M OD UL TUTO R SKENARIO KETIGA

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Tim Kurikulum Pendidikan Preklinik Program Pendidikan Dokter Universitas Islam Malang 2009–2010

SKENARIO KETIGA
Tenggelam Dalam Darah…

URAIAN SCENARIO
Tn. HTM, 28 tahun, kuli bangunan, dibawa ke RS dalam kondisi sesak setelah terjatuh dengan dada membentur batu pondasi bangunan. Dalam perjalanan ke rumah sakit, sesak Tn. HTM memberat dan kondisi tubuhnya makin melemah. Hasil pemeriksan fisik menunjukkan keadaan umum yang lemah, nampak sesak dan kesakitan berat, \ disertai sianotik pada wajah, tangan dan kaki. Tensi 100/60 mmhg, Nadi 110x/menit, irreguler, RR 32 x/menit, asimetris, dengan T.ax. 36,5oC. Didapatkan hematome pada thorax kanan dan fraktur costa 5 - 6 tanpa luka terbuka. Gerakan dinding dada dan suara vesikuler paru kanan menurun dengan perkusi paru kanan yang pekak disertai pergeseran apex jantung dan trachea. Apa yang terjadi pada Tn. HTM & bagaimana keseimbangan asam basanya?

1. IDENTIFIKASI KATA SULIT
HTM = Hemato-Thorax-Masif Kuli bangunan = pekerjaan yang berisiko mengalami trauma akibat kecelakaan kerja apabila tidak menjalankan pekerjaan dengan hati-hati Sesak = Gejala yang timbul akibat gangguan proses respirasi yang ditandai oleh peningkatan Kecepatan respirasi/RR Keadaan umum = Kondisi umum/kondisi pasien secara keseluruhan. N: Baik, sadar dan mampu beraktifitas normal Kasus lemah, sesak & kesakitan = kondisi pasien berat &/ membahayakan jiwa Sianotik = Sianosis = diskolorasi/perubahan warna kulit dan membran mukosa (menjadi biru) akibat konsentrasi berlebihan dari hemoglobin yang tereduksi dalam darah (peningkatan kadarCO2) oleh berbagai sebab. N: Tidak terjadi sianotik di area tubuh manapun Kasus Sianotik pada wajah, tangan dan kaki = peningkatan kadar CO2 pada wajah tangan dan kaki akibat penurunan perfusi ke jaringan perifer (penurunan tekanan darah) dan penurunan jumlah oksigen di jaringan perifer (hipoksia jaringan) akibat gangguan pengembangan dan atau perlukaan paru. Tensi = tekanan darah = tekanan aliran darah yang terbentuk dari resultante kerja jantung dan resistensi perifer. Dinilai melalui tekanan yang dibutuhkan untuk menahan arteri radialis dari awal bunyi korotkoff I s.d. IV. N: Sistole 90 – 120mmhg, Diastole 50 – 80 mmhg. Kasus 100/60 mmhg = Hipotensi yang mengarah pada Pre-Syok akibat nyeri, sesak dan hipoksia.

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Heart Rate = Kecepatan denyut jantung yang dinilai dari jumlah siklus (sistole & diastole) per-menit pada apex jantung menggunakan metode auskultasi. N: 60 – 100 x/menit, reguler, dengan suara siklus sistole dan diastole yang jelas. Nadi = kecepatan denyutan jantung yang dinilai dari jumlah benturan vaskuler pada tangan pemeriksaan dengan metode palpasi pada arteri carotis leher, atau arteri radialis tangan, atau arteri dorsalis kaki. N: 60 – 100 x/menit, reguler, yang kuat, dan bersesuaian dengan HR. Kasus 110, irreguler = Takikardia dengan jarak antar denyut yang tidak sama timbul akibat sesak & kompensasi tubuh akibat hipoksia RR = respiratory rate = kecepatan respirasi yang dinilai dari 1 siklus (inspirasi & expirasi) gerakan dada (kontraksi otot dada) atau gerakan abdomen (kontraksi otot diapragma) dalam 1 menit . N: 12 – 18 x/menit dengan gerakan dada atau gerakan abdomen yang simetris. Kasus 32x/min, asimetris = tachipnea disertai gangguan pada dinding dada dan atau paru disalah satu sisi (kanan) T.ax = temperatur axillla = suhu badan diukur dengan meletakkan termometer axilla pada ketiak selama 3 – 5 menit. N: 36,0oC - 37,5 oC Kasus 36,5oC = normal cenderung rendah. Dapat timbul akibat syok yang membuat extremitas (tangan dan kaki) menjadi dingin dan berkeringat termasuk di axilla. Hematome =Lebam= luka yang timbul akibat pecahnya pembuluh darah dibawah kulit. Kasus lebam pada dada menunjukkan adanya trauma benda tumpul pada dada. Makin besar ukuran lebar, makin besar gaya/trauma yang diterima dada. Costa = Iga = rib Fraktur = pecah/patah/kerusakan/dikontinuitas tulang ditandai dengan krepitasi & nyeri Kasus fraktur costa 5 - 6 tanpa luka terbuka = menunjukkan gaya yang terjadi tidak merobek permukaan kulit dada namun diteruskan kebelakang dada sehingga terjadi pecahnya pembuluh darah bawah iga dan atau penusukan iga yang patah sehingga merobek paru dan pleura. Suara vesikuler paru = suara paru yang terdengar dengan stetoskop saat proses inspirasi dan ekspirasi. N: vesikuler, jelas pada seluruh lapangan paru (atas, tengah, bawah) kanan dan kiri Kasus Suara vesikuler paru kanan menurun = gangguan proses inspirasi dan atau expirasi sehingga suara paru tidak terbentuk dengan baik dan atau terjadi hambatan penghantaran suara paru sehingga suara paru terdengar menurun. Perkusi paru = Proses pemeriksaan paru dengan memukulkan jari pada permukaan paru kanan dan kiri N: Sonor pada seluruh lapangan paru (atas, tengah, bawah) kanan & kiri Kasus perkusi paru kanan yang pekak = terjadi perubahan kepadatan jaringan dibawah jari yang dipukul (ada timbunan darah) sehingga suara perkusi paru jadi pekak Thorax = dinding dada Extremitas atas = tangan Ipsilateral = sisi yang sama dengan sisi yang sakit Apex jantung = Ujung jantung (ventrikel) N: Intercostal Space (ICS) V(5), Mid-Clavicular-Line (MCL) Sinistra (kiri). Kasus pergeseran apex jantung akibat penimbunan darah sisi kanan thorax. Trachea : pipa nafas yang menghubungkan hidung dengan paru N: Posisi Ditengah Kasus pergeseran trachea akibat penimbunan darah pada sisi kanan thorax.

