Transcript 3-Sports-Med.-Cardia..

Cardiac Pre-Participation Exam
and Abnormalities
Jamie B. Varney, M.D.
CAQ Sports Medicine
Pikeville Medical Center
Orthopedics and Sports Medicine
Guidelines
• AAFP,AAP,AMSSM,AOSSM,AOASM publish
guidelines to follow1
• AHA has specific recommendations2
• 36th Bethesda Recommendations3
• Seattle Criteria EKG Interpretation4
AHA Recommendations2
• Medical history*
▫ Personal history
 Exertional chest pain/discomfort
 Unexplained syncope/near-syncope†
 Excessive exertional and unexplained dyspnea/fatigue,
associated with exercise
 Prior recognition of a heart murmur
 Elevated systemic blood pressure
*Parental verification is recommended for high school and middle school
athletes
†Judged not to be neurocardiogenic (vasovagal); of particular concern
when related to exertion
AHA Recommendations2
 Family history
 Premature death (sudden and unexpected, or
otherwise) before age 50 years due to heart
disease, in 1 relative
 Disability from heart disease in a close relative
<50 years of age
 Specific knowledge of certain cardiac conditions in
family members:
 hypertrophic or dilated cardiomyopathy
 long-QT syndrome or other ion channelopathies,
 Marfan syndrome
 clinically important arrhythmias
AHA Recommendations2
▫ Physical examination
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Heart murmur ††
Femoral pulses to exclude aortic coarctation
Physical stigmata of Marfan syndrome
Brachial artery blood pressure (sitting position) †††
†† Auscultation should be performed in both supine and standing
positions (or with Valsalva maneuver), specifically to identify
murmurs of dynamic left ventricular outflow tract obstruction
†††Preferably taken in both arms
Cardiac Exam
• Vital signs
▫ Resting pulse
▫ Resting BP, preferably both arms
• Auscultation
▫ Rate and Rhythm
▫ Murmurs
 Supine and standing or with valsalva
• Palpation of Apical Impulse
• Pulses
▫ Femoral
▫ Radial
▫ Assess for delay (Coarctation)
Vital Signs
• Bradycardia may be normal
• Low BP not uncommon
• If asymptomatic with appropriate response to
exercise likely no further evaluation needed
• Keep in mind that children/adolescents have
different normal values for elevated BP
▫ Age and height percentile tables 5
Murmurs
Grade
1
2
3
4
5
6
Barely audible
Soft but easily heard
Loud but not accompanied by a thrill
Loud and associated with a palpable thrill
Associated with a thrill and heard with
the stethoscope partially off the chest
Audible without a stethoscope
Cardiac Timing
6
Murmurs
7
Innocent/Functional
Pathologic
• Less than Grade 3
• Systolic
• Decrease from supine to
standing
• Grade 3 or greater
• Any diastolic component
• Increases with standing or
valsalva
• Decreases with squatting
Murmur of HCM
• Systolic heard best at lower left sternal border
• Increases with standing or valsalva
• Decreases with squatting
• NO PARTICIPATION including lifting until full
cardiac workup
Murmur of Aortic Stenosis
• Systolic ejection murmur
• Crescendo/Decrescendo
• Radiates to Carotids
• NO PARTICIPATION including lifting until full
cardiac workup and see Bethesda
recommendations3
Mitral Valve Prolapse
• Mid-systolic click
• Late systolic murmur
36th Bethesda Recommendation3
• Whatever cardiac condition you discover these
recommendations are extremely helpful in
evaluation and recommendations
Need for EKG/Echo/EST
• AHA - Only if identified risk or suspicious
finding2
• Cost inefficient to screen everyone
• European Society of Cardiology recommends
EKG (high rate AVRD in Italy)
• Seattle EKG Criteria group investigating
• Special consideration for athletes > 35 “masters
athletes” with CAD as primary cause of SCD
• EKG/Echo first is suspect cardiac abnormality
(before stress)
