Crushing substernal chest pain = MI until proven otherwise. Atypical equivalents: toothache and bad belly ache. Treatment = MONA: Morphine, Oxygen, Nitro, Aspirin.
The Primary Pearl
CRUSHING SUBSTERNAL CHEST PAIN = THINK MI. This is the most-tested EMS association. Lock it in permanently.
Classic Sign
- Crushing substernal chest pain — the classic sign of a heart attack
- Toothache — referred pain from inferior ischemia via vagal pathways; don't dismiss it
- Bad belly ache (epigastric pain) — inferior MI commonly confused for GI complaint
Treatment — M.O.N.A.
M
Morphine
Pain relief & preload reduction. Use per protocol.
O
Oxygen
Titrate to SpO₂ 94–99%. Avoid hyperoxia.
N
Nitro
Hold if hypotensive, RV infarct, or Viagra/Cialis use.
A
Aspirin
324 mg PO — antiplatelet. Give early, give fast.
Sudden onset chest discomfort with radiation = angina pectoris. Lasts 3–5 min (up to 15 min). No death of cardiac muscle (unlike MI). Unstable angina does NOT resolve with nitro. Prinzmetal = calcium-driven spasm.
Angina vs. MI — The Critical Difference
Angina Pectoris
No death of cardiac muscleTransient ischemia — fully reversible
Duration3–5 min; sometimes up to 15 min
BP EffectElevation in blood pressure
PresentationSudden onset chest discomfort, pain radiating, possible epigastric pain + labored breathing
MI (Heart Attack)
Death of cardiac muscleIrreversible necrosis — infarction
Duration>15–20 min; does not self-resolve
BP EffectMay drop if pump fails
TreatmentMONA + cath lab activation
Three Types of Angina
| Type | Trigger | Nitro? | Pearl |
|---|---|---|---|
| Stable Angina | Activity / exertion | Resolves with nitro + rest | Predictable, reproducible — occurs with activity, relieved with rest |
| Unstable Angina | At rest; crescendo attacks | Does NOT go away with nitro | ACS equivalent — treat aggressively, transport immediately |
| Prinzmetal's Angina | Coronary artery spasm | May respond | Caused by a calcium disturbance — calcium controls muscle contraction |
Treatment
- Treatment for angina pectoris = M.O.N.A. (same as MI framework)
- Prinzmetal spasms are thought to be a calcium disturbance — calcium governs muscle contraction responsibility
NREMT TRAP: Unstable angina does NOT go away with nitro. If it doesn't resolve — it's not stable. Treat as ACS.
JVD = right-side failure. Causes of right-side failure with JVD: PE, tension pneumothorax, cardiac tamponade, COPD. #1 cause of right-side failure = left-side failure. #1 cause of left = MI. #1 cause of pulmonary edema = left failure. Wet lungs → think MI.
The Chain — Memorize This
- JVD present? → Think right-side failure first
- Right-side failure seen with COPD patients (cor pulmonale — chronic RV strain)
- #1 cause of right-side failure = left-side failure
- #1 cause of left-side failure = MI
- #1 cause of pulmonary edema = left-side failure
- Wet lungs on auscultation? → Think MI driving left failure driving the fluid back into the lungs
- Left-side failure symptoms: pulmonary edema AND right-side failure
Right-Side Failure — JVD Causes
| Condition | Why JVD? | Key Differentiator |
|---|---|---|
| Pulmonary Embolism (PE) | Obstruction raises RV afterload → backs up | Sudden onset SOB, tachycardia, risk factors (DVT, immobility, OCP) |
| Tension Pneumothorax | Mediastinal shift compresses SVC | Absent breath sounds, tracheal deviation, hypotension, JVD |
| Cardiac Tamponade | Pericardial fluid compresses RV filling | Beck's Triad: JVD + muffled heart tones + hypotension |
| COPD | Chronic pulmonary HTN → cor pulmonale | Hypercarbic, barrel chest, prolonged expiratory phase |
Left-Side Failure → Pulmonary Edema
WET LUNGS = THINK MI. Left ventricle fails → backs up into pulmonary vasculature → fluid leaks into alveoli → crackles/rales on auscultation. Follow the chain upstream.
Sudden onset of shortness of breath → think PE. PE causes right-side failure and JVD. It is one of the four conditions that cause JVD with right-side failure.
The Primary Pearl
SUDDEN ONSET SHORTNESS OF BREATH = THINK PULMONARY EMBOLISM. If SOB came on fast with no warning — PE is on your differential until ruled out.