Pengaruh fraktur pada metabolisme kalsium dan fosfat (termasuk magnesium) 6. HTM sesak? 4. Mengapa dan bagaimana terjadinya sianotik & sesak nafas pada Tn. Bagaimana Status asam basa Tn. Apa yang terjadi pada Tn. HTM? 6. Peran pH pada fungsi tubuh manusia 3. Bagaimana mekanisme terjadinya takikardia & peningkatan denyut nadi Tn. Apa pengaruh gangguan paru pada keseimbangan asam basa? 3. Konsep dasar reaksi CO2 + H2O  H2CO3  H+ + HCO32. Penyakit yang menyebabkan gangguan keseimbangan asam basa 8. Peran respirasi pada keseimbangan Asam basa 4. Pengaruh fraktur pada proses asam basa (peran tulang pada proses asam basa) 7. HTM? 5. Mengapa timbul perkusi paru yang pekak dan pergeseran trachea? 10. Mekanisme kompensasi pada gangguan keseimbangan asam basa 9. Mengapa Tn. HTM? 8. Penatalaksanaan gangguan keseimbangan asam basa (overview aja) . Mengapa timbul penurunan gerakan dinding dada & suara vesikuler paru kanan? 9. Peran ginjal pada keseimbangan Asam basa 5. HTM? 7.2. PENENTUAN PROBLEM LIST UTAMA 1. BRAIN STORMING Bacalah tentang: 1. HTM? 2. Mengapa dan bagaimana terjadinya kondisi umum lemah & kesakitan pada Tn. HTM? LAIN-LAIN 3. Bagaimana pengaruh fraktur 5 dan 6 pada kondisi Tn.

toluene) Dipertahankan o/ BUFFER BUFFER FISIOLOGIS Open Buffer (CO2 bs dilepaskan) Closed Buffer (CO2 canNOT excape) OPEN BUFFER SYSTEM H2CO3 H + HCO3 + - Ginjal (hasilkan & buang HCO3-) Alkalosis Metabolik Ingesti alkali Acid Loss (diuretic use.+ H+ (pH 6. & mereabsorbsi HCO3H2O + CO2 Carbonic anhydrase H2CO3  HCO3. gastric suction) Respirasi Pertahankan kadar CO2 darah ⇑ CO2 / ⇑ H+ nafas cepat.+ H+ (weak Base) Hemoglobin Buffer (intraRBC) HbH  Hb. membentuk.Loss = Asam.4) HANYA MENGIKAT TAPI TIDAK BISA MEMBUANG EXCESS ASAM/BASA Ginjal Sekresi/buang H+ (fosfor.35 – 7.+ H+ (pH 6.+ H+ (weak acids) R-NH2  R-NH3. u/ buang CO2 ⇓ CO2 / ⇓ H+ nafas dangkal. Gain = basa Sekresi H+ reabs Na & HCO3Sekresi H+ reabs Na & HCO3- LIVER Buang Excess Asam/basa dlm bentuk urea Bentuk Urea dg menggunakan HCO3- . etyleneglicol.4. renal failure) Alkoholic ketoasidosis Intoxication (Methanol.+ H+ HCO3. CONCEPT MAPPING Asidosis Respiratorik Pada Hipercapnea/hiperkarbia Pada Hipoksia/anoksia Obstruksi Sal nafas (upper/lower) Defek alveolar berat Status asmatikus Ventilatory restriction (gawat thorax Penggunaan sedatif Depresi SSP Peny. vomiting. laktat & keton) di Tub Proximal & ductus colectivus Membuang.3) Oxy-HbH  Oxy-Hb. dpt cepat/lambat u/⇑ CO2 & H+ CO2 oleh Paru HCO3buffer o/ Ginjal & Liver CLOSED BUFFER SYSTEM Phosfate Buffer (TULANG) Ikat produksi asam/basa pada proses mineralisasi & demineralisasi Tulang HCl + Na2HPO4  NaH2PO4 + NaCl NaOH + NaH2PO4  Na2HPO4 + H2O (intraseluler & urine) Protein Buffer (intraseluler) R-COOH  RCOO. Neuromuskular HOMEOSTASIS Aktivitas Enzym Fisiologis tubuh Rx-Rx Metabolisme Alkalosis Respiratorik Hiperventilasi Fever Anxiety Brain disorder EKS CAI ELE pH darah 7. aspirin. dalam.45 Jaringan (Hasilkan CO2) CO2 + H2O Paru (Buang CO2) Asidosis Metabolik Diabetic ketoasidosis Uremia Lactic acidosis Bicarbonate loss (Diare. urat.

Cegah Infeksi . tulang & periosteum Fase fibrosis .Latihan untuk bergerak & batuk bila sudah memungkinkan - Tindakan Gawat Thorax Penentuan jenis luka/Dx Perbaikan fungsi vital/ resusitasi Pembersihan & penutupan luka Rontgen thorax Antibiotik (bl perforasi/terbuka) Tindakan pneumo/hemotho Analgetik k.Pasang penyalir (udara & air) .Pecah vask. ⇑ H2CO3  HCO3.Tutup luka tembus .Pungsi tamponade jantung . gangguan asam basa • • Pelepasan mediator nyeri Perubahan struktur dada ↓ gerak nafas/gerakan dada Robekan Paru kanan Ubah Tekanan negatif pleura & paru Gangguan kemampuan pengembangan paru.MAPPING KASUS UMUM Trauma Individu - Gawat Thorax (Dx & Tx cepat &tepat) Thorax instabil (flail/gail/frail chest) Obstruksi jalan nafas Hematothorax masif Tamponade jantung Pneumothorax (desak/ventil atau terbuka) Kebocoran tracheobronchial Trauma paru akut Tindakan WAJIB Gawat Thorax .fragmen tulang menempel Fase penulangan/osifikasi .Sel kondroblast kondroid tulang rawan .Sel osteoblast osteoid tulang Fase Penyatuan klinis .Sianosis + H2O + ⇑CO2  Fase hematome .p anestesi blok costa - Sesak Nafas Gangguan Ventilasi (dangkal) Pertukaran O2-CO2 di alveoli paru ⇓⇓ Acute Respiratory Distress Syndrome + . sesak nafas & nyeri + Gangguan sistem tubuh & perangsangan Simpatis Syok.Penebalan tulang sesuai garis tekanan & tarikan tulang Fase Konsolidasi . Mesenkim osteogenik .bentuk kalus fibrosis . ganggu proses inspirasi gangguan pertukaran O2 & CO2 di paru Hipoksia paru & jaringan perifer vaskuler paru pecah Perdarahan masuk ke Cavum pleura Hematothorax proses desak ruang menggeser trachea & jantung kearah paru yang sehat (kiri) sesak gagal nafas Paru yang terluka mengempis & terisi darah suara vesikuler paru ↓ .Demineralisasi Tulang .Pembentukan lamellar tulang & pengembalian kekkuatan tulang Fraktur Costae + Metabolisme Calsium & Fosfor pd Fraktur & asam basa.penimbunan Kalsium/mineralisasi Callus tulang .Bebaskan jalan nafas . hipotensi. ) Sekresi H+ & NH4+ Asidosis Respiratorik Kompensasi Metabolik MAPPING KASUS KHUSUS Tn HTM Jatuh Trauma Thorax Kanan diskontinuitas tulang Trauma Benda Tumpul (Batu) Kerusakan vaskuler dekat rongga dada Darah masuk rongga thorax (hematothorax Proses desak ruang Kerusakan vaskuler bawah kulit tanpa kerusakan kulit Ekstravasasi cairan Plasma ke interstitial LEBAM/ HEMATOME dinding dada Gaya yg besar fraktur + Patahan Iga menusuk Paru Gangguan Hemodinamik.bentuk jar.Tangani flail chest (opx pemasangan shark plate) . takikardia.Nyeri hebat .+ ⇑ H+ pH ⇑⇑ (Asidosis Respiratorik) Lini Pertama H+ dibuffer oleh BASA Non-HCO3-Buffer (darah & Intrasel) Kompensasi Renal (⇑ pembentukan & ⇑ reabsorbsi HCO3-.CO2 darah ⇑⇑ .

