LAPORAN HASIL PRATIK TATANAN NYATA PADA PASIEN Ny. S DENGAN DIAGNOSA ARITMIA DI RUANG KEMUNING RSUD KAB. JOMBANG
Dosen Pembimbing : Supriliyah, S.Kep., Ns
Disusun oleh kelompok 11: 1.
Tita Heni Febrianti
(151001041)
2.
Usha Meilasari
(151001042)
3.
Verra Shintya Putri
(151001043)
4.
Vina Ismawati
(151001044)
SEKOLAH TINGGI ILMU KESEHATAN STIKES PEMKAB JOMBANG PROGRAM STUDI S1 KEPERAWATAN TAHUN 2016/2017
i
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LEMBAR PENGESAHAN ASUHAN KEPERAWATAN TATANAN NYATA RSUD JOMBANG PV. KEMUNING R. 2
Nama kelompok
:Kelompok 11
Anggota Kelompok
: 5.
Tita Heni Febrianti
(151001041)
6.
Usha Meilasari
(151001042)
7.
Verra Shintya Putri
(151001043)
8.
Vina Ismawati
(151001044)
Asuhan keperawatan pada Ny. S diagnosa medis “Aritmia” di Ruang Kemuning kelas 2 RSUD Jombang yang dilaksanakan padatanggal 09 Juni 2017 telah disahkan s ebagai Laporan tatanan nyata Semester IV Prodi S1 Keperawatan STIKES PEMKAB JOMBANG
Jomban, 12 Juni 2017 Mengetahui Pembimbing Lahan
Dosen Pembimbing
Wiwik Luciani.,Amd, Kep
Supriliyah.,S.Kep.,Ns
NIP. 197303111997032004 197303111997032004
NIK.
Mengetahui Kepala Ruangan Kemuning
Wiwik Luciani.,Amd, Kep
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KATA PENGANTAR
Puji syukur penulis panjatkan ke hadirat Allah SWT yang telah melimpahkan, rahmat taufik dan hidayah-Nya sehingga penulis dapat menyelesaikan tugas Tatanan Nyata dengan judul “Laporan Pendahuluan dan Asuhan Keperawatan Aritmia Pada Ny. S Di RSUD JOMBANG” dalam bentuk makalah. Dengan selesainya masalah ini, tidak lupa penulis mengucapkan terimakasih kepada : 1. Ketua STIKES PEMKAB JOMBANG, drg. Budi Nugroho, MPPM 2. Ketua program studi S1 Keperawatan STIKES PEMKAB JOMBANG, Dr. Sestu Retno D.A.,S.Kp,M.Kes 3. Dosen pembimbing Supriliyah.,S.Kep.,Ns 4. Pembimbing Lahan Wiwik Luciani.,Amd, Kep Penulis menyadari bahwa penyusunan makalah ini masih ada kekurangan maupun kesalahan, untuk itu penulis mengharapkan kritik dan saran yang membangun untuk penyempurnaan. Semoga makalah ini dapat bermanfaat bagi pembaca. Atas perhatiannya penulis ucapkan terimakasih.
