Hyperkalemia. Objectives Definition Brief review of potassium regulation processes Causes Clinical Manifestations Therapy Proposals for standardized management.

Hyperkalemia

Objectives

• Definition• Brief review of potassium regulation processes• Causes• Clinical Manifestations• Therapy• Proposals for standardized management

Definition

• Hyperkalemia = plasma K+ concentration > 5.0mmol/L

• Critical hyperkalemia = plama K+ concentration > 6.5 mmol/L

• UNM Lab Ranges: Normal 3.5-5.1 Critical 6.5 for women, 7 for men

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

Causes of Hyperkalemia

I. Potassium release from cells

II. Decreased renal loss

III. Iatrogenic

(Consider pseudohyperkalemia)

Potassium release from cells

• Intravascular hemolysis• Tumor Lysis Syndrome• Rhabdomyolysis• Non-gap metabolic acidosis• Hyperglycemia• Severe Digitalis toxicity• Hyperkalemic periodic paralysis• Beta-blockers• Succinylcholine; especially in case massive trauma, burns

or neuromuscular disease

Decreased renal loss • Renal failure• Decreased distal flow• Decreased K+ secretion

Impaired Na+ reabsorptionadrenal insufficiencyadrenal enzyme deficiencyhyporeninemic hypoaldosteronismdrugs: ACEi, NSAIDS, heparin, K+-sparing

diuretics, trimethoprim, pentamidinetubulointerstitial diseasedistal type 4 RTA

Enhanced Cl- reabsorptionCyclosporineGordon’s syndrome

Clinical Manifestations• 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 wavesProlonged PR interval and QRS durationAV conduction delayLoss of P wavesProgression of QRS duration leading to sine wave patternVentricular fibrillation or asystole

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 BE COUNTED ON; cardiac toxicity does not correlate well with

plasma K+ concentration.MUST OBTAIN STAT ECG.

2. Determine underlying cause(s) once patient treated to maintain stability

If K+ high and ECG normal, consider pseudohyperkalemiaUsually, chronic hyperkalemia is due to impaired K+ excretionReview medications, oral and all IV therapiesEvaluate effective circulating volumePatients 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.

Emergent Therapy1. 10 ml of a 10% solution calcium gluconate infused over 2-3 minutes.

onset of action several minutes, lasts 30 – 60 minutes2. 10-20 units regular insulin with 25-50 g glucose IV

onset action 15-30 minutes, lasts several hours. K+ drops 0.5-1.5 mmol/L.no glucose if patient hyperglycemic

3. Nebulized or parental Beta-agonistonset action 30 minutes, lasts 2-4 hours. K+ drops 0.5 to 1.5 mmol/L.

4. IV NaHCO3 as isotonic solution of 3 amps per liter 5% dextroseIdeally reserved for severe hyperkalemia associated with metabolic acidosis avoid in

patients with ESRD; not tolerated and they seldom respond. Little medical evidence for use.

5. Loop and thiazide diuretics if renal function adequate and not dehydrated6. Cation exchange resin, ie Kayexalate. 25-50 g mixed with 100 ml 20% sorbitol orally, or

30-60 min retention enema with 50 g resin in 150 ml H20.onset 1-2 hours and lasts 4-6 hours. K+ drops 0.5-1.5 mmol/L

7. DialysisPeritoneal is only 15% as effective as hemodialysis

Algorithmic management of hyperkalemia.

Sood M M et al. Mayo Clin Proc. 2007;82:1553-1561

© 2007 Mayo Foundation for Medical Education and Research

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 telemetry4. Policy if K+ <6.5 and no ECG changes present, treat with kayexalate and

repeat K+ level and ECG in 4-6 hours. No need other interventions.5. Policy if K+ < 6.5 and ECG changes present, administer CaGluconate,

Insulin/Glucose, Nebulizer Rx, and Kayexalate. Consider consult ICU team.6. Policy if K+ > 6.4, regardless of presence of ECG changes, administer

CaGluc, Insulin/Glucose, Nebulizer Rx, and Kayexalate. Repeat ECG and K+ level in 1 hour. Consider consult ICU team.

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.