Sudden Cardiac Death (SCD)
• Estimated prevalence 1:200,0002
• Most athletes who die suddenly have no
symptoms
• Difficult to detect risk prior to event
• Any athlete with any suspected risk can not
participate until evaluated properly
Causes of SCD8
• Hypertrophic Cardiomyopathy (HCM) 36% another
% possible HCM
• Coronary Artery Anomalies 17%
• Myocarditis 6%
• Arrhythmogenic right ventricular dysplasia 4%
• Mitral valve prolapse 4%
• Aortic Stenosis 3%
• Coronary Atherosclerosis 3%
• Ion Channelopathies 3%
• Ideopathic Dilated Cardiomyopathy 2%
• Aortic rupture (Marfan syndrome) 2%
• Other 2%
Causes in Absence of Structural
Disease
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Commotio Cordis
Long QT Syndrome
Brugada Syndrome
Catecholaminergic polymorphic VT
Challenges in Screening
• Large population
• Low prevalence2
▫ Estimated 0.3% underlying congenital heart
disease
EKG Interpretation: Seatle Criteria4
• Online Training Module9
• Committee to establish normal and abnormal
findings on EKG for Athletes
Normal EKG Findings in Athletes4
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Sinus Bradycardia >30 bpm
Sinus Arrhythmia
Ectopic Atrial Rhythm
Junctional Escape Rhythm
1st Degree AV block (PR>200ms)
Mobitz Type I (Wenckebach) 2nd Degree AV block
Incomplete RBBB
Isolated QRS voltage criteria for LVH
▫ Unless also non voltage criteria present
 Left atrial enlargement, Left axis deviation, ST depression, Twave inversion, pathological Q waves
• Early Repolarisation (ST elevation, J-point elevation)
• Convex ST segment elevation with T wave inversion in V1V4 in African Americans
Abnormal EKG Findings in Athletes4
• T-Wave Inversion
▫ >1mm in 2 or more leads excluding III, aVR, V1
• ST Depression
▫ ≥0.5mm in 2 or more leads
• Pathologic Q waves
▫ >3mm or >40 ms in 2 or more leads except III and aVR
• Complete LBBB
▫ QRS ≥120 ms, predominantly negative QRS in V1 and
upright R wave in leads I and V6
• IVCD
▫ QRS ≥ 140 ms
• Left Axis Deviation
▫ (-30 to -90 degrees)
Abnormal EKG Findings in Athletes4
• Left Atrial Enlargement
▫ Prolonged P wave > 120 ms in lead I, II with depth
≥1mm and ≥40 ms duration in V1
• Right Ventricular Hypertrophy
▫ R in V1 and S in V5 >10.5 mm AND right axis deviation
> 120 degrees
• Ventricular Pre Excitation
▫ PR <120 ms, Delta wave and wide QRS >120 ms
• Long QTc
▫ Male ≥ 470 ms Female ≥ 480 ms
• Short QTc ≤320 ms
Abnormal EKG Findings in Athletes4
• Brugada-Like Pattern
▫ High take off and downsloping ST segment elevation
followed by negative T wave in 2 or more leads V1-V3
• Profound Bradycardia < 30BPM or pauses ≥ 3sec
• Atrial tachyarrhythmias
▫ SVT, Afib, Aflutter
• PVC’s ≥ 2 per 10 sec
• Ventricular Arrhythmias
▫ Couplets, Triplets, Non-sustained V-Tach
Hypertrophic Cardiomyopathy
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0.2% of general population2, 3
Family history in 30 %10
90% of those with HCM have abnormal EKG10
Typically asymmetric hypertrophy with LV wall
thickness > 16mm3
• Athlete’s Heart has symmetric hypertrophy and
thickness generally < 12mm3
• HCM Phenotype can develop over 3-4 yrs 3
Diagnosis of HCM
• Characteristic murmur
• EKG
▫ Dramatically increased voltage
▫ Prominent Q waves
▫ Deep T-wave inversion
• Echo
• Exercise testing or Stress Echo
HCM
11
HCM
12
HCM Recommendations
3
• Athletes with definite or probable HCM should
not compete in athletics except possibly Low
Intensity
• Independent of symptoms, age, or treatment
Coronary Artery Anomalies
• May present with angina or syncope
• Typically diagnosed with angiography or
possibly Cardiac CT/MR
• Exclude from sports unless corrected3
▫ 3 months after correction may participate unless
 Previous MI
 Or abnormal maximal exercise test
