⭐ High YieldTreatment threshold changed in 2025: Stage 1 HTN now treated at 130/80 if 10-yr ASCVD risk ≥10%. White coat HTN: elevated in office, normal at home. Masked HTN: normal in office, elevated at home (worse prognosis).
Primary vs Secondary HTN
Primary (Essential)
Secondary
Frequency
90–95%
5–10%
Onset
30–50s, gradual
Any age, abrupt
Family Hx
Often +
Usually –
Causes
Genetics, diet, obesity
Renovascular, PA, OSA, renal disease, pheochromocytoma, coarctation, thyroid
Screen for secondary HTN if: Age <30, sudden onset, resistant to 3+ meds, hypokalemia (think primary aldosteronism), or episodic hypertension + headache + sweating (pheochromocytoma).
HTN Urgency vs Emergency
Urgency
Emergency
BP
>180/120
>180/120
End-Organ Damage
None
YES
Symptoms
HA, anxiety
Chest pain, SOB, neuro changes, papilledema
Goal
Reduce 25% over 24–48h (outpatient)
Reduce 25% in 1h (IV meds, ICU)
Treatment
Oral labetalol, amlodipine, captopril
IV labetalol, nitroprusside, nicardipine
⚠️ DO NOT drop BP too fast in HTN emergency → risk of watershed infarction, AKI.
First-Line Treatment by Population
Population
Preferred Agent(s)
Why
General (non-Black)
Thiazide, ACEi/ARB, CCB
Equal first-line efficacy
Black patients
Thiazide + CCB
ACEi/ARB less effective monotherapy (low renin)
Diabetes
ACEi or ARB
Renoprotective, reduce proteinuria
CKD
ACEi or ARB
Nephroprotection
HFrEF
ARNI + BB + MRA + SGLT2i (GDMT)
Mortality benefit
Post-MI
BB + ACEi/ARB + Statin
Reduce remodeling, mortality
Angina (CAD)
BB (first-line antianginal) or CCB
Reduce myocardial O₂ demand
BPH
Alpha-blocker (terazosin, doxazosin)
Treats both BPH and HTN
Pregnancy
Methyldopa, labetalol, nifedipine
Safe for fetus; ACEi/ARB CONTRAINDICATED
⭐ High YieldACEi + ARB = never combine (↑risk of AKI, hyperkalemia). ACEi/ARB: CONTRAINDICATED in pregnancy (teratogenic — bilateral renal agenesis). ACEi side effect: dry cough → switch to ARB.
Lifestyle Modifications (Non-Pharmacologic)
DASH Diet ↓BP by ~8–14 mmHg. Low sodium (<2.4g/day), high K+, Ca2+, Mg2+, fruits, vegetables.
Exercise Aerobic 90–150 min/week. ↓BP by ~5–8 mmHg.
Weight Loss ↓1 kg → ↓BP ~1 mmHg. Goal BMI <25.
Limit Alcohol Men ≤2 drinks/day; Women ≤1/day.
Stop Smoking Major CV risk reduction. Varenicline or NRT.
⭐ Key ConceptStable plaque = thick fibrous cap, smaller lipid core. Vulnerable plaque = thin cap, large lipid core. ACS caused by PLAQUE RUPTURE, not just stenosis. A 40% stenotic plaque can rupture and cause MI!
Troponin: Normal EKG: ST depression/T-wave inversion or normal Pattern: New onset, rest angina, crescendo angina Pathology: Plaque rupture + partial thrombus
NSTEMI
Troponin: ✅ Elevated EKG: ST depression, T-wave inversion, or normal NO ST elevation Pathology: Plaque rupture + partial thrombus
STEMI
Troponin: ✅ Elevated EKG: ≥1mm ST elevation in 2+ contiguous leads, or new LBBB Pathology: Complete occlusion, transmural ischemia
⭐ Key Troponin PointsTroponin rises 3–6h after onset, peaks at 12–24h. Use high-sensitivity troponin (serial at 0h and 3h). Troponin can also rise in PE, myocarditis, SIADH, demand ischemia (type 2 MI). UA vs NSTEMI: TROPONIN is the differentiator.
ACS Initial Management — MONA + BASH
MONA (Immediate)
M
Morphine — for pain (if no response to NTG); use cautiously
O
Oxygen — only if SpO₂ <90%! Don't give O₂ routinely
N
Nitrates — SL NTG q5 min x3; avoid if RV infarct, PDE5i use, hypotension
Artery: RCA (85%) or LCx (15%) Leads: II, III, aVF Reciprocal: I, aVL Get right-sided leads! (RV infarct)
🔵 Lateral
Artery: LCx Leads: I, aVL, V5, V6 Reciprocal: II, III, aVF Often with anterior/inferior
🟠 Posterior
Artery: LCx or RCA Leads: V7–V9 (posterior leads) Reciprocal: V1–V3 ST DEPRESSION R-wave dominant in V1–V2
🟣 Right Ventricle
Artery: RCA With inferior STEMI Leads: V1, V4R Avoid nitrates + diuretics! Give fluids.
✅ STEMI Treatment
PCI within 90 min (door-to-balloon) If no PCI: Thrombolytics within 12h if door-to-balloon >120min Absolute CI to lytics: Prior ICH, active bleed, BP >185/110
⚠️ Cocaine-Induced MI: Give phentolamine (alpha-blocker) or benzodiazepines. AVOID β-blockers — causes unopposed α-stimulation → worsens vasoconstriction!
DAPT (Dual Antiplatelet Therapy) Duration
Scenario
Regimen
Duration
Stable CAD, medical management
ASA 81mg alone
Indefinite
Stable CAD, BMS (bare metal stent)
ASA 81mg + Clopidogrel
≥1 month
Stable CAD, DES (drug eluting stent)
ASA 81mg + Clopidogrel
6–12 months
ACS (any type)
ASA 81mg + Ticagrelor (preferred) or Prasugrel
≥12 months
ACS + high bleed risk
ASA 81mg + Clopidogrel
6–12 months
⭐ P2Y12 Hierarchy in ACSTicagrelor > Prasugrel > Clopidogrel. Prasugrel: AVOID if prior TIA/stroke, age ≥75, weight <60kg. Clopidogrel: prodrug requiring CYP2C19 metabolism (poor metabolizers respond less). After PCI: NEVER stop DAPT early without cardiology consult (in-stent thrombosis risk).
HFrEF vs HFpEF
Feature
HFrEF (Systolic)
HFpEF (Diastolic)
EF
<40% (reduced)
≥50% (preserved)
HFmrEF
EF 41–49% — mildly reduced
Problem
Can't squeeze (systolic dysfunction)
Can't fill (diastolic dysfunction, stiff ventricle)
⭐ Key DifferenceNYHA = symptom severity (can go up or down). ACC/AHA Stage = disease progression (only goes forward, never backward).
GDMT — Guideline-Directed Medical Therapy for HFrEF (EF <40%)
PILLAR 1 ARNi / ACEi / ARB
Sacubitril/valsartan (Entresto) — preferred If not tolerated: ACEi or ARB ↓Mortality ~20%
PILLAR 2 Beta-Blocker
Carvedilol (α+β) Metoprolol succinate (β1) Bisoprolol (β1) ONLY these 3 have mortality benefit!
PILLAR 3 MRA
Spironolactone or Eplerenone ↓Mortality, ↓hospitalization Monitor K+; use if K+ <5.0, eGFR >30
PILLAR 4 SGLT2i
Dapagliflozin or Empagliflozin ↓Hospitalization and mortality Regardless of DM status!
⭐ Additional HFrEF AgentsIvabradine (Corlanor): HR >70 on max β-blocker, EF ≤35%, sinus rhythm. Vericiguat: Recent hospitalization, adds to GDMT. Hydralazine + Isosorbide dinitrate: If ACEi/ARB/ARNI not tolerated OR Black patients with persistent symptoms. Diuretics (furosemide): NOT proven to reduce mortality but essential for symptom relief (preload).
Device Therapy: ICD if EF ≤35% after ≥3 months GDMT. CRT if EF ≤35% + LBBB + QRS ≥150ms. LVAD for Stage D awaiting transplant.
HFpEF Management (EF ≥50%)
✅ Proven Benefit:
SGLT2i — Only proven mortality benefit in HFpEF (empagliflozin, dapagliflozin)
Diuretics — for symptom relief (edema, dyspnea)
Treat underlying HTN aggressively
Treat AFib (rate control)
Weight loss if obese
Exercise rehabilitation
❌ Not Proven in HFpEF:
ACEi/ARB — no mortality benefit (may help symptoms)
Murmur: Harsh systolic crescendo-decrescendo at LLSB
Maneuver
Effect on LVOTO
Murmur
Valsalva (strain phase)
↓Preload → WORSE obstruction
LOUDER
Standing up
↓Preload → WORSE
LOUDER
Squatting
↑Preload → BETTER
Softer
Lying flat (passive leg raise)
↑Preload → BETTER
Softer
Handgrip
↑Afterload → BETTER
Softer
Memory Trick
HOCM murmur = OPPOSITE of most other murmurs. Things that ↑preload (squatting, lying down) → LESS obstruction → softer. Things that ↓preload (Valsalva, standing) → MORE obstruction → louder.
❌ AVOID: Digoxin, vasodilators (nitrates, ACEi), diuretics (↓preload worsens LVOTO), CCBs with LVOTO (except verapamil which is ↑preload). Do NOT dehydrate HCM patients!
✅ TREAT: BB (first-line), Verapamil (alternative), Mavacamten (Camzyos — new cardiac myosin inhibitor for obstructive HCM), Disopyramide (add-on). Septal myectomy or alcohol septal ablation for refractory. ICD for high-risk patients (FH sudden death, NSVT, ↓EF, severe hypertrophy >30mm).
Takotsubo (Stress) Cardiomyopathy
Also called "Broken Heart Syndrome" or apical ballooning syndrome.
Feature
Details
Demographics
Post-menopausal women (90%)
Trigger
Emotional stress (death of loved one) or physical stress (surgery, illness)
Presentation
Mimics anterior STEMI — chest pain, ST elevation, troponin elevation
Coronary arteries
NORMAL on angiography
Echo
Apical ballooning, hyperdynamic base
Mechanism
Catecholamine surge → stunned myocardium
Prognosis
Usually resolves in weeks; recurrence 5–10%
Treatment
Supportive. BB for prevention of recurrence. Anticoagulation if apical thrombus. AVOID catecholamines (worsen).
⭐ Board PearlTroponin elevated but coronaries clean → think Takotsubo (or myocarditis). ST elevation + echo showing apical ballooning → Takotsubo not STEMI.
Dilated Cardiomyopathy (DCM) — Key Causes
Alcohol Most common reversible cause. Improves with abstinence. Dilated, ↓EF.
Peripartum Last month of pregnancy to 5 months postpartum. Often recovers with treatment.
Doxorubicin (Adriamycin) Dose-dependent cardiotoxicity. Can occur years after chemo. Check ECHO before/during chemo.
Viral Myocarditis Coxsackievirus B most common. Fever + CP + ↑troponin. MRI confirms. Supportive tx.
Hemochromatosis Iron deposition in myocardium. Treat with phlebotomy or deferoxamine.
MOA: Block Na-K-2Cl cotransporter in thick ascending loop of Henle
Use: Symptom relief in HF, pulmonary edema, hypertensive urgency
Side Effects: Hypokalemia, hypomagnesemia, hyponatremia, ototoxicity (high dose IV), hyperuricemia
Key: Torsemide has better oral bioavailability than furosemide. Metolazone combined for refractory edema.
Antianginal Agents
Nitroglycerin (NTG): NO → vasodilation (venous > arterial). Short-acting SL for acute relief. Long-acting for prevention (nitrate-free interval 10–12h to prevent tolerance).
Ranolazine: Blocks late Na+ channel → ↑Ca2+ not overloaded → ↑myocardial relaxation. Add-on for refractory angina. No effect on BP/HR.
Ivabradine: If funny (If) channel blocker → ↓HR without affecting contractility or BP. Use in stable CAD if BB intolerant.
⛔ NTG: avoid within 24h of PDE5 inhibitors (sildenafil) → profound hypotension!
Antiplatelet / Anticoagulant Quick Reference
Agent
Class
MOA
Key Points
Aspirin
Antiplatelet
Irreversible COX-1 inhibition → ↓TXA₂
81mg for CVD prevention/secondary prevention. 325mg acute ACS.
Clopidogrel
P2Y12 blocker
Irreversible P2Y12 block. Prodrug (CYP2C19).
Cheaper; poor metabolizers respond less. Hold 5d before surgery.
Ticagrelor
P2Y12 blocker
Reversible P2Y12 block (NO hepatic activation)
Preferred in ACS. CI: history of ICH, severe hepatic impairment. Hold 5d pre-surgery.
Prasugrel
P2Y12 blocker
Irreversible P2Y12 block (more potent prodrug)
Avoid: prior TIA/stroke, age ≥75, weight <60kg. Most potent P2Y12.
UFH
Anticoagulant
Activates antithrombin III → inhibits Xa + IIa
ACS, monitored by aPTT. Reversible with protamine. HIT risk.
Enoxaparin (LMWH)
Anticoagulant
Activates ATIII → mainly inhibits Xa
Monitor anti-Xa (not aPTT). Renally cleared. CI in severe renal failure. Partial reversal with protamine.
UWorld-Style Practice Questions
A 68-year-old woman with a 10-year history of type 2 diabetes and hypertension presents with a blood pressure of 156/94 mmHg on two office visits. She is currently on no medications. Her eGFR is 55 mL/min/1.73m² and urinalysis shows 2+ proteinuria. She denies chest pain, shortness of breath, or visual changes.
