---

High-Yield Emergency Medicine Topics

1. Cardiovascular Emergencies

• ACS - STEMI vs NSTEMI, Killip classification, thrombolytics vs PCI
• Aortic dissection - Stanford/DeBakey classification, BP management
• Cardiac tamponade - Beck's triad, pulsus paradoxus, emergency pericardiocentesis
• Arrhythmias - AF, VT, VF, SVT - when to cardiovert vs defibrillate
• Heart failure - acute pulmonary edema management

2. Respiratory Emergencies

• Tension pneumothorax - needle decompression landmarks
• Status asthmaticus - stepwise management, MgSO4 dosing
• Pulmonary embolism - Wells score, PERC rule, massive PE management
• ARDS - Berlin criteria, low tidal volume ventilation

3. Neurological Emergencies

• Stroke - tPA window (4.5 hrs), NIHSS, hemorrhagic vs ischemic
• Status epilepticus - Benzodiazepines → phenytoin → propofol/midazolam
• Meningitis - empiric antibiotics (don't delay for LP), dexamethasone
• Raised ICP - osmotherapy, head positioning, hyperventilation (temporizing)

4. Trauma

• ATLS primary survey - ABCDE, permissive hypotension in penetrating trauma
• Hemorrhagic shock - 4 classes, damage control resuscitation (1:1:1)
• Head injury - GCS scoring, surgical thresholds (EDH vs SDH)
• Spinal injury - NEXUS criteria, Canadian C-spine rule

5. Toxicology

• Organophosphate poisoning - SLUDGE/DUMBELS, atropine + pralidoxime
• Paracetamol overdose - Rumack-Matthew nomogram, NAC protocol
• Opioid/Benzodiazepine overdose - reversal agents, doses
• TCA overdose - sodium bicarb for wide QRS, avoid physostigmine
• Digoxin toxicity - ECG changes, Fab fragments

6. Metabolic/Endocrine

• DKA - diagnostic criteria, insulin protocol, K+ replacement pitfalls
• Hyperosmolar state (HHS) - distinguishing from DKA
• Adrenal crisis - hydrocortisone dosing
• Thyroid storm - Burch-Wartofsky score, PTU vs methimazole, SSKI timing

7. Renal/Electrolytes

• Hyperkalemia - ECG changes, calcium gluconate vs chloride, treatment ladder
• Hyponatremia - correction rate (max 8-10 mEq/24h), ODS risk
• Rhabdomyolysis - CK thresholds, aggressive IVF

8. Procedural/Airway

• RSI - drug doses (succinylcholine vs rocuronium), failed airway algorithm
• ACLS algorithms - VF/pVT, PEA/asystole, post-ROSC care
• Ultrasound in EM - FAST exam, RUSH protocol, cardiac tamponade

9. Infectious/Sepsis

• Sepsis-3 criteria - qSOFA, SOFA, fluid resuscitation bundles
• Neutropenic fever - empiric antibiotic coverage
• Necrotizing fasciitis - LRINEC score, surgical emergency

10. Obstetric Emergencies

• Eclampsia - MgSO4 dosing, labetalol/hydralazine for BP
• Ectopic pregnancy - beta-hCG discriminatory zone, methotrexate criteria
• PPH - 4 T's (tone, tissue, trauma, thrombin), uterotonics

---

Exam Strategy Tips

• Pattern questions are common: ECG + clinical scenario, toxidrome identification, "what do you do next?"
• Know exact drug doses for: atropine, adenosine, epinephrine, amiodarone, labetalol, tPA
• Scoring systems are frequently tested: GCS, NIHSS, Wells, CURB-65, Killip, Rankin
• "Do first" questions - always think airway → breathing → circulation before specific treatment

---

---

SVT with Aberrancy vs. VT - The High-Yield EM Breakdown

What is SVT with Aberrancy?

