Acute Coronary Syndrome: Pathophysiology, Assessment, and Management
Objective. Learner will describe the pathophysiology of unstable angina, NSTEMI, and STEMI, and demonstrate a complete, systematic cardiac patient assessment and evidence-based prehospital management sequence.
This lesson, its worked examples and its practice questions has not yet been verified by a licensed clinician in the field or by a certification or approval body. It is a study draft and may contain errors. Do not use it to make decisions about any patient or medication. Always follow your instructor, your supervising professional, and current official references and regulations.
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Acute Coronary Syndrome: Pathophysiology, Assessment, and Management
Acute coronary syndrome (ACS) is an umbrella term covering a spectrum of conditions caused by reduced blood flow through one or more coronary arteries. ACS includes unstable angina (UA), non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Understanding where each condition falls on this spectrum guides your prehospital decisions and can directly save a patient's life.
Pathophysiology: From Plaque to Infarction
Atherosclerosis is the underlying disease. Over years, lipid-laden plaques build up inside coronary artery walls. A vulnerable plaque can rupture, exposing its inner contents to flowing blood. Platelets recognize this disruption as an injury, adhere to the site, and begin aggregating. The coagulation cascade activates, and a thrombus (clot) forms rapidly.
- Unstable angina: The thrombus partially occludes the vessel. Blood flow is reduced but not fully cut off. Myocardial cells are stressed but not yet dying. The patient has chest pain at rest or with minimal exertion; the 12-lead ECG may show ST depression or T-wave changes, or it may appear normal. Cardiac biomarkers (troponin) are not elevated.
- NSTEMI: Similar partial occlusion, but now enough ischemia exists to cause actual cell death in a subendocardial region. The 12-lead may show ST depression or T-wave inversions. Troponin will rise, but there is no ST elevation on the 12-lead.
- STEMI: A complete or near-complete occlusion causes transmural (full-thickness) ischemia and cell death. The 12-lead shows ST elevation in two or more contiguous leads corresponding to the affected artery's territory. This is a time-critical emergency; every minute of occlusion destroys more myocardium.
The key concept: time is muscle. The faster perfusion is restored, the more myocardium survives.
Systematic ACS Assessment
Scene safety and general impression: Note the patient's position, skin color, and any signs of distress on approach.
Primary assessment: Airway, breathing, circulation. Identify and treat life threats immediately. Attach the cardiac monitor early.
SAMPLE history (Signs/Symptoms, Allergies, Medications, Pertinent past history, Last oral intake, Events leading up):
- Medications: note anticoagulants, nitrates, erectile dysfunction drugs (phosphodiesterase-5 inhibitors are a contraindication to nitroglycerin).
- Past history: prior MI, bypass surgery, stents, or heart failure affects your treatment plan.
OPQRST pain assessment (Onset, Provocation/Palliation, Quality, Radiation, Severity, Time):
- Classic ACS pain: substernal pressure or squeezing, radiation to the left arm, jaw, or back, onset at rest or with exertion, unrelieved by positional changes.
- Atypical presentations are common, especially in women, elderly patients, and diabetic patients, who may report only fatigue, nausea, dyspnea, or epigastric discomfort without classic chest pain. Never dismiss these presentations.
Physical exam: Assess skin (pale, cool, diaphoretic suggests poor perfusion), lung sounds (crackles may indicate early pulmonary edema), and jugular venous distension. Check for equal radial pulses.
Vital signs: Blood pressure in both arms if posterior or right-ventricular MI is suspected. Heart rate and rhythm, respiratory rate, oxygen saturation, and blood glucose as clinically indicated.
12-lead ECG acquisition: Obtain and transmit as early as possible — ideally within 10 minutes of patient contact for suspected ACS. Identify ST changes, and alert the receiving facility immediately if STEMI criteria are met. Right-sided leads (V4R) and posterior leads should be considered when inferior STEMI is identified to detect right-ventricular involvement.
Prehospital Management
Management follows current AHA/ACC and local medical direction guidelines. The core prehospital interventions are often remembered as MONA (used loosely as a memory tool, though clinical priority order matters):
Oxygen: Administer supplemental oxygen only when indicated. Current evidence supports oxygen for patients with SpO₂ below 94%, respiratory distress, or signs of heart failure. Routine high-flow oxygen for all ACS patients is not supported by current evidence and may be harmful to normoxic patients.
Aspirin: Give aspirin (typically a chewable dose per local protocol) as early as possible to inhibit platelet aggregation, unless the patient has a true aspirin allergy or active bleeding contraindication. Confirm no allergy.
Nitroglycerin: May relieve ischemic chest pain by causing coronary and peripheral vasodilation. Do not give if: systolic BP is below the threshold in your protocol, patient has taken a phosphodiesterase-5 inhibitor within the timeframe specified by your protocol, suspected right-ventricular infarction, or bradycardia with hypotension. Always follow your medical direction orders.
Analgesia: Pain relief (opioid analgesia per protocol and medical direction) may be appropriate if nitroglycerin does not relieve pain. Pain increases sympathetic tone and myocardial oxygen demand.
STEMI reperfusion: The goal is minimizing total ischemic time. Prehospital STEMI notification to the receiving cath lab allows the interventional team to prepare, dramatically reducing door-to-balloon time. Follow local systems-of-care protocols for direct cath lab activation.
Safety Points
- Always reassess vital signs after each intervention, especially nitroglycerin.
- Right-ventricular infarction (inferior STEMI with ST elevation in V4R) is extremely preload-dependent; nitroglycerin can cause life-threatening hypotension in these patients.
- Atypical presentations must be taken seriously — do not anchor on a "non-cardiac" explanation without objective data.
- Continuous cardiac monitoring is mandatory throughout transport; ACS patients are at high risk for lethal dysrhythmias.
- Early notification to the receiving hospital is not optional for STEMI — it is a patient-safety intervention.
- Stay within your scope of practice; consult medical direction for any medication or intervention questions.
Key terms10
Materials: ACS pathophysiology diagram, SAMPLE/OPQRST worksheets, simulation manikin with 12-lead capability, AHA or NAEMSP prehospital ACS reference materials, poster paper and markers
Check: Learner completes the ACS patient assessment scenario within the allotted time, obtains all critical history elements, correctly acquires the 12-lead, and delivers an accurate radio report; instructor uses a structured 20-point scenario rubric with 80% pass threshold.
Practice check8
Answer each question, then check it. Nothing is recorded; this is your own practice.
