A 72-year-old woman with a history of hypertension (on atenolol 50 mg daily) and recurrent urinary tract infections presents with a 3-day history of fever, dysuria, and confusion. On examination, she is febrile (38.5°C), hypotensive (92/58 mmHg), and tachycardic (118/min). Laboratory investigations reveal: serum potassium 6.9 mEq/L, sodium 128 mEq/L, creatinine 2.8 mg/dL (baseline 1.0), blood glucose 420 mg/dL, arterial pH 7.18, HCO₃⁻ 12 mEq/L, and positive blood cultures. ECG shows peaked T waves. What is the PRIMARY mechanism of hyperkalemia in this patient?

Explanation

## Clinical Scenario Analysis This patient presents with **urosepsis** complicated by **acute kidney injury (AKI)**, **hyperglycemia**, **metabolic acidosis**, and **hyperkalemia**. Multiple mechanisms contribute to K⁺ elevation, but the **PRIMARY driver** in this acute setting is **metabolic acidosis**. ## Pathophysiology of Hyperkalemia in Acidosis **Key Point:** In metabolic acidosis, **H⁺ ions shift intracellularly** to buffer the acidosis. To maintain electroneutrality, **K⁺ shifts extracellularly**, raising serum K⁺ by approximately **0.6 mEq/L for every 0.1 unit decrease in pH**. ### Mechanism: $$\text{Intracellular: } H^+ + K^+ \leftrightarrow \text{Extracellular: } H^+ + K^+$$ This occurs **within minutes** and is the **most immediate cause** of hyperkalemia in acute metabolic acidosis. ## Why Each Mechanism Is Present But Not Primary | Mechanism | Present? | Contribution | Onset | |---|---|---|---| | **Metabolic acidosis** | ✓ Yes (pH 7.18) | **PRIMARY** | Minutes | | **AKI/reduced renal perfusion** | ✓ Yes (Cr 2.8) | Secondary | Hours–days | | **Hyperglycemia** | ✓ Yes (glucose 420) | Minimal (osmotic effect is modest) | Hours | | **Beta-blocker effect** | ✓ Yes (atenolol) | Contributory (reduces β₂-mediated K⁺ uptake) | Hours | **High-Yield:** While **AKI** is the most important **chronic** mechanism (impairs renal K⁺ excretion), **metabolic acidosis** is the **acute** mechanism that explains the **rapid onset** of hyperkalemia in this septic patient. ## Clinical Pearl: The Acidosis–Hyperkalemia Link **Clinical Pearl:** The severity of hyperkalemia in sepsis correlates with the **degree of acidosis**, not hyperglycemia alone. Treating the acidosis (fluids, insulin, bicarbonate in severe cases) will lower K⁺ faster than treating hyperglycemia. ## Mnemonic for Hyperkalemia Causes **Mnemonic:** **HARDUPS** — **H**yperaldosteronism (low), **A**cidosis, **R**enal failure, **D**iabetic ketoacidosis, **U**se of drugs (ACEi, K-sparing diuretics), **P**oor intake (rare), **S**ample hemolysis (pseudohyperkalemia). In this case, **A** (acidosis) is the primary acute mechanism; **R** (renal failure) is secondary. [cite:Harrison 21e Ch 280; Robbins 10e Ch 24]