Gangguan Keseimbangan

Cairan dan Elektrolit

Bag/SMF Anestesiologi dan Terapi Intensif FK

Undip/RSDK
Semarang
 GANGGUAN KESEIMBANGAN CAIRAN

KOMPENSASI DEKOMPENSASI

Kekurangan :
1. Pemasukan kurang
2. Pengeluaran berlebih

Kelebihan:
1. Pemasukan lebih
2. Pengeluaran kurang
 Disturbances of fluid homeostasis
• Disturbance of fluid balance (intake≠output)

– Dehydraton, Overhydration (hyperhydration)

• Disturbance of osmolarity (electrolyte intake≠water

intake)

– Isonatremic (isotonic)
– Hyponatremic (hypotonic)
– Hypernatremic (hypertonic)
 Dehydration
• Signs: increased thirst (except: advanced age, hypotonic
dehydration), weakness, decreased skin turgor, dry mucous
membranes, empty neck veins, decreased urine output,
elevated Htk, fever, tachycardia, hypotension, decreased
CVP,lethargy, stupor, coma

• Mild (loss: 4% of body weight): decresed skin turgor, sunken

eyes, dry mucous membranes
• Moderate (loss: 5-8 % of body weight): + oliguria, orthostatic
hypotension, tachycardia
• Severe (loss: 8-10 % of body weight): + hypotension,
decreased level of consciusness, stupor
 Dehydration
Isotonic Hypertonic Hypotonic

Se Na n + -
Se osmolarity n + -
Hb + + +
Htk + + +
Blood volume - - -
Thirst mod. increase increased no
 Isotonic dehydration
• Intracellular fluid volume remains constant

• External loss: vomiting, diarrhoea, haemorrhage,

burning

• Internal loss: ileus, ascites, pleural effusion

• Therapy: volume replacement wiht isotonic solution

 Hypertonic dehydration
• Extracellular + intracellular fluid loss; elevated
osmolarity

• Causes: inadequate replacement of hypotonic fluid

loss, osmotic diuresis (diabetes), decreased ADH
secretion, high fever, heat stroke, massive diarrhoea

• Therapy: slow water replacement, hypotonic solutions

are contraindicated in the first phase of replacement
 Hypotonic dehydration
• Decreased extracellular fluid volumen, elevated
intracellular fluid volume

• Causes: inadequate fluid replacement with hypotonic

solution, elevated ADH secretion + extracellular fluid
loss, diuretics, vomiting

• Usually no thirst

• Therapy: Isotonic fluid replacement, Na replacement in

case of severe hyponatraemia
4. DEHIDRASI
Derajat dehidrasi:
Dewasa Bayi dan Anak
Dehidrasi ringan 4 % BB 5 % BB
Sedang 6 % BB 10 % BB
Berat 8 % BB 15 % BB

Tanda klinis:
Ringan Sedang Berat
Defisit 3-5 % 6-8 % ≥ 10 %
Hemodinamik takikardia takikardia takikardia
nadi lemah nadi sangat lemah nasi tak teraba
volume collapse akral dingin
hipotensi ortostatik sianosis
Jaringan lidah kering lidah keriput atonia
turgor turun turgor kurang turgor buruk
Urine pekat jumlah kurang oliguria
SSP mengantuk apatis coma
Stadium Syok (Kehilangan Cairan)
1. Stadium Kompensasi
fungsi organ vital bertahan dengan peningkatan
reflek simpatis

2. Stadium Dekompensasi
gangguan perfusi jaringan

3. Stadium Irreversibel
kerusakan & kematian sel.
Stadium Kompensasi
A. Resistensi sistemik meningkat
Distribusi selektif aliran darah ke organ primer.
Resistensi arteriol meningkat  diastolik
meningkat.
B. Denyut jantung meningkat  COP naik.
C. Sekresi vasopresin, RAA meningkat ginjal
menahan air dan Na dalam sirkulasi.
Stadium Dekompensasi
a. Perfusi jaringan buruk  O2 sangat turun 
metabolisme anaerob  laktat naik  laktat
asidosis, CO2 menumpuk  asidemia 
kontraktilitas miokard terhambat.
b. Gangguan pompa Na/K tingkat sel  gangguan
membran sel, lisosom & mitokondria  sel
rusak.
c. Aliran darah lambat, rusaknya rantai kinin dan
sistem koagulasi  agregasi trombosit 
tendensi perdarahan.
Stadium Dekompensasi
d. Pelepasan mediator vaskuler : histamin,
serotonin, sotokin (TNFα dan IL1), xanthin
oksidase  O2 radikal & faktor agregasi
trombosit.
Vasodilatasi arteriol, permeabilitas kapiler
meningkat  venous return turun  preload
turun  COP turun.
Manisfestasi klinis :
Takikardi, TD sangat turun, perfusi perifer
buruk, asidosis, oliguria, kesadaran turun.
Stadium Irreversible
Syok berlanjut  sel rusak dan mati  MOF.
Cadangan ATP akan habis, terutama di jantung dan
hepar  tubuh kehabisan energi.

