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Electrolytes
AHD September 1, 2011
SODIUM
Physiology
General Approach
 Increased



concentration
Excess total body amount
Shifts among compartments
Relative fluid loss
 Decreased



concentration
Depleted total body amount
Shifts among compartments
Relative fluid gain
Sodium
 Normal


40-50 mEq/kg
98% in extracellular fluid space
 Normal


total body sodium content
concentration ~ 140 mEq/L
1/3 fixed in bone
2/3 readily exchangable
Sodium
 Moves
passively into cells along the
concentration gradient; pumped actively
out of cells, against the gradient
 When physiologic changes cause
disequilibrium between intracellular and
extracellular spaces, movement of water is
the primary correction (if concentration of
the solute increases, water moves into that
space to restore equilibrium)
Controllers
 Renin



released in response to ↓ circulating intravascular volume or decreased BP
Catalyses angiotensin I → angiotensin II
Angiotensin II stimulates aldosterone
 Aldosterone

Enhances Na reabsorption and K excretion at
the distal nephron; water passively follows
Controllers, cont’d
 ADH



(aka vasopressin)
Released in response to ↑ serum osmolality;
also released due to ↓ intravascular volume or
arterial pressure
Most potent stimulus is volume depletion: may
be released even if hypotonic, if volume ↓↓
Stimulates renal water reabsorption
(enhances tubular water permeability), thus
decreasing urine output
Hyponatremia
Definition
 Na
< 135 mEq/L
 Severe hyponatremia: Na < 125 mEq/L
 Significant mortality: Na < 115 mEq/L
 Generally
occurs when something impairs
normal free water excretion
Symptoms
 Depend
on rapidity of decline, and on level
 If acute: symptoms occur if Na < 120
mEq/L; if chronic, levels may be lower
 Also depends on volume status
 Sx: nausea, malaise, muscle cramps,
lethargy, ↓ LOC, headache, ataxia,
seizures, coma
 Mortality of acute severe hyponatremia
with CNS changes is ~50% in adults
Symptoms, cont’d
 Neuro
sx are due to intracerebral osmotic
fluid shifts and brain edema
 The brain adapts to decreased Na thru
movement of interstitial fluid into the CSF,
and thru loss of intracellular K and organic
osmolytes (to decrease brain edema)
 These products take longer to re-shift
during correction… hence slow correction!
Causes of Hyponatremia
Causes
 Water
gain +/- Na loss (>water loss)
 Alteration in the distribution of body water
 Aberrant lab measurement
Determining cause
 Serum
Na level
 Serum osmolality:



 If


Hypotonic (< 275) = true hyponatremia
Isotonic (275-295)
Hypertonic (>295)
hypotonic:
Volume status
Measure Urine Na
“False” hyponatremia
 Sampling
Error
 Pseudohyponatremia (isotonic
hyponatremia)


Hyperlipemia
Hyperproteinemia (e.g. multiple myeloma)
 Redistribution

(hypertonic hyponatremia)
Hyperglycemia, mannitol (increased solute
concentration causes water movement,
diluting sodium)
Hypotonic Hyponatremia
 Hypovolemic




hyponatremia
Loss of water + Na (more Na than water)
GI: e.g. diarrhea
Renal: RTA, diuretics
Third spacing: burns, pancreatitis
Hypotonic Hyponatremia
 Euvolemic






hyponatremia
SIADH
Psychogenic polydipsia
Reset osmostat e.g. elderly, brain injury
Hypothyroidism, adrenal insufficiency
Ecstasy
Medications e.g. NSAIDS, carbemazepine,
TCAs, cyclophosphamide, morphine,
sulfonylureas, etc.
Hypotonic Hyponatremia cont’d
 Hypervolemic


hyponatremia
Occurs when Na is retained, but retention of
water exceeds that of Na
Causes:
• CHF
• Cirrhosis
• Nephrotic syndrome

↓ renal perfusion → secretion of ADH and
aldo → ↑ tubular resorp of Na and water
Hypotonic Hyponatremia cont’d
 Hypervolemic


hyponatremia
If urinary Na > 20: renal failure
If urinary Na < 20:
• CHF – low flow state seen by kidneys = ADH
• Nephrotic syndrome – low protein (urinary loss)
• Cirrhosis – decreased protein production
Diagnosis
 Urine


osmolality
Polydipsia, reset osmostat: UOsm < 100
If > 100 mOsm/kg, indicates ↑ ADH
 Serum
osmolality
 Urine sodium