Jombang, 10 Juni 2017
Penulis
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DAFTAR ISI
HALAMAN ............................................... ..................................................................... ............................................ ............................................ ............................ ...... i LEMBAR PENGESAHAN ............................................. ................................................................... ............................................ ........................... ..... ii KATA PENGANTAR ............................................. ................................................................... ............................................ ................................... ............. iii DAFTAR ISI ......................... ................................................ ............................................. ............................................ ............................................ ......................... ... iv BAB I PENDAHULUAN 1.1 Latar Belakang ............................ ................................................... ............................................. ............................................ ............................. ....... 1 1.2 Rumusan Masalah ........................ .............................................. ............................................ ............................................ ............................. ....... 1 1.3 Tujuan ..................................................... ........................................................................... ............................................ ........................................ .................. 2 BAB II TINJAUAN TEORI 2.1 Definisi ......................... ................................................ .............................................. ............................................. ........................................... ..................... 3 2.2 Epidemiologi ........................................... ................................................................. ............................................ ........................................ .................. 3 2.3 Etiologi ............................................ .................................................................. ............................................ ............................................. ......................... .. 4 2.4 Patofisiologi ............................................ .................................................................. ............................................ ........................................ .................. 4 2.5 WOC ....................................................... ............................................................................. ............................................ ........................................ .................. 6 2.6 Manifestasi Klinis ......................................................... ............................................................................... ........................................ .................. 7 2.7 Pemeriksaan Penunjang ............................................ .................................................................. ........................................... ..................... 8 2.8 Jenis-Jenis Aritmia ............................................ .................................................................. ............................................ ............................. ....... 8 2.9 Penatalaksanaan ........................................... .................................................................. ............................................. ................................ .......... 10 2.10 Prognosis .......................................... ................................................................. ............................................. ........................................... ..................... 11 BAB III ASKEP TEORI 3.1 Pengkajian ........................ ............................................... ............................................. ............................................ ........................................ .................. 14 3.2 Pemeriksaan Fisik ......................................... ............................................................... ............................................. ................................. .......... 15 3.3 Pemeriksaan Persistem Pers istem .......................................... ................................................................ ............................................ ......................... ... 15 3.4 Diagnosa Banding .......................................... ................................................................. ............................................. ................................ .......... 18 3.5 Intervensi ............................................ ................................................................... ............................................. ........................................... ..................... 19 3.6 Implementasi .......................................... ................................................................ ............................................ ........................................ .................. 20 3.7 Evaluasi ........................................... ................................................................. ............................................ ............................................. ......................... .. 21 BAB IV ASKEP KASUS 4.1 Pengkajian ........................
22
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4.5 Intervensi ............................................ ................................................................... ............................................. ........................................... ..................... 28 4.6 Implementasi .......................................... ................................................................ ............................................ ........................................ .................. 29 4.7 Evaluasi ........................................... ................................................................. ............................................ ............................................. ......................... .. 30 BAB V PENUTUP 5.1 Kesimpulan .................................................... ........................................................................... .............................................. ................................ ......... 32 5.2 Saran ............................................ .................................................................. ............................................ ............................................ ............................. ....... 32 DAFTAR PUSTAKA
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BAB I PENDAHULUAN
1.1 Latar Belakang
Masalah kesehatan yang berpengaruh terhadap sistem kardiovaskuler sertamenuntut asuhan keperawatan dapat dialami oleh orang pada berbagai tingkat usia. Sistem kardiovaskuler mencakup jantung, sirkulasi atau peredaran darah dan keadaan darah, yang merupakan bagian tubuh yang sangat penting karena merupakan pengaturan yang menyalurkan O2 serta nutrisi ke seluruh tubuh. Bila salah satu organ tersebut mengalami gangguan terutama jantung, maka akan mengganggu semua si stem tubuh. Aritmia adalah suatu tanda atau gejala dari gangguan detak jantung atau irama jantung. Aritmia timbul bilamana penghantaran listrik pada jantung yang mengontrol detak jantung mengalami gangguan, ini dapat terjadi bila sel saraf khusus yang ada pada jantung yang bertugas menghantarkan listrik tersebut tidak bekerja dengan baik. Aritmia juga dapat terjadi bila bagian lain dari jantung menghantarkan sinyal listrik yang abnormal. Aritmia jantung (heart arrhythmia) (heart arrhythmia) menyebabkan menyebabkan detak jantung menjadi terlalu cepat, terlalu lambat, atau tidak teratur. Aritmia jantung umumnya tidak berbahaya. Kebanyakan orang sesekali mengalami detak jantung yang tidak beraturan kadang menjadi cepat, kadang melambat. Namun beberapa jenis aritmia jantung dapat menyebabkan gangguan kesehatan atau bahkan sampai mengancam nyawa. Aritmia dan HR abnormal tidak harus terjadi bersamaan. Aritmia dapat terjadi dengan HR yang normal, atau dengan HR yang lambat (disebut bradiaritmia - kurang dari 60 per menit). Aritmia bisa juga terjadi dengan HR yang cepat (disebut tachiaritmia - lebih dari 100 per menit).
1.2 Rumusan Masalah
1. Apa definisi dari aritmia ? 2. Apa etiologi dari aritmia? 3. Bagaimana patofisiologi dari aritmia ? 4. Apa manifestasi klinis dari aritmia ?
