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Murmurs and the Cardiac Physical Exam Carolyn A. Altman Texas Children’s Hospital Advanced Practice Provider Conference Houston, TX April 6 , 2018

TCH APP Conference April 2019multitonal) 34 CongenitalHeartDefects Atrial&Septal&Defect& Patent&Ductus&Arteriosus& Ventricular&Septal&Defect& PulmonaryStenosis Aortic&Stenosis 35 CHD:AtrialSeptalDefect

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Murmurs  and  the Cardiac    Physical  Exam

Carolyn  A.  Altman  Texas  Children’s  Hospital  Advanced  Practice  Provider  Conference  Houston,  TX  April  6  ,  2018

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The  Cardiac  Physical  Exam

Before  applying  a  stethoscope…..  

Some  pearls  on    • General  appearance  • Physical  exam  beyond  the  heart  

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Jugular  Venous  Distention Pallor

Cyanosis

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Work  of  Breathing

Normal  infant  breathing  

Quiet  Tachypnea  

Increased  Rate,  Work  of  Breathing

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Beyond  the  Chest

Clubbing    

Observed  in  children  older  than  6  mos  with  chronic  cyanosis  

Loss  of  the  normal  angle  of  the  nail  plate  with  the  axis  of  the  finger  

Abnormal  sponginess  of  the  base  of  the  nail  bed  

Increasing  convexity  of  the  nail  

Etiology:  ?  sludging

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Chest

❖ Chest  wall  development  and  symmetry  

❖ Long  standing  cardiomegaly  can  lead  to  hemihypertrophy  and  flared  rib  edge:  Harrison’s  groove  or  sulcus    

 

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Ready  to  Examine  the  Heart

Palpation  

Auscultation  

General  overview  

Defects  

Innocent  versus  pathologic

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Cardiac  Palpation  

❖ Consistent  approach:    palm  of  your  hand,  hypothenar  eminence,  or  finger  tips  

❖ Precordium,  suprasternal  notch  

❖ PMI?  

❖ RV  impulse?  

❖ Thrills?  

❖ Heart  Sounds?

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Cardiac    Auscultation  

Where  to  listen:  

★ 4  main  positions  

★ Inching  

★ Ancillary  sites:  don’t  forget  the  head  in  infants

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Cardiac  Auscultation  

Focus  separately  on    

v Heart  sounds:    

• S2  normal  splitting  and  intensity?    

• Abnormal  sounds?  Clicks,  gallops  

v Murmurs  

v Rubs  

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Cardiac  Auscultation

Etiology  of  heart  sounds:  Aortic and pulmonic valves actually close silently

Heart sounds reflect vibrations of the cardiac structures after valve closure

Sudden deceleration of retrograde flow of the column of blood in the aorta and pulmonary artery when the elastic limits of the tensed valve leaflets are met

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Cardiac  Auscultation

S2  

❖ Physiologic  splitting  of  S2:  Increased  systemic  venous  return  and    increased  pulmonary  capacitance  during  inspiration  causes  delayed  closure  of  the  pulmonary  valve  

❖ S2  cannot  be  considered    “normal”  unless  physiologic  splitting  is  heard  

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S2:  normal  splitting Single  S2:    Pulmonar  Hypertension

Wide,  fixed  splitting:  ASD Paradoxical  Splitting  of  S2:  LBBB,  severe  LVOTO

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S2  HInts

❖ If  splitting  persists  while  patient  supine,  try  sitting  position-­‐  less  volume  in  heart  may  normalize  splitting  

❖ Listen  for  splitting  at  mid  to  ULSB  in  kids  

❖ Infants:  Mid  to  LLSB  ❖ Splitting  of  S2  if  the  HR  is  over  160  

hard  to  hear:  gently  blowing  a  breath  in  the  baby’s  face  will  slow  HR

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Cardiac  Auscultation:  S1  

❖ Physiologic  splitting  of  S1:    

❖ Can  be  heard  in  children  with  slower  heart  rates.    

