Pediatric CVS

PHYSIOLOGY Exam Exam No. 3 No. Lecture No. __| Pediatric CVSCVS PHYSIOLOGY 3 Lecture No. | Pediatric

     

UERMMMCI  College  of  Medicine   Subject:   PHYSIOLOGY   Date:     (Thursday)  September  25,  2014   Title:     (3._)  Pediatric  CVS   Lecturer:     Dr.  Cacas   Batch/section:       2018A   Sem/  A.Y.:     1st/A.Y.  2014-­‐2015   Transcribers:  Empamano,  D.,  Encarnacion,  R.,  Erlano,  J.,  Esperanza,  R.,  Hernandez,  E.   Trans  Subject  head:  Falloria,  K.     Outline   SV   Stroke  Volume     CHD   Congenital  Heart   I. Fetal  Circulation     Disease/Disorder   A. Fetal  Blood  Flow  Patterns     COA   Coarctation  of  Aorta   B. Fetal  Cardiac  Output   CHF   Congestive  Heart  Failure   i. Dimensions  of  Cardiac  Chambers     C. Fetal  Vascular  Pressure     Fetal  Circulation   D. Fetal  Pulmonary  Vascular  Resistance       II. Transitional  Circulation     Parts  No  Longer  Present  Upon  Childbirth:     A. Removal  of  Placenta     1. Umbilical  Cord  –  attached  to  the  placenta,  comprised   B. Lung  Expansion     of  3  vessels  (2  arteries  and  1  oxygen-­‐rich  vein)     III. Neonatal  Circulation     ! If  upon  inspection  only  a  single  artery  is  present,  it   A. Difference:  Neonatal  and  Fetal  Circulation     may  be  a  prognosis  for  presence  of  a  kidney   B. Circulatory  Adaptations     problem.   C. Pulmonary  Vascular  Resistance     2. Ductus  Venosus  –  shunts/directs  the  fetal  blood   D. Fetal  and  Neonatal  Development     coming  from  the  placenta  to  the  right  side  of  heart   IV. Congenital  Heart  Disorder     (specifically  blood  coming  from  left  umbilical  vein  to   V. Suspecting  a  Heart  Problem  in  an  Infant     inferior  vena  cava  (IVC))   A. Causes     ! Closes  eventually;  its  closure  is  a  result  of  the   B. Basic  Tools  and  Lab  Exams     eventual  lack  of  blood  return  from  placenta   VI. Pediatric  ECG   3. Foramen  Ovale  –  shunts/directs  blood  from  (right     atrium)  RA  to  (left  atrium)  LA   Objectives   ! Located  within  interatrial  wall     4. Ductus  Arteriosus  –  shunts/directs  blood  from  PA  to   1. Discuss  and  compare  fetal  from  neonatal  circulation.     aorta   2. Identify  the  changes  in  the  circulation  of  blood  after     birth.     Shunts  acts  to  detour  blood  and  hence  is  not  a  usual  route.   3. Discuss  some  conditions  associating  with  unsuccessful   Its  ability  to  redirect  blood  flow  is  due  to  less   extrauterine  transition.     resistance/pressure.  Ductus  Venosus,  Foramen  Ovale,  and   4. Give  pointers  on  the  differences  between  fetal  and   Ductus  Arteriosus  are  the  three  main  shunts  used  by  in   adult  ECG   fetal  circulation.  Although  note  that  the  latter  2  are     considered  the  main  shunts.     Acronyms  Used  in  the  Trans        A.  Fetal  Blood  Flow  Patterns     !!!BEFORE  ANYTHING  ELSE!!!     RA     Right  Atrium   RV   PA   SVC   CVO   HR     LA   LV   PV   IVC   CO  

Right  Ventricle   Pulmonary  Artery   Superior  Vena  Cava   Combined  Ventricular  Output   Heart  Rate   Left  Atrium   Left  Ventricle   Pulmonary  Vein   Inferior  Vena  Cava   Cardiac  Output  

Empamano | Encarnacion | Erlano | Esperanza | Hernandez A.Y. 2014-2015

Page 1 of 10 Physiology | Pediatric CVS

PHYSIOLOGY 3.XX: Pediatric CVS  

 

