Pediatric Cardiac Exam and Athletic Clearance Del McOmber MD Pediatric Heartcare Partners 2-27-15

Pediatric Cardiac Examand

Athletic ClearanceDel McOmber MD

Pediatric Heartcare Partners

2-27-15

Cardiac physical examination can be amongst the most diagnostic if

done correctly and carefully

© Knowledge of cardiac physiology and auscultation techniques/maneuvers can often determine a diagnosis, or help to form a strong differential diagnosis

Physical examination--

© Evaluating signs throughout the body for evidence of hemodynamic sufficiency or insufficiency

© More difficult to assess in infants and children

© Exam findings should be often easier to hear in cooperative younger children and in adolescents than in adults

GENERAL EXAMINATION GUIDELINES

The patient:

© Should have their shirt(s) off, or wear an examination gown

© Females nine years old and older should wear a gown with the opening in the front

© Should be calm and quiet

The stethoscope:

© Should be your own!!!© Should have a separate bell and diaphragm© Bell allows in all sounds© Diaphragm lets in middle and high

frequency sounds, attenuates low pitched sounds

The stethoscope (cont.):

© Bell should be used relatively lightly (avoid diaphragm effect)

© Diaphragm should be small enough to fit on the chest of the patient

© Should have tubing which is short (16-18 inches)

© Should have earpieces that are comfortable and snug

The environment:

© Should be quiet (patient, family, clinic attendants, exam room, surrounding areas)– May briefly disconnect ventilator or occlude

suction devices– Brief bilateral occlusion of infant’s nares (warn

the parents first)© Should be well lit

INSPECTION:

© Chest observation gives clues to cardiopulmonary disease

© Can be insensitive

INSPECTION (cont.):

© Asymmetry can indicate RVE© Increased A-P chest diameter indicates

chronic air trapping/hyperinflation© Pectus deformities--usually no significant

cardiopulmonary consequences© Kyphoscoliosis--can have cardiopulmonary

effect

Apical Impulse:

© Visualization to assess ventricular size/thickness

© Normally distinct and located at 4ICS at/inside the midclavicular line

Apical Impulse (abnormal):

© Hyperdynamic impulse in normal location: think increased cardiac output or LVH

© Hyperdynamic and downward/leftwardly displaced: think LVE

© Indistinct impulse associated with RVH© Precordial heave is seen with RVE

LV/apical impulse (PMI):

© Found w/ the fingertips with the patient upright

© Note interspace location, relation to the midclavicular/anterior axillary line, amplitude compared to RV impulse

LV/apical impulse (abnormal):

© Strong impulse is due to increased cardiac output or LVH

© Downward/leftward displacement--LVE (with or without LVH)

Thrills:

© Palpation of a loud murmur© Found in the precordial, suprasternal, or

carotid artery area© If low intensity murmur, probably just a

pulsation and NOT a thrill

AUSCULTATION: the bread and butter of the business

Auscultation Areas

Where to listen:

© Apex/5LICS (mitral area)© Left lower sternal border/4LICS (tricuspid

and secondary aortic area)© Right middle sternal border/2RICS (aortic

area)© Left middle sternal border/2LICS

(pulmonary area)

Where to listen (cont.):

© Left and right infraclavicular areas© Left anterior axillary line© R and L axillae© R and L interscapular areas of back (for

pulmonary/aortic collaterals)

Where to Listen (Other sites):

© Lungs© Cranium (temples/orbits/fontanelle)© Liver© Neck (carotid area)© Abdomen© Lumbar/abdominal region over renal area© Mouth/trachea with respiration© Femoral artery

How to listen:

© Have a system, e.g. method of inching© Listen systematically: S1, S2, systolic

sounds, systolic murmurs, diastolic sounds, diastolic murmurs

Normal heart sounds

23

Heart Sounds

• S1 – onset of the ventricular contraction• S2 – closure of the semilunar valves• S3 – ventricular gallop• S4 – atrial gallop• Other – opening snap, ejection sound• Murmurs

S1:

© May be due to acceleration/deceleration phenomena in the LV near the A-V valves

