HYPERKALEMIA

Introduction
 Potassium is an important ion in body, which is required
for functions of cells, especially nerve and muscle cells.

 It comes in body through food. The average daily potassium

intake in a typical diet is 70 mEq.

 Under normal conditions, excretion equals intake, with

approximately 90% of potassium excreted in the urine the
remainder in the stool.

 The normal serum level of potassium is 3.5 to 5 mmol/L

 Hyperkalemia is a disorder that occurs when the serum

potassium in the blood rises to >5.5 mEq/L.
Potassium Distribution
 The intracellular preponderance of potassium is the
result of a sodium-potassium (Na+- K+ ) exchange
pump on cell membranes that moves Na+ out of cells
and moves K+ into cells in a 3:2 ratio.

 ROLE : to create a voltage gradient across cell

membranes in ”excitable” tissues (i.e., nerves and
muscles).
 The total body potassium in healthy adults is about
50–55 mEq per kg body weight.

 In a 70 kg adult: total body potassium 3,500 mEq,

with 70 mEq (2%) in extracellular fluid.

 Because the plasma accounts for about 20% of the

extracellular fluid, the potassium content of plasma
will be about 15 mEq, which is only 0.4% of the total
body potassium.

 Plasma K+ is only the “tip of the iceberg” in terms of

evaluating total body potassium.
Illustration of the small fraction of total body K+ that is present outside cells. This example pertains
to a 70 kg adult with an estimated total body K+ of 50 mEq/kg body weight. Each gold bar
represents 100 mEq of K+ .
Serum Potassium
 The relationship between total body K+ and serum
(plasma) K+ forms a curvilinear shaped curve, with the flat
portion of the curve in the region of potassium deficiency
 In an averaged-size adult with a normal serum K+ of 4
mEq/L, a total body K+ deficit of 200–400 mEq is
required to produce a decrease in plasma K+ of 1
mEq/L,
 While a total body K+ excess of 100–200 mEq is
required to produce a similar (1 mEq/L) increase in
plasma K+.
 Therefore, for a given change in serum K+ , the change
in total body K+ is twofold greater with hypokalemia
than with hyperkalemia.
 The larger deficit associated with hypokalemia is due
to the large pool of intracellular K+ that can replenish
extracellular K+ when K+ is lost.
Mechanisms of regulation

 Renal regulation

 Transcellular shift between the

intracellular and extracellular
compartments
Renal regulation
 Potassium excretion in urine is primarily a function of K+
secretion in the distal nephron, which is controlled by
plasma K+ and (primarily by ) aldosterone.

 Aldosterone:
 Released by the adrenal cortex in response to an increase
in plasma K+ (and angiotensin II),
 Increases K+ excretion in the urine by stimulating K+
secretion in the distal nephron.
 Also promotes sodium and water retention.
 The diuretic spironolactone (potassium-sparing diuretic)
acts by blocking the actions of aldosterone in the kidneys.
Transcellular shifts
 Sodium-potassium ATPase
 Both insulin and epinephrine increase the activity of
sodium-potassium pump.

 Potassium channels
 ECF osmolality↑→H2O leaves cell→ ICF K+↑→ K+ moves
out of cell through K+ channels →ECF K+
 Exercise

 Potassium-hydrogen exchange to maintain electrical

neutrality
 In acidosis
 In alkalosis
Functions of potassium
 Maintain the osmotic integrity of cells
 Osmotic pressure in ICF
 Maintain acid-base balance
 Through potassium-hydrogen exchange
 Contribute to the reactions that take place in cells
 Transform carbohydrates into energy
 Convert amino acid to protein
 Change glucose into glycogen
 Play a critical role in the excitability of skeletal,
cardiac, and smooth muscle.
 Hyperkalemia (serum K+ >5.5 meq/L) can be a life-
threatening condition.

Etiology
 Transcellular shift (Potassium release from cells),
 Impaired renal excretion of potassium.
 Excessively rapid administration

 A spot urine K + can be useful to ascertain the source of

hyperkalemia . A high urine K+ (>30 mEq/L) suggests a
transcellular shift, and a low urine K+ (<30 mEq/L)
indicates impaired renal excretion.
PSEUDOHYPERKALEMIA
 Hyperkalemia that is present ex vivo (in the blood sample),
but not in vivo.
CAUSE
 K+ release due to traumatic hemolysis during the
venipuncture(20%) .
 K+ release from muscles during fist clenching
 potassium release from clot formation in the blood collection
tube in patients with severe leukocytosis (>50,000/mm3) or
severe thrombocytosis (platelet count >1 million/mm3).
 When pseudohyperkalemia is suspected, a repeat blood
sample should be obtained using precautions to mitigate
the suspected problem (e.g., minimize suction when
withdrawing blood).
TRANSCELLULAR SHIFT
The conditions associated with K+ movement out of
cells include
 Acidosis,
 Tumor lysis syndrome,
 Drugs, (β-blocker, digitalis, succinylcholine)
 Blood transfusions
 Tissue injury such as burns and crushing injuries
(Rhabdomyolysis)
 Extreme exercise or seizures
 Hyperglyemia
 Sepsis
Impaired Renal Excretion
 The capacity for urinary K + excretion is great enough to
prevent a sustained increase in serum K+ in response to a
K+ load. As a result, hyperkalemia always involves a defect
in renal K+ excretion.
 The common causes of impaired renal K+ excretion
include
 Renal failure: hyperkalemia usually doesn’t occur
until the GFR drops below 10 mL/min, but it can appear
earlier when renal failure is the result of interstitial
nephritis
 Adrenal insufficiency: Adrenal insufficiency
impairs renal potassium excretion, but hyperkalemia is
seen only in chronic adrenal insufficiency.
 DRUGS: Drugs that impair renal potassium excretion
represent a common source of hyperkalemia.
 Angiotensin-converting enzyme inhibitors,
 Angiotensin receptor blockers,
 Potassium sparing diuretics,
 Nonsteroidal antiinflammatory drugs.

