C2B Podcast 23 - Hyperkalemia
Curbside to Bedside
English - November 19, 2019 00:15 - 40 minutes - 32.7 MB - ★★★★★ - 17 ratingsAlternative Health Health & Fitness Science ems foamems paramedic criticalcare emergencymedicalservices emt foamed medicine nursing prehospitalmedicine Homepage Download Apple Podcasts Google Podcasts Overcast Castro Pocket Casts RSS feed
Previous Episode: Diabetic Ketoacidosis
Next Episode: C2B Podcast 24 - Needle Thoracostomy
Hyperkalemia Intro
Potassium is primarily an intracellular ion responsible for maintenance of the resting membrane potential for normal cell conduction. Serum measured potassium is typically between 3.5 and 5.0 mEq/L. Serum K greater than 5.0 mEq/L is generally considered the threshold for hyperkalemia. Potassium is mostly excreted via the kidneys, and the "classic" hyperkalemia patient is one who has missed several dialysis appointments complaining of paralysis or diffuse weakness.
Causes of HyperK
Most commonly, renal failure. Transcelluar shift DKA Acidosis Other acid-base disturbances Medications RAAS or ACE inhibitors
Effects of HyperK
Most drastically affect cardiac myocytes Conduction between myocytes is depressed, leading to slower conduction and widened QRS complexes, however, the rate of repolarization is increased. Leads to ominous “sine wave” pattern on ECG. Arrythmogenic May produce classic tall, “peaked” T waves on ECG. Stepwise ECG changes in hyperkalemia: 5.5-6.5 mEq/L - Peaked T Waves 6.5-7.5 mEq/L - P waves amplitude becomes smaller and PR intervals prolong 7.5-8.0 mEq/L - QRS becomes wide ECGs are not always sensitive for hyperkalemia. Patients may have a critical K with no changes on the ECG. Skeletal muscle tissue is also sensitive to hyperkalemia, and patients may present with weakness or paralysis as a result. Nondescript symptoms such as muscle cramps, diarrhea, vomiting, nausea, and focal paralysis may also be present - but are also not reliable findings.
Management
Prioritized by a strategy of: Stabilization of cardiac cell membranes Shifting potassium back into the cells Eliminating potassium Calcium (Chloride or gluconate) administered to stabilize cell membranes Stabilizing effect is transient and relatively short lived Calcium Chloride contains roughly 3 times the amount of elemental calcium as compared to Ca gluconate, but is associated with severe complications if extravasation occurs. Effects (narrowing of QRS complex, return of more hemodynamic stability) occurs within minutes Calcium Chloride - generally, 1 gram is administered over 3 minutes. Calcium Gluconate - 1 gram over 2-3 minutes Repeat either q5min Albuterol / Beta 2 agonists These act on beta 2 receptors to assist in moving potassium back into the intracellular space Albuterol - 10-20mg (inhalation), with most effect noted in 30 minutes IV Insulin Drives K back into the cells (shift) Generally administered with dextrose unless the patient’s BGL is below 250mg/dL 10 units IVP followed by 25G dextrose Incidence of hypoglycemia is high, and this therapy should be administered cautiously Dialysis Treating reversible cause d/c RASS or ACE inhibiting medicaitions Volume administration