MONA mnemonic in nursing: ACS treatment explained

LS
By Lindsay Smith, AGPCNP
Updated August 26, 2026

Reviewed for clinical accuracy · Methodology: NIH, NCBI, AANP guidelines

When a patient arrives in the emergency department clutching their chest, nurses need to act fast. There is no time to flip through reference materials or second-guess the sequence of interventions. That is where the MONA mnemonic comes in.

MONA stands for Morphine, Oxygen, Nitrates, Aspirin – the four medications historically given in the initial management of acute coronary syndrome (ACS). The mnemonic is taught in nursing school, tested on the NCLEX, and used as a quick mental framework in cardiac care settings. Understanding what each component does, why it is given, and how current guidelines have refined its use will make you a more confident and clinically accurate nurse.

What MONA stands for

LetterMedicationPurposeStanding in the 2025 ACS guideline
MMorphinePain relief (used selectively – see below)No Class of Recommendation; analgesic options table only
OOxygenCorrect hypoxemia if SpO₂ < 90%Class 1 (LOE C-LD) below 90%; Class 3: No Benefit (LOE A) at 90% or above
NNitratesVasodilation, reduce cardiac workloadNo Class of Recommendation; analgesic options table only
AAspirinAntiplatelet therapy, prevent further clot formationClass 1 (LOE A)

Detailed breakdown of each component

M – Morphine

Morphine has been used in cardiac emergencies for decades. As an opioid analgesic, it reduces the perception of chest pain, decreases anxiety, and may lower sympathetic nervous system activation – all of which can reduce the heart’s oxygen demand during an acute event.

However, current clinical guidelines have significantly narrowed the role of morphine in ACS, and this is an important teaching point.

Earlier practice involved giving morphine routinely to ACS patients in pain. Research over the past decade has raised concerns. Evidence from the CRUSADE registry and other studies indicated an association between morphine use and higher rates of adverse clinical outcomes, including increased mortality in patients with non-ST elevation myocardial infarction (NSTEMI). The proposed mechanism is that morphine slows gastric and intestinal motility, which can delay the absorption and pharmacodynamic effect of oral P2Y12 inhibitors such as clopidogrel and ticagrelor.

The 2025 ACC/AHA/ACEP/NAEMSP/SCAI acute coronary syndromes guideline — which replaced the separate 2013 STEMI and 2014 NSTE-ACS documents that most nursing textbooks still cite — reflects this evidence in a way worth understanding precisely. The guideline assigns morphine no Class of Recommendation at all. It does not appear in a numbered recommendation; it appears only in the guideline’s table of analgesic treatment options for cardiac chest pain, alongside nitroglycerin and intravenous fentanyl, with the instruction to use it “for relief of pain that is resistant to other maximally tolerated anti-ischemic medications.” The suggested dosing is 2–4 mg IV, repeated every 5–15 minutes if needed, with doses up to 10 mg considered.

Two details matter for exam and bedside purposes. First, fentanyl (25–50 μg IV, up to 100 μg) sits in the same table as a co-equal option, so the framework is no longer morphine-specific. Second, the guideline is careful about the P2Y12 interaction: it records the pharmacodynamic delay as real while noting that “the clinical relevance of these pharmacodynamic findings remains disputed.” The guideline’s own emphasis is that opiates should not be used to mask ongoing ischemic symptoms — pain that persists despite nitrates is a signal to pursue rapid revascularization, not a signal to escalate analgesia.

As a nursing student, the key takeaway is this: morphine is in the mnemonic, and you should know what it is and why it was used – but you should also know that modern bedside practice has shifted toward more cautious, selective use based on the patient’s clinical picture and your facility’s current protocols.

O – Oxygen

Oxygen was once given routinely to all ACS patients, on the assumption that more oxygen was always better during a cardiac event. Current evidence and guidelines have challenged that assumption.

