GANGGUAN PADA KESEIMBANGAN

ELEKTROLIT
dr. Andi Sulistyo Haribowo, Sp.PD.
SPESIALIS PENYAKIT DALAM
Program Studi Pendidikan Dokter
UNIVERSITAS ISLAM MALANG
2012

FLUIDS and ELECTROLYTES

ELECTROLYTES
Functions of Electrolytes
Contribute most of the osmotically active
particles in body fluids
Provide buffer systems for pH regulation
Provide the proper ionic environment for
normal neuromuscular irritability & tissue
function

DISTRIBUTION OF ELECTROLYTES

CATIONS AND ANIONS IN BODY FLUIDS

Figure 27.2

DISTRIBUTION OF MAJOR
ELECTROLYTES

Na+ and CL- predominate in extracellular fluids

(interstitial fluid and plasma) but are very low
in the intracellular fluid (cytoplasm)
K+ and HPO42- predominate in intracellular fluid
(cytoplasm) but are in very low concentration in
the extracellular fluids (interstitial fluid and
plasma)
At body fluid pH, proteins [P -] act as anions;
total protein concentration [P -] is relatively
high, the second most important anion, in the
cytoplasm, [P-] is intermediate in blood plasma,
but [P-] is very low in the interstitial fluid

DISTRIBUTION OF MINOR
ELECTROLYTES

HCO3- is in intermediate concentrations in all

fluids, a bit lower in the intracellular fluid
(cytoplasm); it is an important pH buffer in the
extracellular comparments
Ca++ is in low concentration in all fluid
compartments, but it must be tightly
regulated, as small shifts in Ca++ concentration
in any compartment have serious effects
Mg++ is in low concentration in all fluid
compartments, but Mg++ is a bit higher in the
intracellular fluid (cytoplasm), where it is a
component of many cellular enzymes

REGULATION OF ELECTROLYTES

Major Cations in body fluids

Sodium

(Na+)
Potassium (K+)
Calcium (Ca++)
Magnesium (Mg++)

PRINCIPLES OF ELECTROLYTE
DISTURBANCES

Implies an underlying disease process

Treat the electrolyte change, but seek the

cause

Clinical manifestations usually not specific to

a particular electrolyte change, e.g.,
seizures, arrhythmias

PRINCIPLES OF ELECTROLYTE
DISTURBANCES

Clinical manifestations determine urgency

of treatment, not laboratory values

Speed and magnitude of correction

dependent
on clinical circumstances

Frequent reassessment of electrolytes

required

ELECTROLYTES & THEIR IMBALANCES

SODIUM (NA+)

Sodium balance
Sodium = major cation in extracellular fluid (ECF)
Sodium = most common problem with electrolyte balance

Key to balance: ingestion via G-I tract = excretion via kidney

Aldosterone controls sodium levels via the kidney

Remember aldosterones antagonist = ANP

Sodium contributes to resting membrane potential
Sodium rushing into cell via open channels causes
depolarization of nerves and muscles

DISORDERS OF SODIUM
BALANCE
Na+

is the most abundant electrolyte in the

ECF.
Na+

and accompanying anion Cl- are

responsible for normal osmotic activity of the
ECF.

All

gain/loss of Na+ is accompanied by

gain/loss of water.

HYPONATREMIA

Hypovolemic hyponatremia
Vomiting
Diarrhea
Diuretics
Adrenal insufficiency

Normovolemic hyponatremia
Syndrome of inappropriate secretion of antidiuretic hormone
Renal failure
Water intoxication

Hypervolemic hyponatremia
CHF
Liver failure
Nephrotic syndrome

CLINICAL MANIFESTATIONS OF
HYPONATREMIA

Neurologic
Seizure
Coma
Agitation

Gastrointestinal
Anorexia
Nausea/vomiting

Muscular
Cramps
weakness

Headache
Cerebral edema

Confusion

TREATMENT OF HYPONATREMIA
Fluid

restriction

Administration

of hypertonic saline and an

osmotic or loop diuretic

!!!Correction

of serum sodium levels too

rapidly can result in neurologic damage and
central pontine myelinolysis!!!

