Pediatric Cardiac Exam and - PowerPoint Presentation

1. Pediatric Cardiac ExamandAthletic ClearanceDel McOmber MDPediatric Heartcare Partners2-27-15

2. Cardiac physical examination can be amongst the most diagnostic if done correctly and carefullyKnowledge of cardiac physiology and auscultation techniques/maneuvers can often determine a diagnosis, or help to form a strong differential diagnosis

3. Physical examination--Evaluating signs throughout the body for evidence of hemodynamic sufficiency or insufficiencyMore difficult to assess in infants and childrenExam findings should be often easier to hear in cooperative younger children and in adolescents than in adults

4. GENERAL EXAMINATION GUIDELINES

5. The patient:Should have their shirt(s) off, or wear an examination gownFemales nine years old and older should wear a gown with the opening in the frontShould be calm and quiet

6. The stethoscope:Should be your own!!!Should have a separate bell and diaphragmBell allows in all soundsDiaphragm lets in middle and high frequency sounds, attenuates low pitched sounds

7. The stethoscope (cont.):Bell should be used relatively lightly (avoid diaphragm effect)Diaphragm should be small enough to fit on the chest of the patientShould have tubing which is short (16-18 inches)Should have earpieces that are comfortable and snug

8. The environment:Should be quiet (patient, family, clinic attendants, exam room, surrounding areas)May briefly disconnect ventilator or occlude suction devicesBrief bilateral occlusion of infant’s nares (warn the parents first)Should be well lit

9. INSPECTION:Chest observation gives clues to cardiopulmonary disease Can be insensitive

10. INSPECTION (cont.):Asymmetry can indicate RVEIncreased A-P chest diameter indicates chronic air trapping/hyperinflationPectus deformities--usually no significant cardiopulmonary consequencesKyphoscoliosis--can have cardiopulmonary effect

11. Apical Impulse:Visualization to assess ventricular size/thicknessNormally distinct and located at 4ICS at/inside the midclavicular line

12. Apical Impulse (abnormal):Hyperdynamic impulse in normal location: think increased cardiac output or LVHHyperdynamic and downward/leftwardly displaced: think LVEIndistinct impulse associated with RVHPrecordial heave is seen with RVE

13. LV/apical impulse (PMI):Found w/ the fingertips with the patient uprightNote interspace location, relation to the midclavicular/anterior axillary line, amplitude compared to RV impulse

14. LV/apical impulse (abnormal): Strong impulse is due to increased cardiac output or LVHDownward/leftward displacement--LVE (with or without LVH)

15. Thrills:Palpation of a loud murmurFound in the precordial, suprasternal, or carotid artery areaIf low intensity murmur, probably just a pulsation and NOT a thrill

16. AUSCULTATION: the bread and butter of the business

17. Auscultation Areas

18. 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)

19. Where to listen (cont.):Left and right infraclavicular areasLeft anterior axillary lineR and L axillaeR and L interscapular areas of back (for pulmonary/aortic collaterals)

20. Where to Listen (Other sites):LungsCranium (temples/orbits/fontanelle)LiverNeck (carotid area)AbdomenLumbar/abdominal region over renal areaMouth/trachea with respirationFemoral artery

21. How to listen:Have a system, e.g. method of inchingListen systematically: S1, S2, systolic sounds, systolic murmurs, diastolic sounds, diastolic murmurs

22. Normal heart soundsLUBDUP

23. 23Heart SoundsS1 – onset of the ventricular contractionS2 – closure of the semilunar valvesS3 – ventricular gallopS4 – atrial gallopOther – opening snap, ejection soundMurmurs

24. S1:May be due to acceleration/deceleration phenomena in the LV near the A-V valves Best heard at the apex and LLSBOften sounds single unless slow heart rate

25. S1 (cont.):If split heard better at the apex, may actually be S4 or ejection clickTends 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

26. Decreased S1:Slowed ventricular ejection rate/volumeMitral insufficiencyIncreased chest wall thicknessPericardial effusionHypothyroidism

27. Decreased S1 (cont.): CardiomyopathyLBBBShockAortic insufficiencyFirst degree AV block

28. Other Abnormal S1 (cont.):Increased S1:Increased cardiac outputIncreased A-V valve flow velocity (acquired mitral stenosis, but not congenital MS)Wide splitting of S1:RBBB (at tricuspid area)PVC’sVT

