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Mengapa tekanan darah lebih tinggi semakin jauh arteri?

Mengapa tekanan darah lebih tinggi semakin jauh arteri?


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Mengapa tekanan darah pada amnya lebih tinggi di arteri distal?


Kerana gelombang tekanan yang dipantulkan dan kekakuan saluran darah. Gelombang tekanan ke depan dari jantung bergerak lebih cepat daripada darah itu sendiri dan dipantulkan pada kawasan meruncing dan bercabang. Gelombang mundur ini melambatkan aliran darah ke depan, dan pada masa yang sama, ketika bertemu dengan gelombang tekanan ke depan seterusnya, gelombang tekanan ke depan bertambah ... tekanan yang lebih tinggi dari jauh ... Dan sekarang anda tahu, dan mengetahui adalah separuh pertempuran ...


Sistem kardiovaskular dipengaruhi oleh tiga jenis tekanan. Ini adalah:

  • Heamodinamik - disebabkan oleh pengecutan jantung, yang akan memberikan pandangan tekanan yang lebih tinggi lebih dekat dengan aorta seperti dalam jawapan Kevin dan pemikiran pertama saya juga.
  • Kinetik - disebabkan oleh tindakan otot rangka dalam pergerakan dalam memerah terutamanya urat untuk mengembalikan darah ke jantung.
  • Hidrostatik - gabungan ketumpatan dan graviti cecair yang membawa kepada tekanan pada endotelium kapal. Tekanan pada titik tertentu sebanding dengan isi padu cecair di atasnya. Ini bermakna tekanan paling tinggi di bahagian bawah kapal.

Arteri sudah tentu boleh dianggap sebagai satu tiub panjang kerana kekurangan injap, oleh itu tekanan hidrostatik boleh menjadi penting dalam menyumbang kepada jumlah tekanan darah. Sekiranya tekanan hidrostatik lebih signifikan daripada tekanan heamodinamik maka ini akan menjelaskan mengapa tekanan menjadi lebih tinggi semakin jauh arteri - ketika berdiri di sana terdapat lebih banyak darah yang menekannya.


Jururawat Penjagaan Kritikal. 2002; 22: 60-79


20.2 Aliran Darah, Tekanan Darah, dan Ketahanan

Aliran darah merujuk pada pergerakan darah melalui pembuluh, jaringan, atau organ, dan biasanya dinyatakan dalam bentuk jumlah darah per unit waktu. Ia dimulakan oleh penguncupan ventrikel jantung. Pengecutan ventrikel mengeluarkan darah ke arteri utama, mengakibatkan aliran dari kawasan tekanan tinggi ke kawasan tekanan rendah, kerana darah menemui arteri dan arteriol yang lebih kecil, kemudian kapilari, kemudian venula dan urat sistem vena. Bahagian ini membincangkan sebilangan pemboleh ubah kritikal yang menyumbang kepada aliran darah ke seluruh badan. Ia juga membincangkan faktor-faktor yang menghalang atau memperlambat aliran darah, suatu fenomena yang dikenali sebagai daya tahan.

Seperti yang dinyatakan sebelumnya, tekanan hidrostatik adalah daya yang diberikan oleh bendalir akibat tarikan graviti, biasanya terhadap dinding bekas di mana ia berada. Salah satu bentuk tekanan hidrostatik adalah tekanan darah, kekuatan yang diberikan oleh darah ke dinding saluran darah atau ruang jantung. Tekanan darah boleh diukur dalam kapilari dan vena, serta saluran peredaran pulmonari walau bagaimanapun, istilah tekanan darah tanpa sebarang deskriptor khusus biasanya merujuk kepada tekanan darah arteri sistemik-iaitu, tekanan darah yang mengalir dalam arteri peredaran sistemik. Dalam praktik klinikal, tekanan ini diukur dalam mm Hg dan biasanya diperoleh menggunakan arteri brakial lengan.

Komponen Tekanan Darah Arteri

Tekanan darah arteri di saluran yang lebih besar terdiri daripada beberapa komponen yang berbeza (Gambar 20.10): tekanan sistolik dan diastolik, tekanan nadi, dan tekanan arteri min.

Tekanan Sistolik dan Diastolik

Apabila tekanan darah arteri sistemik diukur, ia dicatat sebagai nisbah dua nombor (mis., 120/80 adalah tekanan darah dewasa normal), dinyatakan sebagai tekanan sistolik terhadap tekanan diastolik. Tekanan sistolik adalah nilai yang lebih tinggi (biasanya sekitar 120 mm Hg) dan mencerminkan tekanan arteri akibat penyingkiran darah semasa pengecutan ventrikel, atau sistol. Tekanan diastolik adalah nilai yang lebih rendah (biasanya sekitar 80 mm Hg) dan mewakili tekanan arteri darah semasa relaksasi ventrikel, atau diastole.

Tekanan nadi

Seperti yang ditunjukkan dalam Gambar 20.10, perbezaan antara tekanan sistolik dan tekanan diastolik adalah tekanan nadi. Sebagai contoh, seseorang dengan tekanan sistolik 120 mm Hg dan tekanan diastolik 80 mm Hg akan mempunyai tekanan nadi 40 mmHg.

Secara amnya, tekanan nadi mestilah sekurang-kurangnya 25 peratus daripada tekanan sistolik. Tekanan nadi di bawah paras ini digambarkan sebagai rendah atau sempit. Ini mungkin berlaku, sebagai contoh, pada pesakit dengan jumlah strok yang rendah, yang mungkin dilihat dalam kegagalan jantung kongestif, stenosis injap aorta, atau kehilangan darah yang ketara berikutan trauma. Sebaliknya, tekanan nadi tinggi atau lebar adalah perkara biasa pada orang yang sihat selepas melakukan senaman yang berat, apabila tekanan nadi rehat mereka 30–40 mm Hg boleh meningkat buat sementara waktu kepada 100 mm Hg apabila isipadu strok meningkat. Tekanan nadi tinggi yang berterusan pada atau melebihi 100 mm Hg mungkin menunjukkan daya tahan berlebihan di arteri dan boleh disebabkan oleh pelbagai gangguan. Tekanan nadi rehat tinggi kronik boleh merosakkan jantung, otak, dan buah pinggang, dan memerlukan rawatan perubatan.

Maksud Tekanan Arteri

Tekanan arteri min (MAP) mewakili tekanan "purata" darah dalam arteri, iaitu, daya purata yang mendorong darah ke dalam saluran yang melayani tisu. Mean adalah konsep statistik dan dikira dengan mengambil jumlah nilai dibahagi dengan jumlah nilai. Walaupun rumit untuk diukur secara langsung dan rumit untuk dikira, MAP dapat dihampiri dengan menambahkan tekanan diastolik ke sepertiga tekanan nadi atau tekanan sistolik dikurangi tekanan diastolik:

Dalam Rajah 20.10, nilai ini adalah lebih kurang 80 + (120 − 80) / 3, atau 93.33. Biasanya, MAP berada dalam julat 70–110 mm Hg. Sekiranya nilainya jatuh di bawah 60 mm Hg untuk jangka masa yang panjang, tekanan darah tidak akan cukup tinggi untuk memastikan peredaran ke dan melalui tisu, yang mengakibatkan iskemia, atau aliran darah tidak mencukupi. Keadaan yang dipanggil hipoksia, pengoksigenan tisu yang tidak mencukupi, biasanya mengiringi iskemia. Istilah hipokemia merujuk kepada tahap oksigen yang rendah dalam darah arteri sistemik. Neuron sangat sensitif terhadap hipoksia dan mungkin mati atau rosak sekiranya aliran darah dan bekalan oksigen tidak cepat pulih.

Nadi

Setelah darah dikeluarkan dari jantung, serat elastik di arteri membantu mengekalkan kecerunan tekanan tinggi ketika mengembang untuk menampung darah, kemudian mundur. Kesan pengembangan dan penyambungan semula ini, yang dikenali sebagai nadi, dapat diraba secara manual atau diukur secara elektronik. Walaupun kesannya berkurang dari jarak jauh dari jantung, unsur-unsur komponen sistolik dan diastolik nadi masih jelas hingga ke tahap arteriol.

Kerana nadi menunjukkan degup jantung, ia diukur secara klinikal untuk memberi petunjuk keadaan kesihatan pesakit. Ia direkodkan sebagai rentak seminit. Kadar dan kekuatan nadi penting secara klinikal. Denyut nadi yang tinggi atau tidak teratur boleh disebabkan oleh aktiviti fizikal atau faktor sementara yang lain, tetapi juga menunjukkan keadaan jantung. Kekuatan nadi menunjukkan kekuatan pengecutan ventrikel dan output jantung. Sekiranya nadi kuat, maka tekanan sistolik tinggi. Sekiranya lemah, tekanan sistolik akan turun, dan campur tangan perubatan mungkin diperlukan.

