Angina Pectoris vs. Myocardial Infarction: Recognition and Emergency Response

Core Review

Coronary Artery Disease Spectrum

Angina and myocardial infarction exist on a spectrum of coronary artery disease (CAD) — both involve reduced blood flow to the myocardium, but the nature and consequences differ:

Angina Pectoris

Definition: Angina is chest pain or discomfort resulting from myocardial ischemia — an imbalance between myocardial oxygen demand and supply. It is a SYMPTOM, not a disease. The underlying disease is coronary artery disease.

Stable Angina (Classic, Exertional):

• Etiology: Fixed atherosclerotic narrowing of one or more coronary arteries. At rest, blood flow is adequate. With exertion (or emotional stress), oxygen demand exceeds the narrowed vessel's supply capacity → ischemia → pain.
• Pain characteristics:
  • Location: Substernal (behind the sternum, "elephant sitting on my chest"). May radiate to left shoulder, left arm (ulnar aspect), neck, jaw, or back.
  • Quality: Pressure, squeezing, tightness, heaviness. Typically NOT sharp or stabbing.
  • Duration: 1-5 minutes (rarely >10-15 minutes)
  • Provoking factors: Exertion, emotional stress, cold weather, heavy meals
  • Relieving factors: REST (pain usually resolves within 1-3 minutes of stopping activity), nitroglycerin (resolves within 1-3 minutes of sublingual administration)
  • Associated symptoms: Dyspnea (shortness of breath), diaphoresis (less prominent than MI)
• Pattern: Predictable, reproducible. The patient knows "if I walk up one flight of stairs, I get the pain."

Unstable Angina:

• Definition: Angina that occurs at rest, is new-onset, is increasing in frequency/duration/severity, or is not relieved by the patient's usual nitroglycerin dose
• Clinical significance: Unstable angina is a MEDICAL EMERGENCY — it represents an acute coronary syndrome (plaque rupture with partial thrombosis) and carries a high risk of progression to MI
• In the dental setting, any angina episode should be treated as potentially unstable until proven otherwise

Myocardial Infarction

Definition: MI is myocardial necrosis (death of heart muscle) caused by prolonged ischemia, typically from thrombotic occlusion of a coronary artery.

Pain Characteristics — Classic Presentation:

• Location: Substernal (same as angina) — BUT the pain is MORE SEVERE and more prolonged
• Quality: Crushing, heavy pressure, squeezing. Patients often describe it as the "worst pain of my life."
• Duration: PROLONGED — typically >20-30 minutes. Does NOT go away with rest.
• Response to nitroglycerin: DOES NOT RELIEVE the pain (or provides only partial, temporary relief). This is a KEY distinguishing feature from stable angina. If a patient takes 3 doses of nitroglycerin over 15 minutes with no relief, suspect MI.
• Associated symptoms (more prominent than in angina):
  • Nausea and vomiting (diaphragmatic/inferior wall MI stimulates vagus nerve)
  • Profound diaphoresis ("cold sweat" — a highly predictive sign)
  • Dyspnea (pulmonary congestion from left ventricular dysfunction)
  • Sense of impending doom (patients often say, "I think I'm dying" — this is a real clinical finding)
  • Palpitations
  • Lightheadedness/syncope (low cardiac output)
• NOT relieved by rest: Unlike angina, resting does not stop the pain
• May occur at rest: Unlike stable angina, MI can occur without exertion (often in the early morning hours due to circadian variation in platelet aggregability and fibrinolytic activity)

Atypical Presentations:

• Silent MI: No pain or minimal symptoms. More common in diabetics (autonomic neuropathy), elderly, and women.
• Women: More likely to present with atypical symptoms — fatigue, dyspnea, nausea/vomiting, back pain, jaw pain. Chest pain may be absent or less prominent.
• Elderly: May present with confusion, syncope, or weakness rather than typical chest pain.
• Diabetics: Higher incidence of silent MI due to cardiac autonomic neuropathy.

