ASD, VSD, TOF lecture

Question 1

ASD types

Answer 1

1. Ostium Secondum
2. Ostium Primum
3. Sinus Venosis

Question 2

ASD stats

Answer 2

Patent Foramen Ovale
Very common if small
Up to 20% of adults
Rarely of any clinical significance

Question 3

ASD. Problems arise if:

Answer 3

RV Volume Overload
Large shunt volume (2:1, Qp:Qs)
Pulmonary Hypertension
Paradoxical Embolization

Question 4

ASD EKG/ ECG

Answer 4

EKG reflects presence or absence of RVE, Pulmonary Hypertension and Atrial size

Echocardiography is test of choice, start with TTE and most will need TEE, especially for closure details (size, shape and exact location of defect)

Question 5

ASD signs and symptoms

Answer 5

Symptoms are dyspnea, usually exertional
Signs are subtle until RV volume overload or pulmonary hypertension develop.
Abnormality of second heart sound is key, it is Fixed Split (still happens in forced expiration)
Other findings are a SEM (systolic ejection mumur, usually crescendo decrescendo) Flow Murmur because of increased volume causing turbulence across pulmonic valve

Question 6

ASD treatment

Answer 6

Most ASD’s do not require treatment

Treatment may be Percutaneous Closure Device or Surgery (for Sinus Venosis and Primum)

Question 7

VSD congenital vs acquired

Answer 7

Congenital most common
Acquired mostly post AMI, rarely a complication of IE

[After an MI- cause: acute necrosis (takes a few days)]

Question 8

congenital VSD

Answer 8

One of the most common Congenital Defects, but due to spontaneous closure in childhood they account for only 10% of Adult Congenital defects.

(often a flow murmur that kids grow out of )

Question 9

VSD types

Answer 9

1. Infundibular VSD (Type I)
2. Membranous VSD (Type II)
3. Inlet VSD (Type III), AV Canal
4. Muscular VSD (Type IV)

Question 10

The direction and severity of the shunt associated with VSD are determined by

Answer 10

its functional size and by the ratio of pulmonary to systemic vascular resistance.

Question 11

VSD sizes

Answer 11

Small or restrictive VSDs are those with an orifice dimension less than or =25% of the aortic annulus diameter, this results in small L>R shunts with no LV volume overload or pulmonary hypertension (PH)

Moderate sized defects, >25% and less than 75%, cause moderate shunts with mild/moderate volume overload of the pulmonary arteries, LA and LV with no or mild PH

Large VSDs, =>75% cause moderate to large L>R shunts with LV volume overload, and over time cause severe PH

Question 12

Progressive PH –>

Answer 12

may cause Eisenmenger Syndrome from Eisenmenger Complex (VSD plus severe PH)
This causes R>L shunts with desaturation of O2, and mostly irreversible Right Heart Failure

Question 13

VSD clinical manifestations

Answer 13

follow the size and flow, small VSDs are often without symptoms, moderate and large may develop CHF and Eisenmengers Syndrome

Question 14

VSD PE findings

Answer 14

PE demonstrates a loud pansystolic murmur at the LSB, 3-4 ICS.
Other findings follow the prresence or absence of PH, LV volume overload and associated congenital abnormalities.
Small VSDs are called “maladie de Roger”

Question 15

VSD EKG

Answer 15

EKG-normal if VSD small (65%), RBBB and IVCD may be present in larger defect, and RVE with RA abnormality develop with Eisenmengers.

Question 16

VSD most helpful test?

Answer 16

TTE is the most helpful test, directly demonstrating the size, location and flow (direction and volume) characteristics

Question 17

VSD Prognosis

Answer 17

excellent for small defects and guarded for large defects with CHF and PH and Eisenmengers.
87% 20 year survival has been documented for the entire group of VSDs.

Question 18

TOF 4 parts

Answer 18

1. Pulmonic Valve, or Subvalvular Stenosis
2. VSD
3. Overriding Aorta (over ventricular septum)
4. RVH (concentric)

Question 19

TOF stats

Answer 19

Described in 1888 by Etienne-Louis Arthur Fallot with 3 cyanotic patients
4-5 /10,000 Live Births
7-10% of cases of CHD (Congenital Heart Disease)
Equal male: female
One of the most common lesions requiring intervention in the first year of life

Question 20

TOF course

Answer 20

RV Systolic pressure rises to systemic levels, causing a R>L shunt and cyanosis
The pulmonic valve stenosis is multifactorial including sub valvar apparatus and actual valve stenosis in many cases
There may be pulmonary artery stenosis or branch stenosis

Question 21

Overriding Aorta-

Answer 21

a congenital anomaly in which the aorta is displaced to the right over the VSD rather then the LV, this results in blood flow from both ventricles into the aorta

Question 22

TOF Associated Cardiac Features

Answer 22

1. 25% have a right sided aortic arch
2. 9% have coronary anomalies (LAD arising from RCA)
3. Occasional aorticoopulmonary collaterals
4. Occasional PDA

Question 23

TOF pathophysiology consequences- dependent on

Answer 23

degree of RVOT obstruction

Question 24

TOF 3 main Clinical Presentations:

Answer 24

1. Children with severe obstruction and inadequate pulmonary flow present in the immediate newborn period with profound cyanosis
2. Children with moderate obstruction and balanced pulmonary and systemic flow may be noticed during elective evaluation of a murmur. These children will present with hypercyanotic “tet” spells when RVOT is obstructed during periods of aggitation.

(look for kids that squat to relieve the pressure shunting)

3. Children with minimal obstruction may present with pulmonary overcirculation and heart failure.

Question 25

TOF PE

Answer 25

PE- Usually the RVOT obstruction causes the dominant murmur, not the VSD.
Echocardiography provides a nearly complete evaluation of all elements of the TOF.