Denyutan nadi dapat diraba secara manual dengan meletakkan hujung jari di seberang arteri yang berjalan dekat dengan permukaan badan dan menekan dengan ringan. Walaupun prosedur ini biasanya dilakukan menggunakan arteri radial di pergelangan tangan atau arteri karotid biasa di leher, mana-mana arteri cetek yang boleh dipalpasi boleh digunakan (Rajah 20.11). Tapak umum untuk mencari nadi termasuk arteri temporal dan muka di kepala, arteri brachial di lengan atas, arteri femoral di paha, arteri popliteal di belakang lutut, arteri tibial posterior berhampiran kawasan medial tarsal, dan arteri dorsalis pedis di kaki . Pelbagai peranti elektronik komersial juga tersedia untuk mengukur nadi.

Pengukuran Tekanan Darah

Tekanan darah adalah salah satu parameter kritikal yang diukur pada hampir setiap pesakit dalam setiap persekitaran penjagaan kesihatan. Teknik yang digunakan hari ini telah dibangunkan lebih daripada 100 tahun yang lalu oleh seorang doktor perintis Rusia, Dr. Nikolai Korotkoff. Aliran darah bergelora melalui saluran boleh didengari sebagai detik lembut semasa mengukur tekanan darah bunyi ini dikenali sebagai bunyi Korotkoff . Teknik mengukur tekanan darah memerlukan penggunaan sphygmomanometer (manset tekanan darah yang dipasang pada alat pengukur) dan stetoskop. Tekniknya adalah seperti berikut:

  • Klinik membungkus manset kembung dengan erat di lengan pesakit pada tahap jantung.
  • Klinik menekan pam getah untuk menyuntikkan udara ke dalam manset, meningkatkan tekanan di sekitar arteri dan memotong aliran darah ke lengan pesakit untuk sementara waktu.
  • Doktor meletakkan stetoskop pada kawasan antekubital pesakit dan, sambil secara beransur-ansur membenarkan udara dalam manset keluar, mendengar bunyi Korotkoff.

Walaupun terdapat lima suara Korotkoff yang dikenali, hanya dua yang biasanya dirakam. Pada awalnya, tidak ada suara yang terdengar karena tidak ada aliran darah melalui pembuluh darah, tetapi ketika tekanan udara turun, manset mengendur, dan aliran darah kembali ke lengan. Seperti yang ditunjukkan dalam Gambar 20.12, suara pertama yang didengar melalui stetoskop — suara Korotkoff pertama — menunjukkan tekanan sistolik. Apabila lebih banyak udara dilepaskan dari cuff, darah dapat mengalir dengan bebas melalui arteri brachial dan semua bunyi hilang. Titik di mana suara terakhir didengar direkodkan sebagai tekanan diastolik pesakit.

Sebilangan besar hospital dan klinik mempunyai peralatan automatik untuk mengukur tekanan darah yang menggunakan prinsip yang sama. Inovasi yang lebih terkini ialah instrumen kecil yang melilit pergelangan tangan pesakit. Pesakit kemudian memegang pergelangan tangan di atas jantung sementara alat mengukur aliran darah dan mencatat tekanan.

Pembolehubah yang Mempengaruhi Aliran Darah dan Tekanan Darah

Lima pemboleh ubah mempengaruhi aliran darah dan tekanan darah:

  • Keluaran jantung
  • Pematuhan
  • Isipadu darah
  • Kelikatan darah
  • Panjang dan diameter saluran darah

Ingat bahawa darah bergerak dari tekanan tinggi ke tekanan rendah. Ia dipam dari jantung ke arteri pada tekanan tinggi. Sekiranya anda meningkatkan tekanan pada arteri (selepas bebanan), dan fungsi jantung tidak mengimbangi, aliran darah akan benar-benar menurun. Dalam sistem vena, hubungan yang bertentangan adalah benar. Peningkatan tekanan dalam urat tidak mengurangkan aliran seperti yang berlaku di arteri, tetapi sebenarnya meningkatkan aliran. Oleh kerana tekanan pada urat biasanya agak rendah, untuk darah mengalir kembali ke jantung, tekanan di atria semasa diastol atrium mesti lebih rendah. Ia biasanya menghampiri sifar, kecuali apabila atria mengecut (lihat Rajah 20.10).

Keluaran Jantung

Output jantung adalah pengukuran aliran darah dari jantung melalui ventrikel, dan biasanya diukur dalam liter per minit. Apa-apa faktor yang menyebabkan peningkatan jantung meningkat, dengan peningkatan kadar denyutan jantung atau strok atau kedua-duanya, akan meningkatkan tekanan darah dan melancarkan aliran darah. Faktor-faktor ini termasuk rangsangan simpatik, epinefrin katekolamin dan norepinefrin, hormon tiroid, dan peningkatan kadar ion kalsium. Sebaliknya, sebarang faktor yang menurunkan output jantung, dengan menurunkan denyut jantung atau jumlah strok atau kedua-duanya, akan menurunkan tekanan arteri dan aliran darah. Faktor-faktor ini termasuk rangsangan parasimpatis, peningkatan kadar ion kalium, penurunan kadar kalsium, anoksia, dan asidosis.

Pematuhan

Pematuhan adalah kemampuan setiap ruang untuk berkembang untuk menampung peningkatan kandungan. Pipa logam, misalnya, tidak patuh, sedangkan belon adalah. Semakin besar kepatuhan arteri, semakin efektif ia dapat berkembang untuk menampung lonjakan aliran darah tanpa peningkatan daya tahan atau tekanan darah. Vena lebih sesuai daripada arteri dan boleh mengembang untuk menahan lebih banyak darah. Apabila penyakit vaskular menyebabkan arteri menjadi kaku, pematuhan berkurangan dan rintangan terhadap aliran darah meningkat. Hasilnya adalah lebih banyak turbulensi, tekanan yang lebih tinggi di dalam kapal, dan pengurangan aliran darah. Ini meningkatkan kerja jantung.

Pendekatan Matematik kepada Faktor-faktor yang Mempengaruhi Pengaliran Darah

Jean Louis Marie Poiseuille ialah seorang doktor dan ahli fisiologi Perancis yang mencipta persamaan matematik yang menerangkan aliran darah dan hubungannya dengan parameter yang diketahui. Persamaan yang sama juga berlaku untuk kajian kejuruteraan aliran cecair. Walaupun memahami matematik di sebalik hubungan antara faktor yang mempengaruhi aliran darah tidak diperlukan untuk memahami aliran darah, ia boleh membantu mengukuhkan pemahaman tentang hubungan mereka. Sila ambil perhatian bahawa walaupun persamaan itu kelihatan menakutkan, memecahkannya kepada komponennya dan mengikuti perhubungan akan menjadikan perhubungan ini lebih jelas, walaupun anda lemah dalam matematik. Fokus pada tiga pemboleh ubah kritikal: jejari (r), panjang kapal (λ), dan kelikatan (η).

  • π ialah huruf Yunani pi, digunakan untuk mewakili pemalar matematik iaitu nisbah lilitan bulatan kepada diameternya. Ini biasanya dinyatakan sebagai 3.14, walaupun jumlah sebenarnya meluas hingga tak terhingga.
  • ΔP mewakili perbezaan tekanan.
  • r 4 adalah jejari (setengah dari diameter) kapal hingga daya keempat.
  • η adalah huruf Yunani eta dan mewakili kelikatan darah.
  • λ adalah huruf Yunani lambda dan mewakili panjang saluran darah.

Salah satu perkara yang membolehkan persamaan ini kita lakukan ialah mengira rintangan dalam sistem vaskular. Biasanya nilai ini sangat sukar untuk diukur, tetapi dapat dikira dari hubungan yang diketahui ini:

Sekiranya kita menyusunnya sedikit,

Kemudian dengan menggantikan persamaan Pouseille dengan aliran darah:

Dengan memeriksa persamaan ini, anda dapat melihat bahawa hanya ada tiga pemboleh ubah: kelikatan, panjang kapal, dan jejari, kerana 8 dan π adalah kedua-dua pemalar. Perkara penting yang perlu diingat adalah: Dua pemboleh ubah ini, kelikatan dan panjang kapal, akan berubah perlahan di dalam badan. Hanya satu daripada faktor ini, jejari, boleh diubah dengan cepat oleh vasokonstriksi dan vasodilatasi, dengan itu memberi kesan secara mendadak kepada rintangan dan aliran. Selanjutnya, perubahan kecil dalam radius akan sangat mempengaruhi aliran, kerana dinaikkan ke daya keempat dalam persamaan.

Kami telah mempertimbangkan secara ringkas bagaimana output jantung dan jumlah darah mempengaruhi aliran darah dan tekanan langkah seterusnya adalah untuk melihat bagaimana pemboleh ubah lain (pengecutan, panjang kapal, dan kelikatan) diartikulasikan dengan persamaan Pouseille dan apa yang dapat mereka ajarkan kepada kita mengenai kesan aliran darah .

Isipadu Darah

Hubungan antara jumlah darah, tekanan darah, dan aliran darah secara intuitif jelas. Air hanya dapat mengalir di sepanjang dasar sungai di musim kemarau, tetapi cepat-cepat mengalir dan di bawah tekanan hebat setelah hujan lebat. Begitu juga dengan penurunan jumlah darah, tekanan dan aliran menurun. Apabila jumlah darah meningkat, tekanan dan aliran meningkat.