Q: What is the most appropriate first-line antihypertensive for this patient?
✅ ACE Inhibitor or ARB (e.g., Lisinopril or Losartan)
This patient has Stage 2 HTN, T2DM, and CKD with proteinuria. ACEi/ARBs are preferred in diabetic patients with CKD because they: • ↓Intraglomerular pressure (dilate efferent arteriole) → slow CKD progression • ↓Proteinuria • Proven mortality benefit in diabetic nephropathy
Key point: Thiazides are less effective in CKD (eGFR <30 use loop diuretics). CCBs can be added as second agent. Never combine ACEi + ARB. Monitor K+ and creatinine 1–2 weeks after starting.
A 55-year-old man presents to the ED with crushing substernal chest pain radiating to his left arm for 2 hours. EKG shows 2mm ST elevation in leads V1–V4. Troponin is elevated at 4.2 ng/mL. He receives aspirin 325mg, ticagrelor, heparin drip, and sublingual nitroglycerin. His BP is 100/70 mmHg and HR is 98 bpm. The nearest PCI-capable center is 45 minutes away.
Q: What is the next most appropriate step in management?
✅ Activate cath lab and transfer for emergent PCI (door-to-balloon within 90 minutes)
This is an anterior STEMI (V1-V4 → LAD territory). Primary PCI is the preferred reperfusion strategy if achievable within 90 minutes (door-to-balloon or first-medical-contact-to-balloon).
Since the PCI center is 45 min away (total transfer time likely <120 min), transfer for PCI is appropriate.
Thrombolytics indicated if: PCI not available within 120 minutes of first medical contact AND no contraindications (no prior ICH, BP <185/110, no active bleeding).
Note: This patient has borderline hypotension — avoid additional nitrates. Do NOT give beta-blockers with hypotension. Watch for cardiogenic shock (most common complication of anterior STEMI).
A 72-year-old woman with hypertension and obesity presents with 4 months of progressive dyspnea on exertion and bilateral ankle swelling. Echo shows EF of 60%. NT-proBNP is 650 pg/mL. BNP 85 pg/mL. She has bilateral basilar crackles and 2+ pitting edema to the knees. Her BP is 148/90 mmHg.
Q: What is the diagnosis and what medication class has proven mortality benefit?
HFpEF is diagnosed when: HF symptoms + signs of congestion + EF ≥50%.
This patient: Dyspnea, edema, crackles (congestion), EF 60% (preserved), NT-proBNP elevated (>300), underlying HTN (most common cause of HFpEF).
ONLY proven mortality benefit in HFpEF: SGLT2i (empagliflozin and dapagliflozin per EMPEROR-Preserved and DELIVER trials).
Management: • SGLT2i (first-line for mortality) • Furosemide for symptom relief • Aggressive HTN control • Weight loss • Treat AFib if present
Note: ACEi, ARB, BB, MRA do NOT have proven mortality benefit in HFpEF (unlike HFrEF).
A 22-year-old college basketball player collapses during a game. He is resuscitated and brought to the ED. His father died suddenly at age 35 "from a heart problem." Exam reveals a harsh systolic murmur at the left lower sternal border that becomes louder when he stands up and softer when he squats down. Echo shows asymmetric septal hypertrophy measuring 22mm.
Q: What is the diagnosis, and which medication is the preferred initial treatment?
Classic HOCM presentation: • Young athlete, exertional syncope • Positive family history (AD inheritance — sarcomere mutations) • Murmur LOUDER with standing/Valsalva (↓preload → worse LVOTO) • Murmur SOFTER with squatting (↑preload → less obstruction)
Treatment: • Beta-blocker (first-line) or Verapamil if BB not tolerated • Mavacamten (Camzyos) — new cardiac myosin inhibitor — approved for symptomatic obstructive HCM • ICD for prevention of SCD (this patient had SCD event!) • Septal myectomy or alcohol septal ablation for refractory cases
This patient clearly needs an ICD given survived cardiac arrest + positive family history.
A 65-year-old man with HFrEF (EF 30%) on carvedilol, lisinopril, and furosemide presents for routine follow-up. His BP is 118/76, HR 68, and he has minimal edema. He is in sinus rhythm. Labs: K+ 4.2 mEq/L, Na+ 138, eGFR 52 mL/min/1.73m².
Q: What two additional medications should be added to optimize his HFrEF management?
✅ Switch Lisinopril to Sacubitril/Valsartan (Entresto/ARNi) AND add an SGLT2 Inhibitor (Dapagliflozin or Empagliflozin)
He is currently on 2 of 4 GDMT pillars. Missing: • Pillar 1 upgrade: ARNi (sacubitril/valsartan) has greater mortality benefit than ACEi → switch (washout ACEi 36h before starting to prevent angioedema) • Pillar 3: MRA (spironolactone) — K+ 4.2 and eGFR 52 = appropriate to add • Pillar 4: SGLT2i (dapagliflozin or empagliflozin) — indicated in all HFrEF regardless of diabetes
Also consider: EF ≤35% → evaluate for ICD eligibility (this patient: EF 30%, on GDMT — if EF remains ≤35% after 3+ months, ICD indicated for primary prevention of SCD).
A 58-year-old woman presents with chest pain that occurs exclusively at rest, typically between 2–4 AM. Each episode lasts 15–20 minutes and resolves spontaneously. She smokes 1 PPD. EKG during an episode shows transient ST elevation in leads II, III, aVF. Between episodes, EKG is normal. Coronary angiography shows no significant stenosis.
Q: What is the diagnosis and first-line treatment?
Key features: • Resting chest pain (NOT exertional) • Early morning timing (2–8 AM) — circadian variation in coronary vasomotor tone • Transient ST elevation during episodes (looks like STEMI but resolves!) • Normal coronary arteries on angiography • Smoking is a major trigger (also cocaine, hyperventilation, cold exposure)
Click a medication (left), then click its matching mechanism (right).
Sacubitril/Valsartan
Ranolazine
Ivabradine
Spironolactone
Mavacamten
Blocks If (funny) channel → ↓HR only
Inhibits neprilysin + blocks AT1 receptor
Cardiac myosin inhibitor — ↓LVOTO in HCM
Blocks late Na+ channel → ↓Ca2+ overload
Blocks aldosterone receptor → K+ retention
Match the STEMI Territory to the Coronary Artery
V1–V4 ST elevation
II, III, aVF ST elevation + V4R changes
I, aVL, V5, V6
V1–V3 ST depression (reciprocal only)
RCA → inferior STEMI + RV infarct
Posterior STEMI (LCx/RCA) — get posterior leads
LAD → anterior STEMI
LCx → lateral STEMI
Match the HF Medication to its Indication/Role
Furosemide
Ivabradine
Hydralazine + Isosorbide Dinitrate
Carvedilol
Tafamidis
HFrEF + HR >70 on max β-blocker, sinus rhythm
α+β blocker — one of 3 BB with HFrEF mortality benefit
Transthyretin amyloid cardiomyopathy (ATTR)
Symptom relief only — NO mortality benefit in HF
HFrEF if ACEi/ARB/ARNI not tolerated OR Black patients
0/0
Questions answered correctly Click choices, then "Check Answer"
EKG Rhythm Recognition — 15 Questions
Q1 of 15 — What rhythm is shown?
📋 Key features: Rate 72/min · Regular R-R intervals · Upright P wave before every QRS · PR interval 160ms · Narrow QRS <80ms · Normal T waves
✅ A) Normal Sinus Rhythm (NSR)
Criteria for NSR: (1) Regular P waves at rate 60-100 bpm, (2) P wave upright in II, inverted in aVR, (3) Normal PR interval 120-200ms, (4) Every P followed by QRS, (5) Narrow QRS <120ms. Rate 72 = normal (60-100). PR 160ms = normal. Everything is within normal limits. Remember: No P wave → not sinus. Irregular → think AFib or PACs. Rate >100 → sinus tachycardia. Rate <60 → sinus bradycardia.
Q2 of 15 — What rhythm is shown?
📋 Key features: Rate 130/min · Regular · P wave before every QRS · Narrow QRS · Short TP interval (P waves may appear to "ride" the T waves at higher rates)
✅ B) Sinus Tachycardia
Rate 100-150 bpm + normal P waves before every QRS = Sinus Tachycardia. Distinguishing from SVT: sinus tach has visible upright P waves (not buried/retrograde), gradual onset/offset, and commonly has an underlying cause (fever, pain, anxiety, hypovolemia, hypoxia, PE, anemia, medications). Clinical pearl: Sinus tachycardia is a RESPONSE — always find the cause. Treatment = treat the cause, NOT the rhythm itself. Never cardiovert sinus tachycardia!
Q3 of 15 — What rhythm is shown?
📋 Key features: Rate 42/min · Regular · Normal P wave before each QRS · Normal PR interval · Narrow QRS · Long R-R intervals
✅ C) Sinus Bradycardia
Rate <60 + normal P before every QRS = Sinus Bradycardia. Common causes: athletes (physiologic), vagal tone, hypothyroidism, hypothermia, inferior MI (RCA supplies SA node), medications (β-blockers, CCBs, digoxin, amiodarone). Symptomatic bradycardia (AMS, hypotension, CP, acute HF) → ACLS bradycardia algorithm: Atropine 0.5mg IV first, then TCP or dopamine/epinephrine drip if atropine fails. Key differentiator from 3rd degree block: Every P is followed by a QRS with constant PR interval.
Q4 of 15 — What rhythm is shown?
📋 Key features: Irregularly IRREGULAR rhythm · No distinct P waves · Fine fibrillatory baseline · Narrow QRS complexes at variable intervals · No consistent R-R pattern
✅ A) Atrial Fibrillation
Classic triad: (1) Irregularly irregular rhythm, (2) No distinct P waves (replaced by chaotic fibrillatory baseline), (3) Narrow QRS (unless aberrant conduction or WPW). Most common sustained arrhythmia. Management: Unstable → synchronized cardioversion. Stable → rate control (BB or diltiazem). CHA₂DS₂-VASc ≥2 → anticoagulation (DOACs preferred: apixaban, rivaroxaban, dabigatran). Don't confuse with: MAT has 3+ distinct P wave morphologies; Flutter has regular sawtooth waves; frequent PACs still has underlying sinus P waves with normal beats between ectopics.
Q5 of 15 — What rhythm is shown?
📋 Key features: Regular sawtooth-pattern between QRS complexes · Atrial rate ~300/min · Ventricular rate ~150/min · 2:1 block · Narrow QRS · Best seen in inferior leads (II, III, aVF)
✅ C) Atrial Flutter with 2:1 block
Classic features: Sawtooth flutter waves (F waves) at 300 bpm. AV node usually conducts every 2nd (2:1 → rate 150), 3rd (3:1 → rate 100), or 4th wave (4:1 → rate 75). Clinical pearl: Unexplained rate of exactly 150 bpm → think flutter with 2:1 block! Look for "hidden" flutter waves in the T waves or ST segment. Can look like sinus tach. Get vagal maneuvers or adenosine to slow the rate and reveal flutter waves. Management same as AFib (rate control, anticoagulation, cardioversion if unstable).
Q6 of 15 — What rhythm is shown?
📋 Key features: Rate 185/min · Regular · Narrow QRS complexes · No visible P waves (buried in QRS or just after) · Abrupt onset · Retrograde P waves may appear just after QRS
✅ C) SVT — Supraventricular Tachycardia (AVNRT most common)
Narrow complex tachycardia at 150-250 bpm, abrupt onset/offset, P waves not visible (buried in QRS) or just after QRS (retrograde P, called "pseudo-r'" in V1 or "pseudo-S" in II). AVNRT: AV node re-entry — most common SVT. AVRT: Accessory pathway (WPW). Treatment: Stable → Vagal maneuvers first → Adenosine 6mg IV rapid push (flush fast!) → 12mg x2. Unstable → Synchronized cardioversion 50-100J. Rate 150 with P waves hidden → think SVT vs flutter. Key: adenosine will terminate SVT but only slow flutter temporarily (revealing flutter waves).
Q7 of 15 — What rhythm is shown?
📋 Key features: Rate 158/min · Regular · Wide QRS complexes (>120ms) · Monomorphic wide complex tachycardia · AV dissociation (independent P waves "marching through") · Fusion and capture beats
✅ B) Ventricular Tachycardia (VT)
Wide complex tachycardia = VT until proven otherwise! Criteria for VT: (1) AV dissociation (P waves independent of QRS — most specific finding), (2) Fusion beats (partial capture), (3) Capture beats, (4) QRS >140ms, (5) Extreme axis deviation (northwest axis). Brugada Criteria: If no RS complex in any V lead → VT. Management: Pulseless VT → ACLS cardiac arrest (defibrillate). VT with pulse, unstable → Synchronized cardioversion 100J. Stable → Amiodarone 150mg IV over 10 min, Lidocaine 1-1.5mg/kg. Never give adenosine to wide complex tachycardia unless certain it's SVT!
Q8 of 15 — What rhythm is shown? (Patient is unresponsive, no pulse)
📋 Key features: Chaotic disorganized waveform · No identifiable P waves, QRS, or T waves · Irregular amplitude and frequency · Rapid undulations · No organized electrical activity
✅ B) Ventricular Fibrillation (VF)
VF = chaotic disorganized electrical activity, no effective cardiac output, IMMEDIATELY FATAL without treatment. Immediate action: SHOCK FIRST (200J biphasic), then CPR 2 min, then recheck rhythm. While CPR ongoing: Epinephrine 1mg IV q3-5min, Amiodarone 300mg (or Lidocaine 1-1.5mg/kg) for refractory VF. Differentiating from artifact: VF has consistent chaos even when you move leads; patient is unresponsive; no pulse. Torsades: twisting QRS axis you can see morphology changing. Fine VF can look like asystole — treat as VF if any doubt.
