Acute Coronary Syndrome: Initial Management and the MONA Approach

Acute coronary syndrome (ACS) is one of the most time-critical emergencies in both prehospital and in-hospital medicine. Every year, tens of thousands of patients in Austria alone present with acute chest pain – and a significant proportion of these presentations turn out to be ACS. Rapid recognition, correct risk stratification, and targeted initial therapy directly determine the extent of myocardial loss, complication rates, and survival. This article covers the structured initial management of ACS: from initial diagnostics through differentiated pharmacological management to the decision pathways of reperfusion therapy.

Definition and Spectrum of Acute Coronary Syndrome

The term ACS encompasses a continuum of acute coronary events based on a shared pathophysiology: rupture or erosion of an atherosclerotic plaque with subsequent thrombus formation and impairment of coronary blood flow. Clinically, three entities are distinguished:

• ST-Elevation Myocardial Infarction (STEMI): Complete thrombotic occlusion of a coronary artery with transmural ischemia. The ECG shows persistent ST elevations. Immediate reperfusion is mandatory.
• Non-ST-Elevation Myocardial Infarction (NSTEMI): Incomplete occlusion or distal embolization with subendocardial ischemia. Troponin is elevated; the ECG may show ST depressions, T-wave inversions, or may be unremarkable.
• Unstable Angina Pectoris (UAP): Clinical presentation consistent with ACS without troponin elevation. The transition to NSTEMI is fluid.

The distinction between STEMI and NSTEMI/UAP is the central first decision point, as it determines the subsequent management pathway.

Clinical Presentation and Recognition

Typical and Atypical Symptoms

The classic presentation – retrosternal pressure-like chest pain radiating to the left arm, dyspnea, diaphoresis, and a sense of impending doom – is by far not the only one. Certain patient populations frequently present with atypical symptoms:

• Elderly patients: Dyspnea as an anginal equivalent, confusion, syncope
• Women: Nausea, vomiting, epigastric pain, isolated fatigue
• Diabetic patients: Painless or silent ischemia due to autonomic neuropathy
• Postoperative patients: Symptoms are masked by analgesia and sedation

The key is to consider ACS in the differential diagnosis whenever there is unexplained thoracic symptomatology, new-onset dyspnea without a pulmonary cause, or accompanying autonomic symptoms.

Differential Diagnoses

Not every chest pain is ACS. The most important life-threatening differential diagnoses – the so-called "Big Five" of acute chest pain – must be systematically ruled out:

• Acute coronary syndrome
• Aortic dissection
• Pulmonary embolism
• Tension pneumothorax
• Boerhaave syndrome (esophageal rupture)

Pericarditis, myocarditis, hypertensive crisis, and gastroesophageal causes should also be included in the differential diagnosis. A focused history, physical examination, and the 12-lead ECG allow for rapid narrowing of the diagnosis in most cases.

Initial Diagnostics

12-Lead ECG: The Key Diagnostic Tool

The 12-lead ECG is the single most important investigation when ACS is suspected and should be obtained and interpreted within 10 minutes of first contact. This time requirement applies both in the prehospital setting and in the emergency department.

What you need to look for:

• ST elevation ≥ 1 mm in at least two contiguous leads (≥ 2 mm in V1–V3 in men, ≥ 1.5 mm in women) → STEMI diagnosis
• New left bundle branch block (LBBB) with typical symptoms → treat as STEMI (although the modified Sgarbossa criteria should be used for more precise evaluation)
• ST depressions, T-wave inversions → NSTEMI/UAP possible
• Posterior STEMI: Isolated ST depressions in V1–V3 may mask a posterior infarction. In this case: obtain posterior leads (V7–V9).
• Right ventricular infarction: In inferior STEMI (II, III, aVF), always obtain right precordial leads (V3R, V4R).

If the initial ECG is unremarkable but clinical suspicion persists: serial ECG recordings every 15–30 minutes, as ST changes may develop dynamically.

Troponin

High-sensitivity troponin (hs-cTn) is the biomarker of choice for detecting myocardial injury. Current ESC algorithms recommend a 0h/1h or 0h/2h protocol for rapid rule-in/rule-out strategy in suspected NSTEMI.

Important to understand:

• Troponin elevation is not specific for ACS. Pulmonary embolism, myocarditis, sepsis, renal insufficiency, and Takotsubo cardiomyopathy also cause troponin elevations.
• For the STEMI diagnosis, do not wait for troponin results – the diagnosis is made clinically and electrocardiographically, and reperfusion must not be delayed.

