M OD UL TUTO R SKENARIO KETIGA

Nama Tutor NPP / Kelompok

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Tim Kurikulum Pendidikan Preklinik Program Pendidikan Dokter Universitas Islam Malang 20092010

SKENARIO KETIGATenggelam Dalam Darah

URAIAN SCENARIOTn. 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 SULITHTM = 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.

2. PENENTUAN PROBLEM LISTUTAMA 1. Apa yang terjadi pada Tn. HTM? 2. Bagaimana Status asam basa Tn. HTM? LAIN-LAIN 3. Mengapa Tn. HTM sesak? 4. Mengapa dan bagaimana terjadinya kondisi umum lemah & kesakitan pada Tn. HTM? 5. Mengapa dan bagaimana terjadinya sianotik & sesak nafas pada Tn. HTM? 6. Bagaimana mekanisme terjadinya takikardia & peningkatan denyut nadi Tn. HTM? 7. Bagaimana pengaruh fraktur 5 dan 6 pada kondisi Tn. HTM? 8. Mengapa timbul penurunan gerakan dinding dada & suara vesikuler paru kanan? 9. Mengapa timbul perkusi paru yang pekak dan pergeseran trachea? 10. Apa pengaruh gangguan paru pada keseimbangan asam basa?

3. BRAIN STORMINGBacalah tentang: 1. Konsep dasar reaksi CO2 + H2O H2CO3 H+ + HCO32. Peran pH pada fungsi tubuh manusia 3. Peran respirasi pada keseimbangan Asam basa 4. Peran ginjal pada keseimbangan Asam basa 5. Pengaruh fraktur pada metabolisme kalsium dan fosfat (termasuk magnesium) 6. Pengaruh fraktur pada proses asam basa (peran tulang pada proses asam basa) 7. Penyakit yang menyebabkan gangguan keseimbangan asam basa 8. Mekanisme kompensasi pada gangguan keseimbangan asam basa 9. Penatalaksanaan gangguan keseimbangan asam basa (overview aja)

4. CONCEPT MAPPINGAsidosis 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. Neuromuskular HOMEOSTASIS Aktivitas Enzym Fisiologis tubuh Rx-Rx Metabolisme Alkalosis Respiratorik Hiperventilasi Fever Anxiety Brain disorder

EKS CAI ELE

pH darah 7,35 7,45

Jaringan (Hasilkan CO2) CO2 + H2O Paru (Buang CO2) Asidosis Metabolik Diabetic ketoasidosis Uremia Lactic acidosis Bicarbonate loss (Diare, renal failure) Alkoholic ketoasidosis Intoxication (Methanol, etyleneglicol, aspirin, 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, vomiting, gastric suction)

Respirasi Pertahankan kadar CO2 darah CO2 / H+ nafas cepat, dalam, u/ buang CO2 CO2 / H+ nafas dangkal, 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- + H+ (weak acids) R-NH2 R-NH3- + H+ (weak Base) Hemoglobin Buffer (intraRBC) HbH Hb- + H+ (pH 6.3) Oxy-HbH Oxy-Hb- + H+ (pH 6.4) HANYA MENGIKAT TAPI TIDAK BISA MEMBUANG EXCESS ASAM/BASA

Ginjal Sekresi/buang H+ (fosfor, urat, laktat & keton) di Tub Proximal & ductus colectivus Membuang, membentuk, & mereabsorbsi HCO3H2O + CO2 Carbonic anhydrase H2CO3 HCO3- + H+ HCO3- Loss = Asam, Gain = basa Sekresi H+ reabs Na & HCO3Sekresi H+ reabs Na & HCO3-

LIVER Buang Excess Asam/basa dlm bentuk urea Bentuk Urea dg menggunakan HCO3-

MAPPING KASUS UMUMTrauma 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 akutTindakan WAJIB Gawat Thorax - Bebaskan jalan nafas - Pasang penyalir (udara & air) - Tutup luka tembus - Tangani flail chest (opx pemasangan shark plate) - Cegah Infeksi - Pungsi tamponade jantung - Latihan untuk bergerak & batuk bila sudah memungkinkan

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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.p anestesi blok costa

