Clinicopathologic conference- Ventricular septal defect
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Transcript of Clinicopathologic conference- Ventricular septal defect
8/14/2019 Clinicopathologic conference- Ventricular septal defect
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khaikwan, nophawanlariosa, michael jeromele, manliao, karen isabellibres, kimberlypandac, therese rondellpangan, efrea lyndee
perocho, zichri kerensantos, edilberto de belenthanathada, sunklangtonagaya, sarahyee, ma. stephaniezamora, mary rose sugar
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CASE 1
During a routine athletic physical, a 15year old boy is found to have a systolicthrill that is palpable at the lower left
sternal border accompanied by a harsh,pansystolic murmur that is heard best atthe site of the thrill. He is asymptomaticand has no evidence of hypertension,
cyanosis or edema. An electrocardiogramand chest radiograph are normal.
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Clinical Scenario
Male, 15 year old
Presence of systolic thrill palpable atthe lower left sternal border
Accompanying sign: harsh, pansystolicmurmur heard best at site of thrill
Asymptomatic
No hypertension, cyanosis or edema ECG Normal
Chest radiography Normal
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Position of the Heart
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Pulmonary and Systemic
Circulation
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Pericardium
The pericardium is the set of membranesaround the heart. It is actually composedof three layers of membranes.
Visceral pericardium- the innermost Parietal pericardium- the middle,
Fibrous pericardium- the outer one is theextra one and is tough.
Pericardial Activity- tiny space betweenthe visceral pericardium and the parietalpericardium.
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Chambers of the Heart
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Valves of the Heart
4 valves
One way flow
Leaky valve=heart murmur
2 atrioventricular valves
>Left AV valve-bicuspid or mitral
>Right AV valve-tricuspid
2 semilunar valves>Pulmonic semilunar valve
>Aortic Semilunar valve
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Valves of the Heart
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Atrioventricular Valves
1. Right AV valve
Between the right atrium and right ventricle
Also called the tricuspid valve because it has threecusps
Cusps close when right ventricle contracts…preventingblood from going back up into the right atrium
2. Left AV valve
Between the left atrium and the left ventricle
Also called the bicuspid valve because it only has 2
cusps Also called the mitral valve
Cusps close when left ventricle contracts…preventingblood from back-up into the left atrium
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Semilunar Valves
1. Pulmonary semilunar valve
When right ventricle contracts,
blood is forced through this valve toenter pulmonary trunk.
2. Aortic semilunar valve
When left ventricle contracts, bloodis forced through this valve to enterthe aorta.
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Cardiac Conduction
System The cardiac conduction system
generates and transmits impulsesthat stimulate contraction of themyocardium.
Under normal circumstances, theconduction system first stimulate the
contraction of the atria and then theventricles.
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Cardiac Cycle
Refers to the events of one complete heartbeat. The length of the cardiac cycle is usually about0.8 sec.
Systole (contraction of the muscle)- there isventricular pumping, the chambers of the heartbecome smaller as the blood is ejected. Occurssecondary to the depolarization of cells.
Diastole (relaxation of the muscle)- there isventricular filling, the heart chambers fill withblood in preparation for subsequent ejection.
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Cardiac Output
Volume of blood ejected per minute
-Each ventricle ejects approximately
70ml of blood/beat Averages between 4-8L/min
CO=Stroke volume x Heart rate
=70ml x 60 beats/min=4,200 ml/min
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Anatomy of the
Interventricular Septum The interventricular septum is the wall of the heart intermediate to
the right and left ventricles. Its surface markings correspond to theanterior and posterior interventricular grooves. It runs obliquely tothe left and slightly inferiorly from posterior to anterior. Due to thisangulation, the right ventricle tends to lie anteriorly and the leftventricle posteriorly.
Throughout most of its surface area, the septum is as muscular asthe left ventricle. It tends to bulge into the chamber of the rightventricle producing a concavity on the left ventricular side. Nearerto the aortic valve orifice beneath the margins of the right andposterior leaflets, the septum becomes thinner and more fibrous. This region is termed the pars membranacea septi, or themembranous part of the interventricular septum. It is oval in shape.