-

  Figure  1.  Fetal  Circulation     NOTE:  Adults  have  a  system  in  series;  Neonates  have   shunts  allowing  unequal  parallel  circulation     Features  of  Fetal  Circulation:     1. Has  shunts     a. Placenta   b. Ductus  Venosus     c. Foramen  Ovale   d. Ductus  Arteriousus     2. Has  low  Pulmonary  blood  Flow     a. Despite  RV  resistance     b. Diverted  to  Patent  Ductus  Arteriousus   c. Nutritional  requirement  for  lungs  to  develop     *     Components  of  the  Fetal  Blood  Flow  Patterns   *Scheme  of  Fetal  Circulation  at  the  end  of  trans      1.  Placenta     - A  complete  but  a  temporary  organ  as  it  only  persists   until  about  42  weeks;  beyond  that  it  disintegrates   - Structure:  has  separate  maternal  and  fetal  capillary   unit;  hence  no  direct  mixture  of  blood  in  womb  occurs   (which  is  good  due  to  immunological  reasons)   - Organ  with  the  lowest  vascular  resistance  in  hence   promotes  flow     - Site  of  exchange  of  everything  (nutrients,  gas,  waste)     o Exchange  occurs  via  perfusion,  the  process  of   delivering  blood  to  a  capillary  bed  of  biological   tissue   o As  it  is  the  site  of  gas  exchange,  it  acts  as  the   fetal  lung   - Receives  the  largest  amount  of  combined  ventricular   output  (CVO)  or  blood  that  comes  from  both  RV  and   LV  (55%)     o Aorta  receives  blood  coming  from  LV  (since  the   blood  normally  goes  to  aorta  after  LV)  and   2018-A

 

from  RV  (since  the  blood  from  PA  is  shunted  to   aorta  via  ductus  arteriosus)   o Blood  from  aorta  then  enters  the  placenta   Needs  to  be  checked  for  any  abnormalities  (esp.   perfusion  abnormalities)  upon  delivery  of  child   o Adult  Circulation:     Deoxygenated  blood  via  superior  vena  cava   (SVC)  and  IVC  !  RA  !  RV!  PA!  lungs  for   oxygenation  !  oxygenated  blood  via  PV  !  LA   !  LV!  Aorta  !  the  rest  of  the  body   o Fetal  Circulation:     " CVO:   1. ~65%  carried  over  and  brought   back  to  the  placenta  for  re-­‐ oxygenation     2. Rest  are  utilized  by  the  body  of  the   fetus  (perfuse  fetal  organs  and   tissues)  

  2.  Ductus  Venosus     -­‐ Shunts  oxygenated  blood  from  left  umbilical  vein  to   inferior  vena  cava   o Oxygenated  blood  has  the  highest  PO2  of  32   mmHg   -­‐ Pathway  of  blood  coming  from  umbilical  vein   o 50%  goes  to  hepatic  circulation  and  then  to  IVC   o 50%  shunted  to  IVC  via  ductus  venous,   bypassing  the  liver   o At  IVC,  blood  shunted  by  ductus  venosus   partially  mixes  with  the  blood  from  IVC  return   (which  includes  50%  of  the  blood  that  came  to   umbilical  vein  and  went  to  hepatic  circulation).     Blood  in  the  IVC  then  enters  RA.     3.  IVC     -­‐ Drains  blood  from  the  lower  part  of  the  body  so  that   the  deoxygenated  blood  may  eventually  be  returned   to  the  placenta  for  reoxygenation   -­‐ Also  receives  blood  shunted  via  ductus  venosus   -­‐ Oxygen  saturation  in  IVC  is  high  because  blood  in   here  is  a  mixture  of  deoxygenated  IVC  return  and   shunted  oxygenated  blood   -­‐ Blood  from  IVC  enters  RA.  From  RA,  blood  is  either   shunted  to  LA  via  foramen  ovale  or  goes  to  RV  via   tricuspid  valve.   o From  LA,  blood  goes  to  LV  then  to  ascending   aorta.  From  ascending  aorta,  blood  will  perfuse   the  upper  part  of  the  body.   o From  RV,  blood  goes  to  PA     4.  SVC     -­‐ Drains  blood  from  upper  part  of  the  body,  including   the  brain  (contributes  to  15%  of  CVO)     o Blood  drained  by  the  SVC  has  lesser  oxygenation   than  the  IVC  return   -­‐ Blood  from  SVC  enters  RA.  From  RA,  blood  enter  RV   through  tricuspid  valve.  From  RV  to  PA.   o From  PA  only  8-­‐10%  flows  through  the  lungs   for  nourishment  of  the  organ.  

EMPAMANO, ENCARNACION, ERLANO, ESPERANZA, HERNANDEZ

2OF10

PHYSIOLOGY 3.XX: Pediatric CVS  

  o

o

The  rest  of  the  blood  from  PA  is  shunted  to   descending  aorta.   " Shunting  is  due  to  high  intrapulmonary   pressure  in  lungs.  The  pressure  is   brought  about  by  the  lungs  being  filled   with  fluids  and  that  in-­‐utero,  the  fetus   does  not  have  to  breathe  in  gas  and  use   the  lungs.   There  is  lesser  blood  flow  in  the  PA  since  in   fetal  circulation,  it  is  constricted  and  has  high   vascular  resistance.  

