Keseimbangan cairan dan

elektrolit
M. JUFRI MAKMUR
RSU RADEN MATTAHER/FK UNJA
JAMBI
Cairan tubuh
Dalam keadaan normal, keseimbangan cairan, elektrolit, dan
asam/basa selalu dipertahankan dalam keadaan stabil

Keseimbangan ini (physiologic homeostasis) tergantung pada banyak

proses physiologi yang mengatur cairan masuk/keluar tubuh (haus,
produksi urine, konsentrasi urin dll) dan perpindahan air dan
larutannya dalam bagian-bagian tubuh (body compartments) (proses
difusi, osmosis, transport aktip elektrolit dll)
KOMPARTEMEN CAIRAN
 Seluruh cairan tubuh didistribusikan diantara
dua kompartemen utama, yaitu :
1. Cairan intraselular (CIS/ICF)
2. Cairan ekstra selular (CES/ECF)
Fluid Compartments
 Intracellular fluid – fluid inside cells [ICF]
 Extracellular fluid – fluid outside cells
and all other body fluids --- ¼ is plasma
[intravascular fluid], remaining ¾ is
interstitial fluid. Small amount is
localized as CSF, serous fluid, synovial
fluid, humors of eye & endo/perilymph of
ears
 BODY FLUID VOLUME

Body fluid
60% water
Intracelluler extracelluler
2/3(40%) 1/3(20%)
(28 lt in 70 kg (14 lt in 70 kg
young adult) young adult)

Interstitial Transcelluler
Plasma
1-3%
15% (10.5 lt in 70 kg 5% (3.5 lt in
(Cerebrospinal)
young adult) 70 kg young adult)
(aqueous humor)
Komposisi Cairan Tubuh
 1. Pelarut (solvent): air (H2O)
 2. Terlarut (solut): elektrolit, non elektrolit
 Elektrolit:
Substansi yang berdisosiasi
(terpisah) di dalam larutan dan akan
menghantarkan arus listrik.
 Non-elektrolit :
Substansi seperti glokusa dan urea
yang tidak berdisosiasi dalam
larutan.
Keseimbangan elektrolit
 Cations – ions bermuatan positip
 Anions – ions bermuatan negatip
 Molekul organik
 Non-electrolytes: glucose, urea,
creatinine
 Movement of body fluids
“ Where sodium goes, water follows.”

Diffusion – movement of particles down a

concentration gradient.

Osmosis – diffusion of water across a

selectively permeable membrane

Active transport – movement of particles up

a concentration gradient ; requires energy
Difusi:
Difusi adalah proses dimana
partikel yang terdapat dalam cairan
bergerak dari konsentrasi tinggi ke
konsentrasi rendah sampai terjadi
keseimbangan.
 Osmosis:
Osmosis adalah bergeraknya pelarut
bersih seperti air, melalui membran
semipermeabel dari larutan yang
berkonsentrasi lebih rendah ke
konsentrasi yang lebih tinggi yang
sifatnya menarik.
Transport Aktif:

Bahan bergerak dari konsentrasi rendah ke

tinggi.
Diperlukan Energi.
Banyak zat terlarut penting ditransport secara
aktif melewati membran sel meliputi: natrium,
kalium, hidrogen, glukosa dan asam amino.
Tarnsport aktif adalah vital untuk
mempertahankan keunikan komposisi baik ECF
maupun ECF.
Fluid compartments

ICF
Fluid compartments

ICF

Interstitial
Plasma

ECF
Fluid compartments

ICF

Interstitial
Plasma

ECF
Fluid compartments
Capillary
Membrane

ICF

Interstitial
Plasma

ECF
Fluid compartments
Capillary
Membrane

ICF

Interstitial
Plasma

ECF
Fluid compartments
Capillary
Membrane Cell Membrane

ICF

Interstitial
Plasma

ECF
Colloid osmotic pressure
Capillary Capillary membrane freely permeable to
Membrane water and electrolytes but not to large
molecules such as proteins (albumin).

Interstitial
Plasma

ECF
Colloid osmotic pressure
Capillary Capillary membrane freely permeable to
Membrane water and electrolytes but not to large
molecules such as proteins (albumin).

