Cardiovascular medications nursing reference: digoxin toxicity, antihypertensives, antiarrhythmics

Cardiovascular pharmacology is among the highest-yield NCLEX content areas – and the most commonly tested in clinical settings. Nurses administer antihypertensives, antiarrhythmics, and cardiac glycosides daily across med-surg, telemetry, cardiac step-down, ICU, and outpatient cardiology. The consequences of administering these drugs incorrectly, or failing to recognize toxicity, are immediately life-threatening.

This reference covers three major domains: antihypertensives (ACE inhibitors, ARBs, beta-blockers, calcium channel blockers, diuretics), antiarrhythmics (Vaughan-Williams classification, amiodarone, adenosine), and digoxin. For each drug class, you’ll find mechanism, key side effects, hold parameters, and the specific NCLEX facts examiners test. Use it alongside the heart failure nursing guide, the hypertension nursing reference, and the atrial fibrillation nursing guide for integrated clinical coverage.

Fast-scan: cardiovascular drug class overview

Antihypertensives

Hypertension affects nearly half of US adults and is a primary driver of cardiovascular morbidity and mortality. The 2025 AHA/ACC high blood pressure guideline, which replaced the 2017 ACC/AHA guideline (JNC 8 in 2014 was the last of the Joint National Committee reports), names thiazide-type diuretics, ACE inhibitors, ARBs, and dihydropyridine calcium channel blockers as first-line drug classes (Jones 2025; James 2014). Beta-blockers remain essential for specific co-indications such as heart failure with reduced ejection fraction, angina, and post-MI care. Nurses must understand not only the drug but the patient context that determines drug selection.

ACE inhibitors

Mechanism: ACE inhibitors (angiotensin-converting enzyme inhibitors) block the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. Without angiotensin II, aldosterone secretion drops, blood pressure falls, and the kidneys retain less sodium and water. The result is reduced afterload, reduced preload, and protection against maladaptive cardiac remodeling – which is why these drugs are first-line in both hypertension and heart failure with reduced ejection fraction.

Drug names – suffix pattern: All ACE inhibitors end in “-pril”: lisinopril, enalapril, ramipril, captopril, fosinopril. The suffix alone is an NCLEX signal to apply ACE-I nursing considerations.

Key side effects and nursing considerations:

Dry cough – The most common reason patients stop ACE inhibitors. Bradykinin accumulates when ACE is inhibited (bradykinin is normally broken down by ACE), and bradykinin accumulation in the airways triggers a persistent, non-productive cough. This is a pharmacological effect, not an allergy. The clinical response: switch to an ARB, which doesn’t affect bradykinin. On NCLEX, “patient taking lisinopril reports a dry cough” → discontinue the ACE-I, switch to an ARB.

Hyperkalemia – ACE inhibitors reduce aldosterone, which means potassium excretion decreases. Monitor potassium levels, especially in patients with CKD or those taking potassium supplements, potassium-sparing diuretics (spironolactone), or NSAIDs. Dangerous hyperkalemia combinations: ACE-I + potassium-sparing diuretic – see the drug interaction table below.

Angioedema – A rare but potentially life-threatening reaction. Swelling of the lips, tongue, larynx, or pharynx can cause airway obstruction. Angioedema occurs more commonly in Black patients and may appear months to years after starting the drug – it is not always an early reaction. Nursing action: Stop the ACE inhibitor immediately, call the provider, assess airway, prepare for potential epinephrine administration. This is a hard hold – the drug is permanently discontinued, not held temporarily. ARBs may also cause angioedema in susceptible individuals, though the risk is lower.

First-dose hypotension – Especially pronounced in patients who are volume-depleted or on concurrent diuretics. Have the patient sit or lie down after the first dose; advise rising slowly.

Fetal toxicity – ACE inhibitor labels carry a boxed warning: drugs acting on the renin-angiotensin system cause injury and death to the developing fetus, mainly in the second and third trimesters (oligohydramnios, fetal renal failure, skull hypoplasia). The old A/B/C/D/X letter categories were removed from US labels under the 2015 Pregnancy and Lactation Labeling Rule. Stop the drug as soon as pregnancy is detected and notify the provider.