29. 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

30. S2 splitting (normal): Normally split due to different impedance of systemic and pulmonary vascular bedsAudible 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

31. S2 splitting (normal, cont.):Respiratory variation causes  splitting on inspiration:  pulmonary vascular resistance When supine, slight splitting can occur in expirationWhen upright, S2 usually becomes single with expiration

32. S2 splitting (abnormal):Persistent expiratory splittingASDRBBBMild valvar PSIdiopathic dilation of the PAWPW

33. S2 splitting (abnormal, cont.):Widely fixed splittingASDRBBB

34. S2 splitting (abnormal, cont.):Wide /mobile splittingMild PSRVOTOLarge VSD or PDAIdiopathic PA dilationSevere MRRBBBPVC’s

35. S2 splitting (abnormal, cont.):Reversed splittingLBBBWPWPaced beatsPVC’sASPDALV failure

36. 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 ToFLoud (not single) A2: CoA or AI

37. Extra heart sounds

38. S3 (gallop): Usually physiologicLow 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

39. S3 (cont.):Best heard with patient supine or in left lateral decubitusIncreased by exercise, abdominal pressure, or lifting legs LV S3 heard at apex and RV S3 heard at LLSB

40. S3 (abnormal):Seen with Kawasaki’s disease--disappears after treatmentIf prolonged/high pitched/louder:can be a diastolic flow rumble indicating increased flow volume from atrium to ventricle

41. S4 (gallop): Nearly always pathologicCan be normal in elderly or athletesLow pitched sound in late diastoleDue to elevated LVEDP (poor compliance) causing vibrations in stiff ventricular myocardium as it fillsMakes “Ten-nes-see” rhythm

42. S4 (cont.): Better heard at the apex or LLSB in the supine or left lateral decubitus positionOccurs separate from S3 or as summation gallop (single intense diastolic sound) with S3

43. S4 Associations:CHF!!!HCMsevere systemic HTNpulmonary HTNEbstein’s anomalymyocarditis

44. S4 Associations (cont.):Tricuspid atresiaCHBTAPVRCoAAS w/ severe LV diseaseKawasaki’s disease

45. Click: Usually pathologic Snappy, high pitched sound usually in early systole Due to vibrations in the artery distal to a stenotic valve

46. Can be associated with:Valvar aortic stenosis or pulmonary stenosisTruncus arteriosusPulmonary atresia/VSDBicuspid aortic valveMitral valve prolapse (mid-systolic click)Ebstein’s anomaly (can have multiple clicks)

47. Does NOT occur w/ supravalvar or subvalvar AS, or calcific valvar AS.

48. Friction rub: Creaking sound heard with pericardial inflammation Classically has 3 components; can have fewer than 3 components Changes with position, louder with inspiration

49. 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!!

50. Cardiac exam and murmur general descriptors: Various combinations used for all normal and abnormal heart sounds

51. General descriptors:Heart sound splittingGrade/intensityPhaseShapePitch

52. General descriptors (cont.):Timing within the phaseDuration within the phaseCharacter/qualityLocation of maximum intensity on the precordium Radiation of murmur

53. MANEUVERS

54. Routine positions--Supine and standing or sitting examinations should be performed on all patients

55. Other physical maneuvers

56. Squatting:Increases afterload/systemic vascular resistance, initially increased venous return, increased stroke volume, decreased HRReduces the murmur of AS w/ HCM Increases the murmur of MR

57. 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

58. 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

59. 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

60. Other maneuvers: Transient arterial occlusionBreath-holding in end-expiration in the upright position or leaning forwardDeep breath inspiration in upright positionLower extremity elevation (passive) while lying downExercise (running in place)

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

62. Vital signs: Temperature Respiratory rate Heart rate Blood pressure Oxygen saturations Weight and height

63. 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)

64. Lungs (cont.):Possible signs of increased pulmonary blood flowTachypneaDyspneaRetractionsFlaringGruntingPanting

65. 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)

66. Edema (cont.):Locations:PeriorbitalScrotalPre-sacralHand/foot areaNonpitting pedal/hand edema or lymphedema in a newborn: think Turner’s or Noonan’s syndrome