PE in Context
- PE is one of the four causes of JVD with right-side failure: PE, Tension Pneumothorax, Cardiac Tamponade, COPD
- PE obstructs pulmonary blood flow → increased RV afterload → RV backs up → elevated venous pressure → JVD
- Classic triad: sudden SOB + tachycardia + pleuritic chest pain
- Risk factors: DVT, prolonged immobility, post-surgical, OCP use, malignancy
- Prehospital: supportive care — O₂, IV access, monitor, transport urgently
COPD patients can't blow off CO₂ → hypercarbic (pCO₂ >45) → acidotic. Normal blood gases = 35–45. Hypercarbic = over 45. Right-side failure common. Target SpO₂ 88–92%.
Core COPD Pearls
- COPD patients are hypercarbic — their damaged lungs trap CO₂. They can't blow it off.
- Hypercarbic = acidotic — CO₂ + H₂O → carbonic acid → respiratory acidosis
- Normal pCO₂ = 35–45 mmHg. Hypercarbic = above 45 mmHg.
- Right-side failure (cor pulmonale) is seen with COPD patients — chronic pulmonary hypertension strains the RV → JVD, peripheral edema
Blood Gas Quick Reference
| Parameter | Normal | COPD Patient |
|---|---|---|
| pCO₂ | 35–45 mmHg | >45 mmHg (hypercarbic) |
| pH | 7.35–7.45 | <7.35 (respiratory acidosis) |
| SpO₂ target | 94–99% | 88–92% only — avoid hyperoxia |
Oxygen Warning
Do NOT give 100% O₂ unmonitored to a known COPD patient. Target 88–92% SpO₂ only. Hyperoxia can blunt their hypoxic respiratory drive and cause hypoventilation.
Stage 1 = bronchospasm. Stage 2 = inflammation. Shark fin on capnogram = bronchospasm/asthma. Dyspnea + wheezing + cough = asthma signs. Absence of wheezing = imminent death. Severe = epinephrine. Drug class = Beta-2.
Signs & Symptoms
- Dyspnea, wheezing, and cough — the three classic signs of asthma
- First question to ask an asthma patient: "Have you ever been intubated?" — prior intubation signals severe disease history and high-risk patient
Asthma Stages
Stage 1 — Bronchospasm
Smooth muscle contraction narrows airways
Treat: Beta-2 agonists (albuterol)
Capnogram: Shark fin waveform
Stage 2 — Inflammation
Mucosal edema + mucus production follows
Treat: Steroids, Atrovent (ipratropium)
Capnogram Pearl
- Shark fin on the capnogram = asthma / bronchospasm. The delayed CO₂ expiration from obstructed airways creates a sloped, shark-fin-shaped waveform instead of a normal square plateau
- Bronchospasms show like a shark fin on the capnogram — this is the direct quote from the source material. Know it for the exam.
Pulsus Paradoxus
- Severe asthma with pulsus paradoxus: pulse becomes weaker as you inhale
- Cause: air trapped in lungs increases intrathoracic pressure → compresses heart → stops/weakens pulse during inhalation
- Also causes: tachycardia and decreased O₂ saturation
Imminent Death & Treatment
ABSENCE OF WHEEZING IN AN ASTHMA PATIENT = IMMINENT DEATH. No air movement at all = severe air trapping. Pre-arrest emergency. Treat immediately.
| Drug | Class | Role |
|---|---|---|
| Albuterol | Beta-2 agonist | First-line bronchodilator |
| Steroids | Corticosteroid | Anti-inflammatory (inhaler component) |
| Atrovent (ipratropium) | Anticholinergic | Bronchodilator + dries secretions (inhaler component) |
| Epinephrine | Alpha + Beta | Severe / respiratory arrest — dilates bronchioles, constricts vessels |
Tall skinny male + sudden onset SOB = spontaneous (closed) pneumothorax. Closed pneumothorax often has a history of smoking. Marfan syndrome = genetic disease in tall skinny people causing arterial wall weakness → aneurysms.
The Body Habitus Pearl
TALL SKINNY MALE + SUDDEN ONSET SOB = SPONTANEOUS PNEUMOTHORAX (CLOSED). The tall, thin body type creates elongated lung tissue under increased mechanical stress — predisposed to bleb rupture.