  5.  Brain  and  Coronary  Circulation     -­‐ Receives  blood  with  highest  oxygen  saturation  (PO2  of   28  mmHg)   o Perfused  mostly  by  the  blood  that  passes   through  the  LV  (REMEMBER!  LV  output   exclusively  supplies  the  upper  part  of  the   body.)   o REMEMBER!  Blood  that  supplies  the  lower  half   of  the  body  comes  from  the  RV  output,  which  is   less  oxygenated  (PO2  of  24  mmHg),  hence  the   lower  half  of  the  body  receives  less  oxygenated   blood.     *The  blood  from  the  LV  output  comes  from  the  IVC  mixed   blood.     # 1/3  of  IVC  blood  is  directed  by  the  crista  dividens   to  pass  through  the  foramen  ovale  and  to  LA   # 2/3  of  IVC  enters  the  RV  and  then  PA   *Since  blood  is  oxygenated  in  the  placenta,  there  is  higher   oxygen  saturation  in  the  IVC  (70%)  than  in  the  SVC  (40%).     B.  Fetal  Cardiac  Output       • Fetal  cardiac  output  (CO)  highly  depends  on  HR;  when   HR  drops,  as  in  fetal  distress,  CO  falls     o Unlike  adult  heart,  fetal  heart  is  unable  to   increase  stroke  volume  (SV)  when  heart  rate   (HR)  falls  due  to  still  unclear  reasons   o Adult  CO  =  HR  x  SV  (contractility  +  relaxation  of   heart)     • Fetal  CO  is  a  result  of  CVO   o Fetal  CO=    ~450  ml/kg/min   o Fetal  CO  can  only  be  spoken  of  in  terms  of  the   total  output  of  both  ventricles—CVO—since  RV   output  is  not  equal  to  LV  output,  unlike  that  of   adult  circulation.   • RV  is  more  active  than  LV  in  fetus.   o Fetal  RV  output  is  1.3x  LV  output.     o RV  is  pumping  against  systemic  blood  pressure,   thus  performing  greater  volume  of  work  than  the   LV.   o Results  in  RV  Dominance,  right  axis  deviation  (in   ECG)  and  better  developed  musculature     o Reflected  in  newborn  ECG;  showing  greater  RV   force  than  the  adult     2018-A

 

CVO  Influences  Dimensions  of  Cardiac  Chambers   • Proportions  of  CVO  is  reflected  in  the  relative   dimensions  of  the  chambers  and  vessels     • Branches  of  the  PA  are  expected  to  be  small  since  the   lungs  receive  only  15%  of  CVO     • In-­‐utero,  RV  handles  55%  of  CVO  while  LV  handles   45%.  Since,  output  is  about  the  same,  RV  and  LV  have   identical  sizes.   • Also  due  to  foramen  ovale,  pressure  in  RA  is  identical   with  that  of  LA.   • Due  to  closure  of  foramen  ovale  in  adults,  LV   performs  more  than  RV.    LV  is  hence  bigger  than  RV   in  dimensions.       C.    Fetal  Vascular  Pressure       • RA  and  LA  pressure  are  equal  due  to  a  big  opening,   foramen  ovale.     • Afterload  of  fetal  ventricles:     o RV:  Low  compared  to  LV  because  it  ejects  mostly   into  the  low  resistance  umbilical-­‐placental   circulation     o LV:  High  compared  to  RV  because  it  ejects  into   the  high  resistance  upper  body  circulation       D.    Fetal  Vascular  Pressure       Fetus  vs.  Late  Gestation   In  the  Fetus     • Resistance  of  pulmonary  vessels  is  high  in  utero  but   decreases  progressively  until  term   • PA  is  constricted,  anatomically  thicker  tunica  media,   (medial  smooth  muscle  is  exaggerated  in  smaller   arteries)   o Smooth  muscles  constrict  the  vessels  causing   resistance  in  blood  flow.   Late  Gestation     • Only  50%  of  PAs  associated  with  respiratory   bronchioles  are  mascularized     • PAs  within  the  alveolar  wall  are  not  mascularized     • Contain  pericytes  and  intermediate  cells       Factors  That  Regulate  The  Tone  of  Fetal  Pulmonary   Circulation     1. Mechanical  effects  –  mechanical  compression  of   alveoli  that  also  compresses  blood  vessel  causing   increase  blood  vessel  resistance     2. Distension  of  the  lungs     3. Oxygenated  state  –  oxygen  is  a  potent  vasodilator     4. Vasoactive  substances     Table  X.  Vasomotor  Mechanism   Cause  Vasoconstriction   Cause  Vasodilation   • Physical   • NO   • Decrease  O2   • Increase  O2   • Leukotrienes   • PGI2   • Thromboxane  A2   • PGD2  

EMPAMANO, ENCARNACION, ERLANO, ESPERANZA, HERNANDEZ

3OF10

PHYSIOLOGY 3.XX: Pediatric CVS  

  • • •

Endothelin  A  activation   • Platelet  derived  growth   factor  (PDGF)   Platelet  activating   factor  (PAF)   AA  metabolites  

ET  B  activation  

3. 4.