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7. Bagaimana asuhan keperawatan dari aritmia ? 1.3 Tujuan 1. Untuk mengetahui definisi dari aritmia ? 2. Untuk mengetahui etiologi dari aritmia ? 3. Untuk mengetahui patofisiologi dari aritmia ? 4. Untuk mengetahui manifestasi klinis dari aritmia? 5. Untuk mengetahui pemeriksaan penunjang aritmia? 6. Untuk mengetahui penatalaksanaan medis dari aritmia? 7. Untuk mengetahui asuhan keperawatan dari aritmia ?
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BAB II TINJAUAN TEORI
2.1 Definisi
Gangguan irama jantung atau aritmia merupakan komplikasi yang sering terjadi pada infark miokardium. Aritmia atau disritmia adalah perubahan pada frekuensi dan irama jantung yang disebabkan oleh konduksi elektrolit abnormal atau otomatis (Doenges, 1999). Aritmia timbul akibat perubahan elektrofisiologi selsel miokardium. Perubahan elektrofisiologi ini bermanifestasi sebagai perubahan bentuk potensial aksi yaitu rekaman grafik aktivitas listrik sel (Price, 1994). Gangguan irama jantung tidak hanya terbatas pada iregularitas denyut jantung tapi juga termasuk gangguan kecepatan denyut denyut dan konduksi (Hanafi, 1996). 1996). Kelainan irama jantung dibagi atas dua kelompok besar yaitu irama jantung yang terlalu lamba (bradi-aritmia) dan irama jantung yang terlalu cepat (taki-kardi). Bradiaritmia terjadi karena gagalnya pembentukan impuls di nodal SA dan konduksi listrik yang tidak normal ke ventrikel.sedangkan mekanisme yang mendasari taki-aritmia adalah gangguan automaticity, triggered activity dan re-entry.
2.2 Epidemiologi
Data yang diperoleh dari seorang ahli jantung dan pembuluh darah Fakultas Kedokteran Universitas Indonesia, dr. Sjaharuddin Harun (2004), menyebutkan bahwa gangguan irama jantung jenis atrial fibrilasi dapat meningkatkan resiko terserang stroke lima kali lipat dibandingkan populasi dengan irama jantung normal sehingga hal ini dapat menurunkan kualitas hidup penderitanya. Sejauh ini, atrial fibrilasi memberikan
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akibat sindrom koroner akut dan merupakan penyebab 50 % kematian mendadak, yang biasanya terjadi 1 jam setelah onset infark miokard. 2.3 Etiologi
1. Peradangan jantung, misalnya demam reumatik, peradangan miokard (miokarditis karena infeksi). 2. Gangguan sirkulasi koroner (aterosklerosis koroner atau spasme arteri koroner), misalnya iskemia miokard, infark miokard. 3. Karena obat (intoksikasi) antara lain oleh digitalis, quinidin dan obat-obat anti aritmia lainnya. 4. Gangguan keseimbangan elektrolit (hiperkalemia, hipokalemia). 5. Gangguan pada pengaturan susunan saraf autonom yang mempengaruhi kerja dan irama jantung. 6. Ganggguan psikoneurotik dan susunan saraf pusat. 7. Gangguan metabolik (asidosis, alkalosis). 8. Gangguan endokrin (hipertiroidisme, hipotiroidisme). 9. Gangguan irama jantung karena kardiomiopati atau tumor jantung. 10. Gangguan irama jantung karena penyakit degenerasi (fibrosis sistem konduksi jantung).
2.4 Patofisiologi
Rangsangan jantung secara normal disalurkan dari sentrum implus pacu nodus SA (sinoatrial) melalui atrium, sistem hantaran antrioventrikular (AV), berkas serabut Purkinje, dan obat ventrikel. Dalam keadaan normal, pacu untuk denyut jantung dimulai di denyut nodus SA dengan irama sinur 70-80 kali per menit, kemudian di nodus AV dengan 50 kali per
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Aritmia terjadi karena gangguan pemberian implus (otomatisitas abnormal atau gangguan konduksi). Gangguan dalam pembentukan pacu antara lain : 1. Gangguan dan irama sinus, seperti takikardi sinus, bradikardi sinus dan aritmia sinus. 2. Debar ektopik dan irama ektopik :
Takikardi sinus fisiologis, yaitu pekerjaan pekerjaan fisik, emosi, dan waktu makan sedang dicerna.
Takikardi pada waktu istirahat yang merupakan gejala penyakit, seperti demam, hipertiroidisme, anemia, lemah miokard, miokarditis, dan neurosis jantung.