67. Liver:Measure at midclavicular line where it crosses the 9th costal cartilageCan be right-sided (situs solitus), left-sided (situs inversus), or midline (situs ambiguous--measured subxiphoid)

68. Liver (cont.):Measurements:2-3 cm below the RCM in the infant2 cm below the RCM from 1-3 years of age 1 cm below the RCM from 4-5 years of ageUse warm, gentle hands

69. Liver--abnormal:Hepatomegaly caused by systemic venous congestionRight-sided CHF: liver enlarges, becomes firm, loses distinct edgePulsatile liver: tricuspid regurgitation or other cause of elevated R sided pressuresHard liver may be more serious than large, soft liver

70. 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

71. Infective endocarditis:Splenomegaly New/changing murmur Fever Positive blood cultures Neurologic changes Peripheral signs of embolic phenomena

72. Ascites: Severe right or right AND left sided CHF--from Fontan anastomosis, dilated cardiomyopathy

73. Nutrition/muscle mass: Wasting (systemic, bitemporal)--from poor nutrition/high metabolic demand (CHF)

74. Skin: Sweating and pallor (diaphoresis) --associated with increased adrenergic tone

75. 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

76. Arterial Pulses:Assess for rate, rhythm, volume, characterEvaluate radial, brachial, femoral, pedal (dorsalis pedis or posterior tibialis) pulses Also palmar and plantar pulses in newbornsCongenital absence of dorsalis pedis in 10% of population Simultaneous evaluation of both radial pulses and R radial plus a femoral pulse

77. Rate: Bradycardic (conditioning, heart block, digoxin toxicity) Normal Tachycardic (CHF, excitement, fever, anemia, arrhythmia)

78. Rhythm: RegularIrregular (can be sinus arrhythmia with respiratory variation or PAC/PVC’s)Regularly irregularIrregularly irregular (arrhythmia)

79. Volume:Bounding/water hammer (pulse pressure >30 mmHg in infant, >50 mmHg in child)FullNormalThready low output states: shock, severe CHF, large VSD or PDAL sided obstruction: AS, aortic atresia, HLHSAbsent

80. 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

81. INNOCENT MURMURS

82. INNOCENT MURMURS:Also known as flow, benign, normal, nonpathologic, functional, inorganic, or physiologicOccur in up to 77% of neonates, 66% of children, and can be increased to up to 90% with exercise or using phonocardiography

83. General “Rules” of Innocent Murmurs:Grade I-III intensityNo thrills associated at any area of precordiumOnly minimal transmissionNot harshBrief duration (usually early to mid-systole)

84. More General “Rules” of Innocent Murmurs:Never solely diastolicNever loudest at the RUSB/R baseNo clicksNormal S2

85. Occur at areas of mismatch of normal blood flow volumes with decreasing vessel caliber sizee.g. LVOT, RVOT, branch PA’s, etc.Better heard in children due to their thinner chest walls with greater proximity of stethoscope to vessel

86. Having more than one innocent murmur in a patient is normal, too!

87. Vibratory Systolic Murmur (Still’s Murmur):Most common innocent murmur of childhoodNeeds maneuvers  normal ECG to differentiate from subAS, HOCM, VSD

88. Still’s Murmur (Characteristics):Location—max at LLSBRadiation—may radiate to LMSB, apex, and R-L base (“hockey-stick” distribution), although may not completely radiateTiming—mid-systoleIntensity—grade I-IIPitch—mid to low

89. 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

90. Still’s Murmur (Characteristics, cont.):Age range—uncommon in infancy, commonly age 2 to 6 years, rare in teensEtiology—unknown, may be associated with LV ejectionSimilar murmur seen with LV false tendons (but does not tend to diminish as much when upright)

91. Innocent Pulmonary Systolic Murmur:Need to differentiate from ASD, PS, subAS, VSD, and true/organic PPS

92. Innocent Pulmonary Systolic Murmur (Characteristics):Location—LUSBRadiation—possible to hear at LMSBTiming—early to mid-systole with peak in mid-systole

93. Innocent Pulmonary Systolic Murmur (Characteristics, cont.):Intensity—grade I-IIIPitch—mid to high-pitchedCharacter—soft, blowing, somewhat grating, diamond-shaped