Mahasiswa dapat menjelaskan mekanisme kompensasi pada gangguan keseimbangan asam basa 8. Tengah = grading pH dan contoh-contoh larutannya Kanan = Reaksi asam-basa dalam cairan. Mahasiswa dapat menjelaskan peran respirasi pada keseimbangan Asam basa 3. PENENTUAN LEARNING OBJECTIVE 1. jenis asam kuat dan asam lemah Kiri Bawah: Using the definitions proposed by Bronsted. Mahasiswa dapat menjelaskan penatalaksanaan gangguan keseimbangan asam basa 6. Mahasiswa dapat menjelaskan peran ginjal pada keseimbangan Asam basa 5. an acid is a substance that can donate H+ ions and a base is a substance that can accept H+ ions . Mahasiswa dapat menjelaskan Pengaruh fraktur pada proses asam basa (peran tulang pada proses asam basa) 7. Mahasiswa dapat menyebutkan penyakit-penyakit yang menyebabkan gangguan keseimbangan asam basa 9. Mahasiswa dapat menjelaskan pengaruh gagal nafas pada keseimbangan Asam Basa 4. SELF DIRECTED LEARNING Konsep dasar pH Kiri = cara menghitung pH. Mahasiswa dapat menjelaskan pengaruh fraktur pada metabolisme kalsium dan fosfat (termasuk magnesium) 6. Mahasiswa dapat menjelaskan fisiologi peran pH pada fungsi tubuh manusia 2.5.

Penambahan asam akan menggeser reaksi untuk membentuk HA sedangkan pengurangan asam (akibat penambahan alkali kuat) akan menyebabkan pergeseran reaksi menjadi H+ + A-. PHOSPHAT & UREA) . yang menunjukkan bahwa stabilitas pH penting untuk mempertahankan reaksi dalam tubuh untuk berjalan secara optimal BUFFER CONCEPTS (ROLE OF BICARBONAT. Hasil titrasi asam kuat dalam larutan buffer menunjukkan perubahan kecil pH walaupun sudah ditambahkan sejumlah besar asam (gambar tengah).Gambar kiri (fig 3): Contoh buffering dari suatu Reaksi HA  H+ + A. Kurva di gambar kanan (fig 5) menunjukkan hubungan antara aktifitas enzym dan pH..

dengan enzym carbonic anhydrase. CO2 lalu berikatan dengan H2O dengan bantuan enzym carbonic anhydrase menghasilkan HCO3(bikarbonat) dan H+. DI PARU (BAWAH) Bikarbonat dalam plasma akan diambil oleh eritrosit & berikatan dengan H+ dengan bantuan enzym carbonic anhydrase akan berubah menjadi CO2 & H2O yang kemudian berdifusi kedalam alveolus untuk dilepaskan sebagai udara EXpirasi Gambar 6 Transport Karbondioksida dalam darah dan Buffer Hemoglobin Buffer Hemoglobin saat mengangkut karbondioksida dalam sel darah merah. akan diubah sesuai reaksi hendelson hasselbach. gambar atas DIJARINGAN (ATAS) CO2 dari proses katabolisme di jaringan masuk ke eritrosit sehingga meningkatkan kadar CO2 dalam eritrosit. H+ yang terbentuk akan diikat oleh hemoglobin (dalam bentuk Hb (hemoglobin) maupun Oxy-Hb (oksihemoglobin).RED BLOOD CELL BUFFER MECHANISM (CLOSED BUFFER SYSTEM) Peran Cl-bicarbonate antiporter dalam mempertahankan elektrostatik potensial dalam eritrosit & pada asam basa S. Bikarbonat kemudian dikeluarkan ke dalam plasma dengan menukarnya dengan ion Cl. Buffer selain bikarbonat disebut sebagai NBB (non bikarbonat buffer) yang menjadi penetral pH line pertama .D. H+ yang ada akan diikat oleh Hemoglobin.

Liver pembentukan urea & buffer Bikarbonat . protein plasma.Respirasi mengendalikan kadar CO2 . fosfat dll) .Non Bikarbonat buffer (hemoglobin. H+. HCO3-.Intake makanan yang mengandung OH-.Faktor yang mempengaruhi pH darah: .Ginjal Mengendalikan kadar H+. CO2 . bikarbonat dan urea .

At the initial fi ltrate pH of around 7. secreted H + ions interact with phosphate buffers and net acid excretion occurs. In the more distal nephron.4 (similar to plasma). Bicarbonate reabsorption depends on the secretion of H + ions into the lumen of the tubule. As bicarbonate is reabsorbed. the new bicarbonate generated in the renal cells by carbonic anhydrase is added to the blood. When buffered acid excretion occurs. . there is a much greater supply of bicarbonate base (HCO3) than of phosphate base (HPO42−).These H+ ions are recycled by carbonic anhydrase and there is no net acid excreted.RENAL HANDLING OF ACID BASE BALANCE Bicarbonate reabsorption Bicarbonate is freely filtered in the glomerulus. Early in the nephron. but most of the filtered bicarbonate is subsequently reabsorbed to maintain normal plasma bicarbonate concentration and therefore the plasma pH. whereas that of the phosphate system is 6. secreted H + ions are used to reabsorb bicarbonate. the end result is the excretion of acid. Hydrogen ion secretion and its effects • When secreted H + ions interact with bicarbonate in the fi ltrate. This happens because the p K a of the bicarbonate system is 6.1. when this bicarbonate reabsorption is complete. urinary pH falls and the buffers accept H + ions.8. • When secreted H + ions interact with a urinary buffer (mainly phosphate or NH 3 ). the end result is bicarbonate reabsorption.

