pp prinsip terapi cairan dan elektrolit
TRANSCRIPT
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Prinsip Terapi Cairan dan Elektrolit
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Body water content
• Body weight of adult male 55-60%, female 50-55%, newborn 75-80%– Lbh rendah pd jar. Lemak cairan tubuh total pd
obes lbh rendah dr pd yg tdk obes. – Loss of 20% - fatal– Elderly - decreases to 45-50% of body weight• decreased muscle mass, smaller fat stores, and
decrease in body fluids
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Body Fluid Compartments• 2/3 (65%) of TBW is intracellular (ICF)• 1/3 extracellular water–25 % interstitial fluid (ISF)– 5- 8 % in plasma (IVF intravascular fluid)–1- 2 % in transcellular fluids – CSF, intraocular
fluids, serous membranes, and in GI, respiratory and urinary tracts
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Compartments• Intracellular (ICF)– Fluid within the cells themselves –2/3 of body fluid– Located primarily in skeletal muscle mass–Provide nutrients for metabolism:• Kation utama: kalium, anion utama:
fosfat. Protein jg banyak.•Moderate levels of Mg, So4
–Membantu dalam metabolism seluler
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Compartments• Extracellular (ECF)– 1/3 of body fluid– Comprised of 3 major components• Intravascular : fluid within the blood vessels–Plasma
• Interstitial : the fluid that surrounds the cells–Fluid in and around tissues. Ex: lymph
• Transcellular: which is fluid found in the cerebrospinal column,
pericardial envelope, synovial joints, or intraocular space
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Compartments
• Extracellular–Provide Nutrients for cell functioning• Kation: Na (utama), kalium, Ca, Mg• Anion: Cl, bikarbonat, albumin
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Compartments• Intravascular Component– Plasma• fluid portion of blood
– Made of:• water• plasma proteins• small amount of other substances
• Interstitial component– Made up of fluid between cells• Surrounds cells • Transport medium for nutrients, gases, waste products
and other substances between blood and body cells • Back-up fluid reservoir
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Compartments• Transcellular component– 1% of ECF– Located in joints, connective tissue, bones, body
cavities, CSF, and other tissues– Potential to increase significantly in abnormal
conditions
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• Fluid normally shifts between the ICF and ECF compartment each and every day, to help keep our bodies in homeostasis.
• The principles involved in this shifting are osmosis, diffusion, and filtration.
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Regulation of Fluids in Compartments• Osmolalitas: perbandingan antara jmlh solut&air• Solut yg biasa mempengaruhi: natrium, kalium,
glukosa, urea• Makin tinggi osmolalitas makin tinggi tek. osmosis• Osmosis– Movement of water through a selectively
permeable membrane from an area of low solute concentration to a higher concentration until equilibrium occurs
– Movement occurs until near equal concentration found
– Passive process
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Regulation of Fluids in Compartments• Diffusion– Movement of solutes from an area of higher
concentration to an area of lower concentration in a solution and/or across a permeable membrane (permeable for that solute)
– Movement occurs until near equal state– Passive process
• Filtration is caused from pressure on the capillaries(tek. Hidostatik), and it moves both water and solutes.
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Regulation of Fluids in Compartments• Active Transport– Allows molecules to move against concentration
and osmotic pressure to areas of higher concentration
– Active process – energy is expended Na / K pump– Exchange of Na ions for K ions – More Na ions move out of cell– More water pulled into cell– ECF / ICF balance is maintained
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Distribution Of Volume in E.C.F. Freely permeableto both water andsolutes,but onlyslightly permeableto protein
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Arterial end:capillary
fluids tend to leave theplasma under the influence
of hydrostatic pressure.
.Venous end:osmotic pressure,is greater and so the
fluids tend to return to
the circulation.Balance of fluid movementsbetween the plasma and the
interstitial space.Starling~s
Hypothesis.
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Fluid Volume Shifts
• Fluid normally shifts between intracellular and extracellular compartments to maintain equilibrium between spaces
• Fluid not lost from body but not available for use in either compartment – considered third-space fluid shift (“third-spacing”)
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Causes of Third-Spacing
• Burns• Peritonitis• Bowel obstruction• Massive bleeding into joint or cavity• Liver or renal failure• Lowered plasma proteins• Increased capillary permeability• Lymphatic blockage
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Treatment
• Treat underlying cause if possible• Monitor I & O more frequently• Daily weights• Measure abdominal girth in ascites• Measure extremities if necessary • Monitor lab values – albumin level important
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Gangguan keseimbangan air
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Hipovolemia • Suatu keadaan dimana berkurangnya vol.
cairan tubuh yg akhirnya menimbulkan hipoperfusi jar.