Interstitial
Plasma

ECF
Colloid osmotic pressure
Capillary Capillary membrane freely permeable to
Membrane water and electrolytes but not to large
molecules such as proteins (albumin).
The albumin on the plasma side gives
rise to a colloid osmotic pressure
gradient favouring movement of water
H2O into the plasma
Interstitial
Plasma

H2O

ECF
 Colloid osmotic pressure
Capillary Capillary membrane freely
Membrane
permeable to water and
electrolytes but not to large
H2O molecules such as proteins
(albumin) .
H2O
Interstitial The albumin on the plasma side
Plasma

120/80 gives rise to a colloid osmotic

pressure gradient favouring
H2O movement of water into the plasma
This is balanced out by the
H2O
hydrostatic pressure difference

ECF
Cell Membrane
Cell Membrane

H2O

ICF
H2O
Interstitial

Cell membrane is freely permeable to H20 but

Cell Membrane
Cell Membrane

H2O

ICF
H2O
Interstitial
Na+

Cell membrane is freely permeable to H20 but Na and K are pumped

across this membrane to maintain a gradient!
Cell Membrane
Cell Membrane

H2O

ICF
H2O
Interstitial
Na-

Cell membrane is freely permeable to H20 but Na and K are pumped

across this membrane to maintain a gradient!
Cell Membrane
Cell Membrane

H2O

ICF
H2O
Interstitial
Na-

[K+] =150

Cell membrane is freely permeable to H20 but Na and K are pumped

across this membrane to maintain a gradient!
Cell Membrane
Cell Membrane

H2O
Na+= 144
ICF
H2O
Interstitial
Na-

[K+] =150

Cell membrane is freely permeable to H20 but Na and K are pumped

across this membrane to maintain a gradient!
Cell Membrane
Cell Membrane

H2O Na+= 10
Na+= 144
ICF
H2O
Interstitial
Na-

[K+] =150

Cell membrane is freely permeable to H20 but Na and K are pumped

across this membrane to maintain a gradient!
Cell Membrane
Cell Membrane

H2O Na+= 10
Na+= 144
ICF
H2O
Interstitial
Na-

[K+] =150

Cell membrane is freely permeable to H20 but Na and K are pumped

across this membrane to maintain a gradient!
 Balance
 Fluid and electrolyte homeostasis is
maintained in the body
 Neutral balance: input = output
 Positive balance: input > output
 Negative balance: input < output

37
Regulation of Fluids:
Renal sympathetic nerves
Renin-angiotensin-
aldosterone system
Atrial natriuretic peptide (ANP)
Composition of Body Fluids:
Cations Anions
150

100

ECF
Na+
50 Cl-

HCO3-
0
Ca 2+

Mg 2+ Protein
50 PO43-

ICF
K+ Organic
anion

100

150
Osmolarity = solute/(solute+solvent)
Osmolality = solute/solvent (290~310mOsm/L)
Tonicity = effective osmolality
Plasma osmolility = 2 x (Na) + (Glucose/18) + (Urea/2.8)
Plasma tonicity = 2 x (Na) + (Glucose/18)
Regulation of Fluids:

Hydrostatic pressure v.s. Oncotic pressure

 Albumin is the major determining oncotic pressure
Keseimbangan Elektrolit
 Def: konsentrasi tiap jenis elektrolit dalam
kompartemen cairan tubuh selalu normal dan
dipertahankan secara relatip tetap konstan
 Electrolytes larut dalam cairan tubuh
 Natrium merupakan kation predominan di
ECF, dan Chlorida merupakan anion
predominan di ECF
 Bicarbonate juga terdapat di ECF
Keseimbangan Elektrolit
 Kalium merupakan kation predominan di
ICF, dan Posfat merupakan anion
predominan di ICF
 Kation secara aktif di reabsorbsi (ginjal),
sedang anion secara pasif mengikuti
proses elektrokimia
 Aldosterone bekerja di tubulus ginjal untuk
mengatur kadar Natrium dan Kalium
Aktifitas Osmotik
Aktifitas osmotik menunjukkan jumlah
partikel solut didalam larutan
Osmolaritas, adalah aktifitas osmotik
per volume larutan, dinyatakan
dalam miliosmol/liter (mOsm/L)
Osmolalitas, adalah aktifitas osmotik
per-kg air (mOsm/kg H2O)
Basic Definitions
 MW (Molecular Weight) = sum of the
weights of atoms in a molecule
 mEq (milliequivalents) = MW (in mg)/
valence
 mOsm (milliosmoles) = number of
particles in a solution
Osmolalitas Plasma (mOsm/L):
Posm=2[Na+] + [glukosa]/18 + [BUN]/2,8

