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Vodno-Elektrolitni Narushuvanja
Vodno-Elektrolitni Narushuvanja
Professor K.Cakalaroski
29.11.2019 1
BODY FLUIDS AND ELECTROLYTES
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Water Balance
70-kg male
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Normal Intake
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“Normal” Output:1400-2300 mL/d
• Urine: 800-1500 mL
• Stool: 250 mL
• Insensible loss: 600-900 mL (lungs and skin).
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Electrolyte Requirements
• Potassium:
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Glucose Requirements
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Internal Balance
1. Acid-Base
2. Insulin
3. Mineralcorticoids
4. Catecholamines
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1. Acid-Base
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Internal Balance
2. Insulin
• Insulin stimulates K+ uptake by muscle and
hepatic cells.
3. Mineralcorticoids
• Aldosterone makes cells more receptive to
the uptake of K+ and increases renal
excretion of K+.
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4. Catecholamines
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External Balance
Renal Potassium Excretion
• GI Potassium Excretion
• Fecal excretion of K+ normally is small, but
with diarrhea disorders, K+ loss increases
significantly.
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Hypokalemia
(K+ < 3.6 mmol/L)
Mechanisms: Due to inadequate intake, loss, or intracellular shifts
Inadequate Intake. Oral or IV
GI Tract/Skin Loss : vomiting, diarrhea, excess sweating, villous
adenoma, fistula
Renal Loss : Diuretics and other medications (amphotericin B, high-dose
penicillins,aminoglycosides, cisplatin), diuresis other than diuretics
(osmotic, eg, hyperglycemia or ethanol-induced), vomiting (from
metabolic alkalosis from volume depletion), renal tubular disease
(renal tubular acidosis type 1 [distal], and 2 [proximal]), Bartter
syndrome (due to increased renin and aldosterone levels),hypo-
magnesemia,natural licorice ingestion, mineralocorticoid excess
(primary and secondary hyperaldosteronism, Cushing syndrome,
steroid use), and ureterosigmoidostomy
Redistribution (Intracellular Shifts). Metabolic alkalosis (each 0.1
increase in pH ,lowers serum K+ approximately 0.5-1.0 mmol/L, due
to intracellular shift of K+), insulin administration, beta-adrenergic
agents, familial periodic paralysis, treatment of megaloblastic anemia
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Symptoms
• Muscle weakness,flaccid paralysis
• Polyuria, polydipsia (tubulopathy)
Signs
• Decreased motor strength, orthostatic
hypotension, ileus
• ECG changes
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Treatment:
• The therapy depends on the cause.
• A history of hypertension, GI symptoms, or use of
certain medications may suggest the diagnosis.
• A 24-h urine for potassium may be helpful if the
diagnosis is unclear.
• Levels <20 mmol/d suggest extrarenal loss or
redistribution,
• >20 mmol/d suggest renal losses.
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Treatment:
A serum potassium level of 2 mmol/L probably represents a
deficit of at least 200 mmol in a 70-kg adult;
• to change potassium from 3 mmol/L to 4 mmol/L takes
about 100 mmol of potassium in a 70-kg adult.
Treat underlying cause.
• Hypokalemia potentiates the cardiac toxicity of digitalis. In
the setting of digoxin use, hypokalemia should be
aggressively treated.
• Treat hypomagnesemia if present. It will be difficult to
correct hypokalemia in the presence of hypomagnesemia.
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Rapid Correction.
• Give 7.45% KCl, IV.
• Monitor heart with replacement >20 mmol/h.
• IV potassium can be painful and damaging to
veins.
• Patient <40 kg: 0.25 mmol/kg/h x2 h
• Patient >40 kg: 10.0 mmol/h x2 h
• Severe [<2 mmol/L]: Maximum 40 mmol/h IV in
adults
• In all cases check a stat potassium following each
2-4 h of replacement.
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Slow Correction.
• Give KCl orally
• Adult: 20-40 mmol two to three times a day
(bid or tid)
• Pediatric patients: 1-2 mmol/kg/d in divided
doses
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Potassium disorders
Treatment of Hypokalemia
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Hyperkalemia
• Potassium is released from cells at times of stress,
injury, acidosis; but the kidney is able to regulate
potassium well, and hyperkalemia is rarely a
problem.
• However, in the presence of renal failure hyper
kalemia becomes a common problem.
• It is generally treated if there is an abrupt rise from
normal to > 6.5 mmol/liter or if any level is associ-
ated with EKG changes.
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Hyperkalemia
(K+ >5.2 mmol/L)
Mechanisms: Most often due to iatrogenic or inadequate renal
excretion of potassium.