Manisfestasi klinis :
Nadi tak teraba, TD tak terukur, anuria,
tanda-tanda kegagalan organ.
 CARA PENGELOLAAN:
A. Berdasar Derajat Dehidrasi :
- BB 50 kg ---> DH. Berat (10%) = 10% x 50 L=5 L
Vol Pemberian Cairan = seluruh Defisit atau 2/3 bagian.

- Kecepatan infus tergantung :

Klinis / tingkat Dehidrasi & Kondisi Jantung.

- DH. Ringan / sedang : dibagi rata / 24 Jam

- DH. Berat & Syok : Rehidrasi cepat
- 20 - 40 ml/kg BB dalam 1-2 Jam
- 50% dari sisa devisit dalam 8 Jam
- Sisanya defisit dalam 16 Jam
Tahap berikutnya
- Ditambah kebutuhan dasar
(2 ml / kg BB/Jam)
PERDARAHAN
Penggantian bila dipakai :
Kristaloid : 3 kali volume darah yang hilang.
Koloid : Sesuai jumlah darah yang hilang.
( Gelatin, Hestastarch)
Darah : Sesuai jumlah darah yang
hilang.
 Hyperhydration
• Signs: oedema, increased skin turgor, elevated
CVP, distended neck veins, pulmonary oedema
Isotonic Hypertonic Hypotonic
SeNa n + -
Se osmolarity n + -
Hb - - -
Htk - -- (-)
Blood volume + + +
 Isotonic hyperhydration
• Intracellular fluid volume remains constant

• Causes: renal failure, heart failure; decreased

oncotic pressure, increased isotonic fluid
intake

• Therapy: decrease intake, diuretics

 Hypertonic hyperhydration
• Infrequent

• Causes: renal failure, excessive hypertonic fluid

input

• Increased thirst, fever, convulsion, coma

• Therapy: diuretics, dialysis + slow replacement with

hypotonic solutions
 Hypotonic hyperhydration
• Intracellular fluid volume is also increased
• Water poisoning
• Causes: heart failure, near drowning (fresh-water),
increased input of hypotonic solutions (TUR syndrome)

• Symptomes: weakness, nausea, vomiting,altered mental

status

• Therapy: diuretics + fluid replacement with isotonic

solution (+ Natrium)
 Electrolyte Imbalances
Sodium!
Normal range – 135 to 145 mEq/L
- Primary regulator of ECF volume (a loss or gain
of sodium is usually accompanied by a loss or
gain of water)
 Hyponatraemia
• Serum Na < 135 mmol/l
• Causes:
– Water problem (excess of water relative to sodium)
– Water excretion by the kidney is impaired
– Pseudohyponatraemia (hyperlipidaemia, hyperproteinaemia)

• Symptoms:
– Cerebral oedema
– Nausea, vomiting, lethargy, confusion, seizures, coma

• Therapy:
– Hypertonic saline (Se Na < 125 mmol/l)
– Isotonic saline (se na > 125 mmol/l)
– Increase rate of se Na level should be less than 2 mmol/h (cave:
Central pontin myelinolysis)
 Hypernatraemia
• Se Na > 145 mmol/l
• Causes: inadequate water intake and increased free
water loss; intake of hypertonic sodium solution
• Symptoms:
– Increased thirst
– Central nervous system abnormalities (confusion,
weakness, lethargy, seizures, coma)
• Therapy: water repletion, correction rate of Na level
should be no greater than 2 mmol/h (cave: cerebral
oedema)
 All About Potassium
• Major Intracellular electrolyte
• 98% of the body’s potassium is inside the cells
• Most abundant cation of ICF, helps maintain ICF
volume
• Influences both skeletal and cardiac muscle activity
• Key role in the resting membrane potential and
action potential of neurons and muscle fibers
• Normal serum potassium concentration – 3.5 to
5.5 mEq/L.
 Hyperkalemia
• Serum Potassium greater than 5.5 mEq/L
- More dangerous than hypokalemia because
cardiac arrest is frequently associated with
high serum K+ levels
 Hyperkalaemia
• Se K > 5 mmmol/l

