Laporan Pendahuluan Asma Bronkhial

TINJAUAN TEORITIS ASMA BRONKHIAL

1. Pengertian

Asma bronchial adalah penyakit jalan nafas obstruktif intermiten, reversibel dimana trakea dan bronkhi berespon secara hiperaktif terhadap stimulasi tertentu. (Smelzer Suzanne : 2001)

Asma bronchial adalah suatu penyakit dengan ciri meningkatnya respon bronkus terhadap berbagai rangsangan dengan manifestasi adanya penyempitan jalan nafas yang luas dan derajatnya dapat berubah-ubah baik secara spontan maupun hasil dari pengobatan (The American Thoracic Society).

Asma bronchial adalah suatu penyakit pernapasan dimana terjadi penigkatan respon saluran pernapasan yang menimbulkan reaksi obstruksi pernapasan akibat spasme otot polos bronkus. (Sjaifoellah, 2001: 21)

Asma bronchial adalah penyakit pernafasan objektif yang ditandai oleh spasme akut otot polos bronkus. Hal ini menyebabkan obstruksi aliran udara dan penurunan ventilasi alveolus. (Elizabeth, 2000: 430)

Asma bronchial adalah suatu gangguan yang komplek dari bronkial yang dikarakteristikan oleh periode bronkospasme (kontraksi spasme yang lama pada jalan nafas). (Polaski : 1996).

Asma adalah gangguan pada jalan nafas bronkial yang dikateristikan dengan bronkospasme yang reversibel. (Joyce M. Black: 1996).

Dari berbagai deinisi diatas dapat disimpulkan bahwa asma bronchial adalah suatu penyakit gangguan jalan nafas obstruktif yang bersifat reversible, ditandai dengan terjadinya penyempitan bronkus, reaksi obstruksi akibat spasme otot polos bronkus, obstruksi aliran udara, dan penurunan ventilasi alveoulus dengan suatu keadaan hiperaktivitas bronkus yang khas.

2. Etiologi

Sampai saat ini etiologi dari asma bronchial belum diketahui. Berbagai teori sudah diajukan, akan tetapi yang paling disepakati adalah adanya gangguan parasimpatis (hiperaktivitas saraf kolinergik), gangguan Simpatis (blok pada reseptor beta adrenergic dan hiperaktifitas reseptor alfa adrenergik).

Gambar 1.1  Bronkhus pada penderita asma.

Berdasarkan penyebabnya, asma bronkhial dapat diklasifikasikan menjadi 3 tipe, yaitu :

1. Ekstrinsik (alergik)

Ditandai dengan reaksi alergik yang disebabkan oleh faktor-faktor pencetus yang spesifik, seperti debu, serbuk bunga, bulu binatang, obat-obatan (antibiotic dan aspirin) dan spora jamur. Asma ekstrinsik sering dihubungkan dengan adanya suatu predisposisi genetik terhadap alergi. Oleh karena itu jika ada faktor-faktor pencetus spesifik seperti yang disebutkan di atas, maka akan terjadi serangan asma ekstrinsik.

2.  Intrinsik (non alergik)

Ditandai dengan adanya reaksi non alergi yang bereaksi terhadap pencetus yang tidak spesifik atau tidak diketahui, seperti udara dingin atau bisa juga disebabkan oleh adanya infeksi saluran pernafasan dan emosi. Serangan asma ini menjadi lebih berat dan sering sejalan dengan berlalunya waktu dan dapat berkembang menjadi bronkhitis kronik dan emfisema.

3. Asma gabungan

Bentuk asma yang paling umum. Asma ini mempunyai karakteristik dari bentuk alergik dan non-alergik.

Ada beberapa hal yang merupakan faktor predisposisi dan presipitasi timbulnya serangan asma bronkhial.

1. Faktor predisposisi

Genetik. Dimana yang diturunkan adalah bakat alerginya, meskipun belum diketahui bagaimana cara penurunannya yang jelas. Penderita dengan penyakit alergi biasanya mempunyai keluarga dekat juga menderita penyakit alergi. Karena adanya bakat alergi ini, penderita sangat mudah terkena penyakit asma bronkhial jika terpapar dengan foktor pencetus. Selain itu hipersentifisitas saluran pernafasannya juga bisa diturunkan.

2. Faktor presipitasi

3. Alergen

dimana alergen dapat dibagi menjadi 3 jenis, yaitu :

1)      Inhalan, yang masuk melalui saluran pernapasan

Contohnya: debu, bulu binatang, serbuk bunga, spora jamur, bakteri dan polusi.

2)      Ingestan, yang masuk melalui mulut.

Contoh: makanan dan obat-obatan.

3)      Kontaktan, yang masuk melalui kontak dengan kulit

Contoh: perhiasan, logam dan jam tangan.

Perubahan cuaca

Cuaca lembab dan hawa pegunungan yang dingin sering mempengaruhi asma. Atmosfir yang mendadak dingin merupakan faktor pemicu terjadinya serangan asma. Kadang-kadang serangan berhubungan dengan musim, seperti musim hujan, musim kemarau, musim bunga. Hal ini berhubungan dengan arah angin serbuk bunga dan debu.

Stress

Stress/gangguan emosi dapat menjadi pencetus serangan asma, selain itu juga bisa memperberat serangan asma yang sudah ada. Disamping gejala asma yang timbul harus segera diobati penderita asma yang mengalami stress/gangguan emosi perlu diberi nasehat untuk menyelesaikan masalah pribadinya. Karena jika stressnya belum diatasi maka gejala asmanya belum bisa diobati.

Lingkungan kerja

Mempunyai hubungan langsung dengan sebab terjadinya serangan asma. Hal ini berkaitan dengan dimana dia bekerja. Misalnya orang yang bekerja di laboratorium hewan, industri tekstil, pabrik asbes, polisi lalu lintas. Gejala ini membaik pada waktu libur atau cuti.

Olahraga/ aktifitas jasmani yang berat

Sebagian besar penderita asma akan mendapat serangan jika melakukan aktifitas jasmani atau olahraga yang berat. Lari cepat paling mudah menimbulkan serangan asma. Serangan asma karena aktifitas biasanya terjadi segera setelah selesai aktifitas tersebut.

3. Anatomi dan Fisiologi Sistem Penapasan Manusia

Anatomi sistem pernapasan

Sistem pernafasan adalah suatu sistem yang dimulai dari tempat masuknya udara melalui hidung, hingga udara akan mengalami suatu pertukara gas di paru-paru, dan dibentuk oleh organ-organ pernapasan.Sistem Pernafasan meliputi saluran sebagai berikut:

  • Rongga Hidung
  • Farinx
  • Larinx
  • Trakhea
  • Rongga Thoraks
  • Paru-paru
  • Lobus Paru
  • Bronkhus Pulmonalis

Fisiologi pernafasan

Fungsi paru-paru ialah pertukaran gas Oksigen dan Karbon Dioksida.Pada pernapasan melalui paru-paru atau pernapasan externa, Oksigen berasal dari udara yang masuk melalui hidung dan mulut, pada waktu bernapas; oksigen masuk melaui trakhea dan pipa bronkhial ke alveoli dan mempunyai hubungan yang erat dengan darah di dalam kapiler pulmonalis.Hanya satu lapisan membran yaitu membran alveoli-kapiler, yang memisahkan oksigen dari darah. Oksigen menembus membran ini dan diangkut oleh haemoglobin sel darah merah dan dibawa ke jantung kemudian dipompa oleh arteri ke seluruh bagian tubuh. Darah meninggalkan paru-paru pada tekanan oksigen 100 mmHg dan pada tingkat ini hemoglobinnya 95% jenuh oksigen

Di dalam paru-paru, karbon dioksida menembus membran alveoli-kapiler dari kapiler darah ke alveoli dan setelah melalui pipa bronkhial dan trakhea, dikeluarkan melalui hidung dan mulut. Pernapasan jaringan atau pernapasan interna, darah yang telah menjenuhkan hemoglobinnya dengan oksigen (oksihemogloin), mengitari seluruh tubuh dan akhirnya mencapai kapiler, di mana darah bergerak sangat lambat. Sel jaringan mengangkut oksigen dari hemoglobin untuk memungkinkan oksigen berlangsung dan darah menerima, sebagai gantinya, hasil buangan oksidasi, yaitu karbon dioksida.

4. Patofisiologi

Perubahan jaringan pada asma tanpa komplikasi terbatas pada bronkus dan terdiri dari spasme otot polos, edema mukosa, dan infiltrasi sel-sel Radang yang menetap dan hipersekresi mucus yang kental. Keadaan ini pada orang-orang yang rentan terkena asma mudah ditimbulkan oleh berbagai rangsangan, yang menandakan suatu keadaan hiveraktivitas bronkus yang khas.Orang yang menderita asma memilki ketidakmampuan mendasar dalam mencapai angka aliran uadara normal selama pernapasan (terutama pada ekspirasi). Ketidakmampuan ini tercermin dengan rendahnya usaha ekspirasi paksa pada detik pertama, dan berdasrkan parameter yang berhubungan aliran.

Asma ditandai dengan kontraksi spastik dari otot polos bronkus yang menyebabkan sukar bernafas. Penyebab yang umum adalah hipersensitivitas bronkhioulus terhadap benda-benda asing di udara. Reaksi yang timbul pada asma tipe alergi diduga terjadi dengan cara sebagai berikut : seorang yang alergi mempunyai kecenderungan untuk membentuk sejumlah antibody IgE abnormal dalam jumlah besar dan antibodi ini menyebabkan reaksi alergi bila reaksi dengan antigen spesifikasinya. Pada asma, antibody ini terutama melekat pada sel mast yang terdapat pada interstisial paru yang berhubungan erat dengan brokhiolus dan bronkhus kecil. Bila seseorang menghirup alergen maka antibody IgE orang tersebut meningkat, alergen bereaksi dengan antibodi yang telah terlekat pada sel mast dan menyebabkan sel ini akan mengeluarkan berbagai macam zat, diantaranya histamin, zat anafilaksis yang bereaksi lambat (yang merupakan leukotrient), faktor kemotaktik eosinofilik dan bradikinin. Histamine yang dihasilkan menyebabkan kontraksi otot polos bronkiolus. Apabila respon histaminnya berlebihan, maka dapat timbul spasme asmatik. Karena histamine juga merangsang pembentukan mucus dan meningkatkan permeabilitas kapiler, maka juga akan terjadi kongesti dan pembengkakan ruang intestinum paru, sehingga menyebabkan tahanan saluran napas menjadi sangat meningkat. Selain itu olahraga juga dapat berlaku sebagai suatu iritan, karena terjadi aliran udara keluar masuk paru dalam jumlah beasr dan cepat. Udara ini belum mendapat perlembaban (humidifikasi), penghangatan, atau pembersihan dari partikel-partikel debu secara adekuat sehingga dapat mencetuskan asma.

Pada asma, diameter bronkhiolus menjadi semakin berkurang selama ekspirasi dari pada selama inspirasi. Hal ini dikarenakan bahwa peningkatan tekanan dalam intrapulmoner selama usaha ekspirasi tak hanya menekan udara dalam alveolus tetapi juga menekan sisi luar bronkiolus. Oleh karena itu pendeita asma biasanya dapat menarik nafas cukup memadai tetapi mengalami kesulitan besar dalam ekspirasi. Ini menyebabkan dispnea, atau ”kelaparan udara”. Kapsitas sisa fungsional paru dan volume paru menjadi sangat meningkat selama serangan asma karena kesulitan mengeluarkan udara dari paru-paru. Setelah suatu jangka waktu yang panjang, sangkar dada menjadi membesar secara permanent, sehingga menyebabkan suatu ”barrel chest” (dad seperti tong).

5. Tanda dan Gejala

Gejala-gejala yang lazim muncul pada asma bronchial menurut Suzanne Smeltzer (2001: 612) adalah batuk, dispnea, dan mengi. Biasanya pada penderita yang sedang bebas serangan tidak ditemukan gejala klinis, tapi pada saat serangan penderita tampak bernafas cepat dan dalam, gelisah, duduk dengan menyangga ke depan, serta tanpa otot-otot bantu pernafasan bekerja dengan keras. Gejala klasik dari asma bronkial ini adalah sesak nafas, mengi ( whezing ), batuk, dan pada sebagian penderita ada yang merasa nyeri di dada. Gejala-gejala tersebut tidak selalu dijumpai bersamaan. Pada serangan asma yang lebih berat , gejala-gejala yang timbul makin banyak, antara lain : silent chest, sianosis, gangguan kesadaran, hyperinflasi dada, tachicardi dan pernafasan cepat dangkal . Serangan asma seringkali terjadi pada malam hari.

Selain gejala tersebut, ada beberapa gejala menyertainya :

  1. Takipnea
  2. Gelisah
  3. Diaphorosis
  4. Nyeri di abdomen karena terlihat otot abdomen dalam pernafasan
  5. Fatigue ( kelelahan)
  6. Tidak toleran terhadap aktivitas: makan, berjalan, bahkan berbicara.
  7. Serangan biasanya bermula dengan batuk dan rasa sesak dalam dada disertai pernafasan lambat.
  8. Ekspirasi selalu lebih susah dan panjang disbanding inspirasi
  9. Sianosis sekunder
  10. Gerak-gerak retensi karbondioksida seperti : berkeringat, takikardia, dan pelebaran tekanan nadi.
  11. Seragan dapat berlangsung dari 30 menit sampai beberapa jam dan dapat hilang secara spontan.

Ada beberapa tingkatan penderita asma yaitu :

  1. Tingkat I :
  • Secara klinis normal tanpa kelainan pemeriksaan fisik dan fungsi paru.
  • Timbul bila ada faktor pencetus baik di dapat alamiah maupun dengan test provokasi bronkial di laboratorium.
    2.
  1. Tingkat II :
  • Tanpa keluhan dan kelainan pemeriksaan fisik tapi fungsi paru menunjukkan adanya tanda-tanda obstruksi jalan nafas.
  • Banyak dijumpai pada klien setelah sembuh serangan.
  1. Tingkat III:
  • Tanpa keluhan.
  • Pemeriksaan fisik dan fungsi paru menunjukkan adanya
  • bstruksi jalan nafas.
  • Penderita sudah sembuh dan bila obat tidak diteruskan mudah diserang kembali.
  1. Tingkat IV :
  • Klien mengeluh batuk, sesak nafas dan nafas berbunyi wheezing.
  • Pemeriksaan fisik dan fungsi paru didapat tanda-tanda obstruksi jalan nafas.
  1. Tingkat V :
  • Status asmatikus yaitu suatu keadaan darurat medis berupa serangan asma akut yang berat bersifat refrator sementara terhadap pengobatan yang lazim dipakai.
  • Asma pada dasarnya merupakan penyakit obstruksi jalan nafas yang reversibel. Pada asma yang berat dapat timbul gejala seperti : Kontraksi otot-otot pernafasan, cyanosis, gangguan kesadaran, penderita tampak letih, takikardi.

6. Komplikasi

Berbagai komplikasi menurut Arief Mansjoer (2000: 477) yang mungkin timbul adalah :

1. Pneumo thoraks

Pneumothoraks adalah keadaan adanya udara di dalam rongga pleura yang dicurigai bila terdapat benturan atau tusukan dada. Keadaan ini dapat menyebabkan kolaps paru yang lebih lanjut lagi dapat menyebabkan kegagalan nafas.

Kerja pernapasan meningkat, kebutuhan O2 meningkat. Orang asam tidak sanggup memenuhi kebutuhan O2 yang sangat tinggi yang dibutuhkan untuk bernapas melawan spasme bronkhiolus, pembengkakan bronkhiolus, dan m ukus yang kental. Situasi ioni dapat menimbulkan pneumothoraks akibat besarnya teklanan untuk melakukan ventilasi.

2. Pneumomediastinum

Pneumomediastinum dari bahasa Yunani pneuma “udara”, juga dikenal sebagai emfisema mediastinum adalah suatu kondisi dimana udara hadir di mediastinum . Pertama dijelaskan pada 1819 oleh Rene Laennec , kondisi ini dapat disebabkan oleh trauma fisik atau situasi lain yang mengarah ke udara keluar dari paru-paru , saluran udara atau usus ke dalam rongga dada .

3.Emfisema subkutis

4.Ateleltaksis

Atelektasis adalah pengkerutan sebagian atau seluruh paru-paru akibat penyumbatan saluran udara ( bronkus maupun bronkiolus ) atau akibat pernafasan yang sangat dangkal.

5.Aspergilosis

Aspergilosis merupakan penyakit pernafasan yang disebabkan oleh jamur dan tersifat oleh adanya gangguan pernafasan yang berat. Penyakit ini juga dapat menimbulkan lesi pada berbagai organ lainnya, misalnya pada otak dan mata. Istilah Aspergilosis dipakai untuk menunjukkan adanya infeksi Aspergillus sp.

Aspergilosis Bronkopulmoner Alergika (ABPA) adalah suatu reaksi alergi terhadap jamur yang disebut aspergillus, yang menyebabkan peradangan pada saluran pernafasan dan kantong udara.

6.Bronkopulmonar alergik

7.Gagal nafas

8.Bronchitis

Bronkhitis atau radang paru-paru adalah kondisi di mana lapisan bagian dalam dari saluran pernapasan di paru-paru yang kecil (bronchiolis) mengalami bengkak. Selain bengkak juga terjadi peningkatan produksi lendir (dahak). Akibatnya penderita merasa perlu batuk berulang-ulang dalam upaya mengeluarkan lendir yang berlebihan, atau merasa sulit bernafas karena sebagian saluran udara menjadi sempit oleh adanya lendir.

9.Fraktur iga

7. Prognosis

  1. Pada umunya bila segera ditangani dengan adekuat prognosa adalah baik.
  2. Asma faktor imunologi (faktor ektrensik) yang muncul semasa kecil prognosanya lebih baik daripada yang muncul semasa dewasa.
  3. Angka kematian meningkat bila tidak ada fasilitas kesehatan yang memadai.

8. Pemeriksaan Diagnostik

a. Spirometri

Untuk menunjukkan adanya obstruksi jalan nafas reversible, cara yang paling cepat dan sederhana diagnosis asma adalah melihat respon pengobatan dengan bronkodilator. Pemeriksaan spirometer dilakukan sebelum dan sesudah pamberian bronkodilator aerosol (inhaler atau nebulizer) golongan adrenergik. Peningkatan FEV1 atau FVC sebanyak lebih dari 20% menunjukkan diagnosis asthma. Tidak adanya respon aerosol bronkodilator lebih dari 20%. Pemeriksaan spirometri tidak saja penting untuk menegakkan diagnosis tetapi juga penting untuk menilai berat obstruksi dan efek pengobatan. Benyak penderita tanpa keluhan tetapi pemeriksaan spirometrinya menunjukkan obstruksi.

b.Uji Provokasi bronkus

Menurut Heru Sundaru dalam bukunya H.Slamet Sogiono, dkk (2001: 24-25) “Dilakukan jika spirometri normal, maka dilakukan uji provokasi bronkus dengan allergen, dan hanya dilakukan pada pasien yang alergi terhadap allergen yang di uji”.

c.Pemeriksaan sputum

Pemeriksaan sputum dilakukan untuk melihat adanya:

  • Kristal-kristal charcot leyden yang merupakan degranulasi dari kristal eosinopil.
  • Spiral curshmann, yakni yang merupakan cast cell (sel cetakan) dari cabang bronkus.
  • Creole yang merupakan fragmen dari epitel bronkus.
  • Netrofil dan eosinopil yang terdapat pada sputum, umumnya bersifat mukoid dengan viskositas yang tinggi dan kadang terdapat mucus plug.

d.Pemeriksaan Coninofit total

e.Uji kulit

Dilakukan untuk mencari faktor alergi dengan berbagai alergen yang dapat menimbulkan reaksi yang positif pada asma.

f.Elektrokardiografi

Gambaran elektrokardiografi yang terjadi selama serangan dapat dibagi menjadi 3 bagian, dan disesuaikan dengan gambaran yang terjadi pada empisema paru yaitu :

  • Perubahan aksis jantung, yakni pada umumnya terjadi right axis deviasi dan clock wise rotation.
  • Terdapatnya tanda-tanda hipertropi otot jantung, yakni terdapatnya RBB (Right bundle branch block).
  • Tanda-tanda hopoksemia, yakni terdapatnya sinus tachycardia, SVES, dan VES atau terjadinya depresi segmen ST negative.

g.Pemeriksaan kadar Ig E total dan Ig E spesifik dalam sputum

Pemeriksaan Ig E dalam serum juga dapat membantu menegakkan diagnosis asma, tetapi ketetapan diagnosisnya kurang karena lebih dari 30 % menderita alergi.

h.Foto dada ( scanning paru)

Dengan scanning paru melalui inhalasi dapat dipelajari bahwa redistribusi udara selama serangan asma tidak menyeluruh pada paru-paru.

i.Analisis gas darah

  • Analisa gas darah pada umumnya normal akan tetapi dapat pula terjadi hipoksemia, hiperkapnia, atau asidosis.
    Kadang pada darah terdapat peningkatan dari SGOT dan LDH.
  • Hiponatremia dan kadar leukosit kadang-kadang di atas 15.000/mm3 dimana menandakan terdapatnya suatu infeksi.

9. Penatalaksanaan Medis

Menurut Internasional consensus report or diagnisis and treatment of asthma penatalaksanaan asma bronchial terdiri atas :

  1. Edukasi penderita
  2. Menilai dan memonitor besarnya penyakit secara objektif dengan mengukur fungsi paru
  3. Menghindari pengobatan jangka panjang ntuk pencegahan
  4. Merencanakan pengobatan untuk serangan  akut
  5. Menmghindari dan mengendalikan pencetus asma bronchial
  6. Penanganan lanjutan secara teratur

Adapun penatalaksanaan menurut pendapat lain terbagi menjadi 2, yaitu :

  1. Pengobatan farmakologik
  • Bronkodilator : obat yang melebarkan saluran nafas. Terbagi dalam 2 golongan :

1)      Simpatomimetik/ andrenergik (Adrenalin dan efedrin).

Nama obat :Orsiprenalin (Alupent), Fenoterol (berotec) dan Terbutalin (bricasma).

Obat-obat golongan simpatomimetik tersedia dalam bentuk tablet, sirup,suntikan dan semprotan. Yang berupa semprotan: MDI (Metered dose inhaler). Ada juga yang berbentuk bubuk halus yang dihirup (Ventolin Diskhaler dan Bricasma Turbuhaler) atau cairan broncodilator (Alupent, Berotec, brivasma serts Ventolin) yang oleh alat khusus diubah menjadi aerosol (partikel-partikel yang sangat halus ) untuk selanjutnya dihirup.

2)      Santin (teofilin)

Nama obat :Aminofilin (Amicam supp), Aminofilin (Euphilin Retard) dan Teofilin (Amilex).

Efek dari teofilin sama dengan obat golongan simpatomimetik, tetapi cara kerjanya berbeda. Sehingga bila kedua obat ini dikombinasikan efeknya saling memperkuat.

Cara pemakaian : Bentuk suntikan teofillin / aminofilin dipakai pada serangan asma akut, dan disuntikan perlahan-lahan langsung ke pembuluh darah. Karena sering merangsang lambung bentuk tablet atau sirupnya sebaiknya diminum sesudah makan. Itulah sebabnya penderita yang mempunyai sakit lambung sebaiknya berhati-hati bila minum obat ini. Teofilin ada juga dalam bentuk supositoria yang cara pemakaiannya dimasukkan ke dalam anus. Supositoria ini digunakan jika penderita karena sesuatu hal tidak dapat minum teofilin (misalnya muntah atau lambungnya kering).

  • Kromalin

Kromalin bukan bronkodilator tetapi merupakan obat pencegah serangan asma. Manfaatnya adalah untuk penderita asma alergi terutama anak-anak. Kromalin biasanya diberikan bersama-sama obat anti asma yang lain, dan efeknya baru terlihat setelah pemakaian satu bulan.

  • Ketolifen
    Mempunyai efek pencegahan terhadap asma seperti kromalin. Biasanya diberikan dengan dosis dua kali 1mg / hari. Keuntungnan obat ini adalah
    dapat diberika secara oral.
  1. Pengobatan non farmakologik:
  • Memberikan penyuluhan
  • Menghindari faktor pencetus.
  • Pemberian cairan.
  • Fisiotherapy.
  • Beri O2 bila perlu.

TINJAUAN TEORITIS ASUHAN KEPERAWATAN ASMA BRONKHIAL

Menurut Dongoes (1999: 152) teoritis asuhan keperawatan pada asma bronchial meliputi:

1. Pengkajian

a.Aktivitas dan Istirahat

Gejala: Keltihan, kelemahan, malaise, ketidakmampuan untuk melakukan aktivitas sehari-hari karena sulit bernapas, ketidakmampuan untuk tidur (perlu tidur dalam keadaab duduk tinggi), dispnea pada saat istirahat atau respons terhadap aktivitas atau latihan.

Tanda: Keletihan, gelisah, insomnia, kelemahan umum,/ kehilangan masa otot.

b.Sirkulasi

Gejala:   Pembengkakan pada ekstermitas bawah

Tanda:   Peningkatan TD, peningkatn frekiuensi jantung/ takikardi berrat (disritmia), distensi vena leher, edema dependen (tidak berhubungan dengan penyakit jantung), bunyi jantung redup.

c.Integritas Ego

Gejala:     Peningkatan faktor resiko, perubahan pola tidur.

Tanda:     Ansietas, ketakutan, peka rangsang.

d.Makanan dan Cairan

Gejala: mual, muntah, ketidakmampuan untuk makan karena distress pernapasan.

Tanda: Turgor kulit bengkak, edema dependen, berkeringat, penurunan berat badan, penurunan massa otot/ lemak subkutan (emfisema), palpasi abdominal dapat menyebabkan hepatomegali.

e.Higiene

Gejala:     Penurunan kemampuan / peningkatan kebutuhan bantuan melakukan aktivitas sehari-hari.

Tanda:     Kebersihan buruk, bau badan.

f.Pernapasan

Gejala:     Napas pendek, khisunya saat kerja, cuaca atau episode berulangnya napas, dada rasa tertekan, ketidakmampuan untuk bernapas “lapar udara” kronis, riwayat pneumonia berulang, terpajan dalam polusi kimia/ iritan peranapasan dalam jangka panjang atau debu/ asap, faktor keluarga atau keturunan, penggunaan oksigen pada malam hari atau terus menerus.

Tanda:

  • Pernapas:   biasanya cepat, fase ekspirasi memanjag, penggunaan obat Bantu napas.
  • Perkusi:      hiperresonan, kesulitan bicara, kalimat lebih dari 4 atau 5 sekaligus.

g.Keamanan

Gejala: Riwayat reaksi alergi atau sensitive terhadap zat/ faktor lingkungan, adanya/ berulangnya infeksi, kemerahan/ berkeringat.

h.Seksualitas

Gejala: Penurunan libido.

i.Interaksi Sosial

Gejala:     Hubungan ketergantungan, kurangnya system pendukung (kegagalan dukungan diri/ terhadap pasangan/ orang terdekat), penyakit lama atau ketidakmampuan membaik.

Tanda:     Ketidakmampuan untuk membuat/ mempertahankan suara karena distress pernapasan, keterbatasan mobilitas fisik.

j.Penyuluhan/ Pembelajaran

Gejala: Penggunaan atau penyalahgunaan obat pernapasan, kesulitan menghentikan merokok, penggunaan alcohol, kegagalan untuk membaik

2. Diagnosa Keperawatan

  1. Tidak efektifnya bersihan jalan nafas b.d bronkospasme, peningkatan produksi secret (secret tertahan tebal, sekresi kental), penurunan energi atau kelemahan ditandai dengan kesulitan bernapsa, perubhan kedalaman/ kecepatan pernapasan, penggunaan otot aksesori, bunyi napas tidak normal (mis: mengi (ronki krekels), batuk, (menetapa), dengan atau tanpa produksi sputum).
  2. kerusakan pertukaran gas b/d ganguan suplai oksigen ( obstruksi jalan napas oleh sekresi, spasme bronkus, jebakan udara), kerusakan alkoli di tandai dengan despanea, bingung, gelisah, ketidak mmpuan, membuang secret, nilai GDA tak normal (hitoksia dan hiperkapnea ), perubahan tanda vital, penurunan toleransi terhadap aktivitas.
  3. perubahan nutrisi kurang dari kebutuhan tubuh b/d dispnea, kelemahan, efek samping obat atau produksi sputum atau anoreksia, mual atau muntah ditandai dengan penurunan berat badan atau kehilangan masa otot, tunus otot buruk atau, kelemahan, gangguan senasi pengecap, keengganan untuk makan (kurang tertarik pada makanan).
  4. resiko tinggi terhadap infeksi b/d tidak adekuatnya pertahanan (penurunan kerja silya, mantapnya secret), tidak adekuatnya imunitas( kerusakan jaringan, peningkatan pemajanan pada lingkungan), proses penyakit kronis Atau malnutrisi.
  5. Koping individu tidak efektif b.d kurang sosialisasi, ansietas, depresi, kurang informasi/ tidak mengenal sumber informasi, salah mngerti tentang  informasi, kurang mengingat/ keterbatasan kognitif ditandai dengan pertanyaan tentang informasi, pernyataan maslah/ kesalahan konsep, tidak akurat mengikuti instruksi, terjadinya komlpikasi yang dapat dicegah.

3. Intervensi

Diagnosis 1

  • Auskultasi bunyi napas, catat adanya bunyi napas, mis: mengi, krekels, ronki.

Rasional :       beberapa derajat spasme bronkus terjadi dengan opstruksi jalan napas dan dapat atau tak dimaniprestasikan adanya bunyi napas adventesus, mis : penyebaran atau krekels basah ( bronchitis bunyi nafas teredup dengan ekpresi mengik ( empesema ), atau tak pedanya adanya bunyi napas ( napas berat )

  • Kaji atau pantau prekuesi fernapasan. Catat rasio inspirasi  atau ekspirasi

Rasional:     pernapasan dapat merambat dan perekuinsi ekspirasi memanjang di banding inspirasi..