❖ Varies  with  respiration  as  does  S2  

❖ Soft  S1:    low  cardiac  output,  tachycardia  

❖ Loud  S1:  hyperdynamic  (fever,  exercise),  mitral  stenosis  

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Cardiac  Auscultation  

Gallops:  S3  or  S4  

❖ Short,  low  pitched  diastolic  sounds  

❖ Abnormal  ventricular  function

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Auscultation:  S3  Gallop  

❖ Mid  way  thru  diastole    

❖ Muscle  tensing  at  end  of  rapid,  early  filling  which  occurs  with  ventricular  relaxation  

❖ Later  than  split  S2  

❖ Earlier  than  S4

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Auscultation:  S4  Gallop  

❖ If  impaired  ventricular  relaxation,  less  filling  of  the  ventricles  during    during  early  diastole  and  more  during  atrial  contraction    

❖ Hypertrophic  cardimyopathy,  eg  

❖ S4  is  thus  a  sound  generated  late  in  diastole  

❖ Very  close  to  S1,  can  mistake  for  split  S1  or  S1-­‐  ejection  click

S1-Ej click S4

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S3  and  S4  Gallops

❖ Heard  best  with  bell  since  low  pitched  

❖ Can  extinguish  the  sound  by  pressing  too  hard  (turning  bell  into  diaphragm)  

❖ Usually  heard  over  mitral  area,  if  LV  dysfunction  

❖ Listen  in  left  lateral  decubitus  position  too  

❖ If  RV  dysfunction-­‐may  hear  best  at  LLSB

S4

S3

S1-Ej click

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Other  Extra  Heart  Sounds  

❖ Ejection  Click:  opening  of  the  aortic  or  pulmonary  valve  

❖ Mid-­‐systolic  click:  MVP  

❖ Opening  snap  of  MS  

❖ Listen  for  difference  in  timing,  cadence

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How  to  Characterize  Murmurs  

❖ Timing  

❖ Site  of  maximum  intensity  

❖ Intensity  

❖ Radiation  

❖ Pitch:  

❖ Associated  findings:  clicks,  rumbles,  precordial  activity  

❖ Different  from  previous  in  your  patient  

❖ Innocent  or  pathologic

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Timing  of  Murmurs  

Systolic  ?    Diastolic?  or  Continuous  ?    

❖ Systolic  occurs  as  the  heart  contracts  

❖ Diastolic  as  the  heart  relaxes  

❖ Continuous  murmurs  continue  from  systole  into  diastole  

❖ Find  S2  and  listen  to  whether  the  murmur  comes  before  it,  after  it,  or  through  it  

❖ Inching  the  stethoscope  can  help  with  timing

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Murmurs:  Timing

Systolic  murmurs:  

❖ Regurgitant  murmurs:  Begin  with  S1  

❖ Ejection  murmurs:  Begins  shortly  after  S1  

❖ Mid-­‐systolic:  MVP

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Regurgitant  Systolic  Murmurs

❖MR,  TR,  VSD  

❖Begin  with  S1:  “coincident  with  S1”  

❖Often  holosystolic

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Systolic  Ejection  Murmurs

❖AS/PS,  Still’s,  pulmonary  flow  

❖Begin  after  valve  opens,  so  hear  S1  then  murmur  

❖ Should  be  able  to  hear  S2  distinctly  

❖ Early  systolic  ejection  click  if  semilunar  valve  stenosis

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Mid  Systolic  Murmurs

❖Mitral  valve  prolapse  

❖Click  ushers  in  murmur

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Diastolic  murmurs

Aortic  or  pulmonary  regurgitation:  

❖High  pitched  

❖Decrescendo

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Diastolic  murmurs

Diastolic  rumbles:  

❖ Increased  volume  across  MV  or  TV  

❖ Low  pitched  filling  noise  

❖ Absence  of  silence

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Continuous  Murmurs

❖ Start  during  systole,  continue  past  S2  

❖ Louder  in  systole:  PDA,  AVM,  shunts  

❖ Louder  in  diastole:  venous  hums,  coronary  fistula

PDA Coronary fistula AVM

Venous Hum

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Murmurs  by  location  of  greatest  intensity:

Helpful  in  figuring  out  what  is  generating  the  murmur  

❖ URSB:  Aortic  stenosis  ❖ ULSB:  Pulmonary  

stenosis,  pulmonary  flow,  ASD  

❖ LLSB:  VSD,  Still’s,  TR  ❖ Apical:  Mitral

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Characterize  Murmurs:

Grading  system  allows  accurate  communication  between  caretakers  

❖ Grade  I:  is  there  something  there?    ❖ Grade  II:  Ok,  I  can  hear  it  ❖ Grade  III:  Boy,  that’s  loud  ❖ Grade  IV:  Associated  with  a  thrill,  knock  your  socks  

off  loud  ❖ Grade  V:  Audible  with  scope  off  chest  ❖ Grade  VI:  Audible  without  stethoscope

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Characterize  Murmurs:

Important  to  follow  trends:    ❖ Is  an  aorto-­‐pulmonary  shunt  murmur  getting  softer?  

