Cardiovascular Problems

17.1 Exercise-Associated Collapse (EAC)/Syncope

Am Fam Phys 1999;60:2001; Phy Sportsmed 2003;31:23; Clin Auton Res 2004;14S:1-26; Phy Sportsmed 2005;33:28

Causes: Exercise (see Diff Dx).

Epidem:

Exertional-related syncope represents only a minority (3-20%) of all syncope.
1 in 20,000 athletes presenting w syncope has a serious cardiac condition.
In one study, 85% of EAC occurred after completion of an event. The 15% of EAC which occurred before completion were more likely to have an organic etiology.

Pathophys:

Syncope: sudden and temporary loss of consciousness associated w a loss of postural tone.

Exercise-related syncope:

Syncopal episode occurring during or in the immediate postexertional period.
Can signal sudden death and warrants thorough investigation.

Exercise-associated collapse (EAC): broadens the definition and includes athletes who are unable to stand/walk unaided due to lightheadedness, faintness, dizziness, or syncope. It specifically
excludes orthopedic injuries. It is most commonly caused by postural hypotension.

Postural hypotension:

During exercise, an increase in stroke volume (SV) increases cardiac output.
Muscle contractions are crucial in maintaining venous return and end-diastolic volume (EDV).
After exercise, lack of muscular contractions decreases EDV and SV.
This causes a reflex vagal response, leading to vasodilatation, bradycardia, and, hence, hypotension.
Severe postural hypotension may lead to neurocardiogenic syncope.

Sx:

Must differentiate between true syncope vs collapse from exhaustive effort, heat injuries, or metabolic conditions (hypoglycemia, hyponatremia):
- True syncope elicits a history of quick recovery.
- Collapse due to exhaustive effort usually presents with prolonged periods of semiconsciousness.
Determine timing of syncopal event in relation to event:
- Orthostatic hypotension after exercise is more benign.
- Sudden loss of consciousness during exercise is ominous (suggests cardiac or arrhythmic etiology).
Other prodromal symptoms should be elucidated: palpitations (suggesting arrhythmia), chest pain (ischemia, aortic dissection), wheezing/pruritus (anaphylaxis).
Elicit history of high-risk behaviors, eating disorders, murmurs, medications, and family history of sudden death.

Si:

Vitals signs:

For on-site events: vital signs, check rectal temperature to r/o heat injuries, and consider testing for sodium and/or glucose levels to r/o hyponatremia and hypoglycemia.
Office setting: orthostatic blood pressures and BP in arm and leg.

Neuro exam:

Mental status and ability to walk, especially for on-site events.
Mental status changes indicate a more serious condition, such as heat stroke or hyponatremia.

Assess for features of Marfan’s syndrome (Med Sci Sport Exerc 1998;30:S387):

Tall, thin stature with disproportionately long arms:
- Arm span to height ratio >1.05.
Unusually long lower half of body:
- Upper-to-lower segment ratio <0.85.
Long, double-jointed fingers; elongated thumb:
- Wrist sign: thumb and little finger overlaps considerably when wrapped around wrist.
- Thumb sign: apposed thumb across palm extends beyond ulnar margin.
Curvature of the spine (scoliosis).
Chest wall abnormalities (pectus excavatum or pectus carinatum).
Murmur of MVP, MR, AR/AI.

Cardiac exam: W auscultation in supine, standing and squatting positions. Document murmurs, clicks, gallops, and pathological splits.

Systolic murmurs that accentuate w standing suggests HCM.

Crs: Benign course if found to be related to postural hypotension. However, syncope can be a precursor to sudden cardiac death and should be thoroughly investigated.

Cmplc: Seizures, sudden cardiac death.

Diff Dx:

Neurocardiogenic syncope from postural hypotension (most common).
Supraventricular tachyarrhythmias.
Hypertrophic cardiomyopathy (see 17.3).
Myocarditis/pericarditis (see 17.4).
Valvular heart disease (Aortic stenosis, MVP, see 17.5).
Long QT syndrome (see 17.6).
Coronary artery anomalies.
Atherosclerotic coronary artery disease.
Right ventricular dysplasia.
Exertional hyponatremia (see 22.3).
Hyperthermia, heat stroke (see 2.8).
Hypoglycemia.
Hyponatremia.
Seizure.