Dalam keadaan normal, jumlah darah sedikit berbeza. Jumlah darah yang rendah, dipanggil hipovolemia , mungkin disebabkan oleh pendarahan, dehidrasi, muntah, melecur teruk, atau beberapa ubat yang digunakan untuk merawat hipertensi. Adalah penting untuk menyedari bahawa mekanisme pengawalseliaan lain dalam badan adalah sangat berkesan untuk mengekalkan tekanan darah sehingga seseorang individu mungkin tidak menunjukkan gejala sehingga 10-20 peratus daripada jumlah darah telah hilang. Rawatan biasanya termasuk penggantian cecair intravena.

Hipervolemia, jumlah cecair yang berlebihan, mungkin disebabkan oleh pengekalan air dan natrium, seperti yang terlihat pada pesakit dengan kegagalan jantung, sirosis hati, beberapa bentuk penyakit ginjal, hiperaldosteronisme, dan beberapa rawatan steroid glukokortikoid. Memulihkan homeostasis pada pesakit ini bergantung pada membalikkan keadaan yang mencetuskan hipervolemia.

Kelikatan Darah

Kelikatan adalah ketebalan cecair yang mempengaruhi kemampuan mereka untuk mengalir. Air bersih, misalnya, kurang likat daripada lumpur. Kelikatan darah berkadar langsung dengan rintangan dan berkadar songsang dengan aliran oleh itu, sebarang keadaan yang menyebabkan kelikatan meningkat juga akan meningkatkan daya tahan dan penurunan aliran. Sebagai contoh, bayangkan meneguk susu, kemudian milkshake, melalui penyedut minuman bersaiz sama. Anda mengalami lebih banyak rintangan dan oleh itu lebih sedikit aliran dari milkshake. Sebaliknya, sebarang keadaan yang menyebabkan kelikatan menurun (seperti ketika milkshake mencair) akan menurunkan daya tahan dan meningkatkan aliran.

Biasanya kelikatan darah tidak berubah dalam jangka masa yang singkat. Dua penentu utama kelikatan darah adalah unsur terbentuk dan protein plasma. Oleh kerana sebahagian besar unsur yang terbentuk adalah eritrosit, sebarang keadaan yang mempengaruhi eritropoiesis, seperti polisitemia atau anemia, boleh mengubah kelikatan. Oleh kerana kebanyakan protein plasma dihasilkan oleh hati, sebarang keadaan yang menjejaskan fungsi hati juga boleh mengubah sedikit kelikatan dan oleh itu mengubah aliran darah. Keabnormalan hati seperti hepatitis, sirosis, kerosakan alkohol, dan toksisitas ubat mengakibatkan penurunan kadar protein plasma, yang menurunkan kelikatan darah. Walaupun leukosit dan platelet biasanya merupakan komponen kecil unsur yang terbentuk, terdapat beberapa keadaan yang jarang berlaku di mana pengeluaran berlebihan yang teruk boleh memberi kesan kepada kelikatan juga.

Panjang dan Diameter Kapal

Panjang kapal berkadar langsung dengan ketahanannya: semakin lama kapal, semakin besar rintangan dan semakin rendah alirannya. Seperti jumlah darah, ini masuk akal secara intuitif, kerana luas permukaan kapal yang meningkat akan menghalang aliran darah. Begitu juga, jika kapal dipendekkan, rintangan akan berkurang dan aliran akan meningkat.

Panjang saluran darah kita meningkat sepanjang zaman kanak-kanak apabila kita membesar, sudah tentu, tetapi tidak berubah pada orang dewasa di bawah keadaan fisiologi normal. Selanjutnya, pengedaran vesel tidak sama dalam semua tisu. Tisu adiposa tidak mempunyai bekalan vaskular yang meluas. Satu paun tisu adiposa mengandungi kira-kira 200 batu kapal, manakala otot rangka mengandungi lebih daripada dua kali ganda. Secara keseluruhan, kapal berkurang hanya semasa kehilangan jisim atau amputasi. Seorang individu dengan berat 150 paun mempunyai kira-kira 60,000 batu kapal di dalam badan. Menambah sekitar 10 paun menambah dari 2000 hingga 4000 batu kapal, bergantung pada sifat tisu yang diperoleh. Salah satu faedah besar pengurangan berat badan adalah tekanan yang berkurang ke jantung, yang tidak perlu mengatasi rintangan kapal sejauh beberapa batu.

Berbeza dengan panjang, diameter saluran darah berubah di seluruh badan, sesuai dengan jenis kapal, seperti yang telah kita bincangkan sebelumnya. Diameter setiap kapal yang diberikan juga sering berubah sepanjang hari sebagai tindak balas kepada isyarat saraf dan kimia yang mencetuskan vasodilatasi dan vasokonstriksi. Nada vaskular kapal adalah keadaan kontraktil otot licin dan penentu utama diameter, dan dengan itu rintangan dan aliran. Kesan diameter salur pada rintangan adalah songsang: Memandangkan isipadu darah yang sama, diameter yang meningkat bermakna darah yang bersentuhan dengan dinding salur darah berkurangan, sekali gus mengurangkan geseran dan rintangan yang lebih rendah, seterusnya meningkatkan aliran. Diameter yang menurun bermaksud lebih banyak darah yang menyentuh dinding pembuluh darah, dan daya tahan meningkat, seterusnya aliran menurun.

Pengaruh diameter lumen pada rintangan adalah dramatik: Peningkatan atau penurunan diameter yang sedikit menyebabkan penurunan atau peningkatan rintangan yang besar. Ini kerana daya tahan berkadar songsang dengan jari-jari saluran darah (setengah dari diameter kapal) dinaikkan ke daya keempat (R = 1 / r 4). Ini bermaksud, sebagai contoh, bahawa jika arteri atau arteriole menyempit kepada setengah daripada radius asalnya, daya tahan terhadap aliran akan meningkat 16 kali. Dan jika arteri atau arteriol mengembang kepada dua kali jejari awalnya, maka rintangan dalam vesel akan berkurangan kepada 1/16 daripada nilai asalnya dan aliran akan meningkat 16 kali ganda.

Peranan Diameter Kapal dan Luas Kawasan dalam Aliran Darah dan Tekanan Darah

Ingatlah bahawa kita menggolongkan arteriol sebagai pembuluh rintangan, kerana memandangkan lumennya yang kecil, mereka secara dramatik memperlambat aliran darah dari arteri. Sebenarnya, arteriol adalah tempat rintangan terbesar di seluruh rangkaian vaskular. Ini mungkin kelihatan mengejutkan, memandangkan kapilari mempunyai ukuran yang lebih kecil. Bagaimana fenomena ini dapat dijelaskan?

Gambar 20.13 membandingkan diameter kapal, luas luas keratan rentas, tekanan darah rata-rata, dan halaju darah melalui saluran sistemik. Perhatikan di bahagian (a) dan (b) bahawa luas keratan rentas tempat tidur kapilari badan jauh lebih besar daripada jenis kapal lain. Walaupun diameter kapilari individu jauh lebih kecil daripada diameter arteriol, terdapat lebih banyak kapilari dalam badan daripada jenis saluran darah yang lain. Bahagian (c) menunjukkan bahawa tekanan darah menurun secara tidak sekata apabila darah bergerak dari arteri ke arteriol, kapilari, venula dan vena, dan menghadapi rintangan yang lebih besar. Walau bagaimanapun, tapak penurunan paling mendadak, dan tapak rintangan terbesar, adalah arteriol. Ini menjelaskan mengapa vasodilasi dan vasoconstriction arteriol memainkan peranan yang lebih penting dalam mengawal tekanan darah berbanding vasodilatasi dan vasoconstriction saluran lain.

Bahagian (d) menunjukkan bahawa kecepatan (kelajuan) aliran darah menurun secara mendadak ketika darah bergerak dari arteri ke arteriol ke kapilari. Kadar aliran perlahan ini membolehkan lebih banyak masa untuk proses pertukaran berlaku. Apabila darah mengalir melalui urat, kadar halaju meningkat, kerana darah dikembalikan ke jantung.

Gangguan pada.

Sistem Kardiovaskular: Arteriosklerosis

Pematuhan membolehkan arteri mengembang ketika darah dipompa melaluinya dari jantung, dan kemudian merosot setelah lonjakan berlalu. Ini membantu melancarkan aliran darah. Pada arteriosklerosis, kepatuhan dikurangkan, dan tekanan dan daya tahan di dalam kapal meningkat. Ini adalah penyebab utama hipertensi dan penyakit jantung koronari, kerana ia menyebabkan jantung bekerja lebih keras untuk menghasilkan tekanan yang cukup besar untuk mengatasi daya tahan.

Arteriosklerosis bermula dengan kecederaan pada endotelium arteri, yang mungkin disebabkan oleh kerengsaan akibat glukosa darah tinggi, jangkitan, penggunaan tembakau, lipid darah yang berlebihan, dan faktor lain. Dinding arteri yang sentiasa tertekan oleh darah yang mengalir pada tekanan tinggi juga lebih cenderung untuk cedera—yang bermaksud hipertensi boleh menggalakkan arteriosklerosis, serta akibat daripadanya.