• SVT with baseline wide QRS - pre-existing fixed BBB (RBBB or LBBB present even in sinus rhythm)
• SVT with aberrancy - "functional" block in a bundle branch that occurs only during tachycardia (rate-related, because one bundle branch hasn't finished repolarizing when the next impulse arrives)

---

Why Does It Matter in EM?

Golden Rule for EM exams: When in doubt, treat as VT. ~80% of WCT is VT. Giving verapamil to VT can kill the patient.

---

The Big Classification - Start Here

---

ECG Features That Suggest VT (not SVT with Aberrancy)

Clinical context (most important)

• Structural heart disease - prior MI, cardiomyopathy, cardiac surgery, infiltrative disease → strongly favors VT
• Age >50 with CAD history → almost always VT
• A young patient with no cardiac history, palpitations since childhood → more likely SVT with aberrancy

ECG features favoring VT

• AV dissociation = P waves marching through independently at a different rate from QRS = pathognomonic for VT
• Fusion beat = partial capture of ventricle by sinus impulse merging with VT beat = proves AV dissociation = VT
• Capture beat = sinus impulse completely captures the ventricle producing a narrow beat amid wide beats = VT

---

The Brugada Algorithm (Most Tested ECG Algorithm)

1. Absence of RS complex in ALL precordial leads? → Yes = VT
2. RS interval >100 ms in ANY precordial lead? → Yes = VT
3. AV dissociation present? → Yes = VT
4. Morphology criteria for VT in both V1-V2 AND V6? → Yes = VT
5. If all 4 are NO → SVT with baseline wide QRS or SVT with aberrancy

---

Morphology Criteria in Detail (Step 4 of Brugada)

If RBBB pattern (R' in V1):

If LBBB pattern (S in V1):

---

Other Causes of Wide-Complex Tachycardia (don't forget)

• Antidromic AVRT (WPW) - delta waves, accessory pathway conducts antegrade
• Pre-excited AF - irregular, very fast, life-threatening - avoid AV nodal blockers
• Hyperkalemia - sine wave pattern, no discrete P waves
• Flecainide/class IC toxicity - drug-induced conduction slowing
• Fascicular tachycardia - relatively narrow WCT, RBBB + left axis, responds to verapamil (exception to the rule)

---

EM Management Algorithm

Wide Complex Tachycardia
         |
    Haemodynamically unstable? (hypotension, shock, pulmonary oedema, chest pain)
         |
       YES → Synchronized DC cardioversion immediately
         |
        NO
         |
    Apply Brugada criteria + clinical context
         |
    VT likely (>80% chance) → IV Amiodarone 150 mg over 10 min, then 1 mg/min
         |
    SVT with aberrancy confirmed? → Adenosine 6 mg IV rapid push
         |
    Still uncertain? → Treat as VT (never give CCBs or beta-blockers)

Exam trap: Adenosine can be used diagnostically even in WCT - if it terminates the rhythm or transiently shows underlying SVT pattern, it confirms SVT with aberrancy. It will not harm VT (just transiently blocks AV node, may cause brief AV dissociation visible on monitor).

---

High-Yield Exam Summary

---

---

Pulmonary Embolism - Complete EM Exam Guide + Latest 2026 Guidelines

---

🔴 BREAKING: 2026 AHA/ACC Guideline (Brand New!)

• Introduces the AHA/ACC Acute PE Clinical Categories (replaces older massive/submassive/low-risk terminology)
• Strong recommendation for Pulmonary Embolism Response Teams (PERTs) as a new care standard
• Encourages more outpatient management of low-risk PE
• Addresses catheter-directed therapies more explicitly for intermediate/high-risk PE

---

Classification - Start Here

Classic Classification (ESC-based, still widely used in exams)

2026 AHA/ACC New PE Clinical Categories

---

Clinical Features

• Dyspnoea + Chest pain (pleuritic) + Haemoptysis

• Tachycardia (most sensitive sign)
• Unexplained dyspnoea at rest or exertion
• Pleuritic chest pain
• Syncope (suggests massive PE with RV failure)
• Signs of DVT (unilateral leg swelling)

