



  • There is a low rate of adverse cardiac events with MVP.



  • Approximately 5 percent of the population has MVP.



  • Women are more likely than men to have MVP.



Presentation




  • The majority of patients with MVP are asymptomatic.



  • Patients may become symptomatic due to autonomic difficulties or natural progression of the abnormal anatomy.



  • Patients with autonomic-associated symptoms may present with:




    • Palpitations



    • Anxiety



    • Excess fatigue



    • Syncope/near syncope



  • Patients with natural progression of underlying abnormal anatomy may present with typical symptoms of heart failure.



Physical Examination




  • Particular focus should be given to the cardiac examination.



  • The hallmark finding of MVP is a late systolic click; a late apical murmur may or may not be associated with the click.



  • The emergency physician should also pay attention to the sequelae of heart failure.



Essential Diagnostics




  • The patient with suspected MVP should immediately be placed on continuous cardiac monitoring, including pulse oximetry and blood pressure monitoring.



  • An EKG should be performed immediately.



  • Echocardiography should be performed in the ED.




    • Specific criteria have been described to aid in the diagnosis of pathologic MVP.28



  • Basic laboratory testing should include cardiac markers, basic electrolytes, thyroid studies, and possibly a D-dimer (based on presentation and clinical suspicion).



  • Chest x-ray (PA and lateral) should be performed in patients with suspected progression of known disease to evaluate for heart failure.



ED Treatment




  • No treatment is needed for asymptomatic patients.



  • Patients with autonomic-associated MVP that have returned to baseline typically do not require emergent treatment.



  • Patients with progression of underlying anatomic abnormalities should have treatment based on the extent of heart failure present.



  • Most athletes with MVP may continue to participate in sports as long as they are asymptomatic and there is no personal or family history of significant cardiac events.29



Disposition




  • Asymptomatic patients may be safely discharged from the ED to follow-up with a PCP.



  • Patients with autonomic-associated symptoms of MVP that have returned to baseline may also be discharged from the ED.



  • These patients should avoid caffeine and other stimulants until seen by a PCP or by cardiology (as an outpatient).




    • These patients should also avoid exercise until seen for follow-up.



  • These patients may be discharged with twenty-four-hour cardiac monitoring.



  • Emergency physicians are not advised to start this patient group on long-term management medications (e.g., beta blockers).



  • Patients with progression of underlying anatomic abnormalities should be admitted to cardiology for further management of heart failure.



  • These patients may benefit from emergent consultation with cardiovascular surgery to evaluate the need for emergent valve replacement.



Pediatric Considerations




  • The characteristic click and murmur of MVP are commonly seen in the pediatric population. If these are incidental findings the patient may be advised to refrain from exercise until seen by a pediatrician or pediatric cardiologist.



Pearls and Pitfalls




  • MVP has a low risk of adverse cardiac events.



  • Most athletes may continue sports participation as long as they are asymptomatic and have no personal or family history of significant cardiac events.



Hypertrophic Cardiomyopathy (HCM)



General Description




  • This is the most common cause of SCD in young athletes in the United States.



  • It is characterized by an increase in left ventricular size.



  • It may affect any portion of the left ventricle, but most commonly the intraventricular septum.



  • A family history of SCD before the age of 35 should raise suspicion of a familial component to the presentation.



  • Multiple alleles causing HCM have been identified.




    • Genotype testing is increasingly used to identify at-risk athletes, particularly those with a concerning family history.



Mechanism




  • The left ventricular wall increases in thickness due to genetics, pathologic conditions, exercise, or a combination of factors.



  • Left ventricular cavity diameter may also change due to the previously mentioned factors.




    • Normal left ventricular wall thickness is less than 11 mm.



    • Measurements between 12–15 mm are considered indeterminate.



    • Left ventricular wall thickness of greater than 15 mm is considered frank hypertrophy.



  • This increase in wall thickness may not be symmetric around the ventricle, further limiting cardiac output.



  • Many athletes have changes in both left ventricular wall thickness and cavity diameter.



  • A small percentage of athletes also have changes to the right ventricle.



Presentation




  • Patients with hypertrophic cardiomyopathy may present to the ED with a variety of symptoms ranging from chest pain, dyspnea (at rest or with exertion), decreased exercise tolerance, near syncope/syncope, to sudden cardiac arrest.



Physical Examinations




  • Always check vital signs first.



  • A thorough cardiopulmonary examination is mandatory.




    • Cardiac auscultation listening for murmurs.




      • An outflow murmur present with Valsalva but not at rest is pathognomonic for HCM.



    • Also assess for signs of heart failure.




      • Listen to lung sounds.



      • Assess for jugular venous distention (JVD) and for peripheral edema.



Essential Diagnostics




  • An EKG should be performed immediately.




    • Among individuals with hypertrophic cardiomyopathy, 90–95 percent have EKG changes.30



    • Left ventricular hypertrophy is the most common (using standard criteria).



  • Routine lab testing (CBC, CMP, cardiac biomarkers, coagulation studies) should be sent to monitor patient status and to evaluate for possible triggering etiologies.



  • Chest x-ray (PA and lateral) should be performed to evaluate cardiac size.



  • An echocardiogram should be performed to more clearly delineate cardiac parameters.




    • Echocardiogram measurement is considered the current gold standard for determining wall thickness.



ED Management




  • Patients experiencing SCD should have the basic principles of ACLS followed.18



  • In stable patients, further management should be based upon symptoms and acuity of presentation.



Disposition




  • Patients who are otherwise stable may be considered for discharge with close outpatient follow-up with cardiology.




    • Decision to discharge vs. admit will be determined by the acuity of the presentation and should be done in consultation with a cardiologist.



  • Patients should be instructed to not engage in any physical activity until they have followed up with cardiology.

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Feb 13, 2017 | Posted by in EMERGENCY MEDICINE | Comments Off on Arrhythmias and Sudden Cardiac Arrest in Athletes

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