Ingat bahawa kecederaan tisu menyebabkan keradangan. Apabila keradangan menyebar ke dinding arteri, ia melemahkan dan melecet, menjadikannya kaku (sklerotik). Akibatnya, kepatuhan dikurangkan. Lebih-lebih lagi, trigliserida dan kolesterol yang beredar dapat meresap di antara sel lapisan yang rosak dan terperangkap di dalam dinding arteri, di mana sel-sel tersebut sering disatukan oleh leukosit, kalsium, dan serpihan selular. Akhirnya, pembentukan ini, dipanggil plak, boleh menyempitkan arteri cukup untuk menjejaskan aliran darah. Istilah untuk keadaan ini, aterosklerosis (athero- = “bubur”) menerangkan mendapan tepung (Rajah 20.14).

Kadang-kadang plak boleh pecah, menyebabkan air mata mikroskopik di dinding arteri yang membolehkan darah bocor ke tisu di sisi lain. Apabila ini berlaku, platelet bergegas ke tapak untuk membekukan darah. Gumpalan ini dapat menyekat arteri dan - jika terjadi pada arteri koronari atau serebral - menyebabkan serangan jantung atau strok secara tiba-tiba. Sebagai alternatif, plak boleh terputus dan bergerak melalui aliran darah sebagai embolus sehingga menyekat arteri yang lebih jauh dan lebih kecil.

Walaupun tanpa penyumbatan total, penyempitan kapal menyebabkan iskemia — pengurangan aliran darah — ke kawasan tisu “hilir” saluran penyempitan. Iskemia seterusnya menyebabkan hipoksia - penurunan bekalan oksigen ke tisu. Hipoksia yang melibatkan otot jantung atau tisu otak boleh menyebabkan kematian sel dan gangguan fungsi otak atau jantung yang teruk.

Faktor risiko utama untuk kedua arteriosklerosis dan aterosklerosis adalah usia lanjut, kerana keadaan cenderung berkembang dari masa ke masa. Arteriosklerosis biasanya ditakrifkan sebagai kehilangan pematuhan yang lebih umum, "pengerasan arteri," manakala aterosklerosis ialah istilah yang lebih khusus untuk pembentukan plak di dinding vesel dan merupakan jenis arteriosklerosis tertentu. Terdapat juga komponen genetik yang berbeza, dan hipertensi dan / atau diabetes yang ada sebelumnya juga meningkatkan risiko. Walau bagaimanapun, kegemukan, pemakanan yang buruk, kekurangan aktiviti fizikal, dan penggunaan tembakau semuanya merupakan faktor risiko utama.

Rawatan termasuk perubahan gaya hidup, seperti penurunan berat badan, berhenti merokok, senaman yang kerap, dan mengamalkan diet rendah natrium dan lemak tepu. Ubat untuk mengurangkan kolesterol dan tekanan darah mungkin diresepkan. Untuk arteri koronari yang tersumbat, pembedahan adalah wajar. Dalam angioplasti, kateter dimasukkan ke dalam kapal pada titik penyempitan, dan kateter kedua dengan ujung seperti belon diembungkan untuk melebarkan bukaan. Untuk mengelakkan kejatuhan kapal berikutnya, tiub mesh kecil yang disebut stent sering dimasukkan. Dalam endarterektomi, plak dikeluarkan secara pembedahan dari dinding kapal. Operasi ini biasanya dilakukan pada arteri karotid leher, yang merupakan sumber utama darah beroksigen untuk otak. Dalam prosedur pintasan koronari, salur cetek yang tidak penting dari bahagian lain badan (selalunya vena saphenous besar) atau salur sintetik dimasukkan untuk mencipta laluan di sekitar kawasan arteri koronari yang tersumbat.

Sistem vena

Tindakan mengepam jantung mendorong darah masuk ke arteri, dari kawasan tekanan tinggi ke kawasan tekanan rendah. Sekiranya darah mengalir dari vena kembali ke jantung, tekanan di urat mesti lebih besar daripada tekanan di atria jantung. Dua faktor membantu mengekalkan kecerunan tekanan ini antara urat dan jantung. Pertama, tekanan di atria semasa diastole sangat rendah, sering menghampiri sifar ketika atria santai (atrial diastole). Kedua, dua "pam" fisiologi meningkatkan tekanan pada sistem vena. Penggunaan istilah "pam" membayangkan peranti fizikal yang mempercepatkan aliran. Pam fisiologi ini kurang jelas.

Pam Otot Skeletal

Di kebanyakan kawasan badan, tekanan dalam urat boleh ditingkatkan dengan penguncupan otot rangka di sekelilingnya. Mekanisme ini, yang dikenali sebagai pam otot rangka (Rajah 20.15), membantu urat tekanan rendah mengatasi daya graviti, meningkatkan tekanan untuk memindahkan darah kembali ke jantung. Apabila otot kaki mengecut, contohnya semasa berjalan atau berlari, mereka memberi tekanan pada urat berdekatan dengan injap sehala yang banyak. Tekanan yang meningkat ini menyebabkan darah mengalir ke atas, membuka injap lebih tinggi daripada otot yang berkontraksi sehingga darah mengalir. Pada masa yang sama, injap yang lebih rendah daripada otot-otot yang berkontrak menutup, darah tidak boleh merembes ke bawah ke arah kaki. Rekrut tentera dilatih untuk melenturkan kaki sedikit sambil memerhatikan untuk jangka masa yang lama. Kegagalan untuk melakukannya boleh menyebabkan darah mengumpul di anggota bawah dan bukannya kembali ke jantung. Akibatnya, otak tidak akan menerima cukup darah beroksigen, dan individu itu mungkin kehilangan kesedaran.

Pam Pernafasan

Pam pernafasan membantu aliran darah melalui urat toraks dan perut. Semasa menghirup, jumlah toraks meningkat, sebahagian besarnya melalui penguncupan diafragma, yang bergerak ke bawah dan menekan rongga perut. Ketinggian dada yang disebabkan oleh pengecutan otot interkostal luaran juga menyumbang kepada peningkatan jumlah toraks. Peningkatan isipadu menyebabkan tekanan udara dalam toraks berkurangan, membolehkan kita menyedut. Selain itu, apabila tekanan udara dalam toraks menurun, tekanan darah dalam vena toraks juga berkurangan, jatuh di bawah tekanan dalam vena perut. Ini menyebabkan darah mengalir di sepanjang tekanannya dari vena di luar toraks, di mana tekanannya lebih tinggi, ke kawasan toraks, di mana tekanan sekarang lebih rendah. Ini seterusnya mendorong pengembalian darah dari urat toraks ke atria. Semasa menghembus nafas, ketika tekanan udara meningkat di dalam rongga toraks, tekanan pada vena toraks meningkat, mempercepat aliran darah ke jantung sementara injap di urat menghalang darah mengalir ke belakang dari urat toraks dan perut.

Hubungan Tekanan dalam Sistem Vena

Walaupun diameter kapal meningkat dari venula yang lebih kecil ke urat yang lebih besar dan akhirnya ke venae cavae (tunggal = vena cava), jumlah luas keratan rentas sebenarnya menurun (lihat Gambar 20.15a dan b). Vena individu berdiameter lebih besar daripada venula, tetapi jumlahnya jauh lebih rendah, jadi jumlah luas keratan rentas mereka juga lebih rendah.

Perhatikan juga bahawa, ketika darah bergerak dari venula ke urat, tekanan darah rata-rata menurun (lihat Gambar 20.15c), tetapi halaju darah sebenarnya meningkat (lihat Rajah 20.15). Kecerunan tekanan ini memacu darah kembali ke jantung. Sekali lagi, kehadiran injap sehala dan otot rangka dan pam pernafasan menyumbang kepada peningkatan aliran ini. Oleh kerana kira-kira 64 peratus daripada jumlah darah berada dalam urat sistemik, tindakan yang meningkatkan aliran darah melalui urat akan meningkatkan pengembalian vena ke jantung. Mengekalkan nada vaskular di dalam urat menghalang urat dari sekadar mengembang, melancarkan aliran darah, dan seperti yang akan anda lihat, vasokonstriksi sebenarnya meningkatkan aliran.

Peranan Venokonstriksi dalam Rintangan, Tekanan Darah, dan Aliran

Seperti yang telah dibincangkan sebelumnya, vasokonstriksi arteri atau arteriole menurunkan radius, meningkatkan daya tahan dan tekanan, tetapi menurunkan aliran. Venoconstriction, sebaliknya, mempunyai hasil yang sangat berbeza. Dinding vena nipis tetapi tidak teratur oleh itu, apabila otot licin di dinding tersebut mengecut, lumen menjadi lebih bulat. Semakin lumen bulatan, semakin sedikit kawasan permukaan darah, dan semakin kurang daya tahan kapal. Vasokonstriksi meningkatkan tekanan dalam urat seperti yang berlaku di arteri, tetapi pada urat, tekanan meningkat meningkatkan aliran. Ingat bahawa tekanan di atria, di mana darah vena akan mengalir, sangat rendah, mendekati sifar untuk sekurang-kurangnya sebahagian fasa relaksasi kitaran jantung. Oleh itu, venokonstriksi meningkatkan pengembalian darah ke jantung. Kaedah lain untuk menyatakan ini adalah bahawa venokonstriksi meningkatkan preload atau peregangan otot jantung dan meningkatkan pengecutan.


