Fluid and Electrolyte Disorders

Fluid and
Electrolyte
Disorders
Marc Imhotep Cray, MD

Hyponatremia and Hypernatremia
A normal sodium concentration [Na+] is

from 135 to 145 mEq/L
 A [Na+] under 135 mEq/L is hyponatremia
 A [Na+] over 145 mEq/L is hypernatremia
 Important to consider overall volume status

of patient, as well as, whether or not this is an
acute or chronic process
Marc Imhotep Cray, MD 2

Hyponatremia & Hypernatremia (2)
 [Na+] is based not only on gain or loss of

sodium  but also on gain or loss of free
water disturbances in either can lead to
[Na] abnormalities
 changes in total body water are more common
 Important regulatory hormones include ADH

and aldosterone

Hyponatremia
 Hyponatremia can be caused by following:

1. Net Na+ loss in excess of net free water loss
2. Net free water gain in excess of net Na+ gain
(e.g., SIADH)
3. Free water shift (pseudohyponatremia)
N.B. Severe, symptomatic hyponatremia ([Na+]

<120 mEq/L) is almost always caused by SIADH

Hyponatremia (2)
Free water shift--traditionally referred to as

pseudohyponatremia observed in a
hyperosmotic hyperglycemic state 
intracellular free water shifts extracellularly
to maintain osmotic balance
 Extracellular free water shift induces a dilutional
state for Na+  hence, hyponatremia
o total body sodium, however, is not reduced hence,
term pseudohyponatremia

Hyponatremia (3)
 Hyponatremia assoc. w hyperglycemia can

be corrected by control of hyperglycemia
alone
 Hyponatremia assoc. w hyperglycemia may

be corrected as follows:
 For each 100 mg/dL of Glu over normal (e.g.,
nml is ≈ 100 mg/dL), add 2.4 mEq/L of Na+ as a
correction

Hyponatremia (4)
Hyponatremia can be further classified into

hypovolemic, euvolemic, or hypervolemic
 Hypovolemic hyponatremia:
 Caused by hypotonic to hypertonic fluid loss plus
concomitant pure free water or relatively hypotonic
fluid replacement
 Stated another way hypovolemic hyponatremia
occurs when pt. has lost volume and sodium, but
has lost more sodium

Hyponatremia (5)
 Examples of hypovolemic hyponatremia

include
o hypotonic fluid loss (diarrhea, sweating, and
respiration) in which urine sodium would be low
(kidney trying to actively reabsorb sodium and water)
o hypertonic fluid loss (diuretics, aldosterone

insufficiency), in which urine sodium would be
high (kidney cannot reabsorb sodium or water)

Hyponatremia (6)
Euvolemic hyponatremia: Usually caused by excess

free water reabsorption= SIADH
Causes of SIADH are many, including

 Malignancy
 Pulmonary or CNS lesions
 Antipsychotic, antidepressant & antiepileptic drugs
 Pain medications
 Acute nausea and vomiting
 Pain
 A classic example is a smoker w small cell carcinoma of

lung) which can secrete ADH (among other hormones)
Hyponatremia (7)
 Hyponatremia caused by SIADH is considered

euvolemic--even though body is reabsorbing large
amounts of water-- b/c accumulation of volume can
stimulate intravascular pressure-sensing receptors
(baroreceptors) to induce a natriuretic effect to
enhance sodium and water excretion
 In other words ↑ ADH stimulated water reabsorption is
countered by ↓ activity of RAAS and SANS and ↑ levels of
BNP such that ECV & ECF volume are maintained near
normal

Hyponatremia (8)
 Other causes of euvolemic hyponatremia include

 excessive ingestion of free water
o overwhelms maximal ability of kidneys to
excrete water
 poor oral intake
o caused by need of kidneys to pull out solutes
w free water excretion
o Limited solute intake (poor oral intake as in alcoholics
[“beer potomania”] or “tea and toast diet”) limits ability
of kidneys to excrete free water