The 2025 ACS guideline is unusually direct here, and it carries two separate recommendations that students should learn as a pair:

  • Give oxygen when SpO₂ is below 90% (Class 1, LOE C-LD). In patients with ACS and confirmed hypoxia, supplemental oxygen to raise saturations to at least 90% is recommended to improve myocardial oxygen supply and reduce anginal symptoms.
  • Withhold oxygen when SpO₂ is 90% or above (Class 3: No Benefit, LOE A). In patients with ACS and saturations at or above 90%, routine supplemental oxygen is not recommended, because it does not improve cardiovascular outcomes.

The second of those is the stronger statement, and it is the one most often missed. A Class 3: No Benefit designation carried at Level of Evidence A is close to the firmest verdict a guideline can issue — it rests on randomized data, principally DETO2X-AMI, which gave routine oxygen at 6 L/min to 6,629 patients with suspected MI and saturations of 90% or above and found no reduction in one-year all-cause mortality and no reduction in rehospitalization with MI. That null result held even in the subgroup with lower baseline saturations of 90–94%. An earlier trial in STEMI patients with saturations of 94% or above found not just an absence of benefit but a possible increase in myocardial injury and infarct size, consistent with the proposed mechanism that hyperoxia drives coronary vasoconstriction and oxidative stress.

In practice, nurses monitor oxygen saturation continuously in suspected ACS. If the patient is maintaining adequate saturations on room air, oxygen is withheld. If saturations drop below threshold, supplemental oxygen is applied – typically starting with nasal cannula at 2-4 L/min and adjusting based on response.

This shift from routine to targeted oxygen therapy is a clinically significant change that many nursing students are not fully taught because older textbooks still reflect the previous standard. Knowing the updated guidance demonstrates clinical currency and is likely to appear in NCLEX questions framed around evidence-based practice.

N – Nitrates

Nitrates are vasodilators – they relax the smooth muscle in blood vessel walls, causing vasodilation. In the context of ACS, their primary benefits are:

  • Reducing preload by dilating venous vessels, which decreases the volume of blood returning to the heart
  • Reducing afterload through arterial dilation, which lowers the resistance the heart pumps against
  • Relieving coronary artery spasm and improving blood flow to ischemic myocardium
  • Reducing the patient’s perception of chest pain and pressure

A point of precision that trips people up: nitrates carry no numbered Class of Recommendation in the 2025 ACS guideline. Like morphine and fentanyl, nitroglycerin appears in the guideline’s analgesic options table rather than as a formal recommendation, and the guideline states plainly that analgesic therapies “have not been shown to improve clinical outcomes in patients with ACS.” Nitrates are a symptom-relief tool with a long track record, not a mortality intervention. Older references that describe nitrates as Class I are carrying forward the framing of the retired 2013 and 2014 guidelines.

Sublingual nitroglycerin is dosed at 0.3 or 0.4 mg (tablet or spray) every 5 minutes as needed, up to three doses, and only in hemodynamically stable patients with a systolic BP of 90 mmHg or above. Intravenous nitroglycerin starts at 10 μg/min and is titrated to pain relief and hemodynamic tolerance; the guideline positions it for persistent anginal pain after oral nitrate therapy, or when ACS is accompanied by hypertension or pulmonary edema. Tachyphylaxis can develop after roughly 24 hours of IV infusion.

Nurses must be aware of the contraindications to nitrate administration. The most critical is recent use of phosphodiesterase-5 (PDE5) inhibitors – combination with nitrates can cause severe, potentially fatal hypotension. The guideline gives agent-specific washout intervals rather than one blanket number, which is worth memorizing as three values:

PDE5 inhibitorAvoid nitrates within
Avanafil (Stendra)12 hours
Sildenafil (Viagra), vardenafil (Levitra)24 hours
Tadalafil (Cialis)48 hours

Nitrates should also be avoided in suspected right ventricular infarction, where the heart depends on preload to maintain output, in systolic BP below 90 mmHg, and where a nitrate would drop systolic BP more than 30 mmHg below the patient’s baseline — a threshold that catches the hypertensive patient whose “normal-looking” post-dose reading is still a dangerous fall for them.