Additional Initial Measures

• Monitoring: Continuous ECG monitoring, pulse oximetry, non-invasive blood pressure measurement
• Intravenous access: At least one large-bore peripheral IV line
• Baseline labs: Complete blood count, renal function, electrolytes, coagulation panel, BNP/NT-proBNP if heart failure is suspected
• Chest X-ray: For differential diagnosis (pneumothorax, aortic dissection, pulmonary congestion), but must not delay initiation of therapy

Pharmacological Initial Management: The MONA Approach – And Why It Requires a Differentiated View

The acronym MONA (Morphine – Oxygen – Nitro – Aspirin) has established itself as a mnemonic for initial ACS therapy. In modern emergency medicine, however, this approach is no longer uncritically applied as standard therapy for every ACS. Each component has clear indications and contraindications.

M – Morphine (Analgesia)

Severe pain in ACS is not only distressing but hemodynamically relevant: pain increases sympathetic tone, raises heart rate, and increases myocardial oxygen consumption.

• Dosing: Morphine 2–5 mg IV as a bolus, titrated to pain relief. May be repeated every 5–10 minutes.
• Alternative: Piritramide (widely used in Austria) 3.75–7.5 mg IV, titrated.
• Caution: Morphine can delay the absorption of oral antiplatelet agents (due to reduced gastrointestinal motility). This effect has been documented for oral ticagrelor and clopidogrel. When in doubt, administer an antiemetic (e.g., ondansetron 4 mg IV).
• Contraindications: Hypotension, respiratory depression, known allergy.

O – Oxygen

Routine oxygen administration for every ACS patient is no longer recommended. Current evidence shows that hyperoxia in normoxemic patients provides no benefit and may even be harmful through coronary vasoconstriction and formation of reactive oxygen species.

• Indication: SpO₂ < 90% or signs of hypoxemia (dyspnea, cyanosis)
• Target SpO₂: 94–98%
• Administration: Nasal cannula 2–6 L/min or mask as needed

N – Nitroglycerin

Nitroglycerin reduces preload, decreases myocardial oxygen consumption, and can relieve coronary vasospasm.

• Dosing: 0.4–0.8 mg sublingually (spray or capsule), may be repeated after 5 minutes if needed. For persistent symptoms: IV administration at 10–200 µg/min, titrated to blood pressure and symptoms.
• Absolute contraindications:
  • Systolic blood pressure < 90 mmHg or drop > 30 mmHg from baseline
  • Use of PDE-5 inhibitors (sildenafil within 24 hours, tadalafil within 48 hours)
  • Right ventricular infarction (preload-dependent!)
  • Severe aortic stenosis or hypertrophic obstructive cardiomyopathy

A – Aspirin (Acetylsalicylic Acid)

Aspirin remains the cornerstone of acute antiplatelet therapy and should be administered as early as possible.

• Dosing: 150–300 mg orally (have the patient chew it for faster absorption) or 150–250 mg IV if nausea/vomiting or swallowing difficulty is present
• Contraindications: Known aspirin allergy (clopidogrel as an alternative), active gastrointestinal bleeding

Supplementary Pharmacological Therapy

Beyond MONA, the following measures are part of guideline-based ACS initial management:

Dual Antiplatelet Therapy (DAPT):

• In addition to aspirin, a P2Y12 inhibitor is administered.
• Ticagrelor 180 mg loading dose (preferred for STEMI and NSTEMI)
• Clopidogrel 600 mg loading dose (for contraindications to ticagrelor, high bleeding risk, or concurrent oral anticoagulation)
• Prasugrel 60 mg loading dose (option for STEMI prior to PCI, not in patients > 75 years or weight < 60 kg, contraindicated in patients with prior stroke/TIA)
• Timing: For STEMI, the P2Y12 inhibitor can be administered in the prehospital setting. For NSTEMI, the optimal timing (before vs. after coronary angiography) is debated – when in doubt, consult with the receiving cardiology team.

Anticoagulation:

• Unfractionated Heparin (UFH): 60–70 IU/kg IV (max. 5000 IU) as a bolus
• Alternatively: Enoxaparin 0.5 mg/kg IV (for STEMI) or 1 mg/kg SC (for NSTEMI)
• Fondaparinux 2.5 mg SC is an option for NSTEMI with a favorable bleeding profile

Beta-Blockers:

• No longer routinely recommended in the acute phase
• Indicated for tachycardia and hypertension without signs of heart failure
• Contraindications: Heart rate < 60/min, systolic blood pressure < 120 mmHg, AV block, acute heart failure, right ventricular infarction
• If indicated: Metoprolol 2.5–5 mg IV slowly, titrated

