WATER AND ELECTROLYTES

DISTURBANCES
BODY WATER:
sodium (Na +) DOMINAN,
chloride (Cl), oxygen (O2), hydrogen
(H+), bicarbonate (HCO3),
calcium (Ca2+), potassium (K+),
sulfate (SO42), and phosphate
(PO43)
KIDNEY
HOMEOSTATIS
volume,
Electrolyte concentration,
acid-base balance of body fluids;
detoxify and eliminate wastes;
regulate blood pressure regulating fluid
volume.

skin and lungs
The also play a role in fluid and electrolyte
balance. Sweating results in loss of sodium
and water
every breath contains water vapor.

Mineral functions
Source of life
Basic component
enzyme and hormone functions
cells, tissues, bones, blood and body fluids
component
Help every life aspects: hormone and energy
production, dygestion, nerve transmition and muscle
contraction
Adjust pH, metabolism, cholesterol and blood
glucose.
Vitamins and enzyme activators

FLUIDS COMPARTMENS
INTRA CELLULER
EXTRA CELLULER
PLASMA
INTERSTITIAL
IN PATHOLOGIC
CONDITIONS:
THIRD ROUND
organs:
INTRAPERITONEAL
THORAX
OTHERS
FLUID EXCHANGE
BETWEEN BLOOD PLASMA AND INTERSTITIAL FLUID
OBJECTIVE: FLUID, ELEKTROLYTES AND PROTEIN
CONCENTRATION BALANCE
TWO PAIRS FORCES INFLUENCE:
THE FORCE THAT MOVE LUID FROM BLOOD VESSELS TO THE
INTERSTITIAL
PLASMA HYDROSTATIC PRESSURE
TISSUE OSMOTIC PRESSURE

THE FORCE THAT MOVE FLUID INTO BLOOD VESSELS
PLASMA PROTEIN ONCOTIC PRESSURE
INTERSTITIAL FLUID HIDROSTATIC PRESSURE
pH of body fluid
pH = 7.0
pH = 7.35
pH = 7.35 pH = 7.45
Sistem Buffer
sistem carbonic acidbicarbonate (the most
important, work in lung)
haemoglobineoxyhaemoglobine system
(work in red blood cells) haemoglobine
bind to free H+, the blood flow through lung
and the H+ combined with CO2.
Protein Buffer (in ECF and ICF)
Phosphat system (especially in ICF)
BUFFERING
1. Bicarbonate:
HCl + NaHCO3 H2O + NaCl
NaOH + H2CO3 NaHCO3 + H2O
2. Hb
Protein Proteinate- + H+
N+ + Proteinate Na-Proteinate
(extracell)
K+ + Proteinate K-Proteinate
(intracell)

BUFFERING
3. phosphate
Na2HPO4 +HCl NaCl + NaH2PO4
Keseimbangan Asam-Basa
<6.8 Dangerous to life
<7.2 seriously damage of cell functions
<7.35 acidosis
7.35 to 7.45 normal
>7.45 alkalosis
>7.55 seriously damage of cell functions
>7.8 Dangerous to life
pH influence on enzyme actions
ANION GAP CONSEPT
Total kations (Na+, K+, Ca++, Mg++ etc.) ar
always comparable with total anion (Cl-,
HCO3-, PO4-, SO4=, proteinate= etc.)
Routine measured: Na+, K+, Cl- and HCO3-)
Anion concentration always < kation
This difference called anion gape
ANION GAP
Anion gap = [Na+ + K+]-[Cl- + HCO3-]
Ex: for normal electrolytes levels
Anion gap = [140+4] [100 + 28]
= 16 mEq/L
K+ is seldom measured in clinical practice
anion gap = [Na+] [Cl- + HCO3-] = 12 4
mEq/L
What happent to anion gape in too acid or too
basic conditions?
pH = pK + log HCO3-
pCO2

PH = pK + log HCO3-
pCO2
Anion gap >>
Pathophysiologic Consept of Acid-
Base
Acidemia:
Acidosis (MA dan RA)
alkalemia,
Alkalosis (MA dan RA)
Compensation
Acidemia
PH arteri <7.35, More H+ ion in blood
ECF content >, H+ Ion into ICF. To get
extracellular elektricity of neutral intracel
pH the number of equivalent K+ leave the
cell relatif hyperkalemia.
Acidosis
> konsentrasi ion H+ sistemik.
Bila paru gagal mengeliminasi CO2 atau bila
produk asam-asam volatile (asam karbonat)
atau nonvolatile (asam laktat) hasil
metabolisme terakumulasi, konsentrasi ion H+
naik.
Acidosis dapat juga terjadi pada diare berat
hilang anion basa bikarbonat atau
ginjal gagal mensekresikan H+ atau
mereabsorbsi bikarbonat
Alkalosis
H+ level < in the body
Causes:
Lost of CO 2 during hyperventilation,
Lost of nonvolatile acids during vomit, or
more basic intake hidrogen ion consentration >