Before giving any nitrate, nurses assess and document the patient’s blood pressure, heart rate, and which PDE5 inhibitor the patient has taken and when.

A – Aspirin

Aspirin is the most consistently supported component of the MONA framework, and it is the only one of the four that the 2025 guideline backs with a numbered recommendation. An initial oral loading dose followed by daily low-dose aspirin is Class 1, LOE A, given to reduce death and major adverse cardiovascular events. That combination — the strongest class at the strongest level of evidence — puts aspirin in a different category from the other three letters, all of which are symptom-directed rather than outcome-improving.

Aspirin works by irreversibly inhibiting cyclooxygenase-1 (COX-1), an enzyme involved in the production of thromboxane A2. Thromboxane A2 promotes platelet aggregation and vasoconstriction – exactly the processes driving clot formation in ACS. By blocking this pathway, aspirin reduces platelet activity and helps prevent the existing thrombus from growing larger.

The standard ACS loading dose is 162–325 mg of non-enteric-coated aspirin, chewed where possible to achieve a faster onset of antiplatelet action. The pharmacology behind that instruction is well characterized: in Feldman and Cryer’s crossover study of 325 mg buffered aspirin, chewing the tablet produced 50% inhibition of serum thromboxane B2 in about 5 minutes, against roughly 12 minutes when the same tablet was swallowed intact. The guideline also directs that a loading dose be given even to patients already taking daily aspirin, which is a point students routinely get wrong.

After the loading dose, patients continue on a maintenance dose of 75–100 mg of non-enteric-coated aspirin daily. That range is not arbitrary — it comfortably exceeds the minimum dose needed to suppress platelet thromboxane A2, leaving headroom for individual variation in drug response. Continuing full-dose aspirin (300–325 mg daily) for 30 days after the loading dose was tested against low-dose maintenance in patients referred for an invasive strategy and proved no better at reducing major adverse cardiovascular events, while causing more minor and gastrointestinal bleeding. If a patient cannot take anything by mouth, rectal or intravenous aspirin are options where available.

Emergency departments and many pre-hospital protocols now direct paramedics and emergency responders to administer aspirin to patients with suspected ACS before hospital arrival. Nurses need to establish whether aspirin has already been given to avoid double-dosing.

Contraindications to aspirin include confirmed aspirin allergy, active or recent gastrointestinal bleeding, and severe thrombocytopenia. Where a history of aspirin hypersensitivity is reported, the 2025 guideline’s preference is aspirin desensitization wherever possible, so that the patient can still receive dual antiplatelet therapy — not simply dropping aspirin and substituting something else. A P2Y12 inhibitor is recommended in all ACS patients regardless of aspirin hypersensitivity history, and it should be loaded as early as possible in anyone who cannot take aspirin at presentation.

Clinical context: when and where MONA is used

ACS is the umbrella term for conditions caused by reduced blood flow to the heart muscle, including unstable angina, NSTEMI, and STEMI (ST-elevation myocardial infarction). The MONA mnemonic applies primarily to the initial stabilization phase – the first minutes to hours after a patient presents with suspected ACS.

The settings where nursing students are most likely to encounter MONA include:

  • Emergency departments: The ED is often the first point of clinical contact. Nurses triage chest pain patients rapidly, obtain a 12-lead ECG within 10 minutes of arrival, and initiate ACS protocols if indicated.
  • Cardiac care units (CCU) and step-down units: Patients stabilized in the ED are transferred here for monitoring and further management.
  • Medical-surgical floors: Nurses on general medical floors need to recognize signs of ACS deterioration and understand the initial management before transfer.
  • Pre-hospital and transport: Paramedics use MONA-based protocols. Nurses working in transport or community settings may encounter patients mid-protocol.