ARBs (angiotensin receptor blockers)

Mechanism: ARBs block the angiotensin II receptor (AT1 receptor) directly, preventing angiotensin II from binding and exerting its vasoconstricting, aldosterone-stimulating effects. The outcome is nearly identical to ACE inhibition – reduced blood pressure, reduced aldosterone, kidney protection – with one important difference: ARBs do not affect bradykinin levels, so they do not cause the dry cough that frequently ends ACE-I therapy.

Drug names – suffix pattern: All ARBs end in “-sartan”: losartan, valsartan, irbesartan, olmesartan, candesartan.

Key considerations:

• Same indication as ACE inhibitors: hypertension, heart failure, diabetic nephropathy, post-MI
• Hyperkalemia risk is similar to ACE-I – monitor potassium, avoid K+-sparing diuretics without close monitoring
• Angioedema risk exists but is lower than with ACE inhibitors; however, patients with prior ACE-I angioedema should be closely monitored if switched to an ARB
• Never combine an ARB with an ACE inhibitor – dual RAAS blockade significantly increases the risk of hyperkalemia, hypotension, and renal failure without meaningful clinical benefit
• Fetal toxicity – same boxed warning as ACE inhibitors; stop when pregnancy is detected

ARNI (sacubitril/valsartan, Entresto): In HFrEF, the angiotensin receptor-neprilysin inhibitor reduced cardiovascular death or HF hospitalization compared with enalapril in PARADIGM-HF (McMurray 2014), and the 2022 AHA/ACC/HFSA guideline recommends an ARNI in place of an ACE inhibitor or ARB for NYHA class II–III HFrEF (Heidenreich 2022). Because neprilysin also breaks down bradykinin, the label contraindicates combining it with an ACE inhibitor and requires a 36-hour washout after the last ACE inhibitor dose to limit angioedema risk.

For nursing students managing patients on blood pressure medications, the hypertension nursing reference covers patient education and lifestyle modification in detail.

Beta-blockers

Mechanism: Beta-blockers competitively antagonize catecholamines (epinephrine, norepinephrine) at beta-adrenergic receptors. Beta-1 blockade in the heart reduces heart rate (negative chronotropy) and contractility (negative inotropy), lowering cardiac output and blood pressure. Beta-2 blockade causes bronchospasm – clinically relevant in patients with asthma or COPD.

Drug names – suffix pattern: Most beta-blockers end in “-olol”: metoprolol, atenolol, propranolol, carvedilol (exception – but widely used). Carvedilol is also an alpha-1 blocker, causing additional vasodilation.

Key side effects and nursing considerations:

Hold for heart rate <60 bpm – Standard nursing practice. Before administering any beta-blocker, assess the apical heart rate for one full minute. If HR is below 60 (or per the provider’s specific parameters), hold the dose and notify the provider. Document this assessment. This is one of the most frequently tested NCLEX nursing actions for cardiac medications.

Never abruptly discontinue – Stopping a beta-blocker suddenly leads to rebound adrenergic stimulation – upregulation of beta-receptors has occurred during chronic blockade. Abrupt withdrawal causes rebound hypertension, tachycardia, angina, and potentially MI. Taper doses over 1–2 weeks under provider supervision. NCLEX priority: if a patient says they’ve been stopping and starting their metoprolol based on how they feel, this is a safety concern requiring immediate patient education and provider notification.

Caution in decompensated heart failure – Beta-blockers are evidence-based for stable, compensated heart failure (carvedilol, metoprolol succinate, and bisoprolol are the three with mortality benefit). Starting one, or raising the dose, during acute decompensation adds negative inotropy at the worst moment, and the carvedilol label contraindicates it in decompensated HF requiring IV inotropes. In patients already on chronic therapy who are admitted with mild decompensation, the 2022 HF guideline recommends continuing existing guideline-directed therapy, beta-blockers included, unless the patient is hemodynamically unstable or another contraindication applies, so do not hold it without a provider order (Heidenreich 2022). The heart failure nursing guide covers this distinction in clinical context.

Contraindicated in reactive airway disease – Beta-2 blockade causes bronchoconstriction. Avoid non-selective beta-blockers (propranolol) in asthma or COPD. Selective beta-1 agents (metoprolol, atenolol) are relatively safer but should still be used cautiously.