© Best heard at the apex and LLSB© Often sounds single unless slow heart rate

S1 (cont.):

© If split heard better at the apex, may actually be S4 or ejection click

© Tends to be more low-pitched and long as compared to S2

© Differentiate S1 from S2 by palpating carotid pulse:- S1 comes before and S2 comes after carotid

upstroke

Decreased S1:

© Slowed ventricular ejection rate/volume© Mitral insufficiency© Increased chest wall thickness© Pericardial effusion© Hypothyroidism

Decreased S1 (cont.):

© Cardiomyopathy© LBBB© Shock© Aortic insufficiency© First degree AV block

Other Abnormal S1 (cont.):© Increased S1:

- Increased cardiac output- Increased A-V valve flow velocity (acquired

mitral stenosis, but not congenital MS)© Wide splitting of S1:

- RBBB (at tricuspid area)- PVC’s- VT

S2:

© From closure vibrations of aortic and pulmonary valves

© Often ignored, but it can tell much © Divided into A2 and P2 (aortic and

pulmonary closure sounds)© Best heard at LMSB/2LICS © Higher pitched than S1--better heard with

diaphragm

S2 splitting (normal):

© Normally split due to different impedance of systemic and pulmonary vascular beds

© Audible split with > 20 msec difference © Split in 2/3 of newborns by 16 hrs. of age,

80% by 48 hours © Harder to discern in heart rates > 100 bpm

S2 splitting (normal, cont.):

© Respiratory variation causes splitting on inspiration: pulmonary vascular resistance

© When supine, slight splitting can occur in expiration

© When upright, S2 usually becomes single with expiration

S2 splitting (abnormal):

© Persistent expiratory splitting- ASD- RBBB- Mild valvar PS- Idiopathic dilation of the PA- WPW

S2 splitting (abnormal, cont.):

© Widely fixed splitting- ASD- RBBB

S2 splitting (abnormal, cont.):

© Wide /mobile splitting- Mild PS- RVOTO- Large VSD or PDA- Idiopathic PA dilation- Severe MR- RBBB- PVC’s

S2 splitting (abnormal, cont.):

© Reversed splitting- LBBB- WPW- Paced beats- PVC’s- AS- PDA- LV failure

Single S2:

© Single S2 occurs with greater impedance to pulmonary flow, P2 closer to A2

© Single and loud (A2): TGA, extreme ToF, truncus arteriosus

© Single and loud (P2): pulmonary HTN!!© Single and soft: typical ToF© Loud (not single) A2: CoA or AI

Extra heart sounds

S3 (gallop):

© Usually physiologic© Low pitched sound, occurs with rapid

filling of ventricles in early diastole © Due to sudden intrinsic limitation of

longitudinal expansion of ventricular wall © Makes Ken-tuck-y rhythm on auscultation

S3 (cont.):

© Best heard with patient supine or in left lateral decubitus

© Increased by exercise, abdominal pressure, or lifting legs

© LV S3 heard at apex and RV S3 heard at LLSB

S3 (abnormal):

© Seen with Kawasaki’s disease--disappears after treatment

© If prolonged/high pitched/louder:- can be a diastolic flow rumble indicating

increased flow volume from atrium to ventricle

S4 (gallop):

© Nearly always pathologic© Can be normal in elderly or athletes© Low pitched sound in late diastole© Due to elevated LVEDP (poor compliance)

causing vibrations in stiff ventricular myocardium as it fills

© Makes “Ten-nes-see” rhythm

S4 (cont.):

© Better heard at the apex or LLSB in the supine or left lateral decubitus position

© Occurs separate from S3 or as summation gallop (single intense diastolic sound) with S3

S4 Associations:

© CHF!!!© HCM© severe systemic HTN© pulmonary HTN© Ebstein’s anomaly© myocarditis

S4 Associations (cont.):

© Tricuspid atresia© CHB© TAPVR© CoA© AS w/ severe LV disease© Kawasaki’s disease

Click:

© Usually pathologic © Snappy, high pitched sound usually in early

systole © Due to vibrations in the artery distal to a

stenotic valve

Can be associated with:

© Valvar aortic stenosis or pulmonary stenosis© Truncus arteriosus© Pulmonary atresia/VSD© Bicuspid aortic valve© Mitral valve prolapse (mid-systolic click)© Ebstein’s anomaly (can have multiple

clicks)

Does NOT occur w/ supravalvar or subvalvar AS, or calcific

valvar AS.