MONA is one piece of a larger ACS management picture. Alongside these four medications, patients receive anticoagulation (typically heparin or low-molecular-weight heparin), additional antiplatelet agents (such as clopidogrel, ticagrelor, or prasugrel), and urgent cardiac catheterization with possible percutaneous coronary intervention (PCI). Time-to-treatment for STEMI is measured in minutes. The metric has moved on from the older “door-to-balloon” language: the 2025 guideline frames the target as first medical contact (FMC) to first device activation within 90 minutes, which starts the clock at the paramedic’s arrival rather than at the hospital door and therefore holds the whole system accountable, not just the emergency department.

Nurses are central to meeting these targets. Knowing the MONA framework helps you move through initial stabilization efficiently while the broader treatment team mobilizes.

Common mistakes to avoid

Giving oxygen to every ACS patient. Many students assume oxygen is always beneficial in cardiac emergencies. The 2025 guideline is clear in both directions: give supplemental oxygen when SpO₂ is below 90%, and withhold it when SpO₂ is 90% or above, where routine oxygen carries a Class 3: No Benefit designation at Level of Evidence A. Assess first, then decide.

Treating MONA as a fixed sequence. The letters form a convenient memory aid, but clinical priorities may differ. Aspirin is often given first because it has the strongest evidence and fewest contraindications. Assess blood pressure before any nitrate. Ask about PDE5 inhibitors before every nitrate administration.

Assuming morphine is still routine. Many older resources and some simulation labs still present morphine as a standard first-line intervention. In current practice it is given selectively, and understanding why reflects genuine clinical understanding.

Forgetting contraindications. Especially for nitrates – always check blood pressure and PDE5 inhibitor use before administration. This is a common NCLEX test point.

Not chewing the aspirin. Always specify that the loading dose should be chewed, not swallowed. This is clinically meaningful, not just a detail.

MONA is one of many mnemonics you will use in nursing. Others that overlap with cardiac and critical assessment skills include:

  • The VEAL CHOP mnemonic – used in labor and delivery to interpret fetal heart rate patterns
  • The HELLP syndrome mnemonic – for recognizing postpartum preeclampsia
  • PR interval interpretation – essential reading for any nurse working in cardiac care, since understanding ECG basics supports your ability to recognize the changes that prompt ACS interventions
  • The ABC mnemonic – the primary survey framework (Airway, Breathing, Circulation, Disability, Exposure) that structures rapid patient assessment before any targeted intervention like MONA can begin
  • The RACE and PASS mnemonics – fire safety response mnemonics tested in nursing fundamentals alongside MONA. Both are emergency protocols that require the same practiced, automatic recall: in a high-acuity situation, you cannot reconstruct the sequence from scratch.

Building a solid library of mnemonics makes clinical reasoning faster and more reliable, particularly in high-pressure settings where recall speed matters.

Summary

MONA stands for Morphine, Oxygen, Nitrates, Aspirin – the four medications historically central to initial ACS management. Measured against the 2025 ACS guideline, the four letters no longer carry equal weight. Aspirin is the only one backed by a formal recommendation, at Class 1 with Level of Evidence A, given to reduce death and major adverse cardiovascular events. Oxygen carries two recommendations pointing in opposite directions depending on the saturation: give below 90%, withhold at 90% or above. Nitrates and morphine carry no Class of Recommendation at all and sit in the guideline’s analgesic options table, where they relieve symptoms without having been shown to improve outcomes. Understanding that hierarchy is what the mnemonic itself cannot teach you.

Understanding not just what MONA stands for, but why each component is used and how current evidence has refined that use, is what separates a confident, evidence-based nurse from one who is simply reciting a mnemonic.

Frequently asked questions

What does MONA stand for in nursing?

MONA stands for Morphine, Oxygen, Nitrates, and Aspirin – the four medications historically used in the initial management of acute coronary syndrome (ACS). Each letter represents a drug class and its rationale: morphine for pain relief, oxygen for correcting hypoxemia, nitrates for vasodilation and reduced cardiac workload, and aspirin for antiplatelet therapy to limit further clot formation.