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Sesak Nafas Gangguan Ventilasi (dangkal) Pertukaran O2-CO2 di alveoli paru Acute Respiratory Distress Syndrome + - Nyeri hebat - CO2 darah - Sianosis + H2O + CO2

Fase hematome - Demineralisasi Tulang - Pecah vask. tulang & periosteum Fase fibrosis - bentuk kalus fibrosis - fragmen tulang menempel Fase penulangan/osifikasi - bentuk jar. Mesenkim osteogenik - Sel kondroblast kondroid tulang rawan - Sel osteoblast osteoid tulang Fase Penyatuan klinis - penimbunan Kalsium/mineralisasi Callus tulang - Penebalan tulang sesuai garis tekanan & tarikan tulang Fase Konsolidasi - Pembentukan lamellar tulang & pengembalian kekkuatan tulang

Fraktur Costae +

Metabolisme Calsium & Fosfor pd Fraktur & asam basa.

H2CO3

HCO3- + H+

pH (Asidosis Respiratorik)

Lini Pertama H+ dibuffer oleh BASA Non-HCO3-Buffer (darah & Intrasel)

Kompensasi

Renal ( pembentukan & reabsorbsi HCO3-, ) Sekresi H+ & NH4+

Asidosis Respiratorik Kompensasi Metabolik

MAPPING KASUS KHUSUSTn 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, sesak nafas & nyeri + Gangguan sistem tubuh & perangsangan Simpatis Syok, takikardia, hipotensi, 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, 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

5. PENENTUAN LEARNING OBJECTIVE1. Mahasiswa dapat menjelaskan fisiologi peran pH pada fungsi tubuh manusia 2. Mahasiswa dapat menjelaskan peran respirasi pada keseimbangan Asam basa 3. Mahasiswa dapat menjelaskan pengaruh gagal nafas pada keseimbangan Asam Basa 4. Mahasiswa dapat menjelaskan peran ginjal pada keseimbangan Asam basa 5. Mahasiswa dapat menjelaskan pengaruh fraktur pada metabolisme kalsium dan fosfat (termasuk magnesium) 6. Mahasiswa dapat menjelaskan Pengaruh fraktur pada proses asam basa (peran tulang pada proses asam basa) 7. Mahasiswa dapat menjelaskan mekanisme kompensasi pada gangguan keseimbangan asam basa 8. Mahasiswa dapat menyebutkan penyakit-penyakit yang menyebabkan gangguan keseimbangan asam basa 9. Mahasiswa dapat menjelaskan penatalaksanaan gangguan keseimbangan asam basa

6. SELF DIRECTED LEARNING

Konsep dasar pH Kiri = cara menghitung pH. Tengah = grading pH dan contoh-contoh larutannya Kanan = Reaksi asam-basa dalam cairan, jenis asam kuat dan asam lemah Kiri Bawah: Using the definitions proposed by Bronsted, an acid is a substance that can donate H+ ions and a base is a substance that can accept H+ ions

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

BUFFER CONCEPTS (ROLE OF BICARBONAT, PHOSPHAT & UREA)

RED BLOOD CELL BUFFER MECHANISM (CLOSED BUFFER SYSTEM)Peran Cl-bicarbonate antiporter dalam mempertahankan elektrostatik potensial dalam eritrosit & pada asam basa S.D. gambar atas DIJARINGAN (ATAS) CO2 dari proses katabolisme di jaringan masuk ke eritrosit sehingga meningkatkan kadar CO2 dalam eritrosit. CO2 lalu berikatan dengan H2O dengan bantuan enzym carbonic anhydrase menghasilkan HCO3(bikarbonat) dan H+. Bikarbonat kemudian dikeluarkan ke dalam plasma dengan menukarnya dengan ion Cl. H+ yang ada akan diikat oleh Hemoglobin. 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, dengan enzym carbonic anhydrase, akan diubah sesuai reaksi hendelson hasselbach. H+ yang terbentuk akan diikat oleh hemoglobin (dalam bentuk Hb (hemoglobin) maupun Oxy-Hb (oksihemoglobin). Buffer selain bikarbonat disebut sebagai NBB (non bikarbonat buffer) yang menjadi penetral pH line pertama

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

RENAL HANDLING OF ACID BASE BALANCE

Bicarbonate reabsorptionBicarbonate is freely filtered in the glomerulus, but most of the filtered bicarbonate is subsequently reabsorbed to maintain normal plasma bicarbonate concentration and therefore the plasma pH. Bicarbonate reabsorption depends on the secretion of H + ions into the lumen of the tubule.These H+ ions are recycled by carbonic anhydrase and there is no net acid excreted.

