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CV Final Material > AVSD/VSD/ASD > Flashcards

AVSD/VSD/ASD Flashcards

1
Q

4 month old male who presents to clinic for evaluation of a heart murmur that was first
heard at 2 weeks of age.
• He has been sweating and tiring with feeds and has not been growing as well lately. Still has good activity level.
• No cyanosis, edema, or syncope. He was a term vaginal delivery. Mom had advanced maternal age but no perinatal complications.

– HR 154 (120-140 is goal) – RR 45 – BP 78/40 – Pulse ox: 98% – Weight 4 kg (birth weight 3 kg, low wt gain) – Length 64 cm is normal;

What is concerning about this?

A

These are signs for CHF; tachycardia/tachypnea/ murmur and low wt gain despite normal growth

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2
Q

Same baby as before, on physical exam

– Gen: alert, NAD
– HEENT: + up slanting palpebral fissures, + epicanthal folds, flat nasal bridge, no perioral cyanosis, short neck
– Lungs: CTA bilaterally, + tachypnea, subcostal retractions
– CV: active precordium, normal S1 and S2, II/VI systolic murmur heard best at LSB, 2+/4+ pulses bilaterally
– Abdomen: + bowel sounds, non-distended, soft, liver edge palpable 4 cm below RCM (should be 1 cm)
– Ext: warm and well-perfused, CR < 3 seconds. No clubbing, cyanosis, or edema.

Genetic syndrome?

A

Down syndrome; trisomy 21

upward slanting eyes, epicanthic folds, flat facies

systolic murmur at LSB and the liver palpable 4 cm below suggests cardiac anomalies

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3
Q
A
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4
Q

What cardiac defect is present in 40% of pts with Down syndrome?

A

AV Septal or Endocardial Cushion Defect

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5
Q

How many endocardial cushions do we have, when do they appear?

A

4 endocardial cushions
– superior,
– inferior,
– 2 lateral cushion
• Appear at end of the 4th week of gestation

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6
Q

Endocardial cushions appear at end of the 4th week of gestation
– Initially, AV canal only gives access to the

A

primitive left ventricle

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7
Q

• In 5th week, AV canal enlarges to the_____ and blood flow into both the primitive right and left
ventricle

A

right

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8
Q

Fusion of superior and inferior cushions result in

A

division of AV canal into right and left AV orifices (end of 5th week)

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9
Q

Endocardial cushions participate in formation of the
membranous portion of________ and in closure of _______

A

interventricular septum

primum septum

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10
Q

AV septal defects
1. AV valve leaflest insert at same level of:

  1. See unwedged ________ displacement of aortic valve
  2. Elongated _______
  3. Cleft in the ______
A

cardiac crux
anterior displacement of the aortic valve
– Elongated LVOT
– Cleft in left AV valve

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11
Q

AVSD is spectrum disease. We have a tongue of tissue dividing the common AV valve into a R and L component via connecting the _______ and ______ bridging leaflets centrally

A

anterior and posterior

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12
Q

What happened embroyologically to cause the defect seen?

A

this is an AVSD… d/t endocardium cushion defect

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13
Q

24 y/o M presents to your office after moving to this area for Graduate school
– No significant PMHx known except was told he had a murmur during childhood
• Never hospitalized/ No surgeries/ No medications
– Does remember needing to take antibiotics prior to dental visits
• Active lifestyle – working out 2-3 times a week without fatigue or intolerance
Gen: Well nourished, young adult
• HEENT: MMM, EOMI, clear pharynx, no JVD or cervical lymphadenopathy
• Lungs: CTA bilaterally, no accessory muscle
• Abd: Soft, NT, ND, (+)BS
• Ext: no C/C/E, WWP, intact distal pulses
• Heart: Faint thrill over the precordium, no RV lift, and you hear a harsh holosystolic sound from S1 to S2

Dif Dx?

A
  1. VSD
  2. Mitral regurg and tricuspid regurg
  3. Severe pulmonic stenosis

All cause holosystolic murmurs from S1 to S2

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14
Q

You hear a harsh holosystolic murmur on exam of a patient goes from S1 to S2… whats your next step?