ammonia can diffuse back from both these sites into the thin descending limb. In the early distal tubule. metabolize glutamine to produce ammonia and. H + ions are buffered by phosphate and NH 3 . more distally.mediated phosphorylation of its cytoplasmic tail. Tubular handling of H+ and HCO3− Proximal tubule Of the filtered bicarbonate. Na + /H + exchange is linked to sodium reabsorption and is dependent ultimately on the activity of the basolateral Na + /K + ATPase. • Type A intercalated cells secrete H + ions. Some sodium . this is performed by an apical H + ATPase . The NHE3 Na + /H + exchanger can also transport NH4+ into the tubule. these cells secrete bicarbonate. as the tip of the loop of Henle is alkaline. principally those in the proximal tubule. It can also diffuse into the acidified distal tubules where it is protonated to NH4+ and excreted in the urine. secreted H + ions either contribute to the reabsorption of any remaining bicarbonate or interact with urinary buffers to allow acid excretion. and is inhibited by cAMP and protein kinase A . Present only in the connecting tubule and cortical collecting duct. Most H + ions enter the fi ltrate via the NHE3 Na + /H + exchanger at the apical membrane of the tubular cells. Subsequently. The mechanisms responsible are similar to those in the proximal tubule and again involve carbonic anhydrase. The bicarbonate generated in the cell exits basolaterally via the A E1 HCO3 Cl− − anion exchanger. The principal cells play no direct role in acid – base handling. but their role in normal acid – base homeostasis is unclear. Loop of Henle A further 10 – 15% of fi ltered bicarbonate is reabsorbed in the thick ascending limb of the loop of Henle. promoting H + secretion by type A intercalated cells. but their reabsorption of sodium generates a negative potential in the lumen. the H + ATPase performs this role. . which diffuses in from the medullary interstitium. Also. NH4+ in the filtrate dissociates to form NH 3 and this diffuses into the interstitium. NH4+ can be transported out of the lumen in place of K + on the NKCC2 co . This protein is one of a family of molecules with 10 – 12 transmembrane regions.current fashion. Carbonic anhydrase in the proximal tubule cell cytoplasm and the tubular lumen facilitates the reabsorption of bicarbonate by recycling the secreted H + ions. Secreted H + ions that interact with buffers are not recycled and the new bicarbonate formed in the cell enters the blood. Distal nephron Here. The connecting tubule and cortical collecting duct contain two types of intercalated cells that are rich in carbonic anhydrase. The basolateral Na + 3HCO3−co-transporter ( NBC ) carries most of the bicarbonate out of the cell and into the peritubular plasma. Most proximal tubule H + secretion serves this purpose and does not contribute to net acid excretion. ultimately. • Type B intercalated cells are similar to functionally inverted type A cells with a basolateral H + ATPase and an apical AE1 HCO3 Cl− − exchanger. NH 3 enters the fi ltrate from the tubular cells by simple diffusion and is protonated in the lumen to form NH4+.transporter.Ammonia handling and acid – base balance Tubular cells. 80% is reabsorbed in the proximal tubule.dependent (HCO 3 ) − /Cl − counter .transport may also occur. but also to a lesser extent by a H + /K + ATPase similar to that in the stomach. The bicarbonate enters the blood and the NH4+ ions (which effectively carry a H + ion) are excreted in the urine. In the thick ascending limb of the loop of Henle. to be recycled in a counter . which cannot diffuse out of the tubules. glucose and bicarbonate. Na + /H + exchange still mediates most H + secretion but. Principally.

The NH3 is lipid soluble and easily passes any membrane. In adult person. are present in the base form (RCOO.3 the NH3/NH4+ ratio is 1/100. This diffusion trapping of charged molecules such as NH4+ is called non ionic diffusion . In normal conditions only a small amount of nitrogen is used to produce hepatic glutamate.3) of NH3/NH4+ has the consequence that in gastric juice with a pH of 1. so it reaches the tubular fluid of the collecting ducts and form NH4+ at the low pH (Fig. the (pH-pK). whereas alkalosis stimulates hepatic urea production from hepatic glutamate. This is not so in an alkaline urine. amino acid load is from 90 g of protein (16% nitrogen) daily equals to 14. pyruvic acid etc. and almost all ammonia is in the NH4+ form. The NH4+-secretion into the tubular fluid makes use of the Na+-H+-antiporter. . so virtually all ammonia must be NH4+. there is 5% NH3 of the total. The NH4+ in the proximal tubule cells is in equilibrium with minimal amounts of NH3 at low pH.(and a minimal amount of SO42-) is excreted in the urine. where NH4+ substitutes H+. organic acids such as lactic acid. where a major portion is reabsorbed and accumulated in the interstitial fluid (Fig. In the proximal tubules. Bicarbonate of the extracellular fluid reacts with H+ from hepatic phosphoric and sulphuric acid to form carbon dioxide and water.a general elimination principle for many charged metabolites and drugs.The most important urinary buffer is NH3/NH4+. Most of the phosphoric acid is H2PO4-.difference is -8.3. Even in body fluids with a pH of 7. On a mixed diet the production and excretion of non-volatile acids and bases results in a net excretion of acids equal to the daily net production of non-volatile acids..4 g nitrogen (1 mol) corresponds to 1000 mmol of NH3/NH4+. 17-6). Excretion of NH4+reduces the excretion of other positive ions. and a second by oxidative deamination of glutamic acid forming α –ketoglutarate that is metabolised. According to the equation: 2 NH4+ + 2 HCO3- CO(NH2)2 + CO2 + 3 H2O One mol of nitrogen daily produces 500 mmol urea. With a urine pH of 6. The degree of reabsorption of the water-soluble urea depends upon the tubular flow rate. This is because the synthesis of NH3/NH4+ in the tubule cells is controlled by the acid-base status of the body.5. Secretion of NH4+in the collecting ducts involves a special mechanism. renal glutamate produces NH4+ and α-ketoglutarate. The high pK (=9. which is an excellent atoxic ammonia store that can transfer ammonia to the proximal tubules of the kidneys in cases of acidosis. The NH4+ passes with the tubular fluid to the thick ascending limb of the Henle loop. The H2PO4. glutaminase. 17-5). At a urinary pH of 8. α-hydroxybutyric acid. The charged molecule cannot pass the membrane and it is trapped in the tubular fluid and eliminated in the urine.of Fig. 17-5). One molecule of NH4+is produced by deamination of one glutamine molecule by the enzyme. which is equal to the typical urinary urea excretion (daily urea filtration flux is 900 mmol). Acidosis stimulates NH4+-production from renal glutamate. The α-ketoglutarate is metabolised into bicarbonate.