•   Conditions  That  Can  Cause  Medial  Thickening   -­‐ Or  increase  pulmonary  vascular  resistance       1. Fetal  hypoxemia     2. Hypertension  (Pulmonary  HPN  add  pressure)     3. Altered  fetal  blood  flow   4. NSAID  treatment  of  mother       In  conditions  like  hypoxia  or  HPN  that  will  limit  blood   flow,  altered  fetal  blood  flow  will  cause  intermediate  cells   or  pericytes  to  transform  into  smooth  muscle.  Tunica   media  will  thicken  and  compromise  the  lumen  of  blood   vessel  in  that  the  radius  of  the  vessel  changes  to  add   resistance.     Persistent  Fetal  Circulation   $ The  developed  tunica  media  of  fetal  blood  vessels  may   cause  persistent  fetal  circulation     o Persistent  fetal  circulation  –  blood  is  still  shunted   from  PA  to  descending  aorta  via  the  ductus   arteriousus  thus  diminishing  blood  flow  to  the   lungs.  There  is  less  supply  of  O2.     Transitional  Circulation     • Pertains  to  changes  in  circulation  after  birth       • Period  of  adjustment  and  preparation  for  shifting  from   fetal  to  neonatal       • Primary  changes:     o Shift  of  blood  flow  for  gas  exchange  from   placenta  to  the  lungs     o Placental  circulation  disappears  and  brief   hypoxia  occurs  due  to  severing  of  the  umbilical   chord   o Establishment  of  Pulmonary  (Series)  Circulation         A.  Effects  of  Removal  of  Placenta       1. Increase  in  systemic  vascular  resistance     o Result  of  removal  of  very  low  resistance   placenta  (shunt  1)   o Slows  heart  rate,  and  Increases  in  pressure  of   aorta,  LA  and  LV   2. Closure  of  ductus  venosus  (shunt  2)  –  due  to  cessation   of  flow  to  umbilical  vein  and  lack  of  blood  return  to   placenta     B.  Effects  of  Lung  Expansion       1. LA  pressure  increases  due  to  increased  PV  return  to  the   LA     2018-A

 

2.

5.

6. 7. 8.

Functional  closure  of  foramen  ovale  due  to  increased   pressure  in  the  LA  in  excess  of  RA  pressure     RA  pressure  falls  due  to  closure  of  ductus  venosus     Closure  of  ductus  arteriosus  due  to  increase  LA   pressure  and  decrease  RA  pressure     o Also  a  result  of  increased  arterial  O2  saturation     o Rise  in  level  of  O2  becomes  stimuli  for  ductus   arteriosus  to  constrict  and  obliterate  (lumen   disappears  and  blood  cannot  flow)     Reduction  of  pulmonary  vascular  resistance  in  lungs     o Dilation/Non-­‐constriction  of  intrapulmonary   arteries  due  to  amniotic  fluid  decreases   pulmonary  vascular  resistance       o Pulmonary  blood  flow  increases  due  to  decrease   in  pulmonary  vascular  resistance  in  lungs     LV  is  now  responsible  for  delivering  blood  into  the   entire  systemic  circulation  due  to  closure  of  ductus   arteriosus  causing  greater  work  for  LV     Systemic  CO  increases  to  almost  200%  (~350   mL/kg/min)  since  LV  now  deliver  the  entire  systemic   CO   Marked  increase  in  LV  performance  achieved  through  a   combination  of  hormonal  and  metabolic  signals   o Increase  in  level  of  circulation  of  catecholamine   and  myocardial  receptors  (β-­‐adrenergic)   through  which  catecholamine  have  their  effect  →   becomes  the  dominant  ventricle  →  rise  in  LV   afterload      