Hydrogen ion secretion and its effects When secreted H + ions interact with bicarbonate in the fi ltrate, the end result is bicarbonate reabsorption. When secreted H + ions interact with a urinary buffer (mainly phosphate or NH 3 ), the end result is the excretion of acid. When buffered acid excretion occurs, the new bicarbonate generated in the renal cells by carbonic anhydrase is added to the blood. Early in the nephron, secreted H + ions are used to reabsorb bicarbonate. In the more distal nephron, when this bicarbonate reabsorption is complete, secreted H + ions interact with phosphate buffers and net acid excretion occurs. This happens because the p K a of the bicarbonate system is 6.1, whereas that of the phosphate system is 6.8. At the initial fi ltrate pH of around 7.4 (similar to plasma), there is a much greater supply of bicarbonate base (HCO3) than of phosphate base (HPO42). As bicarbonate is reabsorbed, urinary pH falls and the buffers accept H + ions.

Ammonia handling and acid base balanceTubular cells, principally those in the proximal tubule, metabolize glutamine to produce ammonia and, ultimately, glucose and bicarbonate. The bicarbonate enters the blood and the NH4+ ions (which effectively carry a H + ion) are excreted in the urine. NH 3 enters the fi ltrate from the tubular cells by simple diffusion and is protonated in the lumen to form NH4+, which cannot diffuse out of the tubules. The NHE3 Na + /H + exchanger can also transport NH4+ into the tubule. In the thick ascending limb of the loop of Henle, NH4+ can be transported out of the lumen in place of K + on the NKCC2 co - transporter. Also, as the tip of the loop of Henle is alkaline, NH4+ in the filtrate dissociates to form NH 3 and this diffuses into the interstitium. Subsequently, ammonia can diffuse back from both these sites into the thin descending limb, to be recycled in a counter - current fashion. It can also diffuse into the acidified distal tubules where it is protonated to NH4+ and excreted in the urine.

Tubular handling of H+ and HCO3Proximal tubule Of the filtered bicarbonate, 80% is reabsorbed in the proximal tubule. Most proximal tubule H + secretion serves this purpose and does not contribute to net acid excretion. Carbonic anhydrase in the proximal tubule cell cytoplasm and the tubular lumen facilitates the reabsorption of bicarbonate by recycling the secreted H + ions. Most H + ions enter the fi ltrate via the NHE3 Na + /H + exchanger at the apical membrane of the tubular cells. This protein is one of a family of molecules with 10 12 transmembrane regions, and is inhibited by cAMP and protein kinase A - mediated phosphorylation of its cytoplasmic tail. Na + /H + exchange is linked to sodium reabsorption and is dependent ultimately on the activity of the basolateral Na + /K + ATPase. The basolateral Na + 3HCO3co-transporter ( NBC ) carries most of the bicarbonate out of the cell and into the peritubular plasma. Some sodium - dependent (HCO 3 ) /Cl counter - transport may also occur. Loop of Henle A further 10 15% of fi ltered bicarbonate is reabsorbed in the thick ascending limb of the loop of Henle. The mechanisms responsible are similar to those in the proximal tubule and again involve carbonic anhydrase. Distal nephron Here, secreted H + ions either contribute to the reabsorption of any remaining bicarbonate or interact with urinary buffers to allow acid excretion. H + ions are buffered by phosphate and NH 3 , which diffuses in from the medullary interstitium. Secreted H + ions that interact with buffers are not recycled and the new bicarbonate formed in the cell enters the blood. In the early distal tubule, Na + /H + exchange still mediates most H + secretion but, more distally, the H + ATPase performs this role. The connecting tubule and cortical collecting duct contain two types of intercalated cells that are rich in carbonic anhydrase. Type A intercalated cells secrete H + ions. Principally, this is performed by an apical H + ATPase , but also to a lesser extent by a H + /K + ATPase similar to that in the stomach. The bicarbonate generated in the cell exits basolaterally via the A E1 HCO3 Cl anion exchanger. Type B intercalated cells are similar to functionally inverted type A cells with a basolateral H + ATPase and an apical AE1 HCO3 Cl exchanger. Present only in the connecting tubule and cortical collecting duct, these cells secrete bicarbonate, but their role in normal acid base homeostasis is unclear. The principal cells play no direct role in acid base handling, but their reabsorption of sodium generates a negative potential in the lumen, promoting H + secretion by type A intercalated cells.