Pathophysiology:

1. Atherosclerotic plaque rupture (or erosion)
2. Platelet adhesion, activation, and aggregation at the rupture site
3. Thrombus formation (platelet-rich "white" thrombus + fibrin/red cell "red" thrombus)
4. Coronary artery occlusion (partial or complete)
5. Myocardial ischemia → if prolonged (>20-30 minutes) → irreversible necrosis
6. Necrosis begins in the subendocardium (most vulnerable to ischemia) and extends toward the epicardium as time progresses ("wavefront phenomenon")
7. Time = Muscle: Every minute of untreated occlusion results in more irreversible myocardial damage. This is why rapid recognition and EMS activation are critical.

Emergency Management: Angina in the Dental Chair

Step 1: RECOGNIZE

• Patient reports substernal chest pressure/pain
• Patient has a known history of angina
• The patient may say, "I think it's my angina"

Step 2: STOP TREATMENT

• Remove instruments and materials
• Reassure the patient

Step 3: POSITION THE PATIENT

• Upright or semi-upright (reduces venous return, decreasing cardiac preload and workload)
• Do NOT place supine (increases venous return, increases cardiac workload, may worsen ischemia)

Step 4: ADMINISTER NITROGLYCERIN

Protocol for the patient's OWN nitroglycerin (if the patient carries it):

1. Administer ONE dose of the patient's own nitroglycerin (sublingual tablet, 0.3-0.6 mg, or spray, 0.4 mg)
2. Wait 3-5 minutes
3. If pain persists, administer a SECOND dose (wait 3-5 minutes)
4. If pain persists, administer a THIRD dose (wait 3-5 minutes)
5. If pain persists after THREE doses (total of ~15 minutes), suspect MI → ACTIVATE EMS

If the patient does NOT carry their own nitroglycerin:

• The dental office emergency kit should contain nitroglycerin (sublingual tablets or spray)
• Administer per the same protocol

Nitroglycerin Mechanism:

• Nitroglycerin is a vasodilator (nitric oxide donor)
• Dilates coronary arteries → increases myocardial oxygen supply
• Dilates systemic veins → reduces venous return (preload) → decreases cardiac workload → decreases myocardial oxygen demand
• Dilates systemic arteries (at higher doses) → reduces afterload → decreases cardiac workload

Nitroglycerin Contraindications/Precautions:

• Systolic BP <90 mmHg (nitroglycerin can cause further hypotension)
• Patients taking phosphodiesterase-5 inhibitors (sildenafil/Viagra, tadalafil/Cialis, vardenafil/Levitra) within the past 24-48 hours — these drugs potentiate nitroglycerin's vasodilatory effects and can cause life-threatening hypotension
• Severe aortic stenosis
• Increased intracranial pressure

Step 5: MONITOR VITAL SIGNS

• Blood pressure (before and after each nitro dose)
• Pulse rate
• Check if pain resolves → If YES (pain resolves within 1-3 minutes of nitroglycerin and rest): This is consistent with stable angina. The patient may rest and, once stable, may be dismissed (with recommendation to see their physician).
• If NO (pain persists after 3 nitro doses): Activate EMS — suspect MI.

Step 6: ADDITIONAL INTERVENTIONS FOR PERSISTENT PAIN (Suspect MI)

• Aspirin: 325 mg (chewable), chewed and swallowed. Aspirin inhibits platelet aggregation (irreversible COX-1 inhibition) and reduces mortality in MI. Chewing accelerates absorption.
• Oxygen: 2-4 L/min via nasal cannula. Titrate to SpO₂ ≥94%. Routine oxygen is no longer recommended for all MI patients (may cause vasoconstriction), but is appropriate if the patient is hypoxemic or dyspneic.
• Activate EMS: Call 911 immediately. Do not transport the patient by private vehicle.
• Prepare for cardiac arrest: Have AED readily available. Monitor the patient continuously.

