HYPERKALEMIA

SAMIR EL ANSARY

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Causes

of

hyperkalemia

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

causing

hyperkalemia

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 <6Indicates 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 changesBecause 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 hemodialysisis 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.

Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145161011512

9555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY

GOOD LUCK

SAMIR EL ANSARY

ICU PROFESSOR

AIN SHAMS

CAIRO

elansarysamir@yahoo.com