Lab Values NCLEX Practice Questions

The goal is to stabilize the myocardium, shift potassium into cells, and remove it from the body.

• A (incorrect): IV potassium chloride is contraindicated because it would raise an already lethal level.
• B (correct): IV calcium gluconate does not lower potassium but stabilizes the cardiac cell membrane within minutes to prevent lethal dysrhythmias, making it first-line when ECG changes such as peaked T waves are present.
• C (correct): Regular insulin with 50% dextrose drives potassium intracellularly within 10-20 minutes; the dextrose prevents hypoglycemia.
• D (incorrect): Spironolactone is potassium-sparing and retains potassium, worsening the problem; a loop diuretic such as furosemide would be appropriate instead.
• E (correct): Hemodialysis definitively removes potassium and is indicated in CKD or anuric clients who do not respond to medical therapy.
• F (correct): Sodium polystyrene sulfonate or patiromer binds potassium in the GI tract for elimination.

Pearl: remember 'C BIG K Drop' (Calcium, Bicarb, Insulin plus Glucose, Kayexalate/binder, Diuretic/Dialysis). Peaked T waves are the earliest ECG sign of hyperkalemia. A potassium above 6.0 mEq/L is a critical value requiring immediate action.

The therapeutic range for digoxin is 0.5-2.0 ng/mL; a level of 2.8 ng/mL is toxic. Nausea, anorexia, visual disturbances such as yellow-green halos or blurred vision, and bradycardia are classic signs of digoxin toxicity.

• A (incorrect): Administering the scheduled dose would add drug to an already toxic level and could trigger fatal dysrhythmias.
• B (incorrect): Increasing fluids does not address the toxicity and ignores the abnormal level and bradycardia.
• C (correct): The toxic level combined with an apical pulse below 60/min means the nurse must hold the dose and notify the provider, who may order the antidote digoxin immune Fab for life-threatening toxicity.
• D (incorrect): Waiting 4 hours delays care for a client with confirmed toxicity and a low heart rate, which is unsafe.

Pearl: always count the apical pulse for a full minute before giving digoxin and hold for a rate under 60/min in adults. Hypokalemia potentiates digoxin toxicity, so a potassium below 3.5 mEq/L (hypokalemia) increases the risk even when the digoxin level appears borderline.

The therapeutic range for lithium is 0.6-1.2 mEq/L. A level of 2.1 mEq/L is toxic (toxicity begins above 1.5 mEq/L). The client shows moderate-to-severe toxicity: a coarse tremor, ataxia, vomiting, and confusion.

• A (correct): The nurse must hold the lithium and notify the provider; treatment includes hydration, and hemodialysis for severe cases.
• B (incorrect): Restricting sodium and fluids is dangerous and would raise the lithium level further, because low sodium and dehydration cause the kidneys to retain lithium.
• C (incorrect): Reassuring the client is inappropriate. A fine tremor can be an expected early side effect, but a coarse tremor with confusion and ataxia signals true toxicity, not a harmless finding.
• D (incorrect): Giving the next dose would worsen the toxicity and risk seizures and coma.

Pearl: lithium and sodium compete for reabsorption, so anything that lowers sodium or causes volume loss (low-salt diet, vomiting, diuretics, sweating, dehydration) increases the lithium level. Teach clients to maintain steady salt and fluid intake and to report vomiting or diarrhea.

Warfarin is monitored with the INR. A normal INR is about 0.8-1.1, and the therapeutic range for atrial fibrillation is 2.0-3.0 (higher, roughly 2.5-3.5, for a mechanical heart valve). An INR of 5.5 is supratherapeutic and raises bleeding risk, but the client is not bleeding.

Current evidence-based guidance (ACCP/CHEST, ACC) for an INR of 4.5-10 with NO bleeding is to withhold warfarin and recheck the INR serially, resuming at a lower dose once it returns to range. Routine vitamin K is NOT recommended at this level and often causes overcorrection and warfarin resistance. Vitamin K (phytonadione) is reserved for an INR greater than 10 without bleeding or for clinically significant/major bleeding, where prothrombin complex concentrate or fresh frozen plasma may also be added.

