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14.10: Faktor Fisik - Gas Terlarut - Geosains

14.10: Faktor Fisik - Gas Terlarut - Geosains


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14.10: Faktor Fisik - Gas Terlarut

14.10: Faktor Fisik - Gas Terlarut

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Pengantar

Probe oksigen terlarut memberikan pendekatan yang mudah untuk pengukuran langsung oksigen molekuler. Membran mengisolasi elektroda dari sampel, dan oksigen terdeteksi saat berdifusi melintasi membran. Probe dapat digunakan untuk mengukur setiap sistem di mana oksigen hadir. Kalibrasi sensor mudah dicapai jika pengetahuan tentang konsentrasi oksigen atau kelarutan pada kondisi tertentu diketahui.

Kelarutan Oksigen dari atmosfer menjadi air

Kelarutan oksigen dalam air dicapai dengan larutan fisik yang tidak melibatkan interaksi kimia antara senyawa. Kesetimbangan kelarutan adalah fungsi dari faktor-faktor berikut:

  • konsentrasi oksigen dalam fase gas pada antarmuka air-atmosfer
  • gaya tarik menarik antara molekul air dan molekul oksigen
  • energi kinetik molekul air dan oksigen

Perubahan fisik suhu dan tekanan memiliki efek nyata pada faktor kelarutan.

Pengaruh Perubahan Tekanan

Persentase konsentrasi molekul oksigen di udara pada dasarnya konstan di atmosfer yang dekat dengan bumi (sekitar 21% volume dan 23% berat). Jumlah sebenarnya molekul oksigen per satuan volume udara tergantung pada suhu dan tekanan udara. Udara dapat dimampatkan, dan, pada suhu konstan, berat jenis gas akan berubah volume dalam perbandingan terbalik dengan tekanan. Efek praktisnya adalah bahwa jumlah oksigen pada antarmuka udara dan air berkurang dengan menurunnya tekanan udara, atau karena persentase konsentrasi oksigen di udara tetap konstan, konsentrasi sebenarnya oksigen pada antarmuka udara-air adalah berbanding lurus dengan tekanan atmosfer (Hukum Henry). Di Denver, Colorado, (ketinggian sekitar 5000') konsentrasi oksigen pada antarmuka adalah sekitar 84% dari yang akan ada di permukaan laut.

Pengaruh Perubahan Suhu

Pada tekanan konstan, volume berat jenis udara berubah dalam perbandingan langsung dengan suhu mutlak (Skala Kelvin = Derajat Celcius + 273 atau Skala Rankin = Derajat Fahrenheit + 460). Saat udara mendingin dari 100 o F ke 0 o F volume berkurang 17,9%, dan pada 0 o F konsentrasi oksigen per satuan volume adalah 21,8% lebih besar daripada pada 100 o F. Jadi, konsentrasi oksigen pada antarmuka udara-air meningkat dengan penurunan suhu udara.

Suhu air juga penting karena dua faktor lain:

  • Jumlah uap air di udara pada antarmuka udara-air meningkat dengan meningkatnya suhu air, yang mengakibatkan penurunan konsentrasi oksigen pada antarmuka. Penurunannya sekitar 6% karena suhu air berubah dari 32 o F menjadi 100 o F.
  • Setelah oksigen dilarutkan dalam air, suhunya sama dengan air. Baik energi kinetik molekul air maupun O2 molekul berbanding lurus dengan suhu mutlak. Energi kinetik yang lebih tinggi cenderung mengatasi gaya tarik menarik antara molekul air dan oksigen dan berkontribusi pada penurunan kelarutan oksigen pada suhu air yang lebih tinggi.

Efek Bahan Terlarut

Adanya bahan terlarut dalam air berpotensi dapat menurunkan kelarutan oksigen jika bahan terlarut berinteraksi dengan air untuk menurunkan gaya tarik menarik antara air dan oksigen. Misalnya, garam anorganik terlarut, seperti natrium klorida, kalium klorida, atau natrium sulfat, mengurangi kelarutan oksigen dalam air.

Teori

Sebuah probe oksigen molekuler polarografi terdiri dari dua logam dari bangsawan yang berbeda yang berfungsi sebagai elektroda. Logam yang lebih mulia adalah katoda. Jika potensial sekitar 0,5 volt diterapkan pada dua elektroda (negatif ke katoda) dan elektroda direndam dalam elektrolit, molekul oksigen terlarut dalam elektrolit akan berdifusi ke permukaan katoda dan mengambil elektron yang, dalam kombinasi dengan air, akan menghasilkan ion hidroksil. Pada dasarnya pada saat yang sama, ion hidroksil akan melepaskan elektron di anoda dan membentuk oksida. Transfer elektron yang dihasilkan membentuk aliran arus melalui sirkuit eksternal dan dapat ditampilkan pada meter milivolt atau mikroampere.

Elektroda Oksigen bermembran menawarkan keuntungan sebagai berikut:

  1. Membran membungkus kedua elektroda dalam volume elektrolit yang ditangkap, memastikan kekuatan dan kemurnian elektrolit yang konstan sehingga ion-ion yang mungkin "meracuni" probe tidak ada.
  2. Membran mengecualikan bahan yang tidak berdifusi melaluinya. Akibatnya, sebagian besar bahan dalam sampel yang mungkin "meracuni" katoda, atau dapat menyebabkan keluaran yang salah dari sistem elektroda dikecualikan. Gangguan potensial terbatas pada gas reaktif yang berdifusi melalui membran, seperti klorin.

Bahan dan Desain Probe

Katoda untuk probe gaya polarografi biasanya platinum, anoda umumnya perak, dengan elektroda direndam dalam larutan elektrolit kalium klorida. Untuk aplikasi probe yang nyaman, sistem elektroda tertutup dalam wadah dengan katoda dan membran diposisikan untuk paparan sampel. Hanya area membran yang bersentuhan dengan katoda yang perlu terpapar sampel.

Orientasi Membran

Untuk mengoptimalkan kinerja probe bermembran, katoda terletak berdekatan dengan membran. Katoda diberi permukaan cembung sehingga membran dapat ditarik secara dekat di atas katoda. Permukaan platina dikasar untuk memungkinkan akses elektrolit yang diperlukan ke permukaan katoda. Fitur utama dalam orientasi membran dan katoda adalah bahwa membran harus dekat dengan katoda dan orientasi tidak boleh berubah selama pengoperasian probe.

Area Anoda

Seperti yang ditunjukkan di bawah teori, perak di permukaan anoda diubah menjadi perak oksida sebagai penentuan hasil oksigen. Ketika perak tidak tersedia di permukaan anoda karena telah dilapisi dengan oksida perak atau produk reaksi lainnya, sensitivitas probe menurun. Oleh karena itu, untuk memberi probe masa pakai yang lebih lama, area perak relatif terhadap katoda harus seluas mungkin.

Ketebalan Membran dan Area Katoda

Oksigen molekuler mencapai katoda dengan difusi melalui membran Teflon. Untuk ketebalan membran tertentu, pada suhu tertentu, jumlah molekul oksigen yang melewati membran per satuan waktu berbanding lurus dengan jumlah molekul yang ada per satuan luas antarmuka air-ke-Teflon (kadang-kadang disebut sebagai tekanan parsial) atau:

NT = f (O2)

  • nT adalah jumlah molekul oksigen yang tiba di katoda per detik per cm persegi luas katoda pada Temperatur t.
  • HAI2 adalah konsentrasi molekul oksigen pada antarmuka air-ke-Teflon.

Teflon menawarkan ketahanan terhadap difusi oksigen. Jadi, pada suhu tertentu dan konsentrasi oksigen yang tetap pada antarmuka air-ke-Teflon, jumlah molekul oksigen yang tiba di katoda per satuan waktu berbanding terbalik dengan ketebalan membran, D.

NT = f [O2 x (1/H)]

Dari hubungan tersebut, terlihat bahwa untuk mendapatkan sensitivitas maksimum untuk probe perlu dibuat luas katoda yang praktis dan membuat membran teflon setipis praktis. Pertimbangan praktis untuk ukuran katoda adalah hubungannya dengan ukuran probe keseluruhan, yang biasanya ditentukan oleh tempat probe harus ditempatkan. Ketebalan membran harus mengenali tingkat respons yang diinginkan dan kinerja kasar. Membran tipis memberikan respon cepat selain sensitivitas karena keseimbangan difusi tercapai lebih cepat, tetapi membran tebal lebih keras dan akan memberikan pelayanan yang lebih lama.

