How to Use an AED (Automated External Defibrillator) - Complete Guide

What Is an AED?

• Semi-automatic AED - analyzes the rhythm and charges automatically, but requires the user to press a button to deliver the shock.
• Fully automatic AED - detects, charges, and delivers the shock without any button press - all bystanders must stay clear during charging.

Before You Begin - Recognize Cardiac Arrest

• Sudden collapse and unresponsiveness
• No normal breathing (absent or only gasping)
• No pulse when checked for less than 10 seconds
• Loss of consciousness

Step-by-Step AED Use

Step 1 - Assess the Scene and the Person

• Make sure the environment is safe before approaching.
• Tap the person's shoulders firmly and shout, "Are you okay?"
• Check for normal breathing and pulse for no more than 10 seconds.
• If unresponsive with no breathing/no pulse, act immediately.

Step 2 - Call for Help

• Call 911 (or local emergency number) immediately, or direct a bystander to call while you stay with the victim.
• If others are present: one person performs CPR, another locates and retrieves the AED.
• If you are alone: call first, then get the AED if one is nearby.

Step 3 - Start CPR Immediately

• Place the heel of your hand on the center of the chest (lower half of the sternum).
• Push hard and fast - at least 2 inches deep, at a rate of 100-120 compressions per minute.
• Ratio: 30 compressions to 2 rescue breaths.
• Minimize interruptions - keep compressions going until the AED is ready.

Step 4 - Turn On the AED

• Open the AED case - many models turn on automatically when opened.
• If not automatic, press the power button.
• Follow the voice prompts - the AED guides you through every step with clear spoken instructions.

Step 5 - Prepare the Chest

• Remove all clothing from the chest - expose the bare skin completely.
• The chest must be dry. If wet, dry it quickly with a cloth.
• If the person has a hairy chest, the pads may not stick. Use the razor (usually in the AED kit) to shave the pad placement areas.
• Remove any medication patches or metallic objects from the pad zones.

Step 6 - Apply the Electrode Pads Correctly

• Peel the backing off and press pads firmly to bare skin - no air pockets.
• If pads might touch each other (small child or small chest), place one pad in the center of the chest and the other on the back between the shoulder blades.
• If the patient has an implanted pacemaker or ICD (visible as a lump under the skin), place the pad at least 2 inches away from it.
• Plug the pad connector cable into the AED if it is not pre-connected.

Step 7 - Let the AED Analyze the Heart Rhythm

• The AED will announce: "Analyzing rhythm - do not touch the patient."
• Stop CPR and make sure nobody touches the person during analysis - even minor movement can interfere with rhythm detection.
• The AED determines automatically whether a shockable rhythm (VF or pulseless VT) is present.

Step 8 - Deliver the Shock (If Advised)

• If a shock is needed, the AED will announce "Shock advised" and will charge automatically to a preset energy level.
• During charging on a semi-automatic AED: resume CPR while it charges. Stand clear just before the shock.
• On a fully automatic AED: stand clear immediately during charging - it will deliver the shock on its own.
• Loudly call out "Stand clear!" and visually confirm no one is touching the patient or the surface they are lying on.
• On a semi-automatic: press the flashing SHOCK button to deliver the shock.
• The shock will cause a sudden muscle contraction in the patient.

Step 9 - Resume CPR Immediately After the Shock

• Do NOT pause to check the pulse or re-analyze the rhythm immediately after the shock.
• Start chest compressions again right away - 30 compressions to 2 ventilations.
• Continue for 5 cycles (approximately 2 minutes) of CPR.
• This is critical because the heart may be stunned after defibrillation and needs compression support to regain full pumping function.

Step 10 - Reassess and Repeat if Needed

• After 2 minutes of CPR, the AED will prompt you to stop and re-analyze.
• If another shock is needed, follow Steps 7-9 again.
• If no shock is advised, check for a pulse and signs of circulation.
• Continue CPR + AED cycles until:
  • Emergency medical services (EMS) arrive and take over.
  • The person shows clear signs of life (normal breathing, coughing, movement).
  • You are physically unable to continue.

