FLUID AND ELECTROLYTES

BINDIYA MANGAR
24TH FEBRUARY, 2023
BODY WATER

Osmosis: the process by which a solvent (e.g. water) moves through a

semipermeable membrane from an area of less concentrated solution
to an area of more concentrated solution.
For example, if the plasma is hypotonic, the RBC’s become relatively
hypertonic causing water to enter into the RBC’s which can
eventually lead to hemolysis.
BODY WATER

Diffusion: the spontaneous movement of molecules from a region of

higher concentration to a region of lower concentration
For example, oxygen across the alveolar capillary membrane down
the concentration gradient.
Our body is divided into an
intracellular and an extracellular
compartment by the cell
membrane
• The cell membrane is
impermeable to charged
particles e.g. Na+ and K+
however they can pass through
using the Na/K ATP-ase pump.
• Small nonpolar molecules such
as urea, CO2 and water can
easily cross the cell membrane
The extracellular compartment is
divided into an interstitial
compartment and a plasma
compartment.
• The membrane separating the
two is the capillary wall which is
highly permeable to Na+, K+
and nonpolar molecules.
• Albumin and cellular
components like RBC’s, WBC’s
and platelets are restricted from
crossing this membrane
The cell membrane and the
capillary wall are permeable
to water.
• The osmolality of the
body is the same
throughout the body.
• The size of the various
compartments is
determined by the
number of osmoles in the
compartment.
 BODY WATER
Our body is made up of about 60% of water. The average man is 70kg, therefore, 70kg x
0.60 = 42 litres of water. The average TBW for females are 50%.
The water content is not fixed at 60%. This percentage decreases as you become older or
are fatter. In infancy ~ 70% total body water. Elderly have about 50% of TBW.
Muscle is about 75% water and fat is about 10% water
100kg man = 70kg original weight + 30kg of fat
100kg man = (70kg x 0.60) + (30kg x 0.10) = 45L of TBW
Typically, calculators do not account for fat. Just using gender and mass over estimates
TBW.
BODY WATER

Everything in the body is either intracellular or extracellular.

Intracellular – 2/3 TBW (~28 liters)
Interstitial space and plasma make up the remaining 1/3 TBW
~ 11 liters are in the interstitial space (75%)
~ 3 liters are in the plasma space (25%)

Question: is the osmolality in vomit or diarrhea different from the osmolality in the
plasma?
This lady weighs 180kg, how would you estimate her
TBW?

For lean females ~ 50% TBW

However, since she’s obese, her TBW ~40%

180kg x 0.4 = 72 liters

This man weighs 60kg, how would you estimate his TBW?

The average TBW for a lean male is 60%

However, he is an athelete and therefore would have

higher TBW ~70%

60kg x 0.7 = 42 liters

A patient with acute cholecystitis has a T-tube placed in the gall
bladder to allow drainage. The patient then has a cardiac arrest. In the
chaos of resuscitation, an intern pushes an amp of NaHCO3 into the
T-tube and then pulls the T-Tube out.
Assuming the hole sealed itseld behind the tube, what will happen to
the gall bladder volume?
IV FLUIDS USES

Treating sepsis and Replacing fluid Adjusting

shock losses osmolality

Serving as carrier
Increasing urine
fluids for medicine Nutrition
output
and electrolytes
TYPES OF IV FLUIDS
Dextrose solutions

They differ
based on
where the
Crystalloids
fluid ends up.

Plasma expanders
• Dextrose solutions distribute across the entire body.
• Crystalloids remain in the extracellular compartments.
• Plasma expanders remain in the plasma.
DEXTROSE SOLUTIONS

Provide water and some nutrition

Primary use: for treatment of hypernatremia and hypoglycemia
Secondary use: maintenance of fluids
Dextrose solutions distribute across the entire TBW similar to how TBW is
distributed physiologically.
◦ 2/3 goes to the intracellular space
◦ 1/4 goes to the interstitial space
◦ 8% goes to plasma space
D5W

D5W is 5% glucose: 5 grams of glucose per 100mL

Osmolality: 277 mmol/L
Normal osmolality: 275-295
WHY DON’T WE ADMINISTER STERILE WATER IV?