94. Innocent Pulmonary Systolic Murmur (Characteristics, cont.):Variation—louder when supine, fever, exercise, anemiaAge range—most commonly age 8-14 years, but early childhood to young adultsEtiology—normal ejection vibrations into MPA

95. Physiologic Peripheral Pulmonic Stenosis (PPS):Need to differentiate from valvar PS, ASD, true/organic PPS, and ToF

96. Physiologic PPS (Characteristics):Location—LUSBRadiation—LMSB, bilateral axillae, mid-back, approximately same intensity over entire precordiumTiming—early to mid-systole

97. Physiologic PPS (Characteristics, cont.):Intensity—grade I-IIPitch—high-pitchedCharacter—blowing, not harsh, diamond-shapedVariation—none

98. 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

99. Supraclavicular or Brachiocephalic Systolic Murmur (Carotid Bruit):Need to differentiate from supravalvar or valvar AS, CoA, bicuspid AoVBruit is French for “noise”

100. Carotid Bruit (Characteristics):Location—suprasternal notch, supraclavicular areasRadiation—carotids, below claviclesTiming—early to mid-systole

101. Carotid Bruit (Characteristics, cont.):Intensity—grade I-III, ?IV (may have a faint localized thrill)Pitch—mid-pitchedCharacter—may be slightly harsh

102. Carotid Bruit (Characteristics, cont.): Variation—decreased intensity with hyperextension of shoulders; louder with anxiety, anemia, or trained athletes w/ resting bradycardiaAge range—children and young adultsEtiology—unknown, ? turbulence at takeoff of carotid or brachiocephalic vessels

103. Venous Hum:Most common continuous innocent murmur, and probably the second most common innocent murmurNeed to differentiate from AS/AI, AVM, anomalous left coronary artery arising from the PA, or PDA if L-sided

104. Venous Hum (Characteristics):Location—anterior neck to mid-infraclavicular area, R side > L sideRadiation—may go to LMSBTiming—continuous with diastolic accentuationIntensity—grade I-IIIPitch—mid to low

105. Venous Hum (Characteristics, cont.):Character—soft, whispering, roaring, or blowing, distant-soundingVariation—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

106. Venous Hum (Characteristics, cont.):Age rangepre-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

107. Mammary Souffle:Occurs in certain circumstances of breast development/activity and disappear otherwiseDifferentiate from PDA, AVM, or AS/AISouffle is French for “breath”

108. Mammary Souffle (Characteristics):Location—heard over/just above breasts in late pregnancy or in lactating womenRadiation—noneTiming—may be systolic only, systole with diastolic spill-over, or continuous with late systolic accentuation (most common)

109. Mammary Souffle (Characteristics, cont.):Intensity—grade I-IIIPitch—mid to highCharacter—blowing or breath-likeVariation—obliterated by increased stethoscope pressure or compressing the tissue on both sides of the stethoscope

110. Mammary Souffle (Characteristics, cont.):Age range—rare (hopefully!) in pediatric populationEtiology—increased blood flow to the relatively smaller mammary blood vessels

111. “I wouldn't ever set out to hurt anyone deliberately unless it was, you know, important — like a league game or something.”Dick ButkusFirst…do no harm

112. EpidemiologyCollege and Professional Athletes500,000 participants each yearCompetitive Athletics:“Several million high school students participate in competitive athletics each year in the United States”.‘Other’ Organized Sports Participation25 million children and young adults

113. EpidemiologyIncidence of Sudden Cardiac Death:Organized High School/College Athletes1:134,000/Year (Male) (7.47:million/Year)1:750,000/Year (Female) (1.33/million/Year)Marathon Runners1:50,000 Race Finishers (Mean Age 37yo)In brief, ~ 300 deaths/year.But the media attention and legal implications, make these events standout.

