GANGGUAN PADA KESEIMBANGAN ELEKTROLIT

Report
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
Figure 27.2
•
•
•
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
•
•
•
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
 Major




Cations in body fluids
Sodium (Na+)
Potassium (K+)
Calcium (Ca++)
Magnesium (Mg++)
 Implies
 Treat
an underlying disease process
the electrolyte change, but seek the
cause
 Clinical
manifestations usually not specific to
a particular electrolyte change, e.g.,
seizures, arrhythmias
 Clinical
manifestations determine urgency of
treatment, not laboratory values
 Speed
and magnitude of correction dependent
on clinical circumstances
 Frequent
reassessment of electrolytes required

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 aldosterone’s antagonist = ANP
Sodium contributes to resting membrane potential
 Sodium rushing into cell via open channels causes
depolarization of nerves and muscles

 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.



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

Neurologic
• Seizure
• Coma
• Agitation

Gastrointestinal
• Anorexia
• Nausea/vomiting

Muscular
• Cramps
• weakness
•
•
•
Headache
Cerebral edema
Confusion
 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!!!
 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

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
 Tremulousness
 Irritability
 Ataxia
 Mental
 Coma
confusion
d/t cerebral water loss
 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!!!
 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
 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
 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


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
Saladin’s Anatomy & Physiology fourth edition McGraw Hill
Potassium balance in the body
Costanzo Physiology second edition Saunders
27-30
 Causes
•
•
•
•
•
•
Gastrointestinal losses
Systemic alkalosis
Diabetic ketoacidosis
Diuretic therapy
Sympathetic nervous system stimulation
Administration of beta-adrenergic receptor
agonists
 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
 Extrarenal




depletion
diarrhea
laxative abuse
sweat losses
fasting or inadequate intake
 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
 Renal

metabolic acidosis





losses
RTA Type I and II
DKA
Carbonic anhydrase inhibitor therapy
Ureterosigmoidostomy
No acid-base disorder


Mg deficiency
Drugs

Autonomic neuropathy

Skeletal muscle weakness

Increased sensitivity to Digoxin

Cardiac
• Decreased myocardial contractility
• Electrical conduction abnormalities
• Arrhythmias
• Tachycardia
• Ventricular fibrillation
Copyright 2008 by Pearson Education, Inc.
•
Prolonged PR interval
•
Prolonged T interval
•
Widening of QRS
•
Flattened T wave
 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
 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)
 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
 Areflexia
 Weakness
 Paralysis
 Paresthesia
 Cardiac
conduction abnormalities
•
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
 Etiology
– renal failure,
transcellular shifts, cell
death, drugs,
pseudohyperkalemia
 Manifestations
–
cardiac, neuromuscular
 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
 Treatment



Stop potassium!
Get and ECG
Hyperkalemia with ECG changes is a medical
emergency
 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
 Treatment

Therapy directed at actual removal of potassium
from the body



sodium polystyrene sulfonate (Kayexalate)
dialysis
Determine and correct the underlying cause

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
 Regulated
within
narrow range
Elevated extracellular
levels prevent
membrane
depolarization
 Decreased levels lead
to spontaneous action
potential generation

 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
27-51
 Causes:
•
•
•
•
•
•
Decreased serum albumin concentration
Chelation of calcium by citrate
Rhabdomyolysis
Hypoparathyroidism
Pancreatitis
Renal failure
 Neuromuscular
•
•
•
irritability
Tetany
Laryngospasm
Hyperactive deep tendon reflexes
 Weakness
 Vasodilation
 Myocardial
dysfunction
 Bradycardia
 Heart block
 Calcium
replacement
 Intraoperative
– hyperventilation and
respiratory alkalosis
 Causes:
•
Calcium mobilization from bone due to
immobility
•
Tumors
•
Hyperparathyroidism
 Anorexia
 Nausea
 Constipation
 Cognitive
depression
 EKG changes
•
•
•
Prolonged PR interval
Shortened QT interval
PVC’s
 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.
 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
 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

27-61
 Serum
magnesium less than 1.5mEq/L
 Causes:
•
•
•
•
•
•
•
•
Inadequate intake of magnesium
TPN
Gastrointestinal losses
Pancreatitis
Parathyroid hormone disorders
Hyperaldosteronism
Ketoacidosis
Chronic alcoholism
 CNS
irritability
•
Seizures
•
Hyperreflexia
•
Skeletal muscle spasm
 IV
administration of magnesium sulfate
 Serum
magnesium level greater than 2.5
mEq/L
 Causes:
•
Iatrogenic administration
•
•
•
Preeclampsia
Antacids/laxatives
Renal failure
 CNS
depression
 Skeletal
stupor
muscle weakness
coma
respiratory failure
 Decreased
peripheral vascular tone
 Decreased
myocardial contractility
 Tocolysis
 Prolonged
 Widened
PQ interval
QRS
 Supportive
 Fluid
care
loading
 Diuresis
 Acute
hypermagnesemia –IV calcium to
counter the elevated magnesium levels
•
•
•
Phosphate (PO4---)
▫ 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
27-70
 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
 Involved
in acid–base buffering system, ATP
production, and cellular uptake of glucose
 Maintenance
 Essential
function
requires adequate renal functioning
to muscle, RBCs, and nervous system
 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
 Management

Identify and treat underlying cause

Restrict foods and fluids containing PO43

Adequate hydration and correction of hypocalcemic
conditions
 Low
serum PO43 caused by

Malnourishment/malabsorption

Alcohol withdrawal

Use of phosphate-binding antacids

During parenteral nutrition with inadequate
replacement
 Manifestations

CNS depression

Confusion

Muscle weakness and pain

Dysrhythmias

Cardiomyopathy
 Management



Oral supplementation
Ingestion of foods high in PO43
IV administration of sodium or potassium phosphate
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