Sterile water is extremely hypotonic.

This would cause water to move into the RBC’s and lead to
hemolysis  anemia and AKI
 CRYSTALLOIDS

Are the standard solutions used for fluid replacement and maintenance. They
remain in the extracellular compartment, ¾ goes to interstitial space and ¼ goes to
the plasma.
They can either be balanced solutions or saline.
Balanced solutions: attempts to recreate the plasma concentration of all the
essential electrolytes e.g. Ringers, Hartmanns and Plasma-lyte.
Saline: a mixture of sodium, chloride and water. It comes in different
concentrations - 0.225%, 0.45%, 0.9% and 3%. The most isotonic is normal saline
(0.9%).
 SALINE
Most commonly used IVF
◦ Volume resuscitation
◦ Hypotonic saline for maintenance fluids, often mixed with dextrose solutions
◦ 3% saline used for hyponatremia

0.9% NS = 0.9g of NaCl per 100ml = 154 mmol of Na and 154 mmol of Cl ion
each liter.
pH of NS – 5.5
Long infusions of NS  non-anion gap metabolic acidosis
PLASMA EXPANDERS

These remain in the plasma

Blood components – FFP, PRBC and platelets
Colloids – purified albumin and synthetic osmotic agents
(hydroxyethyl starch)
 REGULATION OF VOLUME AND WATER

TBW = 42 litres
Osmolality of body = 285 mOsm/kg
The renin-angiotensin-aldosterone system regulates volume and the water-ADH-thirst
axis that regulates osmolality via the hypothalamus.
The RAAS monitors perfusion using multiple baroreceptors in the body. It regulates
volume by controlling the amount of sodium in the body.

The water-ADH-thirst axis regulates osmolality by controlling the amount of water in the
body.
THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

Hypovolemia is detected by a number of baroreceptors and stretch receptors

throughout the body.
The liver produces angiotensinogen which is converted to angiotensin 1 by renin
(produced by the juxtaglomerular complex of kidneys). Angiotensin 1 is
converted to angiotensin II by ACE in the lungs. Angiotensin II stimulates
aldosterone production.
 RAAS

Plasma volume is increased by sodium reabsorption in the kidneys.

Increased sodium in the ECF draws water from the ICF and the increased
osmolality stimulates ADH and thirst.

Blood pressure is increased by increasing cardiac output, by sympathetic

nervous system and increased vascular resistance through angiotensin II,
sympathetic activity and ADH.
 WATER-ADH-THIRST AXIS

Hypotonic plasma  no thirst, no ADH  water loss

Hypertonic plasma  thirst and ADH  water retention
ADH acts on the kidneys.
Note: the medullary interstitium is the saltiest place in the body. It has an osmolality
of about 1200 mOsm/kg and it is generated through the counter current exchange and
the thick ascending limb of the loop of Henle. This high concentration would draw in
a lot of water however, the collecting ducts are impermeable to water UNTIL ADH
unlocks them. With ADH, the tubules become permeable to water and water flows
into the highly concentrated medullary interstitium.
Thin descending loop of Henle –
concentration of the ultrafiltrate:
medullary hypertonicity (impermeable
to Na+)  passive reabsorption of H2O)

Thick ascending limb of the loop of

Henle – impermeable to H2O  urine
becomes less concentrated. Reaborption
of Na, K and Cl.
ADH

Increases in osmolality immediately causes an increase in ADH

Decreases in volume and blood pressure do not cause an increase in
ADH unless it’s a DRAMATIC decrease.
 OSMOLALITY VS. TONICITY
Osmolality is the concentration of all particles in a solution whether they are active or inactive.
Inactive solute – does not draw water with it e.g. urea, ethanol, glucose + insulin
Active solute – draws water with it e.g. Na, glucose

Urea is a small molecule that can pass through membranes and should be an ineffective osmole, however, during
dialysis when there is rapid removal of urea, the intracellular compartment becomes hyperosmolar and urea becomes
an active osmole, drawing water into the cells  dialysis disequilibrium syndrome

Tonicity is the concentration of all the osmotically active particles in a solution.