The most important urinary buffer is NH3/NH4+. This is because the synthesis of NH3/NH4+ in the tubule cells is controlled by the acid-base status of the body. Acidosis stimulates NH4+-production from renal glutamate, whereas alkalosis stimulates hepatic urea production from hepatic glutamate. In adult person, amino acid load is from 90 g of protein (16% nitrogen) daily equals to 14.4 g nitrogen (1 mol) corresponds to 1000 mmol of NH3/NH4+. According to the equation: 2 NH4+ + 2 HCO3- CO(NH2)2 + CO2 + 3 H2O One mol of nitrogen daily produces 500 mmol urea, which is equal to the typical urinary urea excretion (daily urea filtration flux is 900 mmol). The degree of reabsorption of the water-soluble urea depends upon the tubular flow rate. In normal conditions only a small amount of nitrogen is used to produce hepatic glutamate, which is an excellent atoxic ammonia store that can transfer ammonia to the proximal tubules of the kidneys in cases of acidosis. In the proximal tubules, renal glutamate produces NH4+ and -ketoglutarate. One molecule of NH4+is produced by deamination of one glutamine molecule by the enzyme, glutaminase, and a second by oxidative deamination of glutamic acid forming ketoglutarate that is metabolised. The NH4+ in the proximal tubule cells is in equilibrium with minimal amounts of NH3 at low pH. The NH4+-secretion into the tubular fluid makes use of the Na+-H+-antiporter, where NH4+ substitutes H+. The NH4+ passes with the tubular fluid to the thick ascending limb of the Henle loop, where a major portion is reabsorbed and accumulated in the interstitial fluid (Fig. 17-5). Secretion of NH4+in the collecting ducts involves a special mechanism. The NH3 is lipid soluble and easily passes any membrane, so it reaches the tubular fluid of the collecting ducts and form NH4+ at the low pH (Fig. 17-5). The charged molecule cannot pass the membrane and it is trapped in the tubular fluid and eliminated in the urine. This diffusion trapping of charged molecules such as NH4+ is called non ionic diffusion - a general elimination principle for many charged metabolites and drugs. Excretion of NH4+reduces the excretion of other positive ions. The -ketoglutarate is metabolised into bicarbonate. Bicarbonate of the extracellular fluid reacts with H+ from hepatic phosphoric and sulphuric acid to form carbon dioxide and water. The H2PO4- (and a minimal amount of SO42-) is excreted in the urine. 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. With a urine pH of 6.5, organic acids such as lactic acid, -hydroxybutyric acid, pyruvic acid etc., are present in the base form (RCOO- of Fig. 17-6). Most of the phosphoric acid is H2PO4-, and almost all ammonia is in the NH4+ form. This is not so in an alkaline urine. At a urinary pH of 8, there is 5% NH3 of the total. The high pK (=9.3) of NH3/NH4+ has the consequence that in gastric juice with a pH of 1, the (pH-pK)- difference is -8.3, so virtually all ammonia must be NH4+. Even in body fluids with a pH of 7.3 the NH3/NH4+ ratio is 1/100.