A

Echo

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15
Q

VSD classified according to their relationship to anatomic landmarks on the

A

right side of the septum

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16
Q

Four types of VSD

A

Membranous
– Outlet/subarterial
– Trabecular muscular
– Inlet

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17
Q

Inlet type VSD is commonly associated with

A

Downs

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18
Q

Most common location of VSD

A

Perimembranous

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19
Q

Quick review on location of VSD: better image

A
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20
Q

VSD’s with significant shunts can result in 4 major complications:

A

– CHF secondary to large volume L–>R shunt
– LV dysfunction as a late consequence of chronic volume overload
– Pulmonary HTN with eventual reversal of the shunt to R–>L
(Eisenmenger’s syndrome)
– Bacterial endocarditis

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21
Q

Magnitude of the VSD shunt determined by

A

VSD size and pulmonary vascular resistance

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22
Q

In VSD, a_________ defect has resistance to shunt at the VSD; creates a gradient between LV and RV

A

Restrictive

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23
Q

Survival in pts with VSD:

Spontaneous closure = ______
• 25 year survival

– Small =
– Moderate =
– Large =
– Eisenmenger =

A

normal

– Small = 96%
– Moderate = 86%
– Large = 61%
– Eisenmenger = 42%

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24
Q

Some comlications of small VSD in adulthood

A

– Spontaneous closure = 10%
– Endocarditis = 11%
– Aortic regurgitation = 20%
– Arrhythmias = 9%
• Double chamber RV
• Exercise intolerance

