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Atrial Septal Defects ( ASD )

Atrial Septal Defects ( ASD ) happens when there is a failure to close the communication between the right and left atria.

 

One of the most common type of congenital heart defects ASD along with PDA is generally regarded as benign and often curable congenital heart defects Prevalence quoted in literature
- ASD constitute about 10 % of congenital cardiac defects and 22-40 % of congenital heart disease in adults
- ASD are the 2nd most common Cong HD in children with an incidence of 0.07 % to 0.2 % and have a female to male ratio of 2 : 1
- About 1 % of children with moderate to large ASD will experience symptoms which usually do not happen until late childhood or older ASD can happen with other congenital heart defects.

 

Types of ASD-

 

Ostium secundum -most common ASD type defect accounts for 75 % to 80 % of ASD cases true defect of the atrial septum and involves the region of fossa ovalis relatively central in the atrial septum and is separated from SVC , IVC and tricuspid mitral valves by a rim of atrial septal tissue OS-ASD defects of sizes < 6 mm or smaller in diameter are likely to close spontaneously in the 1st year of life OS-ASD is the only ASD which is potentially amenable to percutaneous device closure Some OS-ASD defects can be seen in familial clusters and autosomal dominant mode of inheritance has been noted Secundum defects are often seen in genetic syndromes as Holt-Oram , Ellis van Creveld , Noonan , Down , Budd-Chiari and Jarcho-Levine

 

Ostium primum- 2nd most commonest ASD this is a much more complicated defect involves the endocardial cushion and is often associated 
with mitral regurgitation due to an anterior leaflet cleft associated with extreme left axis deviation on ECG rather than right axis deviation which is commonly seen in other ASDs.

 

In patients with trisomy 21 , secundum and primum defects are the most type of congenital heart defects.

 

Sinus venosus – third most common subtype superiorly located and almost always associated with
 anomalous pulmonary venous drainage.

 

Coronary sinus ASD – least common suntype associated with persistent left superior vena cava due to partial or complete unroofing of the tissue which separates the coronary sinus from the left atrium causing a shunt through the defect of the coronary sinus orifice.

 

What happens – An atrial septal defect allows communication between the left and 
right sides of heart due to defect in the intra-articular septum.

 

How much blood is going to flow and in which direction will be determined by
 size of the defect type of defect relative diastolic filling properties of the left and right ventricle patient specific factors

It will not always be possible to measure the diameter of the defect as all ASDs may not be circular- but when measurable an ASD must be atleast 10 mm in diameter to cause a significant left to right shunt.

 

Cardial hemodynamic normal -in ASD blood shunts oxygenated blood from LA to the deoxygenated blood pool in RA.

Abnormal pulmonary over-circulation contributes to pulmonary vasculature remodeling and elevation of PVR ( pulmonary vascular resistance ) eventually leading to pulmonary arterial hypertension ( PAH )

 

In some patients when the pulmonary vascular pressure is equal or exceeds systemic levels- a shunt reversal ( right to left ) happens with peripheral desaturation with cyanosis – this is called Eisenmenger syndrome.

 

ECG – tall P wave ( rt atrial enlargement ) incomplete right bundle branch block pattern & rt axis deviation right ventricular hypertrophy ( pulmonary hypertension ) rt ventricular conduction delay ( rSR pattetn in V1 with a tall R ) adult patients may show AF / atrial flutter.

 

CXR- often normal in patients with PAH – cardiomegaly and increased 
pulmonary vascularity rt heart dilatation would be seen better in lateral films.

 

Incidental finding – asymptomatic patients with small defect may not show any symptoms where as those with larger defects may present early significant defects are associated with increased morbidity and mortality ASDs are often picked up when patients undergo echocardiography ( for e.g for a heart murmur , abnormal CXR , abnormal ECG ‘ rSr’ pr ‘rsR’ QRS configuration in rt precordial leads.