Myocarditis
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Be suspicious in athletes with febrile illnesses
Diffuse EKG repolarization abnormalities
Pericardial friction rub
Those with probable or definite myocarditis
should be removed from sports for minimum of
6 months3
• Must have complete evaluation prior to return
▫ Normal EKG, Echo, no arrhythmias on Holter or
EST, normalization of inflammatory markers 3
Myocarditis
13
Arrhythmogenic right ventricular
dysplasia (ARVD)
• Fatty infiltration of right ventricular
myocardium
• Mortality at 10 yrs 20%7
• More common in Italy (most common cause of
SCD)
• Exercise induced palpitations, syncope
• EKG
▫ QRS duration in V1 > 110 msec
▫ Epsilon wave in V1 or V2
▫ T-wave inversion in right precordial leads
ARVD
14
Epsilon Wave
15
ARVD Recommendations
3
• No participation except perhaps low intensity
• Cautious with activities due to risk of syncope
▫ Freeweights, swimming, scuba
Mitral Valve Prolapse
• Can participate in all sports unless the following
exist3 (may participate in low intensity)
▫ History of syncope documented to be
arrythmogenic
▫ Family history of SCD caused by MVP
▫ SVT and VT worsened by exercise
▫ Moderate/severe mitral regurgitation
▫ Prior embolic event
• Also is minor criterion for Marfans
Commotio Cordis
10
• Cardiac contusion
• Arrhythmia precipitated to external blow to
heart
• At least 70 deaths (40 in baseball)
• Survival rate 10%
Long QT Syndrome
• Be aware that some meds may cause or worsen
▫ Antibiotics, albuterol, antidepressants, stimulants,
etc.
• Genetic testing (Type 1,2,3)
• Limit to low-intensity 3
▫ suspected LQTS associated syncope
▫ Asymptomatic with QTc ≥ 470 in men and 480 in
women
▫ Restrict from swimming and diving if Type 1
▫ LQTS Type 3 who are asymptomatic may do more
Long QT
16
Brugada Syndrome
• RBBB and ST elevation V1-V3
• Type 1 (coved) more concerning or if type 2/3
can be converted to coved with sodium channel
blocker
• Bethesda (2005): Restrict to low intensity3
• No clear exercise relation7 and AHA has looser
guidelines published in 2004 that suggest
avoiding high intensity and risk of loss of
consciousness
17
Brugada
18
Brugada
19
Marfans
• See Bethesda Recs
• Mostly Low intensity only unless Echo abnormal
or family Hx SCD3
1st degree AV Block
20
• PR > 200 msec
• If asymptomatic no further workup/restriction
unless excessive (>300 msec) 3
2nd Degree Type I (Wenckebach)
• Progressive prolonged PR then dropped QRS
complex
• Should be evaluated with Echo/Stress
• If has coexisting bundle branch block may
consider EPS
• If no worsening of EKG or symptoms may
participate3
2nd Degree Type II (Mobitz)
• Random drop of QRS complex without
associated PR prolongation
• Require pacemaker
• No contact sports with pacemaker3
21
3rd Degree AV Block
• AV dissociation
• Require pacemaker3
20
Bundle Branch Blocks
• Recommend Echo / Stress
• Consider EPS for LBBB in children
• May compete if do not develop heart block or
ventricular arrhythmia 3
22
Tachycardias
• Afib
▫ Echo/Stress/Holter
▫ Appropriate increase/decrease in HR may
participate3
• Aflutter
▫ Echo/Stress/Holter
▫ If no structural disease and appropriate
increase/decrease in HR may participate3
• Anticoagulation is contraindication to
contact sports
Tachycardias
• SVT
▫ Echo/Stress/Holter
▫ If treated may compete3
▫ May need stress with treatment to determine if adequate
exercise control
• WPW3
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Echo/Stress/Holter
Consider EPS (especially <20 y/o or symptomatic)
If no tachycardia or structural disease may compete
If has tachycardia and treated may compete
Remember this is not treated with B-blockers, Ca Channel
blockers or Digoxin.