Friction rub:

© Creaking sound heard with pericardial inflammation

© Classically has 3 components; can have fewer than 3 components

© Changes with position, louder with inspiration

Murmur:

© Sounds made by turbulence in the heart or blood stream

© Can be benign (innocent, flow, functional) or pathologic

© Murmurs are the leading cause for referral for further evaluation

© Don’t let murmurs distract you from the rest of the exam!!

Cardiac exam and murmur general descriptors:

© Various combinations used for all normal and abnormal heart sounds

General descriptors:

© Heart sound splitting© Grade/intensity© Phase© Shape© Pitch

General descriptors (cont.):

© Timing within the phase© Duration within the phase© Character/quality© Location of maximum intensity on the

precordium © Radiation of murmur

MANEUVERS

Routine positions--

© Supine and standing or sitting examinations should be performed on all patients

Other physical maneuvers

Squatting:

© Increases afterload/systemic vascular resistance, initially increased venous return, increased stroke volume, decreased HR

© Reduces the murmur of AS w/ HCM © Increases the murmur of MR

Sudden standing:

© Decreased afterload, decreased venous return and stroke volume, increased heart rate, increased SVR):

© Accentuates the murmur and S4 of subAS, MVP, and HOCM

Left lateral decubitus positioning or leaning forward

in an upright position:

© Apex of the heart falls toward the chest wall © Brings out mitral valve and aortic valve

murmurs

Some maneuvers for innocent murmurs (more later):

© Jugular vein compression/turning the head can abolish venous hum

© Lying the patient perfectly flat is the most reliable method of quieting the hum.

© Compression of the subclavian artery or shoulder extension can abolish supraclavicular bruit

Other maneuvers:

© Transient arterial occlusion© Breath-holding in end-expiration in the

upright position or leaning forward© Deep breath inspiration in upright position© Lower extremity elevation (passive) while

lying down© Exercise (running in place)

THE REST OF THE BODY--don’t forget it!!

Vital signs:

© Temperature © Respiratory rate © Heart rate © Blood pressure © Oxygen saturations © Weight and height

Lungs:

© Pulmonary congestion probably nonexistent in infants (more manifest by tachypnea or retractions)

© Cardiac asthma: fine crackles heard in older children associated w/ CHF (coarse crackles indicate a pneumonia)

Lungs (cont.):

© Possible signs of increased pulmonary blood flow- Tachypnea- Dyspnea- Retractions- Flaring- Grunting- Panting

Edema:

© Caused by systemic venous congestion © Seen more in older children and adults

(little evidence of this in infants) © More often seen in renal- or liver-induced

hypoproteinemia (esp. if marked)

Edema (cont.):

© Locations:- Periorbital- Scrotal- Pre-sacral- Hand/foot area

© Nonpitting pedal/hand edema or lymphedema in a newborn: think Turner’s or Noonan’s syndrome

Liver:

© Measure at midclavicular line where it crosses the 9th costal cartilage

© Can be right-sided (situs solitus), left-sided (situs inversus), or midline (situs ambiguous--measured subxiphoid)

Liver (cont.):

© Measurements:– 2-3 cm below the RCM in the infant– 2 cm below the RCM from 1-3 years of age – 1 cm below the RCM from 4-5 years of age

© Use warm, gentle hands

Liver--abnormal:

© Hepatomegaly caused by systemic venous congestion

© Right-sided CHF: liver enlarges, becomes firm, loses distinct edge

© Pulsatile liver: tricuspid regurgitation or other cause of elevated R sided pressures

© Hard liver may be more serious than large, soft liver

Spleen:

© Normally felt in newborns under the LCM © Significant enlargement can indicate

TORCH infection with an associated cardiac lesion

© Isolated splenomegaly is usually not seen w/ CHF

Infective endocarditis:

© Splenomegaly © New/changing murmur © Fever © Positive blood cultures © Neurologic changes © Peripheral signs of embolic phenomena

Ascites:

© Severe right or right AND left sided CHF--from Fontan anastomosis, dilated cardiomyopathy

Nutrition/muscle mass:

© Wasting (systemic, bitemporal)--from poor nutrition/high metabolic demand (CHF)

Skin:

© Sweating and pallor (diaphoresis) --associated with increased adrenergic tone

Cyanosis of the mucus membranes:

© Central--from > 3g reduced Hb in the arterial blood due to cardiac or pulmonary shunting

© Acrocyanosis--from low cardiac output © Differential cyanosis

Arterial Pulses:

© Assess for rate, rhythm, volume, character© Evaluate radial, brachial, femoral, pedal

(dorsalis pedis or posterior tibialis) pulses © Also palmar and plantar pulses in newborns© Congenital absence of dorsalis pedis in 10%

of population © Simultaneous evaluation of both radial

pulses and R radial plus a femoral pulse

Rate:

© Bradycardic (conditioning, heart block, digoxin toxicity)

© Normal © Tachycardic (CHF, excitement, fever,

anemia, arrhythmia)

Rhythm:

© Regular© Irregular (can be sinus arrhythmia with

respiratory variation or PAC/PVC’s)© Regularly irregular© Irregularly irregular (arrhythmia)

Volume:© Bounding/water hammer (pulse pressure

>30 mmHg in infant, >50 mmHg in child)© Full© Normal© Thready

- low output states: shock, severe CHF, large VSD or PDA

- L sided obstruction: AS, aortic atresia, HLHS© Absent

Clubbing:

© Thickening of tissues at the base of the nails © Due to capillary engorgement associated

with chronic hypoxemia and polycythemia. © Seen in cyanotic congenital heart disease

and pulmonary disease © Can reverse after improvement of

hypoxemia, can disappear with anemia

INNOCENT MURMURS

INNOCENT MURMURS:

© Also known as flow, benign, normal, nonpathologic, functional, inorganic, or physiologic

© Occur in up to 77% of neonates, 66% of children, and can be increased to up to 90% with exercise or using phonocardiography

General “Rules” of Innocent Murmurs:

© Grade I-III intensity© No thrills associated at any area of

precordium© Only minimal transmission© Not harsh© Brief duration (usually early to mid-systole)

More General “Rules” of Innocent Murmurs:

© Never solely diastolic© Never loudest at the RUSB/R base© No clicks© Normal S2

Occur at areas of mismatch of normal blood flow volumes with

decreasing vessel caliber size

© e.g. LVOT, RVOT, branch PA’s, etc.© Better heard in children due to their thinner

chest walls with greater proximity of stethoscope to vessel

Having more than one innocent murmur in a patient is normal,

too!

Vibratory Systolic Murmur (Still’s Murmur):

© Most common innocent murmur of childhood

© Needs maneuvers normal ECG to differentiate from subAS, HOCM, VSD

Still’s Murmur (Characteristics):

© Location—max at LLSB© Radiation—may radiate to LMSB, apex,

and R-L base (“hockey-stick” distribution), although may not completely radiate

© Timing—mid-systole© Intensity—grade I-II© Pitch—mid to low

Still’s Murmur (Characteristics, cont.):

© Character—vibratory, groaning, musical, buzzing, squeaking, “guitar-string twanging,” “cooing dove”

© Variation—loudest supine, after exercise, with fever, anemia, or excitement Disappears or localizes to LLSB when upright

Still’s Murmur (Characteristics, cont.):

© Age range—uncommon in infancy, commonly age 2 to 6 years, rare in teens

© Etiology—unknown, may be associated with LV ejection

© Similar murmur seen with LV false tendons (but does not tend to diminish as much when upright)

Innocent Pulmonary Systolic Murmur:

© Need to differentiate from ASD, PS, subAS, VSD, and true/organic PPS

Innocent Pulmonary Systolic Murmur (Characteristics):