A  shunt  may  be  getting    obstructed,  outgrown,  or  PVR  elevated  

❖ Is  the  outflow  tract  obstruction  getting  worse  in  a  patient  with  new  chest  pain?      

❖ Is  the  patient  with  TOF  spelling  or  just  colicky:  the  outflow  murmur  will  get  softer  during  a  spell  as  less  flow  traverses  the  RVOT

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Characterize  Murmurs  by  Pitch:

❖ High  

❖ Low  

❖ Harsh  (multitonal)

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Congenital  Heart  Defects

❖ Atrial  Septal  Defect  ❖ Patent  Ductus  Arteriosus  ❖ Ventricular  Septal  Defect  ❖ Pulmonary  Stenosis  ❖ Aortic  Stenosis

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CHD:  Atrial  Septal  Defect

❖ Anatomy:  described  by  location  in  the  septum  Secundum  Primum  Coronary  Sinus  Sinus  Venosus  

❖ Physiology  and  physical  signs  the  same,  regardless  of  location  of  ASD

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CHD:  Atrial  Septal  Defect  

Physiology:  Amount  of  shunting  depends  on    

v Size  of  defect  v Differences  in  compliance  between  RV  

and  LV-­‐  flow  is  usually  left  to  right

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CHD:  Atrial  Septal  Defect

Palpation:  right  ventricular    impulse  from  increased  RV  volume

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CHD:  Atrial  Septal  Defect  

❖ Widely  split  S2:    v Persistent  separation  

of  A2P2  components  of  S2  throughout  respiratory  cycle  

v Increased  pulmonary  capacitance  or    

v Reciprocal  changes  in  flow  into  the  right  atrium  from  the  defect  or  systemic  veins

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CHD:  Atrial  Septal  Defect

❖ Pulmonary  flow  murmur:    v Large  volume  of  blood  crossing  the  

pulmonary  valve  v ULSB  to  back  v Ejection  v Medium  pitched

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CHD:  Atrial  Septal  Defect  

Diastolic  Rumble:    Consistent  with  at  least  2:1  Qp:Qs  Low  pitched  Listen  with  bell  at  LLSB

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CHD:  Patent  Ductus  Arteriosus  

Physiology:    v In  the  setting  of  low  

pulmonary  vascular  resistance,  flow  is  continuous,  left  to  right    

v If  large  PDA,  PA  pressures  may  be  high:  flow  can  be    

•Left  to  right  •Bidirectional  •All  right  to  left

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CHD:  Patent  Ductus  Arteriosus

Palpation  ❖ RV  impulse  if  pulmonary  hypertension  ❖ Hyperactive  LV  impulse  if  large  volume  

of  flow  PDA

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CHD:  PDA  Murmur

v Continuous  if  low  pulmonary  vascular  resistance  

v Machinery  like  v Accentuated  at  end  systole  v Left  infra-­‐clavicular  area,  back,  and  left  

supraclavicular  areas

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CHD:  Ventricular  Septal  Defect  

Anatomy  described  by  location    Perimembranous  Inlet  Muscular  Doubly  committed-­‐

juxtarterial

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CHD:  VSD

Physiology:  amount  of  shunting  depends  on    

❖ Size  of  defect  

❖ Pulmonary  resistance:  more  shunting  with  decreasing  resistance

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CHD:  VSD

Palpation:    ❖ Quiet  precordium?    ❖ RV  impulse  may  be  present  with  volume  or  pressure  loading  

❖ +/-­‐  thrill:  cannot  determine  size  by  presence  of  thrill

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CHD:  VSD

S2 in VSDs can be ❖ Normally split (typical) ❖ Widely split if very generous amount of flow crossing to fill RV ❖ Single: if pulmonary hypertension with elevated resistance

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CHD:  VSD  Auscultation

Murmur  ❖ Usually  along  LSB  ❖ Very  small  defects  do  not  radiate  ❖ Subpulmonary  VSDs  follow  the  RV    

outflow  to  the  pulmonary  arteries  ❖ “Blowing”  quality  ❖ Start  with  S1

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CHD:  VSD  murmurs  

Holosystolic  murmur:    ❖ Starts  with  S1  

(obscured)    ❖ Ends  with  P2,  S2  split  

normally  ❖ Plateau  shape  ❖ The  smaller  the  defect,  

the  more  high  pitched

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CHD:  VSD  murmur

Short  systolic  murmur  consistent  with  very  small  defect  v Starts  with  S1      v Ends  before  S2,  as  defect  closed  by  ventricular  