Hipertensi primer

Komponen hemodinamik dan fisiologi (contohnya, jumlah plasma, aktiviti sistem renin-angiotensin) berbeza-beza, menunjukkan bahawa hipertensi primer tidak mungkin mempunyai satu sebab. Walaupun satu faktor pada mulanya bertanggungjawab, pelbagai faktor mungkin terlibat dalam mengekalkan tekanan darah tinggi (teori mozek). In afferent systemic arterioles, malfunction of ion pumps on sarcolemmal membranes of smooth muscle cells may lead to chronically increased vascular tone. Heredity is a predisposing factor, but the exact mechanism is unclear. Environmental factors (eg, dietary sodium, stress) seem to affect only genetically susceptible people at younger ages however, in patients > 65, high sodium intake is more likely to precipitate hypertension.

Hipertensi sekunder

Renal parenchymal disease (eg, chronic glomerulonephritis or pyelonephritis, polycystic renal disease, connective tissue disorders, obstructive uropathy)

Other, much rarer, causes include pheochromocytoma, Cushing syndrome, congenital adrenal hyperplasia, hyperthyroidism, hypothyroidism (myxedema), primary hyperparathyroidism, acromegaly, coarctation of the aorta, and mineralocorticoid excess syndromes other than primary aldosteronism. Excessive alcohol intake and use of oral contraceptives are common causes of curable hypertension. Use of sympathomimetics, nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, cocaine, or licorice commonly contributes to worsening of blood pressure control.

Hypertension is defined as resistant when BP remains above goal despite use of 3 different antihypertensive drugs. Patients with resistant hypertension have higher cardiovascular morbidity and mortality (1).

Etiology reference

1. Carey RM, Calhoun DA, Bakris GL, et al: Resistant hypertension: Detection, evaluation, and management: A Scientific Statement From the American Heart Association. Hypertension 72:e53-e90, 2018. doi 10.1161/HYP.0000000000000084


Causes - Atherosclerosis

The exact cause of atherosclerosis isn't known. However, studies show that atherosclerosis is a slow, complex disease that may start in childhood. It develops faster as you age.

Atherosclerosis may start when certain factors damage the inner layers of the arteries. These factors include:

Plaque may begin to build up where the arteries are damaged. Over time, plaque hardens and narrows the arteries. Eventually, an area of plaque can rupture (break open).

When this happens, blood cell fragments called platelets (PLATE-lets) stick to the site of the injury. They may clump together to form blood clots. Clots narrow the arteries even more, limiting the flow of oxygen-rich blood to your body.

Depending on which arteries are affected, blood clots can worsen angina (chest pain) or cause a heart attack or stroke.

Researchers continue to look for the causes of atherosclerosis. They hope to find answers to questions such as:

  • Why and how do the arteries become damaged?
  • How does plaque develop and change over time?
  • Why does plaque rupture and lead to blood clots?

Extreme swings in blood pressure are just as deadly as having consistently high blood pressure

Extreme ups and downs in systolic blood pressure may be just as deadly as having consistently high blood pressure, according to a new study from the Intermountain Medical Center Heart Institute in Salt Lake City.

Following a review of electronic medical records, researchers from the Intermountain Medical Center Heart Institute discovered that patients with systolic blood pressure numbers that varied by as much as 30 or 40 between doctor visits over an extended period of time were more likely to die than those with less extreme variances in their blood pressure.

The systolic blood pressure reading (the upper number) indicates how much pressure blood is exerting against the artery walls when the heart beats. According to the American Heart Association, a normal systolic blood pressure is less than 120. High blood pressure is categorized as above 140.

"Blood pressure is one of those numbers we encourage people to keep track of, as it's one indicator of your health heart," said Brian Clements, DO, an internal medicine specialist with the Intermountain Medical Center Heart Institute, and lead invesigator of the study. "The takeaway from the study is, if you allow your blood pressure to be uncontrolled for any period of time, or notice big changes in your blood pressure between doctor visits, you increase your risk of stroke, heart attack, kidney or heart failure, or even death."

Results of the study of nearly 11,000 patients will be reported at the 2017 American Heart Association Scientific Sessions in Anaheim, CA, on Monday, November 13.

Researchers at the Intermountain Medical Center Heart Institute modeled their study after an analysis of the largest hypertension clinical trial ever conducted -- the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).

They examined visit-to-visit variability of systolic blood pressure in 10,903 patient records from Intermountain Healthcare facilities. The patients were required to have had seven blood pressure measurements between 2007 and 2011. After the date of their seventh recorded systolic blood pressure measurement, the patients were followed for five years, with researchers looking at all causes of mortality.

"The call to action for patients as a result of this study is to do everything they can to control their blood pressure on a regular basis," said Dr. Clements. "Eat healthy foods, exercise regularly, and if your doctor has prescribed you medications for your blood pressure, be sure and take them consistently. Because any time your blood pressure is out of control, you're at higher risk of injury or death."

In most people, systolic blood pressure rises steadily with age due to increased stiffness of large arteries, long-term build-up of plaque, and increased incidence of cardiac and vascular disease, according to the the American Heart Association.

Dr. Clements also recommends that people control their environment when measuring their blood pressure to help reduce additional variables from influencing the measurement.

&bull Sit or lay down for 15 minutes prior to taking your blood pressure. Don't do things that will cause you stress, as that may raise your blood pressure.

&bull Use a blood pressure cuff that fits. Make sure it's not too tight or too large.

"After the ALLHAT study, we were in a unique position because Intermountain Healthcare has such a rich database of records that are perfect for identifying trends and outcomes," said Dr. Clements. "In this case, we're working to identify the cause of the variances in systolic blood pressure and learn if it's an independent predictor of mortality, thus helping clinicians work with their patients to better manage their heart health."

Other members of the research team include Nathan Allred Erik Riessen Benjamin Horne, PhD Raymond O. McCubrey Heidi T. May, PhD and Joseph B. Muhlestein, MD.

The Intermountain Medical Center Heart Institute, which is part of the Intermountain Healthcare system based in Salt Lake City, is one of the premier cardiovascular centers in the country.


Annals of Clinical Hypertension

Seriki A Samue 1* , Adebayo O Francis 1 and Odetola O Anthony 2

*Address for Correspondence: Seriki A. Samuel, Department of Human Physiology, College of Medicine, Bingham University, Karu, Nigeria, Tel: +2348036041121 Email: [email protected]

Tarikh: Submitted: 05 July 2018 Approved: 16 July 2018 Diterbitkan: 17 July 2018

Cara memetik artikel ini: Samuel SA, Francis AO, Anthony OO. Role of the Kidneys in the Regulation of Intra- and Extra-Renal Blood Pressure. Ann Clin Hypertens. 2018 2: 048-058. DOI: 10.29328/journal.ach.1001011

Hak cipta: © 2018 Samuel SA, et al. Ini ialah artikel akses terbuka yang diedarkan di bawah Lesen Atribusi Creative Commons, yang membenarkan penggunaan, pengedaran dan pengeluaran semula tanpa had dalam mana-mana medium, dengan syarat karya asal dipetik dengan betul.

Kata kunci: Hypertension Renin Angiotensin System Natriuresis Sodium balance homeostasis

Abstrak

Hypertension is one of the most common chronic diseases of human, affecting more than one billion people worldwide. When it becomes chronic, hypertension leaves behind cardiac hypertrophy, heart failure, stroke, and kidney disease, resulting in substantial morbidity and mortality. Treatments that effectively reduce blood pressure can prevent these complications. Abnormalities in the production of urine by the kidneys have been implicated in increased vascular resistance, leading to high blood pressure and increased cardiac mass. By matching urinary excretion of salt and water with dietary intake, balance is usually attained, thereby maintaining a constant extracellular fluid volume and blood pressure. Based on the capacity for the kidney to excrete sodium, this blood pressure-altering mechanism should have sufficient advantage to limit intravascular volume and consequently lower blood pressure in response to a range of stimuli from elevated heart rate to increase peripheral vascular resistance. A major determinant of the level of intra- and extra- renal blood pressure is therefore sodium handling, and it is controlled by complex physiological mechanism by hormones, inflammatory mediators, and the sympathetic nervous system. Homoeostasis and favourable influence sodium balance are a basic mechanism of efficacy for diuretics and dietary sodium restriction in hypertension. Renin Angiotensin System (RAS) inhibitors, vasodilators, and β-blockers work to facilitate pressure-natriuresis. Also, WNK signaling pathways, soluble inflammatory mediators, and pathways regulating extra-renal sodium disposition may be the focus towards elimination of sodium and reducing blood pressure in hypertension.

Pengenalan

That the kidney plays a role in hypertension is a knowledge that dates back almost 200 years some a researcher postulated that abnormalities in urine production by the kidney altered blood in such a way that tends to increase vascular resistance, leading to high blood pressure and increased cardiac mass. Many years later, Harry Goldblatt also induced malignant hypertension in dogs by obstructing one of the renal arteries [1]. Arthur Guyton and colleagues also advanced a hypothesis suggesting that the kidney governs the level of blood pressure by regulating extracellular fluid volume in 1970. They argued that balance is normally achieved by matching urinary excretion of salt and water with dietary intake, thereby maintaining a constant extracellular fluid volume and blood pressure [2]. They explained that when blood pressure increases for any reason, renal perfusion pressure also increases thereby enhancing sodium and water excretion, which Guyton referred to as pressure-natriuresis.