Normal: 280 – 290 mOs/L

Decrease Osmolality: < 280
Elevated Osmolality: > 290
Regulation of Fluids:
Renal sympathetic nerves
Renin-angiotensin-
aldosterone system
Atrial natriuretic peptide (ANP)
Normal Plasma Ranges of Electrolytes
Cations Concentration
Sodium 135-145 mEq/L
Potassium 3.5-5.0 mEq/L
Calcium 8.0-10.5 mEq/L
Magnesium 1.5-2.5 mEq/L
Anions
Chloride 95-105 mEq/L
Bicarbonate 24-30 mEq/L
Phosphate 2.5-4.5 mEq/L
Sulfate 1.0 mEq/L
Organic Acids (Lactate) 2.0 mEq/L
Total Protein 6.0-8.4 mEq/L
 GANGGUAN KESEIMBANGAN ELEKTROLIT

Elektrolit : penting menjaga proses

kehidupan di tubuh

Gangguan elektrolit :
•Gangguan metabolisme, Gangguan
potensial listrik jaringan mati
mendadak
GANGGUAN KESEIMBANGAN ELEKTROLIT
 Pada anamnesa, pemeriksaan fisik, lab,
dan treatment perlu ditentukan:
 1. Total cairan tubuh dan distribusinya
(hipovolemi, normovolemi, hipervolemi)
 2. Osmolalitas plasma ( hipotonik, isotonik,
hipertonik)
 3. Kadar elektrolit plasma
 4. Kadar elektrolit di urina
GANGGUAN KESEIMBANGAN ELEKTROLIT

 1. Natrium: Hiponatremi, Hipernatremi

 2. Kalium: Hipokalemi, Hiperkalemi

 3.Kalsium: hipokalsemi, Hiperkalsemi

 NATRIUM
 Gangguan konsentrasi [Na+] paling sering terjadi akibat drpd
gangguan homeostasis H2O, yg menyebabkan perubahan
perbandingan relatip [Na+] terhadap H2O.

 Gangguan keseimbangan [Na+] berhubungan dengan perubahan

volume ECF (hypo/normo/hyper).
Maintenance “effective circulating volume” diatur oleh perubahan
ekskresi Na urin, sedangkan keseimbangan air diatur oleh perubahan
intake/output air
 Kekacauan dapat terjadi akibat kekurangan cairan bersamaan
dengan adanya gangguan keseimbangan [Na+]
Peran sentral Natrium pada keseimbangan cairan
dan elektrolit:
Natrium merupakan kation terpenting untuk mengatur
keseimbangan cairan dan elektrolit karena jumlahnya
yang banyak pada ECF dan menentukan tekanan
osmotik /osmolalitas plasma.

