Potassium II Disorders: Hyperkalemia

Mechanism

Progressive Electrocardiographic Manifestations

Hyperkalemia decreases the electronegativity of the myocardial resting membrane potential, partially inactivating voltage-gated sodium channels and slowing atrial and ventricular conduction. The ECG is the main indicator of severity and biological urgency:

1. Peaked T waves

Symmetrical, narrow, large-amplitude T waves ("tented") in precordial leads. It typically occurs with potassium values between 5.5 and 6.5 mEq/L.

2. Driving Impairment

Progressive flattening of the P wave, prolongation of the PR interval and widening of the QRS. It occurs with potassium between 6.5 and 7.5 mEq/L.

3. Sine Wave

Fusion of the QRS with the T wave, forming a continuous sine wave prior to arrest in asystole or ventricular fibrillation. It occurs with potassium > 8.0 mEq/L.

Three-Step Treatment Algorithm for Severe Hyperkalemia

The therapeutic management of severe hyperkalemia (> 6.5 mEq/L or with any associated electrocardiographic alteration) requires a sequential and immediate approach structured as follows:

Step 1: Stabilization of the Myocardial Membrane (Immediate Action)

It consists of counteracting the depolarizing effect of hyperkalemia on the cardiac action potential. It does not reduce plasma potassium levels, but rather prevents the development of lethal arrhythmias.

• Drug of Choice: 10% Calcium Gluconate via peripheral intravenous route.
• Dosage and Administration: Administer 1 ampoule (10 mL of calcium gluconate) to be passed over a period of 5 to 10 minutes via peripheral vein. Its protective effect begins after 1-3 minutes and persists for 30 to 60 minutes. A second dose may be repeated if electrocardiographic alterations persist 5 minutes after the end of the first dose.
• Care Consideration: In patients receiving digitalis (digoxin) chronically, hyperacute infusion of free calcium may exacerbate cellular digitalis toxicity. In these cases, it is preferred to infuse the calcium diluted in 5% dextrose serum over a longer period (20-30 minutes).
• Central alternative: If the patient has a central venous line, 10% Calcium Chloride can be used, which provides three times as many milliequivalents of elemental calcium as gluconate per milliliter of solution.

Pharmacokinetics

Step 2: Intracellular Redistribution of Potassium (Shift)

It consists of forcing the transient internalization of extracellular potassium into the cells through two independent synergistic mechanisms:

1. Polarizing Solution (Insulin + Glucose): Insulin directly stimulates the activity of the Na⁺/K⁺-ATPase pump in skeletal muscle and liver. It is administered together with hypertonic glucose to avoid severe secondary hypoglycemia.
   • Scheme: Administer 10 units of Regular (Rapid) Insulin by direct intravenous route, accompanied by 50 mL of 50% Dextrose (or 250 mL of 10% Dextrose in rapid infusion). This scheme lowers potassium by approximately 0.5 to 1.2 mEq/L in a period of 30 to 60 minutes, with an effect that persists between 4 and 6 hours.
2. Inhaled Beta-2 Adrenergic Agonists: Salbutamol stimulates cellular adrenergic receptors inducing an increase in cAMP that activates the peripheral Na⁺/K⁺-ATPase.
   • Scheme: Administer 10 to 20 mg of nebulized Salbutamol (dose 4 to 8 times higher than that used in bronchospasm). Its use should be avoided in patients with active arrhythmias or underlying unstable ischemic heart disease.

Step 3: Actual Elimination of Potassium from the Body

To achieve resolution of the clinical condition, the actual excretion of excess milliequivalents of potassium is required:

• Loop Diuretics (Furosemide): Useful in patients with preserved renal function or non-anuric acute kidney injury. Administer 40 to 80 mg of Furosemide intravenously to enhance kaliuresis.
• Cation Exchange Ligands (Patiromer, Sodium Zirconium Silicate - ZS-9): They are oral selective polymeric resins that capture potassium ions in the lumen of the colon in exchange for calcium or sodium cations, allowing their fecal elimination. Sodium zirconium silicate acts upon administration and does not induce colon necrosis historically associated with the old sodium polystyrene sulfonate (Kayexalate).
• Urgent Hemodialysis: It represents the gold standard and the fastest method for the absolute clearance of potassium from the body in patients with refractory acute renal failure, severe decompensated anuria or oliguria.