Membran biasanya memiliki ketebalan 1/2 mil, 1 mil, dan 2 mil. Respons kelas atas berlangsung kira-kira pada tingkat orde pertama. Peningkatan ketebalan membran menurunkan kecepatan molekul oksigen mencapai katoda. Hasilnya, 99% penyelesaian respon kelas atas dicapai dalam waktu sekitar 15, 30, dan 75 detik untuk membran 1/2, 1 dan 2 mil masing-masing.

Respons skala bawah berbeda secara signifikan dengan respons kelas atas. Tingkat respons pada dasarnya adalah urutan kedua. Sifat respons menunjukkan bahwa reaksi internal probe serta difusi melalui membran terlibat. Untuk membran 1 mil, waktu untuk penurunan skala respons 99% adalah fungsi dari paparan awal terhadap oksigen. Dari 10 mg/L respon 99% diperoleh dalam waktu sekitar 1 menit. Dari 100 & mug/L, respons 99% diperoleh dalam waktu sekitar 70 detik, dan dari 10 & mug/L, respons 99% diperoleh dalam waktu sekitar 50 detik. Hasil ini menggambarkan bahwa respon yang sangat baik diperoleh dalam aplikasi seperti pengukuran oksigen dalam air umpan boiler. Probe dapat dikalibrasi pada tingkat oksigen mg/L dan dengan membran 1 mil akan membutuhkan sekitar 1 jam untuk mencapai tingkat pengoperasian & mug/L. Selaput 1/2 mil akan merespon dari mg/L ke level & mug/L dalam waktu sekitar 30 menit.

Respon Probe dan Resistansi Sirkuit

Rangkaian listrik untuk aliran elektron dari anoda ke katoda dilengkapi dengan rangkaian pembacaan. Jika pembacaan dilakukan melalui mikroampere meter tipe galvanometer, hambatannya adalah yang ada pada belitan meter dan resistor yang dirangkai seri. Sebuah meteran yang digunakan untuk layanan ini mungkin secara khas memiliki resistansi internal sekitar 2.000 ohm. Jika pembacaan potensiometri disediakan, input ke sirkuit potensiometri adalah penurunan tegangan melintasi resistansi penutup yang dipilih antara katoda dan anoda probe. Dalam kedua kasus, resistensi hadir dalam rangkaian listrik antara anoda dan katoda.

Tingkat respon untuk probe, ketika terkena perubahan konsentrasi oksigen terlarut, dipengaruhi oleh besarnya tahanan penutupan. Tingkat respons yang disajikan sebelumnya didasarkan pada resistansi penutupan 2.000 ohm. Jika resistansi penutupan diturunkan menjadi 100 ohm, respons skala bawah untuk probe yang menggunakan membran 1/2 mil akan menjadi sekitar 99% selesai dalam 10 detik. Jika, untuk probe yang sama, resistansi penutupan dinaikkan menjadi 25.000 ohm, respons downscale akan menjadi sekitar 99% selesai dalam 120 detik.

Tingkat respons kelas atas dari probe dipengaruhi ke tingkat yang jauh lebih kecil oleh resistansi penutupan.

Efek Suhu pada Arus Keluaran Probe

Ada dua faktor yang berhubungan dengan suhu yang harus dikenali untuk mengkorelasikan output dari probe oksigen terlarut dengan konsentrasi molekul oksigen dalam sampel.

  1. Saat suhu air menurun, energi kinetik molekul air dan oksigen menurun dan daya tarik molekul meningkat. Akibatnya, konsentrasi oksigen yang harus ada dalam air untuk menetapkan konsentrasi oksigen tertentu pada antarmuka air-ke-Teflon meningkat, dan
  2. resistensi terhadap difusi oksigen melalui membran Teflon meningkat seiring dengan penurunan suhu.

Kedua faktor suhu berfungsi untuk menurunkan laju molekul oksigen mencapai permukaan katoda saat suhu menurun. Oleh karena itu, jika pembacaan dari Dissolved Oxygen Analyzer adalah untuk menampilkan pembacaan konsentrasi oksigen yang benar untuk semua sampel yang memiliki konsentrasi oksigen yang sama tetapi pada suhu yang berbeda, kompensasi untuk efek suhu keseluruhan harus dicapai.

Kompensasi suhu dicapai dengan menggunakan termistor yang dirancang sesuai sebagai sensor suhu. Resistansi termistor digunakan untuk mencapai faktor perkalian yang tepat oleh penganalisis. Tampilan konsentrasi oksigen terlarut yang dihasilkan dikoreksi hingga +/- 2% dari konsentrasi sebenarnya ketika sampel berada dalam kisaran suhu 0 o C hingga 50 o C. Lebih dari rentang sampel +/- 10 o C dari kalibrasi suhu, DO bacaan berada dalam +/- 1% dari konsentrasi sebenarnya.

Pengaruh Padatan Terlarut pada Arus Keluaran Probe

Jika garam ditambahkan dan dibiarkan larut dalam sampel air yang mengandung konsentrasi oksigen terlarut tertentu (tetapi tidak jenuh), arus keluaran dari probe akan meningkat. Akibatnya, pengukur tampilan penganalisis akan salah menunjukkan bahwa konsentrasi oksigen terlarut dalam sampel telah meningkat. Alasan peningkatan keluaran oleh probe adalah bahwa keberadaan garam terlarut menurunkan daya tarik molekul air dan molekul oksigen dalam sampel. Hal ini meningkatkan konsentrasi molekul oksigen pada antarmuka air-ke-Teflon. Konsentrasi oksigen dalam sampel tidak berubah.

Data Berguna

Tabel 1 menyajikan perubahan kelarutan oksigen dari atmosfer menjadi air pada ketinggian yang berbeda di atas permukaan laut. Data didasarkan pada tekanan barometrik 760 mm Hg di permukaan laut. Tekanan barometrik (dan konsentrasi oksigen pada antarmuka atmosfer-air) menurun pada ketinggian yang lebih tinggi, dan, sebagai akibatnya, konsentrasi keseimbangan oksigen dalam air menurun. Tekanan barometrik versus data ketinggian yang digunakan adalah:

Ketinggian (Kaki Di Atas Permukaan Laut) Tekanan Barometrik (mm Hg)
0 760
1,000 747
2,000 709
3,000 684
4,000 661
5,000 638
6,000 616

Data pada Tabel 1 harus digunakan dengan pengakuan atas dasar bahwa tekanan barometrik adalah variabel saat area bertekanan tinggi dan rendah bergerak. Pendekatan yang lebih optimal untuk koreksi data kelarutan oksigen adalah dengan memanfaatkan tekanan barometrik aktual di lokasi dan waktu yang diinginkan. Perbaiki data kelarutan oksigen di permukaan laut dengan rasio tekanan barometrik aktual hingga 760 mm Hg.

Kelarutan O2 pada kondisi = Kelarutan760 mm Hg x [Tekanan Barometrik, mm Hg / 760]

Data pada Tabel 2 menunjukkan pengaruh salinitas (dinyatakan sebagai klorinitas) pada air payau atau laut. Padatan terlarut (terutama natrium klorida) bereaksi dengan molekul air dan mengurangi daya tarik molekul antara molekul oksigen dan molekul air. Akibatnya, kelarutan oksigen menurun dengan meningkatnya salinitas.

Data pada Tabel 2 adalah untuk tekanan barometrik 760 mm Hg. Jika tekanan barometrik selain 760 mm Hg, koreksi terhadap tekanan barometrik yang sebenarnya diperlukan.

Tabel 1
Kelarutan Oksigen (mg/L) pada Berbagai Suhu dan Ketinggian
(Berdasarkan Tekanan Barometrik Permukaan Laut 760 mm Hg)


Dari Mana DO Berasal?

Bagaimana oksigen terlarut memasuki air

Oksigen terlarut memasuki air melalui udara atau sebagai produk sampingan tanaman. Dari udara, oksigen secara perlahan dapat berdifusi melintasi permukaan air dari atmosfer sekitarnya, atau bercampur dengan cepat melalui aerasi, baik alami maupun buatan 7 . Aerasi air dapat disebabkan oleh angin (menciptakan gelombang), jeram, air terjun, debit air tanah atau bentuk lain dari air yang mengalir. Penyebab aerasi buatan manusia bervariasi dari pompa udara akuarium hingga kincir air yang diputar dengan tangan hingga bendungan besar.