• Sinus tachycardia (most common)
• S1Q3T3 pattern (S wave in lead I, Q wave + T-wave inversion in lead III)
• T-wave inversion V1-V4 (right heart strain)
• Incomplete/complete RBBB
• Right axis deviation
• Note: normal ECG does NOT exclude PE; these findings increase probability

• Cardiomegaly, basilar atelectasis, pleural effusion
• Westermark's sign - focal oligaemia (hyperlucency from obstructed lobar artery) - <5%
• Hampton's hump - peripheral wedge-shaped opacification (pulmonary infarction) - <5%
• Normal CXR with hypoxaemia = high suspicion for PE

---

Risk Stratification Scores

Wells Score for PE (Original)

• 6 = High risk (78% probability of PE)

• 2-6 = Moderate risk (28%)
• <2 = Low risk (3.4%)
• Dichotomous version: >4 = PE likely (go straight to CTPA); ≤4 = PE unlikely (D-dimer first)

PERC Rule (PE Rule-Out Criteria)

If PERC = 0 (all absent) → PE excluded. No D-dimer needed. If any 1 PERC criterion present → go to D-dimer/Wells pathway

sPESI (Simplified PESI) - for low-risk identification

• sPESI = 0 → low risk, consider early discharge/outpatient treatment

---

Diagnostic Algorithm

• Low probability (Wells 0-1): Check PERC → if 0, PE ruled out; if ≥1, D-dimer
• Moderate probability (Wells 2-6): D-dimer → if negative, PE ruled out; if positive, CTPA
• High probability (Wells ≥7): Go straight to CTPA

Age-Adjusted D-dimer (High Yield!)

• Cutoff = Age × 10 µg/L (FEU units)
• E.g., 70-year-old: D-dimer cutoff = 700 µg/L instead of 500 µg/L
• Reduces unnecessary CTPA in elderly without sacrificing sensitivity

YEARS Algorithm (newer, increasingly used)

• If 0 criteria: D-dimer threshold = 1000 µg/L
• If ≥1 criterion: D-dimer threshold = 500 µg/L (standard)
• If threshold exceeded → CTPA

---

Imaging

---

Treatment

1. Hemodynamically Unstable (Massive/High-Risk PE)

Massive PE (shock/arrest)
    ↓
Immediate anticoagulation (heparin UFH bolus 80 U/kg IV)
    ↓
Systemic thrombolysis - FIRST LINE
  • Alteplase (tPA) 100 mg IV over 2 hours
  • For cardiac arrest: 50 mg rapid bolus
    ↓
If thrombolysis fails/contraindicated:
  • Catheter-directed therapy (CDT) or mechanical thrombectomy
  • Surgical embolectomy (last resort)

• Prior intracranial haemorrhage
• Recent (<3 months) ischaemic stroke
• CNS tumour/AVM
• Recent (<3 months) head trauma/surgery
• Active internal bleeding (not menses)

2. Hemodynamically Stable + RV Dysfunction (Submassive/Intermediate-High Risk)

• Anticoagulation with LMWH or UFH
• Do NOT give routine systemic thrombolysis (risk of major haemorrhage, especially ICH, outweighs benefit in stable patients)
• Rescue thrombolysis if clinical deterioration occurs
• CDT (catheter-directed thrombolysis at low dose, e.g., tPA 2 mg/hr via catheter) - may be considered in selected patients (high bleeding risk for systemic lysis)
• PERT team consultation (per 2026 AHA/ACC guideline)

3. Low-Risk PE

• Anticoagulation - DOACs preferred
• Early discharge/outpatient treatment if sPESI = 0 and no other barriers (supported by 2026 AHA/ACC, ESC, CHEST)
• Hestia criteria can also be used to identify suitability for home treatment

---

Anticoagulation - Drug Choice

• Provoked PE (reversible trigger - surgery, immobilisation): 3 months
• Unprovoked PE or persistent risk factors: ≥3-6 months, consider extended therapy
• Recurrent VTE or antiphospholipid syndrome: Indefinite