• Causes
– Impaired excretion
• Renal failure, mineralocorticoid deficiency,
pseudohypoaldosteronism, drugs (potassium sparing
diuretics, ACE-inhibitors NSAID, cyclosporin)
– Shifts of K out of cells
• Tissue breakdown, acidosis, insulin deficiency
 Hyperkalaemia
• Symptoms:
• Cardiac (peaked T waves, loss of P waves, heart
blocks, ventricular arrhytmias, widening of QRS
complexes, asystole)
• Paresthesias, weakness, paralysis
• Acidosis
 Hyperkalaemia
• Therapy
– Direct antagonism of hyperkalemic effect on cell membrane
polarization
• Calcium gluconate
– Movement of extracellular K into intracellular compartment
• Insulin (+glucose)
• Sodium bicarbonate
• β2-adrenergic agonists
– Removal K from the body
• Loop diuretics
• Sodium polystyrene sulfonate
• Dialysis
 Hypokalaemia
• Se K < 3,5 mmmol/l
• Causes:
– Increased excretion: diarrhoea, renal losses, mineralocorticoid excess,
magnesium depletion
– Shifts of K into cells: drugs (insulin, β2-adrenergic agonists,
theophylline, caffeine), alkalosis, hyperthyreoidism
• Symptoms:
– Cardiac: flat t waves, ST depression, U wave, QT interval prolongation,
arrhytmias
– Muscle paralysis, rhabdomyolysis
– Coma
– Metabolic alkalosis
 Hypokalaemia
• Therapy
– Supplementation of K
– (Knormal-Kmeasured) * ttkg * 0.2 + daily need
– Infusion rate: no more, than 20 (30) mmol/h
– Oral supplementation
– 1 gr potassium-chloride containes 13,4 potassium,
1 gr potassium-citrate containes 9,2 mmol/l
potassium
 Calcium
• More than 99% of the body’s calcium is
located in the skeletal system
• Normal serum calcium level is 8.5 to 10mg/dL
• Needed for transmission of
nerve impulses
• Intracellular calcium is needed
for contraction of muscles
 Calcium 2
• Extracellular needed for blood clotting
• Needed for tooth and bone formation
• Needed for maintaining a normal heart
rhythm
 Hypocalcemia
• Serum Calcium level less than 8.5 mEq/L
 Hypocalcemia 2
• Causes
- Vitamin D/Calcium deficiency
- Primary/surgical hyperparathyroidism
- Pancreatitis
- Renal failure
 Hypocalcemia 3
• Clinical Manifestations
- Tetany and cramps in muscles of extremities
Definition – A nervous affection characterized by
intermitten tonic spasms that are usually
paroxysmal and involve the extremities
 Hypocalcemia 4
• Trousseau’s sign – carpal spasms
 Hypocalcemia 5
• Chvostek’s sign – cheek twitching
 Hypocalcemia 6
• Seizures, mental changes
 Hypocalcemia 7
- EKG shows prolonged QT intervals
 Hypocalcemia 8
• Medical management
- IV/PO Calcium Carbonate or Calcium
Gluconate
- Encourage increased dietary intake of Calcium
- Monitor neurlogical status
- Establish seizure precautions
 Hypercalcemia
• Serum Calcium level greater than 10.5 mEq/L
 Hypercalcemia 2
• Causes:
- Hyperparathyroidism
- Prolonged immobilization
- Thiazide diuretics
- Large doses of Vitamin A and D
 Hypercalcemia 3
• Clinical manifestations:
- Muscle weakness, nausea and vomiting
- Lethargy and confusion
- Constipation
- Cardiac Arrest (in
hypercalcemic crisis,
level 17mg/dL or
higher)
 Hypercalcemia 4
• Management
- Eliminate Calcium from diet
- Monitor neurological status
- Increase fluids (IV or PO)
- Calcitonin
 Calcitonin
- used to lower serum calcium level
- useful for pts with heart disease or renal
failure
- reduces bone resorption
- increases deposit of calcium and phosphorus
in the bones
- increases urinary excretion of calcium and
phosphorus
• Parathyroid pulls, calcitonin keeps