Based on the capacity for the kidney to excrete sodium, this blood pressure-altering mechanism should have sufficient advantage to limit intravascular volume and consequently lower blood pressure in response to a range of stimuli from elevated heart rate to increase peripheral vascular resistance [2]. Furthermore, a permissive modification of the pressure-natriuresis response has been predictably required to perpetuate a chronic elevation in intra-arterial pressure, whereby the equilibrium point for salt and water excretion is shifted to a higher level of arterial blood pressure [3]. Also, a series of kidney cross-transplantation studies have supported a key role for intrinsic functions of the kidney in the pathogenesis of hypertension [4]. Genetically, compatible donor and recipient strains were used to circumvent rejection, with both native kidneys removed such that the full extent of excretory function is provided by the transplanted kidney [4].

Likewise, studies in spontaneously hypertensive rats and Milan hypertensive rats recapitulated these findings. The same principle seems to also hold true in humans where resistant hypertension can be alleviated after successful kidney transplantation [5]. Collectively, these studies point to the fact that a defect in sodium excretion by the kidney confers susceptibility to elevated blood pressure.

Blood pressure and hypertension

Hypertension is one of the most common chronic diseases of human, affecting more than one billion people worldwide [6]. Although elevated blood pressure does not typically cause overt symptoms, the consequences of chronic hypertension, including cardiac hypertrophy, heart failure, stroke, and kidney disease, are responsible for substantial morbidity and mortality. Treatments that effectively reduce blood pressure can prevent these complications [7]. However, in recent times, blood pressures were reduced to target levels in less than 50% of patients receiving hypertension treatment, and this rate was under 40% in individuals who also had chronic kidney disease (CKD) [8].

The reasons for these poor outcomes include health services issues around processes of care, compliance, and patient education. Moreover, the precise cause of hypertension is not apparent in the vast majority of patients with hypertension. Limitations in understanding of hypertension pathogenesis in individual patients are an obstacle to applying individualized approaches for prevention and treatment and to identifying new, specific therapies.

The kidneys and their influence on blood pressure

The kidneys play a central role in the regulation of arterial blood pressure. A large body of experimental and physiological evidence indicates that renal control of extracellular volume and renal perfusion pressure are closely involved in maintaining the arterial circulation and blood pressure. Renal artery perfusion pressure directly regulates sodium excretion a process known as pressure natriuresis, and influences the activity of various vasoactive systems such as the renin–angiotensin–aldosterone (RAS) system [9]. Along with vessel morphology, blood viscosity is one of the key factors influencing resistance and hence blood pressure. A key modulator of blood viscosity is the renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system (RAAS), a hormone system that regulates blood pressure and water balance.

The blood pressure in the body depends upon:

• The force by which the heart pumps out blood from the ventricles of the heart - and this is dependent on how much the heart muscle gets stretched by the inflowing blood into the ventricles.

• The degree to which the arteries and arterioles constrict-- increases the resistance to blood flow, thus requiring a higher blood pressure.

• The volume of blood circulating round the body if the volume is high, the ventricles get more filled, and the heart muscle gets more stretched.

The kidney influences blood pressure by:

• Causing the arteries and veins to constrict

• Increasing the circulating blood volume

Specialized cells called macula densa are located in a portion of the distal tubule located near and in the wall of the afferent arteriole. These cells sense the Na in the filtrate, while the arterial cells (juxtaglomerular cells) sense the blood pressure. When the blood pressure drops, the amount of filtered Na also drops. The arterial cells sense the drop in blood pressure, and the decrease in Na concentration is relayed to them by the macula densa cells. The juxtaglomerular cells then release an enzyme called renin.

Renin converts angiotensinogen (a peptide, or amino acid derivative) into angiotensin-1. Angiotensin-1 is thereafter converted to angiotensin-2 by an angiotensin-converting enzyme (ACE), found in the lungs. Angiotensin-2 causes blood vessels to contract -- the increased blood vessel constrictions elevate the blood pressure. When the volume of blood is low, arterial cells in the kidneys secrete renin directly into circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin-1. Angiotensin-1 is subsequently converted to angiotensin-2 by the enzyme angiotensin converting enzyme found in the lungs. Angiotensin-2m a potent vasoactive peptide causes blood vessels to constrict, resulting in increased blood pressure. Angiotensin-2 also stimulates the secretion of the hormone aldosterone from the adrenal cortex [9].

Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood. This increases the volume of fluid in the body, which also increases blood pressure. If the renin-angiotensin-aldosterone system is too active, blood pressure will be too high. Many drugs interrupt different steps in this system to lower blood pressure. These drugs are one of the main ways to control high blood pressure (hypertension), heart failure, kidney failure, and harmful effects of diabetes. It is believed that angiotensin-1 may have some minor activity, but angiotensin-2 is the major bioactive product. Angiotensin-2 has a variety of effects on the body: throughout the body, it is a potent vasoconstrictor of arterioles [9].

How the kidneys increase circulating blood volume

Angiotensin-2 also stimulates the adrenal gland to secrete a hormone called aldosterone. Aldosterone stimulates more Na reabsorption in the distal tubule, and water gets reabsorbed along with the Na. The increased Na and water reabsorption from the distal tubule reduces urine output and increases the circulating blood volume. The increased blood volume helps stretch the heart muscle and causes it to generate more pressure with each beat, thereby increasing the blood pressure. The circulating blood volume is directly proportional to the stretch of the heart muscle.

The actions taken by the kidney to regulate blood pressure are especially important during traumatic injury, when they are necessary to maintain blood pressure and conserve the loss of fluids. The body stores calcium in the bones, but also maintains a constant level of calcium in the blood. If the blood calcium level falls, then the parathyroid glands in the neck release a hormone called parathyroid hormone. Parathyroid hormone increases calcium reabsorption from the distal tubule of the nephron to restore the blood calcium level. Parathyroid hormone aside from stimulating calcium release from bone also causes calcium absorption from the intestine.

Vitamin D is also required by the body to stimulate calcium absorption from the kidney and intestine. Vitamin D is found in milk products. A precursor to vitamin D (cholecalciferol) is made in the skin and processed in the liver. The last phase in the conversion of an inactive form of cholecalciferol into active vitamin D takes place in the proximal tubule of the nephron. Once activated, vitamin D stimulates calcium absorption from the proximal tubule and from the intestine, thereby increasing blood calcium levels.

Kidney stones are abnormalities usually caused by problems in the kidney’s ability to handle calcium. In addition, the kidney’s role in maintaining blood calcium is important in the bone disease osteoporosis that afflicts many elderly people, especially women.

The kidneys therefore function in the body to:

• Control the composition of the blood and eliminate wastes by filtration/reabsorption/secretion

• Influence blood pressure by renin secretion

• Help regulate the body’s calcium by vitamin D activation

If for any reason, the kidneys fail to function, then renal dialysis methods (artificial filtration methods) becomes the only alternative to assist the patient to survive by cleansing the blood. This is especially necessary when both kidneys fail.

Mechanisms of blood pressure control by the kidneys

1. Intra-renal actions of the renin-angiotensin system in blood pressure control

The renin-angiotensin system (RAS) is a potent modulator of blood pressure, and dysregulation of the RAS results in hypertension. Pharmacological blockade of the RAS with renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors, or angiotensin receptor blockers effectively lowers blood pressure in a substantial proportion of patients with hypertension [10], reflecting the important role for RAS activation as a cause of human hypertension. While in rodents, deletion of RAS genes lowers blood pressure, overexpression causes hypertension [11].

While The distal tubule cells (macula densa) sense the Na in the filtrate, and the arterial cells (juxtaglomerular cells) sense the blood pressure. Studies have shown that chronic infusion of low doses of angiotensin II directly into the kidney caused hypertension with impaired natriuresis due to a shift of the pressure-natriuresis relationship [12]. It is also believed that the existence of local and independent control of RAS activity within the kidney influencing sodium excretion and blood pressure regulation. In this hypothesis, increased circulating levels of angiotensin II are associated with accumulation of angiotensin peptides in the kidney, upregulated expression of angiotensinogen, the primary RAS substrate, in proximal tubule epithelium, and increased excretion of angiotensinogen and angiotensin peptides in urine [13]. In this feed-forward pathway, angiotensin II acting via type 1 angiotensin (AT1) receptors in the kidney induces local activation of the RAS inside the kidney and increases generation of angiotensin II in the lumen of renal tubules, resulting in autocrine and paracrine stimulation of epithelial transporters [14,15].

Recent studies in support of this idea have verified the critical requirement of ACE within the kidney to fully manifest stimulation of sodium transporter expression, renal sodium reabsorption, and hypertension in the setting of RAS activation [16,17] (Figures 1,2).

Rajah 1: Renal mechanism whereby activation of the renin-angiotensin system reduces pressure natriuresis relationship and leads to hypertension [39].

Gambar 2: A model for local control of RAS activity within the kidney- High levels of angiotensin II (ANGII) in circulation, derived from angiotensinogen (AGT) generated primarily by the liver, are associated with increased ANGII in the kidney, up regulation of AGT in the proximal tubule epithelium, increased levels of AGT in the tubular lumen, generation of ANGII requiring angiotensin-converting enzyme (ACE) expression in the brush border of the proximal tubule (PT), and increased excretion of AGT and ANG peptides in urine [39].