Oksigen terlarut juga dihasilkan sebagai produk limbah fotosintesis dari fitoplankton, alga, rumput laut dan tanaman air lainnya 8 .

Oksigen Terlarut dari Fotosintesis

Oksigen terlarut dapat masuk ke dalam air sebagai produk sampingan dari fotosintesis.

Sementara sebagian besar fotosintesis terjadi di permukaan (oleh tanaman air dangkal dan ganggang), sebagian besar proses berlangsung di bawah air (oleh rumput laut, ganggang sub-permukaan dan fitoplankton). Cahaya dapat menembus air, meskipun kedalaman yang dapat dicapai bervariasi karena padatan terlarut dan elemen hamburan cahaya lainnya yang ada di dalam air. Kedalaman juga mempengaruhi panjang gelombang yang tersedia untuk tanaman, dengan merah diserap dengan cepat dan cahaya biru terlihat melewati 100 m. Di air jernih, tidak ada lagi cukup cahaya untuk fotosintesis terjadi di atas 200 m, dan tanaman air tidak lagi tumbuh. Dalam air keruh, zona fotik (penetrasi cahaya) ini seringkali jauh lebih dangkal.

Terlepas dari panjang gelombang yang tersedia, siklus tidak berubah . Selain cahaya yang dibutuhkan, CO2 mudah diserap oleh air (sekitar 200 kali lebih larut daripada oksigen) dan oksigen yang dihasilkan sebagai produk sampingan tetap terlarut dalam air¹⁰. Reaksi dasar fotosintesis akuatik tetap:

Karena fotosintesis akuatik bergantung pada cahaya, oksigen terlarut yang dihasilkan akan mencapai puncaknya pada siang hari dan menurun pada malam hari .


Adanya organisme yang hidup di dalam air tentunya akan mempengaruhi jumlah oksigen yang ada di dalamnya. Seperti yang Anda ketahui, sebagian besar organisme membutuhkan oksigen untuk bertahan hidup. Jika banyak organisme yang ditemukan di dalam air, maka jumlah oksigen di dalamnya akan berkurang karena digunakan untuk bernafas atau bertahan hidup oleh organisme di dalamnya.

Ambil contoh air kolam yang berisi ikan. Awalnya, tanpa ikan, kandungan oksigen di dalam air akan tetap besar sesuai dengan jumlah awalnya. Setelah masuk ke dalam ikan, maka jumlah oksigen secara bertahap akan menipis karena ikan membutuhkan oksigen untuk bernafas. Itulah sebabnya kolam ikan sering mendapatkan suplai oksigen tambahan agar ikan di kolam mendapatkan suplai oksigen yang cukup.

Untuk mengetahui kadar oksigen terlarut dalam air, Anda dapat menggunakan DO meter Mettler Toledo yang secara akurat menunjukkan jumlah oksigen di dalam air. Mettler Toledo akan menyatakan konsentrasi oksigen dalam bilangan relatif dan absolut. Intelligent Sensor Management akan memberikan sinyal digital yang kuat sehingga hasil pengukuran akurat. Dapatkan Mettler Toledo di Hyprowira!


Faktor kimia air

Berbagai bahan kimia yang ada dalam air, keasaman dan kebasaan air, salinitas, tingkat pH dan zat terlarut dapat mempengaruhi reaksi kimia dalam air dan dapat mempengaruhi produktivitas Anda. Berikut adalah beberapa faktor kimia yang mempengaruhi peternakan ikan air tawar Anda.

Fotosintesis

Fotosintesis adalah proses di mana fitoplankton menggunakan sinar matahari dan karbon dioksida untuk menghasilkan makanan. Mereka melepaskan oksigen ke dalam air sebagai produk sampingan, sehingga keberadaan plankton dalam air tidak selalu merupakan hal yang buruk. Namun, jika mereka hadir dalam jumlah besar, air mungkin tampak hijau karena klorofil yang ada di sel mereka. Banyak parameter kualitas air seperti oksigen terlarut, karbon dioksida, siklus pH, dan produk limbah nitrogen diatur oleh reaksi fotosintesis di fitoplankton. Selain meningkatkan jumlah oksigen terlarut dalam air, proses fotosintesis juga menghilangkan beberapa bentuk limbah nitrogen, seperti amonia, nitrat, dan urea.

Proses respirasi plankton yang ada di air juga menambahkan karbon dioksida ke dalam air, tetapi proses fotosintesis biasanya mengimbangi jumlah karbon dioksida yang dihasilkan melalui respirasi. Namun, proses fotosintesis tergantung pada ketersediaan sinar matahari, dan karenanya, selama hari-hari berawan, jumlah karbon dioksida yang terlarut dalam air dapat meningkat.

Gas terlarut

Gas terlarut adalah gas yang bercampur dengan air, seperti oksigen, karbon dioksida, nitrogen, dan amonia, dan diukur dalam bagian per juta (ppm).

Oksigen

Oksigen terlarut dalam air merupakan faktor terpenting dalam budidaya ikan. Pembudidaya ikan harus memastikan bahwa oksigen yang cukup ada di dalam air. Kurangnya oksigen terlarut dalam air dapat mengakibatkan kematian ikan. Ikan membutuhkan oksigen untuk proses respirasi dan jumlah oksigen yang dibutuhkan tergantung pada ukuran, spesies, tingkat aktivitas, tingkat makan dan suhu. Ikan yang lebih kecil membutuhkan lebih banyak oksigen daripada ikan yang lebih besar karena mereka memiliki tingkat metabolisme yang lebih tinggi. Misalnya, ikan bass yang dibesarkan pada suhu 77 o F mengkonsumsi 0,012-0,020 pon oksigen per pon ikan per hari. Tingkat metabolisme juga berlipat ganda untuk setiap kenaikan suhu 18 derajat. Kelarutan oksigen dalam air juga bervariasi dengan suhu dan ketinggian. Lebih banyak oksigen dapat larut dalam air yang lebih dingin dan pada ketinggian yang lebih rendah. Kelarutan oksigen dalam air menurun pada suhu yang lebih tinggi.

Aerasi

Untuk meningkatkan produksi ikan di tambak, mungkin perlu untuk memasok oksigen tambahan ke tambak ikan selama musim panas untuk mempertahankan tingkat oksigen terlarut yang memadai. Dalam sistem re-sirkulasi, seorang petani harus menyediakan pasokan oksigen yang stabil ke kolam. Oksigen biasanya dicampur dengan air melalui difusi langsung pada antarmuka udara-air. Kecuali Anda memiliki cukup banyak angin bertiup di atas kolam Anda, penting bagi Anda untuk menggunakan metode difusi langsung untuk mencampur oksigen dengan air kolam Anda.

Kami telah membahas beberapa metode aerasi dalam artikel kami yang berjudul Budidaya Udang Air Tawar- Mengelola Kualitas Air & Penyakit.

Daftar metode aerasi diberikan di bawah ini untuk kenyamanan Anda.

  1. roda dayung
  2. Agitator
  3. Penyemprot vertikal
  4. Impeller
  5. Pompa airlift
  6. Pompa Venturia
  7. Injeksi oksigen cair
  8. Diffuser udara

JIKA Anda memiliki kolam dalam ruangan, satu-satunya cara Anda dapat menyediakan oksigen yang cukup untuk ikan Anda adalah melalui pompa air dan aerator mekanis karena tidak ada plankton di dalam air untuk proses fotosintesis berlangsung.

Karbon dioksida

Sumber karbon dioksida yang umum di air tambak adalah dari proses respirasi tumbuhan dan hewan air, serta dari air yang berasal dari batuan yang mengandung kapur. Ikan dapat menanggung tingkat 10 ppm, asalkan konsentrasi oksigen terlarut tinggi. Namun, Anda harus mencoba untuk menjaga kandungan karbon dioksida kurang dari 5 ppm. Jika Anda memiliki konsentrasi karbon dioksida yang lebih tinggi di kolam Anda, gunakan beberapa bahan penyangga karbon dioksida atau tembak air ke udara menggunakan pompa untuk mengeluarkan karbon dioksida dan mencampur lebih banyak oksigen ke dalam air. Air mancur sangat cocok untuk tujuan ini.

Nitrogen

Setiap gas terlarut seperti nitrogen diukur dengan persentase yang ada dalam air. Jika jumlah nitrogen lebih dari kadar biasa dalam air, seperti tingkat kejenuhan gas di atas 110%, biasanya dianggap bermasalah. Kejenuhan nitrogen dapat menyebabkan penyakit gelembung gas pada ikan. Aerasi yang cukup diperlukan untuk membuang kelebihan nitrogen dari kolam.

