Hyperkaliemia is the very common medical problem. Its also important topic for all graduate and postgraduate doctors

1. Approach to Hyperkalemia
Dr. Abdullah Al Masum, MD
Assistant Professor of Internal Medicine
Bangabandhu Sheikh Mujib Medical University

2. Objectives
• Definition
• Brief review of potassium regulation processes
• Causes
• Clinical Evaluation
• Laboratory workup
• Therapy
• Proposals for standardized management

3. Definition
• Hyperkalemia = plasma K+ concentration>
5.0mmol/L
• Critical hyperkalemia = plama K+
concentration > 6.5 mmol/L
• Lab Ranges:
 Normal 3.5-5.1
 Critical 6.5 for women & 7 for men

4. Potassium Regulation Review
• Intracellular concentration about 150 mmol/L
• The passive outward diffusion of K+ is the most
important factor that generates the resting
membrane potential.
• Maintenance of steady state requires K+
ingestion = K+ excretion
• Nearly all regulation of renal K+ excretion and
total body K+ balance occurs in the distal
nephron, via principal cells
• Potassium secretion regulated by aldosterone
and plasma K+ concentration

6. Causes of Hyperkalemia
I. Potassium release from cells
II. Decreased renal loss
Ill. Iatrogenic
(Consider pseudohyperkalemia)

7. Potassium release from cells
• lntravascular hemolysis
• Tumor Lysis Syndrome
• Rhabdomyolysis
• Non-gap metabolic acidosis
• Severe Hyperglycemia
• Severe Digitalis toxicity
• Hyperkalemic periodic paralysis
• Beta-blockers
• Others- massive trauma, burns or
neuromuscular disease

8. Decreased renal loss
• Renal failure- AKI , CKD
• Decreased distal flow
• Decreased K+ secretion
Impaired Na+ reabsorption
adrenal insufficiency
adrenal enzyme deficiency
hyporeninemic hypoaldosteronism
drugs: ACEi, NSAIDS, heparin, K+-sparing
diuretics, trimethoprim, pentamidine
tubulointerstitial disease
distal type 4 RTA
Enhanced Cl- reabsorption
Cyclosporine
Gordon's syndrome

9. Clinical Manifestations
• Progressive muscular weakness, which can progress to
flaccid paralysis and hypoventilation.
Secondary to prolonged partial depolarization from the elevated K+, which
impairs membrane excitability.
• Metabolic acidosis, which further increases K+
Secondary to hyperkalemia impairing renal ammoniagenesis and absorption,
and thus net acid excretion.
• Altered electrical activity of heart, cardiac arrhythmias.
ECG changes in order of appearance:
Tall, narrow-based, peaked T waves
Prolonged PR interval and QRS duration
AV conduction delay
Loss of P waves
Progression of QRS duration leading to sine wave pattern
Ventricular fibrillation or asystole

10. Lab evaluation
Serum electrolytes
ECG
RBS
Renal function test
Spot urine k+, osm, creat
CPK
ABG
Others – According to causes