The dominating buffer system in the urine is secondary/primary phosphate. This is because of its urinary concentration and of its pK (6.8) being close to urinary pH (6.5). A healthy person has a renal filtration flux of phosphate of 180 mmol daily. Phosphate is a threshold substance, which is reabsorbed, in the proximal tubules, where parathyroid hormone (PTH) inhibits phosphate reabsorption (Fig. 17-7). With 30 mmol left in the tubular fluid, the secondary/primary phosphate-ratio is 24/6 mmol as calculated in Fig. 17-7. Secretion of H+ during the passage of the fluid through the renal tubules converts HPO42- to the acid form, H2PO4-. Thus, in the final urine, the base/acid-ratio is 10/20. 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). Weak acids are not titrated, because they are minimally dissociated at pH 6.5 to 7.4. Normally, the titratable phosphate acidity is 30 mmol in a 24 hour urine. In our example above, the distal H+ -secretion has titrated 14 mmol of HPO42- to H2PO4-. Acidosis increases the urinary titratable phosphate acidity (towards 50 mmol daily) in order to get rid of the acid. The small amount of bicarbonate in the daily urine (zero to 3 mmol) hardly affects the measured titratable phosphate acidity, 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, and that of the intracellular fluid is comparable in the majority of acute conditions, with extended ECV as the initial distribution volume and the intracellular fluid participating importantly after hours. This is because the alteration of the cellular transport processes takes time. The [H+] of the intracellular fluid volume (ICV) is higher than that of the extended ECV. The intracellular pH is precisely controlled in cells with different functions and needs, and the range of values is 7.0 -7.4 (Fig. 17-8) The buffer bases within the cells are proteins, phosphate and bicarbonate. The precise intracellular control is necessary for the pH-sensitive cellular processes with pH-optima for the enzyme systems. The active transport of H+ out of the cell is a coupled Na+/H+exchange. The energy for this exchange is delivered by the Na+-K+-pump, which maintains the Na+-gradient across the cell membrane (Fig. 17-8). Carbohydrate- and K+-containing meals, insulin, hyperkalaemia, adrenaline and aldosterone stimulate the Na+-K+-pump.

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. 17-8). In disorders with extracellular accumulation of carbon dioxide, CO2 diffuses rapidly into the cells. This causes a shift towards the right. The intracellular buffers buffer the H+. Bicarbonate leaves the cells both directly via capnoforin and via other membrane channels (Fig. 17-8), whereby intracellular bicarbonate falls. Intracellular acid accumulation accompanied by hyperkalaemia may develop, if not compensated by the lungs. The K+-output follows the bicarbonate exit. Non-volatile acid is also buffered intracellularly during metabolic acidosis by movement of H+ into the cell, where it reacts with proteins, phosphate and bicarbonate. During metabolic alkalosis movement of H+ out of the cells in exchange of Na+ (Na+-influx in Fig. 17-8) also buffers non-volatile base.

Closed & Open System Buffer In the closed system, the base concentration is reduced by 1 mM to 23, & the acid concentration is increased by 1 mM, because the reaction is shifted towards formation of CO2 causing a high P-CO2. The acid concentration & Buffer capacity are stated in the pic, which is negligible In an open system such as the body, the ventilation simply eliminates excess CO2 & P-CO2 is kept constant. 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, culminating in the restoration of acid-base balance by the renal excretion of the excess H+.

Response to an increase in the PCO2. Although these changes raise the pH toward normal, acid-base homeostasis will not be restored until ventilation is normalized.

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. The pH of a bicarbonate solution is the concentration ratio of bicarbonate and dissolved carbon dioxide ([HCO3]/[CO2]), as defined in the HendersonHasselbalch equation ( A1). Given [HCO3] = 24 mmol/L and [CO2] = 1.2 mmol/l, [HCO3]/[CO2] = 24/1.2 = 20. Given log20 = 1.3 and pKa = 6.1, a pH of 7.4 is derived when these values are set into the equation ( A2). If [HCO 3] drops to 10 and [CO2] decreases to 0.5 mmol/L, the ratio of the two variables will not change, and the pH will remain constant. When added to a buffered solution, H+ ions combine with the buffer base (HCO3 in this case), resulting in the formation of buffer acid (HCO3 + H+ !CO2 + H2O). In a closed system from which CO2 cannot escape ( A3), the amount of buffer acid formed (CO2) equals the amount of buffer base consumed (HCO3). The inverse holds true for the addition of hydroxide ions (OH + CO2 !HCO3). After addition of 2 mmol/L of H+, the aforementioned baseline ratio [HCO3]/[CO2] of 24/1.2 ( A2) changes to 22/3.2, making the pH fall to 6.93( A3). Thus, the buffer capacity of the HCO3/CO2 buffer at pH 7.4 is very low in a closed system for which the pKa of 6.1 is too far fromthe target pH of 7.4.

