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HISTORY TAKING AND
PHYSICAL EXAMINATION
IN CVS IN PAEDIATRICS
Dr. Raghav Kakar
1.Symptoms – s/o heart
disease?
 Feeding difficulties
 Poor weight gain
 Irritability
 Excessive crying
 Bluish extremities
 Excessive
perspiration
 Wheezing
 Noisy laboured
breathing
 Frequent RTI
 Oliguria
 Breathlessness
 Fatigue and
weakness
 Cough
 Chest pain
 Swelling of feet
 Joint pain
 Painful swelling in
finger pulps
 Syncope
 Involuntary
movements
 Haemoptysis
2. Is it Congenital or Acquired ?
Congenital
 Symptoms from infancy
 Feeding difficulties  FTT
 Recurrent hospital admissions
Acquired
 Rheumatic fever:
 Fever, joint pain, chorea
3. If it is congenital, is it cyanotic or
acyanotic?
Why cyanosis occurs?
What are the types of
cyanosis?
Which one is present in
cyanotic CHDs?
How to differentiate?
4. If it is Cyanotic CHD, what is the actual
CHD ?
PBF
TOF
Tricuspid
Atresia
TGA
Single
ventricle with
PS
PBF
Truncus arteriosus
TAPVC
Single ventricle
without PS
Cyanotic CHD
BASED ON MURMURS, CHANGE IN HEART SOUNDS 
INVESTIGATIONS
5. If it is Acyanotic CHD, what is the actual
CHD ?
 ASD
 VSD
 PDA
 PS
 AS
 CoA
Volume overload (Shunt) Pressure overload (Obstn.)
BASED ON MURMURS, CHANGE IN HEART SOUNDS 
INVESTIGATIONS
ACYANOTIC CHD
6. Is it Rheumatic Fever or
RHD?
 If so, which valves are involved?
 Is there any evidence of pericarditis or
myocarditis?
7. Are there any complications?
CCF
Infective Endocarditis
Pulmonary Hypertension
NADA’s Criteria
 Major :
 Systolic murmur Gr.
III or more in
intensity.
 Diastolic murmur
 Cyanosis
 CHF
 Minor:
 Systolic murmur Gr.
II or less in intensity.
 Abnormal 2nd sound
 Abnormal ECG
 Abnormal CXR
 Abnormal BP
Presence of 1 major or 2 minor criteria suggest
presence of Heart Disease
Perinatal History
 Was the mother immunized against rubella
prior to delivery?
 Was the mother scanned in antenatal period?
 H/o fever with rash in 1st trimester, painful
swelling behind the ear.
Maternal conditions
Maternal
Conditions
Heart Defects to be
expected
Diabetes TGA, VSD, PDA, HOCM
SLE Congenital heart block
Phenylketonuria TOF, VSD, ASD, PDA, CoA
Intake of teratogenic drugs
Drugs Cardiac Defect
Sodium Valproate CoA, HLHS, AS, VSD
Hydantoin PS, ASD, VSD, PDA
Alcohol VSD, PDA, ASD, TOF
Thalidomide TOF, ASD, VSD, TA
Lithium EBSTEIN’S ANAMOLY
Amphetamines ASD, VSD, PDA, TGA
Indomethacin Intrauterine closure of PDA
Vit A TOF, TGA, TA
Vit D Supravalvular aortic stenosis
Postnatal history
 Neonatal cyanosis
 Breathing difficulties
 Feeding problems
 Delay in growth
Family History
 Consanguinity
 Maternal age at conception
 Age of the father
 Heart disease in family
 Hereditary diseases
 PS common in Noonan syndrome
 Rheumatic fever
 Diabetic mother
General Examination
 Dysmorphic features/syndromes :
Disorder/Syndrome Common Cardiac Defect
Down’s ECD, VSD
Edward VSD, PDA, PS
Patau VSD, PDA, Dextrocardia
Noonan PS
Marfan AR, MVP
Turner CoA, AS, ASD
Holt-Oram ASD (Ostium Primum)
 Clubbing
 Infective endocarditis, Cyanotic heart disease
 Odema : pedal/sacral
 Restrictive or severe tricuspid valve diseases
 Sweating on forehead
 Chest and spine deformities
 Shifting of apical impulse in scoliosis/kyphosis
 Skin
 Rheumatic nodules
 Pallor
 Anthropometry :
 Weight
 FTT –CHF, cyanotic heart disease
 Weight might increase due to odema
 Height
 Tall/ short stature
CVS Examination
 Pulse
 BP
 JVP
 Inspection of precordium
 Bony/Spine deformities
 Chest shape
 Trachea central/deviated
 Visible precordial bulge
 Visible pulsations
 Scars, dilated veins, sinuses.