The muscular and membranous parts of the interventricularseptum have different developmental origins. The membranouspart of the septum is the most frequent site for ventricular septaldefects which are usually congenital.
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a. Patent ductus arteriosus (PDA)b. Tetralogy of fallotc. Tricuspid regurgitation
Ventricular septal defect Patent ductus arteriosus Tetralogy of fallot Tricuspid regurgitationMurmur Timing Primary four malformations Murmur
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Murmur
Location: 3rd, 4th and 5th left
interspaces
Radiation: often wide
Intensity: often very loud, with
a thrill
Pitch: high holosystolic
Quality: often harsh
Timing
Continuous murmur in
both systole and diastole,
often with a silent interval
late in diastole. Loudest in
late systole, obscures S2, and
fades in diastole.
Primary four malformations
•Pulmonary stenosis
•Overriding aorta
•Right ventricular hypertrophy
•Ventricular septal defect(VSD)
Murmur
Location: lower left sternal
border
Radiation: to the right of
the sternum, to the xiphoid
area, and perhaps to the left
midclavicular line, but not the
axilla
Intensity: variable Pitch: medium
Quality: blowing
holosystolic
Aids: unlike mitral
regurgitation, the intensity
may increase slightly with
inspiration.
Associated findings
•
S2 may be obscured by the loudmurmur
• Findings vary with the severity of
the defect and with associated
lesions
Location
Left 2nd
interspaceRadiation
Toward the left clavicle
Intensity
Usually loud, sometimes
associated with a thrill
Quality
Harsh, machinery-like
Pitch
Medium
Additional anomalies
1.stenosis of the left pulmonary artery,in 40% of patients
2.a bicuspid pulmonary valve, in 40% of patients
3.right-sided aortic arch, in 25% of patients
4.coronary artery anomalies, in 10% of patients
5.a foramen ovale or atrial septaldefect, in which case the syndrome issometimes called a pentalogy of
Fallot6.an atrioventricular septal defect
7.partially or totally anomalouspulmonary venous return
8.forked ribs and scoliosis
Associated findings
•
the right ventricle impulse isincreased in amplitude and
may be sustained.
•An S3 may be audible along
the lower left sternal boarder.
The jugular venous pressure is
often elevated, with large v
waves in the jugular veins.
Mechanism
A VSD is a congenital
abnormality in which blood flows
from the relatively high-pressure
left ventricle into the low-pressureright ventricle through a hole.
Mechanism
Low oxygenation of blood due to the
mixing of oxygenated and
deoxygenated blood in the left ventricle
via the VSD and preferential flow of themixed blood from both ventricles
through the aorta because of the
Mechanism
When the tricuspid valve
fails to close fully in systole,
blood regurgitates from the
right ventricle to right atrium,producing a murmur. The most
common cause is right
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Ventricular septal
defect• A ventricular septal defect (VSD) is a defect inthe ventricular septum, the wall dividing the left andright ventricles of the heart.
• The ventricular septum consists of an inferior muscularand superior membranous portion and is extensively
innervated with conducting cardiomyocytes. Themembranous portion, which is close tothe atrioventricular node, is most commonly affected inadults and older children.
• Congenital VSDs are collectively the mostcommon congenital heart defects.
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Diagnosis
• Detected by cardiac auscultation(due topathognomonic holo- or pansystolic murmur)-- murmur depends on the abnormal flow of blood from the left ventricle, through the
VSD, to the right ventricle.• Confirmation of cardiac auscultation can be
obtained by non-invasivecardiac ultrasound (echocardiography).
• More accurately measure ventricularpressures-cardiac catheterization.
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PDA
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Patent ductus arteriosus
heart condition that is normal but reverses soon after birth.
Persistent PDA, there is an irregular transmission of bloodbetween two of the most important arteries in close proximity tothe heart.