Hyponatremia (9)
 Euvolemic hyponatremia cont’d…

difference betw. SIADH and others causes
 with SIADH, urine will be concentrated
(reabsorbed all water), but
 urine will be dilute in other conditions
 Additional causes of euvolemic hyponatremia

 hypothyroidism
 hypocortisolism
 nephrogenic syndrome of inappropriate diuresis
Hyponatremia (10)
 Hypervolemic hyponatremia:
hypervolemia is caused by volume overload
from…
 Heart failure
 Liver failure (cirrhosis)
 Kidney failure or
 Hypoalbuminemia (nephrotic syndrome)
…leading to interstitial fluid overload

Hyponatremia (11)
Acute hyponatremia results in ↓ osmoles

in intravascular space leading to water
rushing into cells (osmotic gradient)
 This precipitates cellular swelling and
cerebral edema leading to altered mental
status, headache, vomiting, and seizures

Hyponatremia (12)
 Tx of hyponatremia can involve following:

1. Restrict water and allow kidneys to fix
problem by urinating out excess water,
2. Give salt-containing fluids IV or sodium
tablets to correct sodium, or
3. Give medications (e.g., ADH receptor
antagonists, vaptans, demeclocycline [ADH
antagonist]) to increase free water excretion

Hyponatremia (13)
N.B. Care must be taken not to correct hyponatremia too quickly

 This is b/c w chronic hyponatremia (w ↓ intravascular osmoles)
body has made intracellular adjustments to fewer osmoles
 increasing osmoles in bloodstream rapidly by introducing a large

sodium load from IV fluids will pull water out of cells b/c of osmotic
gradient
 This pull of water out of cells is particularly destructive to

myelin potentially causing a syndrome called osmotic
demyelinating syndrome (ODS) [previously called central pontine
myelinolysis (CPM) ] may cause permanent neurologic
damage or death
Hypernatremia
Hypernatremia can occur from following:

1. Gain of sodium
2. Loss of free water (more common), or less commonly
3. Intracellular free water shift
 It’s not intuitive loss of water could cause hypernatremia

“Wouldn’t people just drink water?”
 That’s true and is why hypernatremia is often seen
in those w altered mental status (e.g., nursing home
pts.) or intubated patients  people who cannot get
access to free water

Hypernatremia (2)
 Another way to lose water is to have

diabetes insipidus (DI) causes
polyuria of very dilute urine
 Sx of hypernatremia include altered
mental status and coma
 DDx of central DI vs nephrogenic DI follows

Hypernatremia (3)
In central DI problem is centrally

located in posterior pituitary gland
 If PP fails to secrete ADH
hypernatremia will result by stopping
water reabsorption in distal nephron 
results in large loss of free water
o Cause sometimes seen after head trauma
o Tx responds to desmopressin (DDAVP/
synthetic ADH) administration

Hypernatremia (4)
 Nephrogenic DI occurs when there is

a problem w receptors at kidney
level:
 there is ADH but kidney can’t use it
 can be caused by chronic lithium use,
hypokalemia, or hypercalcemia, or
mutations of ADH receptors
 Does not respond to desmopressin
admin.

Hypernatremia (5)
Differentiation of two types of DI can be

done by admin. of desmopressin
 In central DI, body will respond to
desmopressin b/c problem is a lack of ADH
and not with receptor pathway
o Urine osmolarity should ↑ by 50%
 If osmolarity does not ↑ by 50%
indicates problem w kidney’s ability to
use ADH and therefore, suggests
nephrogenic DI
Hypernatremia (6)
Tx of nephrogenic DI is a thiazide diuretic

(counterintuitive) but as salt and water is lost
(instead of just water) w diuretic use ↑ RAA
axis activation will cause ↑ sodium (and water)
reabsorption in earlier parts of nephron (e.g.,
upregulation of Na+/H+ exchanger in proximal tubule by
angiotensin II) leading to a net ↓ in water loss

Hypernatremia (7)
If primary polydipsia thought to be in DDx

of dilute polyuria (although this causes
hyponatremia, it would also lead to dilute
urine), then fluid restriction can lead to a
diagnosis
 If patient does not take in fluids w primary
polydipsia urine will concentrate normally (not
the case w DI)