 Palpation
 Apex beat
 Parasternal Heave
 Thrills
 Any palpable pulsations in precordial region
 Percussion
 Auscultation
Pulse
 A pulse is a waveform that is felt by the finger,
produced during cardiac systole which travels
along the arterial tree, at a rate much faster
than that of blood column.
Assessment of pulse
 Rate
 Rhythm
 Volume
 Character
 Pulse deficit
 Condition of vessel wall
 R-F delay
 Symmetry
 Pulse rate :
 Counted for full 1 minute by palpating the radial
artery
 Tachycardia:
 Rheumatic fever
 Congestive cardiac failure
 Arrythmias
 Bradycardia :
 Complete heart block
 Sick sinus syndrome (sino-atrial disease)
 Pulse rhythm:
 Normal sinus rhythm : Regular
 Regularly irregular rhythm :
 Sinus arrhythmias
 Irregularly irregular rhythm
 Atrial Fibrillation
 Atrial Flutter with varying degree of heart block
 Pulse Volume :-
 Assessed by palpating Carotid artery.
 PP gives accurate measurement of pulse vol.
 When Pulse Pressure
 30-60mmHg – Normal vol pulse.
 <30mmHg - Low vol pulse.
 >60mmHg - High vol pulse.
Large Volume Pulse
(Bounding)
Small Volume Pulse
( Weak, Thready )
Aortic Incompetence (AR) CCF
PDA Pericardial effusion
A-V Fistula Constrictive pericarditis
Persistent truncus arteriosus Lower limb in CoA
 Pulse character
 Best assessed in carotid artery
 Hypokinetic Pulse:
 Small weak pulse ( Small vol. And narrow PP)
 Anacrotic Pulse ( Parvus et Tardus ):
 Parvus : low amplitude
 Tardus : slow rising and late peak
 Hyperkinetic
Pulse
 Rapid rise
 High amplitude
 Large vol. &
wide PP
 Collapsing pulse :
 Rapid upstroke
 Rapid downstroke
 Large Stroke
volume
 Pulsus alterans
 Alternating small &
large vol. pulse with
irregular rhythm
 Best appreciated by
palpating radial and
femoral pulses
 Pulsus Paradoxus :
 When the fall in BP is more than 10 mmHg
during inspiration, it is Pulsus paradoxus.
 Pulse Deficit:
 Difference between HR & PR when counted
simultaneously for 1 min.
 Causes : Atrial fibrillation and VPCs
 Radio-radial delay:
 Seen in : Pre Subclavian coarctation, supravalvular
AS
 Radio-femoral delay:
 Seen in : CoA, Aortic embolism
Blood Pressure
 What size cuffs are preffered?
 Width:
 40% of circumference
 Length:
 80-100 % of
circumference
JVP
 Expressed as vertical height from the sternal
angle to the zone of transition of distended and
collapsed JVP.
 The patient is kept at 45 degree.
 The upper level of pulsations in the IJV is
seen.
 JVP – indicator of Rt. Atrial pressure
 Centre of RA is approx 5 cm from sternal
angle.
 Right Atrial Pressure = Vertical ht. Of blood
column + 5 cms (cm of
H20)
 Normal JVP = < 8 cms of H2O or < 6mmHg
 Elevated JVP:
 CCF
 TS, TR
 Constrictive
pericarditis
 Cardiac tamponade
 Fall in JVP:
 Hypovolaemia
 Shock
 Kussmaul’s sign –
 Constrictive
pericarditis
 Cardiac tamponade
 RV failure
 Hepato-Jugular
reflex:
 Right heart failure
 TR
 Friedrich’s sign:
 Rapid fall and rise of
JVP
 TR
 Constrictive
pericarditis
 Precordial bulge :
 Long standing cardiac disease
Visible pulsations
 Carotid Pulsations:
 Hyperdynamic
states
 AR
 CoA
 Suprasternal
pulsations:
 AR
 CoA
 Thyrotoxicosis
 Epigastric
pulsations:
 Pulsations of liverin
CHF with TR
 RVH
 Abdominal aorta
aneurysm
 Tricuspid stenosis
 Back:
 CoA
Scar marks
Palpations
 General rule :
 Fingertips : to feel
pulsations,
 Base of fingers :
Thrills,
 Base of hand ( or
ulnar aspect ) :
Heaves
 Apical Impulse :
 It refers to the lowermost and outermost point of definite
cardiac impulse, which gives maximum thrust to the
palpating finger.
Normal variation in location of apical impulse with
age
Age Position of apical
impulse
Relation to midclavicular
line
Infancy Left 4th ICS Lateral to mid clavicular line
Approx 5 years Left 5th ICS In the Midclavicular line
Older children Left 5th ICS Medial to midclavicular line
 Parasternal Heave :
 A palpable thrust, which lifts the palpating hand.