contraction  v Usually  very  localized,  may  only  hear  in  certain  

positions

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CHD:  VSD

Mitral    Rumble    

vIndicates  at    

       least  2:1  Qp:Qs    

vLow  pitched  

vUse  bell  at  apex  

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CHD:  VSD

Diastolic  rumble      

Can  be  quite  subtle  

Listen  for  absence  of  diastolic  silence  

Compare  right  and  lef  chest

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CHD:  VSD

Very  Large  VSDs          

vAllow  high  pressure  and  high  flow  

v  If  lef  unrepaired:  elevated  PVR  develops,    

         eventually  Eisenmenger  syndrome  

Palpahon  

v  RV  impulse  

v  Palpable  S2  

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CHD:  VSD  

Large  VSDs:  

Systolic  Murmur      

vCan  be  holosystolic,  if    any  pressure  restrichon  

v  If  no  pressure  restrichon,  may  be  no  murmur,  or  a  pulmonary  ouilow  murmur

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CHD:  VSD

 Eisenmenger’s  

v  S2  loud  and  single  

v  Pulmonary  valve  click:  dilated  pulmonary  root  

v  Graham-­‐Steele  murmur:  pulmonary  insufficiency

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CHD:  Tetralogy  of  Fallot  

Physiology:  

v  Balance  between  VSD  flow  and  pulmonary  valve  and  sub  valve    stenosis  

v  “Pink”  tets  have  little  pulmonary  stenosis  

v  Other  extreme:  pulmonary  atresia  with  VSD  

v  PS  typically  progresses  over  time

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CHD:  TOF  

 Palpahon:  

v  RV  impulse  

v  Possible  thrill

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CHD:  TOF  

Systolic  Murmur:  reflects  PS,  not  VSD    

v  MLSB  to  ULSB  to  back  

v  Starts  with  S1,  given  subvalvar  component  

v  As  subps  worsens,  murmur  decreases  in  intensity:  pop-­‐off  through  VSD  to  systemic  circulahon  

v  Listen  for  murmur  to  decrease  in    hypercyanohc  spell

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CHD:  TOF

❖    Systolic  Murmur:  reflects  PS,  not  VSD

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CHD:  TOF  post  repair  

To  and  fro  murmur  ❖ PS/PI    ❖ The  murmur  does  

not  carry  through  S2-­‐not  continuous,  not  the  diastolic  component  

❖ The  diastolic  murmur  is  of  a  different  pitch

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CHD:  Pulmonary  Valve  Stenosis  

❖ Anatomy:  thickened,  possibly  dysplashc  valve  with  limited  systolic  excursion  

❖  Physiology:  usually  slowly  progressive  obstruchon

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CHD:  Pulmonary  Valve  Stenosis

Palpahon:    

v  RV  impulse:  more  than  mild  obstruchon  

v  Thrill  indicates  more  severe  obstruchon  

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CHD:  Pulmonary  Valve  Stenosis  

 Systolic  Ejechon  Click:  

v  Either  at  ULSB,  or  upstream  from  valve  at  LLSB  

v  Increases  in  intensity  with  expirahon  

v  Moves  closer  to  S1  with  increasing  PS

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CHD:  Pulmonary  Valve  Stenosis

Systolic  Murmur:  

v  Louder,  longer,  and  later  peaking  with  increasing  stenosis  

v  ULSB  radiahng  to  back,  axilla  

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CHD:  Aortic  Valve  Stenosis  

Anatomy:    

 Thickened  valve  with  decreased  excursion  

 Ofen  bicommissural    

Physiology:  

Obstruchon  can  be  rapidly  progressive,  parhcularly  in  infants  

 Exercise  increases  the  relahve  stenosis

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CHD:  Aortic  Valve  Stenosis  

Palpahon:    

v  Increased  LV  impulse  with  significant  obstruchon  

v  Thrills  frequently  presents  

vDo  NOT  reflect  severity  

vCan  be  along  LVOT,  ULSB,  carohds,    suprasternal  notch

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CHD:  Aortic  Valve  Stenosis  

 Ejechon  click:  vOpening  of  non-­‐compliant  valve  

v  Moves  earlier  in  systole  with  increasing  severity  of  obstruchon,  may  become  inaudible  

v  Heard  at  apex  (upstream)  or  URSB  (downstream)

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CHD:  Aortic  Valve  Stenosis

 Murmur:  

v  With  increasing  stenosis  and  normal  cardiac  output,    murmur  becomes  louder,  longer,  later  peaking    

vMay  not  have  significant  murmur  if  poor  funchon  (neonatal  AS)  

v  Heard  at  apex  (upstream)  or  URSB  (downstream)

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Innocent  Murmurs:

❖ Learn  to  recognize  the  three  most  common  innocent  murmurs  of  childhood:  ❖  Venous  hums,  ❖  Still’s  murmurs  ❖  Physiologic  pulmonary  branch  stenosis  

in  infancy  

❖ Anything  else  is  not  likely  to  be  normal!