Ductus arteriosus normally seals off within a few days, in PDA,the newborn's ductus arteriosus does not close but remainspatent.
common in neonates with persistent respiratory problems suchas hypoxia, and has a high occurrence in premature children. Inhypoxic newborns, too little oxygen reaches the lungs to produce
sufficient levels of bradykinin and subsequent closing of the DA. Premature children are more likely to be hypoxic and thus have
PDA because of their underdeveloped heart and lungs.
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MOA of PDA
allows a portion of the oxygenated blood from the leftheart to flow back to the lungs (following the pressuregradient from the higher pressure aorta to thepulmonary arteries).
If this shunt amount is substantial, the neonate becomesshort of breath because there is not only the normalamount of unoxygenated blood that has returned fromthe body to go to the lungs but in addition there is theamount shunted through the PDA.
The neonate's work of breathing is increased, using upmore calories and often interfering with feeding ininfancy. This condition as a constellation of findings iscalled congestive heart failure.
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In some cases, such as in transposition of the greatvessels (the pulmonary artery and the aorta), aPDA may need to remain open. In this
cardiovascular condition, the PDA is the only waythat oxygenated blood can mix with deoxygenatedblood. In these cases, prostaglandins are used tokeep the patent ductus arteriosus open.
Exemptions:
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Diagnosis
Usually diagnosed using non-invasive techniques.
Echocardiography, in which sound waves are used to capturethe motion of the heart, and
Associated Doppler studies are the primary methods of detecting PDA.
Electrocardiography (ECG), in which electrodes are used torecord the electrical activity of the heart, is not particularlyhelpful as there are no specific rhythms or ECG patterns whichcan be used to detect PDA.
Chest X-ray may be taken, which reveals the overall size of neonate's heart (as a reflection of the combined mass of the
cardiac chambers) and the appearance of the blood flow to thelungs ---small PDA most often shows a normal sized heart andnormal blood flow to the lungs --- large PDA generally shows anenlarged cardiac silhouette and increased blood flow to thelungs.
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Tetralogy of Fallot
Accounting for about 5% of all congenitalcardiac malformations
is the most common cause of cyanotic
congenital heart disease The four features of the tetralogy are
(1)VSD,
(2) obstruction to the right ventricular
outflow tract (subpulmonic stenosis),(3) an aorta that overrides the VSD, and
(4) right ventricular hypertrophy
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Clinical features
- right-to-left shunting,
- decreased pulmonary blood flow, and increased aorticvolumes.
- If the pulmonic obstruction is mild, the conditionresembles an isolated VSD, because the high left-sidedpressures on the left side cause a left-to-right shunt with nocyanosis.
- , marked stenosis causes significant right-to-leftshunting and consequent cyanosis early in life.
- As patients with tetralogy grow, the pulmonic orificedoes not enlarge, despite an overall increase in the size of theheart.
- patients develop erythrocytosis with attendanthyperviscosity, and hypertrophic osteoarthropathy;
- the right-to-left shunting also increases the risk forinfective endocarditis, systemic emboli, and brain abscesses.
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Tricuspid Regurgitation
In this condition, the valve doesnot close properly and blood flows
back into the right atrium.
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CAUSE
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CAUSE
Right ventricle enlarges and Increase resistance of blood flow from the right ventricle to the lungs
Resistance may be increased by a severe, long-standing lung disorder
Emphysema
Pulmonary Hypertension pulmonic stenosis
left side of the heart disorder (such as mitral valvestenosis)
To compensate, the right ventricle enlarges, stretchingthe tricuspid valve and causing regurgitation.
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Weakness and fatigue.
Pulsations in the neck from theelevated Right Atrial pressure
Discomfort in the right upper part of the abdomen due to an enlarged liver
Heart failure results in accumulation
of fluid in the body, mainly in the legs
Signs and Symptoms
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Physical Diagnosis
Echocardiography
Chest x-ray
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Morphology
- heart is large and "boot shaped" as a result of rightventricular hypertrophy
- the proximal aorta is typically larger than normal,with a diminished pulmonary trunk.