Q9 of 15 — What rhythm is shown?
📋 Key features: Rate 65/min · Regular · P wave before every QRS · Every P is followed by QRS · PR interval consistently prolonged at 260ms · Narrow QRS
✅ B) First-degree AV Block
Prolonged PR interval >200ms (0.20 seconds = 5 small boxes) + every P followed by QRS = 1st degree AV block. NOT a true "block" — conduction is just slowed (usually at AV node). All beats still conduct; just delayed. Causes: Increased vagal tone (athletes), inferior MI (RCA → AV node blood supply), medications (β-blockers, CCBs, digoxin, amiodarone), electrolyte disturbances. Management: Usually benign, no treatment needed. Monitor. Stop/adjust offending medications if symptomatic or PR very prolonged. Does not require pacing.
Q10 of 15 — What rhythm is shown?
📋 Key features: Progressive PR lengthening → dropped QRS → cycle resets · "Group beating" pattern · Narrow QRS in conducted beats · P-P interval constant · R-R intervals get shorter then suddenly lengthen after the dropped beat
✅ B) Mobitz Type I (Wenckebach) — 2nd Degree AV Block
Classic pattern: PR gets LONGER and LONGER until one P wave doesn't conduct (no QRS) → cycle resets with short PR. "Longer, longer, longer, drop — then you have a Wenckebach!" R-R intervals SHORTEN leading up to the dropped beat (despite PR lengthening). Location: AV node (benign). Causes: Inferior MI, increased vagal tone, medications, myocarditis. Management: Usually benign — monitor. If symptomatic → Atropine. Rarely needs pacing (compare to Mobitz II which is more dangerous and DOES need pacing). Key differentiator from Mobitz II: In Wenckebach, PR progressively lengthens. In Mobitz II, PR is CONSTANT then sudden drop.
Q11 of 15 — What rhythm is shown?
📋 Key features: Constant PR interval in conducted beats · Sudden dropped QRS with no warning · P wave not followed by QRS (without prior PR prolongation) · Wide QRS complexes in conducted beats · Unpredictable
✅ B) Mobitz II — 2nd Degree AV Block
Classic pattern: CONSTANT PR interval → sudden unexpected dropped QRS. No progressive PR prolongation. Location: Below AV node (His bundle or bundle branches) → more dangerous. Wide QRS in conducted beats. This is dangerous — can progress suddenly to complete (3rd degree) AV block or asystole without warning. Causes: Anterior MI (septal infarct destroys bundle branches), Lyme disease, myocarditis, infiltrative disease. Management: PACEMAKER indicated (transvenous/permanent). Atropine often ineffective (infranodal block). Transcutaneous pacing as bridge. Never rely on atropine alone for Mobitz II. MemoryAid: Mobitz I = AV node (node is friendly, Wenckebach is benign). Mobitz II = Below AV node (more serious = pacemaker).
Q12 of 15 — What rhythm is shown?
📋 Key features: P waves and QRS complexes completely INDEPENDENT of each other · Regular P-P interval (~rate 80) · Regular R-R interval (~rate 35, slow) · No consistent PR relationship · Wide, slow QRS (ventricular escape)
✅ B) Third-degree (Complete) AV Block
Complete AV dissociation: No impulses conduct from atria to ventricles. P waves "march through" QRS complexes at their own regular rate. Ventricles maintain escape rhythm: junctional escape (narrow QRS, rate 40-60) or ventricular escape (wide QRS, rate 20-40). This is a medical emergency! Patient is usually symptomatic: syncope, hemodynamic compromise, bradycardia. Causes: Inferior MI (right coronary artery → AV node), Lyme disease, medication toxicity (β-blockers, digoxin), congenital, degenerative disease (Lev's/Lenègre). Management: Transcutaneous pacing IMMEDIATELY → Transvenous pacing → Permanent pacemaker. Atropine only if narrow escape rhythm (junctional). IV epinephrine or dopamine as bridge.
Q13 of 15 — What is this bundle branch block?
📋 Key features: Wide QRS >120ms · Broad notched "M-shaped" R wave in leads I, aVL, V5-V6 · No septal Q waves in I or V5-V6 · rS pattern in V1-V2 · ST and T waves are discordant (opposite direction to QRS) in V5-V6
✅ B) Left Bundle Branch Block (LBBB)
LBBB Criteria: (1) QRS ≥120ms, (2) Broad notched or slurred R in I, aVL, V5-V6 ("M" or notched pattern), (3) rS or QS in V1-V3, (4) No septal Q waves in I, V5-V6, (5) ST/T discordance. Clinical importance: New LBBB + chest pain = STEMI equivalent → activate cath lab (Sgarbossa criteria help if needed). Causes: Hypertension (most common), CAD, cardiomyopathy, aortic stenosis. LBBB invalidates ST-segment interpretation for ischemia (everything is distorted). Memory trick: WiLLiaM MaRRoW → W pattern in V1 = LBBB; M pattern in V1 = RBBB... wait that's reversed. Try: "LBBB: lateral leads (I, V5-V6) show broad R; V1 shows rS" = turn it Left → "WiLL" → W in V1, M in lateral.
Q14 of 15 — What is this bundle branch block?
📋 Key features: Wide QRS >120ms · RSR' pattern ("rabbit ears" or "M" pattern) in V1-V2 · Wide, slurred S wave in leads I, V5-V6 · Normal septal Q waves may be present · T wave discordance in V1-V2
✅ B) Right Bundle Branch Block (RBBB)
RBBB Criteria: (1) QRS ≥120ms, (2) RSR' ("rabbit ears" or "M" shape) in V1 or V2, (3) Wide/slurred S in I, V5-V6, (4) T wave inversion in V1-V3. RBBB is often incidental and benign. Causes: Normal variant, PE (acute cor pulmonale), ASD, anterior MI (septal branch), Brugada syndrome. Memory trick: MaRRoW → M in V1 = RBBB; W in V1 = LBBB. Or: R has right angles and RSR' looks like R pattern in V1. New RBBB + anterior MI = proximal LAD occlusion (bifascicular block). Brugada pattern: RBBB + ST elevation in V1-V3 = risk of sudden cardiac death → ICD.
Q15 of 15 — What is shown on this EKG?
📋 Key features: Short PR interval <120ms · Delta wave (slurred upstroke of QRS) · Wide QRS >120ms (pseudo-wide) · These features cause secondary ST/T changes · Patient may have paroxysmal SVT or wide complex AFib
✅ C) Wolff-Parkinson-White (WPW) — Ventricular Pre-excitation
WPW Triad: (1) Short PR <120ms (bypasses AV node delay), (2) Delta wave (slurred QRS upstroke from early ventricular activation), (3) Wide QRS. Mechanism: Accessory pathway (Bundle of Kent) allows impulses to bypass AV node and pre-excite the ventricle. Risk: If AFib develops + WPW → rapid conduction down accessory pathway → VF and sudden cardiac death! AVOID AV-nodal blockers in WPW + AFib: adenosine, verapamil, diltiazem, β-blockers (can increase conduction through accessory pathway → VF). Treatment of WPW + AFib: Procainamide IV or cardioversion. Definitive: Radiofrequency catheter ablation of accessory pathway (curative).
ACLS — Advanced Cardiovascular Life Support Algorithms
VF / Pulseless VT — SHOCKABLE RHYTHM
↓
1. Start High-Quality CPR immediately Push hard (≥2 inches adult), push fast (100–120/min), allow full recoil, minimize interruptions (<10 sec), no hyperventilation (10 breaths/min), 30:2 ratio if 1 rescuer
↓
2. Attach defibrillator — confirm VF/pVT Deliver SHOCK: Biphasic 200J (or device-specific energy), Monophasic 360J Resume CPR IMMEDIATELY after shock — do not check pulse first
↓
3. CPR × 2 minutes + establish IV/IO access
↓
💊 Epinephrine 1mg IV/IO — give as soon as IV/IO established, repeat every 3–5 min No evidence for routine bicarb, calcium, or atropine in VF/VT
↓
Rhythm check: Still shockable?
✅ YES → Shock again (same energy or escalating) → CPR × 2 min → Continue cycles
❌ NO → PEA/Asystole → See non-shockable algorithm OR ROSC → Post-arrest care
↓ (if still shockable after 2nd shock)
💊 Amiodarone 300mg IV/IO (first dose) — for refractory VF/pVT Second dose: 150mg if VF/VT persists Alternative: Lidocaine 1–1.5mg/kg IV (then 0.5–0.75mg/kg q5-10min, max 3mg/kg) Amiodarone or Lidocaine — either can be used (no proven mortality difference)
↓
Consider and treat reversible causes (H's & T's) throughout
⭐ HIGH-YIELD ACLS PEARLS:
• CPR quality is the #1 determinant of survival
• Minimize interruptions — hands off <10 seconds for rhythm checks and shocks
• Push hard enough to depress sternum 2–2.4 inches (5–6 cm)
• Epinephrine improves ROSC rates but not neurological survival
• Drug delivery: Push IV bolus, then 20mL flush, elevate arm 10–20 seconds
• After ROSC: 12-lead EKG, targeted temperature management, consider PCI
PEA / Asystole — NON-SHOCKABLE RHYTHM
⚠️ Asystole: Confirm in 2 leads. Check connections. Treat as non-shockable. PEA (Pulseless Electrical Activity): Organized electrical activity but NO palpable pulse. Always has an underlying cause.
↓
1. Start High-Quality CPR immediately
↓
💊 Epinephrine 1mg IV/IO — as soon as possible, ASAP! Repeat every 3–5 min (Earlier epinephrine in non-shockable rhythms → improved ROSC rates)
✅ YES → Switch to shockable algorithm (VF/VT) → Shock
❌ NO (still PEA/asystole) → Continue CPR cycles with Epi q3-5min
↓
THROUGHOUT: Identify and treat reversible causes (H's & T's)
Consider specific antidotes:
• Suspected hyperkalemia: Calcium chloride 1g or calcium gluconate 3g IV
• Severe acidosis/TCA overdose: Sodium bicarbonate 1 mEq/kg IV
• Suspected PE: Consider thrombolytics (tPA 50mg IV) — CPR 60–90 min after
• Tamponade: Pericardiocentesis
• Tension pneumo: Needle decompression 2nd ICS MCL or 4th/5th ICS AAL
⭐ PEA vs Pseudo-PEA: True PEA = no cardiac activity on echo. Pseudo-PEA = some cardiac activity but insufficient output (may respond to aggressive treatment). Bedside echo during CPR pulse check is valuable — can identify tamponade, severe hypovolemia, massive PE.
Bradycardia — HR <60 bpm
↓
Is the patient symptomatic? (Hypotension, AMS, chest pain, signs of shock, acute HF)
NO — Asymptomatic Observe and monitor Search for underlying cause Consider medication review
YES — Symptomatic ↓ Treat IMMEDIATELY
↓ (symptomatic)
💊 Step 1: Atropine 0.5mg IV — repeat every 3–5 min, max 3mg total First-line for most symptomatic bradycardias ⚠️ Atropine NOT effective for Mobitz II or 3rd degree block (infranodal) — go straight to pacing!
↓ (if atropine insufficient)
Step 2: Transcutaneous Pacing (TCP) • Set rate 60–80 bpm • Increase mA until electrical capture (QRS after each pacing spike) • Verify mechanical capture (palpate pulse at femoral or use pleth) • Sedate patient if conscious (TCP is painful)
Alternative: Dopamine infusion 2–20 mcg/kg/min IV Or: Epinephrine infusion 2–10 mcg/min IV (Use as bridge if TCP unavailable or while preparing transvenous pacing)
Irregular? → AFib: rate control (diltiazem, β-blockers), anticoagulation, consider cardioversion. Flutter: rate control or cardioversion.
WIDE COMPLEX (≥120ms)
Regular? → Probable VT: Amiodarone 150mg over 10 min → Lidocaine → procainamide. If SVT with aberrancy suspected: adenosine (only if regular, monomorphic)
Irregular? → AFib+WPW: Procainamide or cardioversion (NO adenosine/digoxin/CCBs/BBs). Torsades: Magnesium 2g IV, correct QT-prolonging agents.
⭐ ADENOSINE RULES: 6mg IV rapid push directly into antecubital vein + immediate 20mL NS flush + elevate arm. Half-life = 10 SECONDS. Works on AV node (terminates SVT, slows AFib/flutter briefly to reveal flutter waves). NEVER use in WPW+AFib (can cause VF). CAUTION in severe asthma (bronchoconstriction).
🩸 Hemodynamics • Target SBP ≥90 mmHg • MAP ≥65–70 mmHg • IV fluids for hypotension • Vasopressors: Norepinephrine or Dopamine
❤️ 12-Lead EKG • Immediately after ROSC • STEMI or new LBBB? → Emergent PCI • Consider PCI even without ST elevation if cardiac cause suspected
🧠 Targeted Temperature Management (TTM) • For comatose survivors • Target core temp 32–36°C × 24h • Prevent fever (≥38°C) for 72h post-arrest
💊 Post-ROSC Medications: Vasopressors for shock: Norepinephrine 0.1–0.2 mcg/kg/min IV. If bradycardia: Dopamine 5–10 mcg/kg/min or Epinephrine 0.1–0.5 mcg/kg/min. Continue amiodarone infusion (1mg/min × 6h, then 0.5mg/min × 18h) if given during arrest for VF/VT.