Perubahan pada kadar natrium menimbulkan

pergeseran/kompensasi air untuk mempertahankan
keseimbangan, sehingga juga berpengaruh terhadap
vol plasma, tekanan darah, volume cairan interstisial
dan intra seluler
 Sodium (Na+) dalam serum 135 – 145 mEq/L
 Volume total dalam tubuh diperkirakan 40 mEq/kg,
1/3 terikat dalam tulang, 2/3 extracellular (trans-
membrane exchange)
 Normal kebutuhan/h 1-2 mEq/kg/h
 Kation utama cairan extracellular
 HIPONATREMI
Gejala klinis: tidak khas
Gejala edem sel otak, yang timbul bila
hipoosmolalitas dalam plasma terjadi
dengan cepat (air berpindah dari ECF
→ICF)
Pada kadar Na 120 – 125 : nausea-vomit
110 – 120 : letargi-sefalgia
< 110 : kejang-koma
Causes of Hyponatremia
Normal plasma osmolality
Pseudohyponatremia (hyperlipidemia);
rare if measured with ion-specific Na+
electrode
Elevated plasma osmolality
Hyperglycemia
Mannitol, glycerol, radiocontrast agents
Decreased plasma osmolality
Urine maximally diluted:
1. Decreased solute excretion (low protein intake)
2. Excessive water ingestion or intake
Urine not maximally diluted:
1. Normal extracellular volume
a. SIADH, Lung disease, CNS disease, Drugs, Anxiety
b. Adrenal insufficiency (may also have volume depletion)
c. Hypothyroidism
2. Low extracellular volume
a. Extrarenal loss
b. Renal loss: diuretics, sodium-losing nephropathy
3. Increased extracellular volume
a. Congestive heart failure
b. Cirrhosis
c. Nephrotic syndrome
treatment
 Hyponatremi berat ([Na+] <120 meq/L), timbul
mendadak (< 48 h), dan adanya gejala neurologic
(confusion, stupor, coma, atau seizures) harus
dikoreksi secara cepat
 Jika asymptomatic, hyponatremia ringan dan kronis
(> 48 h), tidak perlu dikoreksi secara cepat dan
agresif
HIPERNATREMIA
 Pada hiperNa, cairan intrasel →
ekstrasel → sel dehidrasi → ADH ↑
(kompensasi tubuh) → haus →
intake ↑
ETIOLOGI HIPERNATREMI
1.Kehilangan cairan
1.Insensible loss : demam, luka bakar
2.Melalui ginjal : diuretik, diabetes insipidus
2.Intake ↑
1.Pemberian NaCl hipertonis / Na bicarbonat
2.Hiperaldosteron & sindroma cushing
GEJALA KLINIS HIPERNATREMI
Terutama neurologis ok dehidrasi sel otak
• Twiching
• Lethargi
• Kejang
• Koma
• Kelemahan otot
 TERAPI HIPERNATREMI
 Pada keadaan akut harus segera dikoreksi
 Hipernatremi > 24 jam koreksi hati-hati dan
perlahan, ok koreksi yang cepat & progresif →
edem akut sel otak → kematian
 Dapat dikoreksi dengan cairan oral / parenteral
(dextrosan 5 % )
RUMUS Defisit Cairan :
0,6 (♂) / 0,5 (♀) X BB X Na Plasma
140 - 1
 KALIUM
 Kalium merupakan kation terbanyak di
intraseluler
 Gangguan keseimbangan kalium
merupakan perubahan/pertukaran antara
kalium intra dan ekstra seluler)
 Kadar dlm serum 3,5 – 5,0 mEq/L
 Volume total dalam tubuh 50 mEq/Kg
98% ada di intracellular (chief intracelluler cation)
konsentrasi di ICF 150 mEq mEq/L
konsentrasi di ECF 70 mEq mEq/L

Kebutuhan normal 0.5 – 0.8 mEq mEq/kg/hari

Berperan pada aksi membran potensial sel (syaraf,

otot)
 HIPOKALEMI
Gejala Klinis : sangat bervariasi, berat ringannya
tergantung derajat hipokalemi
1. Otot: mialgia, kelemahan/keram otot (sering extremitas bawah),
hipoventilasi (berat)
2. Jantung : 1. Aritmia
2.EKG : gel T datar, gel U, depresi ST, QT lebar
3.Hipotensi : ↓ resistensi perifer
3. Sal cerna : ileus paralitik
4. Ginjal: 1.Osmolalitas urin ↓
2.pH urin ↑
5. Endokrin : 1.Sekresi aldosteron ↓  eksresi K ↓
2.Gangguan toleransi glukosa ok sekresi insulin
terhambat
DIAGNOSIS HIPOKALEMI

Kalium serum < 3,5 mEq / L

 CAUSES OF HYPOKALEMIA

I. Decreased intake
A. Starvation
B. Clay ingestion
II. Redistribution into cells
A. Acid-base
1. Metabolic alkalosis
B. Hormonal
1. Insulin
2. â2-Adrenergic agonists (endogenous or
exogenous)
3. á-Adrenergic antagonists
C. Anabolic state
1. Vitamin B12 or folic acid
administration (red blood cell
production)
2. Granulocyte-macrophage colony-
stimulating factor (white blood cell
production)
3. Total parenteral nutrition
D. Other
1. Pseudohypokalemia
2. Hypothermia
3. Hypokalemic periodic paralysis
4. Thyrotoxic periodic paralysis
5. Barium toxicity
III. Increased loss
A. Nonrenal
1. Gastrointestinal loss (diarrhea)
2. Integumentary loss (sweat)
B. Renal
1. Increased distal flow: diuretics, osmotic
diuresis, salt-wasting nephropathies
2. Increased secretion of potassium
a. Mineralocorticoid excess
b. Distal delivery of non-reabsorbed
anions: vomiting, nasogastric
suction, diabetic ketoacidosis,
Terapi
 K oral utk pencegahan/terapi (KCL, K-I
aspartate)
 K parenteral, konsentrasi 10 mEq/L, atau 20-
40 mEq/L, kecepatan 10 – 20 mEq/jam,
contoh cairan Tridex, KCL:
• Hipokalemi barat
• Aritmia
• Gagal otot nafas
Obat-obatan yg mempengaruhi
Kalium
 Menurunkan Kalium: diuretik Tiazid
(ekskresi), β2 adrenergik agonist, Insulin,
hormon thyroid (memompa K ke
intraseluler)
Meningkatkan Kalium: ACE-I, ARB,
Spironolakton
 Figure 5 A clinical algorithm for investigating hypokalemia