- The left-sided cardiac chambers are normal sized,
while the right ventricular wall is markedly thickened andmay even exceed that of the left.
- The VSD lies in the vicinity of the membranousportion of the interventricular septum, and the aortic valvelies immediately over the VSD.
- The pulmonary outflow tract is narrowed, and, in a
few cases, the pulmonic valve may be stenotic. - Additional abnormalities are present in many cases,
including PDA or ASD; these are actually beneficial inmany respects, because they permit pulmonary bloodflow.
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Three Major Categories:
Malformations causing a left-to-rightshunt
Malformations causing a right-to-leftshunt
Malformations causing anobstruction
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A.) Left-to-right shunts
Atrial Septal Defect
Ventricular Septal Defect
PDA (Patent Ductus Arteriosus) Arterioventricular Septal Defect
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Atrial Septal Defect
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Atrial Septal Defect
Three major types:
Secumdum ASD – 90% of most cases
Primum ASD – 5% of anomalies Sinus venosus
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Ventricular Septal
Defect
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Ventricular Septal
Defect Membranous VSD – 90% involves themembranous septum
Infundibular VSD – lies below thepulmonary valve
Swiss-cheese septum – multiplemuscular VSD
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PDA (Patent Ductus
Arteriosus)
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Arterioventricular
Septal Defect
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Arterioventricular
Septal Defect Partial AVSD – consist of primum ASDand a cleft anterior mitral leaflet
Complete AVSD – large combined AVseptal defect and a large commonAV valve
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B.) Right-to-left shunts
(cyanotic) Tetralogy of Fallot
Transposition of the Great Arteries
Persistent Truncus Arteriosus Tricuspid Atresia
Total Anomalous Pulmonary VenousConnection
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Tetralogy of Fallot
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Tetralogy of Fallot
Four features of the Tetralogy of Fallot:
VSD
Obstruction to the right ventricularoutflow tract (subpulmonarystenosis)
Aorta that overrides the VSD
Right ventricular hypertrophy
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Transposition of the
Great Arteries
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Truncus Arteriosus
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Tricuspid Atresia
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C.) Obstructive
Congenital Disease Coarctation of the Aorta
Pulmonary Stenosis and Atresia
Aortic Stenosis and Atresia
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Coarctation of the Aorta
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Aortic Stenosis and
Atresia
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Natural History
Small (& even some larger)
lesions often close spontaneously either by
muscular growth or plugging with tricuspidvalve tissue. Larger lesions will eithercause problems due to the size of theshunt (failure to thrive & recurrent chest
infections) or cause irreversible pulmonaryvascular disease. Life expectancy andexercise capacity will therefore berestricted.
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Congenital VSDs are frequently associated
with other congenital conditions, such asDown syndrome.
A VSD can also form a few days after amyocardial infarction (heart attack) due tomechanical tearing of the septal wall,before scar tissue forms, when
macrophages start remodelling the deadheart tissue.
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Epidemiology and
Etiology VSDs are the most common
congenital cardiac anomalies. They are found in
30-60% of all newborns with a congenital heartdefect, or about 2-6 per 10,000 births. It isdebatable whether all those defects are trueheart defects, or if some of them are normalphenomena, since most of the trabecular VSDsclose spontaneously. Prospective studies give aprevalence of 2-5 per 100 births of trabecularVSDs that closes shortly after birth in 80-90% of the cases.
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Prognosis
Transcatheter closure has been undertakenfor muscular defects and a device has just
become available for perimembranousdefects and is under evaluation. This isexcellent for most patients. The vastmajority are able to live a normal and
unrestricted life. Re-operations for residualVSDs are now uncommon.
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Congenital Heart
defects(VSD) Caused by developmental abnormalities. However the genes involved in these defects
have been identified in only a minority of conditions.
Well defined genetic or environmentalinfluence are identifiable in only 10% of thecases of congenital heart ds (VSD…).
There is an association of congenital cardiacmalformations with certain chromosomal
abnormalities: trisomies 13, 15, 18 and 21and the Turner Syndrome.