• Berkurangnya cairan ekstrasel dimana air dan natrium berkurang dlm jumlah yg sebanding
• Yg hilang cairan ekstra sel isotonik kadar Na plasma tetap dlm batas normal
• Terjadi pd: kehilangan air&na melalui sal. Intestinalis:
muntah, diare, perdarahan/ mell. Pipa sal. SondeMelalui ginjal: penggunaan diuretik,
hipoaldosteronismeMelaui kulit&sal. Napas: keringat, luka bakar,
insensible losses
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Penanganan • Pembagian hipovolemi:1.Hipovolemi ringan: ≤20% vol. plasma takikardi2.Hipovolemi sedang: 20-40%%vol. plasma
takikardi& hipotensi ortostatik3.Hipovolemi ringan: ≥40% vol. plasma
takikardi, tek. Darah turun,oliguri, agitasi • Vol plasma 6% dr BB org dewasa.Ex: bb 60kg, hipovolemi ringan ( 20%) vol yg
hilang: 0,36x 20% = 0,72 lt• Jenis cairan: tergantung cairan yg keluar. Bila
darah ganti dgn darah. Jika tdk ada, dpt diberi cairan koloid/kristaloid. Ex: ringer laktat/ NaCl isotonis. Pd diare dianjurkan ringer laktat
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Dehidrasi • Keadaan berkurangnya vol. air tanpa elektrolit(
natrium) atau berkurangnya air jauh melebihi natrium dr cairan ekstrasel peningkatan na dlm ekstrasel shg cairan intrasel akan masuk ke ekstrasel shg ICF berkurang.
• Melibatkan berkurangnya ICF & ECF• Terjadi hipernatremi krn cairan yg keluar
adalah hipotonik
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Edema • Pembengkakan yg dapt diraba akibat
bertambahnya vol. cairan interstitium• Terjadi krn:1.Perubahan hemodinamik dlm kapiler yg
menyebabkan keluarnya cairan intravaskuler ke jar interstitium
2.Retensi natrium di ginjal
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Hipervolemia Volume overloadVol intravaskular meningkat, pd kegagalan otot jantung, penurunan fungsi
ginjal bs edema paruTh/ diuretik, restriksi cairan
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Natrium• Normal 135-145 mEq/L• Major cation in ECF• Regulates voltage of action potential; transmission of impulses
in nerve and muscle fibers• Helps maintain acid-base balance
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hyponatremi• Terjadi bila:
Jumlah asupan cairan melebihi kemampuan ekskresiKetidakmampuan menekan sekresi ADH. Mis: pd kehilangan
cairan melalui saluran cerna/gagal jantung/ sirosis hati.• Berdasarkan prinsip diatas, hiponatremi dibagi:1. Hiponatremi dg ADH meningkat
Vol sirkulasi efektif turun Na keluar berlebihan dr tubuh melalui ginjal: diuretik akut,renal salt wasting. Non ginjal:
diare Peningkatan vol ar bebas elektrolit: gagal jantung, sirosis
ati, perdarahanVol sirkulasi efektif tidak turunSIADH ( synd. Of inappropriate ADH secretion)
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hyponatremi2. Hiponatremi dgn ADH tertekan fisiologisEx: gagal ginjal ekskresi cairan lbh rendah
dibanding asupan respon fisologis: menekan sekresi ADH
3. Hiponatremi dgn osmolalitas plasma normal/ tinggi
• Hiperglikemi cairan intrasel keluar dilusi cairan ekstrasel hipona.
• Pemberian cairan isoosmotik tanpa na. hipona. Dgn osmolalitas plasma normal
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• Menurut waktu terjadinya: hiponatremia kronik/ asimptomatik
Berlangsung lambat > 48 jamGejala: lemas, ngantuk
Hiponatremi akut/ simptomatik/beratKejadian berlangsung cepat <48 jmGejala: kejang, ↓kesadaran
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hyponatremi• Clinical manifestations– ↓ BP, confusion, headache, lethargy, seizures,
decreased muscle tone, muscle twitching and tremors, vomiting, diarrhea, and cramps
• Labs– Increased HCT, K– Decreased Na, Cl, Bicarbonate, UOP with low Na and Cl
concentration– Berat jenis urine ↓ 1.010