Unwin, R. J. et al. (2011) Pathophysiology and management of hypokalemia: a clinical perspective

Nat. Rev. Nephrol. doi:10.1038/nrneph.2010.175
 HIPERKALEMI
 Plasma [K+] >5 meq/L.
 Hiperkalemi berat berpengaruh kepada
fungsi neuromuskuler dan aktifitas listrik
jantung, dengan EKG abnormal
 Dapat berlanjut menjadi heart block,
ventricular fibrillation, bahkan asytole
 Kelemahan otot-otot, paralisis,
hipoventilasi (otot pernapasan)
Etiologi hiperkalemi:
1. Intake ↑ - pisang, jeruk
2. - pemberian K i v
3. - hemolisis yang hebat
4. Tdk akan terjadi hiperkalemi bila ginjal berfungsi dengan baik
5. Perpindahan kalium ke ekstra sel
1.Asidosis 3. intoksikasi digitalis
2.Deff insulin 4. ketoasidosis
6. Eksresi ↓
1.Gagal ginjal 3. diuretik hemat K
2.Insuf adrenal
7. Pseudohiperkalemia
Leukositosis hebat ( > 100.000 / mm3 ) → wkt darah diambil →
K keluar sel
8. Obat-obat
ACE I, ARB, NSAID, aldosteron antagonis
DIAGNOSIS
MAJOR CAUSES OF
HYPERKALEMIA
 I. “Pseudo”-hyperkalemia
 A. Cellular efflux; thrombocytosis, leukocytosis, in vitro hemolysis
 B. Hereditary defects in red cell membrane transport
 II. Intra- to extracellular shift
 A. Acidosis
 B. Hyperosmolality; radiocontrast, hypertonic dextrose, mannitol
 C. β2-adrenergic antagonists (noncardioselective agents)
 D. Digoxin or ouabain poisoning
 E. Hyperkalemic periodic paralysis
 III. Inadequate excretion
 A. Inhibition of the renin-angiotensin-aldosterone axis;
 ↑ risk of hyperkalemia when used in combination
 1. ACE inhibitors
 2. Renin inhibitors; aliskiren (in combination with ACE
 inhibitors or ARBs)
 3. ARBs
 4. Blockade of the mineralocorticoid receptor;
 spironolactone, eplerenone
 5. Blockade of the ENaC; amiloride, triamterene,
 trimethoprim, pentamidine
 B. Decreased distal delivery
 1. Congestive heart failure
 2. Volume depletion
 3. NSAIDs, cyclosporine
 C. Hyporeninemic hypoaldosteronism
 1. Tubulointerstitial diseases; SLE, sickle cell
 anemia, obstructive uropathy
 2. Diabetes, diabetic nephropathy
 3. Drugs; NSAIDs, beta blockers, cyclosporine
 4. Chronic kidney disease, advanced age
 D. Renal resistance to mineralocorticoid
 1. Tubulointerstitial diseases; SLE,
 amyloidosis, sickle cell anemia,
 obstructive uropathy, post-ATN
 2. Hereditary;
 pseudohypoaldosteronism type I
 — defects in the mineralocorticoid
 receptor or ENaC
 E. Advanced renal insufficiency with low GFR
 F. Primary adrenal insufficiency
 1. Autoimmune; Addison’s disease, polyglandular endocrinopathy
 2. Infectious; HIV, CMV, TB, disseminated fungal infection
 3. Infiltrative; amyloidosis, malignancy, metastatic cancer
 4. Drug-associated; heparin, low-molecular-weight heparin
 5. Hereditary; adrenal hypoplasia congenita, congenital lipoid adrenal
 hyperplasia, aldosterone synthase deficiency
 6. Adrenal hemorrhage or infarction; may occur in antiphospholipid syndrome
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. β2-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.
 Terapi hiperkalemi
Mekanis terapi dosis onset durasi ket
me
Stabilisasi calsium 10% Ca 1 – 3 min 30–60 min Dapat diulang
membran gluconate, 10 tiap 5
potensial mL over 10 mt/EKG
min