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2.5 WOC/Pathway
Sres, stimulant (kokain, amfetamin, nikotin kafein) hipoksia, hipovelomia, hipoksemia,hopertiroidisme, gagal jantung kongestif
Obat-obatan (digitalis, verepamil, propanolol, reserpin , metildopa) peningkatan tekanan intracranial, infark miokard, cidera akut medulla spinalis, n eri eri berat erat
B2 System kardiovaskuler
Gangguan Irama Sinus
Sinus Takikardi Sinus Bradikardi Frekuensi jantung
Frekuensi jantung lambat
Jantung tidak dapat mengompensasi
Resiko penurunan curah jantung
meningkat
Waktu pengisisan ventrikel
Suplai darah ke jaringan
B6 Sistem Muskulusskeletal
System persyarafa n
Suplai O2 ke
Suplai darah
Kebutuhan o2 otot jantung
Kelelahan
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Menghasilkan asam laktat
Gangguan perfusi jaringan cerebral cerebral Peradangan
Pelepasan mediator inflamasi
Nyeri dada
2.6 Manifestasi Klinis 1. Perubahan TD ( hipertensi atau hipotensi ); nadi mungkin tidak teratur; defisit nadi;
bunyi jantung irama tak teratur, bunyi ekstra, denyut menurun; kulit pucat, sianosis, berkeringat; edema; haluaran urin menurun bila curah jantung menurun berat. 2. Sinkop, pusing, berdenyut, sakit kepala, disorientasi, bingung, letargi, per ubahan pupil. 3. Nyeri dada ringan sampai berat, dapat hilang atau tidak dengan obat antiangina,
gelisah. 4. Nafas pendek, batuk, perubahan kecepatan/kedalaman pernafasan; bunyi nafas
tambahan (krekels, ronki, mengi) mungkin ada menunjukkan komplikasi pernafasan seperti pada gagal jantung kiri (edema paru) atau fenomena tromboembolitik
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2.7 Pemeriksaan Penunjang 1. EKG : menunjukkan pola cedera iskemik dan gangguan konduksi. Menyatakan
tipe/sumber disritmia dan efek ketidakseimbangan elektrolit dan obat jantung. 2. Monitor Holter : Gambaran EKG (24 jam) mungkin diperlukan untuk menentukan
dimana disritmia disebabkan oleh gejala khusus bila pasien aktif (di rumah/kerja). Juga dapat digunakan untuk mengevaluasi fungsi pacu jantung/efek obat antidisritmia. 3. Foto dada : Dapat menunjukkanpembesaran bayangan jantung sehubungan dengan
disfungsi ventrikel atau katup . 4. Skan pencitraan miokardia : dapat menunjukkan aea iskemik/kerusakan miokard yang
dapat mempengaruhi konduksi normal atau mengganggu gerakan dinding dan kemampuan pompa. 5. Tes stres latihan : dapat dilakukan utnnuk mendemonstrasikan latihan yang
menyebabkan disritmia. 6. Elektrolit : Peningkatan atau penurunan kalium, kalsium dan magnesium dapat
mnenyebabkan disritmia. 7. Pemeriksaan obat : Dapat menyatakan toksisitas obat jantung, adanya obat jalanan
atau dugaan interaksi obat contoh digitalis, quinidin. 8. Pemeriksaan tiroid : peningkatan atau penururnan kadar tiroid serum dapat
menyebabkan.meningkatkan disritmia.