 All of these agents promote hyperkalemia by

inhibiting the renin–angiotensin–aldosterone system.
The hyperkalemia from these drugs often occurs in
combination with K+ supplements or renal
insufficiency.
Manifestations of hyperkalemia
 Gastrointestinal manifestations
 Anorexia, nausea, vomitting, intestinal cramps,
diarrhea
 Cardiovascular manifestations
 Ventricular fibrillation and cardiac arrest
 Neuromuscular manifestations
 Paresthesias
 Weakness
 Muscle cramps
ECG changes in hyperkalemia
 The earliest change - appearance of a tall, tapering
(tented) T wave, most evident in precordial leads V2
and V3.
 As the hyperkalemia progresses, The P wave amplitude
decreases and the PR interval lengthens.
 Eventually, P waves disappear and the QRS complex
widens.
 The final event is ventricular fibrillation or asystole.
ECG abnormalities in
progressive
hyperkalemia.

ECG changes usually begin

to appear when the serum
K+ reaches 7 mEq/L , but
the threshold can vary
widely.
Management of Severe Hyperkalemia
 Severe hyperkalemia is defined as a serum K+ >6.5
mEq/L, or any serum K+ associated with ECG changes.
 The management of this condition has 3 goals:
1. antagonism of the cardiac effects of hyperkalemia,
2. transcellular shift of K+ into cells, and
3. removal of excess K+ from the body.
 Stabilize the Myocardial Membrane
 Elevations in the extracellular potassium
concentration will result in a decrease in membrane
excitability that may be manifested clinically by
impaired cardiac conduction and/or muscle weakness
or paralysis
 Calcium antagonizes the cellular effects of
Hyperkalemia
 The response to calcium is short-lived (20–30
minutes) and it does not reduce the serum K+, so
other measures (e.g., insulin-glucose) should be
initiated to reduce serum K+ levels.
Types of Calcium
 Calcium Gluconate  can be given central or
peripherally
 Calcium Chloride  can only be given via
central line
 Has higher concentration of calcium and if
given peripherally will cause local sclerosis
and gangrene
 In hyperkalemia associated with
circulatory shock or cardiac arrest
Transcellular Shift
 INSULIN-DEXTROSE: Insulin drives K+ into skeletal
muscle cells by activating the membrane Na+- K+
exchange pump.
 A dextrose infusion is advised after insulin-dextrose
(unless the patient is hyperglycemic) because there is a
risk of hypoglycemia at one hour.
 In the setting of hyperglycemia, insulin should be used
without dextrose.
 The insulin effect is temporary (peak effect at 30–60
min), so measures that promote K+ removal should be
started.
2 Agonists (albuterol)
 Drives K2+ intracellular by increasing Na-K
ATPase in skeletal muscle
 The dose of inhaled β2- agonists (e.g.,
albuterol) needed to produce a significant
(0.5–1 mEq/L) drop in serum K+ is at least 4
times the therapeutic dose
 Effects occur in 20-30 min
 ADR-palpitations/arrhythmia
Sodium Bicarbonate (NaHCO3)
 Causes an alkalosis leading to potassium
wasting
 Only works if hyperkalemia 2o to ongoing
severe metabolic acidosis
 Onset few minutes but effects are not long
lasting
 Bicarbonate can form complexes with
calcium, which is counterproductive when
calcium is used to antagonize the membrane
effects of hyperkalemia.
Potassium Removal
Loop Diuretic
 Leads to loss of K+ in urine by inhibiting
NA-K-2CL transporter in Loop of Henle
 Need renal function and volume to get
filtrate to Loop of Henle
CATION EXCHANGE RESIN:
 Sodium polystyrene sulfonate (Kayexalate) is a cation
exchange resin that promotes K+ clearance across the
bowel mucosa.
 It can be given orally (preferred) or by retention enema.
 Kayexalate is usually mixed with sorbitol to prevent
concretions.
 Each gram of resin binds 0.65 mEq of K+, and at least 6
hours is required for maximum effect.
 Uncommon complication - necrotic lesions in the bowel -
mortality rate is high (33%).
HEMODIALYSIS:
 The most effective method of potassium removal is
hemodialysis, which can produce a 1 mEq/L drop in
serum K+ after one hour, and a 2 mEq/L drop after 3
hours.
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