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CHD - ASD Robosa, Dino Rodas, Francis Rodriguez, Shereen

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1 CHD - ASD Robosa, Dino Rodas, Francis Rodriguez, Shereen
Rogelio, Ma. Gracella Salazar, Riccel Salcedo, Von

2 CHD-ASD GL 21 y/o, Female CC: easy fatigability and occasional chest pain

3 CHD-ASD Referred for cardiovascular evaluation prior to employment
Diagnosed to have “heart disease” in childhood PMH: frequent upper respiratory tract infection

4 Physical Examination 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

5 12-L ECG Normal sinus rhythm RVH Incomplete right bundle branch block
Diffuse ST – T changes

6 Chest X ray Cardiomegaly with multi-chamber enlargement
Pulmonary congestion

7 Echo-Doppler: 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

8 Hemodynamic Studies Location Pressure (mmHg) Oxygen Saturation (%)
SVC high 74.9 SVC low 64.2 IVC 81.4 RA high 70.8 RA mid 4 mmHg 87.8 RA low 82.7 RV 17/0 mmHg 88.6 RVOT 10/-1 mmHg 88.7 MPA 35/10 mmHg 89.0 LPA 36/12 mmHg 87.9 PCW 8 mmHg 93.2 LA 9 mmHg -- LLPV --- 97.7 LV 94/4 mmHg 96.8 Aorta 98/66 mmHg 96.4

9 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

10 What is your complete diagnosis?

11 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

12 2. How do you explain the auscultatory findings?

13

14 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 Mid-systolic murmurs - begin at a short interval following S1, end before S2 and are usually crescendo-decrescendo in configuration Crescendo-Decrescendo - the loudness of the murmur increases and then decreases. This configuration is typical of systolic ejection murmurs

15 S2 is wide with fixed splitting
Splitting is both heard on inspiration and expiration Normlal physiologic splitting of S2 – heard on inspiration and disappears on expiration - due to increase in venous return, inhale = more (-) intrathoracic pressure  take longer time to empty  delayed closure of the pulmonic valve

16 Wide splitting Fixed 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)

17 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. MVP - excessive or redundant mitral leaflet tissue, which is commonly associated with myxomatous degeneration and greatly increased concentrations of acid mucopolysaccharide genetically determined collagen disorder A reduction in the production of type III collagen has been incriminated The most important finding is the mid- or late (nonejection) systolic click, which occurs 0.14 s or more after the S1 and is thought to be generated by the sudden tensing of slack, elongated chordae tendineae or by the prolapsing mitral leaflet when it reaches its maximum excursion. Systolic clicks may be multiple and may be followed by a high-pitched, late systolic crescendo-decrescendo murmur, which occasionally is "whooping" or "honking" and is heard best at the apex. The click and murmur occur earlier with standing, during the strain of the Valsalva maneuver, and with any intervention that decreases LV volume, exaggerating the propensity of mitral leaflet prolapse. Conversely, squatting and isometric exercises, which increase LV volume, diminish MVP, and the click-murmur complex is delayed, moves away from S1, and may even disappear. Some patients have a mid-systolic click without the murmur; others have the murmur without a click. Still others have both sounds at different times.

18 The right atrium is enlarged due to volume overload.
Tall P waves (more than 2-3 mm) RVH is also noted, typically as rsR’ pattern of the QRS complexes in the right chest leads ***** nakahide na to… just in case na maghanap….

19 4a. What are the chest x-ray findings in a left to right shunt?

20 Left-to-right shunts Acyanotic Includes: Ventral septal defect
Atrial septal defect Patent ductus arteriosus

21 Pulmonary Vascularity
Left-to-right shunts 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 Yes (convex) Patent Ductus Arteriosus

22 Pulmonary Vascularity
Left-to-right shunts 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 Yes (convex) Patent Ductus Arteriosus

23 RV Enlargement RA 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

24 Increased pulmonary vascularity
Normal PA view PA view (ASD) Dilated MPA Aortic knob SVC MPA RV LV IVC Increased pulmonary vascularity

25 Right ventricular enlargement
Normal Lateral view Lateral view (ASD) Retrosternal space Retrosternal space 2/3 1/3 Normally, the heart occupies only 1/3 of the retrosternal space In the patient, the heart occupies almost 2/3 of the retrosternal space Right ventricular enlargement

26 4b. Differentiate pulmonary arterial from pulmonary venous congestion.

27 Mean PAP over 25 mmHg at rest
Venous Arterial Progressive 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.

28 5. How do you manage this patient?