5 H's & 5 T's to identify after ROSC: Look for correctable causes: Labs (K+, glucose, lactate, troponin, CBC), CXR, 12-lead EKG, POCUS (echo, lung), CT head if neurological cause suspected.
Reversible Causes of Cardiac Arrest — H's & T's
5 H's
Cause
Clue/Fix
Hypoxia
Low SpO₂, cyanosis → 100% O₂, intubate
Hypovolemia
Hemorrhage, dehydration, PE → IV fluids, blood products, stop bleeding
H+ (Acidosis)
ABG pH <7.1, DKA, sepsis, shock → NaHCO₃, treat cause
⭐ Memory trick: H's = things you put IN the body (oxygen, fluids, bicarb, potassium, warmth). T's = things you take OUT or undo (needle for pneumo, needle for tamponade, antidote for toxin, cath for thrombosis).
ACLS Drug Quick Reference
Drug
Indication
Dose
Notes
Epinephrine
Cardiac arrest (any rhythm)
1mg IV/IO q3–5min
Vasopressor — ↑aortic diastolic pressure → coronary perfusion during CPR
NON-SHOCKABLE (Asystole/PEA) Most common peds arrest = ASPHYXIAL → fix hypoxia first!
1. CPR immediately
2. Epinephrine 0.01 mg/kg IV/IO q3–5min (ASAP)
3. Optimize airway/ventilation (100% O₂)
4. Treat H's & T's (hypoxia #1 cause)
5. Consider IO access if no IV within 60 sec
⭐ Key PALS Concepts:
• Pediatric cardiac arrest is almost always SECONDARY to respiratory failure or shock (vs adults where primary cardiac is more common)
• Fix the airway first! Most pediatric arrests are hypoxic in origin
• IO access (tibial or humeral) if IV not obtained within 60 seconds
• Vasovagal rarely causes pediatric arrest; consider structural heart disease (HCM, congenital anomalies)
• Hypoglycemia is common during pediatric arrest — check glucose!
Pediatric Bradycardia (HR <60 with poor perfusion)
⚠️ Key PALS Rule: HR <60 WITH signs of poor perfusion (AMS, cyanosis, hypotension) despite adequate oxygenation/ventilation → START CPR! Unlike adults, the threshold to start CPR for bradycardia is lower in infants and children because they are more heart rate–dependent for cardiac output.
↓
1. First — optimize oxygenation and ventilation! • Apply 100% O₂ via NRB or BVM • Ensure airway open; suction secretions • Many pediatric bradycardias are hypoxic in origin — this alone may resolve the bradycardia
↓
Still bradycardic with poor perfusion despite O₂?
↓ YES
💊 Epinephrine 0.01 mg/kg IV/IO (max 1mg) — repeat q3–5min 💊 Atropine 0.02 mg/kg IV/IO (min 0.1mg, max 0.5mg per dose, max 1mg total) — for increased vagal tone or primary AV block May repeat atropine once
↓
If no response → Cardiac Pacing: Transcutaneous pacing (painful, sedate if possible). Transvenous pacing if TCP ineffective. Consider pacing if complete heart block, Lyme carditis, congenital heart disease.
Hemodynamically UNSTABLE? (Altered LOC, severe respiratory distress, poor perfusion)
UNSTABLE → Synchronized Cardioversion 0.5–1 J/kg (first attempt) 2 J/kg (subsequent attempts)
Sedate/analgesia if possible
If unable to sync or Torsades → defibrillate (unsynchronized)
SVT (most common narrow complex tachycardia in children): • Infants: HR typically 220–300 bpm (often mistaken for sinus tachy!) • Children: HR typically 180–240 bpm • Abrupt onset/offset, no P waves or retrograde P waves • Sinus tach usually <220 infants, <180 older children, has gradual rate variation
SVT Management (stable):
1. Vagal maneuvers — ice bag to face (diving reflex) for infants; Valsalva for older children
2. Adenosine 0.1 mg/kg IV rapid push (max first dose 6mg, max second dose 12mg) + 5–10mL NS flush
3. If adenosine fails or refractory: Amiodarone 5 mg/kg over 20–60 min; OR Procainamide 15 mg/kg over 30–60 min
Wide Complex Tachycardia (VT in children): • Less common than in adults • Causes: Prolonged QT, congenital heart disease, channelopathies, electrolyte abnormalities, myocarditis • Treat as VT: Amiodarone 5 mg/kg IV over 20–60 min OR Procainamide 15 mg/kg IV over 30–60 min • Torsades: Magnesium 25–50 mg/kg IV (max 2g)
Pediatric Shock Recognition & Management
Shock in children: Compensated shock (tachycardia + poor perfusion, but normal BP — children COMPENSATE well until decompensation) vs Hypotensive shock (decompensated = urgent). Normal pediatric BP: Systolic ≥70 + (2 × age in years) mmHg
⚠️ Weight-based dosing: Always calculate based on actual body weight (or estimated weight if unavailable). Use Broselow tape for quick weight estimation. Maximum doses apply — do not exceed adult doses.
Drug
Indication
Dose
Max
Notes
Epinephrine
Cardiac arrest, anaphylaxis, bradycardia
0.01 mg/kg IV/IO 1:10,000 solution = 0.1 mL/kg
1mg
q3–5min in arrest. Anaphylaxis: IM 0.01mg/kg (1:1000)
Atropine
Symptomatic bradycardia, vagal, RSI pretreatment
0.02 mg/kg IV/IO
0.5mg/dose; 1mg total
Minimum dose 0.1mg (paradoxical bradycardia with lower doses)
Adenosine
SVT
0.1 mg/kg IV rapid push
6mg (1st), 12mg (2nd)
Must give rapid IV push + flush immediately
Amiodarone
VF/pVT (arrest), VT, SVT refractory
5 mg/kg IV/IO (arrest: rapid; stable: over 20–60 min)
300mg
Can repeat to max 15 mg/kg/day
Lidocaine
VF/pVT (arrest alternative), VT
1 mg/kg IV/IO
3mg/kg max
Infusion: 20–50 mcg/kg/min. Monitor for toxicity.
Magnesium
Torsades de Pointes, hypomagnesemia
25–50 mg/kg IV
2g
For torsades: rapid push. Slow infusion 15–30 min for stable.
Minimum Systolic BP Formula: ≥70 + (2 × age in years) mmHg for children >1 year old. Below this = hypotensive shock. Broselow Tape: Measures child's length to estimate weight and provide color-coded drug doses — use in ALL pediatric codes.
HOCM vs MVP: Both get worse with ↓ preload and better with ↑ preload — opposite of most valvular murmurs. "Empty heart = bad for both." HOCM heard at LSB/apex. AS heard at RUSB.
Matching — Valve Lesion Identification
Match each clinical finding (left) to the correct valve lesion (right):
Crescendo-decrescendo systolic murmur at RUSB radiating to carotids; syncope; pulsus parvus et tardus
Mitral Regurgitation
Opening snap + low-pitched diastolic rumble at apex; history of rheumatic fever; AFib
Aortic Stenosis
Holosystolic blowing murmur at apex radiating to axilla; S3; laterally displaced hyperdynamic PMI
Mid-systolic click that moves earlier with Valsalva and later with squatting; young woman
Aortic Regurgitation
UWorld/PANCE-Style Questions — Valvular Disease
Q1 — Aortic Stenosis Management
A 72-year-old man has a harsh crescendo-decrescendo systolic murmur at the RUSB radiating to the neck, exertional syncope, and an echocardiogram showing AVA 0.8 cm². What is the most appropriate next step?
B) Aortic Valve Replacement (AVR) — Severe symptomatic AS (SAD: Syncope, Angina, Dyspnea). AVA <1cm² = severe. Once symptomatic: syncope → 3yr survival, HF → 1-2yr survival without AVR. TAVR if high surgical risk. AVOID vasodilators (fixed obstruction → dangerous hypotension). BBs can also precipitate acute decompensation. Definitive treatment = valve replacement.
Q2 — Mitral Valve Prolapse Maneuvers
A 26-year-old woman has a mid-systolic click at the apex. When she squats, the click moves later in systole. Which best explains this?
C) Squatting increases preload → leaflet prolapses LATER. MVP click timing = LV volume: ↑ Volume (squatting, supine) → LV full → better leaflet support → click moves toward S2 (later), murmur shorter. ↓ Volume (standing, Valsalva) → LV empty → earlier prolapse → click moves toward S1 (earlier), murmur longer/louder. Opposite of what you might expect. HOCM has same directional response as MVP (both worse with empty LV).
Q3 — Right-Sided Endocarditis
A 32-year-old IV drug user has 3 weeks of fever, a holosystolic murmur at the LLSB that increases with inspiration, JVD, and pulsatile hepatomegaly. Blood cultures grow S. aureus. Which valve is affected?
C) Tricuspid valve — S. aureus. IVDU → right-sided endocarditis → tricuspid valve. TR murmur = holosystolic at LLSB, increases with inspiration (Carvallo sign). JVD + pulsatile hepatomegaly = right heart signs. S. aureus = most virulent, most common in acute IE and IVDU. Classic complication: septic pulmonary emboli (bilateral cavitary infiltrates on CXR). Treatment: Oxacillin or vancomycin (if MRSA) x 6 weeks.
Q4 — Aortic Regurgitation Signs
A 50-year-old man has a diastolic decrescendo murmur at the LSB, BP 160/52, and a mid-diastolic rumble at the apex without mitral stenosis. Which peripheral sign is IMMUNE-MEDIATED (not embolic)?
C) Osler nodes = immune complex mediated. IE peripheral findings: Osler nodes = PAINFUL fingertip/toe nodules = immune complex (minor Duke criterion). Janeway = PAINLESS hemorrhagic lesions on palms/soles = septic emboli. Splinter hemorrhages = septic emboli. Roth spots = retinal with white center = immune complex. "Osler = Ouch = immune." The AR murmur here + Austin Flint murmur (AR jet vibrating anterior MV leaflet = mid-diastolic rumble) + wide pulse pressure = classic AR. AR causes wide pulse pressure (BP 160/52 = 108 PP).
Q5 — Mitral Stenosis Intervention
A 35-year-old woman with rheumatic mitral stenosis (MVA 1.1 cm², heavily calcified valve, no MR) develops worsening dyspnea and new AFib. What is the most appropriate intervention for her MS?
B) Mitral valve replacement. MVA <1.5cm² = severe MS requiring intervention. However, balloon valvuloplasty (PMBV) is CONTRAINDICATED when the valve is heavily calcified (won't open properly) or when significant MR is present. PMBV ideal: pliable valve, no calcification, no significant MR, no LA thrombus. Since PMBV not feasible → MVR. Also: AFib in MS → anticoagulate (DOAC or warfarin). Rate control with BB or diltiazem (avoid digoxin as monotherapy — doesn't adequately control rate with exertion).
Q6 — Murmur with Hand Grip
A 68-year-old man has a systolic ejection murmur at the RUSB that decreases with isometric hand grip exercise. Which condition does this most likely represent?
C) Aortic Stenosis. RUSB + systolic ejection murmur = AS. Hand grip → ↑ afterload → ↑ LV pressure → less gradient across fixed aortic valve obstruction → AS murmur SOFTER. Compare: MR = hand grip → ↑ afterload → more backflow → MR louder. HOCM = hand grip → ↑ preload/afterload → less outflow obstruction → HOCM softer (but heard at LSB/apex, not RUSB). RUSB + radiates to carotids + ejection quality + decreases with hand grip = classic AS.
Symptoms: Young patient, recent viral URI prodrome (1-2 wks prior), chest pain, dyspnea, fatigue, palpitations, fever
Findings: ↑ Troponin, ↑ BNP, new dilated cardiomyopathy (EF↓), diffuse LV dysfunction. Cardiac MRI: late gadolinium enhancement (gold standard for diagnosis). ECG: diffuse ST changes or heart block.
Tx: Supportive (rest, avoid NSAIDs in first 3 months). GDMT for HFrEF if EF↓. ICD if EF stays <35%.
🦠 Infective Endocarditis
Organisms: S. viridans (subacute, dental, native valve), S. aureus (#1 acute; IVDU, prosthetic), Enterococcus (GI/GU procedures), HACEK (culture-negative), S. bovis/gallolyticus → COLONOSCOPY (colon cancer!)
Duke Criteria: 2 major OR 1 major + 3 minor OR 5 minor = definite IE
Major: (+) blood cx x2, echo vegetation/abscess/new regurg
Minor: fever, vascular phenomena, immunologic phenomena, predisposing heart disease, IVDU
Hypotension, dyspnea, distant heart sounds. Often post-procedure, trauma, malignancy, or uremia
Beck Triad: JVD + Muffled heart sounds + Hypotension. Pulsus paradoxus (>10 mmHg drop in SBP with inspiration). EKG: low voltage + electrical alternans (QRS alternates height). Echo: RA/RV collapse, swinging heart.
Pericardiocentesis (emergent). Avoid diuretics/vasodilators. Maintain HR and preload (IV fluids). Avoid intubation if possible (↓ preload kills these patients).
Aortic Dissection
Sudden, severe "tearing" or "ripping" chest/back pain in hypertensive patient. Pain often maximal at ONSET (vs MI which builds gradually)
Unequal blood pressures in arms (>20mmHg difference). Widened mediastinum on CXR (>8cm or >50% chest width). Pulse deficit. AR murmur if Type A extends to aortic root. CT angiography = gold standard.