If, however, the additionally produced CO2 is eliminated from the system (open system; A4), only the [HCO3] will change when the same amount of H+ is added (2 mmol/L). The corresponding decrease in the [HCO3]/[CO2] ratio (22/1.2) and pH (7.36) is much less than in a closed system. In the body, 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). The lungs normally eliminate as much CO2 as produced by metabolism (15 00020 000 mmol/day), while the alveolar PCO2 remains constant. Since the plasma PCO2 adapts to the alveolar PCO2 during each respiratory cycle, the arterial PCO2 (PaCO2) also remains constant. An increased supply of H+ in the periphery leads to an increase in the PCO2 of venous blood (H+ +HCO3!CO2 +H2O) ( B1). The lungs eliminate the additional CO2 so quickly that the arterial PCO2 remains practically unchanged despite the addition of H+ (open system). The following example demonstrates the quantitatively small impact of increased pulmonary CO2 elimination. 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). This corresponds to only about 0.3% of the normal daily CO2 elimination rate. An increased supply of OH ions in the periphery has basically similar effects. Since OH +CO2 !HCO3, [HCO3] increases and the venous PCO2 becomes smaller than normal. Because the rate of CO2 elimination is also reduced, the arterial PCO2 also does not change in the illustrated example ( B2). At a pH of 7.4, the open HCO3/CO2 buffer system makes up about two-thirds of the buffer capacity of the blood when the PCO2 remains constant at 5.33 kPa. Mainly intracellular non-bicarbonate buffers provide the remaining buffer capacity. Since non-bicarbonate buffers (NBBs) function in closed systems, their total concentration ([NBB base] + [NBB acid]) remains constant, even after buffering. The total concentration changes in response to changes in the hemoglobin concentration, however, since hemoglobin is the main constituent of NBBs. NBBs supplement the HCO3/CO2 buffer in non-respiratory (metabolic) acidbase disturbances, but are the only effective buffers in respiratory acidbase disturbances

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

The Siggaard-Andersen acid-base chart with the 9 conditions of van Slyke Humans can suffer from 4 acid-base disorders: 1. Respiratory acidosis, 2 Respiratory alkalosis, 3 Metabolic acidosis and 4 Metabolic alkalosis. Acidosis (acidaemia) is defined as a disorder with pH in the arterial blood (pH-a) less than 7.35, and alkalosis (alkalaemia or baseosis) is defined as a condition with a pH-a > 7.45. Each of these two disorders has respiratory and metabolic forms. Respiratory acid-base disorders are caused by primary changes of PCO2, and compensated by altered renal excretion of acid in a matter of days. Metabolic acid-base disorders are caused by primary changes in BE, and compensated partially by the lungs in a matter of hours. The final correction of metabolic disorders is always renal and takes several days. These four primary acid-base disturbances and their four compensated or chronic types constitute, together with the normal condition, is called the nine van Slyke conditions (Fig. 17-13). Plotting the measured pH and P-CO2in the acid-base chart allows estimation of the base excess (BE), and combined with the case history, the correct diagnosis can be reached. Please observe that each point on the chart can be reached in several ways. Van Slyke, who made the first apparatus to diagnose acidbase disturbances, emphasised the importance of the case history and common clinical sense. The importance is illustrated by the following three examples. The first example is a case of respiratory acidosis due to chronic obstructive lung disease (COLD in Fig. 17-13) and a metabolic acidosis due to diabetic coma. Without the case history it is difficult to diagnose the primary and secondary events in the development of the patients condition. The second example is a case of respiratory alkalosis due to acute mountain sickness (AMS), complicated by a metabolic alkalosis (AMS in Fig. 17-13), because the patient is loosing acid by vomiting. The third example is a serious case of birth anoxia with a combined respiratory and metabolic acidosis. Instantaneous intubation & oxygenation with 50-40-30 % oxygen can saved the newborn