  Neonatal  Circulation     • At  birth,  fetal  circulation  must  immediately  adapt  to   extrauterine  life  as  gas  exchange  is  transferred  from   the  placenta  to  the  lung   • Heart  rate  slows  as  a  result  of  a  baroreceptor   response  to  an  increase  in  systemic  vascular   resistance  when  the  placental  circulation  is   eliminated     A.  Significant  Differences  between  Neonatal   Circulation  and  that  of  Older  Infants     1. Right-­‐to-­‐left  or  left-­‐to-­‐right  shunting  may  persist   across  the  patent  foramen  ovale   2. In  the  presence  of  cardiopulmonary  disease,   continued  patency  of  the  ductus  arteriosus  may  allow   left-­‐to-­‐right,  right-­‐to-­‐left,  or  bidirectional  shunting   3. Neonatal  pulmonary  vasculature  constricts  more   vigorously  in  response  to  hypoxemia,  hypercapnia,   and  acidosis   4. Wall  thickness  and  muscle  mass  of  the  neonatal  left   and  right  ventricles  are  almost  equal   5. Newborn  infants  at  rest  have  relatively  high  oxygen   consumption,  which  is  associated  with  relatively  high   cardiac  output     At  birth:   • Decreased  pulmonary  vascular  resistance  

EMPAMANO, ENCARNACION, ERLANO, ESPERANZA, HERNANDEZ

4OF10

PHYSIOLOGY 3.XX: Pediatric CVS  

  Due  to  onset  of  ventilation  !  introduction  of   oxygen  into  the  lungs   o Decrease  in  pulmonary  hypoxic  vasoconstriction   o Decrease  in  pulmonary  arterial  pressure   Increased  total  systemic  vascular  resistance   o Due  to  interrupted  flow  to  the  placenta   o

•

  Newborn  Cardiac  Output   • About  350mL/kg/min   • Falls  in  the  first  2  months  of  life  to  about   150mL/kg/min   • More  gradually  to  the  normal  adult  cardiac  output  of   about  75mL/kg/min   • High  percentage  of  fetal  hemoglobin  present  in  the   newborn  may  actually  interfere  with  delivery  of   oxygen  to  tissues  in  the  neonate,  so  increased  cardiac   output  is  needed  for  adequate  delivery  of  oxygen               Congenital  Heart  Disorder/Disease  (CHD)     -­‐ A  heart  related  problem  that  is  present  since  birth  and   often  as  the  heart  is  forming  even  before  birth   -­‐ Causes   a. Genetic  factors   b. Environmental  factors  (eg.  viruses,  certain  drugs,   radiation,  living  in  high  altitudes)   c. Rubella  (German  Measles)   o Contracting  rubella  during  the  first  3  months   of  pregnancy  has  a  high  risk  of  having  a  baby   with  a  heart  defect   d. Medications   e. Alcohol     o Drinking  alcohol  during  pregnancy  can  increase   the  risk  of  heart  defects  and  possibly  cause  fetal   alcohol  syndrome  (FAS)   f. Cocoaine   o Use  of  cocaine  during  pregnancy  increases  the  risk   of  birth  defects   g. Chromosomal  defects   o Certain  chromosomal  defects  such  as  Down   Syndrome  are  associated  with  CHD     Suspecting  a  Heart  Problem  in  an  Infant     Tools  and  Laboratory  Exams  in  Evaluating  Heart   Disorders   1. History/  Physical  Exam   2. Chest  X-­‐ray   3. 15  leads  ECG   4. Arterial  Blood  Gas     A.  Inspection   Note  the  child’s:   2018-A

 

• • • • • • •

General  appearance  and  nutritional  state   Any  obvious  syndrome  or  chromosomal  abnormality   Color  (i.e.,  cyanosis,  pallor,  jaundice)   Clubbing   Respiratory  rate,  dyspnea,  and  retraction   Sweat  on  forehead   Chest  inspection  

  Check  whether:   • In  distress   • Well-­‐nourished  or  undernourished   • Happy  or  cranky   • Obese     B.  Palpation   • Peripheral  pulses   • Precordium     Peripheral  Pulses   1. Count  the  pulse  rate  and  note  any  irregularities  in  the   rate  and  volume   • Normal  pulse  rate  varies  with  patient’s  age  and   status  (younger  the  patient,  faster  the  heart   rate)   • Increase  pulse  rate  may  indicate  excitement,   ever,  CH,  or  arrhythmia   o Bradychardia  may  mean  heart  block,   digitalis  toxicity,  etc.   o Irregularity  of  pulse  suggests   arrhythmias,  but  sinus  arrhythmia  is   normal   2. The  right  and  left  arm  and  an  arm  and  a  leg  should  be   compared  for  the  volume  of  the  pulse   • If  a  good  pedal  pulse  is  felt,  coarctation  of  the   aorta  (COA)  is  effectively  ruled  out  especially  if   blood  pressure  is  normal   • Weak  leg  pulses  and  strong  arm  pulse  suggest   COA   3. Bounding  pulses   • Aortic  run-­‐off  lesions  such  as  PDA,  aortic   regurgitation  (AR),  large  systemic   arteriovenous  fistula,  or  persistent  truncus   arteriosus  (rare)   • May  be  observed  in  premature  infants  due  to   lack  of  subcutaneous  tissue  and  because  many   have  PDA   4. Weak,  thread  pulses   • May  indicate  cardiac  failure  or  circulatory   shock   • In  leg  of  a  patient  with  COA   • Arterial  injuries  from  previous  cardiac   catheterization  may  cause  weak  pulse  in   affected  limb     Chest   1. Apical  Impulse   • Location  and  diffuseness  should  be  noted   • Percussion  in  infants  and  children  is  inaccurate   EMPAMANO, ENCARNACION, ERLANO, ESPERANZA, HERNANDEZ 5OF10