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Penatalaksanaan • Anamnesis teliti ( riw.muntah,diuretik?)• Pf• Px.Gula darah, lipid • Px.Osmolalitas darah• Px.Osmolalitas urine/ BJ• Px. Na, K, Cl dlm urine• Terapi: Hiponatremi akut ( koreksi Na dgn cpt)Rumus: 0,5 x BB (kg) x delta Na (selisih kadar Na yg diinginkan
dgn kadar Na awal)Kadar Na dinaikkan 5meq/L dr kadar awal dlm 1 jm, kmd 1
meg/L tiap jam sampai kadar Na dlm darah mencapai 130meq/L
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• Hiponatremia kronikKoreksi Na dilakukan secara perlahan yaitu
sebesar 0,5 meq/L setiap 1 jam, max 10 meq/L dalam 24 jam
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hypernatremi• Terjadi bila: Defisit cairan tubuh akibat ekskresi air melebihi
ekskresi natrium/ asupan air yg kurang. Ex: pengeluaran air tanpa elektrolit melalui keringat, osmotik diare akibat laktulose, diabetes insipidus sentral
Penambahan Na yg melebihi jumlah cairan dalam tubuh. Ex: koreksi bicnat berlebih pd asidosis metabolik
Masuknya air tanpa elektrolit ke dalam sel. Ex: pd O.R yang berat as.laktat ↑ osmolalitas sel tinggi air masuk dr ekstrasel ke intrasel. Biasanya akan normal dlm 5-15mnt stl istirahat
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Signs/Symptoms
• Early: Generalized muscle weakness, faintness, muscle fatigue,
• Moderate: Confusion, thirst• Late: Edema, restlessness, thirst,
hyperreflexia, muscle twitching, irritability, seizures, possible coma
• Severe: Permanent brain damage, hypertension, tachycardia
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Labs
• Increased serum Na• Increased serum osmolality• Increased urine specific gravity
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Treatment
• Tetapkan etiologi hipernatremi• Turunkan kadar natrium plasma
Defisit cairan: koreksi cairan Diabetes insipidus: (-)vol urin ex: diuretik tiazidDiabetes insipidus nefrogenik: (-) asupan
garam/proteinAsupan Na berlebih: (-) asupan
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Kalium • Normal 3.5-5 mEq/L• Major ICF cation• Vital in maintaining normal cardiac and
neuromuscular function, influences nerve impulse conduction, sintesis protein, helps maintain acid-base balance, control fluid movement in and out of cells by osmosis
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Hipokalemi• Serum potassium level below 3.5 mEq/L• Penyebab: 1. Asupan K kurang2. Pengeluaran kalium yg berlebihan melalui sal. Cerna
(muntah, diare,pakai pencahar) /ginjal(pemakaian diuretik, hiperaldosteronisme primer, pd hipomagnesemia)/ keringat ( bila lat.berat+suhu panas shg keringat sampai 10 ltr.
3. Kalium masuk ke dlm selpd alkalosis ekstrasel, pemberian insulin, ↑ aktivitas beta adrenergik (pemakaian β2 agonis), paralisis periodik hipokalemi, hipotermi
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Signs/Symptoms • Skeletal muscle weakness, ↓ smooth muscle
function, nyeri otot, lelah pd k < 3 meq/L. penurunan lbh berat kelumpuhan, rabdomiolisis
• ↓ BP, EKG changes, aritmia (fibrilasi atrium, takikardi ventrikular) possible cardiac arrest
• Gangguan toleransi glukosa, g3 metabolisme protein• paralytic ileus, diarrhea• Metabolic alkalosis ( prod. NH4 & bikarbonat↑ di
tub. Proksimal)• Mental depression and confusion
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Penatalaksanaan • Indikasi koreksi kalium dibagi:1. Indikasi mutlak ( K segera diberi) Ps. Sdg dlm pengobatan digitalis Ps dgn ketoasidosis diabetik Ps dgn kelemahan otot pernapasan Ps dgn hipokalemi berat ( k<2 meq/L)2. Indikasi kuat ( K diberi dlm wkt tdk terlalu lama) Insufisiensi koroner/ iskemi otot jantung Ensefalopati hepatikum Ps yg akai obt yg sebabkan perpindahan K intrasel ke ekstrasel3. Indikasi sedang ( tdk perlu segera) Hipokalemi ringan ( k antara 3-3,5 meq/L)
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Pemberian kalium oral:
mudahpemberian 40-60 meq naikkan K 1-1,5 meq/L. pemberian 135-160 meq naikkan K 2,5-3,5 meq/L.
