CHD - ASD

CHD - ASDRobosa, Dino

Rodas, FrancisRodriguez, Shereen

Rogelio, Ma. GracellaSalazar, Riccel

Salcedo, Von

GL 21 y/o, Female CC: easy fatigability and occasional chest

pain

CHD-ASD

Referred for cardiovascular evaluation prior to employment

Diagnosed to have “heart disease” in childhood

PMH: frequent upper respiratory tract infection

CHD-ASD

Hyposthenic, narrow AP chest diameter BP 100/80 PR 75/min RR 20/min BMI 15 JVP and CAP – normal (+) Left lower sternal lift On auscultation:

◦ S1 is normal followed by a grade 3/6 crescendo decrescendo murmur.

◦ S2 is wide with fixed splitting◦ (+) Multiple clicks at the apex

Lungs: equal expansion, resonant, no crackles

Physical Examination

Normal sinus rhythm RVH Incomplete right bundle branch block Diffuse ST – T changes

12-L ECG

Cardiomegaly with multi-chamber enlargement

Pulmonary congestion

Chest X ray

ASD, ostium secundum type Markedly dilated right ventricle with good wall

motion and contractility with evidence of RV pressure and volume overload

Dilated right atrium with no evidence of thrombus

Dilated main pulmonary artery Mitral Valve Prolapse, anterior mitral valve

leaflet PR Moderate pulmonary hypertension

Echo-Doppler:

Location Pressure (mmHg) Oxygen Saturation (%)SVC high 74.9SVC low 64.2

IVC 81.4RA high 70.8RA mid 4 mmHg 87.8RA low 82.7

RV 17/0 mmHg 88.6RVOT 10/-1 mmHg 88.7MPA 35/10 mmHg 89.0LPA 36/12 mmHg 87.9PCW 8 mmHg 93.2LA 9 mmHg --

LLPV --- 97.7LV 94/4 mmHg 96.8

Aorta 98/66 mmHg 96.4

Hemodynamic Studies

O2 consumption = 159.2 Hgb = 12.6 g/dL CR = 90 bpm BSA = 1.5 m2

Cardiac Output = 3.88 L/min Cardiac Index = 2.58 L/min QP = 8.83 QS = 3.88 QP/QS = 2.27

Hemodynamic Studies

What is your complete diagnosis?

Etiology: Congenital Heart Disease Anatomy: atrial septal defect, ostium

secundum, dilated right atrium, markedly dilated and hypertrophied right ventricle, dilated main pulmonary artery, anterior mitral valve prolapse

Physiology: NSR, incomplete right bundle branch block, diffuse ST-T changes, moderate pulmonary hypertension, increased right ventricular pressure and overload

Functional Capacity: Class II Objective Assessment: C

2. How do you explain the auscultatory findings?

a. At the base, S1 is normal followed by a grade 3/6cresendo-decresendo murmur– Increased flow across the pulmonic valve is

responsible for a midsystolic pulmonary outflow murmur

– Grade 2–3 mid-systolic murmur at the mid to upper left sternal border with fixed splitting of S2• Ostium secundum ASDs are most common

b. S2 is wide with fixed splitting

• Wide splitting– The split becomes wider when there is delayed

activation of contraction or emptying of the right ventricle resulting in a delay in pulmonic closure

• Fixed splitting– This occurs with delayed closure of the pulmonic

valve when output of the right ventricle is greater than that of the left ventricle (such as occurs in large atrial septal defects, a ventricular septal defect with left to right shunting, or right ventricular failure)

c. At the apex, multiple clicks are heard◦ Midsystolic clicks, occurring with or without a

late systolic murmur, often denote prolapse of one or both leaflets of the mitral valve

Results from the chordae tendineae that are functionally unequal in length

Best heard along the lower left sternal border and at the left ventricular apex

◦ Systolic clicks usually occur later than the systolic ejection sound.

4a. What are the chest x-ray findings in a left to

right shunt?