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25
VSD-Late Post-op Complications
* Endocarditis * Aortic regurgitation * Tricuspid regurgitation * Heart block * LV obstruction
26
In fetal circulation, where is the highest oxygenated blood?
in the IVC
27
What structures in fetal circulation allow shunting?
Ductus venosus to bypass the liver Foramen ovale to bypass the lungs PDA to connect pulmonary artery/aorta for any blood that got through
28
Which direction does shunting occur in fetal devo?
Will occur from high to low resistance.. high resistance is in the lungs
29
How does the brain and body receive oxygenated blood in utero?
Blood then passes into the left ventricle --\> then to the aorta --\>blood is sent to the heart muscle itself in addition to the brain from Ascending aorta and to the body from descending aorta
30
SVC dumps into the RA.. it then has what choices (in regards to fetal circulation)?
Go throuh the FO to the LA bc lungs are high resistance or go into RV then will head out the pulmonary artery and cross over at the PDA, again becuase the lungs are high resistance
31
What changes physiologically at birth in regards to fetal circulation?
Baby takes first breath, expands lungs and drastically reduces pulmonary resistance. Blood no longer goes through foramen ovale because systemic resistance is much higher, goes into RV and then lungs .
32
The Ductus arteriosus stays open in the fetus because low PaO2 and circulating prostaglandins (PGE2) are\_\_\_\_\_\_\_ on the ductus. In the neonate, when pulmonary oxygen saturation increases, there is less circulating PGE2 and :
vasodilatory the ductus closes off
33
What are the consequences of a deficient atrial septum before birth?
none.. this is normal fetal circulation allowing R--\> L shunting
34
A layer of tissue called the ________ acts as a valve over the foramen ovale during fetal development. After birth, the pressure in the right side of the heart drops as the lungs open and begin working, causing the foramen ovale to close entirely
septum primum
35
The septum primum grows down from the superior aspect and the Dorsal endocardial cushions grows up from below... they are supposed to meet at the crux of the heart, but the septum primum gets lazy and doesn't.. OH NO! what does this result in?
Get an atrial septal defect
36
The\_\_\_\_\_\_\_\_atrial septal defect is the most common type of atrial septal defect, and comprises 6–10% of all congenital heart diseases.
ostium secundum
37
Heart sound heard in individuals with ASD?
In individuals with an ASD, there is a fixed splitting of S2. The reason that there is a fixed splitting of the second heart sound is that the extra blood return during inspiration gets equalized between the left and right atrium due to the communication that exists between the atria in individuals with ASD.
38
Explain how splitting of S2 happens in normal individuals (they talked about inspriation and expiration)
During respiratory inspiration, the negative intrathoracic pressure causes increased blood return into the right side of the heart. The increased blood volume in the right ventricle causes the pulmonic valve to stay open longer during ventricular systole. This causes a normal delay in the P2 component of S2. During expiration, the positive intrathoracic pressure causes decreased blood return to the right side of the heart. The reduced volume in the right ventricle allows the pulmonic valve to close earlier at the end of ventricular systole, causing P2 to occur earlier.
39
How does ASD affect oxygenation?
not much affect until RV can't keep up with the increased volume. You will not see hypertrophy of RV... just dilation to accomidate increased volume
40
What kind of shunt is an ASD?
L--\> R and its more of a volume shunt over pressure shunt
41
do you see ASD right away in newborn?
not usually.. takes longer to devo symptoms
42
A discrete, congenital narrowing of the thoracic aorta at the site of insertion of the ductus arteriosus
Coarctation of the Aorta
43
In coarctation of the aorta, what structure will remain open?
ductus arteriousum to allow mixing of blood
44
Pathophysiology of coarctation of Aorta Obstruction to flow results in increased \_\_\_\_\_\_\_ --\> Increased wall stress --\>Compensatory \_\_\_\_\_\_\_ •--\>Congestive heart failure --\>SHOCK, metabolic acidosis, and organ failure
LV afterload ventricular hypertrophy
45
Fetal flow patterns: In fetal life, blood flow through the \_\_\_\_\_\_\_\_\_constitutes only about 10% of the total cardiac output. • The ductal flow is \_\_\_\_\_\_ to \_\_\_\_\_\_\_(pulmonary artery to descending aorta) with only 7% of blood going to the lungs
aortic isthmus right to left
46
Coarctation of aorta: The right heart is carrying ~\_\_\_\_\_ of the volume load of the total cardiac output Assuming the isthumus was completly atretic; what will we see with dem babies?
2/3 there would be blood supply to all tissues, so the babies tend to be term and well-formed with normal birth weights
47
Normally at birth, the ductus constricts and \_\_\_\_\_\_\_\_ increases. • The flow through the isthmus of the aorta\_\_\_\_\_\_\_ The pulmonary resistance\_\_\_\_\_\_ and duct reverses directions
pulmonary blood flow increases drops
48
Why Does Coarctation Develop? • Hemodynamic theory (Also Ductal tissue theory and Genetic substrate (association with syndromes, eg. Turner’s))
– Result of hemodynamic disturbances that reduce the volume of blood through the fetal aortic arch – Isthmus normally receives only 10% of the combined ventricular output, which explains why the isthmus is normally 70-80% the diameter of the neonatal ascending aorta – Explains the common association with VSD, LVOTO, tubular hypoplasia of the transverse arch
49