 

In infancy the presentation may include 
 failure to thrive tachypnoea recurrent respiratory tract infections heart failure respiratory insufficiency requiring ventilatory support

these are ( rare ) as most patients even with large shunts may not have overt symptoms until adulthood

 

Adult patients may present with
 fatigue exercise intolerance palpitations syncope arrhythmia ( atrial fibrillation / flutter ) decompensated right heart failure paradoxical embolus transient ischaemic attack cyanosis.

 

Clinical – ejection systolic murmur over the pulmonary area fixed splitting of the 2nd heart sound rarely features of rt heart failure in adults with pulmonary hypertension.

Complications -atrial dysrhythmias pulmonary hypertension right sided congestive heart failure TIA / Stroke Eisenmenger syndrome

 

Size and types of ASD – Defects with small shunts
( secundum , primum and coronary sinus types ) with a ratio of pulmonary / systemic flow Qp: Qs , < 1.5 do not require treatment
( BMJ Best Practice ) Small ASDs may close spontaneously during childhood Larger ASDs if left untreated would to hemodynamic abnormalities and clinical symptoms

 

 

Why treat – It may be prudent to consider closure even in absence of symptoms as
 uncorrected ASD may lead to pulmonary vascular obstructive disease in adulthood risk of supraventricular arrhythmias prevent development of symptoms during adolescence and adulthood reduce morbidity and mortality associated with ASD.

 

Hence all patients with ASD should be offered an elective closure irrespective of the age

 

The decision to repair and method would depend upon
- clinical and anatomical factors ( e.g size and location )
- magnitude of hemodynamic impact
- presence or absence of Closure can be achieved using 
- surgical techniques
- percutaneous devices

References

  1. Atrial Septal Defect Elisa A Bradley MD and Ali N Zaidi MD Cardiology Clinics, 2020-08-01, Volume 38, Issue 3, Pages 317-324
  2. Rao PS and Harris AD. How to cite this article: Recent advances in managing septal defects: atrial septal defects [version 1; referees: 2 2017, (F1000 Faculty Rev):2042
  3. BMJ Best Practice Atrial Septal Defect ( Summary )
  4. Atrial Septal Defect – Forgotten Treatment GuidelinesDr Suraj Wasudeo Nagre*Grant Medical College, Mumbai, Maharashtra, India Nagre, Acute Chronic Dis 2017, 1:1
  5. David S Celermajer, Atrial septal defects: even simple congenital heart diseases can be complicated, European Heart Journal, Volume 39, Issue 12, 21 March 2018, Pages 999–1001, https://doi.org/10.1093/eurheartj/ehx633
  6. Anaesthesia for percutaneousclosure of atrial septal defectsPatrick A Calvert BCh MA MRCPAndrew A Klein MBBS FRCA Continuing Education in Anaesthesia, Critical Care & Pain | Volume 8 Number 1 2008
  7. Nasr, V.G. and DiNardo, J.A. (2017). Atrial Septal Defect. In The Pediatric Cardiac Anesthesia Handbook (eds V.G. Nasr and J.A. DiNardo). doi:10.1002/9781119095569.ch11
  8. Pathophysiology and Therapy for Atrial
    Septal Defects An overview of this common congenital anomaly and the options for surveillance and treatment. BY MARY SHIELDS, MD; MARIA BALDASARE, MD; DAVID GOLDBERG, MD; AWAIL SADIQ, MD; AND SHELDON GOLDBERG, MD, FACC, FSCAI SEPTEMBER/OCTOBER 2014 CARDIAC INTERVENTIONS TODAY
  9. Atrial septal defectsTal Geva, Jose D Martins, Rachel M Wald www.thelancet.comVol 383 May 31, 2014 http://dx.doi.org/10.1016/
  10. Menillo AM, Lee L, Pearson-Shaver AL. Atrial Septal Defect. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK535440/
  11. Gary Webb, MD and Michael A. Gatzoulis, MD, PhD

 

 

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