ECG
RESPIRATORY TRAPS
SHOCK
NEURO EMERGENCIES
HEMATOLOGY AND IMMUNOLOGY
100

A wide-complex tachycardia at 160 bpm with AV dissociation and fusion beats in a 68-year-old with prior MI

What is Ventricular Tachycardia?

Why:
AV dissociation = atria and ventricles not communicating → ventricular origin.
Fusion beats = sinus impulse partially captures the ventricle → confirms VT.
Exam trap: Most WCT in older ischemic patients = VT until proven otherwise.

100

Sudden dyspnea, clear lungs, hypotension, JVD after long flight.

What is a Massive Pulmonary Embolism?

Why:
Obstructive shock.
RV strain → JVD + hypotension.
Clear lungs differentiate from cardiogenic shock.

100

Warm flushed skin, bounding pulses, hypotension.

 What is Early Septic Shock (Distributive)?

Why:
Peripheral vasodilation → warm shock phase.
SVR drops before cardiac output drops.

100

Worst headache of life, nuchal rigidity

 What is Subarachnoid Hemorrhage?

Why:
Aneurysm rupture → blood irritates meninges → stiff neck.

100

A septic patient becomes hypotensive despite fluids. Labs show elevated lactate and widespread microthrombi consuming clotting factors.

What is Disseminated Intravascular Coagulation (DIC)?

Why:
Sepsis → systemic inflammatory cascade → massive thrombin activation.
Microclots form everywhere → clotting factors and platelets get consumed.
Patient paradoxically bleeds because they “used up” clotting components.
Think: Clotting + Bleeding at the same time.

200

ST depression in V1–V3 with tall R waves and upright T waves

What is a Posterior STEMI?

Why:
Posterior wall infarcts produce reciprocal changes anteriorly.
ST depression + tall R = mirror of ST elevation + Q wave posteriorly.
Trap: Students call this “ischemia.” It’s actually infarction

200

COPD patient becomes drowsy after high-flow oxygen.

What is Hypercapnic respiratory failure from hypoxic drive suppression?

Why:
Chronic CO₂ retainers rely partially on hypoxia to stimulate breathing.
Too much O₂ → ↓ respiratory drive → CO₂ narcosis.

200

Bradycardia, hypotension, warm dry skin after spinal trauma.

 What is Neurogenic Shock?

Why:
Loss of sympathetic tone.
Only shock type with bradycardia

200

Unilateral facial droop, including the forehead.

What is Bell’s Palsy?

Why:
The peripheral lesion affects the entire side.
Stroke spares the forehead.

200

A patient with HIV has a CD4 count of 150 and develops pneumonia from Pneumocystis jirovecii.

What is an Opportunistic Infection due to advanced immunosuppression? 

Why:
A CD4 count below 200 cells/mm³ meets the clinical definition of AIDS.
CD4 cells are essential for cell-mediated immunity, which is responsible for fighting intracellular pathogens (like certain fungi, viruses, and protozoa).
When CD4 levels drop this low, the immune system can no longer defend against organisms that normally wouldn’t cause disease, leading to opportunistic infections.  

300

Polymorphic VT in a patient with prolonged QT after receiving sotalol.

 What is Torsades de Pointes?

Why:
Sotalol prolongs repolarization (Class III effect).
Long QT → early afterdepolarizations → polymorphic VT.
Treatment = magnesium (stabilizes myocardium, shortens QT).

300

Unilateral absent breath sounds, hypotension, tracheal deviation

What is Tension Pneumothorax?

Why:
Air trapping → mediastinal shift → decreased venous return → obstructive shock.
Needle decompression before positive pressure ventilation.

300

Chest trauma, muffled heart sounds, JVD, hypotension

What is Cardiac Tamponade?

Why:
Beck’s triad.
Pericardial pressure restricts ventricular filling.

300

Sudden agitation, hyperthermia, headache, and altered LOC in a college student.

What is Meningitis?

Why:
Infection → cerebral inflammation → ICP rise.
Fever + AMS = infection until proven otherwise. Plus, in a large group, it is also a key clue. 


300

A patient develops hypotension, bronchospasm, urticaria, and angioedema minutes after penicillin.

What is Type I Hypersensitivity (IgE-mediated anaphylaxis)? 

Why:
IgE antibodies bind mast cells.
Re-exposure → mast cell degranulation → histamine release.
Results: vasodilation, capillary leak, bronchoconstriction.

400

Bradycardia, hypotension, inferior STEMI, clear lungs

What is a Right Ventricular Infarction?

Why:
RV infarcts are preload dependent.
Nitro ↓ preload → crash.
Clear lungs + hypotension + inferior STEMI = think RV involvement.

400

Pink frothy sputum, diffuse crackles, hypertensive crisis

What is Acute Pulmonary Edema?

Why:
Left ventricular failure → fluid backs into alveoli.
Hypertension increases afterload → worsens fluid shift.
Nitro decreases preload AND afterload.

400

Cool clammy skin, narrow pulse pressure, crackles

What is Cardiogenic Shock?

Why:
Pump failure.
Fluid overload + low cardiac output.

400

Postictal paralysis on one side.

What is Todd’s Paralysis?

Why:
Transient neuronal exhaustion after seizure.

400

A trauma patient has prolonged bleeding time, normal platelet count, and a history of heavy menses since adolescence.

What is von Willebrand Disease? 

vWF helps platelets adhere to damaged endothelium.
Defect → poor platelet function despite normal count.
Common inherited bleeding disorder.

500

Irregularly irregular rhythm with no P waves in a septic patient now hypotensive.

What is Atrial Fibrillation with RVR secondary to sepsis?

Why:
Sepsis → catecholamine surge → atrial irritability.
Loss of atrial kick + tachycardia worsens shock.
Treat underlying cause first (fluids, infection control).

500

Pediatric patient, rapid onset of stridor, muffled voice, tripod positioning

What is Epiglottitis?

Why:
Upper airway obstruction.
Stridor = inspiratory noise → supraglottic narrowing.
Do NOT aggressively manipulate the airway.

500

Hypotension after starting nitroglycerin in inferior STEMI.

What is Preload-dependent right ventricular failure?

Why:
RV infarcts need preload.
Nitro reduces preload → severe hypotension.

500

Unequal pupils, bradycardia, and hypertension are signs of

What is Cushing’s Reflex from Increased ICP?


500

A patient with sickle cell disease develops chest pain, fever, hypoxia, and new pulmonary infiltrates

What is Acute Chest Syndrome? 

Why:
Sickled RBCs obstruct the pulmonary vasculature.
Inflammation + infection + infarction combine.
The leading cause of death in sickle cell patients.
Treat aggressively: oxygen, fluids, antibiotics, pain control.

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