PHYSIOLOGY 3.XX: Pediatric CVS  

  Normally  at  the  5th  intercostal  space  in  the   midclavicular  line  after  age  7   • Before  age  7,  it  is  found  in  the  4th  intercostal   space  just  left  to  the  midclavicular  line   • Diplacement  of  an  apical  impulse  laterally  or   downward  suggest  cardiac  enlargement   • Usually  superior  to  percussion  in  the  detection   of  cardiomegaly   Point  of  Maximal  Impulse   • Helpful  in  determining  whether  the  right   ventricle  or  left  ventricle  is  dominant   • RV  dominant:  impulse  is  maximal  at  the  lower   left  sternal  border  or  over  the  xiphoid  process   • LV  dominant:  impulse  is  maximal  at  the  apex   • Newborns  and  infants  have  RV  dominance   • Heave:  impulse  is  more  diffuse  and  slow  rising;   often  associated  with  volume  overload   • Tap:  impulse  is  well  localized  and  sharp  rising;   associated  with  pressure  overload   Hyperactive  Precordium   • Presence  characterizes  heart  disease  with   volume  overload  (i.e.,  defects  with  large  left-­‐to-­‐ right  shunts,  severe  valvular  regurgitation)   Thrills   • Vibratory  sensations  that  represent  palpable   manifestations  of  loud,  harsh  murmurs.   • Palpation  is  often  of  diagnostic  value   • Felt  better  with  the  palm  of  the  hand  than  with   tips  of  fingers  in  chest   • Fingers  are  used  to  feel  a  thrill  in  the   suprasternal  notch  and  over  the  carotid  arteries   • Lesions  present  thrills  at  diferent  locations   o Upper  left  sternal  border  originate  from  the   pulmonary  valve  or  pulmonary  artery  (PA)   and  therefore  are  present  in  PS,  PA  stenosis,   or  PDA  (rarely)   o upper  right  sternal  border  are  usually  of   aortic  origin  and  are  seen  in  AS   o lower  left  sternal  border  are   characteristic  of  a  VSD   o suprasternal  notch  suggest  AS  but  may  be   found  in  PS,  PDA,  or  COA   o presence  of  a  thrill  over  the  carotid  artery   or  arteries  accompanied  by  a  thrill  in  the   suprasternal  notch  suggests  diseases  of   the  aorta  or  aortic  valve  (e.g.,  COA,  AS).  An   isolated  thrill  in  one  of  the  carotid   arteries  without  a  thrill  in  the   suprasternal  notch  may  be  a  carotid  bruit   o intercostal  spaces  are  found  in  older   children  with  severe  COA  and  extensive   intercostal  collaterals)   •

2.

3.

4.

  Figure  X.  Normal  Blood  Pressures     C.  Auscultation     Done  to  inspect:   • Heart  rate  and  regularity   • Heart  sounds   • Systolic  and  diastolic  sounds   • Heart  murmurs     First  Heart  Sound   • S1  is  associated  with  the  closure  of  the  mitral  valve   and  tricuspid  valves   • Best  heard  at  the  apex  or  lower  left  sternal  border   • Splitting  of  S1  may  be  found  in  normal  children   however  is  infrequent   • Abnormally  wide  splitting  of  S1  may  be  found  in  right   bundle  branch  block  or  Eibstein’s  anomaly   • Splitting  of  S1  vs.  ejection  click  or  S4   o Ejection  click:  more  easily  audible  at  upper  left   sternal  border  in  PS   o S4  is  rare  in  children     Second  Heart  Sound   • S2  is  in  the  upper  left  sternal  border   • Splitting  of  the  S2:  two  components  are  A2  and  P2   • Must  be  evaluated  in  terms  of  degree  of  splitting  and   intensity  of  the  pulmonary  closure  component  of  the   second  heart  sound  (P2)  in  relation  to  the  intensity  of   the  aortic  closure  component  of  S2  (A2)   • Both  components  are  readily  audible  with  the  bell   Normal  splitting  of  the  S2   $ Degree  of  splitting  varies  with  respiration   o Increasing  with  inspiration   o Decreasing  or  becoming  single  with  expiration   $ Increase  in  systemic  venous  return  to  the  right  side  of   the  heart  during  inspiration  due  to  greater  negative   pressure  in  thoracic  cavity  !  increased  blood  volume   in  RV  prolongs  duration  of  RV  ejection  time  !  delays   closure  of  pulmonary  valve  !  wide  splitting  o  S2   $ Absence  of  splitting  or  widely  split  S2  usually   indicates  abnormality    