Masks hypoglycemia signs – Epinephrine-driven hypoglycemia symptoms – tachycardia, tremor, palpitations – are blunted by beta-blockade. Diabetic patients on insulin or sulfonylureas may have severe hypoglycemia with no warning signs other than diaphoresis (which is cholinergic, not adrenergic, so it’s preserved). Teach patients to monitor blood glucose closely and not to rely on symptoms to detect lows.

Other nursing points: Monitor for fatigue, sexual dysfunction (under-reported and a common reason for non-adherence), cold extremities, and depression.

Calcium channel blockers

Mechanism: CCBs block voltage-gated L-type calcium channels in cardiac and vascular smooth muscle, preventing calcium entry that drives muscle contraction. The specific clinical effect depends on which calcium channels predominate – cardiac versus vascular.

The dihydropyridine vs non-dihydropyridine distinction – high yield for NCLEX:

Dihydropyridines (DHPs) – act preferentially on peripheral vascular smooth muscle. Examples: amlodipine, nifedipine, felodipine. These drugs produce potent vasodilation with minimal direct cardiac effects. They lower blood pressure effectively but can cause reflex tachycardia and are more likely to cause peripheral edema (lower extremity swelling from increased capillary hydrostatic pressure rather than fluid overload). Amlodipine is the most commonly prescribed CCB and one of the most commonly prescribed antihypertensives overall. Short-acting (immediate-release) nifedipine is the exception to avoid for chronic blood pressure control: a meta-analysis linked it to a dose-related increase in mortality in coronary heart disease (Furberg 1995), and long-acting formulations are used instead.

Non-dihydropyridines (non-DHPs) – act on both cardiac and vascular tissue. Examples: diltiazem, verapamil. These drugs slow conduction through the AV node, decrease heart rate, and reduce contractility in addition to causing vasodilation. They are used for rate control in atrial fibrillation and SVT, as well as for hypertension and angina. Their cardiac effects are clinically important: combining a non-DHP CCB with a beta-blocker can cause profound bradycardia or AV block.

Key nursing considerations:

Grapefruit interaction – Grapefruit and grapefruit juice inhibit intestinal CYP3A4, which metabolizes CCBs, so drug levels can rise and cause hypotension, reflex tachycardia, or edema. The size of the effect varies by drug, so check the individual label. Felodipine bioavailability roughly doubles with grapefruit juice, nifedipine AUC roughly doubles, and verapamil exposure rises by about 28–36%; those labels advise avoiding grapefruit. The amlodipine (Norvasc) label states that grapefruit juice has no impact on amlodipine exposure. On NCLEX, grapefruit counseling is the expected answer for felodipine, nifedipine, and verapamil.

Peripheral edema – Common with dihydropyridines, especially amlodipine. Teach patients that the swelling comes from vasodilation and does not mean fluid overload. Elevating legs helps; dose adjustment or switching agents may be needed if severe.

AV node effects with non-DHPs – Monitor heart rate and rhythm. Do not combine verapamil or diltiazem with beta-blockers without close cardiac monitoring – the combination can cause AV block, severe bradycardia, or asystole.

Constipation – A class effect, more prominent with verapamil; counsel patients accordingly.

Thiazide and loop diuretics

Mechanism:

Thiazide diuretics (hydrochlorothiazide, HCTZ; chlorthalidone) inhibit sodium-chloride cotransporters in the distal convoluted tubule, promoting sodium and water excretion. They are mild diuretics – effective enough for hypertension management, not potent enough for acute fluid overload.

Loop diuretics (furosemide, bumetanide, torsemide) inhibit the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle – the most sodium-absorbing segment of the nephron. This makes loop diuretics the most potent diuretics available, capable of producing rapid, large-volume diuresis. Furosemide (Lasix) is the most commonly used.

Key nursing considerations – diuretics:

Hypokalemia – Both thiazide and loop diuretics cause potassium loss. Hypokalemia is dangerous in cardiac patients because it increases cardiac excitability and potentiates digoxin toxicity (covered in depth below). Monitor electrolytes, encourage dietary potassium (bananas, oranges, potatoes, leafy greens), and follow protocols for replacement. Review electrolyte imbalances in nursing for a complete hypokalemia management reference.