Stanford A (ascending aorta) → EMERGENCY SURGERY. Stanford B (descending only) → Medical management: IV labetalol or esmolol (↓HR <60, ↓SBP <120). Nitroprusside for BP but ONLY after BB.
Rheumatic Heart Disease
2-6 weeks after Group A Strep pharyngitis (Strep pyogenes). Children/young adults. Mitral stenosis most common late sequela.
Jones Criteria: MAJOR: Carditis, Polyarthritis, Chorea (Sydenham), Erythema marginatum, Subcutaneous nodules. MINOR: Fever, ↑ESR/CRP, prolonged PR interval. Diagnosis: 2 major OR 1 major + 2 minor + evidence of preceding Strep infection (ASO titer, throat culture)
Penicillin for Strep eradication. ASA/NSAIDs for arthritis. Steroids for severe carditis. Penicillin prophylaxis for years (prevents recurrence → prevents further valve damage).
Cardiac Contusion
Blunt chest trauma (MVC steering wheel injury, fall from height). RV most vulnerable (anterior position)
Most common dysrhythmia: sinus tachycardia, PVCs, afib, VT. EKG: new RBBB, ST changes, arrhythmias. Troponin elevated. Echo: wall motion abnormalities.
Continuous cardiac monitoring x 24-48h. Treat arrhythmias. Anticoagulation controversial (bleeding risk). IABP or surgical repair if severe LV dysfunction.
Endocarditis Prophylaxis Indications (AHA): Prosthetic valves, previous IE, certain congenital heart defects (unrepaired cyanotic, repaired with residual defects), cardiac transplant with valvulopathy. Procedure: Dental procedures causing gingival manipulation. Drug: Amoxicillin 2g PO 30-60 min before. If PCN allergic: Clindamycin 600mg or azithromycin 500mg.
A 22-year-old man presents with sharp chest pain that is worse when lying flat and relieved by sitting forward. He had a flu-like illness 2 weeks ago. Temperature is 38.2°C. EKG shows diffuse ST elevation that is concave upward in multiple leads with PR depression. Troponin is mildly elevated. Echocardiography shows a small pericardial effusion but no cardiac tamponade. What is the most appropriate initial treatment?
✅ B) Ibuprofen + colchicine
This is acute pericarditis: pleuritic chest pain relieved sitting forward, friction rub, diffuse saddle-shaped ST elevation with PR depression, recent viral illness. First-line treatment is NSAID (ibuprofen 600mg TID x 2 weeks) + colchicine 0.5mg BID x 3 months — colchicine dramatically reduces recurrence rate (50% → 10%).
❌ Steroids: reserved for refractory/recurrent cases ONLY — steroids increase recurrence risk if given early. ❌ Pericardiocentesis: only if large effusion causing tamponade. The elevated troponin indicates some myopericarditis (inflammation of epicardium/myocardium) — restrict physical activity until CRP normalizes.
Question 2 of 6
A 45-year-old man with end-stage renal disease on hemodialysis presents with worsening dyspnea and hypotension. He missed his last two dialysis sessions. Exam: BP 82/60 mmHg, HR 118/min, JVP elevated, heart sounds distant and muffled. EKG shows low-voltage QRS complexes that alternate in height. Bedside ultrasound shows a large pericardial effusion with RV collapse during diastole. What is the next best step?
Pericardiocentesis is the only definitive treatment. Remove fluid → immediately restores cardiac output. While preparing: IV fluids to maintain preload (NOT diuretics — furosemide would kill this patient by reducing preload). Avoid anything that drops heart rate or preload.
Cause here: uremic pericarditis (ESRD + missed dialysis = classic). Dialysis can be done after stabilization. Electrical alternans = QRS amplitude alternates due to heart "swinging" in large effusion — pathognomonic for tamponade.
Question 3 of 6
A 68-year-old man presents with 3 weeks of fever, fatigue, and weight loss. He had a dental cleaning 6 weeks ago and has a known bicuspid aortic valve. Exam reveals temperature 38.6°C, a new aortic regurgitation murmur, and painless erythematous lesions on both palms. Blood cultures (3 sets) grow Streptococcus viridans. Which of the following peripheral findings is IMMUNE COMPLEX-mediated (not septic emboli)?
✅ C) Osler nodes
Peripheral manifestations of IE: • Osler nodes = PAINFUL raised nodules on fingertips/toes = immune complex deposition (minor Duke criterion "immunologic phenomena") • Janeway lesions = PAINLESS flat hemorrhagic lesions on palms/soles = septic emboli (major Duke criterion "vascular phenomena") • Splinter hemorrhages = under nails, septic emboli • Roth spots = retinal hemorrhages with white centers, immune complex
This is subacute IE: S. viridans (dental source), native valve (bicuspid AV), 3+ weeks course. Treatment: Penicillin G IV x 4-6 weeks (or ceftriaxone). Add gentamicin for synergy in first 2 weeks.
Question 4 of 6
A 52-year-old hypertensive man presents to the ED with sudden severe "ripping" chest pain that radiates to his back and started 30 minutes ago. BP is 188/96 in the right arm and 154/82 in the left arm. CXR shows a widened mediastinum. CT angiography reveals involvement of the ascending aorta. What is the most appropriate management?
✅ C) Emergency surgical repair
This is Type A aortic dissection (ascending aorta involved — Stanford A, DeBakey I or II) = surgical emergency. Untreated Type A mortality: 1-2% per hour. Risk of rupture into pericardium (tamponade), coronary ostia (MI), aortic root (AR), stroke.
❌ Medical management alone is for Type B (descending only, Stanford B) without complications. While preparing for OR: IV esmolol or labetalol (target HR <60, SBP 100-120). If BP still high after HR controlled → add nitroprusside (never nitroprusside alone — reflex tachycardia increases aortic shear stress). ❌ Heparin is CONTRAINDICATED — dissection can bleed into pericardium.
Question 5 of 6
A 14-year-old girl presents with migratory joint pain, fever, and a skin rash consisting of pale-centered, ring-shaped lesions on the trunk. She had a sore throat 3 weeks ago that was not treated. Auscultation reveals a new mitral regurgitation murmur. ASO titer is markedly elevated. Throat culture is negative now. Which of the following is the MOST specific major Jones criterion?
✅ D) Sydenham chorea
This is Acute Rheumatic Fever (ARF) following GAS pharyngitis. Jones Criteria Major: C-A-N-E-S = Carditis, Arthritis (migratory polyarthritis — most common), chorea (Sydenham), Erythema marginatum, Subcutaneous nodules.
Sydenham chorea is the most specific finding for ARF (it's rarely caused by anything else). It may appear weeks to months after the strep infection. Erythema marginatum (pale-centered ring-shaped rash on trunk) is also highly specific but less common than arthritis.
This patient has: arthritis + carditis (new MR murmur) + erythema marginatum + elevated ASO = 2 major criteria + evidence of Strep → DEFINITE ARF. Treatment: Penicillin (eradicate Strep) + ASA for arthritis + Penicillin prophylaxis monthly IM BZN for years.
Question 6 of 6
A 35-year-old man presents after a high-speed MVC where his chest struck the steering wheel. He complains of anterior chest pain. VS: BP 110/70, HR 102, RR 18, SpO2 97%. EKG shows a new RBBB and frequent PVCs. Troponin is 2.1 ng/mL (ULN 0.04). Echo shows anterior RV wall motion abnormality with preserved LV function. Which of the following is the most appropriate next step?
✅ B) Continuous cardiac monitoring for 24-48 hours
This is myocardial contusion (blunt cardiac trauma). Classic: MVC + steering wheel + elevated troponin + new arrhythmias (RBBB, PVCs) + RV wall motion abnormality (RV most anterior = most susceptible to blunt trauma).
Management: Continuous EKG monitoring x 24-48h for life-threatening arrhythmias (VT/VF). Treat arrhythmias as they arise. Hemodynamic monitoring. ❌ Anticoagulation: contraindicated (hemorrhagic myocardial contusion can worsen). ❌ Cardiac cath: no ischemia pattern (troponin elevation from contusion, not thrombosis). Most contusions are managed supportively with good outcomes.
Introduction to Trauma — Primary Survey, ATLS, & Life-Threatening Injuries
⭐ Golden Hour: Definitive hemorrhage control within 60 minutes of injury = best survival. Primary survey MUST be completed in <2 minutes. Treat each life threat as found — do NOT delay to complete survey.
Memory: BP doesn't drop until Class III (>30% blood loss). Tachycardia is the first sign of hemorrhagic shock (Class I and II). Children and athletes may not show tachycardia until significant blood loss (excellent compensation). Elderly patients on β-blockers cannot mount tachycardic response.
Penetrating or blunt; positive pressure ventilation (most common in intubated patients)
Respiratory distress, absent breath sounds one side, tracheal deviation AWAY from injury, JVD, hypotension.
Clinical diagnosis — do NOT wait for CXR!
Immediate needle decompression: 2nd ICS midclavicular line (or 4th/5th ICS anterior axillary). Then chest tube.
Open Pneumothorax
Large chest wall defect (>2/3 tracheal diameter)
Sucking chest wound, air movement through wound, paradoxical chest movement
Clinical
3-sided occlusive dressing (allows air out, not in). Then chest tube at separate site. DO NOT tape all 4 sides (→ tension pneumo).
Massive Hemothorax
Penetrating or blunt. Intercostal vessels or great vessels.
Absent breath sounds, dullness to percussion, hypotension, shock
CXR: opacification. Chest tube output >1500 mL initial OR >200 mL/hr for 3h = thoracotomy
Large-bore chest tube (36-40 Fr). Thoracotomy if massive (see above). Autotransfusion of blood.
Flail Chest
≥3 consecutive ribs fractured in ≥2 places → free-floating segment
Paradoxical chest wall motion (segment moves IN with inspiration). Hypoxia often from underlying pulmonary contusion (NOT just flail mechanics).
CXR/CT: multiple rib fractures. ABG: hypoxia
Adequate analgesia (epidural preferred), PEEP/PPV to splint internally. Intubation if severe hypoxia. Surgical rib fixation for severe cases.
Cardiac Tamponade
Penetrating (stab > GSW), blunt, or iatrogenic
Beck triad. Pulsus paradoxus. EMD/PEA on EKG.
FAST exam (pericardial fluid). Echo: RV collapse.
Pericardiocentesis (subxiphoid). Resuscitative thoracotomy in traumatic arrest. Emergency pericardial window.
Traumatic Aortic Injury
Rapid deceleration (MVC, fall). Most tears at aortic isthmus (ligamentum arteriosum = fixed point).
Widened mediastinum on CXR, unequal arm BP, sternal fracture, "apical cap," tracheal deviation right
CT angiography (gold standard). CXR screening.
Permissive hypotension (SBP 80-90), BB (reduce dP/dt), TEVAR (endovascular stent graft) = standard of care. Open surgery for type A.
FAST Exam (Focused Assessment with Sonography for Trauma)
1. Pericardial
Subxiphoid view. Fluid between pericardium and heart → tamponade.
2. Right Upper Quadrant
Morrison pouch (hepatorenal space). Most dependent right-sided space → blood pools here first.
3. Left Upper Quadrant
Splenorenal space + perisplenic area. Harder to visualize than RUQ.
4. Pelvis (Pouch of Douglas)
Most dependent space in supine patient. Fluid here = significant bleeding.
E-FAST: Extended FAST adds bilateral lung views for pneumothorax (absent lung sliding = pneumothorax). Sensitivity 90%+ for significant hemoperitoneum. Positive FAST + unstable patient → OR immediately, no CT. Negative FAST + unstable → consider other causes (retroperitoneal, pelvic fracture, thoracic).
Matching — Trauma Injuries & Interventions
Match the trauma scenario (left) to the correct intervention (right):
Absent breath sounds on left, tracheal deviation RIGHT, JVD, hypotension after intubation
Chest tube (36Fr) + possible thoracotomy
GCS = 6, pupils unequal, decerebrate posturing
Needle decompression 2nd ICS MCL → chest tube
Dull to percussion, absent breath sounds, initial chest tube output 1800 mL blood
3-sided occlusive dressing + separate chest tube
Positive FAST exam, hemodynamically unstable despite 2L crystalloid
RSI + intubation, HOB 30°, neurosurgery consult
Sucking chest wound — air moving in and out of chest wall defect
Immediate OR — emergency exploratory laparotomy
UWorld/PANCE-Style Questions — Intro to Trauma
Question 1 of 6
A 28-year-old man arrives by ambulance after a high-speed MVC. He is unresponsive (GCS 6). During transport, he was intubated. In the ED, his BP drops to 70/40 and oxygen saturation is 82% despite 100% FiO₂. On exam, there are absent breath sounds on the right and the trachea is deviated to the LEFT. JVD is present. What is the immediate next step?
✅ B) Needle decompression of the right chest at 2nd ICS midclavicular line
This is tension pneumothorax — the classic post-intubation presentation. Positive pressure ventilation → air forced into pleural space without escape → increasing pressure collapses lung, shifts mediastinum AWAY, compresses great veins → JVD + hypotension + absent breath sounds on affected side + tracheal deviation AWAY from affected side.
This is a CLINICAL diagnosis — do NOT wait for CXR (patient will die). Immediate needle decompression at right 2nd ICS MCL → then chest tube. Trachea deviated LEFT = pathology on RIGHT (deflect = away from problem). ❌ CXR will delay treatment. ❌ FAST does not diagnose pneumothorax (use E-FAST for lung).