HYPONATREMIA

Acute, symptomatic hyponatremia

Correct

no faster than 1 mEq/L per hour for the

first 6-8 mEq/L
No more than 10-12 mEq/L in first 24 hours
5% saline is almost never needed
Calculate the Na deficit

Na mEq = ([Na desired] - [Na measured]) X TBW

TBW = .5 or .6 X weight in KG

CAUSES OF HYPERNATREMIA

Most common cause is water deficiency d/t:

Excessive loss
Inadequate intake

Also may be caused by:

Exogenous Na+ load
Primary hyperaldosteronism
Diabetes insipidus
Renal dysfunction

CLINICAL MANIFESTATIONS OF
HYPERNATREMIA
Tremulousness
Irritability
Ataxia
Mental
Coma

confusion

d/t cerebral water loss

TREATMENT OF
HYPERNATREMIA
Renal

tubular diuretics

Hemodialysis
Treat

central diabetes insipidus with

vasopressin

!!!Correction

of serum sodium level too

rapidly can result in neurologic damage
secondary to cerebral edema!!!

HYPERNATREMIA

Treatment
Severe

ECFV depletion is the priority and should

be corrected with NS first. Subsequent fluid
replacement can be hypotonic
Major complication of overly rapid correction is
cerebral edema
Safe rate is no more than .5- 1 mEq/L per hour
Should take 36-72 to hours to completely correct

HYPERNATREMIA

Treatment
Calculate

the water deficit

H2O deficit = TBW X ([Na meas]- [Na des])/[Na
des]
Important to take into account ongoing losses

insensible losses .5 - 1 liter/24 hours

with fever, these losses increase by 60-80ml/24 hrs for
each degree Farenheit

POTASSIUM REGULATION

Major electrolyte and principle cation in the

extracellular fluid
Regulates

metabolic activities
Required for glycogen deposits in the liver and
skeletal muscle
Required for transmission of nerve impulses, normal
cardiac conduction and normal smooth and skeletal
muscle contraction
Regulated by dietary intake and renal excretion

ELECTROLYTES & THEIR IMBALANCES

POTASSIUM (K+)

Potassium balance
Major intracellular cation
Balance: ingestion = excretion (via kidneys)
Aldosterone primarily controls potassium
It exchanges potassium for sodium
Insulin also regulates potassium
It drives it into cells (with sugar) & thus produces
hypokalemia
pH also affects potassium secretion
Acidosis: more H+ in blood which finds its way into cell
& pushes K+ into blood

Also get kidney to exchange H+ for K+

Acidosis -gives- hyperkalemia

Alkalosis:

less H+ in blood

Kidneys exchange K+ for H+; thus get hypokalemia

The relation between potassium and hydrogen ions in the plasma

Saladins Anatomy & Physiology fourth edition McGraw Hill

Potassium balance in the body

Costanzo Physiology second edition Saunders

POTASSIUM ION REGULATION IN

ECF

27-30

HYPOKALEMIA
Causes

Gastrointestinal losses
Systemic alkalosis
Diabetic ketoacidosis
Diuretic therapy
Sympathetic nervous system stimulation
Administration of beta-adrenergic receptor
agonists

HYPOKALEMIA

Spurious hypokalemia
Marked

leukocytosis
A dose of insulin right before the blood draw

Redistribution hypokalemia
Alkalosis

(K decreases .3 for every .1 increase in

pH)
Increased Beta2 adrenergic activity
Theophylline toxicity
Familial

HYPOKALEMIA

Extrarenal depletion
diarrhea
laxative

abuse
sweat losses
fasting or inadequate intake

HYPOKALEMIA

Renal potassium depletion

urine

potassium > 20 mEq/24 hrs

spot urine with > 20 mEq K/gram creatinine
classified whether they occur with a metabolic
alkalosis

vomiting/NG suction
diuretic tx
Mineralocorticoid excess syndromes

HYPOKALEMIA

Renal losses
metabolic

RTA Type I and II

DKA
Carbonic anhydrase inhibitor therapy
Ureterosigmoidostomy

No

acidosis

acid-base disorder

Mg deficiency
Drugs

CLINICAL MANIFESTATIONS OF
HYPOKALEMIA

Autonomic neuropathy

Skeletal muscle weakness

Increased sensitivity to Digoxin

Cardiac
Decreased myocardial contractility
Electrical conduction abnormalities
Arrhythmias
Tachycardia
Ventricular fibrillation

POTASSIUM

Copyright 2008 by Pearson Education, Inc.