 Seen in RVH and Left atrial enlargement.
 Palpated by ulnar aspect of hand.
 Grading :
I. Instant lift, visible not palpable
II. Visible and palpable, lift can be obliterated
III. Visible and palpable, lift cant be obliterated
 Thrills :
 These are palpable vibrations of murmurs which
accompany any organic murmur of grade 3 or
more.
Percussion
 It is done basically to see enlargement of
dullness of the cardiac region.
 Cardiac causes : Cardiomegaly, pericardial
effusion
Auscultation
 Heart sounds:
 Relative, brief auditory vibrations of variable
intensity, frequency & quality, produced by closure
of heart valves.
S1 Abnormalities
Soft S1 Loud S1 Split Reverse
split
MR MS RBBB RVP
TR TS LVP Ectopic beats
Calcification
of AV valves
High output
states
Pulm.
Hypertension
S2 Abnormalities
Soft S2 Loud S2 Single S2
Loud A2 Loud P2 Absent A2 Absent P2
AS Syst. Htn Pulm. Htn AS PS
PS Aortic
aneurysm
ASD, PDA TOF
Calcified lesions of
semilunar valves
Dilated
aorta
LargeVSD TGA
Splitting of S2
Wide- Fixed Wide-
Variable
Narrow Reverse-split
Early A2/Late P2 VSD Severe
AS
Late A2/Early P2
MR LVP Severe
PS
Aortic stenosis
ASD, RBBB HOCM
 S3 and S4
Causes of S3
Physiological S3 Pathological S3
Children High output states
Young adults CHD – ASD, VSD, PDA
MR, TR, AR
 Opening Snap
 Due to opening of AV valves
 Can be heard at the apex :
 MS, MR
 VSD
 PDA
 Or can be heard at parasternal region :
 Tricuspid stenosis
 Tricuspid regurgitation
 ASD
 Ejection Click :
 It is a sharp, clicking sound arising from the
cardiac valves due to sudden swelling of the
pulmonary artery, abrupt dilatation of aorta or
forceful opening of the aortic cusps.
 Early ejection systolic click is seen in aortic and
pulmonary valve stenosis
 Midsystolic ejection click is seen in floppy mitral
valve.
 Pericardial Rub :
 Due to sliding of 2 inflamed layers of pericardium
 Scratching, grating in character
 Triphasic : during misdystole, mid diastole & pre
systole)
 Best heard along left sternal edge in 3rd & 4th ICS
 MURMURS :
 Occur due to the turbulence caused by either an
increased flow through a normal/stenosed valve
or a normal flow through a stenosed valve/orifice
 Auscultation should be done over precordium,
back and over carotids
 They should be described in the following way
 Pitch
 Timing & character
 Systolic/diastolic
 Area where best heard
 Intensity
 Whether best heard with bell or diaphragm
 Conduction
 Variation with respiration
 Posture in which best heard
 Variation with dynamic auscultation.
 Eg/: murmur of MS is best described as;-
 Low-pitched,
 Mid-diastolic,
 Rumbling murmur,
 Best heard in Apical region,
 in LL position
 with the bell of stethoscope,
 not radiated,
 increases with isometric exercise.
 Systolic murmur
grading
I. Very soft (heard in
quite room)
II. Soft, but easily
audible
III. Moderate, no thrill
IV. Loud with thrill
V. Very loud with thrill,
heard with steth
barely placed on
chest
VI. Loud and audible with
stethoscope just off
the chest wall
 Diastolic murmur
grading
I. Very soft
II. Soft
III. Loud
IV. Loud with thrill
 Early systolic murmur:
 Ejection systolic murmur
 Late systolic murmur
 Pansystolic murmur
 Early diastolic murmur
 Mid diastolic murmur:
 Late diastolic murmur:
 MS
 TS
 Atrial myxomas
 Continuous murmur:
 Named Murmurs:
 Carey-coomb’s :
 Short, Middiastolic
 Best heard at apex
 MS in acute RHD
 Graham-steele :
 High pitched, early diastolic
 Best heard at left sternal border, 2nd ICS
 During expiration in PR
 Gibson’s :
 Continuous machinery murmur of PDA
 Cole-cecil :
 Murmur of AR, heard well in axilla.
 Austin flint:
 Low pitched rumbling mid diastolic murmur
 Best heard at apex in severe AR
 Gallavardin phenomenan :
 The harsh noisy component of ESM of AS.
 Best heard at the right sternal border and radiated to
neck
 Carvallo’s sign :
 Pansystolic murmur of TR, best heard in tricuspid
area.