---

IVC Filter

• Acute PE + absolute contraindication to anticoagulation
• Does NOT reduce PE recurrence or mortality - all guidelines agree

---

Biomarkers in PE

---

Echo Findings in Massive PE

• RV dilatation (RV:LV ratio ≥1.0 on echo or CTPA)
• RV hypokinesis with sparing of the apex (McConnell's sign - RV free wall hypokinesis, apex normal)
• Tricuspid regurgitation, elevated RVSP
• TAPSE <16 mm (RV systolic dysfunction)
• Paradoxical interventricular septal shift ("D-sign")
• Thrombus in right heart

---

High-Yield Exam Summary Table

---

---

Pneumothorax - Complete MD Emergency Medicine Guide

---

Classification

---

Pathophysiology

• Normally, pleural pressure is negative (-3 to -5 cmH₂O) keeping the lung expanded
• Air entry into pleural space → lung collapses (elastic recoil)
• PSP: rupture of subpleural blebs/bullae at the apex → air enters with each breath
• Tension PTX: one-way valve mechanism → air enters pleural space with each breath but cannot exit → progressive build-up → mediastinal shift → kinks SVC/IVC → obstructive shock → cardiac arrest

---

Clinical Features

Simple Pneumothorax

• Sudden pleuritic chest pain (sharp, ipsilateral)
• Dyspnoea (severity varies - mild in PSP, severe in SSP)
• Tachycardia
• Decreased breath sounds ipsilateral
• Decreased chest expansion ipsilateral
• Hyper-resonance on percussion ipsilateral

Tension Pneumothorax (the killer - diagnose clinically, DON'T wait for CXR!)

Exam Trap: Tracheal deviation is a LATE sign and often ABSENT - do not wait for it! Treat on clinical suspicion. In ventilated patients: sudden rise in peak airway pressure + haemodynamic collapse = tension PTX until proven otherwise.

---

Diagnosis

CXR Findings

• Absence of lung markings beyond the visceral pleural line
• Visible pleural edge (white line)
• Ipsilateral lung collapse
• Tension PTX on CXR (if you choose to get one): tracheal deviation, mediastinal shift, depressed ipsilateral diaphragm, contralateral lung compression

Sizing on CXR

• Small: <2 cm rim
• Large: ≥2 cm rim

• Small: <3 cm
• Large: ≥3 cm

CT Chest (gold standard for sizing and characterisation)

• Detects occult PTX not visible on CXR
• Identifies bullae/blebs, underlying lung disease
• Measures PTX size accurately

POCUS (Point-of-Care Ultrasound) - High Yield for EM!

POCUS advantage over CXR: More sensitive (especially in supine trauma patients where air rises anteriorly and is missed on AP CXR). Lung point is pathognomonic.

---

Treatment - The EM Framework

STEP 1: Is it a TENSION pneumothorax?

Tension PTX (shock + absent breath sounds + hyper-resonance)?
                    |
                  YES
                    |
        Immediate decompression - DO NOT get CXR

STEP 2: Immediate Decompression for Tension PTX

• Insert 14-16G angiocatheter perpendicular to chest wall, over the SUPERIOR border of the rib (avoids neurovascular bundle at inferior rib margin)
• A rush of air confirms entry into pleural space
• This converts tension → simple PTX → MUST follow with chest tube

Why MAL is now preferred: Cadaveric studies showed significantly shorter distance from skin to pleural space at 4th/5th ICS MAL vs 2nd ICS MCL, especially in obese patients where 2nd ICS MCL often fails (chest wall too thick for standard 14G needle)

• Incision at 4th/5th ICS, MAL
• Sharp dissection through ICS above the rib
• Finger sweeps pleural space
• Higher success than needle decompression; mandatory before chest tube in trauma

Zone of Safety for Chest Tube / Finger Thoracostomy

• Anterior: Lateral border of pectoralis major
• Inferior: Nipple line (men) / 2 fingerbreadths above inframammary fold (women)
• Posterior: Anterior border of latissimus dorsi