• A (incorrect): Giving the next dose would push the INR even higher and increase bleeding risk.
• B (incorrect): Protamine sulfate reverses heparin, not warfarin, and would not correct a high INR.
• C (incorrect): Increasing the dose is the opposite of what a supratherapeutic INR requires.
• D (correct): Holding the next dose and monitoring the INR is correct, as the guidance above describes.

Pearl: match the antidote to the drug. Vitamin K reverses warfarin and protamine reverses heparin, but reversal is driven by the degree of INR elevation and the presence of bleeding, not by any elevated value. Teach clients to keep vitamin K intake (green leafy vegetables) consistent rather than eliminating it, and to report bruising, bleeding gums, or dark/tarry stools. The INR standardizes the PT (normal PT about 11-13.5 seconds) across laboratories.

IV heparin is monitored with the aPTT. A normal aPTT is about 30-40 seconds, and the therapeutic range is 1.5-2.5 times the control value. With a control of 30 seconds, therapeutic is roughly 45-75 seconds. An aPTT of 95 seconds is far above therapeutic and places the client at high risk for hemorrhage.

• A (incorrect): Vitamin K is the antidote for warfarin, not heparin, and would have no effect on heparin activity.
• B (correct): The nurse stops the infusion and anticipates holding or decreasing the rate per protocol, with protamine sulfate as ordered if bleeding occurs or the elevation is marked.
• C (incorrect): Continuing the infusion is unsafe because the value is supratherapeutic, not therapeutic.
• D (incorrect): Increasing the rate would raise the aPTT even higher and worsen bleeding risk.

Pearl: 'PTT with heParin, PT/INR with warfarin.' Protamine sulfate reverses heparin; vitamin K reverses warfarin. Also monitor for heparin-induced thrombocytopenia by trending the platelet count. A drop of more than 50% from baseline several days into heparin therapy suggests HIT and requires stopping all heparin.

Magnesium sulfate is given for seizure prophylaxis in preeclampsia and is titrated to a therapeutic serum level of 4-7 mEq/L, about 4.8-8.4 mg/dL (the normal serum magnesium is 1.5-2.5 mEq/L). Toxicity progresses predictably: loss of deep tendon reflexes appears first, followed by respiratory depression, and finally cardiac arrest. The nurse stops the infusion for absent deep tendon reflexes, a respiratory rate below 12 breaths/min, or urine output below 30 mL/hr.

• A (incorrect): Deep tendon reflexes of 2+ are normal and reassuring, not a reason to stop.
• B (correct): A respiratory rate of 10/min is below 12 breaths/min, signaling respiratory depression.
• C (incorrect): A serum magnesium of 5.5 mg/dL (about 4.5 mEq/L) is within the therapeutic range for preeclampsia, so it is expected, not toxic.
• D (correct): Absent deep tendon reflexes are the first sign of toxicity.
• E (incorrect): A blood pressure of 148/92 mm Hg reflects the underlying preeclampsia and is not a sign of magnesium toxicity.
• F (correct): Urine output of 20 mL/hr is below 30 mL/hr. Magnesium is renally excreted, so poor output causes accumulation.

Pearl: keep IV calcium gluconate at the bedside as the antidote for magnesium toxicity, and monitor reflexes, respirations, and urine output hourly. The loss of the patellar (knee-jerk) reflex is the classic early warning sign.

Normal ABG values are pH 7.35-7.45, PaCO2 35-45 mm Hg, and HCO3 22-26 mEq/L. Here the pH of 7.30 is acidotic (below 7.35). The PaCO2 of 58 mm Hg is elevated (above 45), which is acidic and matches the direction of the pH change, pointing to a respiratory cause. The HCO3 of 26 mEq/L is at the upper end of normal, so the kidneys have not yet compensated.

• A (incorrect): It is not metabolic acidosis, because that would show a low HCO3 as the primary problem.
• B (incorrect): It is not compensated metabolic alkalosis, because the pH is acidic, not alkalotic.
• C (incorrect): It is not respiratory alkalosis, which would show a high pH with low CO2.
• D (correct): This is uncompensated respiratory acidosis, a hallmark of COPD, in which CO2 retention from hypoventilation drives the pH down.