2. Novel Control Mechanisms and Sites of Action for Aldosterone in Hypertension

AT1 receptors in the zona glomerulosa of the adrenal gland stimulate aldosterone release, making aldosterone a downstream effector of the RAS. Activation of the mineralocorticoid receptor (MR) in aldosterone-sensitive nephron segments stimulates assembly and translocation of the subunits of the ENaC. Mutations in ENaC subunits that impair its degradation result in enhanced membrane density and open probability of the channels, resulting in Liddle’s syndrome, characterized by severe, early onset hypertension resembling hyper-aldosteronism, but with low levels of aldosterone [18]. Similarly, activating mutations in the gene encoding the MR also cause hypertension that is exacerbated by steroid hormone alterations during pregnancy [19]. These syndromes may highlight the capacity for dysregulation of the MR/ENaC signaling pathway in the kidney to promote hypertension.

Aldosterone, in addition to stimulation of sodium reabsorption, promotes secretion of potassium into urine. Shibata et al have shown in their studies that regulated phosphorylation of the MR modulates aldosterone responses in the kidney. They showed that phosphorylation of S843 on the MR prevents ligand binding. This form of the MR is present only in intercalated cells of the collecting duct of the kidney where its phosphorylation is differentially regulated by volume depletion and hyperkalemia. For example, in volume depletion, the MR in intercalated cells is dephosphorylated, resulting in potentiation of chloride and sodium reabsorption, allowing a distinct response to volume depletion [20]. Although the MR is classically activated by aldosterone, recent studies suggest that the small GTPase Rac1 may promote hypertension through an MR-dependent pathway, even in the setting of suppressed aldosterone levels (Figure 3).

Rajah 3: Representation of an aldosterone-responsive epithelial cell. The proteins encoded by aldosterone-induced genes are discussed in the text: ENAC α, β, and γ, CHIF, sgk, and RAS are indicated are their known or putative functions [39].

3. The WNKs: Novel Pathways Regulating Renal Solute Transport

Reliable evidence implicating a predominant role for the kidney in the regulation of blood pressure have defined the genetic basis of virtually all of the known Mendelian disorders associated with abnormal blood pressure phenotypes in humans [20-22]. In each case, these mutations impact sodium and fluid reabsorption along the nephron [21]. One of these disorders is pseudo-hypo-aldosteronism type II (PHAII), a Mendelian syndrome characterized by the unusual combination of hypertension and hyperkalemia, found to be caused by mutations in the genes encoding WNK1 (with no lysine [K]) kinase and WNK4 [22]. This discovery triggered intense study of these unique kinases, identifying roles for WNK1 and WNK4 in the regulation of sodium and potassium flux in the distal nephron. These actions are primarily mediated through control of the relative levels and activities of the thiazide-sensitive Sodium (Na) Chloride Cotransporter (NCC) and/or the Renal Outer Medullary Potassium (K) channel (ROMK) [23,24]. The NCC represents a major pathway for sodium reabsorption in the distal nephron and is the target for thiazide diuretics, which are effective and widely used antihypertensive agents [25]. Thiazides are a mainstay of treatment for PHAII, consistent with findings that NCC over-activity is a key feature of the disorder [26]. It is worth noting that while the actions of WNK4 to suppress ROMK activity have been consistent in these studies, variable effects of WNK4 on NCC activity have been observed, perhaps relating to the relative levels of WNK4 in experimental systems. In this regard, mutations causing accumulation of endogenous WNK4 enhance NCC activity possibly through phosphorylation of STE20/SPS-1-related proline-alanine-rich protein kinase (SPAK), whereas deliberate overexpression of WNK4 appears to target NCC for lysosomal degradation [24,27,28] (Figure 4).

Gambar 4: Mechanisms regulating sodium and potassium flux in the distal nephron [33]

WNK family kinases control the activity of the sodium chloride cotransporter (NCC) and the renal outer medullary potassium channel (ROMK) in distal convoluted tubule (DCT) cells in the kidney. WNK1 phosphorylates and stimulates the SPS1-related proline/alanine-rich kinase (SPAK) and oxidative stress-responsive kinase 1 (OSR1) protein kinases, which in turn, promotes NCC-dependent sodium transport. WNK1 may also inhibit ROMK. WNK4 inhibits ROMK but has been reported to have both stimulating and inhibitory actions on NCC depending on the experimental system used. Levels of WNK4 are regulated by the activity of the cullin 3-KLHL3 ubiquitin ligase, which has also been suggested to modulate WNK1.

4. How sodium and potassium flux in the distal nephron is regulated.

Enhanced activity of NCC through modulation of WNKs seems to be a final common pathway for the development of hypertension in a number of scenarios. For example, β-adrenergic stimulation increases blood pressure by suppressing WNK4 and, in turn, enhancing NCC activity [29]. In addition, calcineurin inhibitors commonly used to treat autoimmune disease and prevent transplant rejection, frequently cause hypertension. Recent studies by Ellison et al indicate that the mechanism of hypertension associated with calcineurin inhibitor use involves stimulation of NCC through upregulation of WNK3 [30].

While the ongoing delineation of WNK functions has provided significant insights into kidney physiology, only a small subset of patients with PHAII have mutations in WNK genes. Using exome sequencing, Lifton’s group uncovered mutations in the kelch-like 3 (KLHL3) and cullin 3 (CUL3) genes in patients with PHAII [31]. Moreover, mutations in these two genes accounted for disease in approximately 80% of individuals affected with PHAII [31]. KLHL3 is one of a family of more than 50 broad-complex, tramtrack, bric-a-brac complex–containing (BTB-containing) kelch proteins, characterized by six-bladed, β-propeller domains for binding specific target proteins. CUL3 provides the scaffold for the complex, which includes BTB-domain proteins such as KLHL3 and a RING domain protein that serves as an E3 ubiquitin ligase, targeting specific protein substrates for ubiquitination [32] (Figure 5).

Gambar 5: Effect of changes in mean arterial pressure during chronic changes in sodium intake after angiotensin-converting enzyme (ACE) inhibition, or when angiotensin II was infused at a constant low dose (5 ng/ kg/min) to prevent angiotensin II from being suppressed when sodium intake was raised. (Redrawn from data in Hall et al, 1980) [33].

Salt sensitivity, defined as an exaggerated change in blood pressure in response to extremes in dietary salt intake, is relatively common and is associated with an increased risk for the development of hypertension. Classic Guytonian models suggest that a defect in sodium excretion by the kidney is the basis for salt sensitivity, with impaired elimination of sodium during high-salt feeding leading directly to expanded extracellular fluid volume, which promotes increased blood pressure [34]. This model presumes that the two major components of extracellular volume within the intravascular and interstitial spaces are in equilibrium. As such, accumulation of sodium would be accompanied by commensurate retention of water to maintain iso-osmolality and would thereby proportionally expand the intravascular volume.

However, studies by Titze et al. recently indicated that sodium handling is more complex than this classical two-compartment model the interstitium of the skin may act as a sodium reservoir, buffering the impact of sodium accumulation on intravascular volume and blood pressure [35]. During high-salt feeding, sodium accumulates in the subdermal interstitium at hypertonic concentrations in complexes with proteoglycans [35,36]. Macrophages infiltrating the interstitial space sense hypertonicity caused by this accumulation of sodium in excess of water, triggering expression of TonEBP, a transcription factor regulating the expression of osmo-protective genes. One of the genes induced downstream of TonEBP is vascular endothelial growth factor-C (VEGF-C) [35], a potent inducer of lymph angiogenesis.

In response to high-salt feeding, Titze’s group found robust lymphatic vessel hyperplasia in the dermal interstitium [35]. Depletion of macrophages, cell-specific deletion of TonEBP from macrophages, or specific blockade of VEGF-C prevented hyperplasia of lymphatic vessels and enhanced the level of sodium-dependent hypertension [35-37] demonstrating that this pathway has a key role in the extrarenal control of sodium and fluid volumes. Elevated plasma level of VEGF-C in patients with refractory hypertension was observed, indicating that this system might be perturbed in the human disorder. However, pre-clinical models predict that reduced levels of VEGF-C would promote hypertension [38]. Nonetheless, chronic hypertension in humans is a complex disorder it is possible that the observed elevation in VEGF-C levels may reflect tissue resistance to VEGF-C or even a compensatory response.

Hypertensive kidney injury and the progression of chronic kidney disease

The kidney remains a major site for hypertensive target organ damage which is second only to diabetic nephropathy as a primary cause for end-stage renal disease (ESRD). Moreover, the presence of chronic kidney disease (CKD), including that caused by hypertension, has been shown to be a strong independent risk factor for adverse cardiovascular outcomes. Nevertheless, major aspects of clinical hypertensive renal disease remain poorly understood such as the marked differences in individual susceptibility to hypertensive renal damage and the apparent variable reno-protective effectiveness of antihypertensive classes [40].