Na is the primary source of tonicity in the ECF
 HYPONATREMIA

True hyponatremia: low serum sodium concentration associated with low

osmolality and low tonicity causing water to move into the cells (cells become
relatively hypertonic).

False hyponatremia: low serum sodium concentration associated with normal

or high osmolality and tonicity. Does not cause water to move into the cells.
◦ Pseudohyponatremia – water doesn’t move at all
◦ Factitious hyponatremia – water moves out of the cells
 PSEUDOHYPONATREMIA

Osmolality and tonicity

are normal
Could be caused by lab
measurement error from
an increase in
immunoglobulin (multiple
myeloma, IVIG) or lipids.
 FACTITIOUS HYPONATREMIA
ECF is hypertonic and there is osmotic movement of water out of the cell diluting the serum sodium 
low sodium reported.
Causes:
1. hyperglycemia – for every 100mg/dL the blood sugar rises over 100, the serum sodium falls 1.6
mmol/L
2. mannitol
3. glycine

Note: hyperglycemia in the presence of insulin doesn’t move water. Glucose in the presence of insulin
is an ineffective osmole.
TRUE HYPONATREMIA

Low serum sodium concentration associated with:

1. low osmolality
2. low tonicity
Which causes water to move into the cells.

Hyponatremia is caused by more water intake than excretion

TRUE HYPONATREMIA

Causes of hyponatremia:
1. Renal failure = no urine output (ADH is irrelevant)
2. Obsessive water drinking (18L/day) with maximal but inadequate
urine output e.g. schizophrenia (ADH is suppressed
3. Normal water intake with decreased urine output (ADH dependent
hyponatremia)
 DETERMINANTS OF URINE VOLUME

Concentration = solute/volume
Volume = solute/concentration

Solute intake = solute output

Solute intake is ~10 mOSm/kg for adults
Fat and carbohydrates are metabolised to water and CO2

The concentration can range from 50-1200 mOsm/kg depending on the ADH level.
Minimal ADH = dilute urine ~14L/day
Maximal ADH = concentrated urine ~ 0.5L/day
 TRUE HYPONATREMIA

1. Tea and toast syndrome: diet rich in carbohydrates = minimal solute because carbohydrates get metabolised
to H2O and CO2.
2. Beer drinkers potomania: alcohol is metabolised to water and CO2
3. Compulsive water ingestion

These are the only causes of hyponatremia with low ADH = low specific gravity
Specific gravity measures the density of the urine and ranges from 1.005 – 1.030. Specific gravity is a proxy for
urine osmolality
Treatment: recognize that low specific gravity is not consistent with volume depletion. A low solute diet limits
urine volume, predisposing to hyponatremia. Patient should have a high solute diet.
ADH

There are two physiologic stimuli for ADH release

1. increased serum osmolality
2. decreased perfusion (volume depletion, hypotension)

Volume depletion can be caused by GI losses (vomiting, diarrhea) or renal losses (diuretics) 
ADH release  decreased urine output
Hyponatremia seen in hypotenstion can be due to heart failure, cirrhosis and nephrotic syndrome.
They all lead to edema and hypervolemia. There is decreased blood pressure and perfusion 
ADH release  decreased urine output.
EUVOLEMIC HYPONATREMIA

Sodium intake = sodium excretion

Water intake > excretion
There will be a high urine sodium concentration. A high urine sodium is a way to
differentiate euvolemic hyponatremia from hyper or hypovolemic hyponatremia.
In this state, the ADH is maximal and fixed.
If the patient exceeds their water intake, they will develop hyponatremia
CONSIDER PATIENTS RESPONSE TO NS

In hypovolemic hyponatremia  sodium improves

In tea and toast syndrome  sodium improves
In hypervolemic hyponatremia  sodium does not improve and patient may
deterioate
In euvolemic hyponatremia  sodium does not improve and may fall. All of the
Na give IV will be excreted in a small volume of urine, the water is retained.
CAUSES OF EUVOLEMIC HYPONATREMIA

Hypothyroidism – check TSH

Adrenal insufficiency – check cortisol
SIADH (syndrome of inappropriate ADH) – low BUN and low uric
acid
CAUSES OF SIADH