Pearl: use ROME to assign the cause: Respiratory Opposite (pH and CO2 move in opposite directions) and Metabolic Equal (pH and HCO3 move together). Compensation is 'none' when the opposite system is still normal, 'partial' when it has shifted but the pH is still abnormal, and 'full' when the pH is back within range. The low PaO2 of 65 mm Hg (normal 80-100) also signals hypoxemia requiring careful, low-flow oxygen in COPD.

Normal sodium is 135-145 mEq/L; a level below 120 mEq/L is a critical value. Severe hyponatremia causes water to shift into brain cells, producing cerebral edema with headache, confusion, and, if untreated, seizures, coma, and death.

• A (incorrect): Eliminating all dietary sodium is inappropriate and does not fix the problem, which is water excess (a dilutional low sodium), not a dietary sodium deficit.
• B (incorrect): Encouraging water intake is dangerous because it further dilutes the already low sodium and worsens cerebral edema. Symptomatic hyponatremia is usually managed with fluid restriction, and for acutely symptomatic severe cases like this, cautious hypertonic (3%) saline is the first-line treatment to raise the sodium.
• C (correct): With a sodium of 118 mEq/L and neurologic symptoms, the priority is client safety, so the nurse initiates seizure precautions while the team corrects the sodium.
• D (incorrect): Having the client drink free water hourly makes the problem worse for the same reason as option B.

Pearl: correct severe hyponatremia slowly (generally no faster than about 8 mEq/L in 24 hours); overly rapid correction can cause osmotic demyelination syndrome (central pontine myelinolysis). Think 'brain' with sodium problems, because the earliest and most dangerous effects of both hyponatremia and hypernatremia are neurologic.

Normal creatinine is 0.6-1.2 mg/dL and normal BUN is 7-20 mg/dL. A creatinine that has risen from 0.9 to 2.4 mg/dL, with a BUN climbing from 18 to 42 mg/dL, indicates acute kidney injury. Aminoglycosides such as gentamicin are nephrotoxic.

• A (incorrect): Administering the next dose would deliver more nephrotoxic drug to failing kidneys and could worsen the injury, especially because the drug is renally cleared and will accumulate.
• B (correct): The nurse holds the next dose and notifies the provider, who will reassess dosing and may order alternative therapy and closer monitoring of levels and renal function.
• C (incorrect): Restricting fluids is generally the opposite of what an injured kidney needs; adequate hydration supports renal perfusion unless the client is fluid-overloaded.
• D (incorrect): Increasing the dose is unsafe and not indicated by these labs.

Pearl: monitor peak and trough levels for aminoglycosides such as gentamicin and trend creatinine and BUN. A normal BUN-to-creatinine ratio is roughly 10:1 to 20:1.

A normal WBC is 5,000-10,000/mm3, and neutropenia is an ANC below 1,500/mm3, with severe neutropenia below 500/mm3. This client's ANC of 400/mm3 is severe, so the nurse implements neutropenic precautions to protect against infection.

• A (correct): Meticulous hand hygiene is a foundational protective measure.
• B (incorrect): A rectal suppository is contraindicated because inserting anything rectally can tear fragile mucosa and introduce bacteria into the bloodstream. Avoid rectal temperatures, suppositories, and enemas in neutropenic clients.
• C (correct): A private room reduces exposure to pathogens.
• D (correct): Monitoring temperature and reporting a fever of 100.4°F (38°C) is critical, because neutropenic fever is a medical emergency that can progress to sepsis quickly, and fever may be the only sign of infection when there are too few neutrophils to mount inflammation.
• E (correct): Avoiding fresh flowers, standing water, and raw fruits and vegetables limits exposure to bacteria and fungi.
• F (correct): Restricting ill visitors is a foundational protective measure.

Pearl: in neutropenia, 'no news is not good news': a single low-grade fever demands immediate provider notification and blood cultures. Calculate ANC as WBC times the percentage of neutrophils plus bands, divided by 100.