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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