Furosemide ototoxicity – High-dose IV furosemide can cause temporary or permanent hearing loss and tinnitus. Risk is highest with rapid IV infusion, high doses, and concurrent use of other ototoxic drugs (aminoglycosides, vancomycin). Administer IV furosemide at a rate no faster than 4 mg/minute. Monitor for tinnitus, dizziness, or hearing changes.

Sulfa cross-reactivity – Furosemide and HCTZ contain a sulfonamide group. Historically, sulfa allergy was considered a contraindication, though current evidence suggests true cross-reactivity is rare. The clinical standard remains to assess allergy history and use clinical judgment. Notify the provider if the patient reports a sulfa allergy before administering.

Mineralocorticoid receptor antagonists (MRAs) – Spironolactone and eplerenone are potassium-sparing diuretics with a mortality benefit in HFrEF: spironolactone cut all-cause mortality by 30% in RALES (Pitt 1999), and eplerenone reduced cardiovascular death or HF hospitalization in patients with mild symptoms in EMPHASIS-HF (Zannad 2011). The 2022 HF guideline limits MRA use to patients with eGFR >30 mL/min/1.73 m² and potassium <5.0 mEq/L, with potassium and renal function rechecked closely after starting. Hyperkalemia is the main nursing concern, especially alongside an ACE inhibitor, ARB, or ARNI.

SGLT2 inhibitors – Dapagliflozin and empagliflozin are now part of standard HFrEF therapy regardless of diabetes status; in DAPA-HF, dapagliflozin reduced worsening HF or cardiovascular death (McMurray 2019). With an ARNI/ACE-I/ARB, an evidence-based beta-blocker, and an MRA, they make up the four drug classes of guideline-directed medical therapy for HFrEF (Heidenreich 2022). Watch for volume depletion when they are combined with loop diuretics, and for genital mycotic infections.

Fluid and electrolyte monitoring – Weigh patients daily (same time, same scale, same clothing). A gain of more than 2–3 pounds overnight indicates fluid retention. Monitor BMP or CMP for sodium, potassium, BUN, creatinine. Hyponatremia is a common side effect, particularly with thiazides in older adults.

Antiarrhythmics

Cardiac arrhythmias result from disrupted impulse formation or abnormal conduction. Antiarrhythmic drugs work by targeting specific ion channels or receptors to normalize these processes. The Vaughan-Williams classification organizes these drugs into four major classes based on their electrophysiological mechanism.

Vaughan-Williams classification – overview:

Class II and Class IV agents are covered in the antihypertensive sections above. The two antiarrhythmics most likely to appear on NCLEX deserve focused attention: amiodarone (Class III) and adenosine, which sits outside the four classic classes. Ventricular arrhythmia management follows the 2017 AHA/ACC/HRS guideline (Al-Khatib 2017), which replaced the 2006 ACC/AHA/ESC document.

Dronedarone (Multaq), an amiodarone analog without iodine, carries a boxed warning: in PALLAS it doubled the risk of death, stroke, and HF hospitalization in permanent atrial fibrillation (Connolly 2011), and it is contraindicated in permanent AF and in recently decompensated or NYHA class IV heart failure.

Amiodarone

Amiodarone is the most complex antiarrhythmic in clinical use. It has properties spanning all four Vaughan-Williams classes – sodium channel blockade, beta-blockade, potassium channel blockade, and calcium channel blockade. This broad mechanism makes it effective against both supraventricular and ventricular arrhythmias, but it also creates a toxicity profile that spans multiple organ systems.

Clinical uses: Ventricular tachycardia, ventricular fibrillation (including ACLS protocols), atrial fibrillation rate and rhythm control. In ACLS, amiodarone or lidocaine may be given for VF or pulseless VT that persists after defibrillation and epinephrine (shock-refractory VF/pVT); the first dose of amiodarone is 300 mg IV/IO, then 150 mg (Wigginton 2025). For the atrial fibrillation clinical context, see the atrial fibrillation nursing guide.