What genetic condiciton is associated with coarctation of aorta?
Turners syndrome
50
In coarcation of the aorta, the % oxygenated blood in the descending aorta is approximately the same as in a normal indivudual yet the blood returning to the IVC in normal individual is 65% oxygenated while with coarctation it's only 50%... why?
The blood in the IVC is still getting oxygenated in coarctation... there is just LESS volume of it reaching the lower half of the body thus it will be more deoxygenated when it goes to IVC (tissues need to pull more oxygen from less blood)
51
What is the pressure difference between arch of the aorta in normal and coarctation of aorta?
normal individual pressure is 80/55..... pressure in coarcation is 120/80 to overcome constriction of aorta
52
Explain the ductal theory of coarctation of aorta
Migration of ductal smooth muscle cells into the aorta with subsequent constriction/narrowing of the aortic lumen – becomes evident as the ductus arteriosus begins to constrict – supported by the fact that neonatal coarctation manifests only after ductal closure • The obstruction appears as an indentation (posterior shelf) in the postero-lateral side of thoracic descending aorta
53
Coarctation of aorta is found in _____ of CHD and more common in male or female?
4-8% male
54
Genetic influence in coarctation of aorta
Turner XO 35% affected, causes sterility, can't be transmitted unless mosaic \*Noonan syndrome
55
Coarctation of aorta is assoicated with what other defects?
Association with Intracardiac Lesions • Bicuspid Aortic Valve, 22-42%, up to 85% • Simple Coarctation, 52%– Without important intracardiac lesions • Complex Coarctation, 48% – Presentation in infancy more likely – VSD (perimembranous, muscular, malalignment) – Valvar aortic stenosis – Subaortic stenosis – Mitral stenosis – Shone’s Complex: multiple left-sided obstructive lesions – Other: AVSD, d-TGA, Taussig Bing, l-TGA, HLHS
56
* Aortic arches arise from the\_\_\_\_\_\_\_ part of truncus arteriosus * Develop to supply the 6 pharyngeal arches during _______ week of gestation
most distal 4th and 5th
57
* Each pharyngeal arch receives an artery and cranial nerve * The\_\_\_\_ aortic arch never forms
5th – Only I, II, III, IV, VI ever exist
58
Each aortic arch is embedded in the\_\_\_\_\_\_\_ of the pharyngeal arches • Each will terminate in \_\_\_\_\_\_\_\_ • Over next several days the arterial pattern becomes modified as some of the aortic arches and dorsal aorta regress
mesenchyme the left and right dorsal aorta
59
Natural history of coarctation of aorta: Death had mean age of \_\_\_\_\_\_ and 75% died by \_\_\_\_\_\_ common causes were:
34 by 46 caused by CFH, aortic rupture, Bacterial endocarditis, intracranial hemorrhage
60
Below are all presentations from which anomaly? 1.Fetal cardiac abnormalities 2.Infant with CHF 3.Child/adolescent with arterial systolic hypertension 4.Child with murmur
Coarctation of aorta
61
Infant with CHF from coarctation of aorta: why would CHF occur?
Coarctation is severe or develops rapidly: LV systolic dysfunction and CHF may occur: – ↓SV, ↑LVEDP, ↑LA pressure, pulmonary venous congestion – Acidosis further ↓myocardial contractility
62
63
Infant with CHF d/t coarctation of aorta: – Pale, irritable, respiratory distress – Differential cyanosis if\_\_\_\_\_\_ shunt •\_\_\_\_\_\_\_\_ pulses in upper and lower extremities, should check all four – LE:
R→L Discrepant ↓amplitude and delayed timing
64
Physical exam of coarcation of aorta Palpation: – Heaving LV impulse at apex if \_\_\_\_\_\_\_ – _______ possible in suprasternal notch
LV volume overload Systolic thrill
65
Auscultation in child with coarcation of aorta: What do we hear at the apex of the heart?
Constant systolic ejection click at apex (bicuspid valve)
66
– Murmurs heard in coarcation of aorta:
• 2-3/6 SEM at LUSB and base, radiating to the left interscapular area posteriorly – In severe CoA, systolic murmur may spill into diastole • Continuous murmurs throughout chest (collaterals) • Associated VSD, mitral stenosis
67
What do we see on chest xray in infant with coarcation of aorta with CHF?
– Pulmonary vascular congestion
68
Describe chest xray of coarctation of aorta
– prominent aortic knob – indentation of the left border of the descending aorta (3 sign) – Rib notching (rare before 10 yrs) • Caused by erosion of inferior surfaces of posterior ribs by dilated/tortuous pulsatile intercostal arteries
69
Extended End to End Anastomosis to fix coarctation of aorta: – Advantage:
no circumferential suture → less recurrence
70
Prosthetic Patch Aortoplasty to fix coarctation... problem with this fix?
• High incidence of late aneurysm formation
71
Subclavian Flap Aortoplasty Requires less extensive aortic mobilization • \_\_\_\_\_\_\_has theoretical growth potential • Sacrifices ______ artery • Ligation of \_\_\_\_\_\_to avoid subclavian steal
Subclavian tissue left subclavian vertebral artery
72
Treatment of choice for infants with coarctation of aorta in early studies
subclavian flap aortoplasty
73
Currently, we do percutaneous tx for coarcation of the aorta; Significant miniaturization of equipment over the last decade has enabled percutaneous treatment of coarctation in all but the smallest of patients. • We prefer to \_\_\_\_\_\_\_\_over angioplasty alone, if an adult-sized stent can be placed
stent the aorta
74
Transcatheter Stent Placement for coarcation of aorta • Pros: • Cons:
– Decrease stenosis related to vessel recoil • Eliminates need for over-dilation – Decrease incidence of late aneurysm formation – Physiologic impact of a rigid aortic segment – Large sheath – Size of available stents/balloons may be limiting

CV Final Material (16 decks)

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