Intravena ( larutan KCL)lewat vena yg besar dgn kec. 10-20meq/jam. Pd aritmia yg berbahaya/kelumpuhan otot napas: 40-100meq/jamlarutkan 20meq dlm 100cc Nacl isotonikJika lewat vena perifer kcl max: 60meq dilarutkan dlm 1000cc NaCl isotonik ( jika >, rasa nyeri,skerotik vena)
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Hyperkalemia • Serum potassium level > 5 mEq/L• Penyebab :
Keluarnya kalium dr intrasel ke ekstraselPd asidosis metabolik, def. insulin, katabolisme jar ↑,
pakai obt penghambat beta adrenergikBer – ekskresi K melalui ginjal hipoaldosteronisme, gagal ginjal, deplesi vol.sirkulasi
efektif
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Signs/Symptoms
• ECG changes – tachycardia to bradycardia to possible cardiac arrest– Tall, tented T waves
• Cardiac arrhythmias• Muscle weakness, paralysis, paresthesia of
tongue, face, hands, and feet, cramping, diarrhea, metabolic acidosis
• Biasa gejala timbul pd K > 7 meq/L atau kenaikan dlm wkt cpt
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Prinsip terapi1. Mengatasi pengaruh hiperkalemi dgn beri kalsium IVKalsium glukonat 10ml IV dlm 2-3 menit dgn monitor EKG. Bila
perub. Ekg msh tampak, Ca glukonat dpt diulang stlh 5 mnt2. Pacu masuk K dr ekstrasel ke intrasel• Insulin 10 unit dlm glukosa 40%, 50ml bolus IV, lalu diikuti
infus dextrose 5% u/ cegah hipoglikemi• Na bikarbonat ( akan ↑ PH sistemik)
ph↑ akan merangsang ion H keluar dr dlm sel dan K msk. tanpa asidosis metabolik: na bicnat 50meq i.v slm 10 mnt
• Alfa 2 agonis (inhalasi/iv) akan rangsang pompa NaK-ATPase, K masuk sel. Albuterol 10-20mg
3. Mengeluarkan kelebihan kalium dr tubuhFurosemid, tiazid, hemodialisis
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Kalsium• Normal 4.5-5.5 mEq/L• Terbagi atas:
40% kalsium terikat protein/Ca tdk terdifusi (80-90% terikat dgn albumin)
Ca yg tdk terikat protein/difussible/ultrafiltrable 15% Ca kompleks & 45% Ca ion bebas
• Keseimbangan Ca dlm tubuh merupakan hub timbal balik dr absorbsi usus (di dodenum,jejenum proks.), ekskresi urin( filtrasi glomerulus, reabsorbsi tubulus), faktor hormonal( vit. D dgn metabolit aktifnya 1,25- dihidroksikolekalsiferol/ kalsitriol & paratiroid
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Causes of Hypocalcemia • Def. vit D
malabsorbsi( pd gastrektomi sebagian, pankreatitis kronik), pd met. Vit D terganggu( peny. Riketsia, g3 ginjal)
• Hipoparathyroidisme ( tdk sengaja terangkat saat op.tyroid, idiopatik sejak anak2, efek toksik lsg dr aminoglikosid)
• Proses keganasan ( karsinoma medular kel. Tiroid kalsitonin meningkatekskresi kalsium urin meningkat)
• Hypomagnesemia• Hyperphosphatemia
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Signs/Symptoms
• Abdominal and/or extremity cramping• Tingling and numbness• Positive Chvostek or Trousseau signs• Tetany; hyperactive reflexes• Irritability, reduced cognitive ability, seizures• Prolonged QT on ECG, hypotension, decreased
myocardial contractility• Abnormal clotting
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Treatment• Gejala belum timbul ( ca> 3,2mg/dl): tingkatkan
asupan Ca dlm makanan 1000mg/hari• Timbul gejala( Ca< 2,8mg/dl) : Ca IV 100-200 mg
Ca-elemental/ 1-2 gr Ca glukonas dlm 10-20 menit, lalu diikuti infus Ca glukonas dlm dextrose/ NaCl isotonis dgn dosis 0,5-1,5 m Ca-elemental/Kg BB dlm 1 jam. Ca infus dpt ditukar dgn Ca oral & kalsitriol 0,25-0,5mg/hr
• Hipomagnesemia dgn fs ginjal N: lar. 10% magnesium sulfat 2 gr selama 10 menit, kmd diikuti 1 gr dlm 100cc cairan/1jam
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Hypercalcemia
• Causes– Mobilization of Ca from bone– Malignancy– Hyperparathyroidism– Immobilization – causes bone loss– Thiazide diuretics– Thyrotoxicosis– Excessive ingestion of Ca or Vit D
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Signs/Symptoms
• Anorexia, constipation• Generalized muscle weakness, lethargy, loss
of muscle tone, ataxia• Depression, fatigue, confusion, coma• Dysrhythmias and heart block• Deep bone pain and demineralization• Polyuria & predisposes to renal calculi• Pathologic bone fractures
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Hypercalcemic Crisis
• Emergency – level of 8-9 mEq/L• Intractable nausea, dehydration, stupor,
coma, azotemia(excessive amounts of nitrogenous waste products in the blood ), hypokalemia, hypomagnesemia, hypernatremia
• High mortality rate from cardiac arrest
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Treatment • Tingkatkan ekskresi Ca lewat ginjal
NaCl isotonis
• Menghambat resorbsi tulangKalsitonin (dgn hambat maturasi osteoklas) 4 IU/kgBB
tiap12 jm IV/IMBifosfonatGalium nitrat
• Mengurangi absorbsi kalsium dr ususGlukokortikoid ( prednison 20-40mg/hr)
• Hemodialisis (pilihan terakhir, kondisi berat)
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terimakasih