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VSD
Mutation of the gene that encodes thetranscription factor TBX5 has been shown tocause VSD and ASD observed in Holt-Oramsyndrome which is a rare condition associated
with heart, arm and hand defects. Developmental errors in mesenchymal tissue
migration: anomalies of outflow tract, failure of fusion and failure of septation.
Other mechanisms include extracellular matrix
abnormalities and situs and looping defects andendocardial cushions defects.
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S d b th l ft
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Second, because the leftventricle normally has amuch higher systolicpressure (~120 mm Hg) thanthe right ventricle (~20 mmHg), the leakage of bloodinto the right ventricletherefore elevates rightventricular pressure andvolume, causing
pulmonary hypertension with
Thi ff t i
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This effect is morenoticeable in patients withlarger defects, who maypresent withbreathlessness, poorfeeding and failure tothrive in infancy. Patientswith smaller defects may beasymptomatic.
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Symptoms
VSD is an acyanotic congenitalheart defect, aka a Left-to-rightshunt, so there are no signs of cyanosis.
V t i l t l
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Ventricular septal
defect is usuallysymptomless at birth. Itusually manifests a few
weeks after birth.
Si
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Signs
Pansystolic /Holosystolic murmur(depending upon the size
of the defect)
CLINICAL MANIFESTATIONS
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CLINICAL MANIFESTATIONS
T b i t f VSD
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Two basic types of VSD
Perimembranous VSD - an opening inthe upper section of the ventricularseptum, near the valves, occurs in 75%of all VSD cases.
Muscular VSD - an opening in the lowersection of the ventricular septum
occurs in up to 20% of all VSD cases.
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NORMAL HEART SOUND
CLICK ME!!!
VENTRICULAR SEPTAL DEFECTSOUND
CLICK ME TOO!!!
P t ti
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Presentation The size of the ventricular septal opening will
affect the type of symptoms noted, theseverity of symptoms, and the age at whichthey first occur. A VSD permits extra blood topass from the left ventricle through to the
right side of the heart, and the right ventricleand lungs become overworked as a result.
The larger the opening, the greater theamount of blood that passes through and
overloads the right ventricle and lungs.
M t t f
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Most common symptoms ofVSD fatigue sweating rapid breathing
heavy breathing congested breathing disinterest in feeding, or tiring while
feeding poor weight gain
Signs of VSD
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Signs of VSD
Murmur- due to the sound of bloodas it passes between the left andright ventricles.
Thrill- palpable murmur
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VSD will produce a
systolic murmur. Theclassic murmur is grade¾, holosystolic, harshand blowing incharacter.It will peak in
midsystole. It is bestheard along the lowerleft sternal border andapex. Smaller defects of small and mediumdefects will typically
produce a louder soundthan a larger defect asthe blood velocity ishigher.
Small left to right
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Small left-to-rightshunt 1st heart sound at the apex is normal;
2nd sound at pulmonary area is splitphysiologically
Grade 2-4/6,medium-to high-pitched,harsh pansystolic murmur heard bestat the left sternal border in the 3rd
and 4th
ICS
Moderate left to right
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Moderate left-to-rightshunt Slight prominence of precordium
Moderate left ventricular heave
Systolic thrill palpable at the lowerleft sternal border between the 3rd and 4th ICS
Grade 3-4/6, harsh pansystolic
murmur
Large ventricular septal
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Large ventricular septaldefects w/ pulmonary
hypertension Precordium is prominent, sternum bulges
Left ventricular thrust and rightventricular heave are palpable
Thrill may or may not be present at thelower left sternal border
S2 usually single or narrowly split, w/
acdentuation of pulmonary component
Harsh, pansystolic murmur
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SIMPLE RECALL
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The most common formsare in the muscular portionof the septum where they
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of the septum where theymay lie posterior (1),apically (2) or anteriorly(3). The perimembranous
(4) form is the next mostcommon. It may extendposteriorly in the septum(inlet) or anteriorly towardsthe aortic valve (subaortic).More rarely (except inAsians) it is situated below
both the aortic andpulmonary valves doublycommitted (5).