Amonia

Ikan mengeluarkan amonia dan urea ke dalam air sebagai limbah. Amonia ada dalam air dalam dua bentuk, NH terionisasi4 dan NH yang tidak terionisasi3 yang sangat beracun. Amonia beracun dapat didegradasi menjadi nitrat yang tidak berbahaya melalui proses biologis. Jika peternakan Anda mengandung banyak ikan di dalam air, Anda mungkin menghadapi risiko peningkatan amonia beracun di air Anda.

Keasaman dan kebasaan air

Tingkat pH normal air kolam Anda dapat berfluktuasi antara 4,5 dan 10. Kondisi ideal untuk pH kolam ikan Anda adalah antara 6,5 ​​dan 9,0. Respirasi ikan dan karbon dioksida yang dilepaskan dari tanaman dapat membuat air menjadi asam, menurunkan tingkat pH air dan mengganggu proses respirasi ikan. Sistem buffering dapat menjaga perubahan tingkat pH yang luas di bawah kontrol. Jika tingkat pH air di bawah 4, air mungkin terlalu asam untuk pertumbuhan ikan, dan harus dinetralkan dengan menambahkan basa, seperti batu kapur atau karbonat. Parameter ini adalah ukuran basa, bikarbonat (HCO3-), karbonat (CO3-) dan, dalam kasus yang jarang, hidroksida (OH-).

Sistem penyangga karbonat penting bagi pembudidaya ikan untuk menjaga kadar karbon dioksida tetap rendah. Ini juga mencegah fluktuasi pH yang luas di siang hari.

Kekerasan

Kesadahan air terutama diukur dengan adanya kalsium dan magnesium dalam air, tetapi ion lain seperti aluminium, besi, mangan, strontium, seng, dan ion hidrogen juga disertakan. Tingkat kekerasan minimum 20 ppm sangat ideal untuk pertumbuhan ikan yang optimal. Jika tingkat kesadahan air terlalu rendah, kapur pertanian tanah harus ditambahkan ke air tambak.

Bahan dan gas lain mungkin juga ada di dalam air. Air harus selalu diuji dan diolah terlebih dahulu sebelum ditambahkan ke kolam atau tangki ikan. Pengolahan air bisa sesederhana aerasi hingga proses penghilangan besi yang kompleks.

Lebih lanjut tentang pengolahan air di blog kami berikutnya jadi teruslah membaca artikel kami.

Berpikir untuk memulai peternakan ikan Anda sendiri? Dapatkan eBook gratis kami, Melepaskan Pengusaha dalam Diri Anda.


Suhu Mempengaruhi Kelarutan

Perubahan suhu mempengaruhi kelarutan padatan, cairan dan gas secara berbeda. Namun, efek tersebut ditentukan secara terbatas hanya untuk padatan dan gas.

Padatan

Pengaruh suhu terhadap kelarutan zat padat berbeda-beda tergantung pada apakah reaksi tersebut endotermik atau eksotermik. Menggunakan prinsip Le Chatelier, efek suhu di kedua skenario dapat ditentukan.

  1. Pertama, pertimbangkan sebuah endotermik reaksi ((Delta<>>>0)): Peningkatan suhu menghasilkan tekanan pada sisi reaktan dari panas tambahan. Prinsip Le Chatelier memprediksi bahwa sistem bergeser ke sisi produk untuk mengurangi stres ini. Dengan menggeser ke arah sisi produk, lebih banyak padatan yang terdisosiasi ketika keseimbangan kembali terbentuk, menghasilkan ditingkatkan kelarutan.
  2. Kedua, pertimbangkan sebuah eksotermis reaksi (((Delta<>><0)): Peningkatan suhu menghasilkan tekanan pada sisi produk dari panas tambahan. Prinsip Le Chatelier memprediksi bahwa sistem bergeser ke arah sisi reaktan untuk mengurangi stres ini. Dengan menggeser ke arah sisi reaktan, lebih sedikit padatan yang terdisosiasi ketika kesetimbangan kembali tercapai, menghasilkan menurun kelarutan.

Cairan

Dalam kasus cairan, tidak ada tren yang pasti untuk efek suhu pada kelarutan cairan.

Gas

Dalam memahami pengaruh suhu terhadap kelarutan gas, pertama-tama penting untuk diingat bahwa suhu adalah ukuran energi kinetik rata-rata. Dengan meningkatnya suhu, energi kinetik meningkat. Energi kinetik yang lebih besar menghasilkan gerakan molekul yang lebih besar dari partikel gas. Akibatnya, partikel gas yang terlarut dalam cairan lebih mungkin untuk lolos ke fase gas dan partikel gas yang ada lebih kecil kemungkinannya untuk larut. Kebalikannya juga benar. Kecenderungannya adalah sebagai berikut: peningkatan suhu berarti kelarutan yang lebih rendah dan penurunan suhu berarti kelarutan yang lebih tinggi.

Prinsip Le Chatelier memungkinkan konseptualisasi yang lebih baik dari tren ini. Pertama, perhatikan bahwa proses melarutkan gas dalam cairan biasanya eksotermis. Dengan demikian, meningkat suhu mengakibatkan stres pada sisi produk (karena panas pada sisi produk). Pada gilirannya, prinsip Le Chatelier memprediksi bahwa sistem bergeser ke arah sisi reaktan untuk mengurangi stres baru ini. Akibatnya, konsentrasi kesetimbangan partikel gas dalam fase gas meningkat, menghasilkan diturunkan kelarutan.

Sebaliknya, menurun suhu mengakibatkan stres pada sisi reaktan (karena panas pada sisi produk). Pada gilirannya, prinsip Le Chatelier memprediksi bahwa sistem bergeser ke arah sisi produk untuk mengkompensasi stres baru ini. Akibatnya, konsentrasi kesetimbangan partikel gas dalam fase gas akan berkurang, menghasilkan lebih besar kelarutan.


Isi

DCS diklasifikasikan berdasarkan gejala. Deskripsi awal DCS menggunakan istilah: "membungkuk" untuk nyeri sendi atau tulang "tersedak" untuk masalah pernapasan dan "terhuyung" untuk masalah neurologis. [1] Pada tahun 1960, Golding dkk. memperkenalkan klasifikasi yang lebih sederhana menggunakan istilah "Tipe I ('sederhana')" untuk gejala yang hanya melibatkan kulit, sistem muskuloskeletal, atau sistem limfatik, dan "Tipe II ('serius')" untuk gejala di mana organ lain (seperti pusat sistem saraf) terlibat. [1] DCS tipe II dianggap lebih serius dan biasanya memiliki hasil yang lebih buruk. [2] Sistem ini, dengan sedikit modifikasi, masih dapat digunakan sampai sekarang. [3] Setelah perubahan metode pengobatan, klasifikasi ini sekarang kurang berguna dalam diagnosis, [4] karena gejala neurologis dapat berkembang setelah presentasi awal, dan DCS Tipe I dan Tipe II memiliki manajemen awal yang sama. [5]

Penyakit dekompresi dan disbarisme Sunting

Istilah disbarisme meliputi penyakit dekompresi, emboli gas arteri, dan barotrauma, sedangkan penyakit dekompresi dan emboli gas arteri umumnya diklasifikasikan bersama sebagai penyakit dekompresi ketika diagnosis yang tepat tidak dapat dibuat. [6] DCS dan emboli gas arteri diperlakukan sangat mirip karena keduanya merupakan hasil dari gelembung gas di dalam tubuh. [5] Angkatan Laut AS meresepkan pengobatan yang sama untuk DCS Tipe II dan emboli gas arteri. [7] Spektrum gejalanya juga tumpang tindih, meskipun gejala dari emboli gas arteri umumnya lebih parah karena sering muncul dari infark (penyumbatan suplai darah dan kematian jaringan).