© Location—LUSB© Radiation—possible to hear at LMSB© Timing—early to mid-systole with peak in

mid-systole

Innocent Pulmonary Systolic Murmur (Characteristics, cont.):

© Intensity—grade I-III© Pitch—mid to high-pitched© Character—soft, blowing, somewhat

grating, diamond-shaped

Innocent Pulmonary Systolic Murmur (Characteristics, cont.):

© Variation—louder when supine, fever, exercise, anemia

© Age range—most commonly age 8-14 years, but early childhood to young adults

© Etiology—normal ejection vibrations into MPA

Physiologic Peripheral Pulmonic Stenosis (PPS):

© Need to differentiate from valvar PS, ASD, true/organic PPS, and ToF

Physiologic PPS (Characteristics):

© Location—LUSB© Radiation—LMSB, bilateral axillae, mid-

back, approximately same intensity over entire precordium

© Timing—early to mid-systole

Physiologic PPS (Characteristics, cont.):

© Intensity—grade I-II© Pitch—high-pitched© Character—blowing, not harsh, diamond-

shaped© Variation—none

Physiologic PPS (Characteristics, cont.):

© Age range—newborns, especially premies. May last 3 – 6 months but not longer (requires further eval if persistent)

© Etiology—small relative size of branch PA bifurcation to MPA at birth with acute angle turbulence and relative obstruction

Supraclavicular or Brachiocephalic Systolic Murmur

(Carotid Bruit):

© Need to differentiate from supravalvar or valvar AS, CoA, bicuspid AoV

© Bruit is French for “noise”

Carotid Bruit (Characteristics):

© Location—suprasternal notch, supraclavicular areas

© Radiation—carotids, below clavicles© Timing—early to mid-systole

Carotid Bruit (Characteristics, cont.):

© Intensity—grade I-III, ?IV (may have a faint localized thrill)

© Pitch—mid-pitched© Character—may be slightly harsh

Carotid Bruit (Characteristics, cont.):

© Variation—decreased intensity with hyperextension of shoulders; louder with anxiety, anemia, or trained athletes w/ resting bradycardia

© Age range—children and young adults© Etiology—unknown, ? turbulence at takeoff

of carotid or brachiocephalic vessels

Venous Hum:

© Most common continuous innocent murmur, and probably the second most common innocent murmur

© Need to differentiate from AS/AI, AVM, anomalous left coronary artery arising from the PA, or PDA if L-sided

Venous Hum (Characteristics):

© Location—anterior neck to mid-infraclavicular area, R side > L side

© Radiation—may go to LMSB© Timing—continuous with diastolic

accentuation© Intensity—grade I-III© Pitch—mid to low

Venous Hum (Characteristics, cont.):

© Character—soft, whispering, roaring, or blowing, distant-sounding

© Variation—disappears when supine, with head turn AWAY from the side listened to, with gentle manual compression of jugular venous return w/ fingers, or w/ Valsalva

Venous Hum (Characteristics, cont.):

© Age range– pre-school through grade school age (very

common)– adol. to young adults (rarely heard, can be seen

w/ increased blood flow states e.g. anemia, pregnancy, thyrotoxicosis)

© Etiology—turbulence in jugular and subclavian venous return meeting in SVC

Mammary Souffle:

© Occurs in certain circumstances of breast development/activity and disappear otherwise

© Differentiate from PDA, AVM, or AS/AI© Souffle is French for “breath”

Mammary Souffle (Characteristics):

© Location—heard over/just above breasts in late pregnancy or in lactating women

© Radiation—none© Timing—may be systolic only, systole with

diastolic spill-over, or continuous with late systolic accentuation (most common)

Mammary Souffle (Characteristics, cont.):

© Intensity—grade I-III© Pitch—mid to high© Character—blowing or breath-like© Variation—obliterated by increased

stethoscope pressure or compressing the tissue on both sides of the stethoscope

Mammary Souffle (Characteristics, cont.):

© Age range—rare (hopefully!) in pediatric population

© Etiology—increased blood flow to the relatively smaller mammary blood vessels

“I wouldn't ever set out to hurt anyone deliberately unless it was,

you know, important — like a league game or something.”

