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ELEKTROLIT
dr. Andi Sulistyo Haribowo, Sp.PD.
SPESIALIS PENYAKIT DALAM
Program Studi Pendidikan Dokter
UNIVERSITAS ISLAM MALANG
2012
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
Figure 27.2
DISTRIBUTION OF MAJOR
ELECTROLYTES
DISTRIBUTION OF MINOR
ELECTROLYTES
REGULATION OF ELECTROLYTES
(Na+)
Potassium (K+)
Calcium (Ca++)
Magnesium (Mg++)
PRINCIPLES OF ELECTROLYTE
DISTURBANCES
PRINCIPLES OF ELECTROLYTE
DISTURBANCES
SODIUM (NA+)
Sodium balance
Sodium = major cation in extracellular fluid (ECF)
Sodium = most common problem with electrolyte balance
DISORDERS OF SODIUM
BALANCE
Na+
ECF.
Na+
All
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
!!!Correction
HYPONATREMIA
CAUSES OF HYPERNATREMIA
CLINICAL MANIFESTATIONS OF
HYPERNATREMIA
Tremulousness
Irritability
Ataxia
Mental
Coma
confusion
TREATMENT OF
HYPERNATREMIA
Renal
tubular diuretics
Hemodialysis
Treat
!!!Correction
HYPERNATREMIA
Treatment
Severe
HYPERNATREMIA
Treatment
Calculate
POTASSIUM REGULATION
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
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
Alkalosis:
less H+ in blood
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
pH)
Increased Beta2 adrenergic activity
Theophylline toxicity
Familial
HYPOKALEMIA
Extrarenal depletion
diarrhea
laxative
abuse
sweat losses
fasting or inadequate intake
HYPOKALEMIA
vomiting/NG suction
diuretic tx
Mineralocorticoid excess syndromes
HYPOKALEMIA
Renal losses
metabolic
No
acidosis
acid-base disorder
Mg deficiency
Drugs
CLINICAL MANIFESTATIONS OF
HYPOKALEMIA
Autonomic neuropathy
Cardiac
Decreased myocardial contractility
Electrical conduction abnormalities
Arrhythmias
Tachycardia
Ventricular fibrillation
POTASSIUM
Prolonged PR interval
Prolonged T interval
Widening of QRS
Flattened T wave
TREATMENT OF HYPOKALEMIA
Slow
IV potassium supplements
Anesthesia
related concerns:
HYPERKALEMIA
HYPERKALEMIA
Causes
CLINICAL MANIFESTATIONS OF
HYPERKALEMIA
Areflexia
Weakness
Paralysis
Paresthesia
Cardiac
conduction abnormalities
QRS widening
ST segment depression
Tachycardia
Ventricular fibrillation
HYPERKALEMIA
Manifestations
cardiac, neuromuscular
TREATMENT OF HYPERKALEMIA
Primary
goal
Anesthesia
related concerns:
HYPERKALEMIA
Treatment
Stop
potassium!
Get and ECG
Hyperkalemia with ECG changes is a medical
emergency
HYPERKALEMIA
Treatment
First
IV Calcium
Temporizing
HYPERKALEMIA
Treatment
Therapy
Determine
CALCIUM (CA++)
Calcium balance
Calcium functions
Structural strength for bones & teeth
Maintains stability of nerve membrane
Required for muscle cell contraction
Necessary for blood clotting
Regulated within
narrow range
extracellular
levels prevent
membrane
depolarization
Decreased levels lead
to spontaneous action
potential generation
Elevated
Terms
Hypocalcemia
Hypercalcemia
27-51
HYPOCALCEMIA
Causes:
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:
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.
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
in ECF
Minimal amount in cell
REGULATION OF BLOOD
MAGNESIUM
27-61
HYPOMAGNESEMIA
Serum
CLINICAL MANIFESTATIONS OF
HYPOMAGNESEMIA
CNS
irritability
Seizures
Hyperreflexia
TREATMENT OF
HYPOMAGNESEMIA
IV
HYPERMAGNESEMIA
Serum
mEq/L
Causes:
Iatrogenic administration
Preeclampsia
Antacids/laxatives
Renal failure
CLINICAL MANIFESTATIONS OF
HYPERMAGNESEMIA
CNS
depression
Skeletal
stupor
muscle weakness
coma
respiratory failure
Decreased
Decreased
myocardial contractility
Tocolysis
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
REGULATION OF BLOOD
PHOSPHATE
27-70
PHOSPHATE
HYPERPHOSPHATEMIA
Manifestations
Calcified
HYPERPHOSPHATEMIA
Management
Identify
Restrict
Adequate
HYPOPHOSPHATEMIA
withdrawal
of phosphate-binding antacids
During
HYPOPHOSPHATEMIA
Manifestations
CNS
depression
Confusion
Muscle
Dysrhythmias
Cardiomyopathy
HYPOPHOSPHATEMIA
Management
Oral
supplementation
Ingestion of foods high in PO43
IV
1995
2010
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