• Pseudo-Hyperkalemia. Due to leukocytosis, thrombocytosis,
hemolysis, poor venipuncture technique (prolonged tourniquet
time)
• Inadequate Excretion. Renal failure, volume depletion,
medications that block potassium excretion (spironolactone,
triamterene,amylorides), hypoaldosteronism (including adrenal
disorders and hyporeninemic states [such as Type IV renal tubular
acidosis], NSAIDs, ACE inhibitors), long-standing use of heparin,
digitalis toxicity, sickle cell disease, renal transplant
• Redistribution. Tissue damage, acidosis (a 0.1 decrease in pH
increases serum K+ approximately 0.5-1.0 mmol/L due to
extracellular shift of K+), beta-blockers, decreased insulin,
succinylcholine
• Excess Administration. Potassium-containing salt substitutes, oral
replacement, potassium in IV fluids
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• Symptoms: Weakness, flaccid paralysis, confusion.
• Signs:
• Hyperactive deep tendon reflexes, decreased motor
strength
• ECG changes, such as, peaked T waves, wide QRS, loss
of P wave, sine wave,
• asystole
• K+ = 7-8 mmol/L yields ventricular fibrillation in 5% of
cases
• K+ = 10 mmol/L yields ventricular fibrillation in 90% of
cases
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Treatment
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Rapid Correction.
• These steps only protect the heart from potassium
shifts, and total body potassium must be reduced
by one of the treatments shown under Slow
Correction.
• Calcium chloride, 500 mg, slow IV push (only
protects heart from effect of hyperkalemia)
• Alkalinize with 50 mmol (1 ampule) sodium
bicarbonate (causes intracellular potassium shift)
• 50 mL D 50%, IV push, with 10-15 units regular
insulin, IV push (causes intracellular potassium
shift)
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Slow Correction
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Treatment
• Restrict Exogenous K+
• Calcium gluconate - 10 to 30 ml of 10% solution over 3 to
5 minutes
• NaHCO3 - 50 to 100 ml of 8.4% solution
• Hyperventilation will also create an alkalosis and drive K+
into cells
• Avoid hypoventilation,
• Glucose - insulin - 500 ml of 10% dextrose plus 10 units
regular insulin or 50 - 100 gm with 10 -20 units regular
insulin
• Furosemide, Bumethanide,ethacrynic acid
• Oral or rectal sodium or calcium polystyrene with sorbitol
• Peritoneal dialysis or hemodialysis
• Transvenous temporary pacemaker
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Sodium Physiology
1. Sodium and its anions make up about 90% of the
total extracellular osmotically active solute.
2. Serum osmolality (mOsm/kg H20) = 2 X [Na+] +
[glucose] + [BUN]
3. For practical purposes, twice the Na+ concentra-
tion equals serum osmolality because urea and
glucose ordinarily are responsible for less than 5%
of the osmotic pressure.
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Hyponatremia
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Hyponatremia
a. Isotonic hyponatremia
occurs when plasma solids dilute the Na+. This occurs
with hyperproteinemia and hyperlipidemia.
b. Hypertonic hyponatremia
occurs with uncontrolled diabetes and with the use of
mannitol. Treat by correcting the fluid deficit initially
with isotonic saline, then give insulin to decrease glucose
and hypotonic saline to correct free water deficit.
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Hyponatremia
(Na+ < 136 mmol/L)
• Hypertonic Hyponatremia.
High osmolality. Water shifts from
intracellular to extracellular in response to
high concentrations of such solutes as
glucose or mannitol.
• The shift in water lowers the serum sodium;
however, the total body sodium remains the
same.
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Hypotonic Hyponatremia.
• Low osmolality. Further classified based on clinical assessment of
extracellular volume status
• Isovolemic.
No evidence of edema, normal BP. Caused by water intoxication
(urinary osmolality < 80 mOsm), SIADH, hypothyroidism,
hypoadrenalism, thiazide diuretics, beer potomania
• Hypovolemic.
Evidence of decreased skin turgor and an increase in heart rate and
decrease in BP after going from lying to standing. Due to renal loss
(urinary sodium >20 mmol/L) from diuretics, postobstructive diuresis,
mineralocorticoid deficiency (Addison disease, hypoaldosteronism) or
extrarenal losses (urinary sodium <10mmol/L) from sweating,
vomiting, diarrhea, third spacing fluids (burns, pancreatitis, peritonitis,
bowel obstruction, muscle trauma)
• Hypervolemic.
Evidence of edema. urinary sodium <10 mmol/L). Seen with CHF,
nephrotic syndrome , renal failure, and liver disease
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Symptoms: Usually with Na+ <125
mmol/L
• severity of symptoms correlates with the
rate of decrease in Na+.
• ?Lethargy, confusion, coma
• ?Muscle twitches and irritability, seizures
• ?Nausea, vomiting
• Signs:
Hyporeflexia, mental status changes
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Treatment: Based on determination
of volume status.
• Evaluate volume status by physical
examination HR and BP lying and standing
after 1 min, skin turgor, edema and by
determination of the plasma osmolality.