  Blood  Pressure  Measurement   • When  possible,  every  child  should  have  his  or  her   blood  pressure  measured  as  part  of  a  physical  exam     2018-A

 

EMPAMANO, ENCARNACION, ERLANO, ESPERANZA, HERNANDEZ

  6OF10

PHYSIOLOGY 3.XX: Pediatric CVS  

  Figure  X.  Splitting  of  Second  Heart  Sound     Abnormal  splitting  of  the  S2   1. Widely  split  and  fixed  S2   ! Found  in  conditions  that  prolong  the  RV   ejection  time  or  shorten  LV  ejection   ! Found  in  ASD  or  partial  anomalous  pulmonary   venous  return  (PAPVR)  and  PS   2. Narrowly  split  S2   ! Found  in  conditions  in  which  pulmonary  valve   closes  early  or  the  aortic  valve  closure  is   delayed   ! Occasionally  found  in  normal  child   3. Single  S2   ! Found  when  (i)  only  one  semilunar  valve  is   present,  (ii)  P2  is  not  audible,  (iii)  aortic   closure  is  delayed,  (iv)  P2  occurs  early   4. Paradoxically  split  S2   ! Found  when  the  aortic  closure  (A2)  follows  the   pulmonary  closure  (P2)  and  therefore  is  seen   when  LV  ejection  is  greatly  delayed     Intensity  of  the  P2   $ Relative  intensity  of  P2  with  A2  must  be  assessed   $ A2  is  usually  louder  than  P2   $ A2  is  the  first  component  of  the  second  heart  sound  at   the  pulmonary  area   $ Increased  intensity  of  P2  is  found  in  pulmonary   hypertension   $ Decreased  intensity  of  P2  is  found  in  conditions  of   decreased  diastolic  pressure  of  PA     Third  Heart  Sound   • Low  frequency  sound  in  early  diastole   • Related  to  rapid  filling  of  ventricle   • Beast  heard  at  apex  of  lower  left  sternal  border   • Commonly  heard  in  normal  children  and  adults   • Loud  S3  sound  is  abnormal  and  audible  in  conditions   with  dilated  ventricles  and  decreased  ventricular   compliance  

Figure  X.  Third  Heart  Sound  

 

-­‐

Generally  implies  a  pathologic  condition  and  is   commonly  present  in  Congestive  Heart  Failure  (CHF)   Summation  gallop  represents  tachycardia  and   superimposed  S3  and  S4  

  Cardiac  Murmurs   Innocent  Murmurs   -­‐ Normal  cardiac  tissue  vibrations   -­‐ High  flow  through  valves   -­‐ Thin  chest  wall  (noise  from  vasculature  is  easier  to   hear)     Pediatric  ECG     Electrocardiogram  (ECG  or  EKG)  is  a  visual  representation   of  the  electrical  conduction  of  the  heart   -­‐ Electric   signal   travels   from   atria   to   the   ventricles,   it   can  be  recorded  on  paper   -­‐ P   wave:   Represents   the   electrical   signal   as   it   travels   through   the   atria,   the   atria   contract   and   blood   is   forced  into  the  ventricles.     -­‐ QRS  waves:  Represent  the  signal  as  it  travels  through   the   ventricles,   which   contract   and   blood   is   forced   into   the  arteries.     -­‐ T  wave:  Represents  the  heart  at  rest  prior  to  the  next   beat.    

 

Figure  X.  Cardiac  Conduction  System    

 

  Fourth  Heart  Sound/  Atrial  Sound   • S4  is  a  relatively  low  frequency  sound  of  late  diastole   (i.e.,  presystole)   • Rare  in  infants  and  children   • When  present,  always  pathologic  and  is  seen  in   conditions  with  decreased  ventricular  compliance  of   CH     Gallop  Rhythm   -­‐ A  rapid  triple  rhythm  resulting  from  the  combination   of  a  loud  S3,  with  or  without  an  S4,  and  tachycardia   2018-A

-­‐

Figure  X.  ECG  Tracings  

 

  Difference  in  Adult  and  Pediatric  ECG   ECG   reading   for   pediatric   patients   is   essentially   the   same   with  adults  except  for  the  ff.  differences:     1.  Increased  HR     -­‐ Relative  tachycardia;  decreases  with  age       2.  Right  Ventricular  Hypertrophy     -­‐ RV   dominance:   work   of   RV   is   greater   in   utero,   carried  within  the  1st  few  weeks  or  months  of  life;   LV  becomes  thicker  at  3  mos.    

