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Case Mapping

Anamnesis: Sesak Batuk BB sulit naik

Pemeriksaan Fisik Keadaan umum : lemah, tampak distress nafas GCS 456, Nadi 176x/menit, RR 74x/menit, t axiler 38,7C TD 100/70 mmHg, JVP Anemia + St. Antropometri: malnutrisi/underweight Jantung: murmur sistolik punctum maksimum di ICS III PSL (parasternal line) kiri, gallop Paru-paru : ronki + (seluruh lap baru) Ekstremitas :edema non pitting EKG : CT scan Brachicephalli Skull Chest X ray Prominence pulmonary artery segment Increased pulmonary vascular marking Bronchopneumoni Ekokardiografi: Ventrikular Septal Defect grade sedang berat

Gagal Jantung Akut dengan ec Ventricular Septal Defect dgn Bronchopneumoni, Down Syndrome, Brachicephalli, Gizi kurang
PenatalaksanaanO2 headbox 8 liter per menit Plug Cefotaxime 3x 100mg (iv) Amikacine 2x30 mg (iv) Furosemide 3x5mg (iv) Captopril 2x1,2 mg (po) Digoxin 2x0,02mg (po)Pamol 3x0,4cc (po) Multivit sirup 1xcth (po) ZnSO4 1x1 mg (po) Diet per NGT 12 x 25 cc Kebutuhan cairan 340 cc restriksi 20% menjadi 320 cc Transfusi PRC I 20 cc selama 24 jam kemudian PRC II 20 cc Nebulizer PZ ditambah Ventolin, suction tiap 4 jam Evaluasi distress nafas

Mapping Komplikasi Gagal Jantung pada VSD VSD


Dilusi darah >> CO2 pada aliran arteri yang >> O2 COP menurun Left to Right shunt Jaringan mengalami hipoksik hipoksia Proses adaptasi dengan Meningkatkan O2 COP inadekuat weakness inadekuat Stroke Volume meningkat HR meningkat Takikardi Perfusi koroner menurun Konsumsi oksigen miokard menurun Asidosis,radical load Aktivasi neuroendokrin Sistem saraf simpatis RAAS ADH, endotelin Curah jantung rendah

Resistensi vaskuler meningkat meningkat

Tahanan dinding meningkat

Remodelling Iskemik Fibrosis Kematian miosit

Transudasi cairan ke ruang interstisiil

Paru-paru Edema paru Ronki +

ekstremitas Edema tungkai

Hipertrofi ventrikel kiri

Fisik Diagnostik :

Pemeriksaan Penunjang
Pemeriksaan laboratorium Pemeriksaan radiologi thorax (Apex down ward,Prominence pulmonary artery segment, Increased pulmonary vascular marking Pemeriksaan Elektrokardiografi Pemeriksaan Ekokardiografi

Mapping Konsep
Anamnesis : Asimtomatik Simtomatik (sesak nafas, kesulitan mengisap susu, infeksi paru berulang, gagal tumbuh kembang, gagal jantung)
Penyebab dan patomekanisme Genetik Lingkungan (radiasi, rokok, obat-obatan (thalidomide), infeksi maternal (rubella PDA), umur ibu (muda, tua), geografis daerah ketinggian (O2 ), gangguan metabolisme (DM) Embriology Anatomy The heart is forming during the first 3 weeks of fetal development. It begins as a hollow tube, then partitions within the tube develop that eventually become the septa (or walls) dividing the right side of the heart from the left. Ventricular septal defects occur when the partitioning process does not occur completely, leaving an opening in the Ventricular septum

Inspeksi, palpasi, perkusi, auskultasi. Normal 1st HS or loud , Widely split and fixed 2nd HS, Ejection systolic murmur) Pemeriksaan Gangguan Tumbuh Kembang

VENTRIKULAR SEPTAL DEFECT

PDA with PH Tetralogy Fallot non cyanotic Innosent murmur

Epidemiologi

Penatalaksanaan Pengendalian

Rehabilitasi

Prevalensi & Insidens


Inciden 20% PJB gejala timbul pada usia 2-6 minggu kehidupan 50% meninggal pada bulan pertama kehidupan INDONESIA : 200 juta penduduk --- 30.000 bayi PJB

Preventif

Promotif

Surgery:Recent treatment: with transcatheter closure Supportif (Medikamentosa, nutrisi)

hypoxic hypoxia (anoxic anoxia), in which the PO2 of the arterial blood is reduced; Venous-to-Arterial Shunts When a cardiovascular abnormality such as an inter-atrial septal defect permits large amounts of unoxygenated venous blood to bypass the pulmonary capillaries and dilute the oxygenated blood in the systemic arteries ("right-to-left shunt"), chronic hypoxic hypoxia and cyanosis (cyanotic congenital heart disease) result. Administration of 100% O2 raises the O2 content of alveolar air and improves the hypoxia due to hypoventilation, impaired diffusion, or ventilation-perfusion imbalance (short of perfusion of totally unventilated segments) by increasing the amount of O2 in the blood leaving the lungs. However, in patients with venous-to-arterial shunts and normal lungs, any beneficial effect of 100% O2 is slight and is due solely to an increase in the amount of dissolved O2 in the blood. Table 33-7. Simplified summary of pathogenesis of major findings in congestive heart failure Abnormality Cause Weakness, exercise "Foward failure " of left ventricle; cardiac output intolerance inadequate to perfuse muscles; especially, failure of output to rise with exercise. Ankle, sacral edema "Backward failure " of right ventricle increased venous pressure increased fluid transudation. Hepatomegaly Increased venous pressure increased resistance to portal flow. Pulmonary congestion "Backward failure " of left ventricle increased pulmonary venous pressure pulmonary venous distention and transudation of fluid into air spaces. Dyspnea on exertion failure of left ventricular output to rise during exercise increased pulmonary venous pressure. Paroxysmal dyspnea, Probably sudden failure of left heart output to keep pulmonary edema up with right heart output acute rise in pulmonary venous and capillary pressure transudation of fluid

Orthopnea

Cardiac dilation

into air spaces. Normal pooling of blood in lungs in supine position added to already congested pulmonary vascular system; increased venous return not put out by left ventricle. (Relieved by sitting up, raising head of bed, lying on extra pillows.) Greater ventricular end-diastolic volume.