Hyperkalemia (Study Outline) 1. Background Definition: Ser…
Hyperkalemia (Study Outline) 1. Background Definition: Serum potassium >5.0 mEq/L (lab-dependent). Pathophysiology: Results from impaired renal excretion, cellular shifts, or excess intake (rare alone). High extracellular K⁺ decreases resting membrane potential → cardiac conduction abnormalities (high-yield). Major causes (high-yield): Decreased excretion: Acute or chronic kidney disease. Hypoaldosteronism (Addison disease, adrenal insufficiency). Medications affecting RAAS: ACE-I/ARBs, potassium-sparing diuretics, NSAIDs. Transcellular shifts: Metabolic acidosis. Insulin deficiency (DKA). Tissue breakdown (rhabdomyolysis, tumor lysis, hemolysis). Pseudohyperkalemia: hemolysis of blood sample (important exam clue). 2. History Often asymptomatic early. Muscle symptoms: weakness, flaccid paralysis, paresthesias. Cardiac symptoms: palpitations, lightheadedness, syncope (if arrhythmias). Etiology clues: Kidney dysfunction (oliguria, history of CKD). Recent medication changes (RAAS drugs). Acidosis, DKA symptoms (polyuria, abdominal pain). Trauma/exertion (rhabdomyolysis). Cancer therapy (tumor lysis). 3. Exam Findings Muscle weakness or decreased reflexes. Bradycardia or irregular pulse (arrhythmias). Signs of underlying cause: Volume depletion (DKA). Muscle tenderness (rhabdo). Hypotension or shock (renal failure, adrenal insufficiency). ECG findings (very high-yield): Peaked T waves (early). Widened QRS, prolonged PR. Sine-wave pattern (pre-arrest). 4. Making the Diagnosis Serum potassium: elevated; confirm if pseudohyperkalemia suspected. Renal function tests: ↑ BUN/Cr in AKI/CKD. Arterial/venous chemistry: metabolic acidosis clues. Additional labs based on cause: CK (rhabdomyolysis). Glucose/ketones (DKA). Complete blood count (hemolysis). ECG: key for assessing severity. Gold Standard: Confirmatory serum potassium measurement with clinical correlation. 5. Management (Exam Concepts) (No real-time treatment or dosing — exam concepts only.) Immediate priorities (concept-based): Stabilize cardiac membrane (high-yield concept). Shift potassium intracellularly (concept). Enhance potassium elimination (concept). Conceptual approaches: Cardiac membrane stabilization: Calcium-based concept (no dosing). Shift K⁺ into cells: Insulin/glucose concept, β-agonist concept. Address acidosis conceptually (e.g., correct DKA). Enhance elimination: Renal excretion principles; GI binding/removal concepts. Dialysis principles for severe/refractory cases (especially CKD/ESRD). Avoid/stop contributors: RAAS drugs, potassium supplements, potassium-sparing diuretics (concept-level). Monitor: serial K⁺ levels, ECG, renal function. Indications for dialysis: severe or refractory hyperkalemia, ECG changes not improving, or concurrent severe AKI/ESRD. QUESTION A 67-year-old man presents to the emergency department with progressive muscle weakness and lightheadedness. He has a history of hypertension, chronic kidney disease stage 4, and heart failure with reduced ejection fraction. His medications include lisinopril, spironolactone, and furosemide. He denies chest pain or recent trauma. Vital signs are: blood pressure 108/67 mmHg, heart rate 52/min, respiratory rate 18/min, and oxygen saturation 97% on room air. On exam, he has decreased deep tendon reflexes and mild flaccid weakness in all extremities. ECG shows tall, peaked T waves and a widened QRS complex. Serum chemistry reveals: Potassium: 7.3 mEq/L (reference: 3.5–5.0) BUN: 48 mg/dL (reference: 7–20) Creatinine: 3.1 mg/dL (baseline: 2.5) Which of the following is the most appropriate next step in management? A) Administer intravenous calcium gluconateB) Administer sodium polystyrene sulfonateC) Initiate hemodialysisD) Administer intravenous insulin with glucose