Quiz: Electrolyte Imbalances

Correct answer: Peaked T waves
Explanation:Elevated potassium levels alter cardiac cell membrane excitability and disrupt repolarization. One of the earliest and most recognizable ECG manifestations of potassium excess is the appearance of tall, narrow, peaked T waves. This change signals increasing risk for dangerous dysrhythmias as potassium continues to rise.

Prominent U waves are associated with potassium deficiency rather than excess.

A prolonged QT interval is more commonly linked to calcium or magnesium imbalances, not potassium excess.

ST-segment depression is associated with myocardial ischemia or other electrolyte disturbances, not the early effects of hyperkalemia.

High-Yield Tip: Tall, peaked T waves are an early warning sign of hyperkalemia.

Correct answer: Hypokalemia
Explanation:Low potassium levels interfere with normal neuromuscular and cardiac function. Potassium is essential for muscle contraction and ventricular repolarization. When potassium levels fall, skeletal muscle weakness and cramping occur, along with delayed cardiac repolarization. This delay produces characteristic ECG findings such as flattened T waves and the appearance of U waves. The use of loop diuretics increases renal potassium loss, making this imbalance consistent with the client's presentation.

Excess potassium causes different ECG changes, including tall, peaked T waves and widened QRS complexes, which are not present in this scenario.

Sodium imbalance primarily affects fluid balance and neurological status and does not produce U waves or muscle cramping patterns linked to potassium deficiency.

Calcium imbalance alters neuromuscular excitability but produces findings such as tetany or prolonged QT intervals rather than U waves.

High-Yield Tip: Flattened T waves with U waves are classic ECG indicators of hypokalemia.

Correct answer: Obtain a stat serum magnesium level
Explanation:Magnesium directly influences neuromuscular stability and cardiac conduction. Tremors, hyperreflexia, and ventricular ectopy suggest magnesium deficiency, which can rapidly progress to life-threatening dysrhythmias. Confirming the serum magnesium level is the immediate priority to guide safe and appropriate replacement therapy and prevent further cardiac instability.

Administering magnesium without confirmation risks inappropriate dosing, particularly if renal function is impaired.

Increasing potassium does not correct the underlying neuromuscular and cardiac effects caused by magnesium imbalance.

Adjusting parenteral nutrition may be necessary later but does not address the immediate risk posed by suspected electrolyte-induced dysrhythmias.

High-Yield Tip: Suspected magnesium imbalance with cardiac changes requires immediate laboratory confirmation before replacement.

Correct answer: Reduced smooth muscle activity
Explanation:Potassium is essential for smooth muscle contraction, including intestinal peristalsis. When potassium levels are low, smooth muscle activity slows, resulting in constipation and decreased bowel sounds. These findings reflect a functional response to electrolyte imbalance rather than structural pathology.

Increased motility would cause diarrhea, not constipation.

Bowel obstruction presents with severe abdominal pain and distention rather than generalized electrolyte-related symptoms.

Fluid volume excess does not explain decreased bowel sounds or constipation.

High-Yield Tip: Hypokalemia decreases gastrointestinal motility and can lead to constipation or ileus.

Correct answer: Hyperkalemia
Explanation:Impaired renal function reduces potassium excretion, leading to potassium accumulation. As potassium levels rise, ECG changes progress from peaked T waves to widened QRS complexes. This finding reflects slowed ventricular conduction and indicates severe hyperkalemia with high risk for ventricular fibrillation or cardiac arrest.

Potassium deficiency causes U waves and flattened T waves rather than QRS widening.

Calcium imbalance affects QT interval duration, not QRS width.

Sodium imbalance primarily affects neurological status rather than cardiac conduction patterns.

High-Yield Tip: Widened QRS complexes are a late and dangerous sign of hyperkalemia.

Correct answer: Administer prescribed phosphate binders with meals
Explanation:In kidney disease, phosphorus excretion is reduced, leading to accumulation and neuromuscular symptoms such as muscle cramps. Phosphate binders taken with meals reduce gastrointestinal absorption of phosphorus, directly addressing the cause of hyperphosphatemia and helping restore electrolyte balance.

Encouraging phosphorus rich foods would worsen the imbalance.

Increasing calcium supplementation alone does not effectively lower serum phosphorus and may increase the risk of calcium phosphate imbalance.

Restricting fluids does not significantly affect phosphorus levels.

High-Yield Tip: Phosphate binders reduce intestinal absorption and are key in managing hyperphosphatemia.

Correct answer: Prepare to administer calcium gluconate
Explanation:Excess magnesium depresses neuromuscular and cardiac function, leading to lethargy, hypotension, and diminished reflexes. In clients with renal failure, magnesium excretion is impaired, increasing the risk of toxicity. Calcium gluconate counteracts the cardiac and neuromuscular effects of elevated magnesium and is the priority intervention when signs of magnesium toxicity are present.

Encouraging magnesium intake would worsen toxicity.

Increasing fluids may support renal clearance but does not reverse acute neuromuscular depression.

Seizure precautions are not the priority because magnesium excess suppresses, rather than stimulates, neuromuscular activity.

High-Yield Tip: Calcium gluconate is the antidote for symptomatic hypermagnesemia.

Correct answer: Impaired oxygen delivery
Explanation:Low phosphorus levels impair energy production and red blood cell function, reducing oxygen release to tissues. Muscle weakness and shallow respirations indicate compromised respiratory muscle function, placing the client at risk for inadequate oxygenation. Recognizing impaired oxygen delivery is the priority because it directly threatens respiratory and systemic function.

Bone demineralization is a chronic effect of phosphorus imbalance, not an acute priority.

Fluid volume overload does not explain muscle weakness or respiratory compromise.

Cardiac tamponade is unrelated to phosphorus disturbances.

High-Yield Tip: Hypophosphatemia compromises oxygen delivery and respiratory muscle function.

Correct answer: Confirm adequate urine output
Explanation:Potassium is excreted by the kidneys, and administering potassium without adequate urine output places the client at high risk for potassium accumulation and sudden hyperkalemia. Ensuring sufficient renal function through urine output assessment is a critical safety step before potassium replacement. This action prevents iatrogenic complications that can lead to life-threatening cardiac dysrhythmias.

Verifying the potassium concentration is important but does not supersede confirming the client's ability to excrete potassium safely.

Pulse oximetry does not directly address the primary risk associated with potassium administration.

Blood pressure assessment is part of routine monitoring but does not determine potassium clearance.

High-Yield Tip: Potassium replacement should never begin unless adequate urine output confirms renal excretion ability.

Correct answer: Perform a focused neurological assessment
Explanation:Hyponatremia causes water to move into brain cells, increasing the risk of cerebral edema. Acute confusion and restlessness are early neurological warning signs that require immediate assessment. A focused neurological evaluation establishes the severity of cerebral involvement and guides urgent intervention to prevent seizures or further deterioration.

Increasing oral fluids would worsen dilutional hyponatremia and increase cerebral swelling.

Slowing the IV rate may be necessary, but assessment of neurological status must occur first to determine urgency and severity.

Administering a diuretic without assessment may further disrupt sodium balance and does not address immediate neurological risk.

High-Yield Tip: In hyponatremia, neurological changes signal cerebral edema and demand immediate assessment.