Alkalemia
Arterial blood pH > 7.45, relatively more
base in blood.
More H+ in ICF insist the to flow into ECF. For
ICF electrical homeostatis (neutralisation) K+
moves from ECF into ICF, relative
hypokalemia.

COMPENSATION
LUNG AND KIDNEY, AND CHEMICAL BUFFER
OF INTRACELLULAR AND INTRACELLULAR
COMPARTMENTS WORK TOGETHER TO
MAINTAIN PLASMA PH AT THE RANGE OF
7.35 to 7.45
ACID/BASE BALANCE
ACID/BASE DISTURBANCES AND
COMPENSATION
Metabolic acidosis/ alkalosis
Respiratory alkalosis
Ketoasidosis

Patofisiologi
Pengaturan konsentrasi elektrolit intraseluler
dan extraseluler tergantung pada:
Keseimbangan intake elektrolit dan output nya di
urin, feses, dan keringat
transport cairan dan elektrolit antara cairan
ekstraseluler dan intraseluler
1. Pengertian imbalance ECF
Gangguan Volume :
air berlebih (Overhydration)ECF
air kurang (Dehydration)
Hipervolemia : kelebihan air dan elektrolit
Hipovolemia : kekurangan air dan elektrolit
2. PENYEBAB OVERHYDRATION?
Kelebihan Na
Kelebihan infus, terutama yang hipertonis
Gangguan pengaturan homeostatik air dan Na:
Chronic renal failure
Congestive heart failure
Kelebihan terapi corticosteroid
Sindroma kekurngan ADH (SIADH)

3. PENYEBAB DEHYDRATION?
Kekurangan intake air dan elektrolit:
Gangguan mekanisme haus
Tak mampu menelan cairan
Kehilangan cairan melalui sekresi atau ekskresi:
Terapi diuretik kuat
Diabetes insipidus
Kehilangan cairan dari saluran GI
Keringat berlebihan

Tanda dan Gejala?
1. OVERHIDRASI:
Peningkatan berat badan tiba-tiba
Edema perifer
Nafas pendek dan paru-paru berbunyi
Perubahan perilaku : bingung, lemah
Pembuluh vena melebar
Pulsa meningkat (>)
BP meningkat
Pengosongan vena lambat
TANDA DEHIDRASI
Berat badan turun tiba-tiba
Turgor kulit menurun
Kekeringan membran mukosa
Kulit kasar
lidah kering
Perubahan perilaku: agitasi(terangsang), capek,
lemah
Vena leher datar pada posisi tidur
Pulsa lemah
Hipotensi Orthostatic
Pengisian vena perifer lambat
Ketidak seimbangan Elektrolit
Setiap mineral berpengaruh pada mineral lain
dalam tubuh
Bila satu mineral tidak seimbang
mempengaruhi keseimbangan mineral-mineral
lain melalui serangkaian reaksi berantai


Misalnya: Bila anda makan 1 tablet Fe
1. Na . Karena perangksangan kelenjar adrenal
2. Magnesium . Karena Na menurunkan Mg
3. Calcium . Karena bila Mg, Ca juga untuk
mempertahankan rasio calcium/ magnesium
4. K . Calcium dan potassium pindah ke arah
berlawanan Bila calcium , potassium .
Ex. If you take Iron tablet
5. Nitrogen . Karena oksiidasi cepat, kannibalisasi
proteins. (proteolisis)
6. Cu . Karena peningkatan laju pernafasan Cu
diperlukan dan digunakan. Bila ratio zinc thd Cu >
Cu availability akan sangat <. At < 1.0, zona cancer
7. Zinc . Bila Cu <, zinc juga < (Memperthankan ratio
Karena Zn diperlukan untuk fungsi kel adrenal,
Fungsi adrenal terganggu. rasa lelah
8. Mn . Karena Zn biasanya bergerak berlawanan
dengan Mn..
A. SODIUM (Na+)