Question 2 of 6
A 19-year-old male is brought in after a stab wound to the left chest. His VS are BP 88/60, HR 128, RR 22. Exam reveals muffled heart sounds, jugular venous distension, and no breath sounds are absent bilaterally. A bedside FAST shows fluid in the pericardial space. What is the next step in management?
✅ C) Emergency pericardiocentesis or resuscitative thoracotomy
Penetrating chest trauma + Beck triad (JVD + muffled sounds + hypotension) + pericardial fluid on FAST = traumatic cardiac tamponade. This is a surgical emergency.
• Pericardiocentesis (subxiphoid, needle) is a temporizing measure if patient is still alive • Emergency thoracotomy (ED thoracotomy) for penetrating chest trauma + loss of vital signs or imminent arrest = can be life-saving (open pericardium, control bleeding, internal cardiac massage)
Penetrating trauma (especially stab wounds) to the chest → think tamponade until proven otherwise. Stab wounds have better survival with ED thoracotomy than GSW because less destructive force. ❌ CT scan — do not delay definitive treatment. ❌ Chest tubes don't drain pericardial blood.
Question 3 of 6
A 40-year-old woman is brought in after an MVC. She has bruising over the left chest and complains of severe chest pain. Exam reveals paradoxical inward movement of the left lateral chest wall during inspiration. SpO₂ is 89% on 15L NRB. CXR shows multiple rib fractures of ribs 4-8 on the left in 2 places each, and a diffuse left lung infiltrate. What is the primary cause of her hypoxia?
✅ B) Underlying pulmonary contusion
This is flail chest (≥3 ribs fractured in ≥2 places = free-floating segment = paradoxical movement). However, the primary cause of hypoxia is NOT the mechanical flail movement — it is the underlying pulmonary contusion (alveolar hemorrhage/edema from the same force).
The diffuse left infiltrate = pulmonary contusion. Contusion causes V/Q mismatch → hypoxia that worsens over 24-48 hours. Management: • Adequate analgesia (epidural ideal — allows breathing) to prevent splinting and atelectasis • PEEP/positive pressure ventilation to pneumatically splint the segment • Intubation if SpO₂ doesn't respond to O₂/NIV • Fluid restriction (contusion worsens with overload) • Avoid over-suctioning
Question 4 of 6
A 35-year-old male is brought in after a fall from a 20-foot ladder. He is confused and disoriented. GCS = 11 (E3V3M5). CT head shows a biconvex (lens-shaped) hyperdense lesion over the right temporal lobe with midline shift. He had a brief loss of consciousness followed by a "lucid interval" and then deteriorated. Which of the following is the most likely diagnosis?
✅ B) Epidural hematoma (EDH)
Classic presentation: Temporal/parietal blow → brief LOC → lucid interval → rapid deterioration → herniation. Mechanism: middle meningeal artery tear (runs in epidural space temporal bone). CT: biconvex/lens-shaped hyperdense (acute blood) lesion that does NOT cross suture lines (epidural space is limited by dural attachments at sutures).
Compare: • EDH: Biconvex, does NOT cross sutures, temporal, arterial bleeding, lucid interval • SDH: Crescent-shaped, CROSSES sutures, bridging vein tear, elderly/alcoholics, more gradual • SAH: "Worst headache of life," blood in cisterns/sulci, thunderclap onset
Treatment: Emergent craniotomy for EDH with midline shift/clinical deterioration. While prepping: elevate HOB 30°, mannitol 1g/kg IV, hyperventilate to pCO₂ 30-35 if herniation signs.
Question 5 of 6
A 58-year-old male presents after a rapid deceleration MVC. CXR reveals a widened mediastinum (>8 cm). He has a BP of 176/88 in the right arm and 148/70 in the left arm. There is no aortic regurgitation murmur. CT angiography shows a contained aortic injury at the isthmus with no extravasation. The patient is hemodynamically stable. What is the definitive treatment of choice?
✅ B) TEVAR (Thoracic Endovascular Aortic Repair)
Blunt aortic injury at the isthmus (most common location — at the ligamentum arteriosum, a fixed point between mobile arch and tethered descending aorta → maximum shear stress with deceleration). Contained injury (pseudoaneurysm) in stable patient → TEVAR is standard of care (superior to open surgery: less mortality, less paraplegia, faster recovery).
While preparing for TEVAR: anti-impulse therapy — IV esmolol/labetalol to reduce HR <80 and SBP 100-120 (reduces aortic wall stress and risk of rupture). If antihypertensive needed after HR control → sodium nitroprusside. ❌ Nicardipine alone = reflex tachycardia → worsens aortic shear stress. ❌ Observation only if truly minimal injury and patient refuses intervention.
Question 6 of 6
A 22-year-old male is involved in a drive-by shooting with a GSW to the abdomen. In the ED, his BP is 74/50, HR is 142. FAST exam shows free fluid in Morrison's pouch and the pelvis. You rapidly transfuse 2 units of PRBCs and his BP improves to 88/60. He remains tachycardic. According to hemorrhagic shock classification, what class of shock is he in and what is the most appropriate next step?
✅ B) Class III shock — activate MTP and prepare for OR
BP dropping to 74/50, HR 142, FAST positive (hemoperitoneum) = Class III hemorrhagic shock (30-40% blood volume loss, BP drops, confused/lethargic). Responds transiently to initial resuscitation but remains tachycardic = TRANSIENT RESPONDER → ongoing bleeding = needs definitive hemorrhage control (surgery).
Massive Transfusion Protocol (MTP): 1:1:1 ratio of PRBC:FFP:Platelets → damage control resuscitation (prevents dilutional coagulopathy, replaces all clotting factors, NOT just red cells). Avoid large crystalloid boluses (dilutes clotting factors, worsens "lethal triad" of hypothermia + acidosis + coagulopathy). Add TXA (tranexamic acid) within 3 hours of injury (reduces mortality).
❌ 4L crystalloid = outdated, harmful. Positive FAST + hemodynamic instability → OR immediately without CT.
Pre-Hospital Medicine — EMS, Triage, & Scene Management
Real-time communication with a physician via radio/phone during patient contact.
Examples: Paramedic calls ED physician before giving thrombolytics in STEMI, asks permission for unusual doses, confirms withholding resuscitation.
Advantage: Flexibility for unusual situations, physician accountability.
Offline (Indirect) Medical Direction
Pre-established standing orders, protocols, and quality improvement programs developed by medical director.
Examples: Protocol to give aspirin to all chest pain patients, protocol to intubate GCS ≤8, standing order for epi in cardiac arrest.
Advantage: Speed — provider acts without calling for orders. Most prehospital care is protocol-driven.
START Triage (Mass Casualty Incident)
START = Simple Triage And Rapid Treatment — assess each patient in <30 seconds. Used for MCI when resources are overwhelmed. Tag colors: RED (Immediate), YELLOW (Delayed), GREEN (Minor/Walking Wounded), BLACK (Deceased/Expectant)
Step
Assessment
Finding
Tag Color
1. Walking?
Can patient walk to designated area?
YES → walking wounded
GREEN (Minor)
2. Breathing?
Open airway — is patient breathing?
NO breathing after repositioning → BLACK YES breathing → go to step 3
BLACK (Deceased)
3. Respiratory Rate
Count breaths for 15 seconds × 4
>30 breaths/min OR <10/min → RED 10-30 → go to step 4
RED (Immediate)
4. Perfusion
Radial pulse OR capillary refill
No radial pulse OR cap refill >2 sec → RED Pulse present + cap refill <2 sec → go to step 5
RED (Immediate)
5. Mental Status
"Follow simple commands" (squeeze my hand, open eyes)
Cannot follow commands → RED Follows commands → YELLOW
RED or YELLOW (Delayed)
Expectant (BLACK) in living patients: In some MCI systems, patients who are unlikely to survive even with immediate care (devastating TBI, 90%+ BSA burns, multi-system failure) may be tagged BLACK to allow resources for salvageable patients. This is the hardest triage decision ethically.
SAMPLE History & Scene Assessment
📋 SAMPLE History
S — Signs & Symptoms A — Allergies M — Medications P — Past medical/surgical history L — Last oral intake E — Events leading up to illness/injury
🚨 Scene Size-Up
1. Scene safety (BSI/PPE first!)
2. Nature of illness / Mechanism of injury
3. Number of patients
4. Additional resources needed?
5. C-spine considerations (trauma mechanism?)
🏥 OPQRST (Pain)
O — Onset P — Provocation/Palliation Q — Quality R — Radiation S — Severity (0-10) T — Time (duration/course)
🧠 NEXUS Criteria (C-Spine)
Clear C-spine if ALL of:
• No midline tenderness
• Normal alertness
• No intoxication
• No focal neuro deficit
• No painful distracting injury Fails ANY → cervical collar
Airway Management Progression (Field)
Device
Provider
Indication
Key Points
Positioning, Jaw Thrust
All
Basic airway obstruction
Jaw thrust preferred in trauma (avoids neck extension)
OPA (Oropharyngeal)
All
Unconscious, no gag reflex
Size: corner of mouth to earlobe. Insert inverted, rotate 180°. Stimulates gag in conscious patients → vomiting.
NPA (Nasopharyngeal)
All
Conscious or semi-conscious, intact gag
Size: tip of nose to earlobe. Lubricate. Contraindicated in basilar skull fracture.
BVM (Bag-Valve-Mask)
All
Apneic or inadequate breathing
E-C clamp technique. 10-12 breaths/min adult. Use with supplemental O₂. 2-provider BVM preferred.
Supraglottic Airway (LMA, King LT, i-gel)
AEMT/Paramedic
Cannot intubate, temporary airway
Easier to insert than ETT. Does not protect against aspiration as well. Used as rescue airway.
Endotracheal Intubation (RSI)
Paramedic
GCS ≤8, airway protection, respiratory failure
Confirm with ETCO₂ (waveform capnography = gold standard) + CXR. RSI medications: etomidate + succinylcholine or rocuronium.
Surgical Airway (Cricothyrotomy)
Paramedic (some systems)
Cannot intubate, cannot oxygenate (CICO)
Located between thyroid and cricoid cartilages. Needle crico (temporizing) → surgical crico. Contraindicated in children <12 (use needle only).
Matching — Pre-Hospital Triage & Scene Assessment
Match each scenario (left) to the correct START triage category (right):
Patient is ambulatory, walking to assembly area with minor lacerations and anxiety
BLACK — Deceased/Expectant
RR = 36/min, radial pulse absent, not following commands
GREEN — Minor (Walking Wounded)
Apneic despite airway repositioning maneuver; no spontaneous breathing
YELLOW — Delayed
RR = 18/min, radial pulse present, cap refill 1 sec, follows commands; has closed femur fracture
RED — Immediate
RR = 22/min, radial pulse present, cap refill <2 sec, follows commands; has painful forearm fracture
YELLOW — Delayed
UWorld/PANCE-Style Questions — Pre-Hospital Medicine
Question 1 of 6
A paramedic arrives at a mass casualty incident involving a building collapse. She finds a 45-year-old male who is not walking. He is breathing spontaneously with a rate of 34 breaths/min. His radial pulse is absent. Using START triage, what is the appropriate triage tag for this patient?
Don't need to check further — RR >30 = RED regardless of circulation/mental status. The absent radial pulse would ALSO make him RED if we continued. He needs immediate intervention (control airway, stop bleeding, IV access, transport first).
Remember: In START, you assign a tag and MOVE ON — do NOT provide treatment beyond opening the airway. Treatment comes after all patients are triaged (unless you can correct a problem in <30 sec).
Question 2 of 6
An EMT is caring for a 68-year-old man with chest pain and diaphoresis. The patient has his own nitroglycerin prescription. His BP is 96/64 mmHg. He wants to take his nitroglycerin. What should the EMT do?
✅ B) Withhold nitroglycerin because the patient's BP is below 100 mmHg
EMTs can assist patients with their own prescribed nitroglycerin (cannot administer from their own kit). However, protocols typically require SBP ≥100 mmHg before assisting with nitroglycerin (vasodilation in hypotension → dangerous drop in BP → cardiogenic shock).
Also contraindicated: recent PDE-5 inhibitor use within 24-48 hours (sildenafil, tadalafil — severe hypotension).
At SBP 96 → withhold, lay flat, administer O₂, establish IV, rapid transport. ❌ Administer from own kit: EMTs do not carry nitroglycerin in their drug kit (paramedics do). ❌ Contact medical control and give anyway: contraindication exists regardless of online medical direction recommendation in many protocols.
Question 3 of 6
A paramedic is called to a scene where a 24-year-old female was found unresponsive in her apartment. Her roommate reports she "takes lots of medications." Exam reveals GCS of 6, pinpoint pupils, RR of 6/min, HR 54, and mottled, cool skin. She has track marks on both arms. Which intervention should be performed FIRST?
✅ B) OPA + BVM ventilation
Classic opioid overdose: pinpoint pupils + decreased LOC + respiratory depression (RR 6 = critical). Airway and breathing ALWAYS come first (ABCDE). RR 6 = respiratory failure → immediate BVM ventilation with OPA to maintain oxygenation/ventilation.
Then: IV/IO access → naloxone 0.4-2mg IV/IM/IN (can titrate). Naloxone reverses opioid-induced respiratory depression. Be prepared for acute withdrawal (agitation, vomiting) after naloxone. Repeated dosing or infusion may be needed (naloxone T½ shorter than most opioids).