Dick Butkus

First…do no harm

Epidemiology

• College and Professional Athletes– 500,000 participants each year

• Competitive Athletics:– “Several million high school students

participate in competitive athletics each year in the United States”.

• ‘Other’ Organized Sports Participation– 25 million children and young adults

Epidemiology

• Incidence of Sudden Cardiac Death:– Organized High School/College Athletes

• 1:134,000/Year (Male) (7.47:million/Year)• 1:750,000/Year (Female) (1.33/million/Year)

– Marathon Runners• 1:50,000 Race Finishers (Mean Age 37yo)• In brief, ~ 300 deaths/year.• But the media attention and legal implications,

make these events standout.

Etiology based on largest US data set

1) HCM – 36%2) Coronary Anomalies 17%3) Increased Cardiac Mass (possible HCM) 10%4) Ruptured Aorta/Dissect 5%5) Tunneled LAD 5%6) Aortic Stenosis 5%7) Myocarditis 3%8) Dilated CM 3%9) Idiopathic Myocdardial scarring 3%10) Arrhythmogenic RV dysplasia 3%

•OTHERS…•MVP•CAD•ASD•Brugada Syndrome•Commotio Cordis•Complete heart block•QT prolongation syndrome•Ebstein’s anomaly•Marfan’s Syndrome•Wolff-Parkinson White Syndrome – WPW•Ruptured AVM•SAH

Screening requirements

• In the US competitive athletes are screened by means of history and physical examination.

• Only Europe mandates a resting ECG.• In 1982 the incidence of SCD in Italy was

4.2/100,000 athletes. In 2004 the incidence of SCD decreased markedly to 0.9/100,000. Due to Arrhythmogenic RV dysplasia.

Pre-Participation Physicals

• History– Screen for medications and drugs of abuse that can

have potential cardiotoxic effects (Beta agonists, Theophylline, TCA’s, Macrolides, Pseudoephedriine, Phenypropanolamine, Tobacco, Alcohol, Cocaine, Amphetamines, Ephedrine, and Anabolic Steroids)

• Questions to ask…************************– Have you ever passed out during or after exercise?– Have you ever been dizzy during or after exercise?– Have you ever had chest pain during or after exercise?– Do you get tired more quickly than your friends do

during exercise?– Have you ever had racing of your heart or skipped heart

beats?

Pre-Participation Physicals

• Yes, more questions – Have you had high blood pressure or high

cholesterol?– Have you ever been told you have a heart

murmur?– Has any family member or relative died of

heart problems or sudden death before age 50?– Have you had a severe viral infection within the

last month (ie. Myocarditis or mononucleosis)

– Has a physician ever denied or restricted your participation in sports for any heart problems?

Pre-Participation Physicals – Cont’d

• Physical Exam– Gen: physical appearance

• ie – Marfan’s Syndrome

Pre-Participation Physicals – Cont’d

• Physical Exam– Vitals:

• BP: Elevated readings confirmed– Proper technique

• Pulse: Rate of rise, Contour, Volume, consistency– Normal– Pulsus Bisferiens – Seen in AS, Aortic regurge, HCM - Coarctation of aorta – ie. HTN in arms, but weak femoral

pulses AND/OR femoral pulse lags behind that of the radial artery

Pre-Participation Physicals – Cont’d

– Standing/Squatting: STANDING decreases venous return and reduces the intensity of innocent murmurs (as well as BAD murmurs of AS).

• BUT, …STANDING accentuates the murmur of obstructive hypertrophic cardiomyopathy!

• Squatting will DECREASE the intensity of the murmur of obstructive hypertrophic cardiomyopathy.

• Therefore, the cardiac exam on athletes first supine, then seated, then standing.

Pre-Participation Physicals – Cont’d

• Indications for echo:– All Diastolic Murmurs– Holosystolic murmurs– Murmurs Grade 3/6 and above– Any murmur that examiner isn’t sure about…ie. CYA?