the titratable phosphate acidity is 30 mmol in a 24 hour urine. The small amount of bicarbonate in the daily urine (zero to 3 mmol) hardly affects the measured titratable phosphate acidity. 17-7. In our example above. the base/acid-ratio is 10/20. where parathyroid hormone (PTH) inhibits phosphate reabsorption (Fig. The active transport of H+ out of the cell is a coupled Na+/H+exchange. Normally. because they are minimally dissociated at pH 6. adrenaline and aldosterone stimulate the Na+-K+-pump. With 30 mmol left in the tubular fluid. The [H+] of the intracellular fluid volume (ICV) is higher than that of the extended ECV. in the proximal tubules.and K+-containing meals.8) being close to urinary pH (6. and that of the intracellular fluid is comparable in the majority of acute conditions.5 to 7. 17-7). and the ammonia buffer is not titrated in acid urine The proton concentrations and buffer bases of the extended ECV and of the ICV The importance of the buffer capacity of the extended ECV. Weak acids are not titrated. which is reabsorbed. which maintains the Na+-gradient across the cell membrane (Fig.4). 17-8) The buffer bases within the cells are proteins. The intracellular pH is precisely controlled in cells with different functions and needs. with extended ECV as the initial distribution volume and the intracellular fluid participating importantly after hours. phosphate and bicarbonate. insulin. Secretion of H+ during the passage of the fluid through the renal tubules converts HPO42.4 (Fig. Carbohydrate.to the acid form.0 -7. the distal H+ -secretion has titrated 14 mmol of HPO42. This is because the alteration of the cellular transport processes takes time. The precise intracellular control is necessary for the pH-sensitive cellular processes with pH-optima for the enzyme systems. in the final urine. . The energy for this exchange is delivered by the Na+-K+-pump. and the range of values is 7. 17-8).5). Acidosis increases the urinary titratable phosphate acidity (towards 50 mmol daily) in order to get rid of the acid. Thus. Phosphate is a threshold substance. the secondary/primary phosphate-ratio is 24/6 mmol as calculated in Fig. Titratable phosphate acidity in the daily urine is the amount of base (mmol) needed to titrate an acidic daily urine back to the pH of plasma and glomerular filtrate (pH 7.4. hyperkalaemia.to H2PO4-.The dominating buffer system in the urine is secondary/primary phosphate. H2PO4-. This is because of its urinary concentration and of its pK (6. A healthy person has a renal filtration flux of phosphate of 180 mmol daily.

whereby intracellular bicarbonate falls. 17-8). . 17-8). which is negligible In an open system such as the body.A bicarbonate-transport protein (capnoforin in the red cell and in many other cell membranes) transfers bicarbonate to the extended ECV by bicarbonate/chloride exchange (Fig. culminating in the restoration of acid-base balance by the renal excretion of the excess H+. Bicarbonate leaves the cells both directly via capnoforin and via other membrane channels (Fig. During metabolic alkalosis movement of H+ out of the cells in exchange of Na+ (Na+-influx in Fig. Although these changes raise the pH toward normal. The chemoreceptors are bathed in extracellular fluid. Rise in P-CO2 of the extracellular fluid is sensed by chemoreceptors & releases a proportionate rise in ventilation & changed pH which is an essential capacity Sequential response to a H+ load. 17-8) also buffers non-volatile base. if not compensated by the lungs. because the reaction is shifted towards formation of CO2 causing a high P-CO2. Intracellular acid accumulation accompanied by hyperkalaemia may develop. where it reacts with proteins. The acid concentration & Buffer capacity are stated in the pic. Response to an increase in the PCO2. phosphate and bicarbonate. The intracellular buffers buffer the H+. the base concentration is reduced by 1 mM to 23. & the acid concentration is increased by 1 mM. Closed & Open System Buffer In the closed system. The K+-output follows the bicarbonate exit. the ventilation simply eliminates excess CO2 & P-CO2 is kept constant. CO2 diffuses rapidly into the cells. Non-volatile acid is also buffered intracellularly during metabolic acidosis by movement of H+ into the cell. acid-base homeostasis will not be restored until ventilation is normalized. This causes a shift towards the right. In disorders with extracellular accumulation of carbon dioxide.

while the alveolar PCO2 remains constant. however. A4). the ratio of the two variables will not change.4 is very low in a closed system for which the pKa of 6.36) is much less than in a closed system. A two-fold increase in the amount of H+ ions produced within the body on a given day (normally 60mmol/day) will result in the added production of 60 mmol more of CO2 per day (disregarding non-bicarbonate buffers). In a closed system from which CO2 cannot escape ( A3).33 kPa. Since non-bicarbonate buffers (NBBs) function in closed systems. An increased supply of OH– ions in the periphery has basically similar effects. the arterial PCO2 (PaCO2) also remains constant.4. The lungs normally eliminate as much CO2 as produced by metabolism (15 000–20 000 mmol/day).5 mmol/L.3 and pKa = 6.2) and pH (7. resulting in the formation of buffer acid (HCO3– + H+ !CO2 + H2O). Mainly intracellular non-bicarbonate buffers provide the remaining buffer capacity.4.2 mmol/l. the arterial PCO2 also does not change in the illustrated example ( B2). The inverse holds true for the addition of hydroxide ions (OH– + CO2 !HCO3–). The total concentration changes in response to changes in the hemoglobin concentration.Bicarbonate/Carbon Dioxide Buffer The pH of any buffer system is determined by the concentration ratio of the buffer pairs and the pKa of the system. NBBs supplement the HCO3–/CO2 buffer in non-respiratory (metabolic) acid–base disturbances. and the pH will remain constant. Since the plasma PCO2 adapts to the alveolar PCO2 during each respiratory cycle.93( A3). making the pH fall to 6. bicarbonate buffering occurs in an open system in which the partial pressure (PCO2) and hence the concentration of carbon dioxide in plasma are regulated by respiration ( B). even after buffering.2. An increased supply of H+ in the periphery leads to an increase in the PCO2 of venous blood (H+ +HCO3–!CO2 +H2O) ( B1). Since OH– +CO2 !HCO3–. [HCO3–] increases and the venous PCO2 becomes smaller than normal.1 is too far fromthe target pH of 7. since hemoglobin is the main constituent of NBBs. The following example demonstrates the quantitatively small impact of increased pulmonary CO2 elimination. This corresponds to only about 0.2 ( A2) changes to 22/3.3% of the normal daily CO2 elimination rate. the aforementioned baseline ratio [HCO3–]/[CO2] of 24/1. When added to a buffered solution. After addition of 2 mmol/L of H+. Thus. but are the only effective buffers in respiratory acid–base disturbances . H+ ions combine with the buffer base (HCO3– in this case). At a pH of 7. Given log20 = 1. If. The corresponding decrease in the [HCO3–]/[CO2] ratio (22/1. as defined in the Henderson–Hasselbalch equation ( A1). their total concentration ([NBB base] + [NBB acid]) remains constant. Because the rate of CO2 elimination is also reduced. In the body. If [HCO 3–] drops to 10 and [CO2] decreases to 0. only the [HCO3–] will change when the same amount of H+ is added (2 mmol/L). [HCO3–]/[CO2] = 24/1.2 = 20. the amount of buffer acid formed (CO2) equals the amount of buffer base consumed (HCO3–). The lungs eliminate the additional CO2 so quickly that the arterial PCO2 remains practically unchanged despite the addition of H+ (open system). The pH of a bicarbonate solution is the concentration ratio of bicarbonate and dissolved carbon dioxide ([HCO3–]/[CO2]). a pH of 7. however. Given [HCO3–] = 24 mmol/L and [CO2] = 1. the open HCO3–/CO2 buffer system makes up about two-thirds of the buffer capacity of the blood when the PCO2 remains constant at 5. the additionally produced CO2 is eliminated from the system (open system. the buffer capacity of the HCO3–/CO2 buffer at pH 7.1.4 is derived when these values are set into the equation ( A2).