Sementara gelembung dapat terbentuk di mana saja di tubuh, DCS paling sering diamati di bahu, siku, lutut, dan pergelangan kaki. Nyeri sendi ("bengkokan") menyumbang sekitar 60% hingga 70% dari semua kasus DCS ketinggian, dengan bahu menjadi tempat paling umum untuk penyelaman ketinggian dan pantulan, dan sendi lutut dan pinggul untuk saturasi dan kerja udara terkompresi. [8] Gejala neurologis muncul pada 10% hingga 15% kasus DCS dengan sakit kepala dan gangguan penglihatan menjadi gejala yang paling umum. Manifestasi kulit hadir pada sekitar 10% sampai 15% kasus. DCS paru ("tersedak") sangat jarang terjadi pada penyelam dan telah diamati lebih jarang pada penerbang sejak diperkenalkannya protokol pra-pernapasan oksigen. [9] Tabel di bawah ini menunjukkan gejala untuk tipe DCS yang berbeda. [10]

(siku, bahu, pinggul, pergelangan tangan, lutut, pergelangan kaki)

  • Nyeri lokal yang dalam, mulai dari yang ringan sampai yang menyiksa. Terkadang nyeri tumpul, lebih jarang nyeri tajam.
  • Gerakan aktif dan pasif dari sendi dapat memperburuk rasa sakit.
  • Rasa sakit dapat dikurangi dengan menekuk sendi untuk menemukan posisi yang lebih nyaman.
  • Jika disebabkan oleh ketinggian, rasa sakit dapat terjadi segera atau hingga beberapa jam kemudian.
  • Gatal, biasanya di sekitar telinga, wajah, leher, lengan, dan tubuh bagian atas
  • Sensasi serangga kecil merangkak di atas kulit (formikasi)
  • Kulit berbintik-bintik atau marmer biasanya di sekitar bahu, dada bagian atas dan perut, dengan rasa gatal (cutis marmorata)
  • Pembengkakan kulit, disertai dengan lekukan kecil seperti bekas luka (pitting edema)
  • Perubahan sensasi, kesemutan atau mati rasa (parestesia), peningkatan sensitivitas (hiperestesia)
  • Kebingungan atau kehilangan ingatan (amnesia)
  • Kelainan visual
  • Perubahan suasana hati atau perilaku yang tidak dapat dijelaskan, ketidaksadaran
  • Kelemahan atau kelumpuhan yang meningkat pada kaki dan inkontinensia tinja
  • Girdling (juga disebut sebagai korset, pita, atau perasaan mengencangkan) di sekitar daerah perut dan/atau dada
  • Sakit kepala
  • Kelelahan yang tidak dapat dijelaskan
  • Malaise menyeluruh, nyeri yang tidak terlokalisir
  • Kehilangan keseimbangan, vertigo, mual, muntah
  • Gangguan pendengaran
  • Batuk kering persisten
  • Nyeri dada yang membakar di bawah tulang dada, diperparah dengan pernapasan

Sunting Frekuensi

Frekuensi relatif dari gejala DCS yang berbeda yang diamati oleh Angkatan Laut AS adalah sebagai berikut: [12]

Gejala menurut frekuensi
Gejala Frekuensi
nyeri sendi lokal 89%
gejala lengan 70%
gejala kaki 30%
pusing 5.3%
kelumpuhan 2.3%
sesak napas 1.6%
kelelahan ekstrim 1.3%
kolaps/tidak sadar 0.5%

Pengeditan Awal

Meskipun timbulnya DCS dapat terjadi dengan cepat setelah menyelam, pada lebih dari setengah kasus, gejala tidak mulai muncul setidaknya selama satu jam. Dalam kasus ekstrim, gejala dapat terjadi sebelum penyelaman selesai. The U.S. Navy and Technical Diving International, a leading technical diver training organization, have published a table that documents time to onset of first symptoms. The table does not differentiate between types of DCS, or types of symptom. [13] [14]

Onset of DCS symptoms
Time to onset Percentage of cases
within 1 hour 42%
within 3 hours 60%
within 8 hours 83%
within 24 hours 98%
dalam waktu 48 jam 100%

DCS is caused by a reduction in ambient pressure that results in the formation of bubbles of inert gases within tissues of the body. It may happen when leaving a high-pressure environment, ascending from depth, or ascending to altitude.

Ascent from depth Edit

DCS is best known as a diving disorder that affects divers having breathed gas that is at a higher pressure than the surface pressure, owing to the pressure of the surrounding water. The risk of DCS increases when diving for extended periods or at greater depth, without ascending gradually and making the decompression stops needed to slowly reduce the excess pressure of inert gases dissolved in the body. The specific risk factors are not well understood and some divers may be more susceptible than others under identical conditions. [15] [16] DCS has been confirmed in rare cases of breath-holding divers who have made a sequence of many deep dives with short surface intervals and it may be the cause of the disease called taravana by South Pacific island natives who for centuries have dived by breath-holding for food and pearls. [17]

Two principal factors control the risk of a diver suffering DCS:

  1. the rate and duration of gas absorption under pressure – the deeper or longer the dive the more gas is absorbed into body tissue in higher concentrations than normal (Henry's Law)
  2. the rate and duration of outgassing on depressurization – the faster the ascent and the shorter the interval between dives the less time there is for absorbed gas to be offloaded safely through the lungs, causing these gases to come out of solution and form "micro bubbles" in the blood. [18]

Even when the change in pressure causes no immediate symptoms, rapid pressure change can cause permanent bone injury called dysbaric osteonecrosis (DON). DON can develop from a single exposure to rapid decompression. [19]

Leaving a high-pressure environment Edit

When workers leave a pressurized caisson or a mine that has been pressurized to keep water out, they will experience a significant reduction in ambient pressure. [15] [20] A similar pressure reduction occurs when astronauts exit a space vehicle to perform a space-walk or extra-vehicular activity, where the pressure in their spacesuit is lower than the pressure in the vehicle. [15] [21] [22] [23]

The original name for DCS was "caisson disease". This term was introduced in the 19th century, when caissons under pressure were used to keep water from flooding large engineering excavations below the water table, such as bridge supports and tunnels. Workers spending time in high ambient pressure conditions are at risk when they return to the lower pressure outside the caisson if the pressure is not reduced slowly. DCS was a major factor during construction of Eads Bridge, when 15 workers died from what was then a mysterious illness, and later during construction of the Brooklyn Bridge, where it incapacitated the project leader Washington Roebling. [24] On the other side of the Manhattan island during construction of the Hudson River Tunnel contractor's agent Ernest William Moir noted in 1889 that workers were dying due to decompression sickness and pioneered the use of an airlock chamber for treatment. [25]

Ascent to altitude Edit

The most common health risk on ascent to altitude is not decompression sickness but altitude sickness, or acute mountain sickness (AMS), which has an entirely different and unrelated set of causes and symptoms. AMS results not from the formation of bubbles from dissolved gasses in the body but from exposure to a low partial pressure of oxygen and alkalosis. However, passengers in unpressurized aircraft at high altitude may also be at some risk of DCS. [15] [21] [22] [26]

Altitude DCS became a problem in the 1930s with the development of high-altitude balloon and aircraft flights but not as great a problem as AMS, which drove the development of pressurized cabins, which coincidentally controlled DCS. Commercial aircraft are now required to maintain the cabin at or below a pressure altitude of 2,400 m (7,900 ft) even when flying above 12,000 m (39,000 ft). Symptoms of DCS in healthy individuals are subsequently very rare unless there is a loss of pressurization or the individual has been diving recently. [27] [28] Divers who drive up a mountain or fly shortly after diving are at particular risk even in a pressurized aircraft because the regulatory cabin altitude of 2,400 m (7,900 ft) represents only 73% of sea level pressure. [15] [21] [29]

Generally, the higher the altitude the greater the risk of altitude DCS but there is no specific, maximum, safe altitude below which it never occurs. There are very few symptoms at or below 5,500 m (18,000 ft) unless patients had predisposing medical conditions or had dived recently. There is a correlation between increased altitudes above 5,500 m (18,000 ft) and the frequency of altitude DCS but there is no direct relationship with the severity of the various types of DCS. A US Air Force study reports that there are few occurrences between 5,500 m (18,000 ft) and 7,500 m (24,600 ft) and 87% of incidents occurred at or above 7,500 m (24,600 ft). [30] High altitude parachutists may reduce the risk of altitude DCS if they flush nitrogen from the body by pre-breathing pure oxygen. [31]

