Change ahead : Revised CMC test plan from AACN’s 2025 study of practice · AACN
Cardiac pharmacology, from GDMT to vasoactive drips
CMC · Section III · pharmacology
Pharmacology is the plan’s biggest single change: the list grows to 15 drug classes, up from 7. Drugs share Section III with procedures and have no weight of their own, so expect them inside many questions rather than in a fixed count.
Pump and vessels: inotropes, vasoactive agents, pulmonary vasodilators.
Lipids: antidyslipidemic agents.
Comfort: sedation and analgesia.
15 questions on cardiac drugs
0 of 15 attempted · 0 correct · 0 missed
Therapeutic Interventions: pharmacology
A patient taking furosemide after an MI has frequent PVCs and a 6-beat run of VT on telemetry. The patient is asymptomatic with BP 128/76. The nurse should FIRST
Answer and why, all 4 options
Synchronized cardioversion is for sustained tachycardia with a pulse, especially if unstable. A 6-beat run that has already stopped leaves nothing to convert.
Prophylactic lidocaine after an MI does not lower mortality and has been abandoned. Giving it skips the correctable cause of the ectopy.
Amiodarone is for sustained or hemodynamically significant VT. Starting it for asymptomatic nonsustained runs treats the rhythm strip and leaves the electrolyte cause in place.
Loop diuretics waste potassium and magnesium, and low levels of either set off ventricular ectopy after an MI. In a stable patient, the first step is to find and correct the electrolyte trigger before considering antiarrhythmics.
Item 1047784
Therapeutic Interventions: pharmacology
A patient on dapagliflozin for HFrEF calls the clinic. Which reported symptom requires immediate evaluation?
Answer and why, all 4 options
More urination in the first days is the expected osmotic diuresis from glycosuria. It is not an emergency.
Perineal pain, swelling and fever in a patient taking an SGLT2 inhibitor raise concern for Fournier gangrene, a rare necrotizing infection of the perineum. It needs emergency evaluation and surgical debridement.
Mild genital itching and redness suggest a fungal infection. This is the common SGLT2 inhibitor side effect and is treated as an outpatient problem.
Glycosuria is how SGLT2 inhibitors work. A positive dipstick confirms the drug is acting and is not a complication.
Item 1049210
Therapeutic Interventions: pharmacology
During PCI, the operator plans intravascular ultrasound of the target artery. Before the IVUS catheter is advanced, the nurse should anticipate administering
Answer and why, all 4 options
IV adenosine causes maximal hyperemia for FFR measurement. It is not used to prepare the vessel for imaging, and it would cause unnecessary AV block.
An intracoronary lytic bolus is for a heavy thrombus burden. Giving it routinely before imaging adds bleeding risk without any purpose.
Intracoronary nitroglycerin dilates the epicardial artery before IVUS. That prevents catheter-induced spasm and lets the vessel size be measured at full diameter, which guides the choice of stent.
Atropine treats vagal bradycardia. It does nothing for coronary spasm or vessel sizing.
Item 1050245
Therapeutic Interventions: pharmacology
A patient on home IV epoprostenol develops flushing, jaw pain, diarrhea, headache, and BP 88/50 a few hours after a new cassette was hung. The patient is afebrile. The MOST LIKELY cause is
Answer and why, all 4 options
A line infection would usually bring fever, chills or site changes. The timing right after a new cassette and the prostacyclin-type symptoms point to the drug.
Worsening RV failure causes edema, rising JVP and exertional symptoms over days. It does not cause flushing and jaw pain within hours of a cassette change.
Flushing, jaw pain, diarrhea, headache and hypotension soon after a new cassette are the classic prostacyclin side effects of too much drug. They suggest a concentration or pump-programming error with the new cassette.
Interruption causes rebound pulmonary hypertension: dyspnea, chest pain, hypoxemia and syncope. It does not cause flushing and diarrhea, which are signs of drug excess.
Item 1050504
Therapeutic Interventions: pharmacology
During PCI, a patient receiving eptifibatide develops persistent oozing at the access site. Platelet aggregation shows no response to ADP, collagen, or epinephrine but a normal response to ristocetin, the same pattern as Glanzmann thrombasthenia. The nurse should anticipate FIRST
Answer and why, all 4 options
Protamine reverses heparin. It has no effect on GP IIb/IIIa blockade, so this choice confuses the two antithrombotics given during PCI.
Eptifibatide blocks the GP IIb/IIIa receptor, which mimics the Glanzmann defect, so ongoing oozing is a drug effect. Stopping the infusion is the first step, and because its effect is reversible, platelet function recovers within hours.
Vitamin K restores vitamin K-dependent clotting factors over hours to days. It has no role in platelet receptor blockade.
Desmopressin releases von Willebrand factor and helps uremic or von Willebrand bleeding. The normal ristocetin response shows von Willebrand function is intact.
Item 1051139
Therapeutic Interventions: pharmacology
A patient with HFrEF on spironolactone and sacubitril/valsartan takes sodium zirconium cyclosilicate 10 g daily for hyperkalemia. Over 1 week, weight rises 2 kg with new ankle edema; K⁺ is 4.8 mEq/L. The nurse should recognize that
Answer and why, all 4 options
Sodium zirconium cyclosilicate exchanges sodium for potassium in the gut. Each 5 g dose carries about 400 mg of sodium, so a patient with HF can gain fluid and develop edema on it.