Acyanotic Includes:

◦ Ventral septal defect◦ Atrial septal defect◦ Patent ductus arteriosus

Left-to-right shunts

Left-to-right shuntsLeft-to-Right Shunt

Chambers

Enlarged

Prominent aortic knob

Dilated MPA

Pulmonary Vascularity

Ventral Septal Defect

LA and LV No Yes ↑

Atrial Septal Defect

RA and RV No Yes (convex) ↑

Patent Ductus

Arteriosus

LA and LV Yes Yes ↑

Left-to-Right Shunt

Chambers

Enlarged

Prominent aortic knob

Dilated MPA

Pulmonary Vascularity

Ventral Septal Defect

LA and LV No Yes ↑

Atrial Septal Defect

RA and RV No Yes (convex) ↑

Patent Ductus

Arteriosus

LA and LV Yes Yes ↑

Left-to-right shunts

RV Enlargement◦ PA view: lateral upward displacement of the

cardiac apex◦ Lateral view: fullness of retrosternal space

RA Enlargement◦ PA view: increased convexity of the lower right

cardiac border

Normal PA view PA view (ASD)

SVC

RV

IVC

Aortic knob

MPA

LV

Dilated MPA

Increased pulmonary vascularity

Right ventricular enlargement

2/31/3

Retrosternal space

Normal Lateral view Lateral view (ASD)

Retrosternal space

4b. Differentiate pulmonary arterial from pulmonary

venous congestion.

Venous ArterialProgressive elevation of pulmonary artery / vein pressure and vascular

resistance Mean PAP over 25 mmHg at rest

Occurs in the setting of elevated left sided filling pressure. The degree of elevation is concordant with the degree of elevation in left atrial pressure.

Pressure overload to the right ventricle, increasing right ventricular workload leading to concentric hypertrophy.

Conditions predisposing to this form of PH are mitral valve disease and LV systolic dysfunction (other causes such as diastolic dysfunction or restrictive cardiomyopathy are more difficult to diagnose noninvasively).

Requires a high index of suspicion and the appropriate diagnostic tests. Physical examination can be nonspecific and even normal in some of these patients.

Advances in Pulmonary Hypertension. Official Journal of the Pulmonary Hypertension Association.

5. How do you manage this patient?

Should include treatment of possible complications:◦ Respiratory tract infections◦ Arrhythmias, atrial fibrillation, supraventricular

tachycardia◦ Pulmonary hypertension, coronary artery disease,

heart failure◦ Infective endocarditis

Medical Management

Harrison’s Principles of Internal Medicine 17th ed.

Operative repair – definitive management with a patch of pericardium OR prosthetic material OR percutaneous transcatheter device closure

should be advised for all patients with uncomplicated secundum atrial septal defects with significant left-to-right shunting

Surgical Management

Harrison’s Principles of Internal Medicine 17th ed.

The mere presence of an ASD may warrant intervention especially if there is a significant shunt (> 2:1)

symptomatic pulmonary hypertension is present [pulmonary artery pressure

(PAP) > 2/3 systemic arterial blood pressure (SABP) or pulmonary arteriolar resistance > 2/3 systemic arteriolar

resistance net left-to-right shunt (Qp:Qs) of at least 1.5:1• RA or RV enlargement – radiographic, cardiac catheterization or there is evidence of pulmonary artery reactivity when

challenged with a pulmonary vasodilator (e.g. oxygen, nitric oxide and/or prostaglandins)

or lung biopsy evidence shows that pulmonary arterial changes are potentially reversible

Indications

Schwartz ‘s Principles of Surgery, 9th ed.http://www.achd-library.com/index.html

Device closure may now be offered as an alternative to surgical closure to patients with secundum ASD of up to 36-38 mm in diameter

Surgical closure may also be offered, and may be especially attractive should the patient prefer the surgical approach, or especially if atrial arrhythmia surgery (atrial maze procedure for atrial fibrillation and radiofrequency or cryoablation for atrial flutter) may be offered concurrently

http://www.achd-library.com/index.html

The following ASD patients require periodic follow up by an ACHD cardiologist

• Those repaired as adults• Elevated pulmonary artery pressures at the time of repair• Atrial arrhythmias pre- or post-operatively• Ventricular dysfunction pre-operatively• Co-existing heart disease (e.g. coronary artery disease,

valvular heart disease, hypertension) • Those with device closure need follow-up in specialized

centers with serial ECGs and echocardiograms to determine the late outcomes of these new techniques

• Endocarditis prophylaxis and aspirin are recommended for 6 months following device closure

http://www.achd-library.com/index.html