moves downward as a piston at the floor of the thorax. At the brush border of the proximal tubule cell. The main elements of ventilation are the respiratory pump. brain stem.reabsorption is accomplished by means of H+ secretion. The ventilatory system is responsible for maintaining the arterial carbon dioxide tension (PaCO2) within normal limits by adjusting minute ventilation (V•) to match the rate of carbon dioxide production. A change in Na+. Inspiratory muscle contraction lowers pleural pressure (Ppl) thereby inflating the lungs (_V).Reabsorption of bicarbonate in the proximal and distal parts of the nephron. and the loads that oppose such action. In the intercalated cells of the collecting ducts.reabsorption. the reabsorption is dependent on a proton-K+-ATPase. Most of the filtered HCO3. Normal Daily filtration flux HCO3-amounts to 4500 mmol. which involves the intracellular space & stimulates production of proton-K+ -ATP-ases. and the elastic recoil of the lungs and chest wall. phrenic and intercostal nerves.ion crosses the basolateral cell membrane in exchange of chloride through a chloride-bicarbonate antiporter. carboanhydrase (CA) catalyses the reaction. spinal cord. The strength of the respiratory pump is evaluated by the pressure generated (_P = Ppl .flux is matched by a similar change in proximal HCO3-reabsorption. so CO2 is formed and can enter the cell easily by diffusion Also within the cell. The cells of the thick ascending limb of the Henle loop also reabsorb HCO3by the same mechanism as in the proximal tubule. including the airway flow resistance. The ventilatory requirement influences the load by altering the frequency and depth of the ventilatory cycle. . HCO3-reabsorption is stimulated. the most important inspiratory muscle.homeostasis alters the HCO3-reabsorption secondarily. Acidosis.enters the distal tubules. whereas alkalosis inhibits HCO3. which is thus not excreted in the urine. The small residue of HCO3. Any change in the filtered HCO3.produced in the cell from CO2 of tubular fluid. The Na+-K+-pump in the basolateral membrane provides the energy for the secretion of H+ into the tubular fluid. The inspiratory decrease in Ppl by the respiratory pump must be sufficient to counterbalance the opposing effect of the combined loads.ion diffuses to the interstitial phase & the renal venous blood back to the body. where it is reabsorbed almost totally through a special mechanism independent of Na+. When the tubular fluid reaches the collecting ducts an important H+secretion is mediated by a proton. The daily tubular secretion of H+ is enormous. For each HCO3. The machinery of the respiratory pump includes the cerebrum. which generates a pressure gradient responsible for air flow. where the luminal membrane contains a Na+-H+-antiporter. Hereby. Both effects favour H+-secretion and thus HCO3. The HCO3. and the muscles of respiration. Main components of the ventilatory system.K+-ATPases of the intercalated cells and the Na+-reabsorption/K+ -secretion of the principal cells.K+-ATPase in the intercalated cells. because we excrete 70 mmol of non-volatile acid and also have to match almost all of the total filtration flux of HCO3-. also favours H+-secretion.Pabd). Most H+ secreted in the proximal tubules is derived from Na+.reabsorption by the opposite mechanisms. raising abdominal pressure (Pabd).H+-exchange through antiporter. CA facilitates the production of (H+ + HCO3-). The diaphragm. This secretion serves to reabsorb the filtered HCO3-.flux is reabsorbed in the proximal tubules. HCO3. This special mechanism is most likely ineffective in distal renal tubular acidosis. Aldosterone stimulates the proton. one HCO3.

.

.

.

2 Respiratory alkalosis. the correct diagnosis can be reached. Please observe that each point on the chart can be reached in several ways. 3 Metabolic acidosis and 4 Metabolic alkalosis. Van Slyke. and alkalosis (alkalaemia or baseosis) is defined as a condition with a pH-a > 7. Acidosis (acidaemia) is defined as a disorder with pH in the arterial blood (pH-a) less than 7. together with the normal condition. 17-13) and a metabolic acidosis due to diabetic coma. The first example is a case of respiratory acidosis due to chronic obstructive lung disease (COLD in Fig. who made the first apparatus to diagnose acidbase disturbances.The Siggaard-Andersen acid-base chart with the 9 conditions of van Slyke Humans can suffer from 4 acid-base disorders: 1. and compensated by altered renal excretion of acid in a matter of days. The second example is a case of respiratory alkalosis due to acute mountain sickness (AMS). Instantaneous intubation & oxygenation with 50-40-30 % oxygen can saved the newborn PENYEBAB UMUM HIPOKSIA/ANOKSIA ASIDOSIS RESPIRATORIK . because the patient is loosing acid by vomiting. is called the nine van Slyke conditions (Fig. Respiratory acid-base disorders are caused by primary changes of PCO2. and compensated partially by the lungs in a matter of hours. emphasised the importance of the case history and common clinical sense.45. 17-13). 17-13). Plotting the measured pH and P-CO2in the acid-base chart allows estimation of the base excess (BE). Each of these two disorders has respiratory and metabolic forms. Metabolic acid-base disorders are caused by primary changes in BE.35. Respiratory acidosis. The importance is illustrated by the following three examples. These four primary acid-base disturbances and their four compensated or chronic types constitute. The third example is a serious case of birth anoxia with a combined respiratory and metabolic acidosis. Without the case history it is difficult to diagnose the primary and secondary events in the development of the patients condition. The final correction of metabolic disorders is always renal and takes several days. and combined with the case history. complicated by a metabolic alkalosis (AMS in Fig.

chronic bronchitis and emphysema). the urinary H+-excretion (mainly NH4+ but also H2PO4-) with a virtually complete reabsorption of filtered bicarbonate.HEMATOTHORAX MASIF PENYEBAB ASIDOSIS RESPIRATORIK PADA KASUS Acute respiratory acidosis with a base excess of zero. one mol of non-carbonic buffer base is eliminated. The slope of the BE -zero line depicts the buffer-base capacity of the extended ECV. artificial ventilation is necessary. Hypoventilation is associated with an impaired ability to eliminate CO2. . anaesthesia. the renal ammonia production. polio. 17-9). For each mol of bicarbonate produced. This is often the case in the terminal phase of chronic obstructive lung disease (ie. near drowning and myasthenia gravis. This is because the high intracellular [H+] increases the glutaminase synthesis and activity. drug overdose. strangulation. Other causes of respiratory acidosis are asthma. Any primary respiratory disorder is compensated renally over days. pulmonary cancer or tuberculosis. 17-9) In severe cases of chronic CO2 accumulation. which means that Base Excess (BE) is unchanged zero (Fig. whereby P-a-CO2 increases and the accumulated CO2 reduces the arterial pH. BE becomes positive during compensation (arrow in Fig. and its compensation Respiratory Acidosis is caused by hypoventilation (or breathing of CO2 containing air). Hereby.