---

Management of Simple/Spontaneous PTX

2024 ERS/EACTS/ESTS Guidelines - Major Paradigm Shift!

BTS 2023 Guideline

• Needle aspiration or tube drainage if patient unsuitable for conservative/ambulatory management
• Recommends surgical pleurodesis + bullectomy for recurrence prevention

---

Full Management Algorithm

PNEUMOTHORAX
      |
 Haemodynamically unstable / Tension?
      |
     YES → Immediate needle decompression (4th/5th ICS MAL)
             → Followed by chest tube (same side)
      |
      NO
      |
   PRIMARY SPONTANEOUS (PSP)
      |
   Clinically stable, minimally symptomatic?
      |
     YES → CONSERVATIVE (2024 ERS guideline)
             Observe 4h, supplemental O2, early follow-up
             Regardless of size if stable
      |
      NO (symptomatic, large, or patient preference for treatment)
           |
        Needle aspiration FIRST (2024 ERS - STRONG recommendation)
           |
        Failed aspiration or SSP?
           |
        Chest tube (intercostal drain)
           |
        Pigtail catheter (8.3-14Fr) equally effective for pure PTX
        Large bore (≥28Fr) if haemothorax or large air leak
   
   SECONDARY SPONTANEOUS (SSP)
      → Almost always requires intercostal drain
      → More aggressive management due to limited respiratory reserve
      → Hospital admission mandatory
   
   TRAUMATIC
      → Drain all (chest tube) if PPV required
      → Small occult PTX (<3.5 cm) may be observed if stable, even on ventilator
      → Large (≥3.5 cm) or symptomatic → chest tube

---

Chest Tube Management

• Drain connected to underwater seal ± suction (-20 cmH₂O)
• Suction if persistent air leak or lung not re-expanding
• Stop suction once air leak resolved → water seal only
• Clamping trial before removal: clamp 4 hours → repeat CXR → remove if no re-accumulation
• Pigtail catheter (Seldinger technique, 8-14Fr): equally effective for pure PTX, significantly less painful - now preferred for spontaneous PTX
• From 2023 meta-analysis: pigtail vs large-bore chest tube - no difference in drainage success but significantly less pain with pigtail (PMID 36802811)

---

Recurrence Prevention

• After first PSP: 30-50% within 2 years
• After second PTX: 50-80% chance of third
• After VATS: < 5%

• Life-threatening tension PTX
• Massive air leak / incomplete re-expansion
• Air leak >4 days after second tube placed
• Associated haemothorax with complications
• Identifiable bullous disease
• Patient preference (2024 ERS: early surgery acceptable option)
• Bilateral simultaneous PTX
• Occupation at risk (pilot, diver)

---

Open Pneumothorax ("Sucking Chest Wound")

• Penetrating trauma creates chest wall defect > 2/3 tracheal diameter → air preferentially enters through wound (less resistance than trachea)
• Immediate management: 3-sided occlusive dressing (Asherman seal or vented chest seal)
  • Seals 3 sides, leaves 4th open → acts as flutter valve (air out, not in)
  • A fully sealed dressing risks converting to tension PTX
• Definitive: Formal chest tube (separate site from wound) + surgical repair of defect

---

Special Situations

PTX in Ventilated Patients

• All PTX on PPV need drainage (even small ones - can rapidly tension)
• Exception: small occult PTX ≤3.5 cm, stable patient - may observe with serial imaging

Iatrogenic PTX (post-subclavian/IJV line)

• Small, asymptomatic: observe, supplemental O2
• Symptomatic or enlarging: needle aspiration or chest tube

Haemopneumothorax

• Large-bore chest tube (28-32Fr) mandatory
• Drain blood to prevent empyema / fibrothorax

PTX in Pregnancy

• Treat aggressively (SSP criteria); foetal hypoxia risk
• VATS safe in pregnancy if needed

Bilateral PTX

• Surgery indicated even at first episode

---

High-Yield Exam Summary

---