hyperkalemia Flashcards
Q: What is hyperkalemia?
A: Hyperkalemia refers to an elevated serum potassium level, usually above 5.5 milliequivalents per liter.
Q: What are the symptoms of mild and severe hyperkalemia?
A: Mild hyperkalemia can be asymptomatic, while severe hyperkalemia can cause life-threatening symptoms like paralysis and cardiac arrhythmias.
Q: What are some common causes of hyperkalemia?
A: Increased potassium intake, transcellular potassium shifts (e.g., medication-induced, metabolic acidosis, tumor lysis, rhabdomyolysis), decreased effective arterial blood volume, reduced renal function, tubular resistance to aldosterone, hyporeninemic hypoaldosteronism, and adrenal insufficiency.
Q: What initial assessment should be performed if hyperkalemia is suspected?
A: Perform an ABCDE assessment to determine if the patient is unstable or stable.
Q: How should you stabilize an unstable hyperkalemic patient?
A: Stabilize airway, breathing, and circulation, obtain IV access, put the patient on cardiac telemetry, monitor vital signs, and provide supplemental oxygen if needed.
Q: What steps should be taken for a stable hyperkalemic patient?
A: Obtain a focused history and physical examination, labs (CMP, blood gas), and a 12-lead ECG.
Q: What are the characteristic ECG changes in hyperkalemia?
A: Tall-peaked T waves, p wave flattening, prolongation of the PR interval, disappearance of P waves, widening of the QRS complex, and a sine-wave appearance.
Q: What is pseudohyperkalemia and how can it occur?
A: Pseudohyperkalemia is a falsely elevated potassium level due to hemolysis or blood clotting during blood collection, or potassium diffusion in stored packed red blood cells.
Q: What mnemonic helps remember the treatment options for hyperkalemia?
A: C BIG K Drop: Calcium gluconate, Beta-agonists or Bicarbonate, Insulin, Glucose, K-binders, and Diuretics or Dialysis.
Q: What is the purpose of calcium gluconate in hyperkalemia treatment?
A: Calcium gluconate helps stabilize the cardiac cell membrane.
Q: How do beta-agonists, bicarbonate, and insulin help in hyperkalemia treatment?
A: They help rapidly shift potassium into cells, temporarily decreasing serum levels.
Q: Why is glucose administered with insulin in hyperkalemia treatment?
A: To prevent hypoglycemia since insulin shifts glucose into cells.
Q: What is the role of K-binders in hyperkalemia treatment?
A: K-binders prevent gastrointestinal absorption of potassium, increasing its fecal excretion.
Q: When is dialysis used in hyperkalemia treatment?
A: For refractory cases that don’t respond to other treatments and for patients with renal failure.
Q: What should be considered when looking for the cause of hyperkalemia?
A: Increased potassium load, transcellular potassium shift, and decreased renal potassium excretion.
Q: What conditions are associated with transcellular potassium shifts causing hyperkalemia?
A: Medication-induced hyperkalemia, metabolic acidosis, tumor lysis syndrome, rhabdomyolysis.
Q: What genetic condition causes hyperkalemia after strenuous exercise?
A: Hyperkalemic periodic paralysis.
Q: How can decreased effective arterial blood volume cause hyperkalemia?
A: By leading to a urine sodium level below 25 millimoles per liter.
Q: What does a urine sodium level greater than or equal to 25 millimoles per liter indicate?
A: It suggests hyperkalemia due to reduced renal function or aldosterone issues.
Q: What are the next steps if a patient has an eGFR ≤ 20?
A: Diagnose hyperkalemia due to reduced renal function, seen in acute kidney injury and chronic kidney disease.
Q: What are the possible causes if serum aldosterone is normal or elevated?
A: Tubular resistance to aldosterone, potentially due to medications or systemic disorders.
Q: What does low serum aldosterone and low renin indicate?
A: Hyporeninemic hypoaldosteronism.
Q: What does normal or high renin with low aldosterone indicate?
A: Adrenal insufficiency, such as primary hypoaldosteronism or Addison disease.
Q: Why might renin levels be high in patients taking ACE inhibitors or ARBs?
A: These medications lower aldosterone levels, leading to potassium retention and compensatory increase in renin.
