ASD Julie Brogdon DO A) 5 weeks - PowerPoint Presentation

Slide1

ASD

Julie

Brogdon

DO

A) 5 weeks

gestation:a Septum primum will begin to grow caudally toward the endocardial cushions. wall

B) Small perforations develop.The gap between free edge of septum primum and endocardial cushion is called ostium/foramen primum.

C) The perforations form the ostium/foramen secundum on the cephalic end of the septum primum. wall

D) The foramen/ostium primum will fuse caudally and close.

E) The septum

secundum

begins to grow both cranially and caudally to the right of the septum primum. It will cover up the ostium/foramen

secundum

.

F) The space left between in the septum

secundum is called the foramen ovale. This allows oxygenated blood coming from placenta to enter the RALALVbody; bypassing the lungs.

E

E

1

The septum primum

and

septum secundum create a flap valve. The higher pressures in the fetal RA push the flexible septum primum open.

At birth expansion of the lungs lowers right heart pressures. At the same time the systemic vascular resistance increases. This causes reversal of the interatrial pressure and the septum primum is held against the septum

secundum

closing the shunt.

ASD: Atrial Septal defects occur when there is failure of closure between the right and left atria. -Can be associated with fetal alcohol syndrome -Second most common congenital heart defect in adults -Persons are usually not symptomatic until adulthood

SECUNDUM ASD-About 70-75% of ASD cases. -At the level of fossa ovalis-Can be due to excess apoptosis of cephalic septum primum or due to incomplete development of septum secundum. -More common in females -Most that are <8mm close spontaneously by 2-5 yo.

PRIMUM ASD -Failure of the free edge of septum primum to fuse with endocardial cushions. Usually leaves a large opening.-Found in 25% of Down Syndrome cases-Associated with anomalies of the AV valves especially cleft in anterior mitral valve leaflet.

Oxygenated blood will shunt from LA

RA due to higher pressures on left side especially with small ASD.

This is an

acyanotic

heart defect where oxygenated blood goes thru to pulmonary circulation. Will cause increased

O2 saturation in the RA, RV, and pulmonary artery.

-L to R shunting will happen mainly in early diastole and in late ventricular systole.

-Even with equal LA and RA pressures as seen with large ASD there is still a L to R shunt due to better compliance of RV.

TYPES OF ASD

Clinical Manifestations

-Most pts with ASD and a significant shunt will become symptomatic and need surgery to correct by age 40

-Common symptoms reported by pts were

atrial arrhythmias

(A-fib and A-flutter especially beyond 3

rd

decade),

exercise intolerance

, and

HF

.

Fatigue

and

dyspnea

were found in more than ½ of pts experiencing symptoms.

-Moderate to severe

pulmonary HTN

is present in <10% of adults at time of dx.

-Overloading on the R side of heart is tolerated quite well for many years. The normal pulmonary vasculature

recruits under perfused vessels to accommodate increased volume. The pulmonary artery pressure will not

change significantly until volume > 2.5x baseline.

-

Eisenmenger syndrome

may develop eventually which is R to L shunting and right ventricular failure typically

with pulmonary HTN. In such cases cyanosis and clubbing can be expected. As it progresses signs of RV failure

may be noted such as hepatic congestion, TR, pedal edema, and elevated JVP.

Physical Exam Findings: -Extra blood volume passing in pulmonic valve will cause a delay in its shutting relative to aortic valve. Will hear wide fixed split S2 on auscultation. (May not be fixed in supine position) May even cause systolic murmur.-If large LR shunt can cause enlarge RV which can produce RV heave most pronounced on LSB and subxiphoid area. -Enlarged pulmonary artery may cause palpable pulmonary artery impulse at LUSB.-S1 split at apex and LLSB with second component of tricuspid closure intensified. -Possible murmurs: *mid-systolic pulmonary flow or ejection (mod-lrg shunts) at 2nd left intercostal space *MR if cleft mitral valve in primum ASD. *diastolic rumble accentuated by inspiration-Pulmonary HTN: may be associated with RV 4th heart sound, mid-systolic ejection click, increased intensity of pulmonic component of S2 but no fixed split, holosystolic murmur of TR if RV and atrial enlargement occurred.

Complications

-Paradoxical embolism. If for example a DVT occurs and part dislodges, it could flow into the RA and bypass lungs

flowng

thru the ASD to the LALVbrain.

-Atrial arrhythmias

LATE complications of large ASD:

-RV dilation

-TR

-R HF

-Pulmonary HTN

-RL shunting

(Eisenmenger syndrome)

-ECG: May be NSR with uncomplicated ASD and small shunt. *BOTH ASDs -may show evidence of atrial arrhythmias especially a-fib but also a-flutter and SVT. -1st degree AV block. -Could see RA enlargement (tall p waves) *Primum ASD: -1st degree AV block more common with primum in association with complete RBBB and LAFB since spatially the defect is near His bundle. -Left axis deviation *Secundum ASD: -RVH- rSR’ in V1, R>S in V1 -Right axis deviation - Notch in R wave of inferior leads II, III, and aVF (“crochetage”) is sensitive and specific findings of ASD.

-Echocardiogram:

imaging modality of choice for the diagnosis of ASD.

-

Transthoracic echocardiography (TTE)

is usually definitive in

secundum

ASD defect diagnosis and assessment. The interatrial septum can be seen in apical four chamber view but incorrect ASD diagnosis may be made when relying solely on two-dimensional and color Doppler in this view. Interatrial septum is best visualized in the subcostal view where the septum is perpendicular to the US beam. This view may not be optimal for obese pts. Other views may be needed to interrogate the entire interatrial septum.

-The ASD size on 2D TTE doesn’t correlate well with the shunt flow. This may be better assessed with Doppler and color flow or 3D TTE.

-Transesophageal ECHO (TEE):

TEE is superior for imaging dx of ALL types of ASD.

-Agitated Saline Contrast:

If after Doppler and 2D TTE there is still inconclusive evidence for ASD injecting agitated saline contrast into peripheral vein and using maneuvers such as Valsalva, cough, or pressing on abdomen can confirm dx. Can be performed with TTE or TEE.

-Chest radiograph:

may show evidence of RA, RV, and pulmonary artery dilation. Atypical findings

sich

as normal

vasculature, pulmonary venous HTN, LA enlargement,

nad

pulmonary edema may be more common in pts >50.

--The increased flow leads to right-sided cardiac and pulmonary artery dilatation evident on chest radiograph and

echocardiographic imaging. The main pulmonary arteries dilate and pulmonary vascularity increases.

These changes may be evident on the chest radiograph, and large vessels in both the lower and upper lobes may be seen.