 Becomes louder during inspiration
 Innocent murmurs:
 Functional/ benign murmurs
 Absence of anatomical/functional abnormalities of
heart and circulation
 Accentuated during periods of febrile illness and
high output states
 Characteristic features :
 Asymptomatic
 Normal cardiac silhouette on chest-xray
 Usually systolic
 Less than grade 3
 No cyanosis
 Normal pulses
 Normal heart sounds
Dynamic auscultation
 During dynamic auscultation, as opposed to
conventional auscultation, the patient is asked
to change position or perform certain activities
that enable the physician to hear the murmurs
and heart sounds.
 Respiration
 Valsalva manouvre
 Muller manouvere
 Standing to squatting
 Squatting to standing
 Passive leg exercise
 Isometric hand grip
 Leaning forward
 Chin turned upwards
 Respiration :
 During inspiration:
 Right sided murmur become louder
 Left sided murmurs become softer or unchained
 Expiration has the opposite effect
 Valsalva manouvre:
 It is an attempted forced expiration in closed
glottis, when both the mouth and nose are closed.
 It increases the intrathoracic pressure
 Murmur of MVP becomes louder
 Systolic murmur of HOCM become louder
 ESM of AS will be decreases
 Standing to squatting:
 It increases blood return and systemic vascular
resistance.
 HOCM becomes soft due to increased diastolic
volume.
 Isometric hand grip:
 Increases systemic circulation
 Murmurs of regurgitation ( MR,VSD) become louder
due to back pressure
 Murmurs of AS become softer due to decreased
gradient across the valve.
Thank you

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history and examination in pediatric CVS

  • 1. HISTORY TAKING AND PHYSICAL EXAMINATION IN CVS IN PAEDIATRICS Dr. Raghav Kakar
  • 2. 1.Symptoms – s/o heart disease?  Feeding difficulties  Poor weight gain  Irritability  Excessive crying  Bluish extremities  Excessive perspiration  Wheezing  Noisy laboured breathing  Frequent RTI  Oliguria  Breathlessness  Fatigue and weakness  Cough  Chest pain  Swelling of feet  Joint pain  Painful swelling in finger pulps  Syncope  Involuntary movements  Haemoptysis
  • 3. 2. Is it Congenital or Acquired ? Congenital  Symptoms from infancy  Feeding difficulties  FTT  Recurrent hospital admissions Acquired  Rheumatic fever:  Fever, joint pain, chorea
  • 4. 3. If it is congenital, is it cyanotic or acyanotic? Why cyanosis occurs? What are the types of cyanosis? Which one is present in cyanotic CHDs? How to differentiate?
  • 5.
  • 6. 4. If it is Cyanotic CHD, what is the actual CHD ? PBF TOF Tricuspid Atresia TGA Single ventricle with PS PBF Truncus arteriosus TAPVC Single ventricle without PS Cyanotic CHD BASED ON MURMURS, CHANGE IN HEART SOUNDS  INVESTIGATIONS
  • 7. 5. If it is Acyanotic CHD, what is the actual CHD ?  ASD  VSD  PDA  PS  AS  CoA Volume overload (Shunt) Pressure overload (Obstn.) BASED ON MURMURS, CHANGE IN HEART SOUNDS  INVESTIGATIONS ACYANOTIC CHD
  • 8. 6. Is it Rheumatic Fever or RHD?  If so, which valves are involved?  Is there any evidence of pericarditis or myocarditis?
  • 9. 7. Are there any complications? CCF Infective Endocarditis Pulmonary Hypertension
  • 10. NADA’s Criteria  Major :  Systolic murmur Gr. III or more in intensity.  Diastolic murmur  Cyanosis  CHF  Minor:  Systolic murmur Gr. II or less in intensity.  Abnormal 2nd sound  Abnormal ECG  Abnormal CXR  Abnormal BP Presence of 1 major or 2 minor criteria suggest presence of Heart Disease
  • 11. Perinatal History  Was the mother immunized against rubella prior to delivery?  Was the mother scanned in antenatal period?  H/o fever with rash in 1st trimester, painful swelling behind the ear.