SIADH: Urine Na > 20-40 mEq/L
Hypovolemia: Urine Na < 25 mEq/L
 Other

TSH, cortisol, albumin, triglycerides, SPEP
Management
Treatment
 Guided



by:
Severity of symptoms
Duration of illness
Volume status
 Immediate,



rapid intervention:
Neurologic dysfunction or seizures
Shock
Severe volume overload
Treatment
 If



 If

Na < 120 and/or the patient is unwell
3% saline (513 mEq/L) at 25-100 ml/hr
Can give lasix to reduce water content and
give more rapid correction
Check lytes q1h
above criteria not met
Replace total body defecit with NS
(154mEq/L)
Guidelines
 Acute

hyponatremia (< 48 hours)
Rate of correction: 1-2 mEq/L per hour
 Chronic

 In

hyponatremia
Rate of correction: < 0.5 mEq/L per hour
general:
Level should not be corrected to above
120mEq/L or by more than 8-10 mEq/L in the
first 24 hours
Formula
 To
estimate the expected change in serum
Na, depending on fluid used:
 Change

[(infusate Na + infusate K) – serum Na] /
[Total body water + 1]
 Total

in serum Na =
body Na defecit =
(Desired [Na] – Actual [Na]) x TBW
Hypovolemic Hyponatremia
 Correct
volume deficits with normal saline
(hypertonic compared with patient’s
serum)
Euvolemic Hyponatremia
 Free
water restriction
 Treat underlying disorder
 SIADH:


May worsen if given normal saline
If refractory: demeclocycline (antagonizes
vasopressin), lithium
Hypervolemic Hyponatremia
 Salt
and fluid restriction
 Diuretics (esp. loop diuretics)
 Dialysis
 Correction of underlying condition
Monitoring
 Check
electrolytes every 2-4 hours
 Carefully monitory neurologic status:
watch for acute worsening
POTASSIUM
Physiology
 Major


Intracellular [K] = 100-150 mEq/L
Extracellular [K] = 3.5-5.0 mEq/L
 Total

intracellular cation
body store = 35-55 mEq/kg
70-75% is found in muscle tissue
Potassium Regulation
 Renal



excretion is 90% of elimination
Filtered freely thru the glomerulus,
reabsorbed in the proximal/asc tubules
Secreted in distal tubule for Na
Healthy kidneys can excrete 6mEq/kg/d
 Some
loss in stool and sweat
 Acid/base status
 Intra- extra cellular shift
Hypokalemia
Symptoms
 Weakness,
paralysis
 Lethargy, depression, irritability
 Decreased DTRs, fasiculations
 Dysrhythmias
 Rhabdomyolysis
 Significant
symptoms if K <2.5 mEq/L
The Asymptomatic Patient
 Treatment
depends on patient
characteristics and potential causes
 Always ensure follow-up and repeat
testing
 Oral replacement (food vs. pharm)
 Rarely have concerning cause
 GOOD HISTORY!
Treatment
 IV
vs. PO
 20 mEq infusion raises serum [K] by ~
0.25 mEq/L
 1.0 mEq/L = 370 mEq defecit
 50% of administered K is excreted in urine
 ? Give magnesium with potassium
Hyperkalemia
Symptoms
 Cardiac:


Heart block, wide-complex tachycardia, v.fib.
Peaked T’s, flat P’s, wide QRS, sine wave
 Neurological

Muscle cramps, weakness, paralysis,
paresthesias, tetany
When to treat:
 Depends
on patient, chronicity, clinical
symptoms
 > 6.0 mEq/L needs some treatment
 > 8.0 always needs all modalities
Kay-Exalate
 PO
or PR
 Works within 2-3 hours
 Works better and faster if given PR
 Caution with patients with volume overload
Insulin/Glucose
 Shifts
location of potassium
 Does not remove potassium from the body
 Works within 10-20 minutes
 Duration of action is 2-4 hours (peak 30
minutes)
 Decreases K by 0.5-1 mEq/L in 1 hour
 K will rebound if no definitive treatment
within 2 hours
 Check glucoscans frequently
Ventolin
 20
mg nebulized
 0.5-1 mEq/L reduction
 Care for side effects
Bicarbonate
 Older
modality
 Effect is shift
 Works in 10-20 minutes, duration of action
is 2 hours
 Very useful in patients with metabolic
acidosis
 Should not be routinely used
Dialysis
 Continually
rising K
 Rebound K elevation (recurrent)
 Severe cardiotoxicity
 Acute renal failure
 Chronic renal failure with rising K
CALCIUM
Definition
 Total


