Perfusion Policies 101: HyperKalemia
Editor’s Note:
Welcome to PERFUSION POLICIES 101. This will be a continuing series provided to assist your programs with that one puzzle piece we all run into now and then- that one time that an unexpected patient condition may give you pause…
The intention here is to disseminate some basic recipes that have probably been implemented at countless institutions, for God knows how long. The usual disclaimers obviously apply:
Due Diligence is the Responsibility of the Reader!
Use the information as you feel fit, recognizing that this is information gleaned from multiple sources, it is recruited from the public domain of the internet, with no implied assurance of accuracy- but is cogent, and based on logical and reasonable clinical rationale.
Frank Aprile ?
The Heart and Hyperkalemia
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Most of the body’s potassium is located intracellularly. Onl a small fraction (=2%) is found in the extracellular compartment. As serum potassium concentration increases, a decreased ratio of intracellular to exrtracellular K+concentration occurs, and results in a decreased resting cell membrane potential. Increased serum Na+ and Ca+ concentrations limit depolarization of the cell membrane. In addition, there is shortening of the action potential duration from increased membrane permeability to K+. Mild hyperkalemia (6.0mEQ/L), with normal renal function generally needs no treatment. Moderate hyperkalemia (6.0-7.0mEq/L), with normal renal function generally resolves with time and no therapy. Severe hyperkalemia (7.0mEq/L), especially with EKG manifestations, requires immediate therapy. Renal excretion accounts for total maintenance of potassium balance.
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Causes of Hyperkalemia
-Cardioplegia solutions
-Transfusion of overaged banked blood
-Renal dysfunction from any cause
-K from cell hemolysis
-Acidosis
-K sparing diuretics ( Spironalactone, Triamterene, Amiloride)
-Ace inhibitors
-Digitalis in high doses
-KCL supplementation
-Drugs causing tumor lysis
-Low insulin production (DM)
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Treatment of Hyperkalemia
- If you get a lab value back that is questionable, be sure to send another sample for a repeat value. In the meantime, alert anesthesia to the possibility of true hyperkalemia, and the necessity for treatment of it.
- Stop all infusions containing K+ (cardioplegic solution, priming solutions, IVs).
- Increase the elimination of K+ from the extracellular fluid:
- Infuse Dextrose and Insulin:
1-2g glucose/kg in children
0.3U R insulin/glucose in children
50g glucose and 15U R insulin in adults
- NaHc03:
1-2mEq/kg children
45mEq adults
- Calcium:
20mg/kg calcium gluconate over 5 min in children
500-1000mg of calcium chloride in adults
- Increase dieresis
- Hemoconcentration on CPB: Hemoconcentrate off as much as pump volume as possible, adding normal saline (for injection) as needed for volume replacement. Recheck K+ and electrolye levels often.
- Hemodialysis for persistent hyperkalemia.
- Emergency cardiac pacing if severe hyperkalemia is causing arrhythmia’s.
- If you are aware preoperatively that your patient is hperkalemic, during CPB you can scavenge the initial flush of cardioplegia to the cell saver.
*Note: All of the above listed procedures are contingent upon approval with both the surgeon and anesthesia.
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HOW TREATMENT OF HYPERKALEMIA IS ACHIEVED
NaHcO3: Correction of acidosis by diminishing the extracellular hydrogen burden and transfer of K+ intracellularly, provides intracellular binding sites for K+ in the form of potassium carbonate, buffers dextrose; corrects acidosis from shift of H+ from intracellular to extracellular.
Hypertonic saline: Correct hyponatremia; counteracts cardiotoxicity; expands extracellular compartment and dilutes K+.
Glucose and insulin: Directly promotes the movement of K+ from extracellular to intracellular compartments.
Calcium: Activates receptor sites of potassium pumps on cell membranes; replaces serum Ca, which is driven intracellularly by administration of insulin.