  • 12. Maternal conditions Maternal Conditions Heart Defects to be expected Diabetes TGA, VSD, PDA, HOCM SLE Congenital heart block Phenylketonuria TOF, VSD, ASD, PDA, CoA
  • 13. Intake of teratogenic drugs Drugs Cardiac Defect Sodium Valproate CoA, HLHS, AS, VSD Hydantoin PS, ASD, VSD, PDA Alcohol VSD, PDA, ASD, TOF Thalidomide TOF, ASD, VSD, TA Lithium EBSTEIN’S ANAMOLY Amphetamines ASD, VSD, PDA, TGA Indomethacin Intrauterine closure of PDA Vit A TOF, TGA, TA Vit D Supravalvular aortic stenosis
  • 14. Postnatal history  Neonatal cyanosis  Breathing difficulties  Feeding problems  Delay in growth
  • 15. Family History  Consanguinity  Maternal age at conception  Age of the father  Heart disease in family  Hereditary diseases  PS common in Noonan syndrome  Rheumatic fever  Diabetic mother
  • 16. General Examination  Dysmorphic features/syndromes : Disorder/Syndrome Common Cardiac Defect Down’s ECD, VSD Edward VSD, PDA, PS Patau VSD, PDA, Dextrocardia Noonan PS Marfan AR, MVP Turner CoA, AS, ASD Holt-Oram ASD (Ostium Primum)
  • 17.  Clubbing  Infective endocarditis, Cyanotic heart disease  Odema : pedal/sacral  Restrictive or severe tricuspid valve diseases  Sweating on forehead  Chest and spine deformities  Shifting of apical impulse in scoliosis/kyphosis  Skin  Rheumatic nodules  Pallor
  • 18.  Anthropometry :  Weight  FTT –CHF, cyanotic heart disease  Weight might increase due to odema  Height  Tall/ short stature
  • 19. CVS Examination  Pulse  BP  JVP  Inspection of precordium  Bony/Spine deformities  Chest shape  Trachea central/deviated  Visible precordial bulge  Visible pulsations  Scars, dilated veins, sinuses.
  • 20.  Palpation  Apex beat  Parasternal Heave  Thrills  Any palpable pulsations in precordial region  Percussion  Auscultation
  • 21. Pulse  A pulse is a waveform that is felt by the finger, produced during cardiac systole which travels along the arterial tree, at a rate much faster than that of blood column.
  • 22. Assessment of pulse  Rate  Rhythm  Volume  Character  Pulse deficit  Condition of vessel wall  R-F delay  Symmetry
  • 23.
  • 24.  Pulse rate :  Counted for full 1 minute by palpating the radial artery
  • 25.  Tachycardia:  Rheumatic fever  Congestive cardiac failure  Arrythmias  Bradycardia :  Complete heart block  Sick sinus syndrome (sino-atrial disease)
  • 26.  Pulse rhythm:  Normal sinus rhythm : Regular  Regularly irregular rhythm :  Sinus arrhythmias  Irregularly irregular rhythm  Atrial Fibrillation  Atrial Flutter with varying degree of heart block
  • 27.  Pulse Volume :-  Assessed by palpating Carotid artery.  PP gives accurate measurement of pulse vol.  When Pulse Pressure  30-60mmHg – Normal vol pulse.  <30mmHg - Low vol pulse.  >60mmHg - High vol pulse.
  • 28. Large Volume Pulse (Bounding) Small Volume Pulse ( Weak, Thready ) Aortic Incompetence (AR) CCF PDA Pericardial effusion A-V Fistula Constrictive pericarditis Persistent truncus arteriosus Lower limb in CoA
  • 29.  Pulse character  Best assessed in carotid artery
  • 30.  Hypokinetic Pulse:  Small weak pulse ( Small vol. And narrow PP)
  • 31.  Anacrotic Pulse ( Parvus et Tardus ):  Parvus : low amplitude  Tardus : slow rising and late peak
  • 32.  Hyperkinetic Pulse  Rapid rise  High amplitude  Large vol. & wide PP
  • 33.  Collapsing pulse :  Rapid upstroke  Rapid downstroke  Large Stroke volume
  • 34.  Pulsus alterans  Alternating small & large vol. pulse with irregular rhythm  Best appreciated by palpating radial and femoral pulses
  • 36.  When the fall in BP is more than 10 mmHg during inspiration, it is Pulsus paradoxus.
  • 37.  Pulse Deficit:  Difference between HR & PR when counted simultaneously for 1 min.  Causes : Atrial fibrillation and VPCs  Radio-radial delay:  Seen in : Pre Subclavian coarctation, supravalvular AS  Radio-femoral delay:  Seen in : CoA, Aortic embolism
  • 38. Blood Pressure  What size cuffs are preffered?
  • 39.  Width:  40% of circumference  Length:  80-100 % of circumference
  • 40. JVP  Expressed as vertical height from the sternal angle to the zone of transition of distended and collapsed JVP.  The patient is kept at 45 degree.  The upper level of pulsations in the IJV is seen.
  • 41.