1. Paraneoplastic diseases
2. Nausea
3. Pulmonary disease – TB, PPV, Pneumonia
4. CNS disease
5. Drugs – SSRI, anti-psychotics, narcotics, sulfonylureas
 COMPENSATED HYPONATREMIA
Intially with hyponatremia, water moves into the cells causing tissue swellins and
intracellular solutes then move extracellulary to restore homeostasis.
Compensated hyponatremia is largely asymptomatic but you may find:
1. unsteady gait
2. slow reaction time
3. increased falls
4. hiccups
 COMPENSATED HYPONATREMIA
If you vigorously treat hyponatremia with 3% NS, water will move out of the
intracellular compartment to the extracellular compartment rapidly and can lead to
cerebral collapse  central pontine myelinolysis syndrome or osmotic demyelination
syndrome.
- flaccid quadriplegia
- respiratory failure
- pseudobulbar palsy
- coma
- death
COMPENSATED HYPONATREMIA

Speed limit for the correction of compensated hyponatremia

- 6 or 10 mmol/L in the first 24 hours
- 8 mmol/L in subsequent days
HYPOVOLEMIA HYPONATREMIA TREATMENT

Correct the hypovolemia with oral or IV fluids.

Corrected volume status  suppressed ADH  increased urine output
You need to monitor patients urine output for sudden increases and replace urine
output with D5W or oral water to prevent the Na from increasing too rapdily.
HYPERVOLEMIC HYPONATREMIA TREATMENTS

- Treat the underlying condition

- Fluid restriction
- Use drugs to block ADH (tolvaptan - PO, conivaptan - IV)
EUVOLEMIC HYPONATREMIA

- Correct underlying conditions

- Fluid restriction
- Vaptans
- Loop diuretics – block the Na-K-2Cl channels which reduces the
osmolality of the medullary interstitium and causes less H2O
reabsorption.
- Increase solute load
TREATMENT OF ACUTE SYMPTOMATIC HYPONATREMIA

Uncompensated hyponatremia – movement of fluid from ECF to ICF  tissue

edema, most importantly cerebral edema.

Severe Symptoms Moderately Severe

• Vomiting • Nausea
• Cardiorespiratory distress • Headaches
• Abnormal and deep • Confusion
somnolence
• Seizures
• Coma (GCS <8)
19 y/o male presents to AE unresponsive. Foley placed and he drains
800mL of clear urine and continues to produce 1L/hr. Urine
osmolality is 50 mmol/L and serum sodium is 112. What is the cause
for his hyponatremia?
- excessive water drinking
HYPERNATREMIA

Thirst is more important than ADH in preventing hypernatremia.

Central diabetes insipidus – the brain does not produce ADH e.g. trauma, stroke, mass lesions,
infections and ischemia. ADH is synthesized by thr hypothalamus and stored in the posterior
pituitary gland. Trauma to these areas cause a triphasic response. Initally there is no ADH and
high urine output then the premade ADH gets released leading to SIADH and urine output
decreases and finally the organ is completely dea d and no ADH is produced.
Treatment: desmopressin
Nephrogenic diabetes insipidus – the kidney does not respond to ADH e.g. loop diuretics,
hypokalemia, hypercalcemia, lithium, ATN and osmotic diuresis
HYPERCALCEMIA IN NEPHROGENIC DIABETES INSIPIDUS
HYPERNATREMIA

Lack of water is necessary for hypernatremia but increased water loss

will help drive the hypernatremia.
Renal loss: diuretics, diabetes insipidus, non-oliguric AKI
Extra-renal loss: diarrhea, skin losses and insensible losses

Gain of sodium can predispose to hypernatremia e.g. hypertonic IVF,

sodium bicarbonate, hyperaldosteronism/Cushings.
 HYPERNATREMIA TREATMENT

If you rapidly correct hypernatremia, there will be a shift of fluid into the cells and
cause cerebral edema.

Correction of hypernatremia: 0.5 mmol/L/hour or 12 mmol/L in 24 hours

 HYPERNATREMIA TREATMENT

Accounting for ongoing losses is essential if the patient has diabetes insipidus and is
polyuric or if the patient has high insensible losses e.g. febrile or an open surgical
wound.