1. normal:
Serum Na 135-145 MEq/L
Serum Na+ Menentukan osmolalitas darah

2. Ketidakseimbangan
Hypernatremia B
Serum Na+ > 145 mEq/L
Serum osmolality > 295 mOsm/kg
Hyponatremia
Serum Na <135 mEq/L
Functions
Maintenance of Membrane Potential
Nutrient Absorption and Transport
Maintenance of Blood Volume and Blood
Pressure

Pengaturan oleh Ginjal
Perubahan GFR atau hemodinamik ginjal
Aldosteron
Atrial natriuretic peptide (ANP)
PENYEBAB HYPERNATREMIA?
Kehilangan air:
Diabetes insipidus
Gangguan pemekatan Ginjal
diarrhea
Menurun intake air meningkat intakeNa+ :
Ketidakmampuan merespon mechanism haus
Susah menelan cairan
Makanan hipertonis kurang minum
Kelebihan penggunaan larutan NaCl atau NaHCO3
hipertonis
Hiperfungsi Adrenal Hyperaldosteronism
PENYEBAB HIPONATREMIA
Peningkatan ambilan air
Enema air
Perangantsangan anti diuretic hormone (ADH)
Psychogenic polydipsia
Kehilangan Na+:
Penggunaan diuretil loop gol thiazide
Kehilangan Na karena penyakit ginjal
Penggantian air tapi bukan elektrolit pad kasus terbakar,
muntah atau diare
Adrenal insufficiency
signs and symptoms Hypernatremia
Perubahan perilaku :
cemas
stupor, coma
Haus berlebihan
Lemah otot
Membran mukosa kering dan lengket
sign and symptoms Hyponatremia
Perubahan perilaku:
Cemas
Convulsions dan coma
Lemah otot
Mual dan cramp perut
Hypotension Postural
B. Potassium (K+)
1. normal:
Serum K+ 3.5 - 5.0 mEq/l
K+ is primarily intracellular (98%)

2. imbalance:
Hyperkalemia Serum K+ > 5.0 mEq/L
Hypokalemia Serum K+ < 3.5 mEq/L
Functions
Maintenance of Membrane Potential
Cofactor for Enzymes (K/Na ATPase, pyruvate
kinase)
Causes hyperkalemia
Increased K+ intake:
Rapid IV administration of K+
Administration of aged blood
Increased oral intake causes hyperkalemia only if
accompanied by decreased K+ excretion
Excessive use of salt substitutes (K+ClB)
Decreased renal excretion of K+:
Acute and chronic renal failure
Kerusakan sel (terbakar dll) K+ keluar dari sel
Asidosis (H+ banyak dalam sel K+ keluar)
Causes hyperkalemia
Decreased production of Aldosterone
Adrenal insufficiency (Addison=s disease)
Excessive use of K+ conserving diuretics: Spironolactone
(Aldactone) and Amiloride (Moduretic)
Movement of K+ into ECF:
Tissue injury (burns, major surgery, or crush injury)
Acidosis B decreased pH with excess H+ in ECF (compensation
causes K+ to shift from cells to ECF)
Insulin deficiency

Causes hypokalemia
Decreased K+ intake:
Anorexia nervosa
Gastrointestinal K+ loss:
Vomiting, gastric suction
Diarrhea, laxative abuse, recent ileostomy
Large sweat loss without K+ replacement
Increased renal excretion of K+:

Hypokalemia (cont)
Use of K+ losing diuretics without K+
replacement Ex.: Furosemide (Lasix),
Bumetanide (Bumex), and HCTZ
Hyperaldosteronism
Entry of K+ into cells:
Alkalosis : increased pH with decreased H+ in ECF
(compensation causes K+ to shift from ECF to
cells)

signs and symptoms hyperkalemia
Mental confusion
GI hyperactivity (abdominal cramping and
diarrhea)
Cardiotoxicity
EKG changes (K+ > 6 mEq/L:
Cardiac arrhythmias bradycardia and heart
block
Cardiac arrest
Sign and symptoms hypokalemia
Muscle weakness/paralysis, flaccid muscles
(lack tone)
Decreased bowel motility (intestinal ileus,
nausea and vomiting)
Polyuria
EKG changes (serum K+ < 3 mEq/L):
Cardiac arrhythmias
Respiratory failure K+ <1.5 mEq/L