114. Etiology based on largest US data setHCM – 36%Coronary Anomalies 17%Increased Cardiac Mass (possible HCM) 10%Ruptured Aorta/Dissect 5%Tunneled LAD 5%Aortic Stenosis 5%Myocarditis 3%Dilated CM 3%Idiopathic Myocdardial scarring 3%Arrhythmogenic RV dysplasia 3%OTHERS…MVPCADASDBrugada SyndromeCommotio CordisComplete heart blockQT prolongation syndromeEbstein’s anomalyMarfan’s SyndromeWolff-Parkinson White Syndrome – WPWRuptured AVMSAH

115. Screening requirementsIn 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.

116. Pre-Participation PhysicalsHistoryScreen 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?

117. Pre-Participation PhysicalsYes, 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?

118. Pre-Participation Physicals – Cont’dPhysical ExamGen: physical appearanceie – Marfan’s Syndrome

119. Pre-Participation Physicals – Cont’dPhysical ExamVitals:BP: Elevated readings confirmedProper techniquePulse: Rate of rise, Contour, Volume, consistencyNormalPulsus 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

120. Pre-Participation Physicals – Cont’dStanding/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.

121. Pre-Participation Physicals – Cont’dIndications for echo:All Diastolic MurmursHolosystolic murmursMurmurs Grade 3/6 and aboveAny 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.

122. Additional TestingEKG’sFindings in Athletes considered WNLSinus Bradycardia – as low as 30-40 bpmVarious A/V blocks occur in up to 33% of athletesFirst Degree (PR>0.2) – Most CommonSecond Degree (Mobitz-1 or Wenkeback) Increased R or S wave voltage without Left axis deviation, QRS prolongation, or LAEU-waves with up-sloping ST segments and normal T wavesIncomplete RBBB

123. Quick abbreviationsARVD = arrhythmogenic right ventricular dysplasiaAS = aortic stenosisCAA = coronary artery anomolyDC = dilated cardiomyopathyHB = heart blockLQTS = long QT syndromeMC = myocarditisMVP = mitral valve prolapseNMS = neurally mediated syncopeTCA = tunneled coronary arteryVP = ventricular preexcitation

124. Exertional SyncopeCV CausesCAA, LQTS, HCM, MC, DC, AS, WPW, NMS, HBAdditional Testing NeededEKG, Echo, Exercise Stress Testing - 64 slice CT scan? for CAA

125. Exertional Chest Pain or dyspneaCV CausesHCM, CAA, Marfan’s, TCA, MVP, MC, ARVD, AS

126. PalpitationsCV CausesWPW, LQTS, MVPNon-CV CausesHyperthyroidism, Supplements, Stimulant meds

127. MECHANISM OF SUDDEN DEATHVentricular Tachycardia and Ventricular FibrillationNormal EKGVentricular TachycardiaPolymorphic Ventricular TachycardiaVentricular Fibrillation

128. Cardiac Pathology in Athletes:Sudden Death in Young People

129. ECG Intervals

130. What do athletes die from?

131. Risk Evaluation

132. HANK GATHERS1967 - 1990

133. Hypertrophic Obstructive Cardiomyopathy

134. Hypertrophic Obstructive Cardiomyopathy

135. ECG of HOCM patient

136. Commotio CordisTraumatic 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

137. Commotio Cordis cont’dMost 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

138. Commotio Cordis

139. Commotio Cordis

140. “Pistol” Pete Maravich

141. Anatomy

142. Coronary Artery anomalies

143. Coronary Artery anomalies

144. Marfan syndrome

145. Marfan syndrome

146. Marfan syndrome

147. Marfan syndrome

148. Marfan syndrome

149. When in Rome…..Arrhythmogenic RV dysplasia (22%) is the most common cause of SCD in athletes.

150. ARVDArrhythmogenic 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.

151. ARVD cont.Global or regional right ventricular dysfunction, and late evolution to right or biventricular heart failure. Incomplete or complete RBBBInverted T waves in the anterior precordial leadsLocalized prolongation of the QRS complex in leads V1 and V2Epsilon waves visible as sharp discrete deflections at the terminal portion of the QRS complex in the anterior precordial leadsUse QRS width in Lead I which is always <120msLead III R>SS wave upstroke in V1 - V3 >55ms was found in 95 percent of ARVD********

152. Arrythmogenic Right Ventricular Cardiomyopathy

153. Arrythmogenic Right Ventricular Cardiomyopathy

154. Arrythmogenic Right Ventricular Cardiomyopathy

155. Long QT syndrome

156. 26th Bethesda Conference Guidelines for Athletic Participation