Doubling the binder would add more sodium and push potassium lower, when the problem is fluid gain.
Spironolactone promotes sodium and water loss. It does not cause edema, so this blames the wrong drug.
A potassium of 4.8 mEq/L is not low. Calling it hypokalemia misreads a level that is in fact well controlled.
Item 1102841
Therapeutic Interventions: pharmacology
Bempedoic acid is being considered for a patient with ASCVD who cannot tolerate statins. Which history item should the nurse report BEFORE it is started?
Answer and why, all 4 options
Treated, stable hypothyroidism does not affect bempedoic acid. Untreated hypothyroidism matters more for statin-related muscle symptoms.
Statin muscle symptoms are the usual reason bempedoic acid is chosen. It is not activated in skeletal muscle, so this history supports the drug rather than ruling it out.
Bempedoic acid raises uric acid and can trigger gout, and it has been linked to tendon rupture. A history of recurrent gout should be reported and weighed before the first dose.
An egg allergy is sometimes raised before propofol or clevidipine. It has no bearing on bempedoic acid.
Item 1103130
Therapeutic Interventions: pharmacology
A patient receives a cangrelor infusion during PCI and will be transitioned to clopidogrel 600 mg. The nurse should give the clopidogrel loading dose
Answer and why, all 4 options
Waiting a day leaves a fresh stent unprotected once cangrelor wears off, which happens within about an hour. That opens a window for stent thrombosis.
Giving clopidogrel with the cangrelor bolus has the same binding problem: the active metabolite reaches a receptor that is already blocked, and the dose is lost.
Clopidogrel given while cangrelor is running cannot bind the receptor. The patient leaves the infusion with no lasting platelet inhibition.
Clopidogrel binds the same P2Y12 receptor that cangrelor occupies. Given during the infusion, it is washed out and fails to inhibit platelets. The loading dose is therefore given right after the infusion stops.
Item 1103402
Therapeutic Interventions: pharmacology
A patient taking flecainide 150 mg twice daily has a creatinine clearance that has fallen from 70 to 25 mL/min over 3 days. QRS has widened from 0.10 to 0.16 s; K⁺ is 4.4 mEq/L and the rhythm is sinus. The MOST likely cause is
Answer and why, all 4 options
Flecainide is partly cleared by the kidney, so a sharp fall in creatinine clearance raises its level. Class IC sodium-channel blockade then widens the QRS in a use-dependent way and can set off VT.
Digoxin toxicity causes AV block, atrial tachycardia with block and bidirectional VT, not isolated QRS widening. Nothing in the stem says the patient takes digoxin.
Hyperkalemia also widens the QRS, but a potassium of 4.4 mEq/L excludes it. This option repeats a reasonable differential without checking the lab value.
Ischemic LBBB would come with symptoms or ECG changes of ischemia. The stem points instead to a renally cleared drug and failing kidneys.
Item 1103436
Therapeutic Interventions: pharmacology
Before coronary CT angiography, a patient has HR 84 in sinus rhythm, BP 128/78 mm Hg and no asthma or AV block. The nurse should anticipate
Answer and why, all 4 options
Furosemide does not protect the kidneys from contrast. Volume depletion can actually raise the risk of kidney injury.
A saline bolus does not slow the heart. Routine pre-hydration is not indicated for a patient without high contrast-kidney risk.
Coronary CT needs a slow, regular rate, typically below about 60 to 65 beats per minute, to limit motion artifact and radiation. Without asthma or AV block, a beta-blocker such as metoprolol is the standard choice.
Atropine speeds the heart rate. That is the opposite of what CT image quality needs.
Item 1103449
Therapeutic Interventions: pharmacology
A 45-year-old has recurrent chest pain at rest between 0300 and 0500 with transient ST elevation that resolves with nitroglycerin. Angiography shows normal coronaries, and provocation testing confirms coronary spasm. The nurse should anticipate long-term therapy with
Answer and why, all 4 options
Aspirin alone does not prevent spasm. At higher doses it can even worsen vasospasm by blocking prostacyclin.
A nonselective beta-blocker leaves alpha-mediated vasoconstriction unopposed and can worsen spasm. It is the classic wrong drug for vasospastic angina.
Stenting a segment that is only spastic does not remove the tendency to spasm. Spasm can recur at the stent edges, and there is no fixed lesion.
Coronary vasospasm is treated long-term with a calcium channel blocker, with nitrates added as needed. Extended-release diltiazem prevents the spasm.
Item 1104580
Therapeutic Interventions: pharmacology
Dofetilide is being started in the hospital for persistent AF. Baseline QTc is 420 ms, K⁺ 4.4 mEq/L and Mg²⁺ 2.1 mg/dL; calculated creatinine clearance is 48 mL/min. The nurse should anticipate a starting dose of
Answer and why, all 4 options
Dofetilide is not given once daily. This choice keeps the full dose and only changes the frequency, which is not how the label adjusts it.
