Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

AV Septal or Endocardial Cushion Defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

right

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

interventricular septum

primum septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happened embroyologically to cause the defect seen?

A

this is an AVSD… d/t endocardium cushion defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

VSD classified according to their relationship to anatomic landmarks on the

A

right side of the septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Four types of VSD

A

Membranous
– Outlet/subarterial
– Trabecular muscular
– Inlet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Inlet type VSD is commonly associated with

A

Downs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Most common location of VSD

A

Perimembranous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Quick review on location of VSD: better image

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Magnitude of the VSD shunt determined by

A

VSD size and pulmonary vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

Restrictive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

VSD-Late Post-op Complications

A
  • Endocarditis
  • Aortic regurgitation
  • Tricuspid regurgitation
  • Heart block
  • LV obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

In fetal circulation, where is the highest oxygenated blood?

A

in the IVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What structures in fetal circulation allow shunting?

A

Ductus venosus to bypass the liver

Foramen ovale to bypass the lungs

PDA to connect pulmonary artery/aorta for any blood that got through

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which direction does shunting occur in fetal devo?

A

Will occur from high to low resistance.. high resistance is in the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does the brain and body receive oxygenated blood in utero?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

SVC dumps into the RA.. it then has what choices (in regards to fetal circulation)?

A

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
Q

What changes physiologically at birth in regards to fetal circulation?

A

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
Q

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 :

A

vasodilatory

the ductus closes off

33
Q

What are the consequences of a deficient atrial septum before birth?

A

none.. this is normal fetal circulation allowing R–> L shunting

34
Q

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

A

septum primum

35
Q

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?

A

Get an atrial septal defect

36
Q

The________atrial septal defect is the most common type of atrial septal defect, and comprises 6–10% of all congenital heart diseases.

A

ostium secundum

37
Q

Heart sound heard in individuals with ASD?

A

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
Q

Explain how splitting of S2 happens in normal individuals (they talked about inspriation and expiration)

A

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
Q

How does ASD affect oxygenation?

A

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
Q

What kind of shunt is an ASD?

A

L–> R and its more of a volume shunt over pressure shunt

41
Q

do you see ASD right away in newborn?

A

not usually.. takes longer to devo symptoms

42
Q

A discrete, congenital narrowing of the thoracic aorta at the site of insertion of the ductus arteriosus

A

Coarctation of the Aorta

43
Q

In coarctation of the aorta, what structure will remain open?

A

ductus arteriousum to allow mixing of blood

44
Q

Pathophysiology of coarctation of Aorta

Obstruction to flow results in increased _______
–> Increased wall stress
–>Compensatory _______
•–>Congestive heart failure
–>SHOCK, metabolic acidosis, and organ failure

A

LV afterload

ventricular hypertrophy

45
Q

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

A

aortic isthmus

right to left

46
Q

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?

A

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
Q

Normally at birth, the ductus constricts and ________ increases.
• The flow through the isthmus of the aorta_______

The pulmonary resistance______ and duct reverses directions

A

pulmonary blood flow

increases

drops

48
Q

Why Does Coarctation Develop?
• Hemodynamic theory

(Also Ductal tissue theory and Genetic substrate (association with syndromes, eg.
Turner’s))

A

– 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
Q

What genetic condiciton is associated with coarctation of aorta?

A

Turners syndrome

50
Q

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?

A

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
Q

What is the pressure difference between arch of the aorta in normal and coarctation of aorta?

A

normal individual pressure is 80/55….. pressure in coarcation is 120/80 to overcome constriction of aorta

52
Q

Explain the ductal theory of coarctation of aorta

A

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
Q

Coarctation of aorta is found in _____ of CHD and more common in male or female?

A

4-8%

male

54
Q

Genetic influence in coarctation of aorta

A

Turner XO

35% affected, causes sterility, can’t be transmitted unless mosaic

*Noonan syndrome

55
Q

Coarctation of aorta is assoicated with what other defects?

A

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
Q
  • Aortic arches arise from the_______ part of truncus arteriosus
  • Develop to supply the 6 pharyngeal arches during _______ week of gestation
A

most distal

4th and 5th

57
Q
  • Each pharyngeal arch receives an artery and cranial nerve
  • The____ aortic arch never forms
A

5th

– Only I, II, III, IV, VI ever exist

58
Q

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

A

mesenchyme

the left and right dorsal aorta

59
Q

Natural history of coarctation of aorta:

Death had mean age of ______

and 75% died by ______

common causes were:

A

34

by 46

caused by CFH, aortic rupture, Bacterial endocarditis, intracranial hemorrhage

60
Q

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

A

Coarctation of aorta

61
Q

Infant with CHF from coarctation of aorta:

why would CHF occur?

A

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
Q
A
63
Q

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:

A

R→L

Discrepant

↓amplitude and delayed timing

64
Q

Physical exam of coarcation of aorta

Palpation:
– Heaving LV impulse at apex if _______
– _______ possible in suprasternal notch

A

LV volume overload

Systolic thrill

65
Q

Auscultation in child with coarcation of aorta:
What do we hear at the apex of the heart?

A

Constant systolic ejection click at apex (bicuspid valve)

66
Q

– Murmurs heard in coarcation of aorta:

A

• 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
Q

What do we see on chest xray in infant with coarcation of aorta with CHF?

A

– Pulmonary vascular congestion

68
Q

Describe chest xray of coarctation of aorta

A

– 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
Q

Extended End to End Anastomosis to fix coarctation of aorta:
– Advantage:

A

no circumferential suture → less
recurrence

70
Q

Prosthetic Patch Aortoplasty to fix coarctation… problem with this fix?

A

• High incidence of late aneurysm formation

71
Q

Subclavian Flap Aortoplasty

Requires less extensive aortic mobilization
• _______has theoretical growth potential
• Sacrifices ______ artery
• Ligation of ______to avoid subclavian steal

A

Subclavian tissue

left subclavian

vertebral artery

72
Q

Treatment of
choice for infants with coarctation of aorta in
early studies

A

subclavian flap aortoplasty

73
Q

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

A

stent the aorta

74
Q

Transcatheter Stent Placement for coarcation of aorta
• Pros:

• Cons:

A

– 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions