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Pengertian, Patofisiologi dan Penatalaksanaan – JEVUSKAPengertian syok septik atau syok sepsis, patofisiologi sepsis dan penatalaksanaan penanganan syok septik. PENDAHULUANSyok septik atau sepsis adalah suatu sindrom respon inflamasi sistemik atau systemic inflammatory response syndrome (SIRS) yang terkait dengan adanya suatu infeksi. Sindrom ini merupakan penyebab kematian tertinggi urutan ke- 1. Amerika Serikat, dan meskipun perkembangan dunia kedokteran, angka mortalitasnya masih belum berubah. Pasien menunjukkan adanya takikardia, takipneu, demam, dan lekositosis, atau bahkan syok septik disertai gagal organ multiple. Seperti halnya SIRS, pelepasan mediator inflamasi sistemik dalam sepsis berakibat terjadinya gangguan dalam mikrosirkulasi, venodilatasi, dan disfungsi miokard dan ginjal. Terapi cairan merupakan hal yang penting dalam penanganan sepsis karena relatif terjadi hipovolemia dan diikuti dengan ekstravasasi cairan dari kompartemen vaskuler. Askep Syok Anafilaktik Pdf CreatorTujuan dari resusitasi cairan dalam sepsis ini adalah untuk mengembalikan tekanan pengisian dan arterial untuk memperbaiki perfusi end- organ dan metabolisme aerob, sementara meminimalkan overhidrasi yang berlebihan, yang dapat mengarah pada edema pulmonal, ileus paralitik, dan sindrom menekan kompartemen. Untuk mencapai tujuan ini, dokter menggunakan beberapa indeks perbedaan untuk mengatur terapi cairan dan terapi lainnya. Askep Syok Anafilaktik Pdf To JpgAskep Pada Pasien Syok downloads at Ebook-kings.com - Download free pdf files,ebooks and documents - ASUHAN KEPERAWATAN PADA PASIEN DENGAN SHOCK. Asuhan Keperawatan Gawat Darurat Syok Hipovolemik downloads at Ebook-kings.com - Download free pdf files,ebooks and documents - PRODI DIII KEPERAWATAN AKES RUSTIDA. MAKALAH \' Askep Gadar Pada pasien Syok\'. Syok anafilaktik(= shock anafilactic) adalah reaksi anafilaksis yang disertai hipotensi dengan atau tanpa penurunan. Usaha yang intensif dibuat untuk menghindari overhidrasi. Namun, untuk mempertahankan hidrasi intravaskuler, terapi cairan dalam sepsis akan menyebabkan keseimbangan cairan positif yang sangat besar. Meskipun diperlukan, terapi cairan belumlah cukup untuk mempertahankan homeostasis fisiologis, dan terapi tambahan seperti pressor atau bahkan inotropik kadang- kadang diperlukan. Patofisiologi sepsis melibatkan dalam pelepasan mediator inflamasi dari netrofil, makrofag, limfosit- T, dan sel- sel endothelial, atau dalam kasus organisme gram- negatif dan positif, endotoksin dan eksotoksin. Target seluler dari mediator- mediator ini akan menstimulasi pelepasan sitokin, eicosanoid, protease, radikal oksigen, dan nitrat oksida (NO) dan katabolitnya. Sitokin menyebabkan diferensiasi sel- T, sel- B, dan sel- sel natural killer, yang mengarah pada kerusakan jaringan secara langsung. Aktivasi dari rangkaian inflamasi ini juga akan menyebabkan mata rantai hiperkatabolisme dan demam. Kerusakan pada sistem kardiovaskuler akan menyebabkan disfungsi miokardium dan hilangnya integritas mikrovaskuler. Aliran cairan transvaskuler yang terjadi dalam mikrosirkulasi dapat disimpulkan dengan persamaan Starling- Landis berikut 2: Jv = Kf ? Di bawah kondisi fisiologis yang normal, persamaan ini hampir mencapai kesetimbangan dan akan mengubah aliran cairan transvaskuler hampir mendekati titik nol. Karena itulah, cairan yang disaring dengan adanya tekanan hidrostatik interstitial dan kapiler dikembalikan dengan adanya perbedaan tekanan onkotik. Pada beberapa keadaan, termasuk sepsis, perubahan ini akan menyebabkan terjadinya filtrasi cairan, sehingga volume intravaskuler akan menurun dan terbentuklah edema. Permeabilitas mikrovaskular, khususnya molekul yang besar, meningkat selama sepsis oleh karena endotoksin dan pelepasan dari mediator inflamasi lainnya. Protein molekul besar lainnya yang normalnya mengisi kapiler pecah dan air akan keluar secara osmosis. Gradiasi onkotik yang telah diperbaiki menjadi kurang efektif meskipun mekanisme peningkatan permeabilitas mikrovaskuler belum lengkap digambarkan, kontraksi endothelial mungkin memainkan peranan penting. Peningkatan tekanan kapiler oleh mediator sistemik , seperti histamin, bradikinin, dan disfungsi myocardial meningkatkan extravasasi cairan. Akhirnya, volume cairan yang besar yang menggantikan kehilangan volume vaskuler menambah dilusi dari protein plasma sehingga menurunkan tekanan onkotik plasma. Hasilnya hubungan dari perubahan pada mikrosirkulasi mengeluarkan extravasasi cairan dan membentuk edema. Venodilatasi yang dihasilkan oleh pengeluaran mediator inflamasi seperti nitrit oksida (NO), menurunkan pengisian ventrikular dan karena itu menurunkan cardiak output dan tekanan arterial.
Normalnya, sistem kardiovaskular menyesuaikan untuk menurunkan preload dan peningkatkan resistensi sistem vaskuler sistemik dan kontraktilitas myocardial dan heart rate, tetapi pada sepsis, mekanisme ini tidak efektif karena respon sirkulasi yang buruk. Akibat dari kurangnya respon ialah sebahagian dari hasil membentuk NO. Cairan diatur untuk menambah aliran balik vena dan meningkatkan cardiak output. Pada pasien yang pada awalnya merespon bolus cairan, cardiak output, hipotensi dan perfusi organ dapat dipulihkan. Bagaimanapun, pada pasien dengan resiko tinggi, luas cairan dengan / tanpa inotropik dan agen vasopressor dibutuhkan untuk mempertahankan aliran balik vena dan perfusi adekuat untuk jaringan vital. Meskipun Cardiak Output meningkat selama resusitasi pasien syok septik, juga terjadi penurunan komplians ventricular, penurunan kontraktilitas, dan disritmia selama terjadi sepsis. Tumor necrosis factor- ? Fungsi sistolik, yang diukur dengan echocardiografi, turun 2. Volume intravaskuler akan menurun akibat peningkatan tekanan kapiler, karena pasien dengan penurunan komplians ventrikel dan konraktilitas miokard memerlukan tekanan pengisian yang lebih tinggi untuk mempertahankan stroke volume yang adekuat. Karenanya, resusitasi cairan merupakan usaha yang penting dalam mempertahankan stabilitas hemodinamik. PETUNJUK AKHIR RESUSITASISejak resusitasi cairan dimulai, dokter sebaiknya menggunakan beberapa petunjuk untuk menjadi pegangan dalam pemberian cairan. Awalnya, output urine, tekanan arteri rata- rata atau mean arterial pressure (MAP), dan denyut jantung dipilih sebagai pegangan untuk terapi cairan. Meskipun petunjuk ini dapat memprediksi volume intravaskuler pada pasien hipovolemik non- sepsis, namun hanya dapat memprediksi perfusi global yang pendek selama sepsis. Monitor invasif lain seperti kateter arteri pulmonal dihubungkan dengan risiko yang lebih tinggi dalam menyebabkan trauma seperti pneumothorax, infeksi, ruptur arteri pulmonal, dan disritmia. Sementara teknik- teknik terbaru telah mulai dicoba dan menunjukkan hasil yang cukup menjanjikan sebagai indeks yang lebih baik untuk resusitasi cairan, monitoring hemodinamik dan pengukuran output urine merupakan cara yang paling sering digunakan oleh para dokter. Pada bagian ini, kita akan mendiskusikan keuntungan dan keterbatasan setiap teknik monitoring. Tekanan Arteri Rata- rata atau Mean Arterial Pressure (MAP). Hipotensi arterial digunakan untuk mengukur beratnya syok septik. Meskipun MAP kurang dari 6. Hg merupakan kriteria syok septik, namun jika lebih dari 6. Hg pada pasien dengan hipertensi kronik juga dapat dianggap sebagai syok septik 7. Resusitasi cairan jarang dapat mengembalikan MAP ke kadar normotensi. Pada kenyataannya, risiko overhidrasi seperti edema pulmonal, edema interstitial, dan sindrome kompartemen abdomen akan terjadi, jika hanya petunjuk di atas yang digunakan sebagai pegangan terapi cairan. Tekanan arterial digunakan sebagai pengukuran adanya syok, daripada digunakan sebagai petunjuk akhir indikator resusitasi. Sebagai tambahan, MAP diikuti dengan paradigma resusitasi untuk menjamin perfusi yang adekuat pada peredaran darah oroner dan serebral. Jika hipotensi masih tetap berlangsung dan indikasi lain dari volume intravaskuler masih normal atau lebih dari normal, harus dipertimbangkan pemberian inotropik seperti pada keadaan kritis. Jika pemberian inotropik ini tidak berhasil, pemberian obat- obatan pressor harus dipertimbangkan. Frekuensi Jantung. Takikardia (frekuensi jantung > 9. Hal ini dapat terjadi karena ada tidaknya volume intravaskuler yang rendah. Pasien- pasien sepsis memperlihatkan keadaan hipermetabolik, meningkatnya denyut jantung disertai demam, katabolisme, dan rendahnya resistensi vaskuler. Bahkan setelah tes pemberian cairan, takikardia tidak menghilang. Bradikardia bisa muncul pada beberapa pasien sepsis. Pengeluaran Urine. Pengeluaran urine yang berjumlah lebih dari 0,5 m. L/kg/jam sering digunakan sebagai patokan terapi cairan. Secara spesifik, jumlah ini mewakili klirens minimum dari sisa metabolisme nitogenous dan asam metabolik yang diproduksi oleh tubuh, dan kemampuan konsentrasi maksimal dari ginjal dalam mengekskresi tambahan metabolik. Meskipun pengeluaran urine ini merupakan prediktor perfusi ginjal yang cukup rasional pada pasien non- sepsis, namun tetap ada keterbatasan dalam penggunaannya sebagai indeks perfusi baik global maupun regional. Kami mendapat laporan bahwa laju filtrasi glomerular turun pada pasien sepsis sebagai akibat tidak adekuatnya resusitasi 8. Pengeluaran urine bisa normal atau meningkat meskipun aliran darah ginjal menurun, karena kadar atrial natriuretik faktor meningkat pada pasien sepsis 8,9. Keadaan hiperosmotik seperti hiperglikemia, atau terapi diuretik seperti furosemide, akan menambah produksi urine meskipun dengan adanya penurunan laju filtrasi glomerular. Faktor penyerta ini sering terjadi pada pasien sepsis. Hipoproteinemia, yang juga ada pada mayoritas pasien sepsis, membantu pembentukan urine meskipun terjadi reduksi yang potensial pada aliran darah ginjal, karena tekanan osmotik koloid plasma yang rendah kurang mampu memfasilitasi terjadinya reabsorbsi onkotik. Tekanan Pengisian Kardial. Tekanan atrium kanan dan tekanan oklusif arteri pulmonal merupakan indikator yang digunakan oleh para dokter untuk memperkirakan preload pada pasien yang berespon buruk terhadap terapi cairan yang diberikan. Di bawah kondisi fisiologis yang normal, tekanan atrium kanan dan tekanan oklusif arteri pulmonal berkorelasi dengan volume end- diastolik ventrikel kiri atau preload jantung. Karena itulah, volume dan tekanan berkorelasi. Untuk memaksimalkan cardiac output, tekanan pengisian ditingkatkan hingga 1. Hg. Namun pada sepsis, tekanan pengisian tidak merefleksikan volume end- diastolik.
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Troubleshoot printing problems (Acrobat 5. Adobe Acrobat Reader 5. Adobe Reader 6. 0- 7. Mac OS)Troubleshoot printing problems (Acrobat 5. Adobe Acrobat Reader 5. Adobe Reader 6. 0- 7. Mac OS). Determining the cause of the problem. Resolving problems printing a specific PDF file from an Acrobat product. Resolving problems printing any PDF file from an Acrobat product. Resolving problems printing any file from any application. This document provides troubleshooting suggestions to help you resolve general printing problems in Adobe Acrobat products. You may find a solution to a specific printing problem by searching the Support Knowledgebase on the Adobe website at. Print another PDF file, such as the first page of Acrobat Help. If that file prints correctly, the PDF file that doesn\'t print correctly may be damaged. Print another type of file (for example, a text file) from another application (such as Microsoft Word,Text. Edit or Simple. Text). The problem could be insufficient memory on the system or the printer, or a poor connection between the computer and the printer. Work through steps 3- 6 to eliminate some likely causes of the problem. If the problem persists, see . Restart the computer, and then print a PDF file. Turn off your printer for at least 1. PDF file. - - If the file prints correctly, the printer\'s memory was too full. Contact your network administrator or consult your network documentation. Print a PDF file to another printer. Make sure that the printer is turned on and connected properly, and then run a self- test on it to make sure that it\'s working correctly. For instructions, see the documentation that came with the printer. You may want to contact your network administrator for assistance. Print the PDF file as an image. Choose File > Print, and then click Advanced. Select Print As Image. Click OK to close the Advanced Print Setup dialog box, and then click Print. Choose File > Print. Choose Acrobat from the pop- up menu (Mac OS X) or Acrobat 5. Mac OS 9. x). Choose Print As Image from the Print Method pop- up menu. Select any other desired printing options, and then click Print. Save the PDF file as a new file. The Save As command causes Acrobat to rewrite the file. Enable the Post. Script error handler. The Post. Script error handler prints a page that lists any Post. Script errors that occur when you print. For help interpreting and resolving Post. Script errors, see document. Choose File > Print, and then choose a Post. Script printer from the Printer Menu. Re- create the PDF file. Print the original source file to the Adobe PDF Printer, or print it as a Post. Script file and then use Distiller to re- create the PDF. If you use Acrobat 6. PDF file to the Adobe PDF printer. Download the PDF file again. Print the PDF file in batches. If you can identify a particular page or object on a page that won\'t print, remove or re- create the page or object. Adjust