If the patient has a relatively low urine output, you multiply the urine output by 0.5
and that is the amount to be replaced.

If the patient is polyuric, you multiply the urine output by 1.0, and that is the amount
to be replaced.
HYPERNATREMIA TREATMENT
To correct hypernatremia, add the water deficit to the ongoing urinary losses and
give that to the patient. Ideal fluid is water by mouth or D5W.
 POTASSIUM

Intracellular K = 140 mmol/L

Extracellular K = 4 mmol/L

A banana has 1 mmol of potassium per inch.

 POTASSIUM REGULATION

1. Intake
2. Cellular distribution depends on 4 factors: insulin, beta-2 recpetors, pH and cell growth and
destruction.
◦ Na-K-ATPase moves 3 Na ions out of the cell in exchange for 2 K ions. Insulin and beta-2 receptors stimulate
the Na-K-ATPase pump. Insulin moves glucose, K and phosphorus into the cell.
◦ With alkalosis, hydrogen ions exit the cell in exchange for K
◦ With acidosis, hydrogen ions go into the cell in exchange for K except for DKA and lactic acidosis. In DKA,
beta-hydroxybutyrate and acetoacetate move into the cell with hydrogen ions, and in lactic acidosis, lactate
moves into the cell with hydrogen ions.
◦ Cell construction decreases extracellular K while cell destruction causes release of K.
◦ Hypertonicity causes water to flow out of the cell and carries K with it.
 POTASSIUM REGULATION
3. Renal excretion: 10-400 mmol/day. All of the potassium in the urine is secreted by
the cortical collecting duct. The cortical collecting duct has two types of cells:
◦ Principal cells secrete potassium
1. Reabsorption of Na down its concentration gradient via the epithelial Na channels (ENaC) since the Na-K-ATPase
maintains a very low Na level intracellularly. The epithelial Na channel (ENaC) is an electrogenic transporter  the
reabsorption of Na generates a negative charge in the tubule. Enhanced Na delivery = more K secretion
2. The negative charge generated in the tubule attracts the positively charged K via two channels.
3. Aldosterone: leads to an increase in the number of the principal proteins involved in K secretion as well as the amount of
K these proteins are able to secrete.
◦ Intercalated cells secrete hydrogen and HCO3
HYPOKALEMIA

Potassium level <3.5 mmol/L

Moderate hypokalemia <3.0 mmol/L
Severe hypokalemia <2.5 mmol/L

Causes of hypokalemia:
1. Decreased intake e.g. anorexia and bulimia
2. Intracellular shift
3. Increased renal excretion
HYPOKALEMIA: INTRACELLULAR SHIFT

1. Rapid cell growth due to treatment of folate or B-12 deficiency causes

increased potassium consumption by the new cells.
2. Beta-2 agonists e.g. tocolytics, asthma and COPD
3. Refeeding syndrome – starvation  total body depletion of K, Mg and phos
 resumption of feeding with carbohydrates  release of insulin  shift K and
Phos into the cells  hypokalemia and hypophosphatemia.
HYPOKALEMIA: GI LOSSES
HYPOKALEMIA: SECONDARY HYPERALDOSTERONISM

Diarrhea  volume depletion  secondary hyperaldosteronism  minimal renal

losses of K
Why does this occur?
Volume depletion  increase Na reabsoprtion proximally  decreased Na
delivery to cortical collecting ducts  decreased K secretion

You need both an increase in Na delivery and hyperaldosteronism to cause K loss.

HYPOKALEMIA: SECONDARY HYPERALDOSTERONISM

Diuretics increase distal delivery of Na as well as volume depletion which leads

to secondary hyperaldosteronism  increased K secretion.