Hypokalemia and Hyperkalemia
 Changes in potassium levels alter resting membrane

potential leading to abnormal cellular activity
 K+ homeostasis is controlled by kidneys, w

aldosterone being key regulatory hormone leading
to excretion of K+ in urine
 Cells also have a H+/K+ exchanger leading to

changes in K+ levels w changes in pH
 acidosis causing cells to take in H+ in exchange for putting
K+ into the bloodstream
 alkalosis causing cells to give H+ to bloodstream in
exchange for taking in K+
Hyperkalemia
 Hyperkalemia is defined as K+ level

higher than 5.0 mEq/L
 Causes: Hyperkalemia can be caused by
many factors main causes involving:
1. Decreased renal excretion
2. Cell lysis, and
3. Transcellular movement

Hyperkalemia (2)
 Causes of ↓ renal excretion include

 renal failure (inability to excrete K+)
 hypoaldosteronism (b/c aldosterone
causes K+ loss in urine), and
 potassium-sparing diuretic use
(prevents elimination of K+)

Hyperkalemia (3)
Cell lysis such as rhabdomyolysis (skeletal

muscle breakdown) or high cell turnover,
such as in some leukemias and
lymphomas can cause hyperkalemia b/c it
is spilling intracellular K+ into bloodstream
Lysis of cells during blood draws

(hemolysis) can lead to elevated K+ of bld
sample (so it is important to keep in mind)

Hyperkalemia (4)
 Transcellular movement of K+, as noted,

can occur w acidosis, as excess H+ in
blood moves into cells in exchange for K+
b/c insulin and sympathetic drive both
activate Na+/K+ ATPases in cells
(promoting K+ uptake in cells)
 loss of either of these can cause hyperkalemia

Hyperkalemia (5)
Clinical Findings:
 Electrocardiographic (ECG) findings include peaked
T waves (from vigorous accelerated repolarization), PR
interval prolongation, QRS widening, and eventually
a sinusoidal tracing
 Ventricular arrhythmias can also occur from abnormal

excitability of the heart
 Muscle weakness can occur b/c of higher resting

membrane potential leading to sodium channels not
being able to reset fully (repolarization not complete)
Hyperkalemia (6)
Treatment:
Tx is threefold:
1. Reduce myocardial irritability to prevent
arrhythmia and death;
2. Move potassium intracellularly to temporarily
reduce potassium, and
3. Promote potassium loss through the urine and
stool
 Rationale for each follows…

Hyperkalemia (7)
Reduction of myocardial irritability is via

calcium administration, which helps stabilize
cell membranes
Potassium can be moved intracellularly by

increasing Na+/K+ ATPase activity via insulin
(and glucose, to prevent hypoglycemia) and
sympathetic stimulation (usually albuterol) or
 by causing an alkalosis and promoting H+/K+
exchange across cell via bicarbonate admin.
Hyperkalemia (8)
Finally, potassium must eventually be

removed from body, usually via
 potassium wasting diuretics (e.g., furosemide)
 potassium-binding resins that bind K+ in
intestines (sodium polystyrene sulfonate
[Kayexalate]) or
 dialysis

Hypokalemia
Hypokalemia is defined as K+ level

less than 3.5 mEq/L
Causes: in general, are opposite of causes of
hyperkalemia, and involve:
1. Increased renal excretion
2. Transcellular movement
3. Gastrointestinal loss
Discussion of each follows…

Hypokalemia (2)
Increased renal excretion is seen w

 hyperaldosteronism from any cause
 hypercortisolism b/c high levels of cortisol can
act on aldosterone receptor, and
 potassium-wasting diuretic use
 Hypokalemia can also be seen in states of ↑
diuresis, such as in DM from glucosuria leading to
polyuria
Transcellular movement
 Hypokalemia can be seen w alkalosis b/c cells
give up some H+ to help replenish lost serum H+ &
exchange it by taking in K+
Hypokalemia (3)
Gastrointestinal loss
 GI fluids are generally K+-rich (stomach
acid and stool) so vomiting and
diarrhea can lead to K+ loss further
exacerbated by volume loss, leading to
RAA axis stimulation and ↑ K+ loss via
aldosterone action