the transparency flattening. Flattening removes transparency information and converts images to a format the printer can interpret. Adjust the transparency flattening to determine if transparency is causing the problem. Choose File > Print, and then click Advanced. Select Transparency Flattening from the list on the left. Adjust the Raster/Vector Balance. If you print to an inkjet printer, drag the Raster/Vector Balance slider to the lowest setting. Select Convert All Text To Outlines. Deselect Clip Complex Regions, click OK, and then click Print. Select the default print settings. Choose File > Print, and then click Advanced. Click OK to close the dialog box, and then click Print. Merge or flatten layers (Acrobat Professional only). Acrobat Professional, however, lets you specify which layer is visible and printable. Merge or flatten the layers in the PDF file to determine if a layer is the problem. Merged layers acquire the properties of the layer into which they are merged. Flattening layers discards any content that isn\'t visible. Make a backup copy of your PDF file. Open the copy and choose Advanced > PDF Optimizer, and then select Discard Objects (Acrobat 7. Clean Up tab (Acrobat 6. Printing in PowerPoint and Turning on Background Images. Printing in PowerPoint and Turning on Background. Turn off your printer. I need to produce a pdf with this. Turn Off Background Printing Pdf FilesSelect Discard Hidden Layer Content And Flatten Visible Layers (Acrobat 7. Remove Hidden Layers Content And Flatten Layers (Acrobat 6. OK. In the Layers palette, choose Options, and then select either Merge Layers or Flatten Layers. Print a composite of the file. When you print a composite file, all the colors print on one plate, regardless of whether individual colors are selected. Start the Printer Setup Utility (Mac OS 1. Print Center (Mac OS 1. Select the printer, and click Delete. Choose a connection method from the top pop- up menu. Select a printer, or enter the printer\'s IP address. Choose the printer model from the Printer Model menu, and then click Add. Open the Chooser from the Apple menu. Select Adobe. PS or Laser. Writer 8, and click Setup. Use an updated printer driver. If you use a Post. Script printer, make sure that it\'s set to Post. Script Level 2 or higher. Refer to the printer documentation for printer specification. Use an updated PPD file. Incorrect or outdated PPD files can increase print times. If you print to a Post. Script printer, use the correct PPD file, or use a generic PPD file. Move the PDF file to a local hard disk. Adobe recommends storing files on a local hard disk when you open, save, or print them to reduce potential problems and damage to your files. Create more free disk space. For instructions about clearing the disk cache, see the documentation for the browser. If you don\'t save printer memory, print jobs require more printer memory. Choose File > Print, and then click Advanced. Choose Post. Script Options from the menu, select Emit PS Form Object, and then click OK. Choose File > Print. Select Save Printer Memory. Print. to a local printer. If the file prints correctly, network- related issues may be the cause. Contact your network administrator for assistance. Connect USB printers directly to the computer. Assign a default printer. Disable background printing. Choose File > Print, and then choose Background Printing from the menu. Select Foreground (no spool file), and then click Print. Continue as follows. If the PDF file prints, allocate more memory to Print Monitor, which is in the Extensions folder, and then reenable background printing. If the problem recurs after you allocate more memory to Print Monitor, reinstall your printer driver from the system software installation disks or from the disks included with your printer. After you resolve the problem, you can reenable background printing. Reduce the monitor resolution (Mac OS 9. If you print to a non- Post. Script printer, reduce the monitor resolution (for example, from 1. You can change the resolution in the Monitors or the Monitors & Sounds control panel. Make sure that the printer is on, and check the physical connections between the printer and the computer- -the solution may be as simple as reconnecting a loose cable. |
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May 2017
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