Cellular K+ Insulin 8 U RI with 50 30 min 4- 6 jam Dapat

mL of D 40, if diulang/ 15
uptake blood sugar
mt
<250

β2-agonist Nebulized 30 min 2–4 h Bersama

insulin, hati2
albuterol, 10–
peny jtg
20 mg in 4 (tachicardi)
mL saline
Na Bicarbonat 150 mEq/ L D5, _ _
250 ml/jam

K+ removal Kayexalate 30–60 g PO in 1–2 h 4–6 h

20% sorbitol

Furosemide 20–250 mg IV 15 min 4–6 h

hemodialisis
PENGOBATAN Management of Hyperkalemia
K+ Meninggi ?

Tidak Ya
Berhenti Apakah nyata?

Tidak Ya
Berhenti Apakah > 6.0 mEq/L atau ada
perubahan EKG

Tidak Ya
Pasien perlu penurunan K+
darurat.

EKG abnormal ?

Tidak Ya
Beri insulin dengan glukosa
Beri kalsium glukonat
dan/atau Ventolin
dgn nebulizer

Lanjutkan dengan Periksa K+ urine,

evaluasi osmolailty, kreatinin

K < 6.0 mEq/L?

Tidak Ya
Ulangi insulin dan glukosa, Beri cation exchange resin atau
pertimbangkan hemodialisis furosemide
Evaluasi lanjutan dan
terapi jangka panjang
 Calcium (Ca++)
 Bagian darpd tulang, mineral paling banyak dalam tubuh,
98 % drp Ca berada didalam tulang
 Kation extraseluler
 Diperlukan pada proses pembekuan darah, saraf dan
fungsi otot
 PTH menyebabkan reabsorbsi dari tulang, meningkatkan
reabsorbsi dari GI tract, dan filtrasi glomerulus, sehingga
Ca dalam darah meningkat
 Calcitonin menghambat osteoclast dan merangsang
osteoblast, sehingga Ca dalam darah menurun
Gangguan keseimbangan Calcium
 Terjadi pada ECF
 Diatur oleh:
• Parathyroid hormone
• ↑Ca++ plasma dengan cara merangsang
osteoclast
• ↑GI absorpsi dan renal retensi
• Calcitonin dari kelejar thyroid
• ↑ Pembentukan tulang
• ↑ eksresi ginjal
105
 Hypercalcemia
 Akibat dari:
• Hyperparathyroidism
• Hypothyroid states
• Renal disease
• Excessive intake of vitamin D
• Milk-alkali syndrome
• Certain drugs
• Malignant tumors – hypercalcemia of malignancy
• Tumor products promote bone breakdown
• Tumor growth in bone causing Ca++ release
106
 Hypercalcemia
 Biasanya didapatkan juga hypophosphatemia
 Efeknya:
• Gejala non spesikfik – fatigue, weakness, lethargy
• Pembentukan batu ginjal, dan batu pankreas
• Kram otot
• Bradycardia, cardiac arrest
• Rasa nyeri
• Pada GI
• Nausea, abdominal cramps
• Diarrhea / constipation
• Metastatic calcification
107
 Hypocalcemia
 Hyperactive neuromuscular reflexes dan tetany bedakan dengan
hypercalcemia
 Convulsions pada keadaan berat
 Penyebab:
• Renal failure
• Kekurangan vitamin D
• Penekanan fungsi parathyroid
• Hypersecresi calcitonin
• Keadaan malabsorption
• Abnormal intestinal acidity dan keseimbangan asam/basa
• Infeksi luas atau inflamasi peritoneal

108
Hypocalcemia
 Diagnosis:
• Chvostek’s sign
• Trousseau’s sign
 Treatment
• IV calcium utk acute
• Oral calcium dan vitamin D utk yg kronis

109
TERIMAKASIH

WASSALAM
 Komposisi
Elektrolit
Ekstraselular
Intraselular
mEq/L Plasma Darah Interstisial

Kation
Na + 15 142 144
K+ 150 4 4
Ca ++ 2 5 2.5
Mg ++ 27 3 1.5
Anion
Cl - 1 103 114
HCO 3 - 10 27 30
HPO 4 = 100 2 2
SO 4= 20 1 1
Asam organik - 5 5
Protein 63 16 6