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SAMIR EL ANSARY
Causes
of
hyperkalemia
Extracellular potassium
redistribution
Can be caused by
Metabolic acidosis, insulin deficiency,
B-adrenergic blockade,
rhabdomyolysis, massive hemolysis,
tumor lysis syndrome, periodic
paralysis
(hyperkalemic form), and
Heavily catabolic states such as
severe sepsis.
States of hypoaldosteronism
include :
Decreased renin-angiotensin system
Activity
(e.g., hyporeninemic
hypoaldosteronism in diabetes,
interstitial nephritis, ACE inhibitors,
nonsteroidal antiinflammatory drugs
[NSAIDs], cyclosporine)
States of hypoaldosteronism
include :
Decreased renin-angiotensin system
Activity
Decreased adrenal synthesis
(e.g., Addison disease, heparin), and
aldosterone resistance
(e.g., high-dose trimethoprim,
potassium-sparing diuretic agents).
Drugs
causing
hyperkalemia
Clinical manifestations of
hyperkalemia
Clinical manifestations of hyperkalemia
are dependent on many other variables
such as calcium,acid-base status, and
chronicity.
The most serious manifestation of
hyperkalemia involves the electrical
conduction system of the heart.
Hyperkalemia disproportionate to
reductions in GFR usually results from
decreases in potassium secretion (due
either to decreases in aldosterone, as
may occur in Addison disease, or to
diabetes with hypo-reninemic hypoaldosteronism) or from marked
decreases in sodium delivery to the
distal nephron, as may occur in severe
prerenal states.
Diagnostic approach to
hyperkalemia
The cause is often apparent after a careful
history and review of medications and
basic laboratory values
including a chemistry panel with
Blood urea nitrogen and creatinine
concentrations.
Effect of heparin on K+
Heparin can cause hyperkalemia by
blocking aldosterone biosynthesis.
Both low-molecularweight heparin and
unfractionated heparin can cause
hyperkalemia.
Pseudohyperkalemia
Serum potassium measurements can
be falsely elevated when potassium is
released during the process of blood
collection from the patient or during the
process of clot formation in the
specimen tube.
These situations do not reflect true
hyperkalemia.
2.7 mEq/L.
Potassium release during the process of
clot formation in the specimen tube from
leukocytes (white blood cell counts
>70,000/mm3) or platelets (platelet count
> 1 ,000,000/mm3) can also become quite
significant and distort serum potassium
measurement results.
In these circumstances, an
unclotted blood sample
(i.e., plasma potassium
determination) should be
obtained.
Severe weakness.
Serum potassium level above 6 mEq/L.
EGG changes may not always be present,
although this level of hyperkalemia
predisposes to rhythm abnormalities.
Treatment of hyperkalemia
The general approach is to use
therapy involving each of the
following
Membrane stabilization:
Calcium antagonizes the cardiac effects of
hyperkalemia.
It raises the cell depolarization threshold and
reduces myocardial irritability.
Calcium is given regardless of serum calcium
levels.
One or two ampules of IV calcium chloride result
in improvement in ECG changes within seconds,
but the beneficial effect lasts only approximately
30 minutes.
The dose can be repeated in absence of
obvious change in ECG or with recurrence of
ECG changes after initial resolution.
Removal of potassium:
Loop diuretics can sometimes cause enough
renal potassium loss in
patients with intact renal function, but usually a
potassium-binding resin must be used (e.g.,
Kayexalate, 30 gm taken orally or 50 gm
administered by retention enema).
The effect of resin on potassium is slow, and the
full effect may take up to 4 to 24 hours.
Acute hemodialysis
is quick and effective at removing potassium
and must be used when the GI tract is
nonfunctional or when serious fluid overload is
already present.
GOOD
LUCK
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
elansarysamir@yah
oo.com