11. January 15, 2006 ◆ Volume73, Number2 www.aafp.org/afp AmericanFamilyPhysician 287
Hyperkalemia
treatment focuses on lowering total body potassium. In
patients who do not require urgent treatment, lowering
total body potassium may be the only step necessary.
Intravenous calcium is administered to stabilize the
myocardium; it lowers the threshold potential, thus
counteracting the toxic effect of high potassium. Cal-
cium does not have any effect on the serum potassium
level. Improvement in the ECG changes should be vis-
ible within two to three minutes of administration of
calcium (Table 52,3). Repeated doses can be given while
other measures are initiated.28
Caution should be used in patients who take digoxin
because calcium has been reported to worsen the myo-
cardial effects of digoxin toxicity.2,3 Some experts sug-
gest using a slower calcium infusion for 20 to 30 minutes
in patients with hyperkalemia who are on digitalis ther-
apy.28-30 An alternative is to consider using magnesium
instead of calcium to stabilize the myocardium.29
Shifting potassium intracellularly is done using insu-
lin or a beta2 agonist (Table 52,3). Insulin typically is
given as 10 units intravenously with 50 mL of 50 percent
glucose to counteract hypoglycemia. Repeated doses can
be given if the potassium level remains elevated.
Inhaled beta2 agonists have a rapid onset of action.
The effect of beta2 agonists is additive to that of insu-
lin administration, and they can be taken together.31
Nebulized albuterol (Ventolin) is taken in a dose of
10 to 20 mg. Intravenous beta2 agonists have been used
in Europe, but they are not approved by the U.S. Food
and Drug Administration.3
Sodium bicarbonate is no longer recommended to
lower potassium, although it may be appropriate in
patients with severe metabolic acidosis.32
loweriNg t o t a l boDy Potassium
Treatments that shift potassium into the cells have no
effect on total body potassium. Potassium can be elimi-
nated by renal excretion, gastrointestinal elimination, or
dialysis. The agents taken to lower total body potassium
can interfere with tests to determine the cause of hyper-
kalemia. Thus, spot urine potassium, creatinine, and
osmolality levels should be obtained before the agents are
initiated; however, treatment should not be delayed while
awaiting results.
Gastrointestinal excretion is accomplished using
sodium polystyrene sulfonate (Kayexalate), which binds
potassium in the colon in exchange for sodium; it can be
given orally or as a retention enema. The enema form is
faster; the oral route can take four to six hours because it
requires the resin to get to the colon before it takes effect.
Sodium polystyrene sulfonate often is given with sorbi-
tol to decrease constipation. However, sorbitol can have
intestinal complications, with reports of bowel necrosis
and perforation in immunocompromised patients.33
Using furosemide (Lasix) with polystyrene reduces the
risk of volume overload because of the sodium that is
exchanged for potassium by the resin (Table 52,3).33
Excretion of renal potassium can be increased
with the use of diuretics, particularly loop diuret-
ics (e.g., furosemide). Patients with decreased kidney
table 4
Diagnostic equations for Hyperkalemia
Test* Formula† Interpretation in hyperkalemia Notes
FEK less than 10 percent indicates renal etiology
FEK greater than 10 percent indicates extrarenal
cause
Values can be increased
in chronic renal failure.
Fractional excretion
of potassium (FEK)
Transtubular
potassium gradient
(UK/SK) 100%
(UCr/SCr)
or
[UK SCr /SK UCr] 100
[(UK) / (Uosm/Sosm)]
SK
or
(UK Sosm) / (SK Uosm)
Gradient less than 6 to 8 indicates renal cause
Gradient greater than 6 to 8 indicates extrarenal
cause.
Values can be increased
in chronic renal failure.
UK = urine potassium; SK = serum potassium; UCr = urine creatinine; SCr = serum creatinine; Uosm = urine osmolality; Sosm = serum osmolality.
*—For the most accurate representation of the kidney’s response to hyperkalemia, these measurements should be drawn before the serum
potassium is corrected.
†—Plasma values for potassium and osmolality are recommended for this equation, but serum values are listedbecause these are more commonly
available.
Information from references 22 and 23.

12. Therapy
1. Determine needed approach - if emergent or not.
Typically, potential fatal hyperkalemia occurs with K+ > 7.5 and associated
with profound weakness.
THIS CANNOT BECOUNTED ON; cardiac toxicity does not correlate well with
plasma K+ concentration.
MUST OBTAIN STATECG.
2. Determine underlying cause(s) once patient treated to
maintain stability
If K+ high and ECGnormal, consider pseudohyperkalemia
Usually, chronic hyperkalemia is due to impaired K+ excretion
Review medications, oral and all IV therapies
Evaluate effective circulating volume
Patients with Kidney disease are highest risk of developing hyperkalemia.
Consider the combination of: HCO3 <20, Cl-> 105, Cr> 1.5, diabetic as high
risk for hyperkalemia.