  • 42.  JVP – indicator of Rt. Atrial pressure  Centre of RA is approx 5 cm from sternal angle.  Right Atrial Pressure = Vertical ht. Of blood column + 5 cms (cm of H20)  Normal JVP = < 8 cms of H2O or < 6mmHg
  • 43.  Elevated JVP:  CCF  TS, TR  Constrictive pericarditis  Cardiac tamponade  Fall in JVP:  Hypovolaemia  Shock
  • 44.  Kussmaul’s sign –  Constrictive pericarditis  Cardiac tamponade  RV failure  Hepato-Jugular reflex:  Right heart failure  TR  Friedrich’s sign:  Rapid fall and rise of JVP  TR  Constrictive pericarditis
  • 45.  Precordial bulge :  Long standing cardiac disease
  • 46. Visible pulsations  Carotid Pulsations:  Hyperdynamic states  AR  CoA  Suprasternal pulsations:  AR  CoA  Thyrotoxicosis  Epigastric pulsations:  Pulsations of liverin CHF with TR  RVH  Abdominal aorta aneurysm  Tricuspid stenosis  Back:  CoA
  • 48. Palpations  General rule :  Fingertips : to feel pulsations,  Base of fingers : Thrills,  Base of hand ( or ulnar aspect ) : Heaves
  • 49.  Apical Impulse :  It refers to the lowermost and outermost point of definite cardiac impulse, which gives maximum thrust to the palpating finger. Normal variation in location of apical impulse with age Age Position of apical impulse Relation to midclavicular line Infancy Left 4th ICS Lateral to mid clavicular line Approx 5 years Left 5th ICS In the Midclavicular line Older children Left 5th ICS Medial to midclavicular line
  • 50.
  • 51.
  • 52.  Parasternal Heave :  A palpable thrust, which lifts the palpating hand.  Seen in RVH and Left atrial enlargement.  Palpated by ulnar aspect of hand.  Grading : I. Instant lift, visible not palpable II. Visible and palpable, lift can be obliterated III. Visible and palpable, lift cant be obliterated
  • 53.  Thrills :  These are palpable vibrations of murmurs which accompany any organic murmur of grade 3 or more.
  • 54. Percussion  It is done basically to see enlargement of dullness of the cardiac region.  Cardiac causes : Cardiomegaly, pericardial effusion
  • 56.  Heart sounds:  Relative, brief auditory vibrations of variable intensity, frequency & quality, produced by closure of heart valves.
  • 57. S1 Abnormalities Soft S1 Loud S1 Split Reverse split MR MS RBBB RVP TR TS LVP Ectopic beats Calcification of AV valves High output states Pulm. Hypertension
  • 58. S2 Abnormalities Soft S2 Loud S2 Single S2 Loud A2 Loud P2 Absent A2 Absent P2 AS Syst. Htn Pulm. Htn AS PS PS Aortic aneurysm ASD, PDA TOF Calcified lesions of semilunar valves Dilated aorta LargeVSD TGA
  • 59. Splitting of S2 Wide- Fixed Wide- Variable Narrow Reverse-split Early A2/Late P2 VSD Severe AS Late A2/Early P2 MR LVP Severe PS Aortic stenosis ASD, RBBB HOCM
  • 61. Causes of S3 Physiological S3 Pathological S3 Children High output states Young adults CHD – ASD, VSD, PDA MR, TR, AR
  • 62.  Opening Snap  Due to opening of AV valves  Can be heard at the apex :  MS, MR  VSD  PDA  Or can be heard at parasternal region :  Tricuspid stenosis  Tricuspid regurgitation  ASD
  • 63.  Ejection Click :  It is a sharp, clicking sound arising from the cardiac valves due to sudden swelling of the pulmonary artery, abrupt dilatation of aorta or forceful opening of the aortic cusps.  Early ejection systolic click is seen in aortic and pulmonary valve stenosis  Midsystolic ejection click is seen in floppy mitral valve.
  • 64.  Pericardial Rub :  Due to sliding of 2 inflamed layers of pericardium  Scratching, grating in character  Triphasic : during misdystole, mid diastole & pre systole)  Best heard along left sternal edge in 3rd & 4th ICS
  • 65.  MURMURS :  Occur due to the turbulence caused by either an increased flow through a normal/stenosed valve or a normal flow through a stenosed valve/orifice  Auscultation should be done over precordium, back and over carotids
  • 66.  They should be described in the following way  Pitch  Timing & character  Systolic/diastolic  Area where best heard  Intensity  Whether best heard with bell or diaphragm  Conduction  Variation with respiration  Posture in which best heard  Variation with dynamic auscultation.
  • 67.  Eg/: murmur of MS is best described as;-  Low-pitched,  Mid-diastolic,  Rumbling murmur,  Best heard in Apical region,  in LL position  with the bell of stethoscope,  not radiated,  increases with isometric exercise.