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17-10). Hyperventilation before underwater swimming eliminates the CO2 stimulus and shifts the oxyhaemoglobin dissociation curve towards the left. This is called totally compensated respiratory alkalosis. simple rebreathing from a bag cures the disorder within minutes. Loss of consciousness below water is often fatal. muscle cells and the myocardial syncytium. These patients often experience tetanic cramps. The equilibrium dislocates towards the right in alkalosis. and the alkalosis inhibits formation and secretion of NH4+.Acute respiratory alkalosis and its compensation The hyperventilation is disproportionately high compared to the CO2 production. The dissociation leads to tetany: Protein + Ca2+ Ca-proteinate + 2 H+. which stimulates the chemoreceptors to hyperventilation (CO2 -wash-out).In cases of asthma-anxiety or hysteria with hyperventilation tetany. whereby the P-a-CO2 falls & the pH increases/alkali (Fig. Acute respiratory alkalosis is compensated by increased renal excretion of bicarbonate. Hereby. which is the result of decreased tubular H+secretion. The Na+-influx reduces the membrane potential and increases the excitability of the tissues. Dissociation of protein molecules occurs in all types of alkalosis in order to liberate H+. After a few days the renal compensation of the respiratory alkalosis is complete. As long as no non-carbonic acid or base is added to the extra-cellular fluid volume. As the P-a-CO2 falls with increasing altitude. which causes tetanic cramps (almost continuous muscular contractions). one mol non-carbonic buffer base is formed. the extracellular base excess remains unchanged (zero). . This is a typical reaction to high altitude. so it takes days to become effective. This is because the low P-a-CO2 reduces the tubular H+-secretion. blackout and grey-out occurs. oxygen is bound firmly to haemoglobin.Ca2+-pumps and opens Na+-channels in the cell membranes of neurons. which means that BE is maintained at zero (Fig. When the P-a-O2 falls below 30 mmHg (4 kPa). . When the alveolar ventilation is doubled. 1710). The renal mechanisms affect the production and activity of cellular enzymes and hormones. The falling extracellular  Ca2+ activates Na +. the Pa-O2 eventually falls below 55 mmHg. and the pH is normal. For each mol of bicarbonate eliminated. Other typical cases are the anxious patient during an attack of asthma or the hysterical hyperventilation in neurotic patients. the P-a-CO2 is halved.

Metabolic acidosis is diagnosed by negative base excess. Acidosis shifts the oxygen dissociation curve to the right (ie. H+-ions from the cells enter the extended ECV and a further bicarbonate infusion is necessary. K+-loss from the cellular pool may lead to K+-deficiency. and a new equilibrium with too much CO2. The iso-base excess-line (-15 mM) is steeper than the base excess-zero line. Kidney disease with destruction of a large number of nephrons reduces the tubular capacity to excrete H+ and NH4+ in the urine. The primary strategy is to eliminate the lack of base of the extended ECV. Administration of an overshoot of Na+-bicarbonate leads to volume expansion. cause excess production. which are surrounded by the extended ECV and stimulated by its hydrogen ion concentration to react with hyperventilation. Hours later. Continuous control of acid-base variables over days is therefore important. Acidosis stimulates K+-loss from the cellular pool. Careful monitoring of acid-base variables is necessary. which diffuses into the cells. Two errors are possible. Diarrhoea causes acidosis by loss of bicarbonate with the faeces. because both types of buffer bases are reduced. . worsening the intracellular acidosis. the cellular K+-efflux may lead to hyperkalaemia. A rapid decrease in [Ca2+] releases tetanic cramps (see alkalosis). This strategy is accomplished by infusion of approximately X mmol bicarbonate (X= negative BE in mM multiplied by extended ECV). Hunger (hunger diabetes). The extended ECV is approximately 20% of the body weight in kg or l. however. Renal tubular acidosis is a damage of tubular cells caused by drugs or immunological reactions . inhibits 2. the Bohr effect). The compensation is shown with an arrow. 17-4). increasing the delivery of oxygen to the tissues. The impaired H+ secretion reduces the tubular bicarbonate reabsorption. which tends to shift the oxygen dissociation curve back towards the left When renal function is normal. lactic acid accumulation or high protein intake with increased production of hydrochloric and sulphuric acid.3-DPG production. Another type of lactic acidosis is caused by decreased hepatic lactate metabolism .often drug-induced. diabetic ketoacidosis. In Fig. which develops over hours as a reduction in Pa-CO2 (Fig. Impaired renal H+-excretion is related to increased loss of bicarbonate in the urine (due to renal failure). Lactic acidosis is caused by increased lactic acid production during exercise.Acute metabolic acidosis: The base excess is reduced. Insulin must be given in diabetic ketoacidosis. because of excess production or impaired H+-excretion. whereas the iso-base excess-line (+15 mM) is less steep than the BE-zero-line. The chloride-bicarbonate antiporter of the intercalated cells of the collecting ducts is probably ineffective (see above).or it may be inherited. 17-11). Any loss of bicarbonate in the urine or faeces is equivalent to an addition of H+to the extracellular fluid (Fig. A patient with metabolic acidosis and a base excess of -15 to -25 mM may have to be treated with bicarbonate infusion. due to the relative low pK-values of essential buffers. When renal K+-secretion is impaired. This hyperventilation is a respiratory compensation. because of K+-efflux from the cells (Fig. This compensation is caused by the chemoreceptors. Chronic acidosis. pulmonary oedema. Rapid infusion of bicarbonate may be dangerous. Oxygen enriched air is administered in cases of lactic acidosis with poor tissue bloodflow. Metabolic Acidosis is caused by accumulation of strong acids in the extended ECV. and causing bicarbonate efflux accompanied by hyperkalaemia. The final correction of a metabolic acidosis is always renal. Strong acids accumulate. The patient with metabolic acidosis suffers from dyspnoea (deep and frequent Kussmaull respiration). 17-11). shock. Correction of the primary disease (insulin to diabetic ketoacidosis) may in itself cure the acidosis by combustion of keto-acids to bicarbonate with the danger of overinfusion with bicarbonate. 17-11 both types of buffers and the total concentration of buffer bases of the extended ECV are clearly reduced and the BE is -15 mM. anoxia or following cardiac arrest.