Spontaneous / Closed Pneumothorax
- Often presents from a history of smoking — emphysematous changes increase bleb formation
- Sudden, sharp unilateral chest pain + acute SOB with no trauma mechanism
- Decreased breath sounds on affected side
Marfan Syndrome
- Marfan syndrome = genetic disease that presents with weakness in the arterial walls
- Affects tall, skinny people — the phenotype is the diagnostic clue
- Arterial wall weakness leads to aneurysms — particularly aortic aneurysm / dissection
- Tall skinny patient + chest/back pain = consider Marfan-related aortic dissection in addition to pneumothorax
Female + child-bearing age + belly pain = ectopic until proven otherwise. Tubal ligation = higher ectopic risk. Transport in position of comfort. Shoulder pain from belly insult = ruptured spleen, ectopic, or liver. Placenta previa = painless bright red bleeding (3rd trimester). Abruption = tearing pain + board-like abdomen + massive hemorrhage (3rd trimester).
Ectopic Pregnancy Pearls
- Any female of child-bearing age with belly pain = ectopic pregnancy until ruled out. Do not skip this differential.
- Tubal ligation increases ectopic risk — scar tissue can trap a fertilized egg in the fallopian tube
- Transport position: position of comfort — do not force supine if it increases pain
Referred Shoulder Pain — Belly Insults
BELLY INSULT → SHOULDER PAIN: Three causes refer pain to the shoulders via diaphragmatic irritation (Kehr's sign):
1. Ruptured spleen
2. Ectopic pregnancy (ruptured)
3. Liver injury
Always think internal hemorrhage when shoulder pain follows an abdominal event.
1. Ruptured spleen
2. Ectopic pregnancy (ruptured)
3. Liver injury
Always think internal hemorrhage when shoulder pain follows an abdominal event.
3rd Trimester Emergencies
| Condition | Trimester | Key Signs | Pearl |
|---|---|---|---|
| Placenta Previa | 3rd trimester | Painless bright red bleeding | Placenta covers cervical os. No pain because no uterine contractions are causing it. |
| Abruptio Placentae | 3rd trimester | Sudden sharp tearing pain, stiff board-like abdomen, vaginal bleeding, massive hemorrhage | Placenta shears off uterine wall — painful, rapid hemorrhage, fetal emergency |
Trauma Patient Rule
- The only reason NOT to disrobe a trauma patient is environmental (cold, hostile environment). Otherwise — fully expose and assess. Missing injuries costs lives.
Type 1 allergic reaction driven by IgE on mast cells and basophils. Most severe route = injection (insects/Hymenoptera). Most dangerous signs = stridor + laryngeal edema. Simple allergic reaction = Benadryl. Anaphylaxis = epinephrine.
Mechanism
- Type 1 hypersensitivity reaction — the antibody driver is IgE
- IgE attaches to mast cells (tissue-fixed) and basophils (mobile cells in circulation)
- Re-exposure to allergen → IgE triggers massive degranulation → histamine flood → systemic vasodilation + bronchoconstriction
Routes of Exposure — Severity Order
| Route | Examples | Severity |
|---|---|---|
| Eating (ingestion) | Peanuts, shellfish, dairy | Variable — absorbed more slowly |
| Absorption (contact) | Latex, topical agents | Moderate |
| Inhaled | Pollen, dust, animal dander | Moderate to severe |
| Injection | Insect stings (Hymenoptera), IV medications | MOST SEVERE — fastest systemic response |
Signs & Symptoms
| System | Signs & Symptoms |
|---|---|
| Skin | Itching, flushed skin, hives (urticaria), swelling of the skin, cyanosis |
| Airway | Stridor, laryngeal edema, bronchospasm — MOST CONCERNING |
| Cardiovascular | Vasodilation, increased heart rate, decreased blood pressure, headache |
| GI / Other | Abdominal cramping, convulsions, tearing, respiratory difficulty |
Treatment — Know the Difference
Simple Allergic Reaction
Benadryl (diphenhydramine)
H1 antihistamine. Good for hives, itching, mild reactions.
NOT sufficient for true anaphylaxis.
Anaphylaxis
Epinephrine — first line, always
Dilates bronchioles (Beta), constricts vessels (Alpha). Dual alpha AND beta activity.
0.3–0.5 mg IM, anterolateral thigh preferred.
MOST CONCERNING SIGNS: Stridor + laryngeal edema. The upper airway is closing. This is a time-critical airway emergency. Give epinephrine immediately — do not reach for Benadryl.
Black widow = immediate redness/swelling + severe big muscle spasms (abdomen, thighs) + possible seizures/paralysis/decreased LOC. Treatment: diazepam + calcium gluconate. Brown recluse = 8-hour delay, small erythematous macule with white ring, tissue necrosis days–weeks later.
