Hyperkalemia

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Wellcome in our new group ..... Dr.SAMIR EL ANSARY

High potassium intake
(e.g., oral potassium replacement, total
parenteral nutrition, and high-dose
potassium penicillin)
can cause hyperkalemia
Usually in the setting of
Low renal potassium excretion.

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.

Low renal potassium excretion
Can be caused by renal failure,
decreased effective circulating
volume (e.g., severe sepsis,
congestive heart failure,
cirrhosis), and states of
hypoaldosteronism.

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 that cause release of
intracellular potassium include
Succinylcholine and, rarely, B-
blockers.

Drugs that block the renin-
angiotensin-aldosterone axis will
result in
Decreased renal potassium
excretion
These include spironolactone, ACE
inhibitors, cyclosporine, heparin
(low molecular weight and
unfractionated), and NSAIDs.

Drugs that impair the process of sodium
and potassium exchange include
Digitalis
Drugs that block sodium and potassium
exchange in the distal nephron include
Amiloride and trimethoprim
.

States of decreased circulatory
volume cause hyperkalemia
Urinary K+ is primarily dependent on
aldosterone action mediated through
activation of the epithelial Na+
channel (E Na C).

In states of volume deficiency, there is
enhanced proximal nephron Na+
reabsorption, hence decreased Na+
availability to epithelial Na+ channel
ENaC.
Even in the setting of high
aldosterone (e.g., congestive heart
failure)
Insufficient Na+ reabsorption occurs to
cause electrogenic K+ secretion.

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.

Profound hyperkalemia can lead to
heart block and asystole.
Initially, the ECG shows
Peaked T waves and decreased
amplitude of P waves followed by
prolongation of QRS waves.

With severe hyperkalemia,
QRS and T waves blend
together into what appears to
be a sine-wave pattern
consistent with ventricular
fibrillation.

A good way to think about
ECG changes in
hyperkalemia
is to imagine
Lifting the T wave, in which
the T gets taller first followed
by flattening of P and QRS.

Other effects of hyperkalemia
include weakness, neuromuscular
paralysis (without central nervous
system disturbances)
And suppression of renal ammonia
genesis, which may result in
metabolic acidosis.

•What degree of chronic kidney
disease
Causes hyperkalemia?
Chronic kidney disease per se is not
associated with hyperkalemia until the
GFR is reduced to approximately 75% of
normal levels
(serum creatinine level >3 mg/dL).

Although more than 85% of filtered
potassium is reabsorbed in the
proximal tubule
Urinary excretion of potassium is
determined primarily by
potassium secretion along the
cortical collecting tubule.

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 hypo-
aldosteronism) or from marked
decreases in sodium delivery to the
distal nephron, as may occur in severe
prerenal states.

Transtubular potassium gradient
(TTKG)
When should it be used?
Transtubular potassium gradient TTKG
was developed to account for the
potentially confounding effect of urine
concentration on the interpretation of the
urine potassium concentration.

The TTKG provides a better clinical
approach to uncover defects in
urinary potassium (UK) excretion as
compared with
UK alone
because the latter fails to account for
plasma potassium concentration and
for medullary water
abstraction.

TTKG is calculated as follows:
Urine K x Serum osm/Serum K x Urine
osm
It is most commonly used in patients with
hyperkalemia
Where a TTKG <6
Indicates an inappropriate renal response
to hyperkalemia, that is
Reduced renal potassium excretion.

Two limitations exist to using the
TTKG:
Urinary sodium must be >25 mEq/L
(so that sodium delivery is not the limiting
factor for K+ secretion).
Na+ is reabsorbed by the cortical
collecting tubule (epithelial Na channel),
then removed from the cell
(Na+,K+-ATPase)
resulting in an increase in cellular K+ that
then moves through a K+ channel into the
urine.

Urine must be hypertonic
(because vasopressin is required for
optimal potassium conductance in the
distal nephron).
TTKG is of limited use in patients with a
varying K+ diet or after acute diuretic
use.

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.

Additional laboratory tests can be
performed if clinical suspicion exists
for
any of the following:
•Pseudohyperkalemia
(look for high white blood cell and platelet
counts)
•Rhabdomyolysis
(look for high creatinine kinase
concentration)

Additional laboratory tests can be
performed if clinical suspicion exists
for
any of the following:
•Tumor lysis syndrome
(look for high lactate dehydrogenase, uric
acid, and phosphorus and low calcium
levels)
•Hypoaldosteronemic state
(look for a TTKG <5 in the setting of
hyperkalemia)

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.

Potassium release from muscles distal to
a tight tourniquet can artifactually
elevate potassium level by as much as
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.

•indications for emergent therapy
EGG changes
Because cardiac arrest can occur at any point
during EGG progression, hyperkalemia with
EGG changes constitutes a medical
emergency.
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.

Shifting potassium into cells:
IV insulin with glucose administration begins to
lower serum potassium levels in approximately 2
to 5 minutes and lasts a few hours.
Correction of acidosis with IV sodium
bicarbonate has a similar duration and time of
onset.

Nebulized p-adrenergic agonists such
as albuterol can lower serum
potassium level by 0.5 to 1.5 mEq/L
with an onset within 30 minutes and
an effect lasting 2 to 4 hours.
Albuterol, however, may be
ineffective in a subset of patients with
end-stage renal disease (from 20%-
40%).

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.
Rarely, when chronic hyperkalemia
is secondary to
hypoaldosteronism
mineralocorticoids can be of use.

•Should glucose always be given
with insulin?
Glucose elevation in the extravascular space
(e.g., with administration of 50% dextrose)
results in K+ movement from the intracellular
to extracellular space.
Thus hyperglycemia in diabetes may cause
hyperkalemia, especially in the absence of
insulin.
After insulin therapy for hyperkalemia,
glucose should not be administered if the
serum glucose concentration is over 175
mg/dL.

•Should glucose always be given
with insulin?
After insulin therapy for
hyperkalemia, glucose should
not be administered if the serum
glucose concentration is over
175 mg/dL.

GOOD LUCK
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
elansarysamir@yahoo.com

Hyperkalemia

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Hyperkalemia