Amiodarone toxicities – multi-organ monitoring table:

Key NCLEX points for amiodarone:

• Its half-life is extremely long: after a single dose the label gives a mean of 58 days (range 15–142), and after chronic oral therapy most patients fall in the 40–55 day range. Adverse effects and drug interactions can persist for weeks to months after the drug is stopped
• Oral amiodarone carries a boxed warning for pulmonary, hepatic, and cardiac (proarrhythmic) toxicity; pulmonary toxicity is the most feared complication
• Drug interactions: amiodarone inhibits P-glycoprotein and CYP enzymes. The amiodarone label says to reduce the warfarin dose by one-third to one-half (prothrombin time can rise 100% within 3–4 days) and to reduce digoxin by half or stop it, then monitor INR and digoxin levels closely
• Monitoring schedule (HRS practical guide, Goldschlager 2007): TSH and LFTs at baseline and every 6 months; CXR at baseline and yearly
• Teach patients sun protection (UPF clothing, broad-spectrum sunscreen) from day one

Adenosine

Adenosine is not classified in the Vaughan-Williams system but is the drug of choice for terminating paroxysmal supraventricular tachycardia (SVT). It works by transiently blocking conduction through the AV node, breaking the reentrant circuit responsible for most SVTs.

Half-life: less than 10 seconds (label) – one of the shortest half-lives of any drug used in clinical practice. This is the pharmacological basis for one of the most technique-dependent nursing skills in cardiac care.

Administration technique – this is where most references stop short:

1. Use a large peripheral vein as proximal to the heart as possible (antecubital preferred). Adenosine must reach the heart before it is metabolized.
2. Draw up adenosine in one syringe and a 20 mL NS flush in a second syringe. Use a stopcock or two-port setup so both can be given in rapid succession.
3. Administer adenosine as a rapid IV bolus – push the full 6 mg dose over 1–2 seconds, then immediately push the saline flush rapidly. The entire sequence must be completed within seconds.
4. Have the patient lie supine before administration. Warn them: “You may feel a brief sensation of chest tightness, flushing, or a feeling of impending doom – this lasts only seconds.” This warning prevents extreme patient distress and is a nursing care standard.
5. Monitor continuous ECG and run a rhythm strip during the push. A pause of a few seconds or transient AV block is expected as the AV node is blocked, and it is usually self-limiting because of the very short half-life. Prolonged asystole and ventricular fibrillation have been reported, so keep resuscitation equipment at the bedside. If the SVT does not convert within 1–2 minutes, give 12 mg rapid IV push; the 12 mg dose may be repeated once (label). Doses above 12 mg are not recommended.

Contraindications (label): Second- or third-degree AV block or sinus node disease (sick sinus syndrome, symptomatic bradycardia) unless a functioning pacemaker is present, and known hypersensitivity. Use with caution in asthma and bronchospastic disease (can cause bronchospasm). Caffeine and theophylline blunt its effect; dipyridamole potentiates it.

Digoxin

Digoxin (Lanoxin) is one of the oldest cardiac drugs still in clinical use, derived from the foxglove plant. It has a narrow therapeutic index – the difference between a therapeutic and a toxic dose is small – which makes it a perennial NCLEX topic and a significant source of preventable adverse events.

Mechanism

Digoxin inhibits the sodium-potassium ATPase (Na/K-ATPase) pump on cardiac myocytes. Normally, this pump moves sodium out of the cell and potassium into the cell. When digoxin blocks this pump:

1. Intracellular sodium rises
2. The sodium-calcium exchanger compensates by pumping sodium out in exchange for calcium in
3. Intracellular calcium rises
4. More calcium is available for each contraction → increased contractile force (positive inotropy)

Simultaneously, digoxin enhances vagal tone at the AV node, slowing conduction – a negative chronotropic effect. This is why digoxin is useful for both conditions it treats: heart failure (needs more force) and atrial fibrillation (needs slower ventricular rate).

Therapeutic range and toxicity threshold

• Label range: the Lanoxin label links levels below 0.5 ng/mL with diminished efficacy and levels above 2 ng/mL with increased toxicity and no added benefit. The 0.8–2.0 ng/mL “therapeutic range” in older references rests on small early studies.
• Current targets are lower: in HFrEF, post hoc analyses of the DIG trial found the lowest mortality at roughly 0.5–0.9 ng/mL, with harm at ≥1.2 ng/mL. For atrial fibrillation, the 2023 ACC/AHA/ACCP/HRS guideline says it is reasonable to target levels below 1.2 ng/mL when levels are measured (class 2a) (Joglar 2023).
• Toxicity: usually seen above 2 ng/mL, though symptoms can occur at lower levels (label)
• Critical caveat: hypokalemia, hypomagnesemia, hypercalcemia, renal impairment, low body weight, and advanced age all make toxicity likelier at “normal” levels
• Timing: per the label, draw the level just before the next scheduled dose or at least 6 hours after the last dose; a sample drawn sooner reads falsely high

