Acute Coronary Syndromes - NREMT: AEMT Level

ST depression and or T-wave inversion (may also be normal early). These changes reflect subendocardial ischemia, distinguishing from STEMI but still requiring urgent evaluation.

Do not give routine oxygen; titrate only if hypoxemic. Routine oxygen can cause vasoconstriction and harm in normoxic patients, per evidence-based guidelines.

Atherosclerotic plaque rupture with platelet thrombus formation. This mechanism leads to partial or complete coronary artery occlusion, resulting in myocardial ischemia or infarction.

Myocardial ischemia spectrum: unstable angina, NSTEMI, STEMI. ACS encompasses a continuum of myocardial ischemia conditions requiring prompt prehospital recognition and intervention to prevent progression to infarction.

Titrate to $94%$ to $99%$ oxygen saturation. This range optimizes oxygen delivery while avoiding hyperoxia-related complications in ACS.

Chew $160$ to $325$ mg aspirin. Aspirin inhibits platelet aggregation, reducing thrombus progression in ACS.

True aspirin allergy or active major bleeding. These conditions increase bleeding risk or cause severe reactions, outweighing aspirin's benefits in ACS.

$0.4$ mg SL every $5$ min, up to $3$ doses if tolerated. Nitroglycerin relieves ischemia by vasodilation, with limits to prevent cumulative hypotension.

Hypotension (systolic BP below local protocol threshold). Low BP exacerbates nitroglycerin-induced vasodilation, risking profound hypotension.

PDE-5 inhibitor use (sildenafil, vardenafil, tadalafil). These drugs synergize with nitroglycerin to cause severe hypotension via cGMP pathway.

Right ventricular infarction (often with inferior STEMI). RV infarction relies on preload; nitroglycerin reduces it, potentially causing cardiogenic shock.

Leads II, III, and aVF. These leads view the inferior heart wall, detecting ischemia in right coronary artery territory.

Leads V1 to V4. These precordial leads assess the anterior wall, indicating left anterior descending artery occlusion.

Angina is ischemia; MI includes myocardial necrosis (cell death). Angina involves reversible ischemia without cell death, while MI results from prolonged ischemia causing irreversible myocardial damage.

Leads I, aVL, V5, and V6. These leads evaluate the lateral wall, often involving circumflex artery pathology.

Ventricular tachycardia and ventricular fibrillation. Reperfusion injury and irritability in infarcted tissue predispose to these life-threatening arrhythmias.

Transport directly to a PCI-capable facility with prearrival activation. PCI provides definitive reperfusion for STEMI, with activation minimizing door-to-balloon time.

Aortic dissection (avoid treatments that delay definitive care). Dissection mimics ACS but requires surgical management; nitroglycerin may worsen it by reducing pressure.

Pressure, squeezing, heaviness, or tightness (not sharp pleuritic). Ischemic pain typically manifests as visceral discomfort due to myocardial oxygen deprivation.

Within 10 minutes of patient contact (as soon as possible). Rapid ECG acquisition enables early STEMI detection and system activation for reperfusion.

Early recognition, 12-lead ECG, and rapid transport to PCI-capable care. Timely ECG and transport facilitate rapid reperfusion, improving outcomes in time-sensitive ACS.

Older adults, women, and patients with diabetes. These groups often have altered pain perception or neuropathy, leading to non-classic presentations.

Diaphoresis. Sympathetic activation in ACS triggers sweating as part of the stress response.

ST-segment elevation in contiguous leads consistent with infarction. ST elevation indicates transmural ischemia, guiding urgent reperfusion therapy decisions in the field.