PENYEBAB UMUM HIPOKSIA/ANOKSIA

ASIDOSIS RESPIRATORIK

HEMATOTHORAX MASIF

PENYEBAB ASIDOSIS RESPIRATORIK PADA KASUS

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

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

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

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

Untuk metabolisme kalsium & Fosfor baca literatur yang disertakan sebelumnya (MODUL TUTOR 2)

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, Luka lecet, Luka robek Kombinasi Luka tusuk, Luka iris, Luka bacok Gun, Shot gun

Fisik

Kematian jaringan Rangsangan otot, saraf. jantung Efek panas, Efek mekanik Kulit kering, keras, coklat, sesuai aliran cairan Kulit pucat, teraba licin

Kimia

7. REPORTING1. Tutor menggali kembali keberhasilan belajar mahasiswa melalui pertanyaan yang mengarah pada kemampuan mahasiswa menjelaskan LO yang ada 2. LO nomor 1 (fisiologi peran pH pada fungsi tubuh manusia), No 2 (peran respirasi pada keseimbangan Asam basa), No 3 (peran ginjal pada keseimbangan Asam basa), No 4 (pengaruh fraktur pada metabolisme kalsium dan fosfat (termasuk magnesium), No 6 (mekanisme kompensasi pada gangguan keseimbangan asam basa) harus tercapai minimal 68% penguasaan materi dasar dalam konsep mapping & mapping kasus 3. LO no 5 (Pengaruh fraktur pada proses asam basa (peran tulang pada proses asam basa)), No 7 (penyakit-penyakit yang menyebabkan gangguan keseimbangan asam basa) & No 8 (Penatalaksanaan gangguan keseimbangan asam basa) 8. DAFTAR PUSTAKA 1. AY Sutedjo, 2007. Buku Saku mengenal penyakit melalui Pemeriksaan laboratorium, Amara Books, Yogyakarta 2. Chang R, 1998. Chemistry, 6th Edition, McGraw Hill, USA 3. Fauci et al., 2008. Harrison's Principles Of Internal Medicine, 17th Ed, McGraw-Hill Companies, Inc. USA 4. Ganong WF, 2003. Review of Medical Physiology, 21th edition, Mc Graw Hill, USA 5. Goldman L, Ausiello D (ed), 2007. Cecil Medicine, 23rd ed, Saunders Elsevier, USA 6. Guyton AC, Hall JE, 2000. Textbook of Medical Physiology, 10th Edition, WB Saunders, Philadelphia, USA 7. Horne MM, Swearingen PL, 2001. Keseimbangan cairan, elektrolit dan asam basa. Edisi terjemahan, Penerbit buku kedokteran EGC, Jakarta 8. Konsil Kedokteran Indonesia, 2006. Standar Kompetensi Dokter, KKI, Jakarta 9. Kumar V, Cotran RS, Robbins SL, 2003. Robins Basic Pathology, 7th edition, WB Saunders Co, Philadelphia, USA 10. la-Rocca JC, Otto SL, 1998. Terapi Intravena, Edisi 2, EGC, Jakarta 11. Murray RK, Granner DK, Mayes PA, Rodwell VW, 2000. Harpers Biochemistry, 25th Edition, McGraw Hill, USA 12. McPhee SJ, Lingappa VR, Ganong WF, Lange JD, 1997. Pathophysiology of Disease, an Introduction to Clinical Medicine, 2nd Edition, Appleton & Lange, USA 13. Park GR, Roe PG, 2000. Fluid Balance & Volume Resuscitation for beginners. Greenwich Medical media, London. 14. Rang HP, Dale MM, Ritter JM, Flower RJ, 2007. Rang And Dales Pharmacology, Churchill Livingstone, USA 15. Runge MS, Greganti MA, Netter FH, 2003. Netters Internal Medicine, Icon Learning System, USA 16. Rose BD, Post TW, 2001. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th Edition, McGraw-Hill, USA. 17. Ferri FF, 2008. Ferri's Clinical Advisor Instant Diagnosis And Treatment, Mosby Elsevier, USA 18. McCann JAS, Holmes NH, Robinson JR, Putterman A, Houska A, Henry K, Bilotta K, Comerford KC, Weinstock D, Foulk L, 2007. Professional Guide to Signs and Symptoms, 5th Edition. Lippincott Williams & Wilkins. USA.