▫ May need repeat stress to document treatment
Vtach
3
• Without structural disease
▫ May compete if ablated and documented improvement
by EPS/Stress/Holter
▫ If treated with medication no competition for at least
two to three months after the last VT episode
 If no recurrences, and the VT is not inducible by
EPS/Stress/Holter may compete.
▫ Asymptomatic athlete with less than 8 to 10 consecutive
ventricular beats of nonsustained monomorphic VT,
rates generally less than 150 beats/min without
worsening with stress/Holter may compete
• With structural heart disease and VT, moderate- and
high-intensity competition is contraindicated
regardless of whether the VT is suppressed or ablated
Summary
• Asking appropriate history is best resource for finding
potential abnormalities
• If there is any concern hold player and work up/refer
• Bethesda Recommendations
• General starting point is EKG/Echo
• Stress/Stress Echo if needed
• Add Holter if arrhythmia is suspected and EPS if
indicated
• If persistent symptoms may consider angiogram or
Cardiac CT/MR to evaluate anatomy
• Evaluate for other sources if work up negative
▫ Respiratory/GI/ Musculoskeletal
References
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American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports Medicine.
Preparticipation Physical Evaluation, 4th Ed., Bernhardt D, Roberts W (Eds), American Academy of Pediatrics,
2010
American Heart Association
Recommendations and Considerations Related to Pre-participation Screening for Cardiovascular Abnormalities
in Competitive Athletes: 2007 Update. Circulation, Mar 2007; 115: 1643 - 1655.
36th Bethesda Conference: Eligibility Recommendations for Competitive Athletes With Cardiovascular
Abnormalities. Journal of the American College of Cardiology Vol. 45, No. 8, 2005
Drezner, J. et al Electrocardiographic Interpretation in Athletes: The ‘Seattle Criteria’
http://www.nhlbi.nih.gov/health-pro/guidelines/current/hypertension-pediatric-jnc-4/blood-pressure-tables.htm
Image http://www.vetgo.com/cardio/concepts/concsect.php?conceptkey=46
Hergenroeder, A. UpToDate. The Preparticipation Sports Examination in Children and Adolescents. (6-17-2014)
Pelliccia, A. ,Link, M. UpTo Date. Risk of Sudden Cardiac Death in Athletes. (3-1-2013)
Seattle Criteria Online Training www.amssmfoundation.org/ECG-Training-Module.php
Mellion, M. et al. Team Physician’s Handbook 3rd edition.Hanley & Belfus Inc. 2002.
HCM Image http://www.doctorwiki.net/2007/01/background-apical-hypertrophic.html
HCM Image 2 http://www.aafp.org/afp/20000501/2683.html
Myocarditis http://www.amc.edu/amr/archives/200408/EKG2_ans.html
ARVD Image http://www.hosp.u-toyama.ac.jp/clla/seiri/ecg/kongetu_ecg/arvd.html
Epsilon Wave Image http://commons.wikimedia.org/wiki/Image:ARVD-Epsilon_wave.png
Long QT Image http://www.emedu.org/ecg/crapsanyallans.php
Brugada Table http://askdrwiki.com/mediawiki/index.php?title=Brugada_syndrome
Brugada Image http://scienceblogs.com/purepedantry/2007/11/the_differential_diagnosis_of.php
Brugada Criteria http://emcrit.org/065-132/074-dysrhythm.htm
AV Block Image http://www.pacemakerproject.com/cardiac_phy/cp_AV_block.htm
Heart Block Image http://www.learnwell.org/EKG200.htm
Bundle Branch Block Image http://forlag.fadl.dk/sample/ppaulev/chapter11/kap.11.htm
All Murmur Sound Courtesy of http://www.egeneralmedical.com/listohearmur.html