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17-12). Cerebral insufficiency is common in alkalosis.has a molecular weight 17 times larger than H+. the acid of choice is an ammonium chloride solution. A patient with metabolic alkalosis is therefore rarely treated with infusion of acids. This increases renal bicarbonate reabsorption and leads to metabolic alkalosis. Protein anions bind Ca2+ during alkalosis. Vomiting (loss of gastric acid and volume depletion). K+ and Mg2+ are corrected. The hypoventilatory compensation is shown with an arrow Metabolic Alkalosis is caused by a primary accumulation of strong bases in the extended ECV. Each OH. and excessive intake of bases towards gastric ulcer can cause this form of alkalosis. K+deficiency. but raises Pa-CO2. This correction is also counteracted by the rise in Pa-CO2. impairing the delivery of oxygen to the tissues. and excess secretion of mineralocorticoid increase the H+-secretion in exchange for Na+ in the distal tubules. so the BE is increased (Fig. The compensation is never total. Careful monitoring with replacement of Na+ and K+ is essential. . when deficits of NaCl. which is the renal plasma concentration threshold for reabsorption. The actual [bicarbonate] is often above 27 mM. since the rise in Pa-CO2and the fall in Pa-O2in itself oppose the hypoventilation.passes the membrane channels comparatively slowly in metabolic alkalosis compared to the H+-transfer of metabolic acidosis. Above this threshold lots of bicarbonate is lost in the urine. Both the [bicarbonate] and the [noncarbonic buffer base] is increased. so OH. whereby the bicarbonate excretion is increased. whereby the bicarbonate excretion is reduced. in order to improve the renal excretion of bicarbonate. Untuk metabolisme kalsium & Fosfor baca literatur yang disertakan sebelumnya (MODUL TUTOR 2) . The final renal correction of metabolic disorders takes several days. Such cases must be treated with NaCl and KCl. when NH3 is used for carbamide (urea) production in the liver. Only rarely is it necessary to infuse acid. Long-term use of thiazides and loop diuretics. In the very few cases. This results in delayed intracellular transfer and buffering of the alkalosis. which stimulates tubular bicarbonate reabsorption. increased metabolism of lactate and citrate (turns into bicarbonate and water). In metabolic alkalosis the kidneys increase H+-secretion less than the bicarbonate filtration. The delayed renal correction increases bicarbonate excretion by reducing its reabsorption.Metabolic alkalosis combined with hypokalaemia and reduced ECV often has increased H+-secretion. reduces the free serum [Ca2+] and triggers tetanic cramps. The hypoventilatory compensation reduces pH. which produce H+. Dissociation of protein molecules may lead to tetany.Acute metabolic alkalosis: BE is increased. and the respiratory centre is depressed. Alkalosis displaces the oxyhaemoglobin dissociation curve to the left. Metabolic alkalosis is difficult to compensate by the body and difficult to treat.

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Luka lecet. sesuai aliran cairan Kulit pucat.TRAUMA : Sifat penyebab Mekanik Jenis penyebab Benda tumpul Benda tajam Senjata api Suhu tinggi Api / Udara Benda padat Benda cair Suhu rendah Udara Arus listrik AC DC / petir Asam kuat Basa kuat Akibatnya Luka memar. Shot gun Fisik Kematian jaringan Rangsangan otot. keras. saraf. jantung Efek panas. Luka iris. Luka robek Kombinasi Luka tusuk. Efek mekanik Kulit kering. Luka bacok Gun. teraba licin Kimia . coklat.

Professional Guide to Signs and Symptoms. KKI. EGC. . Ganong WF. Foulk L. Comerford KC. Saunders Elsevier. Hall JE. No 4 (pengaruh fraktur pada metabolisme kalsium dan fosfat (termasuk magnesium). 1998. Robbins SL. la-Rocca JC. Jakarta 8. Horne MM. WB Saunders. Granner DK. Henry K. Penerbit buku kedokteran EGC. Inc. LO nomor 1 (fisiologi peran pH pada fungsi tubuh manusia). McGraw-Hill Companies. McGraw-Hill. 2007. USA 10. elektrolit dan asam basa. USA 6. USA 18. Ganong WF. 2008. 23rd ed. Rang And Dale’s Pharmacology. No 2 (peran respirasi pada keseimbangan Asam basa). Dale MM. 2000. London. Netter FH. Ritter JM. USA 3. No 6 (mekanisme kompensasi pada gangguan keseimbangan asam basa) harus tercapai minimal 68% penguasaan materi dasar dalam konsep mapping & mapping kasus 3. Kumar V. 2007. 7th edition. 5th Edition. Goldman L. 2nd Edition. 2003. 17th Ed. 2007. USA 4. Edisi terjemahan. Putterman A. USA. 14. Mc Graw Hill. DAFTAR PUSTAKA 1. Philadelphia. Textbook of Medical Physiology. Chemistry. Icon Learning System. Flower RJ. 2006. Otto SL. Mayes PA. Post TW. 21th edition. Jakarta 9. Review of Medical Physiology. USA 5. Jakarta 11. Buku Saku mengenal penyakit melalui Pemeriksaan laboratorium. Robins Basic Pathology. Edisi 2. Amara Books. 2001. Guyton AC. McPhee SJ. Roe PG. Lingappa VR. Clinical Physiology of Acid-Base and Electrolyte Disorders. 1997. 2003. Ferri FF. 6th Edition.7. REPORTING 1. Netter’s Internal Medicine. 25th Edition. No 3 (peran ginjal pada keseimbangan Asam basa). Weinstock D. Rose BD. Holmes NH. Yogyakarta 2. Standar Kompetensi Dokter. WB Saunders Co. Fluid Balance & Volume Resuscitation for beginners. USA 7. 2000. Keseimbangan cairan. Ferri's Clinical Advisor Instant Diagnosis And Treatment. No 7 (penyakit-penyakit yang menyebabkan gangguan keseimbangan asam basa) & No 8 (Penatalaksanaan gangguan keseimbangan asam basa) 8. LO no 5 (Pengaruh fraktur pada proses asam basa (peran tulang pada proses asam basa)). Ausiello D (ed). Chang R. Harrison's Principles Of Internal Medicine. USA 13. McGraw Hill. Lippincott Williams & Wilkins. Mosby Elsevier. Philadelphia. Rodwell VW. Murray RK. 2001. AY Sutedjo. Harper’s Biochemistry. USA 16. Robinson JR. Lange JD. Bilotta K. Runge MS. Cotran RS. 1998. Tutor menggali kembali keberhasilan belajar mahasiswa melalui pertanyaan yang mengarah pada kemampuan mahasiswa menjelaskan LO yang ada 2. Fauci et al. an Introduction to Clinical Medicine. 2000. Cecil Medicine. Churchill Livingstone. Greganti MA. McGraw Hill. Houska A. USA 12. 2008. 17. Appleton & Lange. 10th Edition. USA. McCann JAS. 2007.. Greenwich Medical media. Konsil Kedokteran Indonesia. Pathophysiology of Disease. 5th Edition. Swearingen PL. Terapi Intravena. USA 15. Rang HP. 2003. Park GR.

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