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dan/atau gejala2 yg berkaitan dgnya sebaiknya dievaluasi oleh seorang dokter jantung. Namun, pada kebanyakan orang, PVC biasanya tidak berbahaya dan jarang memerlukan terapi. 3. Atrial fibrilasi (AF). Ini merupakan irama jantung tidak teratur yang sering menyebabkan atrium, ruang atas jantung, berkontraksi secara abnormal. 4. Atrial flutter. Ini merupakan aritmia yang disebabkan oleh satu atau lebih sirkuit yang cepat di atrium. Atrial flutter biasanya lebih terorganisir dan teratur dibandingkan dengan atrial fibrilasi. Aritmia ini terjadi paling sering pada orang dengan penyakit jantung, dan selama minggu pertama setelah bedah jantung. Aritmia ini sering berubah menjadi atrial fibrilasi. 5. Paroxysmal supraventricular tachycardia (PSVT). Suatu HR yang cepat, biasanya dengan irama yang teratur, te ratur, berasal dari atas ventrikel. PSVT mulai dan berakhir dg tiba2. Terdapat dua tipe utama : accessory path tachycardia dan AV nodal reentrant tachycardia (lihat bawah). 6. Accessory pathway tachicardia. HR yang cepat disebabkan oleh jalur atau hubungan extra yang abnormal antara atrium dan ventrikel. Impuls berjalan melewati jalur ekstra selain juga melewati rute biasa. Ini membuat impuls berjalan di jantung dg sangat cepat menyebabkan jantung berdenyut dg cepat. tachycardia . HR yang cepat disebabkan lebih dari satu jalur 7. AV nodal reentrant tachycardia
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10. Long QT syndrome. Interval QT adalah area pd ECG yang merepresentasikan waktu yang diperlukan otot jantung untuk berkontraksi dan kemudian relaksasi, atau yang diperlukan impuls listrik utk meletupkan impuls dan kmd recharge. Jika interval QT memanjang, ini meningkatkan resiko terjadinya “torsade de pointes”, suatu bentuk ventricular tachicardia yang mengancam hidup. Long QT syndrome merupakan suatu kondisi yang diturunkan yang dapat menyebabkan kematian mendadak pada orang muda. Ini dapat diterapi dengan obat2 antiaritmia, pacemaker, electrical cardioversion, defibrilasi, defibrilator/cardioverter implant atau terapi ablasi. 11. Bradiaritmia. Ini merupakan irama jantung yang pelan yang dapat muncul dari kelainan pada sistem konduksi listrik jantung. Contohnya adalah sinus node dysfunction dan blok jantung. 12. Sinus node dysfunction. HR yang lambat yang disebabkan oleh SA node yang abnormal. Diterapi dengan pacemaker. 13. Blok jantung. Suatu penundaan (delay) atau blok total impuls listrik ketika berjalan dari sinus node ke ventrikel. Blok atau delay dapat terjadi pada AV node atau sistem HIS purkinje. Jantung berdenyut ireguler dan sering lebih lambat. Jika serius blok jantung perlu diterapi dengan pacemaker.
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Anti aritmia Kelas 2 (Beta adrenergik blokade) Atenolol, Metoprolol,
Propanolol : indikasi aritmi jantung, angina pektoris dan hipertensi. Anti aritmia kelas 3 (Prolong repolarisation) Amiodarone, indikasi VT, SVT
berulan Anti aritmia kelas 4 (calcium channel blocker) Verapamil, indikasi
supraventrikular aritmia. b. Terapi mekanis Kardioversi : mencakup pemakaian arus listrik untuk menghentikan disritmia
yang memiliki kompleks GRS, biasanya merupakan prosedur elektif. Defibrilasi : kardioversi asinkronis yang digunakan pada keadaan gawat
darurat. Defibrilator kardioverter implantabel : suatu alat untuk mendeteksi dan
mengakhiri episode takikardi ventrikel yang mengancam jiwa atau pada p asien yang resiko mengalami fibrilasi ventrikel. Terapi pacemaker : alat listrik yang mampu menghasilkan stimulus listrik
berulang ke otot jantung untuk untuk mengontrol frekuensi jantung.
2.9 Prognosis
Aterosklerosis
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b.
Infark Miokard Akut Infark miokard adalah kematian otot jantung karena penyumbatan pada arteri koroner. Otot-otot jantung yang tidak tersuplai darah akan mengalami kerusakan atau kematian mendadak.
c.
Kardiomiopati Kardiomiopati
adalah kerusakan
atau
gangguan
otot
jantung
sehingga
menyebabkan dinding-dinding jantung tidak bergerak sempurna dalam menyedot dan memompa darah. Penderita kardiomiopati seringkali berisiko terkena arritmia dan gagal jantung mendadak.
d.
Penyakit Jantung Rematik Penyakit jantung rematik adalah kerusakan pada katup jantung karena demam
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h.
KelainanKatupJantung Katup jantung berfungsi mengendalikan arah aliran darah dalam jantung. Kelainan katup jantung yang dapat mengganggu aliran tersebut, antara lain karena pengecilan (stenosis), kebocoran (regurgiasi), atau tidak menutup sempurna (prolapsis). Kelainan katup dapat terjadi sebagai bawaan lahir maupun karena infeksi dan efeksamping pengobatan.