body Ca = 1.0-1.5 kg
10-20 g/kg body weight
99% is bound in bone
 Intravascular



Ca
50% protein bound
45% free active ions
5% non-ionized
Physiology
 Absorption


– GI tract
Active: vitamin D dependent
Passive – concentration dependent
 Excretion


Mostly GI tract (in stool)
Small amount through kidneys
Physiology
 Changes

in [H+] = changes in [Ca++]
Calcium will bind to protein in place of H+
 Alkalosis



Decreases ionized calcium (relative hypoCa)
pH up 0.1… 3-8% drop in [Ca++]
No effect on total serum Ca
 Acidosis

Increases ionized calcium
Regulation
 Serum



Ca level is maintained by
Parathyroid hormone
Vitamin D metabolites
Calcitonin
Regulation
 Parathyroid




hormone
Secreted in response to low Ca or Mg
Raises serum Ca mostly by stimulating
osteoclasts to increase bone resorption
Indirect action in kidneys to increase Ca
absorption and PO4 excretion
Acts with calcitriol to increase intestinal
absorption
Regulation
 Calcitonin



Influenced by increased Ca
Inhibits osteoclast activity
Potentiates Ca loss at kidneys
 Vitamin

D
Production is upregulated by decreases in Ca
or PO4
Hypocalcemia
Symptoms: Early
 Perioral
numbness
 Paresthesias
 Muscle Cramps
 Mild mental status changes (irritability)
Symptoms: Late
 Chvostek’s
sign (facial nerve)
 Trosseau’s sign (carpal spasm w/ BP cuff)
 Mental status changes
 Seizures
 Tetany
 Hypotension; acute heart failure
 ST, QT prolongation
Causes
 Surgery


Parathyroidectomy
Inadvertent removal of parathyroids (during
thyroidectomy)
 Shifts




in intravascular volume
High volume fluid resuscitation
Dialysis
Transfusions
Plasmapheresis
Causes, cont’d
 Calcium


Citrate (e.g. in dialysate)
Phosphate (e.g. bowel prep)
 Critical


Binders
Illness
Pancreatitis
Sepsis, other causes of shock
 Nutritional

Deficiency
Malnutrition; vitamin D deficiency
Diagnosis
 High




PTH, high phosphate:
Renal failure
Pseudohypoparathyroidism
Rhabdomyolysis
Massive Tumor Lysis
Diagnosis
 High






PTH, Low or normal phosphate:
Vitamin D deficiency
Pancreatitis
Inadequate diet, lack of sunlight
GI malabsorption
Blood transfusions (citrate)
Bisphosphonates
Diagnosis
 Low



PTH; high phosphate
Hypoparathyroidism
Hypomagnesemia
Hypothyroidism
Management
 Symptomatic…


IV calcium
Calcium gluconate
Calcium chloride
 Asymptomatic…


Calcium carbonate
Calcium citrate
 To


PO calcium
increase calcium absorption
Calcitriol (vitamin D)
Treat hypomagnesemia
Hypercalcemia
Symptoms
 Stones
 Bones
 Groans
 Moans
Symptoms, cont’d
 Renal

(Stones)
Polyuria (nephrogenic DI), volume depletion,
acute renal failure, nephrolithiasis
 Skeletal

Osteoporosis, osteomalacia, osteitis fibrosa
cystica, arthritis
 GI

(Bones)
(Groans)
Nausea/vomiting, constipation, abdo pain
Symptoms, cont’d
 Neurologic

(Moans)
Difficulty concentrating, confusion, psychosis,
fatigue, lethargy, muscle weakness
 Cardiovascular

Hypertension, QT interval shortening, Cardiac
arrhythmias
Causes
 PTH

Mediated
1o hyperparathyroidism, MEN, familial
hypocalciuric hypercalcemia, renal failure
 Malignancy