• Do not need to treat hyponatremia from
pseudo-hyponatremia (increased protein or
lipids) or hypertonic hyponatremia
(hyperglycemia),
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Treatment: Based on determination of
volume status.
Life-Threatening. (Seizures, coma) 3-5% NS can be given in
the ICU setting. Attempt to raise the sodium to about 125
mmol/L with 3-5% NS.
Isovolemic Hyponatremia. (SIADH)
• Restrict fluids (1000-1500 mL/d).
• Demeclocycline can be used in chronic SIADH.
Hypervolemic Hyponatremia
• Restrict sodium and fluids (1000-1500 mL/d).
• Treat underlying disorder. CHF may respond to a
combination of ACE inhibitor and furosemide.
Hypovolemic Hyponatremia
• Give D5NS or NS.
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Hypernatremia
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Hypernatremia (Na+ >144 mmol/L)
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Hypernatremia (Na+ >144 mmol/L)
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Hypernatremia (Na+ >144 mmol/L)
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Hypernatremia (Na+ >144 mmol/L)
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Hypernatremia
• Symptoms:
Depend on how rapidly the sodium level has
changed
• Confusion, lethargy, stupor, coma
• Muscle tremors, seizures
• Signs:
Hyperreflexia, mental status changes
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Hypernatremia:
Treatment:
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Hypernatremia:
Treatment:
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• Give free water as D5W, one-half the volume
in the first 24 h and the full volume in 48 h.
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Hypervolemic Hypernatremia
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Treatment of hypernatremia
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Hypercalcemia
(C a2+ > 2.55 mmol/L)
Mechanisms
• Parathyroid-Related. Hyperparathyroidism with secondary
bone resorption
• Malignancy-Related. Solid tumors with metastases (breast,
ovary, lung, kidney), or paraneoplastic syndromes, (squamous
cell, renal cell, transitional cell carcinomas, lymphomas, and
myeloma;PTH rp)
• Vitamin-D-Related. Vitamin D intoxication, sarcoidosis, other
granulomatous disease
• High Bone Turnover. Hyperthyroidism, Paget’s disease,
immobilization, vitamin A intoxication
• Renal Failure. Secondary hyperparathyroidism, aluminum
intoxication
• Other. Thiazide diuretics, milk alkali syndrome, exogenous
intake
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Symptoms
• Stones (renal colic); bones (osteitis fibrosa),
moans (constipation), and groans (neuropsy-
chiatric symptoms e.g confusion), as well as
polyuria, polydipsia, fatigue, anorexia, nausea,
vomiting
Signs
• Hypertension, hyporeflexia, mental status changes
• Shortening of the QT interval on the ECG.
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Treatment:
• Usually emergency treatment if patient is
symptomatic and Ca+2 > 3.24 mmol/L
• Use saline diuresis: D5NS at 250-500 mL/h.
• Give furosemide 20-80 mg or more IV (saline and
furosemide will treat most cases).
• Euvolemia or hypervolemia must be maintained.
Hypovolemia results in calcium reabsorption.
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Other Second-Line Therapies:
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Symptoms
• Hypertension, peripheral and perioral paresthesia,
abdominal pain and cramps, lethargy, irritability (in
infants)
Signs
• Hyperactive DTRs, carpopedal spasm (Trousseau’s sign)
• Positive Chvostek’s sign (facial nerve twitch, can be
present in up to 25% of normal adults).
• Generalized seizures, tetany, laryngospasm
• Prolonged QT interval on ECG
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Treatment
Acute Symptomatic
• 100-200 mg of elemental calcium IV over 10 min
in 50-100 mL of D5W followed by an infusion
containing 1-2 mg/kg/h over 6-12 h
• 10% calcium gluconate contains 93 mg of
elemental calcium.
• 10% calcium chloride contains 272 mg of
elemental calcium.
• Check magnesium levels and replace if low.
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Chronic
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Hypermagnesemia
(Mg2+ > 1.05 mmol/L)
Mechanisms
• Excess Administration. Treatment of
preeclampsia with magnesium sulfate
• Renal Insufficiency. Exacerbated by
ingestion of magnesium-containing antacids
• Others. Rhabdomyolysis, adrenal
insufficiency
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Hypermagnesemia
(Mg2+ > 1.05 mmol/L)
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Hypermagnesemia
(Mg2+ > 1.05 mmol/L)
Treatment:
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Hypomagnesemia
(Mg2+ < 0.75 mmol/L)
Symptoms
• Weakness, muscle twitches, Vertigo
• Symptoms of hypocalcemia
(hypomagnesemia may cause hypocalcemia
and hypokalemia)
Signs
• Tachycardia, tremor, hyperactive reflexes,
tetany, seizures
• ECG may show prolongation of the PR, QT,
and QRS intervals as well as ventricular
ectopy (VES), sinus tachycardia
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Hypomagnesemia
(Mg2+ < 0.75 mmol/L)
Treatment