Risk Stratification in NSTEMI/UAP

While the pathway is clear for STEMI (immediate reperfusion), the NSTEMI/UAP spectrum requires structured risk stratification that determines the timing of invasive diagnostics:

• Immediate invasive strategy (< 2 hours): Hemodynamic instability, cardiogenic shock, life-threatening arrhythmias, recurrent angina despite maximal therapy, mechanical infarction complication
• Early invasive strategy (< 24 hours): Confirmed NSTEMI diagnosis (troponin rise and fall), dynamic ST/T changes, GRACE score > 140
• Invasive strategy (< 72 hours): Diabetes mellitus, renal insufficiency (GFR < 60 mL/min), LVEF < 40%, early post-infarction angina, prior PCI or CABG, GRACE score 109–140

For risk assessment, the GRACE score has been established as a validated tool, incorporating age, heart rate, systolic blood pressure, creatinine, Killip class, ST changes, troponin, and cardiac arrest at admission.

Reperfusion Therapy in STEMI

In STEMI: Time is muscle. Every minute counts, and the management strategy depends on the availability of a cardiac catheterization laboratory.

Primary PCI (Percutaneous Coronary Intervention)

Primary PCI is the preferred reperfusion strategy when it can be performed within 120 minutes of first contact (target: < 90 minutes, ideally < 60 minutes).

• Door-to-balloon time (hospital arrival to balloon inflation): < 60 minutes
• Ideally, direct transport to a PCI center bypassing the emergency department (pre-notification by EMS, direct catheterization lab activation based on the prehospital ECG)

Fibrinolysis

If primary PCI is not available within 120 minutes of first contact, fibrinolysis should be initiated within 10 minutes of STEMI diagnosis (provided there are no contraindications).

Fibrinolytics:

• Tenecteplase (TNK) as a weight-adjusted single bolus (preferred due to ease of administration)
• Alteplase (tPA) as an accelerated regimen over 90 minutes
• In patients ≥ 75 years: consider half-dose tenecteplase

Absolute contraindications to fibrinolysis:

• History of hemorrhagic stroke
• Ischemic stroke within the past 6 months
• CNS neoplasm or arteriovenous malformation
• Major trauma, surgery, or head injury within the past 3 weeks
• Gastrointestinal bleeding within the past month
• Active bleeding or known bleeding diathesis
• Aortic dissection

After successful fibrinolysis (> 50% resolution of ST elevation within 60–90 minutes), coronary angiography should be performed within 2–24 hours. In case of lysis failure (persistent ST elevation, ongoing pain), immediate rescue PCI is indicated.

Complications in the Acute Phase

The most common and dangerous complications in the early phase of ACS that you must be prepared for:

• Ventricular fibrillation / pulseless ventricular tachycardia: The most common cause of prehospital cardiac arrest in ACS. Immediate defibrillation per ACLS algorithm.
• Cardiogenic shock: Persistent hypotension (< 90 mmHg systolic) despite adequate volume resuscitation with signs of end-organ hypoperfusion. Vasopressor therapy (norepinephrine as first-line), early revascularization, consider mechanical circulatory support.
• AV blocks: Particularly in inferior infarction. Usually transient; have transcutaneous pacing ready if hemodynamically significant.
• Acute mitral regurgitation: Due to papillary muscle ischemia or rupture. Clinically presents as a new systolic murmur, acute pulmonary edema.
• Free wall rupture / ventricular septal defect: Rare but lethal complication. Acute hemodynamic decompensation, immediate surgical intervention required.

Structured Handoff

Particularly in ACS, a structured handoff between EMS and the hospital, or between the emergency department and the catheterization lab, is critical. The ISBAR framework (Identify – Situation – Background – Assessment – Recommendation) is an excellent tool:

• I: Name, age, sex
• S: Acute chest pain for X minutes/hours, suspected STEMI/NSTEMI
• B: Cardiovascular risk factors, current medications, allergies
• A: ECG findings, vital signs, medications administered with timing
• R: Catheterization lab activation requested, recommendation for direct admission

Practical Training

Managing acute coronary syndrome requires not only solid knowledge but also well-practiced workflows, rapid decision-making, and confident teamwork – especially when hemodynamic instability or cardiac arrest escalate the situation. In the ACLS Refresher Course by Simulation Tirol, you train exactly these scenarios: from the 12-lead ECG to structured ACS initial management to the management of complications such as ventricular fibrillation and cardiogenic shock. In a safe simulation environment, you can reinforce algorithms, internalize medication dosages, and practice handoffs – so that in a real emergency, you can act confidently and in accordance with current guidelines.