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The diagnosis of a VSD is usually
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suspected clinically by hearing acharacteristic heart murmur. A murmuris a sound generated by abnormallyturbulent flow of blood through theheart. This murmur is the result of blood
being shunted through the VSD from thehigher-pressure left ventricle into thelower-pressure right ventricle.
The loudness of the murmur is relatedto the size of the defect and amount of blood crossing the defect.
Chest x-ray
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yChest X-ray looks to see if there is a large heart with fluid
in the lungs.
Possible result: Small defects have a normal chest X-ray. Large defects with a big shunt have cardiomegaly and
pulmonary plethora.
A chest X-ray can also help follow the progression of
congestive heart failure by looking at the size of theheart and the amount of blood flow to the lungs. Thismay be normal at birth and change with time.
Electrocardiogram-- ECG shows signs of an enlarged left ventricle
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ECG shows signs of an enlarged left ventricle.
Possible result: Small defects have a normal ECG. Large defectswith a big shunt have biventricular hypertrophy due to thepressure load on the RV and the volume load on the LV. If the
shunt decreases due to either the development of pulmonarystenosis or vascular disease then the volume load decreases onthe LV and the left ventricular hypertrophy resolves to leaveright ventricular hypertrophy.
echocardiogramEchocardiogram is used to make a definite diagnosis
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Echocardiogram is used to make a definite diagnosis.
This shows size & position of VSD (arrow) and thus assists with theprognosis. It also allows identification of associated defects (ASD,pulmonary stenosis, aortic, mitral valve & arch lesions) when present.Colour Doppler is especially useful in identifying small defects.
The size of the shunt can be numerically estimated by Doppler flowtechniques but the accuracy is poor and the method rarely usedclinically. A reasonable subjective impression can however be madebased on the LA and LV size which will be enlarged in a large shunt. This may stretch the mitral valve ring causes mitral regurgitation
(LAVVR).
The pulmonary artery pressure can usually accuratelybe assessed using Doppler across the VSD In the
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be assessed using Doppler across the VSD. In theexample the VSD velocity which using the Bernoulliequation (4V2) is equivalent to a pressure difference
between the LV and RV of 64 mm predicating anormal PA pressure in most children.
Cardiac catheterization
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- (rare) concerns of high blood pressure in the lungs esp. moderate-sized defectsCardiac catheterization is used to study the various functions of theheart. Using different techniques, the coronary arteries can be viewedby injecting dye or opened using balloon angioplasty. The oxygenconcentration can be measured across the valves and walls (septa) of the heart and pressures within each chamber of the heart and acrossthe valves can be measured. The technique can even be performed in
small, newborn infants.
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A VSD can be detected by
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A VSD can be detected by… cardiac auscultation.
Classically, a VSD causes a pathognomonicholo- or pansystolic murmu
Auscultation is generally consideredsufficient for detecting a significant VSD.
The murmur depends on the abnormal flowof blood from the left ventricle, through the
VSD, to the right ventricle
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Normal section through the
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Normal section through themiddle
Normal heart front view
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Normal heart front view
VSD
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VSD
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CHF1 knockout mice have ventricular septal defects but no other organpathology
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Sakata Y et al. PNAS 2002;99:16197-16202
©2002 by National Academy of Sciences
Membranous VSD
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Membranous VSD
http://www.embryology.ch/anglais/pcardio/patholcardio03.html#AtrioventrikularerSeptum
defekt
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Muscular VSD
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Muscular VSD
Histological sections of mousehearts
VSD
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VSD
VSD
Cardiomyopathy
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y p y
cardiomyocyte
multinucleation.
