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Balance Cairan Final.
Balance Cairan Final.
1. 2. 3. 4. 5. 6.
7.
Media semua reaksi kimia tubuh Berperan dalam pengaturan distribusi kimia & biolistrik dalam sel Alat transport hormon & nutrien Membawa O2 dari paru-paru ke sel tubuh Membawa CO2 dari sel ke paru-paru Mengencerkan zat toksik dan waste product serta membawanya ke ginjal dan hati Distribusi panas ke seluruh tubuh
60 60
60/50 55/47
Total body fluid is 60% of body weight Intracelluler 2/3 (40%) extracelluler 1/3 (20%)
Interstitial 15%
Plasma 5%
Transcelluler 1-3%
Plasma(mEq/L
142 4 5
Mg2+
Total Anion: ClHCO3Protein Others Total
2
153 103 25 17 8 153
2
154 117 28 9 154
40
210 3 7 45 155 210
lingkungan
Penyakit
Intake (Range)
Output (range)
Air minum = 1400 1800 ml Urine = 1400 1.800 ml Makanan = 700 1000 ml Faeces = 100 ml Oksigenasi = 300 400 ml Kulit = 300 500 ml Nafas = 600 800 ml
TOTAL
= 2400 - 3200 ml
Output (range) Urine = 65 (50-100) Faeces = 5 (2-20) Urine = 90 (50-120) Faeces = 10 (2-40) Urine = 10 (2-20) Faeces = 20 (2-50) Urine = 3(0-10) Faeces = 12 (2-30)
o o o
Merupakan Kehilangan cairan melalui kulit (difusi) & paru-paru Cara mengetahui IWL : Dewasa = 15 cc/kg BB/hari Anak = (30 usia (th)) cc/kg BB/hari Demam : (nilai 36,8 C adalah konstanta)
Input cairan: Air (makan+Minum) Cairan Infus Terapi injeksi Air Metabolisme
= = = =
cc/kgBB/hari) Output cairan: Urine = ......cc Feses = .....cc Muntah/perdarahan/cairan drainage luka/cairan NGT terbuka = .....cc IWL = .....cc
Osmolality plasma Thirst Water ingesti exc Water retensi Osmolaliti plasma Vol sirkulasi ADH water
Melalui kulit
1.
2.
3.
Sistem skor ( dehidrasi akut, mis GE akut ) Pemasangan CUP Ukur kadar Na plasma
defisit cairan = 0,6 X BB {Na plasma _ 1}
140
4.
Ukur hematokrit
defisit cairan = 0,2 X BB {
Ht
_ 1}
Ht N
5.
Ukur BJ plasma
Gejala klinis Muntah Suara serak Kesadaran apatis Kesadaran somnolen, sopor sampai koma. Sistolik 90 mmHg Nadi 120/mnt Nafas kusmaul ( 30/mnt ) Turgor kulit kurang Facies Cholerica Extremitas dingin Jari tangan keriput (washer hand) Sianosis Umur 50 thn Umur 60 thn
Skor 1 2 1 2 2 1 1 1 2 1 1 2 -1 -2
Patogenesis 1. tekanan darah hidrostatik kapiler tekanan koloid osmotik plasma ( alb ) Permeabilitas kapiler
1. 2. 3. 4. Trauma Radang Luka bakar Alergi 1. Sind. Nefrotik 2. Sirosis hepatis 3. Malnutrisi 1. Payah jantung 2. Sirosis hati 3. Obstruksi vena lokal
2.
3.
4.
Pengobatan
Sesuai
penyakit dasar
Simptomatis
Hyperkalaemia
Pseudohyperkalaemia Haemolysis Leucocytosis (>50.000/ml) Thrombocytosis(>1.000.000/ml) Impaired renal excretion Renal failure Drugs: ACE inhibitors K-sparing diuretics NSAIDS
MANIFESTASI KLINIK
OTOT SKELET: PARALYSIS/FLACCID PARALYSIS ARREST PERNAFASAN ILEUS
DYS-RYTHMIA : TACHYCARDIA FIBRILLASI VENTRIKULER SINUS BRADYCARDIA SINUS ARREST RYTHME IDIO-VENTRICULAR LAMBAT
PENGOBATAN
Table 28-4. Treatment of Hyperkalemia 1 Antagonism of membrane action A. Calcium B. Hypertonic Na solution (if hyponatremic) 2. Increased K+ entry into cells A. Glucose and Insulin B. NaHCO3 C. 2-adrenergic agonist D. Hypertonic Na+ solution ( if hyponatremic) 3. Removal of the excess K+ A. Diuretics B. Cation exchange resin C. Hemodialysis or peritoneal dialysis
Burton Davis Rose: Hyperkalemia, in: Clinical Physiology of Acid-Base Balance And Electolyte disorders. 4th edit 1994 p.848.