Digoxin toxicity: the hypokalemia connection – mechanistic explanation

This is one of the most important pharmacology concepts on NCLEX, and understanding the mechanism makes it impossible to forget:

The Na/K-ATPase pump – the same pump that digoxin inhibits – has a binding site that potassium and digoxin compete for. When serum potassium is normal, potassium competes effectively at the binding site, limiting how much digoxin can bind. When potassium is low (hypokalemia), there is less competition – digoxin binds more freely to the pump, amplifying its inhibitory effect. The result: the same digoxin dose becomes effectively more potent, and toxicity occurs at drug levels that would be safe in a normokalemic patient.

This is why diuretics and digoxin require careful co-administration monitoring. Furosemide and thiazides both cause hypokalemia – which potentiates digoxin toxicity. Nurses must monitor both the digoxin level AND the potassium level, and treat hypokalemia aggressively in patients taking digoxin.

Hypomagnesemia also predisposes to digoxin toxicity (the label lists it alongside hypokalemia and hypercalcemia), and diuretics deplete magnesium as well as potassium. Monitor magnesium in addition to potassium.

Toxicity signs and symptoms

The classic triad:

1. Gastrointestinal: Nausea, vomiting, anorexia, abdominal pain – often the first symptoms to appear
2. Visual disturbances: Yellow-green visual halos around objects (xanthopsia), blurred vision, photophobia – highly characteristic of digoxin toxicity and NCLEX-testable
3. Cardiac arrhythmias: Any rhythm can occur, but bradyarrhythmias, AV block, and premature ventricular contractions are most common; bidirectional ventricular tachycardia and atrial tachycardia with AV block are highly suggestive of digoxin toxicity

Neurological symptoms also occur: headache, fatigue, confusion, dizziness – particularly in older adults, who may present with digoxin toxicity predominantly as altered mental status.

Nursing hold parameters and monitoring

• Hold if heart rate is below 60 bpm – digoxin slows AV conduction and can cause dangerous bradycardia. Check apical pulse for one full minute before every dose.
• Monitor digoxin levels, BMP (potassium, magnesium, creatinine – renal function affects digoxin clearance)
• Assess for early toxicity symptoms at every assessment

Treatment of digoxin toxicity

• Discontinue digoxin
• Correct electrolyte imbalances (particularly hypokalemia and hypomagnesemia)
• Continuous cardiac monitoring
• Digoxin immune fab (DigiFab) – the antidote for life-threatening or potentially life-threatening digoxin toxicity. DigiFab is the only digoxin immune fab sold in the US; the older Digibind product was withdrawn from the US market in 2011. The antibody fragments bind free digoxin. Label indications include severe ventricular arrhythmias, progressive bradycardia or second- or third-degree heart block not responsive to atropine, potassium above 5.5 mEq/L in adults with rapidly progressive toxicity, ingestion of 10 mg or more in a healthy adult, and chronic toxicity with steady-state levels above 6 ng/mL. Potassium can fall rapidly after DigiFab, so recheck it frequently. Standard serum digoxin levels drawn after DigiFab are misleading (total digoxin rises, but it is bound to Fab), so the label advises against relying on them until the fragments are cleared.
• IV calcium: traditional teaching held calcium to be contraindicated in digoxin toxicity, and the Lanoxin label warns that rapid IV calcium can cause serious arrhythmias in digitalized patients. A 17.5-year retrospective review found no life-threatening dysrhythmias within 1 hour of IV calcium and no difference in mortality (Levine 2011). DigiFab remains the definitive treatment for hyperkalemia caused by digoxin toxicity; follow the provider’s order and local protocol on calcium.

Drug interactions raising digoxin levels

Quinidine and amiodarone both inhibit P-glycoprotein, which clears digoxin. The Lanoxin label lists quinidine as raising digoxin AUC by 54–83% and advises cutting the digoxin dose by about 30–50%; for amiodarone it lists a smaller rise and a 15–30% cut. The amiodarone label is more conservative: reduce digoxin by half or stop it. In practice, measure a digoxin level before starting either drug, expect the provider to reduce the dose, and recheck levels and watch for toxicity.

