TUGAS Ventricular Septal Defect.docx

8/13/2019 TUGAS Ventricular Septal Defect.docx

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Ventricular Septal Defect (VSD) and the ECGPathophysiology

Shunt flows from high pressure left ventricle to low pressure right ventricle.

Shunt flow follows the left ventricle - right ventricle - pulmonary artery - left atrium - leftventricle route.

ECG changes reflect the hemodynamic changes caused by the shunt flow.

The ECG may be normal if VSD is small.

ECG abnormalities that may be observed in patients with VSD

Right atrial abnormality (RAA).

Left atrial abnormality (LAA).

Right ventricular hypertrophy (RVH).

Complete or incomplete right bundle branch block (RBBB).

Left ventricular hypertrophy (LVH).

If VSD is large, S1S2S3 pattern may be observed.

Katz-Wachtel phenomenon ( sign ): large biphasic (equiphasic) QRS complexes observed in

midprecordial and limb leads. Sum of the amplitudes of R and S waves in leads C2, C3 or C4 is >60mm (6mV).

Katz-Wachtel phenomenon is seen when pulmonary hypertension and the resultant biventricular

hypertrophy developes.

ECG in patients with VSD and Eisenmenger syndrome

Signs of right ventricular hypertrophy are observed more frequently.

Signs of left ventricular hypertrophy may also accompany.

The rhythm is generally sinus.

Right atrial abnormality may be seen.

ECG abnormalities in adult patients who have been operated for closure of the VSD during their

childhood

Right bundle branch block:50-90% if operated by right ventriculotomy

40% if operated by right atrial approach.
http://metealpaslan.com/ecg/rbbben.htmhttp://metealpaslan.com/ecg/rbbben.htm


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Complete atrioventricular (AV) block (very rare).

In this group of patients, the risk of sudden cardiac death has been reported to increase in patients

with left axis deviation on ECG and/or ventricular arrhythmias on Holter monitoring.

ECG 1. The ECG above, belongs to an 11 years old child who has been operated for ASD, VSD and

coarctation of the aorta. Katz-Wachtel phenomenon (biventricular hypertrophy pattern) is also seen.

ECG 2. This ECG belongs to a 49 years old woman who was operated for VSD and pulmonary stenosis.
http://metealpaslan.com/ecg/avb3en.htmhttp://metealpaslan.com/ecg/avb3en.htm


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The subaortic or anterior malalignment type of VSD appears just below the posterior semilunar valvecusps, entirely superior to the tricuspid valve. Subpulmonary VSD appears as echo dropout within theoutflow septum and extending to the pulmonary annulus. One or two of the aortic cusps may be seento be protruding through the defect into the right ventricular outflow tract. The inlet AV septal-type ofVSD extends from the fibrous annulus of the tricuspid valve into the muscular septum; it is oftenentirely beneath the septal tricuspid leaflet.

Muscular defects may appear anywhere throughout the ventricular septum. They may be either largeand single or small and multiple.

The anatomic localization of all VSDs is facilitated by coupling 2D sonograms with a Doppler systemand by superimposing a color-coded direction and velocity of blood flow on the real-time images.

Chest radiography

In patients with small VSDs, the results of chest radiographs are usually normal. With medium-sizeVSDs, minimal cardiomegaly and a borderline increase in pulmonary vasculature may be observed. Inlarge VSDs, the chest radiograph shows gross cardiomegaly with prominence of both ventricles, theleft atrium, and the pulmonary artery. The pulmonary vascular markings are increased, and frankpulmonary edema, including pleural effusions, may be present.

Electrocardiography

The electrocardiogram (ECG) mirrors the size of the shunt and the degree of pulmonary hypertension.

Small restrictive VSDs usually produce a normal tracing. Medium-sized VSDs produce a broad,notched P wave characteristic of left atrial overload. Signs of LV volume overload namely, deep Qand tall R waves with tall T waves in leads V5 and V6 are present. In addition, signs of atrialfibrillation are often present. Large VSDs produce right ventricular hypertrophy with right-axisdeviation. With further progression, the ECG shows biventricular hypertrophy; P waves may benotched or peaked.

Tetralogy of Fallot (ToF) and the ECGComponents of Tetralogy of Fallot (ToF)

Ventricular septal defect (VSD).

Obstruction to right ventricular outflow.

Dextroposition (overriding) of the aorta

Right ventricular hypertrophy.

ECG abnormalities that are frequently observed in patients with ToF

Right atrial abnormality ( RAA ).

Right ventricular hypertrophy ( RVH ).

Right axis deviation .

Right bundle branch block ( RBBB ) is frequently observed after corrective surgery.

Left anterior fascicular block may accompany.


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Atrial arrhythmias are frequently observed after corrective surgery.

Ventricular arrhythmias may be observed after corrective surgery.

If QRS width is > 180 msec, this suggests an increased risk for development of ventriculararryhthmias and sudden cardiac death.

