Pp Prinsip Terapi Cairan Dan Elektrolit

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

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

• 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.

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

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.

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

Distribution Of Volume in E.C.F. Freely permeableto both water andsolutes,but onlyslightly permeableto protein

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

Gangguan keseimbangan air

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

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

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

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

Hipervolemia Volume overloadVol intravaskular meningkat, pd kegagalan otot jantung, penurunan fungsi

ginjal bs edema paruTh/ diuretik, restriksi cairan

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

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)

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

• Menurut waktu terjadinya: hiponatremia kronik/ asimptomatik

Berlangsung lambat > 48 jamGejala: lemas, ngantuk

Hiponatremi akut/ simptomatik/beratKejadian berlangsung cepat <48 jmGejala: kejang, ↓kesadaran

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

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

• Hiponatremia kronikKoreksi Na dilakukan secara perlahan yaitu

sebesar 0,5 meq/L setiap 1 jam, max 10 meq/L dalam 24 jam

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

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

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

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)

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)

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

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

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

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

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)

terimakasih