Nursing monitoring quick reference

NCLEX high-yield bullets

These are the most testable facts from this reference – the ones that appear repeatedly on NCLEX and in clinical practice:

• ACE inhibitor dry cough is caused by bradykinin accumulation – not an allergy. Clinical response: switch to an ARB.
• ACE inhibitor angioedema is a permanent discontinuation. Do not restart, do not switch doses – assess airway and escalate.
• Beta-blockers: NEVER stop abruptly. Rebound tachycardia, hypertension, and MI are the consequences. Taper under supervision.
• Beta-blockers mask hypoglycemia symptoms in diabetics – except diaphoresis. Teach patients to check blood glucose, not rely on symptoms.
• Metoprolol succinate, carvedilol, and bisoprolol are evidence-based for stable HFrEF. Do not start them during acute decompensation; for patients already taking one, follow the provider’s order (the 2022 HF guideline favors continuing it unless the patient is unstable).
• HFrEF guideline-directed therapy has four classes: ARNI (or ACE-I/ARB), evidence-based beta-blocker, MRA, and SGLT2 inhibitor. Allow a 36-hour washout between an ACE inhibitor and sacubitril/valsartan.
• Furosemide ototoxicity: risk increases with high-dose IV, rapid infusion, and aminoglycoside co-administration. Max infusion rate: 4 mg/min.
• Grapefruit inhibits intestinal CYP3A4 and raises levels of felodipine, nifedipine, and verapamil. The amlodipine label reports no effect, so the interaction varies by drug.
• Verapamil or diltiazem + beta-blocker = dangerous combination – high risk of AV block and severe bradycardia.
• Amiodarone monitoring: baseline and yearly CXR, TFTs and LFTs every 6 months, eye exam for any visual symptoms. Half-life is measured in weeks (label mean 58 days after a single dose; 40–55 days for most patients on chronic therapy), so toxicity persists after stopping.
• Amiodarone raises warfarin levels (label: reduce warfarin by one-third to one-half) and raises digoxin levels (amiodarone label: reduce digoxin by half or stop it).
• Digoxin levels: toxicity is usually seen above 2 ng/mL, and current targets are lower (below 1.2 ng/mL in AF; about 0.5–0.9 ng/mL in HFrEF). Hold for HR <60 in adults or per the provider’s parameters.
• Hypokalemia potentiates digoxin toxicity – mechanistically, because potassium competes with digoxin at the Na/K-ATPase binding site. Treat hypokalemia aggressively in patients on digoxin.
• Digoxin toxicity triad: nausea/vomiting/anorexia + yellow-green visual halos + cardiac arrhythmias.
• Digoxin antidote: DigiFab (digoxin immune fab). Digibind left the US market in 2011. Recheck potassium often after DigiFab, because it can drop quickly.
• Adenosine half-life: under 10 seconds. Must be given as a rapid IV bolus over 1–2 seconds followed immediately by a rapid NS flush. Use a large proximal vein. A brief pause of a few seconds is expected; keep resuscitation equipment ready.

Drug interaction quick reference

Further reading

This reference is part of the pharmacology pillar. Continue building your clinical pharmacology knowledge with:

• Psychiatric medications nursing reference – antipsychotics, mood stabilizers, lithium monitoring
• Drug classifications nursing guide – prefix and suffix patterns across all drug classes
• Heart failure nursing reference – clinical application of the cardiac drugs covered above
• Atrial fibrillation nursing guide – amiodarone, digoxin, and rate control in clinical context
• Electrolyte imbalances nursing reference – hypokalemia, hypomagnesemia, and their cardiovascular consequences

References

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2. Jones DW, Ferdinand KC, Taler SJ, et al. “2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults.” Circulation. 2025;152(11):e114–e218. https://doi.org/10.1161/CIR.0000000000001356
3. Joglar JA, Chung MK, Armbruster AL, et al. “2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation.” Circulation. 2024;149(1):e1–e156. https://doi.org/10.1161/CIR.0000000000001193 (digoxin target <1.2 ng/mL, class 2a)
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