Cardiovascular Considerations in an Athlete

Question 1

Normal Physical exam findings of an athlete

Answer 1

• Reversible!!!! Left Ventricular Hypertrophy - LV wall thickness (LVWT) and LV cavity size, permits enhanced filling. - Increased CO maintained at high HR
• Bradycardia•Increased VO2max
• Sinus Arrhythmia
• Transient Split S2 - Changes with inspiration and expiration - Less common in adults

Question 2

Post exercise syncope

Answer 2

Exhaustion, Exercise-induced hyponatremia, heat illness, rapid reduction in preload and functional sympatholysis with elevated contractility and HR

Question 3

Syncope during exercise

Answer 3

More concerning; linked to HCOM, arrhythmogenic right ventricular cardiomyopathy.

Question 4

Screening recommendations for syncope in an athlete

Answer 4

• Until diagnosis or pathologic causes excluded, exercise is generally restricted.
• R/O post vs during; ask bystanders
• Screen for defects (Marfan’s, HCOM etc)

Question 5

Dehydration

Answer 5

• Performance suffers, earlier fatigue
• Can reduce exercise SV and CO, - Especially in the heat but can happen even without hyperthermia
• Less able to tolerate hyperthermia
• Eventually MAP may drop
• When coupled with heat illness can potentially trigger arrhythmias
• Rehydration Strategy (NATA)

Question 6

Sudden cardiac death

Answer 6

• SCD is the leading cause of non traumatic mortality in athletes
• Low overall prevalence ; ~100 to 150/year; OR 2.3 to 4.4/100,000 per year•Black/African American 5.6/100,000 per year
• Athletes aren’t at a greater risk for SCD than general population*

Question 7

Which sports does SCD most often happen in?

Answer 7

Football and basketball

Question 8

How much more does SCD happen in males v females

Answer 8

9x

Question 9

Most common causes of SCD

Answer 9

Youths: HCM (33-50%), Coronary Anomalies (15-20%), Several others each <5%
•Adults: 80% due to undiagnosed CAD, plaque rupture

Question 10

Most common mechanism of death in SCD

Answer 10

• ventricular tachyarrhythmia

- exception of marfan syndrome: usually aortic dissection/ rupture

Question 11

Hypertrophic Cardiomyopathy

Answer 11

• Strong genetic link to HCOM
• (55% of cases with familial relative)
• More common in Black/African Americans
• Ejection murmur changes with position
• Softens during sitting/squatting
• Amplifies during standing/Valsalva
• Persistent Split S2
• No change with breath holds
• S4 Gallop possible too
• Syncope or Dyspnea during exercise
• Persistent hypertrophy despite detraining

Question 12

Coronary Anomalies

Answer 12

• The most common anomalies are left coronary artery origins in the right sinus of Valsalva and right coronary artery origins in the left sinus of Valsalva.
• SCD results from ventricular arrhythmia triggered by ischemia during exercise.
• Coronary blood flow is impaired by the abnormal ostium, compression of the artery and/or coronary spasm triggered by endothelial dysfunction.
• Usually asymptomatic, although angina associated with syncope should raise suspicion

Question 13

Myocardial Bridge definition

Answer 13

• epicardial coronary artery, is tunneled within the myocardium
• characterized by systolic compression of the tunneled segment

Question 14

symptoms of myocardial bridge

Answer 14

• asymptomatic
• atypical or angina-like chest pain
• resting ECGs are frequently normal
• stress testing may induce nonspecific signs of ischemia, conduction disturbances, or arrhythmias
• diagnosed with angiogram
• surgical intervention in some cases

Question 15

potential complications of myocardial bridge

Answer 15

• Angina, myocardial ischemia, myocardial infarction, left ventricular dysfunction, myocardial stunning, paroxysmal AV blockade, as well as exercise-induced ventricular tachycardia and SCD
• there is a high prevelence in heart transplant recipients and in patients with HCOM

Question 16

Marfans syndrome

Answer 16

Marfan’ssyndrome results from a gene mutation overproduction of transforming growth factor beta (TGF-β)

Question 17

Cardiovascular disorders found in patients with marfans

Answer 17

• Aortic tear or rupture - Most often in ascending/thoracic aorta
• Mitral valve prolapse
• Aortic regurgitation
• Arrhythmias (atrial & ventricular)

Question 18

Intervention of marfans syndrome

Answer 18

• Close monitoring
• Medications for arrhythmias
• Surgery to correct defects
• Activity modification

Question 19

Commotio cordis

Answer 19

• Sudden blunt impact (ball, puck, opponent) to the chest causes sudden death in the absence of cardiac damage.
• Most Common Sports - Baseball, ice hockey, lacrosse, football, and martial arts.
• Usually triggers ventricular fibrillation
• 3% of SCD in young athletes
• 35% able to be resuscitated

Question 20

Prevention of Commotio cordis

Answer 20

• Shields not demonstrated to be to effective
• Having Defibrillators present at events
• Educate coaches and players to turn away chest from inside pitches

Question 21

AHA Screening recommendations

Answer 21

• Indicated for any athlete 12-25
• Yes to any of the 14 question warrants further examination before participation in sports.
• AHA does not support the usage of mass ECG screenings - Cost, logistics, low incidence and type 1 errors with ECG

Question 22

ECG Screening in the athlete

Answer 22

• In Italy, a 12-lead ECG and limited stress test is routinely obtained as part of a mandatory comprehensive screening program.
• The International Olympic Committee, mandates medical screening including a baseline ECG•Pre-draft testing with ECG occurs in ≈90% of the 122 major professional sports teams in North America - NBA is the most rigorous

Question 23

ECG athlete facts

Answer 23

• ECGs are abnormal in >90% of patients with HCM
• HCOM most common cause of SCD in patients <35 y/o
• Advanced interpretation can reduce false positive rate
• ECG screening for adults >35 y/o may not be as effective
• Cost savings may be different in a single payer healthcare system

Question 24

ECG Screening athlete “the seattle criteria”

Answer 24

Normal, ECG findings in athletes.- Results from adaptation of the cardiac autonomic nervous system to conditioning.
1. Sinus bradycardia (>= 30 bpm)
2. Sinus arrhythmia
3. Ectopic atrial rhythm
4. Junctional escape rhythm
5. 1°AV block (PR interval > 200 ms)
6. Mobitz Type I (Wenckebach) 2°AV block
7. Incomplete RBBB
8. Isolated QRS voltage criteria for LVH
9. Early repolarisation
10. Convex (‘domed’) ST segment elevation combined with T-wave inversion in leads V1–V4 in black/African athletes
•Reduced the false-positive rate from 17% to 4.2%

Question 25

Physical therapy implications

Answer 25

• Recreational Athletes likely at low risk, increased with uncontrolled risk factors
• Risk of adverse event during exercise including SCD decreases with increased frequency and volume of exercise
• For someone who has never exercised before, recommend gradually increasing activity starting with low <3METs (walking)
• Take Vitals, check for arrhythmias, report undiagnosed findings to PCP
• Utilize PARQ or ACSM Pre-Activity Screen
• Consider SubMax ETT or Response to low-mod exercise: walking, stairs etc
• Effectively educate staff on CPR, have access to defibrillators
• Climate control in clinic/facility, access to water and electrolytes