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BAB III ASUHAN KEPERAWATAN TEORI
3.1. PENGKAJIAN A. Identitas Pasien
Hal-hal yang perlu dikaji pada bagian ini antara lain: Nama, Umur, Jenis Kelamin, Pendidikan, Pekerjaan, Agama, Status Mental, Suku, Keluarga/orang terdekat, alamat, nomor registrasi. B. Keluhan Utama Berisi data pasien singkat dan jelas, 2 atau 3 kata yang merupakan keluhan yang membuat pasien meminta bantuan kesehatan. Jika pengkajian dilakukan setelah beberapa hari pasien MRS maka keluhan
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3.2. PEMERIKSAAN FISIK Tanda-tanda Vital, TB dan BB :
S : ……°C (SUHU. (SUHU. axial, rectal, oral) N : …. x/menit x/menit ( NADI. teratur, tidak teratur, kuat, lemah)
TD : …../…..mmHg (lengan kiri, lengan kanan, berbaring, duduk)
: ….x/menit (regular/ irregular)TB : … cm
RR
BB : …. K g ( cara menghitung berat
badan ideal : TB -100 ( ± 10% dari hasil ).
3.3. PEMERIKSAAN PEMERIKSAAN PERSISTEM a. System pernapasan
Anamnesa : karakteristik batuk (produktif/non produktif), sesak nafas, nyeri dada (PQRST) Hidung
Inspeksi : Napas cupping hidung
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Ekstrimitas atas
Inspeksi : sianosis, clubbing finger
Palpasi : CRT Ekstrimitas bawah
Inspeksi : identifikasi edema pada ektrimitas , clubbing finger Palpasi : identifikasi adanya benjolan pada ekstrimitas c. Persyarafan
1. Uji nervus 1 olfaktorius (pembau) : dengan cara menggunakan bau – bauan (minyak kayu putih, kopi dan tembakau), kemudian meminta klien untuk menutup mata dan membedakan bau – bau – bauan bauan tersebut. 2. Uji nervus II opticus (penghilatan) : mengobservasi apakah terdapat kelainan pada mata misalnya katarak, infeksi konjungtiva atau infeksi lainnya.
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Mulut
Inspeksi : sianosis , stomatitis (+/-) Palpasi : nyeri tekan Abdomen (dibagi menjadi 4 kuadran)
Inspeksi : terdapat luka atau tidak Palpasi : adanya nyeri tekan atau tidak Perkusi : suara perut (tympani / hypertimpani)
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Leher
Inspeksi : bentuk , pembesaran kelenjar tyroid Palpasi : pembesaran kelenjar tyroid , nyeri tekan Ekstrimitas bawah : edema g. System reproduksi
Anamnesa : mengidentifikasi masalah haid h. Persepsi sensori
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3.5 INTERVENSI KEPERAWATAN
NIC Intervensi Intervensi
NOC Aktifitas
Perawatan Jantung Action :
Outcome
Indikator
Keefektifan pompa
1. Disritmia (3)
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tindakan
keperawatan
yang
telah
direncanakan
dan
dilanjutkan
dengan
pendokumentasian semua tindakan yang telah dilakukan beserta hasil-hasilnya. Beberapa petunjuk pada pelaksanaan adalah sebagai berikut : a. Intervensi dilaksanakan sesuai dengan rencana setelah dilakukan validasi. b.Keterampilan interpersonal, intelektual, teknikal, dilakukan dengan cermat dan efisien pada situasi yang tepat. c. Keamanan fisik dan psikologis dilindungi.
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BAB IV ASUHAN KEPERAWATAN KASUS
Pada tanggal 07 Juni 2017 Ny. S yang berusia 44 tahun datang ke RSUD Jombang dengan keluhan berdebar-debar mulai tadi malam, kedua kakinya bengkak ,disertai mual. Setelah di lakukan pengkajian didapatkan didapatkan data TD : 120/90 x/menit, N :82 x/menit S : 38 0C, RR : 24 x/menit. Skala nyeri : 0 ,Takikardi : >120
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D. RIWAYAT PENYAKIT DAHULU
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Leher
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D. Sistem Pencernaan-Eliminasi Alvi
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4: Gerakan aktif,dapat melawan gravitasi serta mampu menahan tahanan
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Perkusi: tidak ada reaksi hebat pada regio frontalis, sinus frontalis dan
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