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Innocent  Murmurs:  Still’s

 Shll’s:  most  common               innocent  murmur    

❖  I-­‐III/VI  SEM  

❖  Sofer  with    standing     or  sinng  

❖  Vibratory,  twanging  

❖  Low  pitched,  best    heard  with  bell

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Still’s  murmur  versus  subaortic  stenosis

Subaortic  stenosis  can  mimic  Still’s:  both  can  be  musical

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Still’s  murmur  versus  Subaortic  Stenosis  

❖ Use  positional  changes  to  help  distinguish  subAS  from  Still’s  

❖ Dynamic  obstruction  in  HCM  accentuated  with  decrease  in  filling:  murmur  gets  louder  with  stand  

❖ Discrete  sub  AS  will  not  usually  get  louder,  but  will  also  not  diminish  with  stand

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Innocent  Murmur:  Venous  Hum  

 Venous  Hum:  innocent  continuous  murmur  

❖ Turbulent  flow  merging    from  internal  jugular  and  subclavian  veins  into  SVC    

❖ Louder  in  diastole    

❖ Disappear  when  patient  lies  supine  or  turns  head  

❖ Audible  along  infraclavicular  area,  and  low  anterior  neck  (not  the  head)    

❖ I-­‐III/VI

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Innocent  Murmur:  Venous  Hum

Continuous  murmur:  whining,  roaring,  whirring,  waterfall

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Venous  Hum  versus  Pathologic  Continuous  Murmurs

❖ PDA  

❖ Coronary  fistula  

❖ Cranial  AVM  

❖ AO-­‐PA  shunt

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Innocent  Murmur:  Peripheral  Pulmonary  Stenosis  

❖ PPS  in  infant  under  6  mos:  same  pitch  as  respirations  

❖ As  loud  or  loudest  in  back  or  axilla  

❖ Systolic,  high  pitched,  blowing  

❖ Relatively  small  branch  Pas  arising  at  acute  angle  from  large  MPA

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PPS  versus  Pathologic  Murmurs  

PPS-­‐distinguish  from      

❖ Tiny  VSD:  better  heard  at  mid  to  LLSB,  not  back/axilla  

❖ PS:  has  a  click  

❖ ASD:  Has  abnl  S2

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Position  Changes

❖ Distinguish  innocent  Still’s  murmurs  from  LVOTO  ❖ Detect  gallops:  apex,  left  lateral  decubitus  ❖ Distinguish  venous  hums  from  non-­‐innocent  

continuous  murmurs  ❖ Mitral  valve  prolapse

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Mitral  Valve  Prolapse  

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Auscultation  

Artificial  valves:  should  be  audible  without  a  stethoscope  

★ Artificial  aortic  valves  should  have  a  mechanical  S2  

★ Artificial  mitral  valves  should  have  a  mechanical  S1  

★ Worry  if  it  goes  away-­‐valve  thrombosis

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Tips  for  better  exams

❖ Quiet  room    ❖ Recognize  that  naptime,  stranger  anxiety,  hunger  

can  adversely  affect  the  situation  ❖ Make  the  child  as  comfortable  as  possible:    ❖ Silent  distracters  to  entertain  the  child-­‐flashlight,  ID  

badge,  toys,  siblings

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Tips  for  Better  Exams

★ Tiny  bodies:    Use  the  right  size  stethoscope  to  minimize  ambient  noise  and  to  accurately  determine  the  presence  and  location  of  a  murmur  

★ Change  the  order  of  the  exam  to  fit  the  child  ★ Warm  hands  and  scopes  

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★ Remember-­‐    

★ Always  not  normal:  RV  impulse,  thrills,  apical  murmurs,  murmurs  that  increase  with  sitting  or  standing,  murmurs  with  extra  heart  sounds,  diastolic  murmurs  

★ Need  to  have  a  normally  split  S2  to  be  normal  

★ If  it  does  not  sound  innocent-­‐  needs  further  evaluation  

★ Thank  you.