Hypokalemia (4)
Clinical Findings:
 Electrocardiographic (ECG) findings include
 presence of a U wave (a small hump after T
wave), and altered membrane potentials
 can also lead to arrhythmias w hypokalemia
 muscle weakness caused by a more negative
membrane resting potential
o Note: hypokalemia or hyperkalemia causes muscle
weakness

Hypokalemia (5)
Treatment:
 K+ repletion and correction of underlying cause
 Avoid alkalinization and use of glucose or insulin
in patients with severe hypokalemia b/c both of
these can increase intracellular K+ uptake and
exacerbate existing hypokalemia

Volume Disorders
Overview:
 The two forms of volume disorders, volume
depletion and volume excess, will be discussed
below, followed by details regarding laboratory
distinction of the two disorders
 First, however, we will review 2 important concepts

in renal physiology
 ECF volume regulation by kidneys and
 ECF volume regulation by ADH

How do kidneys regulate
extracellular fluid volume?
Kidneys regulate ECF volume by adjusting rate of
excretion of Na+
In contrast,
Kidneys regulate body fluid osmolarity and sodium
conc. by altering excretion of free water (=ADH)
NB: This is one of most important concepts in renal
physiology
 In normal state, volume is regulated through sodium
balance, whereas osmolarity and sodium conc. are
regulated through water balance…

Kidneys regulating ECF volume cont’d.
…Thus, it is effective circulating volume (ECV)

that is regulated by body, not ECF volume
b/c body has no way to directly follow ECF volume
levels
 Instead, various pressure and volume sensors
located throughout circulatory system (in atria,
aortic arch, carotid sinus, and afferent arterioles of
kidney) monitor ECV  and, through various
mechanisms, stimulate or inhibit Na+ excretion
o RAAS is most important
 ECV is proportional to ECF  notable exceptions
occur during CHF cirrhosis, and nephrotic syndrome
How does ADH regulate ECF volume?
Under normal conditions, ADH does not work to

regulate ECF volume
 Instead, ADH normally functions to regulate reabsorption of free
water in collecting duct in response to changes in body fluid
osmolarity
 However, when ECV is severely compromised (↓ by 5-

10% of normal) secretion of ADH by posterior pituitary
is stimulated
 Thus, w significant hypovolemia, function of ADH changes to
help preserve volume rather than osmolarity

ADH regulating ECF volume cont’d.
Ability of ADH to sacrifice osmolarity to help maintain

ECV is an exception to rule given above stating 
(ie. water balance is regulated to maintain osmolarity and
sodium balance is regulated to maintain volume)
 When volume is low enough, body abandons rule and

retains sodium and water regardless of osmolarity
o Illustrated by CHF, nephrotic syndrome, and
cirrhosis b/c these three diseases are have ↓ ECV,
hyponatremia commonly occurs in all of them as a
result of chronically high ADH levels
Volume Depletion
Clinical presentation
 In mild volume depletion: Orthostatic
dizziness and tachycardia
 In severe volume depletion: Hypotension,
mental obtundation, cool extremities, severe
oliguria
N.B. Oliguria is earliest and most sensitive

clinical indication of hypovolemia

Volume Depletion (2)
Causes of volume depletion

GI causes of volume depletion: bleeding,
vomiting, diarrhea
Renal causes of volume depletion

o Due to loss of salt and water: Diuretics, acute tubular
necrosis
o Due to loss of water: Diabetes insipidus
Skin and respiratory causes of volume

depletion: sweat, burns
Causes of Volume Excess
Primary renal sodium retention (assoc. w ↑ ECV):

 Acute renal failure
 Cushing syndrome
 Hyperaldosteronism
Secondary renal sodium retention:

 Heart failure
 Liver disease
 Nephrotic syndrome
 In these edematous states, excess volume is sequestered
outside arterial system causes a persistent low-volume
stimulus to which kidney responds by retaining water,
leading to hyponatremia

Laboratory studies to help determine
cause of volume disorder
1. Urine osmolality
 Increased in: Addison disease, congestive heart
failure, shock, hypovolemia,
 Decreased in: Hyperaldosteronism, diabetes insipidus,
excess fluid intake, renal tubular necrosis
2. Serum osmolality
 Increased in: Dehydration, diabetes insipidus,
increased glucose, hypernatremia, methanol
intoxication, ethylene glycol intoxication, and uremia.
 Decreased in: Excess fluid intake, hyponatremia,
SIADH
Further Study
 Fluid and Electrolytes_ SDL Tutorial (Darrow-Yannet Diagrams)

 Electrolyte and Acid-Base Practice Q&A
Textbook:
Kamel KS, Halperin ML. Fluid, Electrolyte, and Acid-Base
Physiology: A Problem-Based Approach, 5th Ed. Philadelphia, PA:
Elsevier, 2017.

Fluid and Electrolyte Disorders

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Fluid and

Marc Imhotep Cray, MD

A normal sodium concentration [Na+] is

 Important to consider overall volume status

Marc Imhotep Cray, MD 2

 [Na+] is based not only on gain or loss of

 Important regulatory hormones include ADH

Marc Imhotep Cray, MD 3

 Hyponatremia can be caused by following:

N.B. Severe, symptomatic hyponatremia ([Na+]

Marc Imhotep Cray, MD 4

Free water shift--traditionally referred to as

Marc Imhotep Cray, MD 5

 Hyponatremia assoc. w hyperglycemia can

 Hyponatremia assoc. w hyperglycemia may

Marc Imhotep Cray, MD 6

Hyponatremia can be further classified into

Marc Imhotep Cray, MD 7

 Examples of hypovolemic hyponatremia

o hypertonic fluid loss (diuretics, aldosterone

Marc Imhotep Cray, MD 8

Euvolemic hyponatremia: Usually caused by excess

Causes of SIADH are many, including

 A classic example is a smoker w small cell carcinoma of

 Hyponatremia caused by SIADH is considered

Marc Imhotep Cray, MD 10

 Other causes of euvolemic hyponatremia include

Marc Imhotep Cray, MD 11

 Euvolemic hyponatremia cont’d…

 Additional causes of euvolemic hyponatremia

Marc Imhotep Cray, MD 13

Acute hyponatremia results in ↓ osmoles

Marc Imhotep Cray, MD 14

 Tx of hyponatremia can involve following:

Marc Imhotep Cray, MD 15

N.B. Care must be taken not to correct hyponatremia too quickly

 increasing osmoles in bloodstream rapidly by introducing a large

 This pull of water out of cells is particularly destructive to

Hypernatremia can occur from following:

 It’s not intuitive loss of water could cause hypernatremia

Marc Imhotep Cray, MD 17

 Another way to lose water is to have

 DDx of central DI vs nephrogenic DI follows

Marc Imhotep Cray, MD 18

In central DI problem is centrally

Marc Imhotep Cray, MD 19

 Nephrogenic DI occurs when there is

Marc Imhotep Cray, MD 20

Differentiation of two types of DI can be

Tx of nephrogenic DI is a thiazide diuretic

Marc Imhotep Cray, MD 22

If primary polydipsia thought to be in DDx

Marc Imhotep Cray, MD 23

 Changes in potassium levels alter resting membrane

 K+ homeostasis is controlled by kidneys, w

 Cells also have a H+/K+ exchanger leading to

 Hyperkalemia is defined as K+ level

Marc Imhotep Cray, MD 25

 Causes of ↓ renal excretion include

Marc Imhotep Cray, MD 26

Cell lysis such as rhabdomyolysis (skeletal

Lysis of cells during blood draws

Marc Imhotep Cray, MD 27

 Transcellular movement of K+, as noted,

Marc Imhotep Cray, MD 28

 Ventricular arrhythmias can also occur from abnormal