Osteolytic bone metastases, multiple
myeloma, lymphoma, sarcoidosis, small cell
lung cancer (paraneoplastic)
Causes, cont’d
 Medications

Thiazide diuretics, lithium, theophylline
toxicity, herbal supplements
 Endocrine

Hyperthyroidism, pheochromocytoma, adrenal
insufficiency
Diagnosis
 Confirm


diagnosis is correct
Check ionized calcium
Correct for albumin level
Diagnosis
 PTH




low
PTHrp high: malignancy
Vit 1,25-D high: lymphoma, sarcoid
Vit 25-D high: herbal supplements
Normal Vit D, PTHrp: bone mets, multiple
myeloma
Diagnosis, cont’d
 PTH


normal or high
Low urinary calcium: familial hypocalciuric
hypercalcemia
Elevated urinary calcium: primary
hyperparathyroidism
Management
 Mild-moderate
(< 3.5 mmol/L) with mild or
no symptoms


May not need to treat
Avoid: thiazides, lithium, volume depletion,
bedrest, high calcium diet
Management
 Acute




Treatment (works in hours)
Aggressive hydration with NS
Loop diuretics (after hydration)
Calcitonin (effective for 48 hours)
Dialysis
Management, cont’d
 Chronic




Treatment (works in days)
IV bisphosphonates
Glucocorticoids
Gallium nitrate
Calcimimetics
MAGNESIUM
Physiology
 Normal



25-35% protein bound
10-15% complexed
50-60% ionized
 Total


serum Mg = 1.5-2.5 mEq/L
body content ~ 24g (2000 mEq)
50-70% in bone – slow exchange
40% ICF (distrib similar to K)
Physiology
 Most
is excreted in stool (60%); remainder
is via urinary excretion
 Regulation is only done via changes in
urinary excretion
Hypomagnesemia
Associations
 Low



Mg is associated with:
HypoK – defective membrane ATPase leads
to urinary loss of K
HypoCa – due to altered Vitamin D Metab
Protein level – extracellular Mg is protein
bound
Symptoms
 Neuromuscular:




Tetany, muscle weakness, cerebellar (ataxia,
nystagmus, vertigo)
Confusion, obtundation, coma
Seizures, irritability, paresthesias
Apathy, depression
 Gastrointestinal

Dysphagia, anorexia, nausea
Symptoms, cont’d
 Cardiovascular

Heart failure, dysrhythmias, hypotension
 Miscellaneous





Hypokalemia
Hypocalcemia
Hyponatremia
Hypophosphatemia
Anemia
Causes

Redistribution


Extrarenal Losses


Post-parathyroidectomy, correction of DKA, IV
glucose/hyperalimentation, refeeding, acute
pancreatitis
NG suction, lactation, profuse sweating, burns,
sepsis, intestinal or biliary fistula, diarrhea
Decreased intake

Alcoholism, malnutrition, small bowel resection,
malabsorption, NG suction
Causes, cont’d
 Medications

Thiazide/loop diuretics, aminoglycosides,
digoxin, cisplatin, cyclosporin
 Increased

Renal Losses
Ketoacidosis; Drugs: loop diuretics,
aminoglycosides, alcohol, cisplatin, Vit D;
SIADH; hyperthyroidism; hyperparathyroid;
hypercalcemia, DKA, hyperaldosteronism,
diuresis, K deficiency, hypophosphatemia,
familial
Diagnosis
 Check




Mg levels if:
Refractory hypoCa or hypoK
Alcoholics
Chronic diuretic use
Patients on digoxin, aminoglycosides,
amphotericin, cisplatin
Management
 Caution
with renal impairment
 Monitor for loss or diminishing DTRs (sign
or hypermagnesemia)
Treatment
 Asymptomatic/chronic


Mg oxide > 120 mg po tid
K sparing diuretics
 Symptomatic

IV MgSO4 to replace body stores:
• 8-12 g in 1st 24 hrs
• Next 3-4 days: 4-6 g/day
• Via very slow infusions
Hypermagnesemia
Symptoms
 Neuromuscular






toxicity
Ileus
Urinary retention
Parasympathetic blockade
Decreased DTRs
Apnea
Flaccid paralysis
Symptoms
 Mental

status changes
Lethargy, confusion, coma
 Cardiovascular

toxicity
Acts as a calcium channel blocker
• Decreased HR, BP; increased PR interval and
QRS duration; prolonged QT; complete heart block
 Metabolic