❌ Don't rush to RSI before trying BVM + naloxone first — naloxone may restore spontaneous breathing, avoiding intubation. ❌ EKG is not the priority when someone is not breathing.
Question 4 of 6
A paramedic is transporting an intubated 55-year-old man in cardiac arrest who achieved ROSC 5 minutes ago. During transport, the patient's SpO₂ drops to 88% and EtCO₂ (waveform capnography) suddenly drops from 40 mmHg to 8 mmHg. Breath sounds are absent on the left. What is the most likely cause and the correct intervention?
✅ B) Right mainstem intubation — pull ETT back 1-2 cm
This is right mainstem bronchus intubation. When the ETT is advanced too far, it enters the right mainstem bronchus (straighter angle from carina) → only ventilates right lung → absent sounds on LEFT → desaturation.
The EtCO₂ dropped from 40 to 8 — initially might seem like arrest, but with ROSC and absent unilateral breath sounds, the cause is mechanical (tube position), not re-arrest. Waveform capnography remains positive (there IS ETCO₂, just low because only one lung ventilated).
Fix: Pull ETT back 1-2 cm, reassess breath sounds bilaterally, confirm with rising SpO₂. Correct ETT depth: ~3× ETT size in children, or at 21-23 cm at the lips in adults.
Tension pneumo would also cause absent breath sounds on one side, but typically with JVD, hypotension, and tracheal deviation — and would show more dramatic hemodynamic instability post-ROSC.
Question 5 of 6
EMS responds to a 58-year-old male with sudden onset crushing chest pain with radiation to the left arm, diaphoresis, and nausea. 12-lead EKG shows 3mm ST elevation in leads II, III, and aVF with reciprocal depression in I and aVL. The closest hospital with a catheterization lab is 65 minutes away. The closest hospital without cath lab is 12 minutes away. The patient is hemodynamically stable. What is the most appropriate prehospital destination decision?
✅ B) Transport directly to the PCI-capable hospital (65 min)
This is an inferior STEMI (ST elevation II, III, aVF = right coronary artery territory). Definitive treatment = primary PCI (door-to-balloon <90 minutes).
Guidelines: If first medical contact to balloon time ≤120 minutes is achievable by going directly to PCI center → bypass non-PCI hospital and go directly. 65 minutes transport + time in ED = still within 120 min window → bypass and go directly.
Pre-notification of receiving hospital reduces time to activation of cath team (cath team assembled before patient arrives). Give aspirin 324mg PO + heparin en route. ❌ Transfer from non-PCI hospital adds time (load-and-go → unload → re-load) often exceeding 120 min total. ❌ Field thrombolytics: only considered if PCI center is >120 min away AND patient is within 12 hours of onset with no contraindications.
Question 6 of 6
A paramedic responds to a 3-year-old child in cardiac arrest. CPR is in progress. The child weighs approximately 15 kg (per Broselow tape). The rhythm shows VF. What is the correct defibrillation dose and epinephrine dose for this child?
Always use Broselow tape in pediatric codes — color-coded dosing avoids calculation errors under stress. Epinephrine concentration: use 1:10,000 solution (0.1 mg/mL) → 0.15mg = 1.5 mL of 1:10,000. Common pediatric error: using adult dose (1mg Epi) = 6.7× overdose → can cause severe hypertension, worsens outcomes.
VF in children is less common than asphyxial arrest (PEA/asystole) — always ensure airway/ventilation is optimized, as hypoxia is the most common cause of pediatric arrest.
Conduction Disorders — Rhythm Reference
Each rhythm is described by the 5-step analysis: Rate → Rhythm → P waves → PR interval (PRI) → QRS. Normal values: PRI 0.12–0.20 s (3–5 boxes), QRS <0.12 s (3 boxes). 6-second strip rate = R waves × 10.
⭐ Mechanism PearlIf the rhythm starts and stops suddenly → think reentry (AVNRT, VT post-MI). If it gradually speeds up and slows down → think automaticity (sinus tach). Triggered activity (afterdepolarizations) → Torsades. Conduction block → AV blocks.
Sinus & Atrial Rhythms
Rhythm
Rate
Rhythm
P waves
PRI
QRS
Key points
Normal Sinus
60–100
Regular
Present, upright, uniform
0.12–0.20
0.08–0.10
Baseline normal
Sinus Tachycardia
100–150
Regular
Present, upright, uniform
0.12–0.20
0.08–0.10
Treat underlying cause (fever, hypovolemia, anemia, PE, pain). Gradual onset; clear P waves
Classic in severe COPD; often mistaken for AFib. CCB/BB if LV preserved
⭐ Sinus Tach vs SVTSinus tach: gradual onset, usually <150, clear P waves, secondary to a cause. SVT: sudden onset, often >150–180, P waves hidden, reentry mechanism.
Sick Sinus Syndrome (Tachy-Brady)
SA node dysfunction — sinus arrest, SA exit block, or persistent bradycardia. Classic elderly presentation: recurrent SVT (often AFib) alternating with bradyarrhythmias. "The node is unreliable — sometimes it pauses, sometimes it races." Treating the tachyarrhythmia is difficult without first pacing (BB/CCB/antiarrhythmics worsen bradycardia). Permanent pacemaker = mainstay; does not reduce mortality but improves QOL.
Supraventricular Tachycardia (SVT)
Rate 150+ | Regular | P waves often non-discernable | QRS 0.08–0.10 (narrow). Paroxysmal SVT = sudden onset/offset, regular. Most common mechanism = reentry. AVNRT (dual AV nodal pathways) ≈ 60% of PSVT; AVRT (accessory pathway) ≈ 30%.
SVT Treatment ladder: 1) Vagal maneuvers (Valsalva at 45°, modified Valsalva w/ leg raise, diving reflex/cold water) → terminates 20–50%. 2) Adenosine 6 mg rapid IV push (1–2 s), then 12 mg if needed — terminates ~90%. Caution in reactive airway disease (bronchospasm). 3) If unstable or adenosine fails → synchronized cardioversion (100 J). Long-term: AV nodal blockers (BB/non-DHP CCB); catheter ablation preferred for recurrent symptomatic.
⚠ AVOID AV nodal blockers (CCB, BB, adenosine, digoxin) in WPW with AFib — blocking the AV node forces conduction down the accessory pathway → faster ventricular rates → can degenerate to VF. Use procainamide; cardiovert if unstable. Definitive Tx: catheter ablation.
Junctional & Premature Beats
Rhythm
Rate
P waves
QRS
Notes
Junctional Escape
40–60
Inverted or absent
0.08–0.10
AV junction is pacemaker
Accelerated Junctional
60–100
Inverted or absent
0.08–0.10
—
Junctional Tachycardia
100+
Inverted or absent
0.08–0.10
Causes: digitalis toxicity, myocarditis, CAD
PAC
—
Early, different morphology
Narrow
Single ectopic atrial beat, irregular R-R
PJC
—
Inverted/absent
Narrow
Single ectopic junctional beat
PVC
—
None (no P)
Wide
Bigeminy/trigeminy = every 2nd/3rd beat. Reassure if benign; eval if frequent/multifocal or >10% burden
AV Blocks
AV block = interruption of impulse from SA → AV node. PR interval is the key. Can be physiologic (↑vagal tone) or pathologic (ischemia, myocarditis, fibrosis, post-surgery).
AV dissociation — none conducted. Mobitz II & 3° → pacemaker. High-grade blocks = emergency
Ventricular Rhythms
Rhythm
Rate
QRS
Treatment
Idioventricular (ventricular escape)
20–40
Wide
Seen post-MI reperfusion; usually none unless unstable
Ventricular Tachycardia
100+
Wide, no P
Stable: amiodarone. Unstable: synchronized cardioversion. Monomorphic (structural) vs polymorphic (ischemia/lytes)
Torsades de Pointes
—
Twisting around baseline
Polymorphic VT + prolonged QT. Give magnesium! Defibrillate if unstable; correct lytes. QT-prolongers: antiarrhythmics, macrolides, fluoroquinolones, antipsychotics
Ventricular Fibrillation
n/a
Fibrillatory, no organized QRS
Lethal — most common cause of SCD (~70% from CHD). Immediate defibrillation + CPR
Brugada Syndrome
Inherited Na+ channelopathy → SCD risk in young healthy people. More common in Southeast Asian males. ECG: ST elevation V1–V3. Presents with syncope/SCD. Treatment: ICD.
Cardioversion: if AFib >48 h or unknown duration → TEE first to exclude LA thrombus, OR ≥4 wks OAC before. Electrical: biphasic 200 J → 360 J. Continue OAC ≥4 wks post (often indefinitely). Unstable (shock, severe hypotension, pulmonary edema, ongoing ischemia) → urgent cardioversion despite thromboembolism risk.
Atrial Flutter
Sawtooth flutter waves (inferior leads II, III, aVF) | ratio variable (2:1, 3:1) | QRS narrow. One irritable atrial focus; atrial rate 250–350 bpm with AV block determining ventricular rate. Stroke risk = equivalent to AFib. Seen in COPD, VHD, ASD, repaired CHD. Catheter ablation = definitive; rate control (BB/non-DHP CCB), anticoagulation, cardioversion.
💡 Interactive ECG tracings with twelve diagnoses are in the 📊 EKG Quiz tab — use this tab as the written reference and that tab to test pattern recognition.
Hypotension
Definition: BP <100/60 in women or <110/70 in men. Etiologies: volume depletion, infection, medications, positioning/activity, pregnancy, cardiovascular disease.
First priority: RULE OUT SHOCK. Assess for multisystem hypoperfusion — markedly ↓BP, tachycardia, tachypnea, poorly perfused skin/extremities, altered mental status, ↓urine output. If no shock, consider SIRS, infection, liver failure, anaphylaxis, adrenal insufficiency, hemorrhage, PE, tamponade. Goal of treatment: perfused organs + treat underlying pathology.
Orthostatic Hypotension
Drop in SBP ≥20 mmHg or DBP ≥10 mmHg within 3 min of standing. Affects up to 24% of those >65.
Orthostatic vitals: lie flat 5 min → BP/HR; stand → BP at 1 and 3 min. Abnormal = SBP↓≥20, DBP↓≥10, + lightheadedness.
Patient education: stand slowly (sit → dangle legs → stand with support), avoid overheating/hot showers, hydrate, move legs when standing still, compression stockings, limit alcohol, feet up if faint.
Postprandial Hypotension
SBP fall ≥20 mmHg within 2 h of eating. Impaired baroreflex-mediated/splanchnic vasoconstriction. Meal modifications: avoid large meals, low-carb meals, avoid alcohol, drink water with meals, avoid sudden standing after eating, semi-recumbent 90 min post-meal if needed, walk between meals.
Vasovagal Syncope ("common faint")
Most common cause of syncope. Neural reflex → self-limited hypotension with relative/severe bradycardia ± vasodilation. Prodrome: lightheadedness, warmth/cold, sweating, palpitations, nausea, visual blurring/whiteout, "whooshing" sounds, pallor. Occurs sitting/standing; brief (1–2 min). Workup: ECG in all syncope; tilt-table confirmatory when atypical.
POTS — Postural Orthostatic Tachycardia Syndrome
Significant tachycardia within 10 min of standing WITHOUT postural hypotension. More common in women, age 20–50. May follow pregnancy, surgery, trauma, chemo, vaccination, or viral infection; associated with joint hypermobility & MVP.
Case 1 — 76-y/o man with dizziness & "black spots" when standing, near-fall getting up from a chair. PMH: HTN, T2DM. Meds: lisinopril, HCTZ, metoprolol. Vitals: supine 132/78 HR 68; standing 1 min 108/66 HR 78; 3 min 106/64 HR 80.
Diagnosis: Orthostatic hypotension. SBP drops 132→106 (↓26, ≥20) on standing with only a blunted HR rise (baroreflex impairment in an older diabetic). Contributors: age, autonomic neuropathy from DM, volume depletion + vasodilation from HCTZ/lisinopril, rate-blunting from metoprolol. Risk: falls/syncope. Management: review/reduce offending meds, slow positional changes, hydration, compression stockings; consider midodrine/fludrocortisone if refractory.
Diagnosis: POTS. Marked tachycardia (HR 72→118, Δ46) on standing without a significant BP drop — distinguishes it from orthostatic hypotension (where BP falls). Often post-viral. Pathophysiology: venous pooling/denervation, hyperadrenergic response, or volume dysregulation. Non-pharm first: ↑salt & fluids, compression, graded exercise, postural training. Pharm by subtype: BB/clonidine (hyperadrenergic) or midodrine/fludrocortisone/pyridostigmine (neuropathic).
Lipid Disorders
⭐ Lipid HypothesisLDL is causal for ASCVD, not just a lab value. Lowering LDL slows plaque progression and stabilizes plaque. In established ASCVD, cholesterol lowering = secondary prevention → ↓mortality & recurrent events.
Lipoproteins (by density)
Triglyceride ↓density; apoproteins ↑density.
Particle
Note
Chylomicrons
Least dense; after fatty meals
VLDL
Very low density
LDL
Carries most cholesterol; ↑LDL = ↑ASCVD risk
HDL
Densest/smallest; ↑HDL = ↓risk
Clinical Manifestations
Most patients asymptomatic. Hypertriglyceridemia → pancreatitis (esp. TG ≥500). May see xanthomas or xanthelasma (lipid plaques on eyelids).
Autosomal dominant/recessive → very high LDL → premature MI/CVA. ~1 in 500. Get family history + genetic testing in patients <40 with LDL >200. Treat: high-intensity statins or PCSK9 inhibitors; monitor for ASCVD closely.