  • 68.  Systolic murmur grading I. Very soft (heard in quite room) II. Soft, but easily audible III. Moderate, no thrill IV. Loud with thrill V. Very loud with thrill, heard with steth barely placed on chest VI. Loud and audible with stethoscope just off the chest wall  Diastolic murmur grading I. Very soft II. Soft III. Loud IV. Loud with thrill
  • 74.  Mid diastolic murmur:
  • 75.  Late diastolic murmur:  MS  TS  Atrial myxomas
  • 77.  Named Murmurs:  Carey-coomb’s :  Short, Middiastolic  Best heard at apex  MS in acute RHD  Graham-steele :  High pitched, early diastolic  Best heard at left sternal border, 2nd ICS  During expiration in PR
  • 78.  Gibson’s :  Continuous machinery murmur of PDA  Cole-cecil :  Murmur of AR, heard well in axilla.  Austin flint:  Low pitched rumbling mid diastolic murmur  Best heard at apex in severe AR
  • 79.  Gallavardin phenomenan :  The harsh noisy component of ESM of AS.  Best heard at the right sternal border and radiated to neck  Carvallo’s sign :  Pansystolic murmur of TR, best heard in tricuspid area.  Becomes louder during inspiration
  • 80.  Innocent murmurs:  Functional/ benign murmurs  Absence of anatomical/functional abnormalities of heart and circulation  Accentuated during periods of febrile illness and high output states  Characteristic features :  Asymptomatic  Normal cardiac silhouette on chest-xray
  • 81.  Usually systolic  Less than grade 3  No cyanosis  Normal pulses  Normal heart sounds
  • 82. Dynamic auscultation  During dynamic auscultation, as opposed to conventional auscultation, the patient is asked to change position or perform certain activities that enable the physician to hear the murmurs and heart sounds.
  • 83.  Respiration  Valsalva manouvre  Muller manouvere  Standing to squatting  Squatting to standing  Passive leg exercise  Isometric hand grip  Leaning forward  Chin turned upwards
  • 84.  Respiration :  During inspiration:  Right sided murmur become louder  Left sided murmurs become softer or unchained  Expiration has the opposite effect
  • 85.  Valsalva manouvre:  It is an attempted forced expiration in closed glottis, when both the mouth and nose are closed.  It increases the intrathoracic pressure  Murmur of MVP becomes louder  Systolic murmur of HOCM become louder  ESM of AS will be decreases
  • 86.  Standing to squatting:  It increases blood return and systemic vascular resistance.  HOCM becomes soft due to increased diastolic volume.  Isometric hand grip:  Increases systemic circulation  Murmurs of regurgitation ( MR,VSD) become louder due to back pressure  Murmurs of AS become softer due to decreased gradient across the valve.

Hinweis der Redaktion

  1. Left side shows the symptoms we come across mostly in Infants...and right side..in older children.... SIGNS : Hepatomegaly-tender, Cardiomegaly, Tachycardia Odema in dependent parts-fluid retention, reduced venous flow,,,,Congestive hepatomegaly, Engorged pulsatile neck veins...Chest Pain—AS, P.Htn
  2. Q.1 –Is it due to cardiac or respi cause? Or a Hb-patthy?.. Time of onset, severity, aggravating factors? Resp causes of cyanosis :- Presence of more than 5g% of REDUCED Hb . Central-soft palate, tongue, floor of mouth, nail bed, ear lobes Peripheral – tip of fingers and toes, tip of nose
  3. Differential cyanosis : Preductal saturation more than post ductal—PDA with reversal of shunt... Reverse differential : PDA with TGV with either PPHN or PREDUCTAL CoA
  4. Symptoms of increasd PBF : Increased RR, sweating while feeding, shortness of breath, failure to thrive
  5. M A T P Endocarditis is a must in RHD........ MILK MAID GRIP, PRONATOR SIGN
  6. Pressing over recurrent laryngeal nerve...also in aortic aneurysm
  7. AMPHETAMINE – NARCOLEPSY, ADHD THALIDOMIDE- IMMUNOMODULATOR
  8. Cyanosis on crying/feeding in cyanotic chd Resp distress Delay growth—poor weight gain— weight affected more than height in acyanotic,
  9. Father age—marfan syndrome—AR....consanguinity—FRIEDRICH’s ATAXIA—HOCM/AF 1% incidence One sibling affecte-3% 1 affected-2-6% 2 affected- 25%
  10. Happy, anxious or sweating?
  11. Sweating in infants with ccf Pallor due to Vasoconstriction in CCF Clubbing – earlies in thumb...widening and thickening of fingenails,loss of the angle
  12. Both height and weight affected in Cyanotic Weight affected more in Acyanotic None affected in Acyanotic due to pressure overload
  13. Rate and rhythm- Radial Artery Volume and character – Carotid artery BP- Brachial artery
  14. Write normal for each age group
  15. Rhythm : It is the spacing of successive beats in time Generated by SA node Extra systoles –regularly irregular
  16. VOLUME—It is the Amplitude of the pulse wave---depends on stroke volume and compliance of arteries ( Carotid artery ::::closest to heart & least subjected to damping & distortion in arterial tree) Absent,,thready,,weak,,,normal,,,bounding.
