Transcript Hyperkalemia

The Lethal Electrolyte
Part I: Hyperkalemia
DEFINITION:
Hyperkalemia
• An abnormal physiological state resulting
from high extracellular concentrations of
potassium.
• In a homeostatic state, 98% of K+ is located
in the intracellular fluid (ICF).
Normal Serum K+ Levels
• Infants
• Children
• Adults
4.1-5.3mm/L
3.4-4.7mm/L
3.5-5.0mm/L
Critical values: <2.5mm/L or >6.5mm/L
Causes
• Decreased secretion or excretion as with renal
failure, acidosis (K+ excretion is exchanged in the
kidney for H+ in order to correct acidotic state),
potassium sparing diuretics and adrenal
insufficency.
• Increased intake of K+ as with salt substitutes,
vitamins, rapid transfusion of aged blood (lysis of
dead blood cells increases extracellular K+).
Causes
• Cellular shift as seen with acidotic states; sepsis,
ketoacidosis and with massive tissue damage;
trauma, burns or tumor lysis (causing intracelluar
K+ to spill into extracxellular fluid).
• NOTE: False elevations in serum K+ may occur
with vigorous pumping of the hand after
application of tourniquet for veinous puncture and
in hemolized samples.
Manifestations
• Irritability, anxiety, weakness to lower
extremities, parethesia, irregular pulse and
cardiac standstill if hyperkalemia is sudden
or severe.
• ECG changes include tall, peaked T waves,
prolonged PR interval, ST depression, loss
of P wave, widened QRS, VF and cardiac
standstill (see fig. 1).
ECG Changes
Potassium’s Effect on Cardiac Muscle
STEP 1: Rapid Depolarization
Na+ channels open and Na+
floods into the cell.
STEP 2: The Plateau
Ca++ flows into cell via slow
calcium channels, stimulating
a contraction.
STEP 3: Repolarization
K+ escapes the cell through
slow potassium channels.
Reduction of Chemical Gradient
The loss of the concentration gradient in hyperkalemia
inhibits repolarization of the cardiac muscle. The muscle is
then paralyzed in the absence of a greater stimulus.
Hyperkalemia’s Effect on the Heart
• The heart is able to
function normally in a
homeostatic state.
• In hyperkalemia cardiac
contractions become weak
and irregular.
• In severe cases the heart
eventually stops in
diastole.
Emergency Treatment
•
•
•
•
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Insulin
Glucose
Ventolin
Calcium
Furosemide
• Sodium
Bicarbonate
• Potassium
Binding Resin
• Hemodialysis
Antidotes
• Insulin & Glucose: Glucose and Insulin shift
K+ into cells and begin having an effect within 30
min. of administrationand and lasting for 4-6
hours after.
Insulin (Humulin, Humulog, Novolin) 5-10U of
regular Insulin IVis accompanied by Glucose
(D50W) 1-2 amps IV to counteract hypoglycemia
NOTE: High concentrations of glucose can cause
thrombosis when given peripherally. Ideally, D50W
should be given via central line.
Beta-Antagonists
• Ventolin: An adrernergic agent that increases
plasma insulin levels therefore aiding in the
cellular shift of K+ into the cells. This treatment
is ideal in patients with renal failure where fluid
overload is a concern.
There are discrepancies regarding effective
dosages. Anywhere from 2.5mg to 20mg
nebulized by mask are suggested with effects seen
within 15-30 min. and lasting for 15 min to 3
hours.
Electrolyte supplements
• Calcium: Increases the threshold potential therefore
restoring the cardiac muscles ability to function and
counteracting the paralytic effect of hyperkalemia.
Effects seen in 1-3 min. and last 30 – 60 min.
Calcium Chloride 5ml of 10% sol. IV over 2 min.
OR
Calcium Gluconate 10 ml of 10% sol. IV over 2 min.
YCH recently changed the vials of Calcium Gluconate
so watch the dose!
Caution in bradycardia
Diuretics
• Furosemide: Increase the loss of K+ through the
kidney. However, the effects take as long as an
hour and the results are in consistent.
Lasix 20-40mg IV slow push
If patient is already taking this medications double
thier daily PO dose and give IV.
Large doses my be required in renal failure.
Alkalinizing Agents
• Sodium Bicarbonate: Neutraizes H+ ions
and raises urine and blood pH. Onset of
effect in 5-10 min. and lasting 1-2 hours.
Sodium Bicarb 1mEq/kg slow IV push or
continuous IV drip
Only use to treat documented metabolic acidosis or
hyperkalemia-induced cardiac arrest.
Blood pH must be monitored to avoid alkalosis.
Binding Resins
• Sodium Polystyrene Sulfonate: Promote the
exchange of K+ for Na+ in the GI tract. Lower
K+ within 1-2 hours of administration with effects
lasting 4-6 hours.
Kayexalate 25-50g mixed with 100 ml Sorbitol
PO or PR. Multiple doses usually necessary.
Kayexalate should never be given to someone with
hypoactive bowel sounds because fluid shifts can
lead to bowel necrosis.
Hemodialysis
• Sometimes the best solution for hyperkalemia,
especially in patients with known renal failure, is
dialysis. This process simulates the chemical
gradient within healthy kidneys and draws out
excess potassium.
• Most hemodialysis patients presenting with
elevated K+ require dialysis for other electrolyte
imbalances as well ie: elevated urea, creatinine.
Further care
• Continuous Cardiac monitoring
• Continuous monitoring of serum potassium
levels
• Correction of the cause, ie: renal failure,
trauma, sepsis, acidosis.
• Appropriate follow up care regarding
diagnosis to prevent recurrence.
Sources
Garth M.D., D. Hyperkalemia from eMedicine.com
last updated July 25, 2001
Martini Ph.D, F. Fundamentals of Anatomy and
Physiology. Prentice Hall, New Jersey, 1998.
Lewis RN, Ph.D., FAAN, S., Heitkemper RN, Ph.D.,
FAAN, M & Dirkson RN, Ph.D., S. Medical
Surgical Nursing. Mosby, Toronto, 1996.
Potter, RN, BSN, MSN, P., & Perry RN, BSN, MSN,
EdD, A. Canadian Fundamentals of Nursing.
Mosby, Toronto, 1997.