Dofetilide is dosed by creatinine clearance: 500 mcg twice daily above 60 mL/min, 250 mcg twice daily for 40 to 60, and 125 mcg twice daily for 20 to below 40. At 48 mL/min, 250 mcg twice daily is the label dose.
500 mcg twice daily is the full dose for clearance above 60 mL/min. At 48 mL/min it raises drug levels and the risk of QT prolongation and torsades.
125 mcg twice daily is the dose for 20 to below 40 mL/min. It underdoses this patient by misreading the clearance band.
Item 1104730
Therapeutic Interventions: pharmacology
A patient with HFrEF (LVEF 30%) and moderate COPD without asthma is euvolemic on sacubitril/valsartan, spironolactone and dapagliflozin. HR is 92 in sinus rhythm and BP 118/72 mm Hg. A beta-blocker was withheld because of the COPD. The nurse should anticipate
Answer and why, all 4 options
COPD without asthma is not a reason to withhold a beta-blocker in HFrEF. A cardioselective, evidence-based agent such as bisoprolol is started at a low dose and titrated, which lowers mortality.
Leaving out the beta-blocker gives up one of the four mortality-reducing drug classes. This mistakes COPD for a contraindication.
Propranolol is nonselective, so it is more likely to cause bronchospasm in COPD. It is also not one of the evidence-based beta-blockers for HFrEF.
Ivabradine is added only when the sinus rate stays at or above 70 on a maximally tolerated beta-blocker. It is not a substitute for a beta-blocker the patient has never tried.
Item 1105092
Therapeutic Interventions: pharmacology
A patient in cardiogenic shock is receiving dobutamine. Which finding indicates the infusion should be REDUCED?
Answer and why, all 4 options
Dobutamine is a beta-agonist and can provoke ventricular arrhythmias. New runs of nonsustained VT are a signal to lower the dose and check potassium and magnesium.
A falling lactate shows tissue perfusion is improving, which is the goal of therapy, not a sign of toxicity.
A cardiac index rising from 1.8 to 2.4 is the intended inotropic effect. It is a reason to continue, not to reduce.
A modest fall in SVR from 1600 is expected with dobutamine's beta-2 effect and a better cardiac output. It matters only if it causes hypotension.
Item 2032772
Therapeutic Interventions: pharmacology
An 80-year-old patient with severe aortic stenosis awaiting TAVR reports dizziness when standing. BP is 96/60 mm Hg. Which new order should the nurse clarify with the provider?
Answer and why, all 4 options
A statin is standard for most older patients with coronary risk and does not cause orthostatic hypotension.
Low-dose aspirin does not affect preload or blood pressure. It is often continued around TAVR.
Telemetry is appropriate for a symptomatic patient with severe aortic stenosis, who is at risk for heart block and arrhythmias.
Nitrates lower preload, and with a fixed aortic outflow obstruction, stroke volume cannot rise to compensate. In a patient who is already orthostatic, a long-acting nitrate risks syncope and hypotension, so this is the order to clarify.
Item 2033170
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GDMT for HFrEF, from the bedside
For reduced ejection fraction, the heart failure guideline (AHA/ACC/HFSA, 2022) rests therapy on four drug classes: renin-angiotensin inhibition with an ARNI preferred, one of three proven beta-blockers, an MRA, and an SGLT2 inhibitor. The decisions that reach the nurse:
Switching to sacubitril/valsartan: the ACE inhibitor stops at least 36 hours before the first dose, because the combination raises the risk of angioedema.
MRA safety: the guideline uses an MRA when eGFR is above 30 mL/min/1.73 m² with potassium under 5.0 mEq/L; a rise past either limit is a reason to hold and report.
Which beta-blocker: carvedilol, metoprolol succinate or bisoprolol. Metoprolol tartrate does not qualify.
SGLT2 inhibitors: watch volume alongside the loop diuretic, hold before planned surgery as the labeling directs, and remember that ketoacidosis can occur with a near-normal glucose.
The same guideline gives SGLT2 inhibitors a weaker (class 2a) place in mildly reduced and preserved ejection fraction.
Drug decisions that cost points
Diltiazem or verapamil for rate control in HFrEF. The same heart failure guideline rates nondihydropyridine calcium channel blockers as harmful when the ejection fraction is reduced.
AV-node blockers in pre-excited atrial fibrillation. With an accessory pathway, adenosine, digoxin, diltiazem, verapamil and IV amiodarone can speed conduction down it; the atrial fibrillation guideline (ACC/AHA/ACCP/HRS, 2023) points to cardioversion when unstable, and procainamide or ibutilide otherwise.
Epoprostenol handled like any infusion. Its half-life is minutes, so a stopped pump or a clamped line can bring rebound pulmonary hypertension; it runs through a dedicated line and is never paused for a flush or a move.
Digoxin toxicity read from the level alone. Toxicity is a clinical picture (nausea, visual change, new rhythms), made worse by hypokalemia; digoxin immune fab is the antidote.
Sedation without its cardiac effects. Dexmedetomidine slows the heart and can lower pressure; propofol lowers pressure, and long high-dose infusions carry propofol infusion syndrome.