Decreased Ca, Increased K, decreased renin
activity
Causes
 Decreased



Renal failure
Volume depletion
Lithium
 Increased

renal excretion
Mg load
Laxatives/antacids/enemas containing Mg,
treatment of preeclampsia/eclampsia, DKA,
tumor lysis, rhabdomyolysis
Causes cont’d
 Increased

renal Mg absorption
Hyperparathyroidism, familial hypocalciuric
hypercalcemia, hypothyroidism,
mineralocorticoid deficiency, adrenal insuff.
 Redistribution

Metabolic acidosis
Diagnosis
 High
serum Mg concentration
 Other tests:





Check other lytes
BUN/Creat
CK, urine myoglobin (if suspect rhabdo)
R/O respiratory acidosis
ECG, cardiac monitor
Management
 Mild

symptoms
IV saline to replete volume
 Moderate/Severe


symptoms
100-200mg of 10% Ca gluconate infusion (24mg/kg/hr)
dialysis
Hypophosphatemia
Definition
 Normal
Phosphate:
 Moderate hypophosphatemia:

0.3-0.8 mmol/l
 Severe

hypophosphatemia:
< 0.3 mmol/l
Physiology
Symptoms
 General:

Malaise, anorexia
 Muscular

Diplopia, weak grips, dysphagia/slurred
speech, respiratory failure, rhabdomyolysis
 CNS

Paresthesias, memory loss, altered mental
status
Symptoms, cont’d
 CVS

Hypotension, angina, decreased cardiac
output, cardiomyopathy (reversible)
 Hematology

Hemolytic anemia, bruising/bleeding – platelet
dysfunction
 Skeletal

Loss of bone density, osteomalacia, bone
pain
Causes
 Decreased

Vitamin D deficiency, antacids (aluminum or
magnesium based), steotorrhea, chronic
diarrhea
 Increased

absorption
urinary excretion:
Hyperparathyroidism, vit D deficiency,
osteomalacia, Fanconi syndrome, osmotic
diuresis, acetazolamide, acute volume
reexpansion
Causes, cont’d
 Internal

redistribution
Increased insulin secretion (refeeding
syndrome), hungry bone syndrome, acute
respiratory alkalosis
Diagnosis
 Check

fractional excretion of phosphate
> 5% = renal phosphate loss
• If PTH high – hyperparathyroidism
• If PTH low – paraneoplastic
• If PTH normal – RTA

< 5% = extrarenal causes
• Check plasma calcium and 1, 25-Vit D levels
Management
 Asymptomatic,

No treatment or oral replacement
(1000 mg/day)
 Critically

ill, moderately low:
0.08-0.16 mmol/kg IV phosphate, over 2-6
hours
 Severe

mild-moderate:
hypoPO4:
0.08-0.16 mmol/kg IV phosphate, over 2-6
hours
Hyperphosphatemia
Definition
Symptoms
 Tetany
 Acute
kidney disease (nonproteinuric)
 Ectopic calcification
 Hypocalcemia (due to precipitation of
calcium with phosphate)
Causes
 Increased

Vitamin D intoxication, phosphate-containing
enemas, acute phosphorus poisoning
 Increased

load (exogenous)
endogenous load
Tumor lysis syndrome, rhabdomyolysis, bowel
infarction, acid-base disorders (lactic acidosis,
DKA, respiratory acidosis)
Causes, cont’d
 Reduced

urinary excretion
Renal failure, hypoparathyroidism,
acromegaly, magnesium deficiency
 Pseudohyperphosphatemia

Multiple myeloma, hemolysis in vitro,
hypertriglyceridemia
Diagnosis
 With

tumor lysis syndrome
 With

↑ CK, ↑ aldolase and myoglobinuria:
rhabdomyolysis
 With

↑ K and ↑ serum uric acid:
metabolic acidosis and big anion gap:
phosphate salt toxicity
Management
 Phosphate-binding

salts
Aluminum hydroxide, magnesium salts,
calcium acetate, sevelamer
 Decrease
 Dialysis
protein intake