13. Emergent Therapy
1. Stabilize cell membrane potential
10 ml of a 10% solution calcium gluconate infused over 2-3 minutes. onset
of action several minutes, lasts 30 - 60 minutes
2. Shift K+ into cells
• 5 units regular insulin with 50ml of 50%glucose IV
• Nebulized or parental Beta-agonist
• IV NaHCO3 as isotonic solution of 3 amps per liter 5% dextrose
Ideally reserved for severe hyperkalemia associated with metabolic
acidosis avoid in patients with ESRD; not tolerated and they seldom
respond. Little medical evidence for use.
3. Remove K+ from body
• Loop and thiazide diuretics if renal function adequate and not dehydrated
• Ion exchange resin, orally, or enema
• Dialysis

15. Proposals for standardized
management
1. No treatment, other than kayexalate, for K 5 . 1 - 6 unless medical
condition strongly predicts the value will continue to increase. Examples:
acute oliguric renal failure, tumor lysis syndrome. Do repeat and f/u on
potassium level.
2. Policy that for any K+ > 6.0, order ECG.
Consider stat repeat K+ if concern pseudohyperkalemia
3. For persistent K+ > 5.1, order telemetry
4. Policy if K+ <6.5 and no ECGchanges present, treat with kayexalate and
repeat K+ level and ECGin 4-6 hours. No need other interventions.
5. Policy if K+ < 6.5 and ECG changes present, administer CaGluconate,
Insulin/ Glu cose, Nebulizer Rx, and Kayexalate. Consider consult ICU
team.
6. Policy if K+ > 6.4, regardless of presence of ECGchanges, administer
CaGluc, Insulin/Glucose, Nebulizer Rx, and Kayexalate. Repeat ECG and
K+ level in 1 hour. Consider consult ICU team.

16. Recap of Major Learning
Points
Hyperkalemia
Make sure it’s real
Determine emergent or not
Rate of rise, degree of hyperkalemia, EKG
Treat emergent cases with calcium gluconate, insulin, dextrose, and
kayexalate +/- dialysis/lasix
Monitor closely for response to treatment—watch for rebound
Fix the cause if possible

17. Case #1
A 56 y/o male presents due to increased swelling in his face,
legs, and abdomen, as well as increasing SOB and DOE. He
is volume overloaded on exam. His labs are listed below. His
serum albumin is 2.5 g/dL. Would you replace or treat
anything?
Na+ K+ Cl- CO2 BUN Creat Gluc Ca2+ Mg2+ Phos
133 5.5 101 18 51 9.5 83 8.2 2.1 6.0

18. Case #1 (continued)
Patient’s EKG

19. Case #1 (continued)
Here’s what the intern did…
Gave 30gm Kayexalate PO
Appropriate
Gave lasix for volume overload, attempt at diuresis and potassium lowering
Appropriate
No insulin/dextrose/calcium gluconate
Probably appropriate
Gave phosphate binders for high phosphorus and DID NOT Rx low calcium
(corrected calcium 9.4 mg/dL--normal)
Very appropriate
Discussed possible hemodialysis with senior
Appropriate

20. Case #1 (continued)
Here’s what the intern did…
Rechecked K+ 12 hours later, still 5.5 mEq/L
Could have rechecked a little sooner
Therfore gave another 30gm of Kayexalate PO
Appropriate
Rechecked K+ 8 hours later, down to 5.1 mEq/L

21. Teaching Points
 Know the systematic approach to assessing and treating
hyperkalemia
 Avoid unnecessary correction of low serum calcium values,
especially when they are spuriously low

22. Case #2
A 57 yr old hypertensive man presented with generalized weakness. ECG
showing - -
a) Write down 2 positive findings
b) What is the likely cause of the ECG changes
c) What immediate 2 measure you will take to prevent death
d) Mention 4 other subsequent mx may be needed
-

23. References
1. Harrisons Principles of Internal Medicine. 17th Edition.
2008.
2. Alfonzo, Annette V.M. Review paper: Potassium
disorders-clinical spectrum and emergency management.
Resuscitation (2006) 70, 10 -25.
3. Sood, Manish M. Emergency Management and
Commonly Encountered Outpatient Scenarios in Patients
With Hyperkalemia. Mayo Clinic Proc. 2007; 82(12): 1553-
1561.
4. Tzamaloukas, A. Pathophysiology and Management of
Fluid and Electrolyte Disturbances in Patients on Chronic
Dialysis with Severe Hyperglycemia. Seminars in Dialysis.
2008; 21(5): 431-439.

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