A 52-year-old man from Delhi presents to the emergency department with acute-onset weakness and numbness in both legs following a road traffic accident with crush injury to the lower limbs. On examination, he has severe muscle pain and dark urine. Serum potassium is 7.2 mEq/L (normal 3.5–5.0), creatinine 3.8 mg/dL, and myoglobin is markedly elevated. An ECG shows peaked T waves and prolonged PR interval. Which of the following best explains the cardiac manifestations observed in this patient?

Explanation

## Pathophysiology of Hyperkalemia-Induced Cardiac Changes ### Resting Membrane Potential and Hyperkalemia **Key Point:** The resting membrane potential (RMP) is primarily determined by the K⁺ concentration gradient across the cell membrane, governed by the Nernst equation: $$E_K = 61 \log \frac{[K^+]_{out}}{[K^+]_{in}}$$ In normal conditions, the RMP is approximately −90 mV. When extracellular K⁺ rises (hyperkalemia), the K⁺ gradient **decreases**, making the RMP less negative (e.g., −70 to −60 mV) — a state of **partial depolarization**. ### Why Option C is Correct Hyperkalemia depolarizes the RMP, **reducing the gap between the resting potential and the threshold potential** (approximately −55 mV). This reduced "safety margin" means cells are closer to threshold and can fire more readily — explaining the **initial increase in excitability** and the appearance of **peaked T waves** (reflecting shortened, accelerated repolarization). As hyperkalemia worsens, sustained partial depolarization causes **inactivation of fast Na⁺ channels** (which require a sufficiently negative RMP to recover), ultimately slowing conduction and producing the **prolonged PR interval** and QRS widening seen on ECG. The phrase "increasing neuronal/cardiac excitability" in Option C refers to this initial phase; the overall mechanism — depolarization of RMP reducing the threshold gap — is the correct and primary explanation for the cardiac manifestations observed here. ### Why the Other Options Are Wrong - **Option A:** Hyperkalemia does NOT primarily act by inhibiting Na⁺/K⁺-ATPase. The pump is not the primary determinant of the acute ECG changes; the direct effect on RMP via the Nernst equation is. Na⁺/K⁺-ATPase inhibition (as with cardiac glycosides) causes intracellular Na⁺ accumulation and hypercalcemia-mediated arrhythmias — a distinct mechanism. - **Option B:** Hyperkalemia **decreases** (not increases) the K⁺ gradient, causing **depolarization** (less negative RMP), not hyperpolarization. Hyperpolarization would occur with hypokalemia. - **Option D:** There is no "rightward shift of the action potential curve" as a recognized mechanism of hyperkalemia. This is a fabricated distractor with no textbook basis. ### ECG Progression in Hyperkalemia | K⁺ Level (mEq/L) | ECG Finding | |---|---| | 5.5–6.5 | Peaked, narrow T waves | | 6.5–8.0 | Prolonged PR interval, widened QRS | | > 8.0 | Sine wave pattern, cardiac arrest | **Clinical Pearl:** Peaked T waves in hyperkalemia reflect **shortened action potential duration** (faster repolarization due to increased K⁺ conductance), not simply increased excitability. The prolonged PR interval reflects slowed AV nodal conduction due to Na⁺ channel inactivation from sustained partial depolarization. *(Guyton & Hall, Medical Physiology, 14th ed.; Ganong's Review of Medical Physiology)* **High-Yield:** Crush injury → rhabdomyolysis → myoglobinuria → acute kidney injury → hyperkalemia → cardiac toxicity. This is a classic NEET PG chain linking trauma to electrolyte disturbance and membrane physiology.