Is morphine still used in ACS treatment?

Morphine is no longer given routinely to all ACS patients. The 2025 ACC/AHA/ACEP/NAEMSP/SCAI acute coronary syndromes guideline assigns morphine no Class of Recommendation at all – it appears only in the guideline’s table of analgesic options for cardiac chest pain, alongside nitroglycerin and IV fentanyl, reserved for pain resistant to other maximally tolerated anti-ischemic medications. Suggested dosing is 2–4 mg IV, repeatable every 5–15 minutes, with doses up to 10 mg considered. Evidence from the CRUSADE registry raised concerns that opiates delay gastric and intestinal absorption of oral P2Y12 inhibitors such as clopidogrel and ticagrelor, though the guideline notes the clinical relevance of that pharmacodynamic effect remains disputed. Its firmer point is that opiates should not be used to mask ongoing ischemic symptoms: pain persisting despite nitrates should prompt rapid revascularization.

When is oxygen given to ACS patients?

The 2025 ACS guideline splits this into two recommendations. Supplemental oxygen to raise saturations to at least 90% is recommended in patients with confirmed hypoxia, meaning SpO₂ below 90% (Class 1, LOE C-LD). In patients with saturations of 90% or above, routine supplemental oxygen is not recommended because it does not improve cardiovascular outcomes (Class 3: No Benefit, LOE A). The second recommendation is the stronger one and rests largely on DETO2X-AMI, which gave routine oxygen at 6 L/min to 6,629 patients with suspected MI and saturations of 90% or above and found no reduction in one-year all-cause mortality or in rehospitalization with MI, including in the 90–94% subgroup. An earlier STEMI trial suggested routine oxygen may increase myocardial injury and infarct size. Nurses assess oxygen saturation first, then decide whether supplemental oxygen is warranted.

What are the contraindications to nitrates in ACS?

The most critical contraindication is recent use of phosphodiesterase-5 (PDE5) inhibitors – combining these with nitrates can cause severe and potentially fatal hypotension. The 2025 ACS guideline gives agent-specific washout intervals rather than one blanket figure: avoid nitrates within 12 hours of avanafil, 24 hours of sildenafil or vardenafil, and 48 hours of tadalafil. Nitrates should also be avoided in suspected right ventricular infarction, where maintaining preload is essential for cardiac output, in systolic BP below 90 mmHg, and where the dose would drop systolic BP more than 30 mmHg below the patient’s own baseline. Nurses must check blood pressure and establish which PDE5 inhibitor the patient took and when before every nitrate administration.

Why is aspirin chewed rather than swallowed in ACS?

Chewing the loading dose of aspirin (162–325 mg, non-enteric-coated) achieves a faster onset of antiplatelet action. In Feldman and Cryer’s crossover study of 325 mg buffered aspirin, chewing produced 50% inhibition of serum thromboxane B2 in about 5 minutes, against roughly 12 minutes when the same tablet was swallowed intact. In the acute setting, those minutes matter – faster platelet inhibition means faster limitation of clot growth. The 2025 ACS guideline also directs that a loading dose be given even to patients already on daily aspirin. This is a commonly tested NCLEX point and a clinically meaningful distinction.

Is MONA tested on the NCLEX?

Yes. MONA and ACS management appear regularly on the NCLEX-RN. Questions typically test whether students know current guideline updates – for example, that oxygen is given only to hypoxemic patients and that morphine is no longer first-line for all ACS presentations. The NCLEX also tests contraindications to nitrates, particularly the PDE5 inhibitor interaction, and the correct aspirin technique (chewed, not swallowed).


This article is for educational purposes and reflects the 2025 ACC/AHA/ACEP/NAEMSP/SCAI acute coronary syndromes guideline, the current standard as of August 2026. Always follow your facility’s protocols and the most current ACC/AHA guidance in clinical practice.

References

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