Although the occurrence of DCS is not easily predictable, many predisposing factors are known. They may be considered as either environmental or individual. Decompression sickness and arterial gas embolism in recreational diving are associated with certain demographic, environmental, and dive style factors. A statistical study published in 2005 tested potential risk factors: age, gender, body mass index, smoking, asthma, diabetes, cardiovascular disease, previous decompression illness, years since certification, dives in the last year, number of diving days, number of dives in a repetitive series, last dive depth, nitrox use, and drysuit use. No significant associations with risk of decompression sickness or arterial gas embolism were found for asthma, diabetes, cardiovascular disease, smoking, or body mass index. Increased depth, previous DCI, larger number of consecutive days diving, and being male were associated with higher risk for decompression sickness and arterial gas embolism. Nitrox and drysuit use, greater frequency of diving in the past year, increasing age, and years since certification were associated with lower risk, possibly as indicators of more extensive training and experience. [32]

Environmental Edit

The following environmental factors have been shown to increase the risk of DCS:

  • the magnitude of the pressure reduction ratio – a large pressure reduction ratio is more likely to cause DCS than a small one. [21][29][33]
  • repetitive exposures – repetitive dives within a short period of time (a few hours) increase the risk of developing DCS. Repetitive ascents to altitudes above 5,500 metres (18,000 ft) within similar short periods increase the risk of developing altitude DCS. [21][33]
  • the rate of ascent – the faster the ascent the greater the risk of developing DCS. NS U.S. Navy Diving Manual indicates that ascent rates greater than about 20 m/min (66 ft/min) when diving increase the chance of DCS, while recreational dive tables such as the Bühlmann tables require an ascent rate of 10 m/min (33 ft/min) with the last 6 m (20 ft) taking at least one minute. [34] An individual exposed to a rapid decompression (high rate of ascent) above 5,500 metres (18,000 ft) has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent. [21][33]
  • the duration of exposure – the longer the duration of the dive, the greater is the risk of DCS. Longer flights, especially to altitudes of 5,500 m (18,000 ft) and above, carry a greater risk of altitude DCS. [21]
  • underwater diving before flying – divers who ascend to altitude soon after a dive increase their risk of developing DCS even if the dive itself was within the dive table safe limits. Dive tables make provisions for post-dive time at surface level before flying to allow any residual excess nitrogen to outgas. However, the pressure maintained inside even a pressurized aircraft may be as low as the pressure equivalent to an altitude of 2,400 m (7,900 ft) above sea level. Therefore, the assumption that the dive table surface interval occurs at normal atmospheric pressure is invalidated by flying during that surface interval, and an otherwise-safe dive may then exceed the dive table limits. [35][36][37]
  • diving before travelling to altitude – DCS can occur without flying if the person moves to a high-altitude location on land immediately after diving, for example, scuba divers in Eritrea who drive from the coast to the Asmara plateau at 2,400 m (7,900 ft) increase their risk of DCS. [38] – diving in water whose surface altitude is above 300 m (980 ft) — for example, Lake Titicaca is at 3,800 m (12,500 ft) — without using versions of decompression tables or dive computers that are modified for high-altitude. [35][39]

Individual Edit

The following individual factors have been identified as possibly contributing to increased risk of DCS:

    – Studies by Walder concluded that decompression sickness could be reduced in aviators when the serum surface tension was raised by drinking isotonic saline, [40] and the high surface tension of water is generally regarded as helpful in controlling bubble size. [33] Maintaining proper hydration is recommended. [41] – a hole between the atrial chambers of the heart in the fetus is normally closed by a flap with the first breaths at birth. In about 20% of adults the flap does not completely seal, however, allowing blood through the hole when coughing or during activities that raise chest pressure. In diving, this can allow venous blood with microbubbles of inert gas to bypass the lungs, where the bubbles would otherwise be filtered out by the lung capillary system, and return directly to the arterial system (including arteries to the brain, spinal cord and heart). [42] In the arterial system, bubbles (arterial gas embolism) are far more dangerous because they block circulation and cause infarction (tissue death, due to local loss of blood flow). In the brain, infarction results in stroke, and in the spinal cord it may result in paralysis. [43]
  • a person's age – there are some reports indicating a higher risk of altitude DCS with increasing age. [15][33]
  • previous injury – there is some indication that recent joint or limb injuries may predispose individuals to developing decompression-related bubbles. [15][44] temperature – there is some evidence suggesting that individual exposure to very cold ambient temperatures may increase the risk of altitude DCS. [15][33] Decompression sickness risk can be reduced by increased ambient temperature during decompression following dives in cold water. [45]
  • body type – typically, a person who has a high body fat content is at greater risk of DCS. [15][33] This is due to nitrogen's five times greater solubility in fat than in water, leading to greater amounts of total body dissolved nitrogen during time at pressure. Fat represents about 15–25 percent of a healthy adult's body, but stores about half of the total amount of nitrogen (about 1 litre) at normal pressures. [46]
  • alcohol consumption – although alcohol consumption increases dehydration and therefore may increase susceptibility to DCS, [33] a 2005 study found no evidence that alcohol consumption increases the incidence of DCS. [47]

Depressurisation causes inert gases, which were dissolved under higher pressure, to come out of physical solution and form gas bubbles within the body. These bubbles produce the symptoms of decompression sickness. [15] [48] Bubbles may form whenever the body experiences a reduction in pressure, but not all bubbles result in DCS. [49] The amount of gas dissolved in a liquid is described by Henry's Law, which indicates that when the pressure of a gas in contact with a liquid is decreased, the amount of that gas dissolved in the liquid will also decrease proportionately.

On ascent from a dive, inert gas comes out of solution in a process called "outgassing" or "offgassing". Under normal conditions, most offgassing occurs by gas exchange in the lungs. [50] [51] If inert gas comes out of solution too quickly to allow outgassing in the lungs then bubbles may form in the blood or within the solid tissues of the body. The formation of bubbles in the skin or joints results in milder symptoms, while large numbers of bubbles in the venous blood can cause lung damage. [52] The most severe types of DCS interrupt — and ultimately damage — spinal cord function, leading to paralysis, sensory dysfunction, or death. In the presence of a right-to-left shunt of the heart, such as a patent foramen ovale, venous bubbles may enter the arterial system, resulting in an arterial gas embolism. [5] [53] A similar effect, known as ebullism, may occur during explosive decompression, when water vapour forms bubbles in body fluids due to a dramatic reduction in environmental pressure. [54]

Inert gases Edit

The main inert gas in air is nitrogen, but nitrogen is not the only gas that can cause DCS. Breathing gas mixtures such as trimix and heliox include helium, which can also cause decompression sickness. Helium both enters and leaves the body faster than nitrogen, so different decompression schedules are required, but, since helium does not cause narcosis, it is preferred over nitrogen in gas mixtures for deep diving. [55] There is some debate as to the decompression requirements for helium during short-duration dives. Most divers do longer decompressions however, some groups like the WKPP have been pioneering the use of shorter decompression times by including deep stops. [56]

Any inert gas that is breathed under pressure can form bubbles when the ambient pressure decreases. Very deep dives have been made using hydrogen-oxygen mixtures (hydrox), [57] but controlled decompression is still required to avoid DCS. [58]

Isobaric counterdiffusion Edit

DCS can also be caused at a constant ambient pressure when switching between gas mixtures containing different proportions of inert gas. This is known as isobaric counterdiffusion, and presents a problem for very deep dives. [59] For example, after using a very helium-rich trimix at the deepest part of the dive, a diver will switch to mixtures containing progressively less helium and more oxygen and nitrogen during the ascent. Nitrogen diffuses into tissues 2.65 times slower than helium but is about 4.5 times more soluble. Switching between gas mixtures that have very different fractions of nitrogen and helium can result in "fast" tissues (those tissues that have a good blood supply) actually increasing their total inert gas loading. This is often found to provoke inner ear decompression sickness, as the ear seems particularly sensitive to this effect. [60]

Bubble formation Edit

The location of micronuclei or where bubbles initially form is not known. [61] The most likely mechanisms for bubble formation are tribonucleation, when two surfaces make and break contact (such as in joints), and heterogeneous nucleation, where bubbles are created at a site based on a surface in contact with the liquid. Homogeneous nucleation, where bubbles form within the liquid itself is less likely because it requires much greater pressure differences than experienced in decompression. [61] The spontaneous formation of nanobubbles on hydrophobic surfaces is a possible source of micronuclei, but it is not yet clear if these can grow large enough to cause symptoms as they are very stable. [61]

Once microbubbles have formed, they can grow by either a reduction in pressure or by diffusion of gas into the gas from its surroundings. In the body, bubbles may be located within tissues or carried along with the bloodstream. The speed of blood flow within a blood vessel and the rate of delivery of blood to capillaries (perfusion) are the main factors that determine whether dissolved gas is taken up by tissue bubbles or circulation bubbles for bubble growth. [61]