HYPOKALEMIA AND THE EKG

Prolonged PR interval

Prolonged T interval

Widening of QRS

Flattened T wave

TREATMENT OF HYPOKALEMIA
Slow

IV potassium supplements

Anesthesia

related concerns:

Increased risk of myocardial irritability K+ <2.6

Avoid hyperventilation of the lungs
Avoid glucose containing IV solutions
Avoid rapid infusion of IV K+ supplements

HYPERKALEMIA

Severe hyperkalemia is a medical emergency

Neuromuscular signs (weakness, ascending
paralysis, respiratory failure)
Progressive ECG changes (peaked T waves,
flattened P waves, prolonged PR interval,
idioventricular rhythm and widened QRS
complex, sine wave pattern, V fib)

HYPERKALEMIA
Causes

Increased total body potassium

Renal failure
Potassium-sparing diuretics
Excessive IV K+ supplements
Excessive use of salt substitutes

Altered distribution of potassium

Metabolic or respiratory acidosis
Digitalis intoxication
Insulin deficiency
Hemolysis
Tissue and muscle damage after burns
Administration on succinylcholine

CLINICAL MANIFESTATIONS OF
HYPERKALEMIA
Areflexia
Weakness
Paralysis
Paresthesia
Cardiac

conduction abnormalities

HYPERKALEMIA AND THE EKG

Narrowing and peaking of T waves

1st degree AV block

QRS widening

ST segment depression

Progression to merging of QRS an

T waves to a sine wave

Tachycardia

Ventricular fibrillation

HYPERKALEMIA

Etiology renal failure,

transcellular shifts, cell
death, drugs,
pseudohyperkalemia

Manifestations
cardiac, neuromuscular

TREATMENT OF HYPERKALEMIA
Primary

goal

Avoid adverse cardiac effects

Insulin and glucose to shift K+ into cells
IV calcium to antagonize cardiac effects of
hyperkalemia

Anesthesia

related concerns:

A serum K+ of 5.5mEq/L is upper limit for elective

procedures

HYPERKALEMIA

Treatment
Stop

potassium!
Get and ECG
Hyperkalemia with ECG changes is a medical
emergency

HYPERKALEMIA

Treatment
First

phase is emergency treatment to

counteract the effects of hyperkalemia

IV Calcium

Temporizing

treatment to drive the potassium

into the cells

glucose plus insulin

Beta2 agonist
NaHCO3

HYPERKALEMIA

Treatment
Therapy

directed at actual removal of potassium

from the body

sodium polystyrene sulfonate (Kayexalate)

dialysis

Determine

and correct the underlying cause

ELECTROLYTES & THEIR IMBALANCES

CALCIUM (CA++)

Calcium balance

Calcium is most abundant mineral in body

Calcium is important as an extracellular cation
Calcium & phosphorus have a reciprocal relationship
Calcium balance is dependent on:
Parathyroid hormone (PTH)
Calcitriol (active vitamin D)
Calcitonin (from thyroid)
98% of calcium reabsorbed at the kidneys

Calcium functions
Structural strength for bones & teeth
Maintains stability of nerve membrane
Required for muscle cell contraction
Necessary for blood clotting

REGULATION OF CALCIUM IONS

Regulated within
narrow range
extracellular
levels prevent
membrane
depolarization
Decreased levels lead
to spontaneous action
potential generation

Elevated

Terms
Hypocalcemia
Hypercalcemia

PTH increases Ca2+

extracellular levels
and decreases
extracellular
phosphate levels
Vitamin D stimulates
Ca2+ uptake in
intestines
Calcitonin decreases
extracellular Ca2+
levels
27-50

REGULATION OF CALCIUM IONS

27-51

HYPOCALCEMIA
Causes:

Decreased serum albumin concentration

Chelation of calcium by citrate
Rhabdomyolysis
Hypoparathyroidism
Pancreatitis
Renal failure

CLINICAL MANIFESTATIONS OF
HYPOCALCEMIA
Neuromuscular

irritability

Tetany
Laryngospasm
Hyperactive deep tendon reflexes

Weakness
Vasodilation
Myocardial

dysfunction
Bradycardia
Heart block

TREATMENT OF HYPOCALCEMIA
Calcium

replacement

Intraoperative

hyperventilation and
respiratory alkalosis

HYPERCALCEMIA
Causes:

Calcium mobilization from bone due to

immobility

Tumors

Hyperparathyroidism

CLINICAL MANIFESTATIONS OF
HYPERCALCEMIA
Anorexia
Nausea
Constipation
Cognitive

depression
EKG changes

Prolonged PR interval
Shortened QT interval
PVCs

TREATMENT OF
HYPERCALCEMIA
Treatment

of underlying cause
Volume expansion
Intraoperative hypercalcemia should be
managed with administration of adequate
fluids and maintenance of urine output.