Lab:

Chemistries: electrolytes, glucose, BUN/CR, CPK (heat injuries, CAD).
Drug screen, if suspected illicit drug use.
EKG: r/o long QT, pre-excitation (WPW), LVH, RVH, ischemia.
GXT: perform after echo. Should be sport-specific, reproduce conditions that led to syncopal event.
Other special tests: Holter/event monitor (arrhythmias), EP studies (WPW, pre-excitation), EEG (seizures).
Tilt table testing: not useful in trained athletes; 2° high false pos.

X-ray:

Echo: If clinically warranted, can assess left ventricular function/size (HCM), PA pressures (RV dysplasia), valvular diseases (MVP), coronary artery anomalies (left coronary ostium).

Rx:

Postural hypotension/neurocardiogenic:
- Acute, on-site events: place athlete in supine position, elevate legs, and administer oral rehydration until vital signs are stable.
- Chronic events: avoid dehydration and consider β-blockers, disopyramide, SSRI, fludrocortisone.
Hypertrophic cardiomyopathy (see 17.3).
Myocarditis (see 17.4).
SVT: consider ablation.

Return to Activity:

If history, physical, EKG, and selected lab tests are diagnostic/suggestive and is:
- Potentially life threatening → restriction and referral.
- Non-life threatening → treat or evaluate/refer, as indicated.
If history, physical, EKG, and selected lab tests are unexplained; restriction from activity and perform Echo/GXT:
- Referral if Echo/GXT is diagnostic.
- Reassurance if normal Echo/GXT with reassuring clinical features (postexertional, nonrecurrent, normal FH, normal cardiac exam.
- Referral if normal/nondiagnostic Echo/GXT w suggestive clinical features.

17.2 Hypertension

J Am Coll Cardiol 1994;24:885; Jama 2003;289:2560, JNV VII, NIH No. 03-5233; 2003; Med Sci Sports Exerc 2004;36:533

Cause:

Primary (95%): essential hypertension.

Secondary (5%): Coarctation of the aorta, Cushing’s syndrome, hyperaldosteronism, hypercalcemia, hyperthyroidism, pheochromocytoma, renal artery stenosis, renal parenchymal disease, various drugs.

Epidem: Occurs in 24-29% of the general adult population, and is the most common cardiovascular condition in competitive athletes (Table 17.1).

Table 17.1 Hypertension Classification by Age

		Normal	Pre-HTN	HTN (Stage 1)	HTN (Stage 2)
Children 6-9 y/o^*
	Systolic	<110-114	110-117	119-130	≥126-130 (129)^**
	Diastolic	<70-75	70-79	80-92	≥87-92 (84)
Children 10-12 y/o^*
	Systolic	<115-120	115-122	124-136	≥132-136 (134)
	Diastolic	<75-76	75-80	85-94	≥91-94 (89)
Adolescents 13-15 y/o^*
	Systolic	<120	120-130	131-143	≥138-143 (149)
	Diastolic	<77-79	77-82	86-96	≥94-96 (94)
Adolescents 16-17 y/o^*
	Systolic	<120	120-135	139-148	≥146-148 (159)
	Diastolic	<80	80-86	89-99	≥97-99 (99)
Adults ≥18 y/o
	Systolic	<120	120-139	140-159	≥160 (180)
	Diastolic	<80	80-89	90-99	≥100 (110)
^Calculated at 50th percentile for height; combined age ranges. Normal: < 90th percentile for age. Pre-HTN: 90-95th percentile for age. Stage 1 HTN: 95-99th percentile, plus 5 mm Hg. Stage 2 HTN: > 99th percentile, plus 5 mm Hg. More detail, see Peds 114;2004:555. ^*Values in parentheses represent classification for severe HTN by the 26th Bethesda Conference.
Classification: JACC 1994;24:886; Jama 2003;289:250; JNC VII; Peds 2004;114:555