Increased size of both cytoplasmand nuclease
Myocyte hypertrophy
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Histology of myocyte
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Clinical Features
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Small VSDs may beasymptomatic
VSDs in themuscular portion of the septum mayclose spontaneouslyduring infancy orchildhood
Large defects causesevere left to rightshunts
ASDs often lead toother cardiacmalformations orsecondary defects
Sequelae of Untreated Large
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gVentricular Septal Defects
Hypertrophied and dilated right ventricle Progressive pulmonary hypertension
Shunt reversal
Infective endocarditis
Vascular changes leading to cardiac failure High output
Subvalvular aortic stenosis (aortic valve incompetence)
Hypertrophied and Dilated
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Right Ventricle
Right QRS axisdeviation
Ejection isforceful but
ineffective
Ventriculararrhythmias
Myocardialischemia leadingto anginal pain
Progressive Pulmonary
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Hypertension
Vascular hyperactivity that leads tochronic vasoconstriction
Dyspnea on exertion
Cyanosis
Severe respiratory insufficiency
Chest pain
Shunt reversal
Effects of Shunt
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Reversal Condition similar to the Tetralogy of
Fallot
Decreased blood flow to the lungs
Cyanosis Increased size of heart
Increased risk of infective
endocarditis
Infective Endocarditis
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High pressure shunts increasehemodynamic trauma to the endocardialsurface
The creation of jet lesions in the rightventricle
Infection of the mural surface of theendocardium
Formation of vegetation (mass of thrombotic debris and organism)
Vascular Changes Leading to
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Cardiac Failure
Heart is enlarged, flabby and itspumps are inefficient
Development of progressive
congestive heart failure Patient experience episodes of
angina pectoris
As disease progresses, sudden deathis common
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T R E A T M E N T
The medical treatment of infants with
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ventricular septal defect (VSD) is directed at
the control of congestive heart failure.
The goals of therapy are:
To relieve symptoms.
To minimize frequency and severity of respiratory infections.
To facilitate normal growth.
Ventricular septum defect in infants is initiallyt t d di ll ith
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treated medically with:
Cardiac glycosides (e.g. 10-20mcg/kg/day)
- increases the strength of the heart muscle todeal with the greater blood volume.
Loop diuretics (e.g. furosemide 1-3 mg/kg/day)
- help remove excess fluid from the body so the
heart doesn't have to work as hard and thepatient feels much better.
ACE inhibitors (e.g. captopril 0.5-2 mg/kg/day)
- used to decrease the work load on the left
ventricle.
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A VSD that either decreases in size or
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closes completely during the first year
of life presents no problems to thepracticing physician.
Older children with VSDs are seldomsymptomatic and require little in theway of medical therapy.
Surgical Therapy
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Surgical closure is typically done before thechild begins preschool.
Surgery is indicated if medications do notwork in the first few months or years of life,especially if the child is not growingadequately even with medications.
Surgery is more urgent if evidence of
pulmonary hypertension has developed.
VSD surgery involves making a cut in the
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g y gchest so a surgeon can stitch the hole
closed or sew a patch of manmadesurgical material (such as Dacron orGore-Tex) over the defect. This preventsshunting (the movement of oxygenatedblood from the left to the right ventricle).Eventually, the tissue of the heart healsover the patch or stitches, and by 6
months after the surgery, the hole will becompletely covered with tissue.
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Surgery is not usually performed in
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g y y pnewborns because small defects will
close spontaneously in 20-25%.
The surgery also is more risky in the
first few months of life; the risk of death from the operation is higher inthe first 6 months of life than later.
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Medical management includes endocarditisantibiotic prophylaxis for all patients with VSDs
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antibiotic prophylaxis for all patients with VSDs.
Respiratory infections require promptevaluation and treatment.
Evaluate children with VSD at least once ortwice yearly to detect changes in the clinicalpicture that suggest the development of pulmonary vascular obliterative changes.
Patients with VSD and pulmonaryl b t ti di h
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vascular obstructive disease who are
deemed inoperable because of irreversibly elevated resistance requiremore intensive support andsymptomatic therapy as cyanosis
progresses and activity becomes morelimited.
Improvement in the symptomsi t d ith th l th i f
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associated with the polycythemia of
Eisenmenger complex (headache,extreme fatigue, and extremedyspnea) may be provided by partialexchange transfusion for RBC volume
reduction.
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