• Features of “Innocent Murmurs”:– Low in intensity and midsystolic in timing, normal splitting,

normal DYNAMIC auscultation, absence of a specific pattern of radiation, asymptomatic.

Additional Testing

• EKG’s– Findings in Athletes considered WNL

• Sinus Bradycardia – as low as 30-40 bpm• Various A/V blocks occur in up to 33% of athletes

– First Degree (PR>0.2) – Most Common– Second Degree (Mobitz-1 or Wenkeback)

• Increased R or S wave voltage without Left axis deviation, QRS prolongation, or LAE

• U-waves with up-sloping ST segments and normal T waves

• Incomplete RBBB

Quick abbreviations• ARVD = arrhythmogenic right ventricular

dysplasia• AS = aortic stenosis• CAA = coronary artery anomoly• DC = dilated cardiomyopathy• HB = heart block• LQTS = long QT syndrome• MC = myocarditis• MVP = mitral valve prolapse• NMS = neurally mediated syncope• TCA = tunneled coronary artery• VP = ventricular preexcitation

Exertional Syncope

• CV Causes– CAA, LQTS, HCM, MC, DC, AS, WPW,

NMS, HB

• Additional Testing Needed– EKG, Echo, Exercise Stress Testing

- 64 slice CT scan? for CAA

Exertional Chest Pain or dyspnea

• CV Causes– HCM, CAA, Marfan’s, TCA, MVP, MC,

ARVD, AS

Palpitations

• CV Causes– WPW, LQTS, MVP

• Non-CV Causes– Hyperthyroidism, Supplements, Stimulant

meds

MECHANISM OF SUDDEN DEATHVentricular Tachycardia and Ventricular Fibrillation

Normal EKG

Ventricular Tachycardia Polymorphic Ventricular TachycardiaVentricular Fibrillation

Cardiac Pathology in Athletes:Sudden Death in Young People

ECG Intervals

What do athletes die from?

Risk Evaluation

HANK GATHERS1967 - 1990

Hypertrophic Obstructive Cardiomyopathy

Hypertrophic Obstructive Cardiomyopathy

ECG of HOCM patient

Commotio Cordis

• Traumatic cause of sudden death via arrhythmia (usually v-fib)

• Caused by blunt force trauma to chest occurring during the vulnerable repolarization period ( usually on the T-wave and can be the QRS period also)

• Some evidence support cardiac injury, but the etiology and electrophysiology have yet to be completely defined

Commotio Cordis cont’d

• Most commonly seen in adolescent baseball players but also unprotected karate kicks to chest, ice hockey, etc.

• Chest protectors and softer core baseballs decrease, but do not eliminate the risk

Commotio Cordis

Commotio Cordis

“Pistol” Pete Maravich

Anatomy

Coronary Artery anomalies

Coronary Artery anomalies

Marfan syndrome

Marfan syndrome

Marfan syndrome

Marfan syndrome

Marfan syndrome

When in Rome…..

• Arrhythmogenic RV dysplasia (22%) is the most common cause of SCD in athletes.

ARVD• Arrhythmogenic Right Ventricular

Dysplasia, also known as arrhythmogenic right ventricular cardiomyopathy, is characterized by replacement of the right ventricular muscle by fatty and fibrous tissue.

• arrhythmias of right ventricular origin that range from isolated premature ventricular beats to nonsustained or sustained VT and ventricular fibrillation.

ARVD cont.• Global or regional right ventricular

dysfunction, and late evolution to right or biventricular heart failure.

• Incomplete or complete RBBB• Inverted T waves in the anterior precordial leads• Localized prolongation of the QRS complex in leads V1 and V2• Epsilon waves visible as sharp discrete deflections at the

terminal portion of the QRS complex in the anterior precordial leads

• Use QRS width in Lead I which is always <120ms• Lead III R>S• S wave upstroke in V1 - V3 >55ms was found in 95 percent of

ARVD********

Arrythmogenic Right Ventricular Cardiomyopathy

Arrythmogenic Right Ventricular Cardiomyopathy

Arrythmogenic Right Ventricular Cardiomyopathy

Long QT syndrome

• 26th Bethesda Conference Guidelines for Athletic Participation