Management of Hyperkalemia
K+ Meninggi ? Tidak Berhenti Tidak Berhenti Tidak
Ya
Apakah nyata? Ya Apakah > 6.0 mEq/L atau ada perubahan EKG Ya Pasien perlu penurunan K+ darurat. EKG abnormal ? Tidak Beri insulin dengan glukosa dan/atau Ventolin dgn nebulizer Lanjutkan dengan evaluasi Periksa K+ urine, osmolailty, kreatinin K < 6.0 mEq/L? Tidak Ulangi insulin dan glukosa, pertimbangkan hemodialisis Ya Beri cation exchange resin atau furosemide Evaluasi lanjutan dan terapi jangka panjang Ya Beri kalsium glukonat
1. Direct membrane antagonism (cardiac toxicity): IV Ca-gluconas, CaCl2 10% 10 ml, over 2-5 minute 2. Transcellular shift of K: a. IV dextrose 50% 50ml + IV 5-10 unit Regular-Insulin b. IV Na.Bicarbonate 50-100mEq infused over 5-10 min 3. Enhanced clearance from body - diuretics: IV frusemide 10-20mg - haemodialysis/CRRT - ion exchange resins (Resonium A PO 15g q 8h or enema 30g q8h)
Etiologi :
1. Tanpa defisit K total tubuh
1. Intake , anoreksia 2. Hilang sal cerna : GE, muntah ginjal : hiperaldosteron, loop diuretik
Gejala Klinis :
1.
Jantung
2. 3.
4.
Pada hipernatremia, cairan intrasel ekstrasel sel dehidrasi ADH (kompetensi tubuh) haus intake
Hypernatraemia ([Na]>150mEq/L)
Hypovolaemia
Euvolaemia
Hypervolaemia
Renal losses Diuretic Osmotic diuresis Diabetes insipidus Extrarenal losses Vomiting, diarrhea Skin, respiratory
Renal losses Diabetes insipidus Extrarenal losses Vomiting, diarrhea Sweating, respiratory
Low ECFV : Isotonic saline, then hypotonic fluids IV (<300ml/h) or PO free water High ECFV: loop diuretics, Replace with hypotonic fluids if necessary Correction Na level should < 0.5mEq/L/h, or <1.0 mMeq /L/h for acute hyper Na Treat underlying condition e.g Diabetes Inspidus: Desmopressin When hypovolemia has been corrected: Current TBW x current [Na] = normal TBW x normal [Na] Current TBW = normal TBW x (140/current[Na]) TBW deficit = normal TBW current TBW = 0.6 BW (kg) current TBW = (0.6xBW)(1 140/current [Na
measure plasma osmolality normal or increased Hypotonic hyponatraemia Pseudohyponatraemia Assess ECF volume
HIPONATREMI
Euvolaemia
diarrhea, vomiting skin losses failure third spacing nephrosis cirrhosis diuretics, renal failure
renal losses
Gejala oleh karena edem sel otak, yang timbul bila hipoosmolalitas dalam plasma terjadi dengan cepat Pada kadar Na 120 125 : nausea-vomit 110 120 : letargi-cephalgia < 110 : kejang-koma
TERAPI
Low ECF asymptomatic: replace with isotonic saline symptomatic: replace with hypertonic saline Normal ECF asymptomatic: frusemide diuresis + isotonic saline symptomatic : frusemide + hypertonic saline High ECF asymptomatic : frusemide diuresis symptomatic: frusemide diuresis + hypertonic saline
Hiponatremi yang disertai hipokalemi (mis,GE) koreksi kalium saja telah langsung mengoreksi Na Larutan NaCl 3 % (~ 513 mEq/L) diberikan bila ada gejala edem serebri Bila gejala edem serebri hilang cukup berikan NaCl isotonis
Dapat terjadi pada hiperparatiroidisme, tumor ganas yg mengeluarkan PTH, Intoksikasi vitaminD, Intoksikasi vit. A, Hipertiroid , Insufisiensi adrenal, Milk Alkali Syndrome
PTH: from parathyroid activate osteoclasts enhance intestinal absorption increase kidney reabsorption
most calcium in bones as calcium phosphate PO4- reabsorbed in proximal tubules regulated by PTH
Etiologi dapat terjadi pada defisiensi vitamin D, makanan kurang lemak, sindrom malabsorbsi (gastrektomi, pankreatitis, obat pencahar), renal insufisiensi, gangguan fungsi hati, obat anti kejang, Hipoparatiroidism, Pseudohipoparatiroidism, Keganasan, Hipofosfatemia. Penatalaksanaan dengan koreksi defisiensi dengan kalsium iv (Ca.Gluconat/ klorida 10%) atau peroral (Ca.Gluconas/ karbonat); dapat disertai pemberian vit.D dosis besar
Rhythm : regular atrial & ventricular hythm Rate : normal limit P wave : normal size & configuration PR interval : normal limit QRS complex : normal limit Segmen ST : prolonged T wave : normal size & configuration, may become flat or inverted Interval QT : prolonged