hypokalemia

As the continuous insulin infusion takes effect, it aggressively forces serum potassium out of the bloodstream and into the intracellular space.

This causes a rapid, dangerous drop in serum potassium levels, hypokalemia.

Hypokalemia alters the resting membrane potential of cardiac myocytes.

It prolongs repolarization, manifesting as prominent U-waves on an EKG, and drastically lowers the threshold for action potentials.

In a patient with a history of massive myocardial infarction and current atrial fibrillation, hypokalemia will trigger lethal ventricular arrhythmias like torsades de pointe.

Unlike sodium, intracellular potassium is 30 times more abundant than extracellular potassium, so small shifts in serum concentration reflect large intracellular changes.

Hypokalemia prolongs the QT interval, causes U waves on electrocardiography, and increases risk of ventricular arrhythmias.

The distal nephron secretes potassium in response to aldosterone, sodium delivery, and urine flow rate, which explains why both diuretics and aldosterone antagonists cause hyperkalemia or hypokalemia, depending on context.

Recognizing whether hypokalemia is due to renal wasting, urine cake on a 20-millibig for eel, or gastrointestinal loss, urine 5-me directs therapy toward the underlying cause.

Revamp, you go from non-ionized to... to ionized because ionized has a charge and has less cns penetration it also helps you increase urinary excretion of the salicylates this is how you get rid of them this is really important so this is the key therapy for most symptomatic patients right alkalinize them target a serum ph 745 to 755 a urine ph greater than 7.5 and use bicarbonate to do that do note that these patients have to be you Normokalemic, their potassium has to be normal because potassium is critical in urinary alkalinization.

Hypokalemia will prevent you from being able to adequately alkalinize the urine.

So ensure potassium is within normal ranges and replete it as you need to because without it, you might not be able to alkalinize that urine effectively.

So alkalinization is the key therapy here, right? Use bicarb and do it.

That is a perfect analogy.

Hypokalemia is entirely optional and highly inconstant in this disease.

A substantial fraction of these patients present perfectly normokalemic.

Which misleads a lot of clinicians.

So hyperkalemia and hypokalemia are common imbalances, and both can cause serious cardiac dysrhythmias.

The classic sign of hyperkalemia on the EKG is a tall, peaked T wave, and hypokalemia often causes frequent PVCs.

Hypokalemia can occur for a wide range of reasons, including diarrhea and vomiting, Cushing syndrome, and even insulin administration.

Remember that insulin unlocks the cell to let glucose enter, and potassium just comes along for the ride.

If you have a patient with hypokalemia who is also taking digoxin, be very aware that they will be at very high risk for significant cardiac arrhythmias.

contributions.

In a contribution entitled, Hypokalemia and Hyperkalemia in Heart Failure, Risk Factor or Risk Marker? By Lars Lund and Barnas Thabor Söderberg from Karolinska Institute in Stockholm, Sweden.

Comment on the recently published paper entitled, Optimal Serum Potassium Concentrations in Heart Failure an Individual Patient Data Meta-Analysis by Rihoy Ono et al.

from the University of Glasgow in the United Kingdom Ono and colleagues reply in a separate

Calcium also changes the QT.

Hypokalemia lengthens the ST segment and so the QT.

Hyperkalemia shortens it.

You mentioned sodium channel blocker toxicity earlier.