Emergency Management: MI (or Suspected MI)

If you suspect MI from the onset (prolonged pain >15-20 minutes, severe, unrelieved by rest, associated nausea/diaphoresis/impending doom, no history of angina, or pain that feels "different" from the patient's usual angina):

1. STOP treatment
2. Activate EMS (911) immediately — do NOT wait
3. Position: semi-upright (30-45°)
4. Administer aspirin: 325 mg chewable
5. Administer oxygen: if SpO₂ <94% or dyspnea present (2-4 L/min)
6. Administer nitroglycerin: ONLY if systolic BP >90 mmHg AND the patient has a known history of angina with their own nitro. One dose; reassess in 3-5 minutes.
7. Monitor vital signs continuously
8. Be prepared to initiate CPR and use the AED if the patient becomes unresponsive with no pulse
9. Document: time of onset, symptoms, vital signs, drugs administered, EMS activation time

Risk Factors for Coronary Artery Disease

The NBDHE may test recognition of CAD risk factors:

Non-Modifiable:

• Age (men >45, women >55)
• Male gender (women's risk increases after menopause)
• Family history of premature CAD (first-degree relative: male <55, female <65)
• Ethnicity (increased risk in South Asian, African American populations)

Modifiable:

• Hypertension (the most important modifiable risk factor for CAD)
• Hyperlipidemia (elevated LDL, low HDL)
• Smoking (dose-dependent risk; risk declines after cessation)
• Diabetes mellitus (accelerates atherosclerosis; considered a CAD equivalent)
• Obesity (especially central/abdominal obesity)
• Physical inactivity
• Unhealthy diet

Dental Treatment Modifications for CAD Patients

• Medication review: Ensure the patient has taken their usual cardiac medications
• Stress reduction protocol: Short appointments, morning scheduling, effective pain control
• Epinephrine in local anesthetic: Use with caution. Maximum: 0.04 mg epinephrine (approximately 2 carpules of 1:100,000). Consider using local anesthetic without vasoconstrictor for basic procedures in unstable patients.
• Elective treatment deferral:
  • Recent MI (<6 months): defer elective treatment; emergency treatment with medical consultation
  • Unstable angina: defer elective treatment
  • Recent coronary artery bypass graft or stent: consult cardiologist
• Anticoagulant/antiplatelet therapy: Many CAD patients take aspirin, clopidogrel, or other antiplatelets, and/or warfarin/DOACs. These typically do NOT need to be discontinued for routine non-surgical dental procedures.

Clinical Application

Scenario 1: A 62-year-old male with known stable angina is undergoing scaling. Midway through, he reports substernal chest pressure and states, "This feels like my usual angina." He carries his own nitroglycerin.

Management: Stop treatment. Position semi-upright. Administer his nitroglycerin (0.4 mg sublingual). Wait 3 minutes. Pain resolves completely. Vital signs stable. The episode is consistent with stable angina. Allow the patient to rest for 10 minutes. Determine whether to continue or dismiss (patient preference and clinical judgment). Document the episode.

Scenario 2: A 58-year-old female during a periodic exam reports sudden onset of substernal chest pain that she describes as "crushing." She is diaphoretic, nauseous, and looks frightened. The pain began 10 minutes ago and is not relieved by rest. She has no history of angina.

Management: This presentation is highly suspicious for MI. ST

1. Activate EMS (911) immediately
2. Position semi-upright
3. Administer aspirin 325 mg chewed
4. Administer oxygen (2-4 L/min)
5. Monitor vital signs
6. Do NOT give nitroglycerin unless her own is available and BP >90 mmHg (since she has no known cardiac history, you do not know if she might have an aortic stenosis or be on PDE-5 inhibitors)
7. Prepare AED
8. Document thoroughly

Common Traps

• TRAP: Assuming chest pain in a dental setting is "just anxiety." Chest pain must be treated as cardiac until proven otherwise.
• TRAP: Placing a patient with chest pain supine. Supine position increases venous return and cardiac workload. Semi-upright is correct.
• TRAP: Not calling 911 when a known angina patient's pain does NOT respond to 3 doses of nitroglycerin. Persistent pain = suspect MI.
• TRAP: Giving nitroglycerin to a patient who has taken Viagra/Cialis within 48 hours. This can cause life-threatening hypotension.
• TRAP: Delaying or deferring EMS activation for a suspected MI because "the patient says it's getting better." MI pain can wax and wane. When in doubt, call 911.