Hypokalemia

Why Give potassium chloride 0.5 mEq/kg by mouth and recheck the level in 30 minutes is correct

• Abrupt, painless, symmetric flaccid quadriparesis on waking after strenuous exercise and a carbohydrate-rich meal, with hyporeflexia but intact sensation, bulbar function, respiration, and mentation, is an attack of hypokalemic periodic paralysis, a skeletal muscle channelopathy
• Total body potassium is normal: insulin and beta-adrenergic tone drive potassium into muscle through Na-K-ATPase, so a serum value of 2.0 mEq/L here reflects a transcellular shift, not a deficit
• Small oral increments restore sarcolemmal excitability while the shift reverses on its own: 0.5 to 1 mEq/kg by mouth, the serum potassium and the strength examination rechecked about every 30 minutes before any further dose, and rarely more than about 200 mEq in 24 hours
• He swallows normally, so the oral route is available; were he unable to swallow, potassium chloride would be infused no faster than 10 mEq/h in 5% mannitol, the preferred vehicle because both dextrose and sodium chloride can deepen the weakness, with saline the fallback only when mannitol is unavailable
• Continuous cardiac monitoring is mandatory whichever route is used, because the potassium can climb from 2.0 mEq/L to frankly hyperkalemic within a few hours as muscle releases the shifted potassium back into the serum

Why the others are wrong

• Infuse potassium chloride at 20 mEq/h until the serum potassium exceeds 4.0 mEq/L - that endpoint, and the cumulative load needed to reach it, belong to a true depletion state; here the sequestered potassium returns to the extracellular space as the attack breaks, so driving the measured level above 4.0 mEq/L adds tens of milliequivalents the patient never lost and produces symptomatic rebound hyperkalemia (the trap is treating the number instead of the mechanism)
• Infuse potassium chloride 10 mEq in 500 mL of 5% dextrose in water over one hour - the increment is reasonable but the vehicle is not: dextrose triggers insulin release, which drives still more potassium into muscle and deepens the paralysis, so potassium in periodic paralysis is given by mouth when the patient can swallow and otherwise in mannitol, never in a glucose-containing fluid (the trap is reaching for the default maintenance fluid)
• Give acetazolamide 250 mg by mouth now and repeat the same dose in six hours - acetazolamide is maintenance prophylaxis that reduces how often attacks occur between episodes, it does not abort an attack already in progress, and it can worsen attacks in some SCN4A-related and thyrotoxic cases; it also leaves the profound hypokalemia and its ECG changes untreated right now (the trap is reaching for the disease-specific drug instead of the one that fixes the physiology at the bedside)
• Give magnesium sulfate 2 g IV over one hour before giving any potassium - magnesium depletion keeps the kidney wasting potassium, so checking and correcting it is the right reflex when hypokalemia from true losses proves refractory, and even then it is given alongside potassium rather than in place of it; this attack is a transcellular shift with normal total body stores, nothing in his history suggests magnesium loss, and holding potassium for an hour leaves the paralysis and ECG changes untreated at a level of 2.0 mEq/L (the trap is applying the refractory-depletion rule to a shift)

Additional high-yield points

• Contrast with diabetic ketoacidosis, where a large potassium load is correct: osmotic diuresis and insulin deficiency have depleted total body stores by 3 to 5 mEq/kg, so insulin is withheld until the potassium is above 3.3 mEq/L and 20 to 30 mEq of potassium is added to each liter of replacement fluid; there the potassium is gone from the body, whereas here it is only hiding inside cells, which is why the same order causes rebound hyperkalemia in this patient
• Screen every adult presenting with a first attack for thyrotoxicosis with TSH and free T4; thyrotoxic periodic paralysis is most common in men of Asian or Latin American descent aged 20 to 40 and stops recurring once the patient is euthyroid
• Once thyrotoxicosis is confirmed, nonselective beta blockade with propranolol is the adjunct that aborts attacks and blunts the rebound hyperkalemia by removing the adrenergic drive on Na-K-ATPase; it is not part of the acute treatment of primary familial hypokalemic periodic paralysis, so it follows the thyroid studies rather than preceding them
• Attacks are provoked by carbohydrate loads, rest after strenuous exercise, alcohol, stress, and glucocorticoids; beta-agonists such as albuterol can precipitate one
• Long-term management is trigger avoidance plus acetazolamide or dichlorphenamide, with a potassium-sparing diuretic as an alternative; dichlorphenamide is the only FDA-approved agent for primary periodic paralysis
• Hyperkalemic periodic paralysis is the mirror image: shorter attacks provoked by fasting or potassium-rich foods, aborted with carbohydrate intake, inhaled albuterol, or IV calcium

Why Prominent U waves after the T wave is correct

• Hypokalemia delays ventricular repolarization, producing T-wave flattening, ST depression, and the characteristic prominent U waves following the T wave.
• Several days of vomiting cause volume depletion that drives renal potassium wasting, matching the low potassium here.
• Severe hypokalemia also warrants magnesium assessment because hypomagnesemia perpetuates the loss.

Why the others are wrong

• Long ST segment with normal T waves — This is the hypocalcemia pattern, in which the QT prolongs through a longer ST segment while the T wave stays normal; a potassium of 2.6 mEq/L instead flattens the T wave and adds a U wave.
• Peaked T waves with QRS widening — These are hyperkalemia changes, the opposite electrolyte disorder; choosing it ignores the measured potassium of 2.6 mEq/L.
• Shortened QT interval with normal T waves — A short QT reflects hypercalcemia, not hypokalemia; hypokalemia actually prolongs repolarization, so this is the wrong direction.
• Osborn J waves at the QRS-ST junction — this extra positive deflection at the J point, where the QRS meets the ST segment, is classically a sign of hypothermia; the extra wave of hypokalemia comes later, as a U wave after the T wave, together with T-wave flattening and ST depression (the trap is putting the extra wave in the wrong place).