Side-by-Side Comparison
| Feature | Black Widow | Brown Recluse |
|---|---|---|
| Symptom onset | Immediate — redness and swelling right away | 8-hour delay — pain, redness, swelling appear later |
| Bite appearance | Immediate redness and swelling at site | Small erythematous macule surrounded by a white ring |
| Key systemic sign | Muscle spasms of large muscle groups (abdomen/stomach, thighs) — ALWAYS the key sign | Chills, fever, nausea/vomiting, joint pain |
| Severe signs | Redness, swelling, progressive muscle spasms of ALL large muscle groups; seizures, paralysis, decreased LOC | Tissue necrosis beginning days to weeks after the bite |
| Treatment | IV muscle relaxants; Diazepam + Calcium Gluconate for spasms; Versed (midazolam) | Supportive — wound care, antibiotics if secondary infection develops |
Black Widow Key Sign
BLACK WIDOW = MUSCLE SPASMS IN THE BIG MUSCLES (stomach muscles / thighs) — THIS IS ALWAYS THE KEY SIGN. Severe abdominal rigidity in a patient who denies trauma? Think envenomation. Treat with diazepam and calcium gluconate for the spasms.
Brown Recluse Timeline
- 8-hour delay before localized pain, redness, and swelling appear
- Tissue necrosis starts days to weeks after the bite — the wound looks like it's getting worse over time
- Systemic signs: chills, fever, nausea/vomiting, joint pain
Alzheimer's signs: shuffling gait, stiffness of body muscles, aphasia (speech disorder), psychiatric disturbances, severe decorticate posturing in end-stage disease.
Signs & Symptoms — Know Each One
| Sign / Symptom | What It Is | Clinical Pearl |
|---|---|---|
| Shuffling gait | Small, dragging steps with reduced arm swing | Classic Alzheimer's presentation — disease associated with this sign |
| Stiffness of body muscles | Increased muscle tone, cogwheel rigidity in advanced stages | Disease associated with this sign |
| Aphasia (speech disorder) | Expressive or receptive language deficits | Disease associated with this sign |
| Psychiatric disturbances | Agitation, hallucinations, paranoia, wandering | Common in mid-to-late stage disease |
| Severe decorticate posturing | Arms flexed, legs extended — indicates deep cortical damage | End-stage finding |
AMS occurs at 6,600 feet. Body becomes alkalotic (hyperventilation blows off CO₂). Least serious altitude illness. Signs: lightheadedness, breathlessness, weakness, headache, nausea, vomiting. Treatment = fluids.
AMS Pearls
| Pearl | Detail |
|---|---|
| Altitude threshold | 6,600 feet — above this altitude, AMS can occur |
| Body response | Alkalosis — hyperventilation caused by hypoxia blows off CO₂, raising blood pH |
| Severity | Least serious of all altitude-related illnesses (AMS < HACE < HAPE) |
| Treatment | Fluids + descend to lower altitude + rest + supplemental O₂ |
Signs & Symptoms
- Lightheadedness
- Breathlessness
- Weakness
- Headache
- Nausea and vomiting
Addison's = hypoadrenalism. Signature sign = hyperpigmentation of the skin. Decreased appetite + weight loss = Addison's. Caused by intense stressor → adrenal/autoimmune disease. Death = cardiopulmonary collapse. HTN history → think MI, stroke, aneurysm.
Addison's Disease (Hypoadrenalism)
| Feature | Detail |
|---|---|
| Cause | Intense stressor on the system → adrenal disease, autoimmune disease, hypoadrenalism |
| Signature sign | Hyperpigmentation of the skin — darkening in skin creases, mucous membranes, scars. See this → think Addison's. |
| Other signs | Progressive weakness, fatigue, decreased appetite, weight loss, vomiting, diarrhea |
| Death from | Cardiopulmonary collapse — adrenal crisis when physiologically stressed |
Diseases Caused by Intense Stressor
- Adrenal disease — cortex destruction → insufficient cortisol/aldosterone
- Autoimmune disease — body attacks its own adrenal tissue
- Hypoadrenalism (Addison's disease) — the clinical syndrome that results
- All three lead to the same endpoint: cardiopulmonary collapse
Hypertension → The Three Dangers
HISTORY OF HYPERTENSION? Think three things downstream:
1. MI — chronic HTN accelerates coronary artery disease
2. Stroke — HTN is the #1 modifiable risk factor for hemorrhagic and ischemic stroke
3. Aneurysm — chronic high pressure weakens arterial walls (especially aortic)
1. MI — chronic HTN accelerates coronary artery disease
2. Stroke — HTN is the #1 modifiable risk factor for hemorrhagic and ischemic stroke
3. Aneurysm — chronic high pressure weakens arterial walls (especially aortic)