Transcript Hyperkalemia

Hyperkalemia
Objectives
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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
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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+ 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
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 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
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 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.
Emergent Therapy
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10 ml of a 10% solution calcium gluconate infused over 2-3 minutes.
onset of action several minutes, lasts 30 – 60 minutes
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
Nebulized or parental Beta-agonist
onset action 30 minutes, lasts 2-4 hours. K+ drops 0.5 to 1.5 mmol/L.
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.
Loop and thiazide diuretics if renal function adequate and not dehydrated
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
Dialysis
Peritoneal 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
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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.
Policy that for any K+ > 6.0, order ECG.
Consider stat repeat K+ if concern pseudohyperkalemia
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For persistent K+ > 5.1, order telemetry
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.
Policy if K+ < 6.5 and ECG changes present, administer CaGluconate,
Insulin/Glucose, Nebulizer Rx, and Kayexalate. Consider consult ICU
team.
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): 15531561.
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.