Salt wasting nephropathies: Bartter syndrome is a genetic abnormality in the

thick ascending loop of Henle (congenital loop diuretic). Gitelman syndrome is a
genetic abnormality in the distal convoluted tubule (congenital thiazide diuretic).
 HYPOKALEMIA: VOMITING

In normal physiology, a hydorgen pump

is located in the stomach. The hydrogen
then travels to the duodenum where it is
exchanged for HCO3. The hydrogen
that enters the circulation binds to
HCO3 and becomes neutralized. And
the hydrogen that remains in the
duodenum also gets neutralized by
HCO3 therefore there is no net
movement of HCO3.
 HYPOKALEMIA: VOMITING

With vomiting, hydrogen and chloride

are lost. The absence of hydrogen in the
duodenum does not activate the proton
pump which causes an increase in HCO3
in the duodenum, and hydrogen to be
secreted into the circulation.
The HCO3 that was secreted into the
circulation by the stomach does not get
neutralized  metabolic alkalosis.
HYPOKALEMIA: VOMITING

To compensate for the increased HCO3, the kidney increases HCO3 excretion.
The HCO3 has a negative charge which attracts the K from the cortical collecting
duct.
HCO3 also pairs with Na  increased Na delivery
Vomiting  volume depletion  increased aldosterone
 HYPOKALEMIA: PRIMARY HYPERALDOSTERONISM
Unregulated and autonomous release of excess aldosterone from the adrenal gland.
- bilateral adrenal hypertrophy
- functional adenoma in a single adrenal gland (Conn’s syndrome)

Primary hyperaldosteronism is a syndrome that consists of:

1. hypertension
2. hypokalemia
3. metabolic alkalosis
4. hypernatremia (increased ENaC stimulation)
APPARENT PRIMARY HYPERALDOSTERONISM

Very similar to primary hyperaldosteronism however, aldosterone levels are low.

Cortisol and aldosterone are very similar molecularly and cortisol can bind to the
mineralocorticoid receptor (MR) and lead to similar actions as aldosterone 
increased synthesis of Na-K ATPase, Enac, K channel and H-ATPase
However in the cortical collecting tubules, there is an enzyme called 11 beta-
hydroxysteorid dehydrogenase that converts cortisol to an inactive cortisone that
cannot bind to MR. Licorice blocks this enzyme and allows cortisol to exhibit the
same effects as aldosterone.
UNREABSORBABLE ANIONS

Chloride (anion) gets reabsorbed in the cortical collecting duct via a paracellular pathway. It has
a negative charge and when it gets reabsorbed, the negative charge on the tubular side gets
diminished  chloride reabsorption competes with K secretion. More chloride reabsorption =
less K secretion and vice versa.
Some anions that pass through the collecting tubule do not get reabsorbed  increased negative
charge on the tubular side  increased K secretion.
UNREABSORBABLE ANIONS
- bicarbonate with vomiting
- bicarbonate with proximal RTA (type 2)
- bicarbonate with medications
- bicarbonate with IVF
- acetate in IVF and TPN
- lactate in IVF and TPN
- ticarcillin
- toluene (glue sniffing)
- phosphates
 POTASSIUM WASTING NEPHROPATHY
1. Polyuria
2. Distal RTA (type 1 RTA) – the intercalated cells of the cortical collecting ducts secrete hydrogen into
the tubules via the H-ATPase. Therefore, hydrogen secretion into the tubules require ATP as well as the
negative charge generated from Na reabsorption. Hydrogen and K compete for this negative charge.
Increased hydrogen secretion will decrease K secretion.
Distal RTA you lose distal hydrogen secretion  K no longer competes with hydrogen for the negative
charge  enhanced K secretion.
3. Hypomagnesemia – the ROMK channel is slowed down by intracellular magnesium. So low Mg =
increased activity of ROMK.
SYMPTOMS OF HYPOKALEMIA

Muscle Weakness Metabolic Effects

• Cramps • Diabetes insipidus

• Rhabdomyolysis • Metabolic alkalosis
• Ileus • Increased ammonia
• Paralysis production
 HYPOKALEMIA ECG CHANGES

1. T wave flattening
2. U waves
3. ST depression
4. Pseudo-QT elongation
With worsening hypokalemia:
- frequent supraventricular and ventricular ectopics
- supraventricular tahcyarrhythmias: fib, flutter, atrial tachycardia.
- potential to develop life-threatening ventricular arrhythmias: VT, VF and Torsades de
Pointes
 HYPOKALEMIA TREATMENT
Calculate the K deficit = 0.3 x Kg x (4 – K measured)
Divide by 13.4 = amount of amps that you need to replace.
So you can mix the amps in NS/RL and give over 2 hours then start the patient on maintenance potassium in the from of
KCl.
KCl is the best K supplement, the Cl gets reabsorbed paracellularly  decreasing the negative charge  decreased K
secretion.