  • Pertahankan polusi lingkungan minuman, mis : debu asap dan bulu bantal yang berhubungn dengan kondisi individu

Rasional:     Pencetus tipe reaksi alergi pernapasan yang dapat mentriger episode akut.

  • Dorong/ Bantu latihan napas abdomen/bibir

Rasional:     Memberikan pasien beberapa cara untuk mengatasi dan mengontrol dipnea dan menurunkan jebakan udara.

  • Tingkatkan masukan cairan sampai 3000ml/ hari sesuai toleransi jantung. Memberikan air hangat.

Rasional: Hidrasi membantu menurunkan kekentalan secret, mempermudah pengeluaran. Penggunaan air hangat dapat menurunkan spasme bronkus.

Kolaborasi

  • Berikan humidifikasi tambahan, mis: Nebuliser ultranik, humidifier aerosol ruangan.

Rasional:     kelembaban menurunkan kekentalan secret mempemudah pengeluaran dan dapat membantu menurunkan/ mencegah pembentukan mukosa tebal pada bronkus.

  • Awasi/ buat grafik seri GDA, nadi oksimetri, foto dada.

Rasional:     Membuat dasar untuk pengawasan kemajuan / kemunduran proses penyakit dan komplikasi.

Diagnosis 2

  • Tinggikan kepala tempat tidur, Bantu pasien untuk memilih posisi yang nyaman untuk bernapas. Dorong napas dalam perlahan atau napas bibir sesuai kebutuhan individu.

Rasional: pengiriman oksigen dapt diperbaiki dengan posisi duduk tinggi dan latihan napas untuk menurunkan kolaps jalan napas, dispnea, dan kerja napas.

  • Kaji/ awasi secar rutin kulit dan  warna membrane mukosa

Rasional:     Sianosis mungkin perifer (terlihat sekitar bibir/ daun telinga). Keabu-abuan dan dianosis sentral mengindikasikan beratnya hipoksemia.

  • Dorong pemgeluaran sputum: penghisapan bila diindikasikan

Rasional:     Kental, tebal, dan banyaknya sekresi adalah sumber utama gangguan pertukaran gas pada jalan napas kecil. Penghisapan dibutuhkan jika batuk tidak efektif.

  • Palpasi Fremirus

Rasional:     Penurunangetaran vibrasi diduga ada pengumpulan cairan atau udara terjebak.

  • Evaluasi tingkat toleransi aktivitas

Rasional:     Selama distress pernapasan berat / akut/ refraktori pasien secara total tidak mampu melakukan aktivitas sehari-hari karena hipoksemia dan dispnea.

Kolaborasi

  • Kaji pemeriksaan laboratorium

Rasional:     Mengevaluasi/ mengatsi kekurangan dan mengawasi keefektifan terapi nutrisi.

  • Berikan oksigen tambahn selam makn sesuai indikasi

Rasional:     menurunka dispnea dan meningkatkan energi untuk makn meningkatkan masukan.

Diagnosis 3

  • Kaji kebiasaan diet, masukan makanan saat ini. Ctat derajat kesulitan makan.

Rasional: pasien distress pernapasn akut sering anoreksia karena dispnea, produksi sputum, dan obat.

  • Auskultasi bunyi usus

Rasional: Penurunan/ hipoaktif bising usus menunjukan penurunan motilitas gaster dan konstipasi yang berhubungan dengan pembatasan masukan cairan, pilihan makanan buruk, penurunan aktiviutas, dan hipoksemia.

  • Berikan perwata oral dengan sering, buang secret, berikan wadah khusus untuk sekali pakai dan tisu.

Rasional:     Rasa tak enak, baud an penbampilan adalah pencegah utama terhadap nafsu makn dan dapat membuat mual dan muntah dengan penigkatan kesulitan napas

  • Dorong periode istirahat selama 1 jam sebelum dan sesudah makan.Berikan makan porsi kecil tapi sering.

Rasional:     Membantu menurunka kelemahan selam waktu makan dan memberikan kesempatan untuk meningkatkan masukan kalori total.

Kolaborasi

  • Konsul ahli gizi nutrisi pendukung tim untuk memberikan makanan yang mudah dicerna, secra nutrisi seimbang.

Rasional:     Metode makan dan kebutuhan kalori didasarkan pada situasi/ kebutuhan individu untuk memberikan nutsisi maksimal dengan upaya minimal pasien/ penyalahgunaan energi.

  • Kaji pemerikasaan laboratorium

Rasional:     Mengevaluasi/ mngatasi kekurangan dan mengawasi keefektifan terapi nutrisi.

Diagnosis 4

  • Awasi shu

Rasional: Demam dapt terjadi karena infeksi / dehidrasi

  • Kaji pentingnya latihan nafas, batuk efektif, perubahn posisi sering dan masukan cairan adekuat.

Rasional:     Aktivitas ini meningkatkan mobilisasi dan pengeluaran secret untuk menurunkan resiko terjadinya infeksi paru.Observasi warna, karakter, bau sputum.

  • Observasi warna,m karakter, bau sputum.

Rasional:     Secret berbau, kuning, atau kehijauan menunjukan adanya infeksi paru.