  17. Thready– low volume with high pulse rate---peripheral circulatory failure
  18. 2 main components of this wave : A) Forward moving wave, B)Reflected wave. Forward wave is generated when the ventricles contract. The wave travels down the large aorta and gets reflected at the bifurcation of aorta into 2 iliac vessels.Normally it returns to the heart during diastole. This returned wave gives a notch.Helps in coronory perfusion. Velocity at which returns is very important.Stiffer the artery, better the return.
  19. Bounding Pulse
  20. Water hammer pulse...corrigan pulse Palpate the wrist in such a way that—webs fall over radial and rest of the arm falls over ulnar artery... Now elevate the whole upper limb above the level of heart and recognize any change in volume.. In water hammer—volume increases from the basal level and pulses strike the palpating hand with strike and force. Abrupt downstroke produces collapsing feel. • Large SV volume → streching of carotid arteries →aortic sinus reflex →reduced peripheral vasc resis
  21. Ventricular premature contractions beats Radial artery with left hand and femoral with right hand simaltaneously
  22. The lateral force exerted by the blood column per unit area of the vascular wall, that is expressed in mmHg. Principle of sphygmomanometry – Turbulant flow through a partially compressed artery Creates noises (Korotkoff’s sounds) Change in intensity correlates with systemic arterial pressures Korotkoff’s sounds : 5 phases 1st appearance of clear, tapping sounds. Represents SBP Tapping sounds are replaced by soft murmurs Murmurs become louder Muffling sounds Disappearance of sounds.Corresponds to DPB
  23. In normal children the pulsations lie behind the sternum and cannot be seen. The vertical distance between the sternal angle (zero point) and the upper border of oscillatory column is meaasured
  24. RIGHT IJV preffered :Straight line course through innominate vein to the svc and right atrium Less likely extrinsic compression from other structures in neck Why not EJV EJV is superficial, prone to kinking, doesnt directly drain into SVC, may hv valves
  25. RIGHT IJV preffered :Straight line course through innominate vein to the svc and right atrium Less likely extrinsic compression from other structures in neck Why not EJV EJV is superficial, prone to kinking, doesnt directly drain into SVC
  26. •KUSSMAUL --Normally during inspiration, there is fall in JVP. But in constrictive pericarditis, there is rise in JVP. HEPATOJUGULAR REFLEX :: Compression over right paraumbilical area or R upper abdomen for 30 secs Normally JVP rises transiently by <3cm ....But falls later even if the pressure is continued Other cases it remains elevated NEGATIVE IN BUDD CHIARI SYNDROME.
  27. BARRELL CHEST : Increased AP diameter FUNNEL CHEST : Depression in lower portion of sternum. Compression of heart & great vessels may produce murmurs. PIGEON CHEST : Sternum is displaced anteriorly. ↑ AP diameter. The costal cartilages adjacent to protruding sternum are depressed.
  28. Pulsations at back : SUZMAN’s Sign : the pulsations prominent over the scapular region, best visualised with patient bending forwward
  29. Right : BT shunting>>>> Midline : Complex cardiac procedure...>>>LEFT: BT Shunting old..PDA ligation,,,CoA Repair 1 .  Repair :  VSD ,  ASD , Tetralogy of Fallot repair 2 .  Palliative: A. Temporary: BT shunt( to allow for pulmonary blood  flow, encourage deviation ofpulmonary tree ) PA banding (  prevent overloading of thepulmonary circulation pending repair of large VSD )
  30. Thrills are palpable vibrations of murmur ,, grade 3 or more
  31. Absent in – OBESE, Pericardial/pleural effusion, pneumothorax SHIFT in : LVH-outward and downward RVH: outwards.....Dextrocardia.....scoliosis ..kyphosis....diaphragmatic hernia
  32. Heaving—Normal, no shift---more than 2/3rd—sustained---Concentric hypertrophy– pressure overload---AS, CoA Hyperdynamic – MR/AR/VSD/PDA—volume overload
  33. Volume Overload  Fast, ill-sustained PS impulse  L→R shunts -ASD, VSD Pressure overload  Slow, sustained PS impulse  PS
  34. Left ventricular pacing
  35. Normally A2 is followed by P2, duration being 30-40 ms
  36. Pericardial knock : Loud, High frequency, Diastolic sound In constrictive pericarditis Due to abrupt halt to diastolic filling of heart.
  37. Changing murmurs : they change in intensity from time to time as seen in Infective endocarditis.
  38. Levine and freeman staging
  39. MR---radiates to axilla...and accentuates during expiration
  40. PDA, AV FISTULA, VENOUS HUM, CoA, TAPVC
  41. Intra pleural and intra thoracic pressure decreases during inspiration Flow to right side of heart increass
  42. Passive leg raise is similar
  43. ‘Use your eyes and hands before before your ears, Start at the periphery and leave the heart to last; and when you come to it, leave the auscultation to the last.’