C. Calcium (Ca++)
1. normal?
Serum Ca++ 8.5-11 mg/dL
Serum Ca++ and serum phosphate vary inversely

2. imbalance?
Hypercalcemia Serum Ca++ > 11 mg/dL
Hypocalcemia Serum Ca++ < 8.5 mg/dL
Physiological functions:
blood to clot,
bones hold up.
nerves fire,
for your brain to function,
for your muscles to contract.
heart beating
Calcium maintains the organization of tissues
Cofactor for Enzymes and Proteins
secretion of hormones (insuline)
causes hypercalcemia?
Ca++ release from bone:
Hyperparathyroidism
Metastatic carcinoma
Multiple myeloma
Thyrotoxicosis
Prolonged immobilization
Increase GI absorption of Ca++
Excessive ingestion of Vitamin D

Causes hypocalcemia:
Decreased intake or decreased GI absorption of Ca++:
Vitamin D deficiency
Chronic insufficient dietary intake of Ca++
Acute pancreatitis
Overuse of antacids
Malabsorption Syndromes
Decrease in physiologically available Ca++:
Hypoparathyroidism
Overuse of phosphate-containing laxatives and enemas (Ex.:
Fleet Phospho-soda)
Increased urinary excretion of Ca++:
Chronic renal failure

signs and symptoms?
hypercalcemmia
Nausea and vomiting
Constipation
Muscle weakness/flaccidity
Depressed deep tendon reflexes
Confusion, lethargy, CNS depression (coma)
Polyuria
Pathological fractures (chronic)
Renal calculi
EKG changes: Shortened QT interval, Cardiac arrest
brittle arteries
Sign and symptoms hypocalcemia
Muscle cramps
Confusion, anxiety
Tetany
Neuromuscular irritability:
Positive Chvostek= s sign muscle spasm at cheek and
corner of mouth in response to tap over facial nerve in front
of ear.
Positive Trousseau= s sign carpal spasms after occlusion of
blood flow to hand with BP cuff for three minutes.
Hyperactive deep tendon reflexes
Convulsions
EKG changes: Prolonged QT interval
Cardiac arrest
D. Magnesium (Mg++)
1. normal?

Serum Mg++ 1.5-2.5 mEq/L
Mg++ is absorbed primarily through the small intestine

2. imbalance:

Hypermagnesemia B Serum Mg++ >2.5 mEq/L
Hypomagnesemia B Serum Mg++ < 1.5 mEq/L
Functions:
structure and the function of the human body
Cell Signaling (involved in more than 300
essential metabolic reactions )
Energy Production
Synthesis of Essential Molecules
Ion Transport Across Cell Membranes
Cell Migration
causes hypermagnesemia
Excessive intake or absorption of Mg++:
Overuse of antacids containing Mg++ (Maalox,
Gelusil, Riopan)
Overuse of laxatives containing Mg++ (Milk of
Magnesia)
Impaired Mg++ excretion:Advanced renal
failure
Adrenal insufficiency (Addison=s disease)
causes hypomagnesemia
Decreased Mg++ intake or absorption:Chronic
diarrhea
Chronic malnutrition
Malabsorption syndrome B Steatorrhea
Small bowel resectionChronic alcoholism
Prolonged IV administration without Mg++
supplementation
Gastrointestinal Mg++ loss:Prolonged diarrhea or
nasogastric suction
Intestinal fistulas
Increased urinary excretion of Mg++:Prolonged
excessive diuretic therapy
signs and symptoms hypermagnesemia
Hypoactive deep tendon reflexes
Drowsiness, lethargy
Mild hypotension
Nausea and vomiting
Respiratory depression (serum Mg++ > 15 mEq/L)
dan paralisis otot
Cardiac arrhythmias (bradycardia, heart block)
Cardiac arrest (serum Mg++ > 25 mEq/L)
signs & symptoms hypomagnesemia
Hyperactive deep tendon reflexes
Coarse tremors
Tetany
Positive Chvosteks (FACE MUSCLE MOVING) and
Trousseaus sign (MUSCLE CRAMP)
Intense confusion
Cardiac arrhythmias
Convulsions
Coma
ALL DUE TO NERVE MUSCLE ALTERATION
conclutions
1. Mineral and fluid and pH imbalance will couse alteration of
other systems functions
2. Imbalance: over><less
3. Alterations and symptoms are depend on minerals / acid-
base imbalance
4. Imbalance of one mineral affects all minerals by massive
chain reactions of mineral imbalance
5. Acid/base imbalance will be compensated (respiratory or
kidney)
6. Be carefull of taking any food supplement containing
minerals!