Pitfalls of giving K IV:

1. phlebitits
2. volume overload if using NS
3. increased insulin release if using dextrose solutions  transient worsening of hypoklaemia.
HYPERKALEMIA

Normal K+: 3.5 – 5.3 mmol/L

Causes of hyperkalemia
◦ Increased intake
◦ Extracellular shift
◦ Decreased potassium excretion
INCREASED INTAKE

Unusal causes of hyperkalemia without concurrent renal failure

◦ Salt substitutes – have K instead of Na, 15 mmol of K per ¼ teaspoon. Usually not an
issue unless patient is on ACEI or aldosterone antagonists which decrease renal excretion
of K.
◦ TPN
◦ Enteral supplements
◦ Blood transfusions: K 12-40 mEq/L – increases as the PRBC ages.
◦ High potassium foods e.g. tomato juice
◦ Penicillin: 1.7 mmol of K per million units
◦ Dialysate
EXTRACELLULAR SHIFT

1. Hyperosmolality e.g. DKA and hyperglycemia

2. Cell destruction e.g. rhabdomyolysis, tumor lysis syndrome,
hypothermia, hemolysis
3. Drugs e.g. beta blockers, digoxin, sux
4. Acidemia
HYPEROSMOLALITY

Hyperglycemia: extracellular hypertonicity  water moves from

intracellular space to extracellular space, dragging K with it.
DIGOXIN

Digoxin poisons the Na/K ATP-ase pump  prevents extracellular K

from entering the cell.
Management: Digoxin immune FAB  binds and neutralizes digoxin
ACIDOSIS

With acidosis, hydrogen ions go into the cell and K goes out  maintains
electroneutrality.
In cases where acidosis is due to beta-hydroxybutyrate, acetoacetate or lactate,
hydrogen ions move into the cell along with these negatively charged ions to
maintain electroneutrality with no need for movement of K out the cell.
DECREAED K EXCRETION

Persistent hyperkalemia is always due to a failure of renal potassium

handling.
◦ Renal failure
◦ Decreased distal Na delivery
◦ eNaC antagonism
◦ Hypoaldosteronism
DECREASED K EXCRETION

Potassium is freely filtered at the glomerulus then reabsorbed in the proximal

tubule and loop of Henle.
All of the potassium in the urine is secreted by the cortical collecting duct.
At the cortical collecting ducts, Na flows down its concentration gradient via the
eNaC channel in the principal cells. This concentration gradient is maintained by
the Na/K ATPase on the basal membrane of the principal cells.
The movement of Na intracellularly generates a negative charge in the tubule 
K enters the tubule via the electrical gradient
DECREASED K EXCRETION

A decreased GFR = decreased distal delivery of Na  no electrical gradient

generated  K retention. NSAIDs can decrease GFR.
The eNaC channel is sensitive and can be blocked by triamterene, amiloride,
trimethoprim and type 1 RTA (electrogenic).
Hypoaldosteronism: aldosterone stimulates the production of all 3 critical
proteins – Na/K ATPase, eNaC and ROMK. Low levels = shut down of the
channels = hyperkalemia. It can be caused by congenital causes (Addison’s
disease), diabetes and drugs (renin inhibitors, ACEI, ARBs, ketoconazole
aldosterone antagonists.
PSEUDOHYPERKALEMIA

WBC >100,000
Platelets >1,000,000
Chronic lymphocytic leukemia
Tourniquets
Cold weather
Tube system e.g. pneumatic tube
HYPERKALEMIA CONSEQUENCES

Muscle weakness and paralysis

ECG changes and cardiac arrhythmias
TREATMENT OF HYPERKALEMIA

Calcium gluconare – to prevent cardiac arrhythmia

Stop intake of K
Induce intracellular shift of K: digoxin antidote for digoxin toxicity (DigFAB);
salbutamol; insulin
Increased excretion of K: diuretics, saline to increase distal Na delivery; kayexalate;
note: kayexalate can cause intestinal necrosis
Dialysis