When to Start a Statin
Use the ASCVD Risk Calculator. Initiate statin for: T1/T2 DM age 40–75 • No CVD, age 40–75, & 10-yr risk ≥7.5% • LDL ≥190 (age >21) • Any ASCVD • Age <19 with familial hypercholesterolemia history.
Fibrates (≥500 to prevent pancreatitis); icosapent ethyl if ASCVD + TG 135–499
HDL
Niacin (raises HDL but no proven CV benefit)
Practice Cases
Case 1 — 58-y/o man with HTN, T2DM, obesity. Lipids: TC 245, LDL 160, HDL 40, TG 180. Most appropriate first-line treatment? A) Statin B) Fibrate C) Omega-3 D) Ezetimibe
A) Statin therapy. Diabetic 40–75 with elevated LDL → statin is first-line (likely high-intensity given DM + risk factors). Ezetimibe is an add-on, not first-line.
Case 2 — 45-y/o woman, family history of hyperlipidemia, LDL 195, TC 275, HDL 55, normal TG. Most likely diagnosis? A) FH B) Hypothyroidism C) Metabolic syndrome D) ASCVD
A) Familial hypercholesterolemia. Isolated very high LDL with strong family history and normal TG/HDL points to FH. Treat with high-intensity statin ± PCSK9i.
Case 3 — 68-y/o man, MI 3 yrs ago, on atorvastatin. LDL 98, TC 160, HDL 40, TG 120. Which is true? A) LDL at target for secondary prevention B) Stop statin C) High risk — further LDL lowering indicated D) Needs HDL therapy
C) High risk — further LDL lowering indicated. Established ASCVD = very high risk; goal LDL <70 (often <55). At LDL 98 on statin → add ezetimibe ± PCSK9i.
Case 4 — 32-y/o woman with muscle aches/weakness after starting atorvastatin 20 mg. Which test for the statin-related side effect? A) LFTs B) TFTs C) CBC D) CK
D) Creatine kinase (CK). Myalgias are the most common statin AE; CK assesses for myopathy/rhabdomyolysis.
Case 5 — Recurrent pancreatitis, TG 800. Best agent to lower TG? A) Gemfibrozil B) Atorvastatin C) Ezetimibe D) Niacin
A) Gemfibrozil (fibrate). Severe hypertriglyceridemia (≥500) → fibrate to prevent pancreatitis. Statins/ezetimibe mainly lower LDL.
Vitals first: SBP <90, tachycardia, tachypnea. Shock Index = HR ÷ SBP; SI >0.9 predicts mortality and need for pressors/fluids/blood.
Narrowed pulse pressure = early sign of hemorrhagic shock (↑SVR → ↑DBP). SvO₂ normal 65–75% (low = inadequate delivery; high in sepsis from impaired extraction).
↓preload from blood/fluid loss. Cold-shock picture, low JVP, narrow PP, oliguria, AMS. Labs: Hgb/Hct (trends best — may be normal early), BUN:Cr >20 (prerenal), lactic acidosis, coagulopathy in severe hemorrhage. Imaging: CXR/PXR, FAST exam, CT if stable. Treatment: stop the bleeding → isotonic IVF → blood (type O-neg or type-specific PRBCs/whole blood). Monitor response: urine output, BP, HR, mental status, warmth, cap refill, pH/base deficit/lactate.
Cardiogenic Shock
Tissue hypoxia from ↓CO despite adequate volume. ↑JVP, pulmonary edema. Echo: ↓LV contractility, dilated/full LV (vs small hyperdynamic LV in hypovolemia). ECG for ischemia (STEMI = ≥1 mm in ≥2 contiguous leads; troponin for NSTEMI/UA). Treatment: ABCs, careful IVF (250 mL challenges), pressors to MAP 65 (norepinephrine 1st-line; milrinone lowers SVR), PCI mainstay for MI, inotrope dobutamine (low CO + high PCWP, no hypotension), mechanical support (IABP, VAD).
Neurogenic: spinal cord injury → loss of sympathetic tone → hypotension + bradycardia (no compensatory tachycardia), warm. IVF + pressors to MAP 85–90 for spinal perfusion (rule out hemorrhage first). Anaphylactic: IgE-mediated vasodilation, angioedema, bronchospasm → IM epinephrine 0.3–0.5 mg q5–15 min, IVF, H1+H2 blockers, albuterol, steroids. Endocrine: adrenal insufficiency (abrupt steroid cessation), myxedema, thyroid storm.
Vasopressors & Inotropes
Agent
Action
Use
Norepinephrine
α > β1 (↑MAP)
1st-line: septic, cardiogenic, neurogenic shock
Epinephrine
α + β
Vasopressor of choice for anaphylaxis; severe shock/resuscitation
Phenylephrine
Pure α
Hyperdynamic septic shock when tachyarrhythmia limits β-agents
Vasopressin
V1 vasoconstriction
Adjunct to NE in distributive shock
Dopamine
Dose-dependent (dopa→β→α)
Alternative pressor; bradycardia
Dobutamine
β1 inotrope, ↓afterload
Low CO + high PCWP without hypotension (cardiogenic)
Milrinone
Inotrope, lowers SVR
Cardiogenic shock (PDE-3 inhibitor)
⭐ Volume FirstVasoactive agents are given only after adequate fluid resuscitation. Continued hypotension with high CO (sepsis) → pressors. Low CO with high filling pressures → inotropes. Septic = 30 mL/kg; cardiogenic = small 250 mL boluses; give less to HF/CKD patients.
Cardiovascular Emergencies — Approach to Chief Complaints
Dx: ECG within 10 min, troponin, CXR (edema, pneumo, widened mediastinum), CBC/CMP/Mg, ±D-dimer. Mgmt: O₂ if hypoxic, aspirin, nitroglycerin (not if hypotensive or RV infarct), IV access, monitoring.
⭐ PearlsAll chest pain is cardiac until proven otherwise. Normal ECG ≠ no ACS. Troponin = injury, not mechanism. NTG response doesn't rule in/out ACS. Epigastric pain can be MI. Women/elderly/diabetics atypical.
Dyspnea on Exertion
Can't-miss: HF, ACS, valvular (AS, MS), PE, arrhythmia. History: acute vs chronic, positional, exertional threshold, weight gain, orthopnea/PND, edema.
Dx: ECG, BNP, CXR (congestion, effusions), CBC/CMP/Mg, ±echo. Mgmt: O₂ if hypoxic, diuretics if overloaded.
⭐ PearlsDyspnea is often cardiac, not pulmonary. DOE = early HF sign. Orthopnea = ↑LV filling pressures. Crackles are LATE; JVD is earlier. PE often = normal CXR + hypoxia.
Palpitations
Can't-miss: VT and other malignant arrhythmias. Dx: ECG (rhythm), electrolytes, TSH, drug screen. Mgmt: monitoring; unstable → synchronized cardioversion; stable → rate/rhythm control.
⭐ PearlsRate kills before rhythm. Hypotension in tachyarrhythmia = unstable → electricity, not meds. AFib w/ RVR → cardiogenic shock. Wide-complex tachycardia = VT until proven otherwise.
Syncope
Can't-miss: arrhythmia, aortic stenosis, HCM, PE, tamponade, hemorrhage. High-risk: exertional syncope, no prodrome, family history of sudden death, structural disease. Dx: ECG, glucose, orthostatics, troponin, electrolytes, TSH, drug screen.
⭐ PearlsCardiac syncope = highest mortality. Exertional = obstruction/arrhythmia. No prodrome = arrhythmia. Family hx sudden death = genetic cardiomyopathy. Syncope is a diagnosis of cause.
Edema
Pitting vs non-pitting; unilateral vs bilateral. Cardiac causes: HF, constrictive pericarditis, VTE. Red flags: rapid onset (acute HF/PE), dyspnea, hypotension (cardiogenic shock), ascites + JVD (R-sided HF). Dx: CMP, BNP, venous US (DVT), ±echo.
ER survival rules: Rule out lethal causes first. Treat instability immediately (electricity > meds when unstable). Think in syndromes & physiology. Reassess after every intervention. Never trust a single data point. Ask "what will kill this patient fastest?" Avoid anchoring/confirmation bias. Normal vitals ≠ stable physiology.
Case Studies
Case 1 — "Pressure and Doom" 62-y/o man, 30 min crushing substernal pressure radiating to left arm/jaw, diaphoretic, nauseated. BP 88/54, HR 112, RR 24, SpO₂ 91% RA. HTN, HLD, T2DM, 40-pk-yr smoking.
Red flags: hypotension (shock), hypoxia, classic ACS presentation. Can't-miss DDx: STEMI/ACS (top), aortic dissection, PE, tamponade. Dx: ECG within 10 min, troponin, CXR (mediastinum), CBC/CMP. Mgmt: aspirin, O₂, IV access, monitoring — avoid nitroglycerin (hypotensive, possible RV involvement); this is cardiogenic shock from likely STEMI → activate cath lab / PCI, cautious fluids, pressors (norepinephrine).
Case 2 — "I can't breathe lying down" 70-y/o woman, 3 days worsening SOB, can't lie flat, sleeping in chair. BP 104/66, HR 108, RR 26, SpO₂ 89% RA. JVD, bilateral crackles, S3, pitting edema. CHF, prior MI, CKD.
Red flags: hypoxia, orthopnea, JVD. Dx: decompensated heart failure (acute pulmonary edema). DDx: ACS trigger, arrhythmia. Dx workup: ECG, BNP, CXR, troponin, CMP. Mgmt: O₂/positioning (consider NIPPV), IV loop diuretics, nitrates if BP tolerates; identify precipitant (ischemia, arrhythmia, nonadherence).
Case 3 — "Passed out at work" 28-y/o man collapses after sudden palpitations, brief LOC. BP 92/60, HR 168 irregular, RR 22, SpO₂ 96%. No PMH. Father died suddenly at 41.
Red flags: syncope + palpitations + exertion, no prodrome, family history of sudden cardiac death → malignant arrhythmia / genetic cardiomyopathy (HCM, WPW, Brugada, channelopathy). Irregular wide/fast rhythm — consider AFib with pre-excitation (WPW). Dx: 12-lead ECG (delta wave?), electrolytes, TSH, troponin, echo. Mgmt: monitoring; borderline-unstable → prepare for synchronized cardioversion; if WPW + AFib AVOID AV nodal blockers.
Case 4 — "Swollen Legs" 66-y/o man, 2 wks progressive bilateral leg swelling + worsening DOE. BP 98/64, HR 102, RR 22, SpO₂ 92%. Massive pitting edema, hepatomegaly, JVD, ascites. COPD, pulmonary HTN, OSA.
Work through this infective endocarditis case as a clinical reasoning exercise. Reveal each answer after you've thought it through.
Part 1 — Presentation
32-y/o man: "Fever and body aches for ~2 weeks, feel exhausted." Temp 38.6°C (101.5°F), HR 112, BP 104/64, RR 18, SpO₂ 97%. Reports progressive fatigue, intermittent fevers/chills, night sweats, ↓appetite, mild exertional dyspnea, diffuse joint aches. Thought it was "the flu."
Task 1: What critical history questions are needed?
Dental extraction 3 weeks ago • History of IV heroin use, last injection 1 month ago • No known heart disease • New: sharp right-sided pleuritic chest pain, dry cough, intermittent abdominal discomfort.
Task 2: Key risk factors & top differentials?
Risk factors: IV drug use, recent dental procedure. DDx: Infective endocarditis (fever + IVDU + dental work — leading), pneumonia (fever, infiltrates), myocarditis, pulmonary emboli (pleuritic pain), TB (night sweats, but acute timeline argues against). Suspicion shifts strongly toward IE.
Part 3 — Physical Exam
Appears ill/fatigued. Cardiac: tachycardia, new holosystolic murmur at LLSB. Skin: small painless erythematous macules on palms/soles; linear reddish-brown streaks under nails. Lungs: scattered RLL crackles. Eyes: retinal hemorrhages with pale centers.
Task 3: Classic findings & leading diagnosis?
Classic IE stigmata: Janeway lesions (painless palm/sole macules), splinter hemorrhages (nail streaks), Roth spots (retinal hemorrhage with pale center), new murmur (valvular involvement). LLSB holosystolic murmur ↑ with inspiration = tricuspid regurgitation. Leading dx: right-sided (tricuspid) infective endocarditis — typical for IVDU.
🧠 FROM JANE — IE peripheral signs
F
Fever
R
Roth spots (retinal hemorrhages, pale center)
O
Osler nodes (painful, fingertips/toes)
M
Murmur
J
Janeway lesions (painless palms/soles)
A
Anemia
N
Nail-bed (splinter) hemorrhages
E
Embolism (septic pulmonary emboli in right-sided IE)
Admit (all IE patients). Empiric: Vancomycin IV + Ceftriaxone IV. Targeted (MRSA): continue IV Vancomycin × 4–6 weeks. Consults: Infectious Disease (ALL cases), Cardiology, Cardiac Surgery if needed. Surgical indications: acute HF, persistent infection after 7–10 days, recurrent emboli, fungal infection, abscess formation.
Task 7: Counseling?
Harm reduction: substance-use treatment referral, avoid IV drug use. Antibiotic prophylaxis for future dental work (indicated given history of IE). Complications to watch: embolic events, HF, recurrence. Long-term follow-up with cardiology/ID.
Cardio Quiz #3 — Hard Final Review
Interactive timed final-review quiz with explanations, topic filters, and scoring. Use the controls inside the quiz to start the timer or review explanations.