Pathophysiology Edit

The primary provoking agent in decompression sickness is bubble formation from excess dissolved gases. Various hypotheses have been put forward for the nucleation and growth of bubbles in tissues, and for the level of supersaturation which will support bubble growth. The earliest bubble formation detected is subclinical intravascular bubbles detectable by doppler ultrasound in the venous systemic circulation. The presence of these "silent" bubbles is no guarantee that they will persist and grow to be symptomatic. [62]

Vascular bubbles formed in the systemic capillaries may be trapped in the lung capillaries, temporarily blocking them. If this is severe, the symptom called "chokes" may occur. [63] If the diver has a patent foramen ovale (or a shunt in the pulmonary circulation), bubbles may pass through it and bypass the pulmonary circulation to enter the arterial blood. If these bubbles are not absorbed in the arterial plasma and lodge in systemic capillaries they will block the flow of oxygenated blood to the tissues supplied by those capillaries, and those tissues will be starved of oxygen. Moon and Kisslo (1988) concluded that "the evidence suggests that the risk of serious neurological DCI or early onset DCI is increased in divers with a resting right-to-left shunt through a PFO. There is, at present, no evidence that PFO is related to mild or late onset bends. [64] Bubbles form within other tissues as well as the blood vessels. [63] Inert gas can diffuse into bubble nuclei between tissues. In this case, the bubbles can distort and permanently damage the tissue. [65] As they grow, the bubbles may also compress nerves, causing pain. [66] [67] Extravascular or autochthonous [a] bubbles usually form in slow tissues such as joints, tendons and muscle sheaths. Direct expansion causes tissue damage, with the release of histamines and their associated affects. Biochemical damage may be as important as, or more important than mechanical effects. [63] [66] [68]

Bubble size and growth may be affected by several factors - gas exchange with adjacent tissues, the presence of surfactants, coalescence and disintegration by collision. [62] Vascular bubbles may cause direct blockage, aggregate platelets and red blood cells, and trigger the coagulation process, causing local and downstream clotting. [65]

Arteries may be blocked by intravascular fat aggregation. Platelets accumulate in the vicinity of bubbles. Endothelial damage may be a mechanical effect of bubble pressure on the vessel walls, a toxic effect of stabilised platelet aggregates and possibly toxic effects due to the association of lipids with the air bubbles. [62] Protein molecules may be denatured by reorientation of the secondary and tertiary structure when non-polar groups protrude into the bubble gas and hydrophilic groups remain in the surrounding blood, which may generate a cascade of pathophysiological events with consequent production of clinical signs of decompression sickness. [62]

The physiological effects of a reduction in environmental pressure depend on the rate of bubble growth, the site, and surface activity. A sudden release of sufficient pressure in saturated tissue results in a complete disruption of cellular organelles, while a more gradual reduction in pressure may allow accumulation of a smaller number of larger bubbles, some of which may not produce clinical signs, but still cause physiological effects typical of a blood/gas interface and mechanical effects. Gas is dissolved in all tissues, but decompression sickness is only clinically recognised in the central nervous system, bone, ears, teeth, skin and lungs. [69]

Necrosis has frequently been reported in the lower cervical, thoracic, and upper lumbar regions of the spinal cord. A catastrophic pressure reduction from saturation produces explosive mechanical disruption of cells by local effervescence, while a more gradual pressure loss tends to produce discrete bubbles accumulated in the white matter, surrounded by a protein layer. [69] Typical acute spinal decompression injury occurs in the columns of white matter. Infarcts are characterised by a region of oedema, haemorrhage and early myelin degeneration, and are typically centred on small blood vessels. The lesions are generally discrete. Oedema usually extends to the adjacent grey matter. Microthrombi are found in the blood vessels associated with the infarcts. [69]

Following the acute changes there is an invasion of lipid phagocytes and degeneration of adjacent neural fibres with vascular hyperplasia at the edges of the infarcts. The lipid phagocytes are later replaced by a cellular reaction of astrocytes. Vessels in surrounding areas remain patent but are collagenised. [69] Distribution of spinal cord lesions may be related to vascular supply. There is still uncertainty regarding the aetiology of decompression sickness damage to the spinal cord. [69]

Dysbaric osteonecrosis lesions are typically bilateral and usually occur at both ends of the femur and at the proximal end of the humerus Symptoms are usually only present when a joint surface is involved, which typically does not occur until a long time after the causative exposure to a hyperbaric environment. The initial damage is attributed to the formation of bubbles, and one episode can be sufficient, however incidence is sporadic and generally associated with relatively long periods of hyperbaric exposure and aetiology is uncertain. Early identification of lesions by radiography is not possible, but over time areas of radiographic opacity develop in association with the damaged bone. [70]

Decompression sickness should be suspected if any of the symptoms associated with the condition occurs following a drop in pressure, in particular, within 24 hours of diving. [71] In 1995, 95% of all cases reported to Divers Alert Network had shown symptoms within 24 hours. [72] This window can be extended to 36 hours for ascent to altitude and 48 hours for prolonged exposure to altitude following diving. [8] An alternative diagnosis should be suspected if severe symptoms begin more than six hours following decompression without an altitude exposure or if any symptom occurs more than 24 hours after surfacing. [73] The diagnosis is confirmed if the symptoms are relieved by recompression. [73] [74] Although MRI or CT can frequently identify bubbles in DCS, they are not as good at determining the diagnosis as a proper history of the event and description of the symptoms. [3]

Differential diagnosis Edit

Symptoms of DCS and arterial gas embolism can be virtually indistinguishable. The most reliable way to tell the difference is based on the dive profile followed, as the probability of DCS depends on duration of exposure and magnitude of pressure, whereas AGE depends entirely on the performance of the ascent. In many cases it is not possible to distinguish between the two, but as the treatment is the same in such cases it does not usually matter. [8]

Other conditions which may be confused with DCS include skin symptoms cutis marmorata due to DCS and skin barotrauma due to dry suit squeeze, for which no treatment is necessary. Dry suit squeeze produces lines of redness with possible bruising where the skin was pinched between folds of the suit, while the mottled effect of cutis marmorata is usually on skin where there is subcutaneous fat, and has no linear pattern. [8]

Transient episodes of severe neurological incapacitation with rapid spontaneous recovery shortly after a dive may be attributed to hypothermia, but may be symptomatic of short term CNS involvement, which may have residual problems or relapses. These cases are thought to be under-diagnosed. [8]

Inner ear DCS can be confused with alternobaric vertigo and reverse squeeze. The history of difficulty in equalising during the dive makes ear barotrauma more likely, but does not always eliminate the possibility of inner ear DCS, which is associated with deep, mixed gas dives with decompression stops. [8]

Numbness and tingling are associated with spinal DCS, but can also be caused by pressure on nerves (compression neurapraxia). In DCS the numbness or tingling is generally confined to one or a series of dermatomes, while pressure on a nerve tends to produce characteristic areas of numbness associated with the specific nerve on only one side of the body distal to the pressure point. [8] A loss of strength or function is likely to be a medical emergency. A loss of feeling that lasts more than a minute or two indicates a need for immediate medical attention. It is only partial sensory changes, or paraesthesias, where this distinction between trivial and more serious injuries applies. [75]

Large areas of numbness with associated weakness or paralysis, especially if a whole limb is affected, are indicative of probable brain involvement and require urgent medical attention. Paraesthesias or weakness involving a dermatome indicate probable spinal cord or spinal nerve root involvement. Although it is possible that this may have other causes, such as an injured intervertebral disk, these symptoms indicate an urgent need for medical assessment. In combination with weakness, paralysis or loss of bowel or bladder control, they indicate a medical emergency. [75]


Limnology (2+1)