EMPAMANO, ENCARNACION, ERLANO, ESPERANZA, HERNANDEZ

7OF10

PHYSIOLOGY 3.XX: Pediatric CVS  

    3.  Right  Axis  Deviation     -­‐ Newborns   normally   have   RAD   compared   with   adult  standard     -­‐ By  3  yrs,  QRS  approaches  the  mean  adult  values  of   +50  degrees       NOTE:     • T  wave  in  V1  is  expected  to  be  negative  but  abnormal   in  adults     • Upright  T  wave  in  neonates  suggests  RV  hypertrophy   which   can   be   considered   normal   within   the   1st   few   days  of  life     • Heart  Rate     o Average  rate  -­‐  120  to  140  beats/min     o Crying   and   Activity   -­‐   May   increase   to   170+   beats/min     o Sleeping  Rates  -­‐  Drops  to  70–90  beats/min       Calculation  of  Heart  Rate  using  ECG  Tracings   1. Choose   the   one   with   the   regular   occurring   R-­‐R   intervals     2. Count  the  small  squares  between  R-­‐R  intervals     3. Divide  1500  by  the  number  of  small  squares     *when   the   heart   rate   is   slow,   count   the   large   boxes,   and   divide  300  by  the  number  of  large  boxes       Table  X.  Heart  Rates  in  Normal  Children  

    RV  Dominance:     -­‐ Right  axis  deviation:  tall  R  waves  in  avR     -­‐ Deep   S   waves:   v5   and   v6,   in   the   extreme   left   chest   leads       Table  X.  Normal  QRS  Axes  

    T-­‐  Axis   • Determined   by   the   same   method   used   in   the   determination  of  QRS   • Normal  children  and  new  borns  has  a  T-­‐axis  of  45⁰  

2018-A

 

•

T   wave   must   be   upright   in   L1   ans   aVf.   (P,   QRS,   &   T   waves   should   be   upright   to   have   a   normal   new   born   tracing).   Intervals  should  also  be  normal  

•   NOTE:   *Each  duration  is  shorter  in  infants  and  increases  with  age.     *QT  interval  are  expected  to  be  0.45  -­‐  0.  47  in  the  first  six   months  of  age.   *Interpretation  will  always  vary  with  the  age   of  the  child.   Always  ask  for  the  age  first.    

  Figure  X.  Position  of  Chest  Leads  in  Children     • Pediatric   ECG   has   three   extra   chest   leads   (V3R,   V4R,   V5R).     • Same  location  but  on  the  opposite  side  of  the  adult’s.     • 15   lead   ECG   is   done   to   pediatric   patients   because   of   the  RV  dominance.   • RV  dominance   o Right  axis  deviation  and/or  anterior  QRS  forces   o Tall   R   waves   in   aVr   and   in   the   right   precordial   leads   o Deep  S  waves  in  L1  and  left  precordial  lead.     NOTE:   *Normal  in  adults:  Small  R  in  the  first  lead  and  goes  higher   and   higher   because   the   right   wave   represents/   reflects   left   ventricle.     *Not   seen   in   babies.   Tall   R   waves   in   the   right   precordial   leads   and   prominent   S   waves   in   the   left   precordial   lead   because   these   are   all   reflective   of   the   forces   of   the   bigger   right  ventricle.            

EMPAMANO, ENCARNACION, ERLANO, ESPERANZA, HERNANDEZ

8OF10

PHYSIOLOGY 3.XX: Pediatric CVS  

  Appendix  

 

Figure  X.  Scheme  of  Fetal  Circulation  (Tortora  &  Derrickson,  2009)      

  2018-A

 

EMPAMANO, ENCARNACION, ERLANO, ESPERANZA, HERNANDEZ

9OF10

PHYSIOLOGY 3.XX: Pediatric CVS  

    # # # # #

V4R  almost  same  level  as  V2.     RAD  L1  aVf     Dominant  R  waves  in  the  right  precordial  lead   T  wave  in  V1  is  usually  negative  and  upright  which  suggests  right  ventricular  hypertrophy.     o Normal  progression  of  R  wave  is  not  seen,  in  fact  it  is  decreasing  in  size  (paliit).     Complete  reversal  of  the  adult  type  RS  progression   o Tall  R  waves  in  V1  and  deep  S  waves  in  V5  and  V6.     o In  adults,  it’s  the  opposite:  small  R  waves  getting  taller,  big  S  waves  getting  smaller)        

  *In  summary:  Tachycardia,  Right  ventricular  hypertrophy  and  deviation  is  seen  as  compared  to  adults’    

2018-A

 

EMPAMANO, ENCARNACION, ERLANO, ESPERANZA, HERNANDEZ

10OF10