  • Tunjukan dan Bantu pasien tentang pembuangan tisu dan sputum.

Rasional: Mencegah penyebaran phatogen melaui cairan.

  • Dorong keseimbangan antar aktivitas dan istirahat.

Rasinonal:   Menurunkan konsumsi/ kebutuhan keseimbangan oksigen, memperbaiki pertahanan pasien terhadap infeksi, meningkatkan penyembuhan.

  • Kolaborasi
  • Dapatkan specimen sputum dengan batuk atau penghisapan untuk pewarnaan  kuman gram, kultur/ sensitivitas.

Rasional:     Dilkaukan untuk mengidentifikasi organisme penyebab dan kerentanan terhadap berbagai antimicrobial.

  • Berikan antimicrobial sesuai indikasi

Rasional: Dapat diberikan untuk organisme khusus yang teridentifikasi dengan kultur dan sesnitivitas, atau diberikan secara profilaktik karena risiko tinggi.

Diagnosis 5

  • Jelaskan / kuatkan penjelasan proses penyakit individual. Dorong pasien/ orang terdekat untuk menanyakan pertanyaan.

Rasional:     Menurunkan ansietas dan dapat menimbulkan perbaikan partisipasipada perencanaan pengobatan.

  • Instruksikan/ kuatkan rasional untuk latihan nafas, batuk efektif, dan latihan kondisi umum.

Rasional:     Napas bibir dan napsa abdominal/ diafragmatik menguatkan otot pernapasan, membantu meminimalkan kolaps jalan napas kecil, dan memberikan individu arti untuk mengontrol dispnea. Latihan kondisi umum meningkatkan toleransi aktivitas, kekuatan otot dan rasa sehat.

  • Tunjukkan teknik penggunaan dosis inhaler.

Rasional:     Pemberian obat ynang tepat meningkatlkan penggunaan dan keefektifan.

  • Tekankan pentingnya perawtan oral/ kebersihan.

Rasional: Menurunkan pertumbuhan bakteri pada mulut, dimana dapat menimbulkan infeksi saluran naas atas.

  • Kaji efek bahaya merokok dan nasehatkan menghentikan rokok pada pasien dan orang terdekat.

Rasional:     Penghentian merokok dapat menghambat/ memperlambat kemajuan PPOM.

  • Berikan Informasi tentang pembatasan aktivitas .

Rasional: Mempunyai pengetahuan ini dapat memampukan pasien untuk membuat pilihan/ keputusan informasi untuk menurunkan dispnea.

4. Evaluasi

Diagnosis 1

  • Mempertahankan jalan nafas pasien dengan bunyi napas bersih/ jelas.
  • Menunjukkan perilaku untuk memperbaiki bersihan jalan napas, mis: Batuk efektif dan mengeluarkan secret.

Diagnosis 2

  • Menunjukkan perbaikan ventilasi dan oksigenisasi jaringan adekuat dengan GDA dalam rentang normal dan bebas gejala distress pernapasan.
  • Berpartisipasi dalam program pengobatan  dalam tingkat kemampuan/ situasi.

Diagnosis 3

  • Menunjukkan penigkatan berat badan menuju tujuan yang tepat.
  • Menunjukka perilaku/ perubahan; pola hidup untuk meningkatkan lingkungan yang aman.

Diagnosis 4

  • Menyatakan pemahaman penyebab/ faktor resiko individu.
  • Mengidentifikasi intervensi untukj mencegah/ menurunkan risiko infeksi
  • Menunjukkan teknik perubahan pola hidup untuk meningkatkan lingkungan yang aman.

Diagnosis 5

  • Menyatakan pemahaman kondisi/ Proses penyakit dan tindakan.
  • Mengidentfikasi hubungan tanda/ gejala yang ada dari proses penyakit dan menghubungkan dengan faktor p-enyebab.
  • Melakukan perubahan pola hidup dan berpartisipasi dalam program pengobatan.

DAFTAR PUSTAKA

  • Price, Silvia A & Wilson, Lorraine M. 2006. Patofisiologi Edisi 6. Jakarta: EGC
  • Corwin, Elizabeth J. 2000. Buku Saku Patofisiologi. Jakarta: EGC
  • Dongoes, Marylin E, dkk. 1999. Rencana Asuhan Keperawatan Edisi 3. Jakarta: EGC
  • Mansjoer, Arif. 2000. Kapita Selekta Kedokteran. Jakarta: Media Aesculapius.
  • Smeltzer, Suzame C. 2001. Buku Ajar Medikal Bedah. Jakarta: EGC
  • Kelompok V. Asuhan keperawatan Asma Bronkhial Pada Klien Ny. P di Ruanmg Nilam (Penyakit Dalam) Rumah Sakit dr. H. M Anshari Sahaleh Banjarmasin Program Studi D3. Keperawatan 2009.
  • http://www.blogspot.com/pelayanan/askep asma bronkhial.html/diakses tanggal 11 April 2010 pukul 20.30
  • http://www.bbkpmska.com/kumpulan askep/asma-bronchial/penunjang-diagnostic/html.diakses tanggal 11 April 2010 pukul 20.30.
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