ECG 1. The ECG of a 7 years old boy who was operated for ToF one year ago. He isunder congestive heart failure therapy

Diagnosis

Hemoglobin and hematocrit values are usually elevated in proportion to the degree of cyanosis.Patients with significant cyanosis have the following, in association with a tendency to bleed:

Decreased clotting factors

Low platelet count

Diminished coagulation factors

Diminished total fibrinogen Prolonged prothrombin and coagulation times

Arterial blood gas (ABG) results are as follows:

Oxygen saturation varies

pH and partial pressure of carbon dioxide (pCO2) are normal unless the patient is in extremisImaging studies include the following:

Echocardiography

Chest radiographs

Magnetic resonance imaging (MRI)Echocardiography has the following attributes:

Color-flow Doppler echocardiography accurately diagnoses ductus arteriosus, muscular VSD, oratrial septal defect


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TUJUAN TERAPI DIET

Memberikan makanan secara bertahap (energi & konsistensi) tanpa memberatkan kerja jantung

Mencegah/mengurangi penimbunan cairan dengan membatasi asupan cairan dan garam natrium

Mengurangi kembung dengan menghindari makanan yang mengandung gas

PRINSIP/SYARAT DIET

. Energi cukup2. Protein cukup : 1 g/kgBB/hari , bila ada insuf renal protein 0,8 /kgBB/hari

3. Cairan: dibatasi, bila ada edema paru keseimbangan cairan harus negatif, cairan yang masuk

(infus & minuman/makanan) lebih sedikit dari pada cairan yang keluar (Urine & IWL)

4. Vitamin, mineral & elektrolit

a. Natrium dibatasi: 15002000 mg/hari

b. Kalium: 20006000 mg/hari

c. Magnesium: 300350 mg/hari

5. Bentuk makanan diberikan secara bertahap sesuai kemampuan dapat dimulai dari lunak bubur, tim

dan nasi

PENATALAKSANAAN MEDIK

a. Terapi Non-Farmakologis

Anjuran umum

1. Edukasi : terangkan hubungan keluhan, gejala dengan pengobatan

2. Aktivitas sosial dan pekerjaan diusahakan agar dapat dilakukan seperti biasa

sesuai kemampuan fisik

3. Gagal jantung berat harus menghindari penerbangan panjang

Tindakan umum

1. Diet rendah garam

2. Hentikan rokok

3. Aktivitas fisik

4. Istirahat baring pada gagal jantung akut, berat, dan eksaserbasi akut

b. Terapi Farmakologis

1. Glikosida jantung

Digitalis, meningkatkan kekuatan kontraksi otot jantung dan memperlambat frekuensi jantung

Efek yang dihasilkan : peningkatan curah jantung, penurunan tekanan vena dan volume darah, dan peningkatan

diurisi dan mengurangi edema.

Ex : Digoxin

- Digoxin memiliki efek inotropik positif(bekerja meningkatkan kontraksi otot jantung ) pada irama sinus dan

menyebabkan perbaikan simptomatis serta menurunkan tingkat perwatan di rumah sakit walaupun tidak

mempengaruhi tingkat mortilitas.

- Penghambat Fosfodiesterase

Hambatan enzim ini menyebabkan peningkatan kadar siklik AMP (cAMP) dalam sel miokard yang akan

meningkatan kadar kalsium intrasel, ex : Mirinon dan Amirinon

2. Diuretik


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Dasar untuk terapi simptomatik. Dosisnya harus cukup besar untuk menghilangkan edema paru dan/atau perifer.

Efek samping utama adalah hipokalemia ( berikan suplemen K+ atau diuretik hemat kalium seperti amilorid)

Ex : Spironolakton, suatu diuretik hemat kalium (antagonis aldosteron), memperbaiki prognosis pada CHF berat.

3. Inhibitor ACE

Menghambat perubahan angiotensin I menjadi angiotensin II, memotong respon neuroendokrin maladaptif,menimbulkan vasodilatasi dan menurunkan tekanan darah. Obat ini dapat memicu gagal ginjal pada stenosis

arteri renalis bilateral.

Efek samping lain : batuk kering persisten

4. Antagonis Reseptor Angiotensin II

Ex : Losartan, menghambat angiotensin II dengan antagonisme langsung terhadap reseptornya. Efek dan

manfaatnya sama seperti inhibitor ACE.

5. -Bloker

Ex : Bisoprolol, Metoprolol, Karvedilol

-Bloker diberikan hanya pada pasien yang stabil, dengan dosis sangat rendah, dinaikkan bertahap. Menurunkan

kegagalan pompa serta kematian mendadak akibat aritmia.

6. Kombinasi Hidralazin dengan Isosorbid Dinitrat

Untuk pasien yang intoleran dengan inhibitor ACE

7. Terapi Umum

Obati penyebab yang mendasari dan aritmia bila ada. Kurangi asupan garam dan air, pantau terapi dengan

mengukur berat badan setiap hari. Obati faktor resiko hipertensi dan PJK dengan tepat.

TUGAS Ventricular Septal Defect.docx

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