4.1. Dissolved gases – Oxygen, Carbon dioxide and other dissolved gases
Dissolved gases
No naturally occurring body of water is free of dissolved gases. Their spatial and temporal distribution is dependent on factors such as precipitation, inflow and outflow, physical factors like temperature, movement of water and chemical factors such as solution processes, combination and precipitation of reactions, complex formation etc.
Among the dissolved gases present in water, oxygen and carbon dioxide are direct indicators of biological activity of water bodies. Gaseous nitrogen only enters the metabolic cycle of a few specific microorganisms. Hydrogen sulphide and methane occur in small localized amounts due to bacterial activity under conditions of low redox potential and are incorporated into the material budget of water bodies by certain bacteria.
The Liebig’s law of minimum states that the yield is dependent on whatever growth factor is at a minimum in proportion to all the other similar factors.
Solubility of Gases in water
The solubility of gases in water decreases with increasing temperature and decrease of pressure. When a gas comes in contact with water, it dissolves in it until a state of equilibrium is reached in which the solution and the emission of the gas are balanced. Total solubility of gas is expressed by Henry’s law. The concentration of a saturated solution of gas is proportional to the pressure at which the gas is supplied.
Condition affecting the solubility of gases in water
Solubility of gases differs widely even when their pressures are equal. It is therefore necessary to find out the solubility constants.
Henry’s law is stated as :
C= K p
Where, C = Concentration of gas in solution
p = Partial pressure of gas
K= Constant of solubility
The following general conditions affect the solubility of a gas:
Saya. Rise in temperature reduces solubility
ii. Increasing concentration of dissolved salts diminishes solubility
aku aku aku. Rate of solubility is greater when the gases are dry than when they contain water vapour
iv. Rate of solubility is increased by wave action and other forms of surface water agitation

A. Oxygen
The main sources of dissolved oxygen in water are:
i) The atmosphere and
ii) By photosynthetic activity of aquatic plants
Atmospheric oxygen enters the aquatic system:
a) By direct diffusion at the surface and
b) Through various forms of surface water agitations such as wave action, waterfalls, and turbulences due to obstructions.
Aquatic chlorophyll bearing plants release oxygen as a byproduct of photosynthesis, which gets distributed into the different layers of lake water by movements. In most lakes the phytoplankton contributes the bulk of the oxygen supply because of the huge amounts of chlorophyll of algae in the epilimnion zone. In shallow waters like ponds and swamps the limnetic photoautotroph may be overshadowed by littoral macrophytes, attached algae, and the benthic algal mats. In small rivulets and brooks the periphyton account for most of the production of oxygen.
The main causes of decrease of oxygen in water are:
Saya. Respiration of animals and plants throughout the day and night and
ii. Decomposition of organic matter – Aerobic bacteria use up of the oxygen of water while decomposing organic matter. Chemical oxidation of sediments also takes place. Purely chemical oxidation may also occur, but most of the oxidative processes in aquatic habitats are probably mediated through bacterial action.
aku aku aku. Reduction due to other gases – A gas may be entirely removed from solution by bubbling another gas through the water in which it is dissolved. In nature, gases like CO2, methane and hydrogen sulphide often accumulate in large amounts and the excess amounts rise in the form of bubbles removing the dissolved oxygen.
iv. By physical process – In summer days the heat warms up the epilimnion zone of the lake, which could account for oxygen depletion of water. The combined effects of all or some of the above mentioned processes may completely deplete oxygen content of the system.
Diel oxygen changes in freshwaters
The concentration of oxygen in an aquatic environment is a function of biological processes such as photosynthesis and respiration and physical processes such as water movement and temperature. Diel variations occur in both day and night hours. Estimates of diel production can be made in natural waters by considering night as the dark bottle and day as the clear bottle. The increase in oxygen from dawn to dusk reflects net primary productivity. The decrease from dusk until dawn represents half the diel respiration. Adding the oxygen that disappeared at night to the day time gain gives a sum that is daily gross primary productivity.

B. Carbon dioxide
i) Sources of carbon dioxide in freshwater
The atmospheric carbon dioxide mixes with the water when it comes in contact with the water surface, as it possesses the highest solubility in water. As the partial pressure of carbon dioxide in air is low, the amount which remains in solution in water at a given temperature is also low.
1. Rainwater and inflowing ground water
Rainwater is charged with 0.55 to 0.60 mg/I CO2 as it falls towards earth. Water trickling through organic soil may become further charged with CO2.
2. Byproduct of Decomposing Organic Matter (DOM)
Carbon dioxide is added to the water as a byproduct of decomposing organic matter which is a common phenomenon in natural waters. Large quantities of the gas are produced in this way. It is found that carbon dioxide is the second largest decomposition product, constituting 3 to 30 per cent of the total gas evolved.
3. Respiration of Animals and Plants
Respiratory processes produce and release carbon dioxide into the water. The quantities so added are governed by the magnitude of aquatic flora and fauna, the relative size of the individual organism and those factors which determine the rate of respiration.
ii) Reduction of carbon dioxide in freshwaters
The principal processes which tend to reduce the carbon dioxide supply are
1. Photosynthesis of aquatic plants
Consumption of free CO2 in photosynthesis depends upon amount of green plants which the water supports, duration of effective day light, transparency of water and the time of year.
Marl forming organisms
The following groups of aquatic organisms are known to form marl (=Crumble : large deposits of calcium and magnesium carbonate) in water bodies aquatic flowering plants like Potamogeton, Ceratophyllum, Nymphaea, Vallisneria many blue-green algae like Rivularia, Lyngbya nana, Lyngbya martesiana, Colacacia. Centrosphaeria facciolaea many species of diatoms mollusks which form calcareous shells insects like Diptera larvae the cray fishes and lime-forming bacteria. All these organisms function in the production of the insoluble carbonates which involves carbon dioxide, calcium and magnesium. Thus the process of lime formation binds up carbon dioxide supplied from circulation and removes the available calcium and magnesium from the system.
Agitation of water
Agitation is a very effective method of releasing free carbon dioxide from water. It is evident from the fact that sometimes when deeper layers of water has large amount of it, the surface water shows very little carbon dioxide.
Evaporation
Evaporation of waters containing bicarbonates results in the loss of half-bound carbon dioxide and precipitation of mono carbonate. The form of loss is greatest in shallow water bodies where evaporation is most effective.
Rise of bubbles from depths
Free carbon dioxide often accumulates in decomposing bottom deposit in such quantities that at frequent intervals increasing internal pressure of gas exceeds the external pressure and the excess gas rises in the form of masses of bubbles to the surface and is lost into the air.

Other dissolved gases
i) Methane
Methane, sometimes called marsh gas, is one of the products of decomposing organic matter at the bottoms of marshes, ponds, rice field and lakes. The methane bacteria are obligate anaerobes. They decompose organic compounds with the production of methane (CH4) through reduction of either organic or carbonate carbon. Conditions favorable for production of methane appear at about the time the dissolved oxygen content is exhausted. This is because methane (CH4), a compound of carbon and hydrogen burns in oxygen forming oxides of carbon and hydrogen ie, carbon dioxide and water.

It has been found that large quantities of methane are produced in marshes and eutrophicated lakes during summer time.
ii) Hydrogen Sulphide
Hydrogen sulphide dissolves very rapidly in water and is thus not dissipated like methane. The bottom water of stratified eutrophic lakes may contain appreciable quantities of the very soluble gas H2S. This is especially marked in lakes of regions of high edaphic sulfate. The reduction of sulfate to sulfide is a phenomenon largely associated with anaerobic sediments. H2S is poisonous to aerobic organisms because it inactivates the enzyme cytochrome oxidase.
iii) Nitrogen
Nitrogen has a low solubility in water. It is such an inert gas that the quantities which occur in lake water are not changed by the chemical and biological processes. The atmosphere usually supplies the greater amounts of nitrogen found in water. The minimum amount occurs in winter, since it is more soluble in cool water.
iv) Ammonia
Ammonia occurs in small amounts in unmodified natural waters. It is exceedingly soluble, 1 volume of water dissolving 1,300 volume of ammonia at 0° C. In lakes, it is the result of the decomposition of organic matter at the bottom. In summer, free ammonia ordinarily increases with depth.
v) Sulphur dioxide
Traces of sulphur dioxide may occur in natural waters.
vi) Hydrogen
Liberation of hydrogen in the anaerobic decomposition of lake bottom deposits seems likely. But, the amount so formed is small.
vii) Carbon Monoxide
Carbon monoxide may occur in the bottom of the hypolimnion in small amount.


Hidrolika

13.2.3.1 Density

Dead oil is defined as oil without gas in solution. Its specific gravity γHai is defined as the ratio of the oil density and the water density at the same temperature and pressure:

API gravity, with a unit of degree ( o ) is defined as:

di mana γHai is the specific gravity of oil at 60°F, and the water density at 60°F is 62.37 lb/ft 3 .

The effect of gas dissolved in the oil should be accounted for in the calculation of the di tempat oil (live oil) density. The oil density can be calculated as follows: (13-5)


Tonton videonya: Кобылян Костя. Слова остались мне Евгений Литвинкович. Х-фактор 6. Третий кастинг