Parathyroid hormone pulls calcium out of the

bone.
Calcitonin keeps it there.
 Magnesium
- Normal serum magnesium level is 1.5 to 2.5 mg/dL
- Helps maintain normal muscle and nerve activity
- Exerts effects on the cardiovascular system, acting
peripherally to produce vasodilation
- Thought to have a direct effect
on peripheral arteries and
arterioles
 Hypomagnesemia
• Serum Magnesium level less than 1.5 mEq/L
 Hypomagnesemia
• Causes
- Chronic Alcoholism

- Diarrhea, or any disruption in small bowel

function
 Hypomagnesemia 2
- TPN

- Diabetic ketoacidosis
 Hypomagnesemia 4
• Clinical manifestations
- Neuromuscular irritability
- Positive Chvostek’s and Trousseau’s sign
- EKG changes with prolonged QRS, depressed
ST segment, and cardiac dysrhythmias
- May occur with hypocalcemia and
hypokalemia
 STARVED
• Starved – possible cause of hypomagnesemia

• Seizures
• Tetany
• Anorexia and arrhythmias
• Rapid heart rate
• Vomiting
• Emotional lability
• Deep tendon reflexes increased
 Hypomagnesemia 5
• Management
- IV/PO Magnesium replacement, including
Magnesium Sulfate
- Give Calcium Gluconate if accompanied by
hypocalcemia
- Monitor for dysphagia, give soft foods
- Measure vital signs closely
 Hypomagnesemia 6
• Foods high in Magnesium:
- Green leafy vegetables
 Hypomagnesemia 7
- Nuts

- Legumes
 Hypomagnesemia 8
• Seafood

• Chocolate
 Hypermagesemia
• Serum Magnesium level greater than 2.5
mEq/L
 Hypermagnesemia 2
• Causes
- Renal failure
- Untreated diabetic ketoacidosis
- Excessive use of antacids and laxatives
 Hypermagnesemia 3
• Clinical manifestations
- Flushed face and skin warmth

- Mild hypotension
 Hypermagnesemia 4
- Heart block and cardiac arrest
- Muscle weakness and even paralysis
 RENAL
• Reflexes decreased (plus weakness and
paralysis)
• ECG changes (bradycardia and hypotension)
• Nausea and vomiting
• Appearance flushed
• Lethargy (plus drowsiness and
coma)
 Hypermagnesemia 5
• Management
- Monitor Mg levels
- Monitor respiratory rate
- Monitor cardiac rhythm
- Increase fluids
- IV calcium for
emergencies
 Phosphorus
- Normal serum phosphorus level is 2.5 to 4.5
mg/dL
- Essential to the function of muscle and red
blood cells, maintanence of acid-base balance,
and nervous system
- Phosphate levels vary inversely to calcium
levels
- High Calcium = Low Phosphate
 Hypophosphatemia
• Serum Phosphorus level less than 2.5 mEq/L
 Hypophosphatemia 2
• Causes
- Most likely to occue with overzealous intake
or administration of simple carbohydates
- Severe protein-calorie
malnutrition (anorexia or
alcoholism)
 Hypophosphatemia 3
• Clinical manifestations
- Muscle weakness
- Seizures and coma
- Irritability
- Fatigue
- Confusion
- Numbness
 Hypophosphatemia 4
• Management
- Prevention is the goal
- IV Phosphorus for severe
- Prevention of infection
- Monitor phosphorus levels
- Increase oral intake of phosphorus rich foods
 Hypophosphatemia 5

Foods rich in Phosphorus:

- Milk and milk products

- Organ meats
- Nuts
- Fish
 Hypophosphatemia 6
- Poultry

- Whole grains
 Hyperphosphatemia
• Serum Phosphorus level greater than 4.5
mEq/L
• Causes
- Renal failure
- Chemotherapy
- Hypoparathyroidism
- High phosphate intake
 Hyperphosphatemia 2
• Clinical manifestations
- Tetany
- Muscle weakness
- Similar to Hypocalcemia because of reciprocal
relationship
 Hyperphosphatemia 3
• Management
- Treat underlying cause
- Avoid phosphorus rich foods