Studies have revealed that time-varying SBP was associated with incident CKD, with a steady increase in risk of incident CKD above an SBP of 120 mmHg. Time-weighted SBP was associated with a more rapid decline of kidney function. Diabetes was the strongest predictor of incident CKD, and more rapid decline of kidney function and worse glycemic control were associated with greater risk, thereby supporting the role of BP and other traditional risk factors like diabetes in the initiation and progression of kidney function decline in hypertensive patients with normal kidney function at baseline [41].

Perbincangan

Sodium handling by the kidney is a major determinant of the level of intra- and extra- renal blood pressure, and its under complex physiological control by hormones, inflammatory mediators, and the sympathetic nervous system. It is self-evident that a basic mechanism of efficacy for diuretics and dietary sodium restriction in hypertension is to favorably influence sodium balance and homeostasis. Other antihypertensive agents such as RAS inhibitors, vasodilators, and β-blockers work through a similar mechanism by facilitating pressure-natriuresis. Recent studies have also suggested that WNK signaling pathways, soluble inflammatory mediators, and pathways regulating extra-renal sodium disposition might also be useful targets for enhancing elimination of sodium and reducing blood pressure in hypertension.

The renin-angiotensin system (RAS) is a powerful modulator of blood pressure, and dysregulation of the RAS causes hypertension. Pharmacological blockade of the RAS with renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors, or angiotensin receptor blockers effectively lowers blood pressure in a substantial proportion of patients with hypertension [10], reflecting the important role for RAS activation as a cause of human hypertension. Similarly, in rodent models, deletion of RAS genes lowers blood pressure whereas overexpression causes hypertension [11].

Kesimpulan

There is essential link between the kidney and blood pressure control. An impaired capacity of the kidney to excrete sodium in response to elevated blood pressure is a major contributor to hypertension, irrespective of the initiating cause. In this regard, novel pathways controlling key sodium transporters in kidney epithelia have a critical impact on hypertension pathogenesis, supporting a model in which impaired renal sodium excretion is a final common pathway through which vascular, neural, and inflammatory responses raise blood pressure. The relationship between sodium intake and changes in body fluid volume reveals the mechanism.

Expanded understanding of the role of the kidney as both a cause and target of hypertension to increase knowledge on key aspects of pathophysiology may help lead to identification of new strategies of regulating both intra-and extra- renal blood pressure to help in the prevention and treatment of hypertension.


Measuring Heartbeat Using a Stethoscope

Auscultation of the heart means to listen to and study the various sounds arising from the heart as it pumps blood. These sounds are the result of vibrations produced when the heart valves close and blood rebounds against the ventricular walls or blood vessels. The heart sounds may be heard by placing the ear against the chest or by using a stethoscope . Two major sounds can be heard:

First heart sound . Produced at the beginning of systole when the atrioventricular (AV) valves close and the semilunar (SL the aortic and pulmonary) valves open. This sound has a low-pitched tone commonly termed the “lub” sound of the heartbeat.

Second heart sound . Occurs during the end of systole and is produced by the closure of the SL valves, the opening of the AV valves, and the resulting vibrations in the arteries and ventricles. Owing to the higher blood pressures in the arteries, the sound produced is higher pitched than the first heart sound. It is commonly referred to as the “dub” sound.

*Measure your heart rate and the heart rate of 2 test subjects over a 30 second period. Multiply by 2 to get your heart rate.


Arterial Lines

Prepare pressurized and heparinized flush solution. (See procedure under Hemodynamic Principles).

Flush pressurized closed transducer tubing with luer-lok connections and ports.

Use tubing with inline blood discard reservoir.

Don sterile gloves, protective gown, and mask.

Assist with skin preparation.

Facilitate immobilization of extremity.

Once catheter is inserted, connect pressure tubing and secure site with sterile occlusive dressing & bandage.

Observe waveform and perform a dynamic response test (square wave test).

Level the transducer with phlebostatic axis (See Hemodynamic Principles.)

Zero transducer to air. (See Hemodynamic Principles.)

Compare arterial line pressure with noninvasive cuff reading of blood pressure.

Prevention of nosocomial infections.

Confirm collateral circulation to the hand through the ulnar artery.

1-2 units heparin/mL reduces risk of catheter occlusion through thrombosis.

Removal of ALL air bubbles promotes better waveforms and reduces danger of air embolism.

Maintains closed system while obtaining blood samples.

Arterial line insertion is a sterile procedure

Reduce normoflora microbes at insertion site.

Facilitates access to artery during insertion.

Prevention of dislodgement of arterial catheter will reduce risk of hemorrhage from an artery.

Determines location of the catheter and degree of waveform dampness.

Transducer should be leveled with right atrium to provided accuracy of blood pressure readings.

Insures representation of the patient's BP on the monitor.

Validates reference point for arterial readings.

  1. Check level of transducer with phlebostatic axis.
  2. During first assessment of shift, zero transducer to air.
  3. Assess waveform for dampness.
  4. Record readings on monitor.
  5. During first assessment of shift, compare reading with noninvasive cuff reading of blood pressure.
  1. Insures accuracy of readings.
  2. Insures representation of patient's BP on monitor.
  3. Dampness may distort systolic and diastolic readings.
  4. Systolic/Diastolic (Mean Arterial Pressure)
  5. Verifies reference point for arterial readings.
  1. Membasuh tangan.
  2. Don nonsterile gloves.
  3. Prepare ABG equipment or blood specimen equipment.
  4. Label all syringes or tubes with the patient's information.
  5. Connect syringe or Vacutainer ® with luer-lok adaptor to port nearest patient.
  6. Suspend alarms.
  7. If tubing contains an inline blood discard reservoir, turn stopcock off distal to reservoir and aspirate blood from arterial line. Turn off stopcock between reservoir and external port.
  8. Turn stopcock of proximal port off to transducer (patient to external port).
  9. If there is no reservoir, fill one tube or syringe of blood for discard.
  10. Then collect blood specimen by Vacutainer ® or syringe for blood gases or lab work.
  11. Close external port insuring tubing is open from transducer to patient.
  12. If an inline blood discard reservoir exists, then eject the blood back through the arterial line into the patient.
  13. Check other stopcocks to insure tubing is open between transducer and patient.
  14. Flush arterial line tubing until blood is gone from tubing.
  15. Assess patient's response to the procedure.
  16. Send blood specimen immediately to lab (If ABG's were collected, the specimen must be sent in ice.)
  1. Prevent nosocomial infection.
  2. Protect self from exposure to body fluids.
  3. Preparation of equipment minimizes time during aspiration of blood in arterial line.
  4. Labels beforehand insures specimen results are attributed to the correct patient.
  5. Nearest port reduces how much blood needs to be discarded.
  6. Reduces distressing sounds for patient.
  7. This aspirates blood into reservoir instead of wasting it.
  8. Now port is available for blood aspiration.
  9. If using syringe, use a 5 ml syringe first to collect discarded blood. Discarded blood is mixed with solution from pressure line, so lab values will not be accurate.
  10. Here is the actual collection of the specimen.
  11. Reduces risk of hemorrhage from patient.
  12. Reduces blood loss associated with specimen collections.
  13. Insures patency of arterial tubing system.
  14. Flushing line reduces potential for thrombosis in arterial catheter.
  15. Generally, this is a painless procedure due to the presence of an arterial line, but especially fragile patients may be affected by the loss of even small volumes of blood.
  16. Analysis should be done as soon as possible to prevent chemical reactions or cell changes from occurring due to time delays.

Mean Arterial Pressure (MAP) = Systolic BP + 2(Diastolic BP)

Systolic Blood Pressure: 90 – 120 mm Hg

Diastolic Blood Pressure: 50 – 80 mm Hg

Mean Arterial Pressure: 70 – 100 mm Hg

Assess tubing for presence of air bubbles (most likely during initial preparation and flushing). Remove air bubbles from nearest port. Flush arterial line pressure tubing (dynamic response test). Assess positioning of patient's extremity, particularly the wrist. The patient may require a padded splint to prevent flexion of the wrist.


Central Venous Catheterization

Patients needing secure or long-term vascular access (eg, to receive antibiotics, chemotherapy, or total parenteral nutrition) and those with poor peripheral venous access require a central venous catheter (CVC). CVCs allow infusion of solutions that are too concentrated or irritating for peripheral veins and allow monitoring of central venous pressure (CVP).

CVCs can be inserted through the jugular, subclavian, or femoral veins or via the upper arm peripheral veins (PICC line). Although the type of catheter and site chosen are often determined by individual clinical and patient characteristics, a jugular CVC or PICC line is usually preferred to a subclavian CVC (associated with a higher risk of bleeding and pneumothorax) or femoral CVC (associated with a higher risk of infection). During cardiac arrest, fluid and drugs given through a femoral vein CVC often fail to circulate above the diaphragm because of the increased intrathoracic pressure generated by cardiopulmonary resuscitation (CPR). In this case, a subclavian or internal jugular approach may be preferred.

Ultrasound guidance for placement of internal jugular lines and PICC lines is now standard care and reduces the risk of complications. Coagulopathy should be corrected whenever feasible prior to CVC insertion, and the subclavian approach should not be used in patients with uncorrected coagulopathy because the venipuncture site cannot be monitored or compressed.

The red arrow points to the tip of a left subclavian venous port catheter (placed appropriately in the lower superior vena cava).