Copyright 2008 by Pearson Education, Inc.

REGULATION OF CHLORIDE &

MAGNESIUM IONS

Chloride ions
Predominant anions in ECF
Magnesium ions
Capacity of kidney to reabsorb is limited
Excess lost in urine
Decreased extracellular magnesium results in
greater degree of reabsorption

27-59

MAGNESIUM
REGULATION
Essential for enzyme activities

Neurochemical activities
Cardiac and skeletal muscle excitability
Regulation
Dietary
Renal

mechanisms
Parathyroid hormone action

50 60% of magnesium contained in bones

1%

in ECF
Minimal amount in cell

REGULATION OF BLOOD
MAGNESIUM

27-61

HYPOMAGNESEMIA
Serum

magnesium less than 1.5mEq/L

Causes:

Inadequate intake of magnesium

TPN
Gastrointestinal losses
Pancreatitis
Parathyroid hormone disorders
Hyperaldosteronism
Ketoacidosis
Chronic alcoholism

CLINICAL MANIFESTATIONS OF
HYPOMAGNESEMIA
CNS

irritability

Seizures

Hyperreflexia

Skeletal muscle spasm

TREATMENT OF
HYPOMAGNESEMIA
IV

administration of magnesium sulfate

HYPERMAGNESEMIA
Serum

magnesium level greater than 2.5

mEq/L
Causes:

Iatrogenic administration

Preeclampsia
Antacids/laxatives

Renal failure

CLINICAL MANIFESTATIONS OF
HYPERMAGNESEMIA
CNS

depression

Skeletal

stupor

muscle weakness

coma
respiratory failure

Decreased

peripheral vascular tone

Decreased

myocardial contractility

Tocolysis

HYPERMAGNESEMIA AND THE

EKG
Prolonged
Widened

PQ interval

QRS

TREATMENT OF
HYPERMAGNESEMIA
Supportive
Fluid

care

loading

Diuresis
Acute

hypermagnesemia IV calcium to
counter the elevated magnesium levels

ANIONS
Phosphate (POCONTD.
)

--4

Buffer ion found in ICF

Assists in acid-base regulation
Helps to develop and maintain bones and teeth
Calcium and phosphate are inversely proportional
Promotes normal neuromuscular action and participates in
carbohydrate metabolism
Absorbed through GI tract
Regulated by diet, renal excretion, intestinal absorption and PTH

Under normal conditions, reabsorption of phosphate occurs at

maximum rate in the nephron

An increase in plasma phosphate increases amount of phosphate in

nephron beyond that which can be reabsorbed; excess is lost in urine

REGULATION OF BLOOD
PHOSPHATE

27-70

OTHER ELECTROLYTE DEFICITS

CA, PO4,4, MG

May produce serious but nonspecific cardiac,

neuromuscular, respiratory, and other effects
All are primarily intracellular ions, so deficits
difficult to estimate
Titrate replacement against clinical findings

PHOSPHATE

Involved in acidbase buffering system, ATP

production, and cellular uptake of glucose

Maintenance requires adequate renal functioning

Essential to muscle, RBCs, and nervous system

function

HYPERPHOSPHATEMIA

High serum PO43 caused by

Acute

or chronic renal failure

Chemotherapy
Excessive ingestion of phosphate or vitamin D

Manifestations
Calcified

deposition: joints, arteries, skin, kidneys,

and corneas
Neuromuscular irritability and tetany

HYPERPHOSPHATEMIA

Management
Identify

and treat underlying cause

Restrict

foods and fluids containing PO43

Adequate

hydration and correction of hypocalcemic

conditions

HYPOPHOSPHATEMIA

Low serum PO43 caused by

Malnourishment/malabsorption
Alcohol
Use

withdrawal

of phosphate-binding antacids

During

parenteral nutrition with inadequate

replacement

HYPOPHOSPHATEMIA

Manifestations
CNS

depression

Confusion
Muscle

weakness and pain

Dysrhythmias
Cardiomyopathy

HYPOPHOSPHATEMIA

Management
Oral

supplementation
Ingestion of foods high in PO43
IV

administration of sodium or potassium phosphate

1995

2010
Saya akan perlakukan teman sejawat saya seperti saudara
kandung
Saya akan memperlakukan teman sejawat saya sebagaimana
saya ingin diperlakukan.