29 Diagnostic An adequate diagnostic workup:
Documents the presence and type of ASD(s) Determines the size (diameter) of the defect(s) Determines the functional importance of the defect either by: shunt size (Qp/Qs) right ventricular size, function and volume overload and right atrial size pulmonary artery pressures and if elevated, pulmonary vascular resistance Identifies other associated conditions that may influence management (e.g. anomalous pulmonary venous connection, significant valve disease; or coronary artery disease)

30 The initial workup should include at a minimum:
A thorough clinical assessment ECG Chest x-ray Transthoracic echo-Doppler evaluation by an appropriately trained individual Transesophageal (TEE) echo/Doppler examination to prove the existence of an ASD, better define its/their location(s) and size(s) and shape(s), assess pulmonary venous connections, and to evaluate the cardiac valves, if this information is not provided by transthoracic echocardiography (TTE) A transesophageal examination is essential to determine if the ASD is suitable for device closure and must be performed prior to the procedure Resting oxygen saturation

31 The diagnostic workup may require:
Heart catheterization (if determination of pulmonary artery pressures and resistances is of concern; to assess pulmonary vascular reactivity; or delineate anomalous pulmonary venous connections) Coronary angiography in patients at high risk of coronary artery disease or in patients over the age of 40 years if surgical repair is planned Magnetic resonance imaging (MRI) to prove the existence of an ASD or to assess pulmonary venous connections if doubts remain after other imaging modalities. MRI can also be used to estimate Qp/Qs Oxygen saturation with exercise if there is any suggestion of pulmonary hypertension. If there is severe pulmonary hypertension or resting desaturation of < 85%, the patient should not be exercised Open lung biopsy should only be considered when the reversibility of the pulmonary hypertension is uncertain from the hemodynamic data. It is potentially hazardous and should be done only at centres with substantial relevant experience in CHD

32 Medical Management Should include treatment of possible complications:
Respiratory tract infections Arrhythmias, atrial fibrillation, supraventricular tachycardia Pulmonary hypertension, coronary artery disease, heart failure Infective endocarditis Respiratory tract infections-prevented only upon correction of ASD Arrhythmias, atrial fibrillation, supraventricular tachycardia-refer to handouts/book Pulmonary hypertension, coronary artery disease, heart failure-refer to CHF handouts/book Infective endocarditis-hidden slide Harrison’s Principles of Internal Medicine 17th ed.

33 Pulmonary Hypertension
Because the pulmonary artery pressure in PAH increases dramatically with exercise, patients should be cautioned against participating in activities that demand increased physical stress O2 supplementation helps to alleviate dyspnea and RV ischemia in patients whose arterial O2 saturation is reduced Anticoagulant therapy (Warfarin) Phosphodiesterase 5 inhibitors (Sildenafil) Prostacyclins (Treprostinil) PHOSPHODIESTERASE-5 INHIBITORS Sildenafil, a phosphodiesterase-5 inhibitor, is approved for the treatment of PAH patients who are NYHA functional classes II and III. Treprostinil, an analogue of epoprostenol, is approved for patients with PAH who are NYHA functional classes II–IV Harrison’s Principles of Internal Medicine 17th ed.

34 Infective Endocarditis
Prevention of Infective Endocarditis: Guidelines From the American Heart Association

35 Surgical Management 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 Harrison’s Principles of Internal Medicine 17th ed.

36 Indications think otherwise if:
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 think otherwise if: PVR > 12 U/mL / significant pulmonary hypertension Eisenmenger – R to L shunting with cyanosis Schwartz ‘s Principles of Surgery, 9th ed.

37 Device closure may now be offered as an alternative to surgical closure to patients with secundum ASD of up to 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

38 Device closure Early and intermediate follow-up is excellent after device closure The intermediate results are comparable to surgery with a high rate of shunt closure and few major complications Longer follow-up is needed to determine the incidence of arrhythmias and thromboembolic complications late after device closur Functional capacity improves and supraventricular arrhythmias are better tolerated and more responsive to pharmacologic management  Surgical closure Following surgical repair, pre-operative symptoms, if any, should decrease or abate Pre-existing atrial flutter and fibrillation may persist . Likewise, atrial flutter and/or fibrillation may arise after repair, but are better tolerated and often more responsive to antiarrhythmic therapy Post-operative ASD patients are especially prone to cardiac tamponade for the first several weeks after surgery

39 Complications with transcatheter closure include:
air embolism (1 to 3%) thromboembolism from the device (1 to 2%) disturbed AV valve function (1 to 2%) systemic/pulmonary venous obstruction (PVO) (1%) perforation of the atrium or aorta with hemopericardium (1 to 2%) atrial arrhythmias (1 to 3%) and malpositioning/embolization of the device requiring intervention (2 to 15%)

40 Those repaired as adults
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


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