Special Situations

Energy Levels (For Healthcare Providers Using Manual Defibrillators)

• Biphasic defibrillator (standard AED type): 120-200 J (manufacturer-specific default, typically ~200 J)
• Monophasic defibrillator: 360 J

After the Event - AED Maintenance

• Replace the electrode pads after each use (single-use only).
• Replace batteries as needed (typically every 4 years or per manufacturer).
• AEDs perform self-checks automatically - if an alarm/beep is triggered, contact the manufacturer.
• Register your AED with the manufacturer to receive safety alerts and recall notices.
• Store it in a clearly marked, easily accessible location and ensure everyone nearby knows where it is.

Key Reminders

1. Speed matters - every minute without defibrillation during VF reduces survival by 7-10%.
2. CPR + AED together dramatically increases survival compared to either alone.
3. You cannot harm someone with an AED - the device will only advise a shock if it detects a shockable rhythm. It will say "No shock advised" for any other rhythm.
4. Modern AEDs also provide CPR feedback via metronome beats or real-time guidance on compression rate and depth, which improves CPR quality and the chance of successful defibrillation.
5. Training is recommended but not required - the voice prompts are designed for untrained bystanders to follow successfully.

NSTEMI - What It Is and How to Diagnose It

What Is NSTEMI?

Spectrum of acute coronary syndromes - from unstable angina to NSTEMI to STEMI (Harrison's Principles of Internal Medicine, 22e)

Pathophysiology (Why It Happens)

1. Plaque rupture with inflammation - thin-capped lipid-rich plaque fissures; inflammatory T-cell response drives thrombosis.
2. Plaque rupture without inflammation - mechanical fissuring.
3. Plaque erosion - present in at least one-third of ACS cases; the overlying endothelium erodes, exposing the subendothelium and triggering thrombus.
4. Spasm or microvascular dysfunction - no thrombosis; epicardial or microvascular spasm, typically on a background of fixed obstruction.

• Left main stenosis: <10%
• Three-vessel CAD: ~35%
• Two-vessel CAD: ~25%
• Single-vessel CAD: ~20%
• No apparent critical stenosis: ~10% (microvascular or spasm)

Clinical Presentation

Symptoms

1. Occurs at rest or with minimal exertion, lasting more than 10 minutes
2. Recent onset (within the prior 2 weeks)
3. Crescendo pattern - distinctly more severe, prolonged, or frequent than previous episodes

• Usually substernal, severe, pressure-like or squeezing
• Radiates to the left arm, left shoulder, neck, or jaw
• Associated with diaphoresis, nausea, shortness of breath

• Dyspnea alone
• Epigastric discomfort / nausea
• Unexplained fatigue or weakness
• Pain only in the jaw, shoulder, or arm

• Diaphoresis, pale/cool skin
• Sinus tachycardia
• S3 or S4 heart sounds
• Basilar lung crackles (rales)
• Hypotension, or in extreme cases, cardiogenic shock

Always exclude life-threatening mimics: pulmonary embolism, aortic dissection, cardiac tamponade.

Diagnosis of NSTEMI

1. History and Risk Factor Assessment

• Age ≥65 years
• Known CAD (stenosis ≥50%)
• Diabetes mellitus
• Hypertension, hyperlipidemia, smoking
• Family history of premature CAD (first-degree relative before age 50)
• Prior MI, PCI, or CABG

2. ECG (12-Lead)

• Wellens' Syndrome - deep symmetric T-wave inversions or biphasic T waves in V2-V3 (sometimes V1-V6), seen when pain-free, with normal/minimally elevated biomarkers. Indicates a critical proximal LAD stenosis - very high risk for imminent large MI. About 15% of unstable angina patients display this sign.
• ST depression in multiple leads + ST elevation in aVR and/or V1 - suggests ischemia from left main or multivessel disease - very high risk.
• Posterior STEMI pattern (ST depression in V1-V3 = mirror image) - always obtain posterior leads (V7-V9) if suspected.

The posterior circulation (circumflex artery) is poorly seen on standard ECG - always consider posterior leads or urgent echocardiography when posterior NSTEMI is suspected.

3. Cardiac Biomarkers (Troponin) - The Definitive Diagnostic Test

NSTEMI = troponin value above the 99th percentile of the upper reference limit, with a rising and/or falling pattern (delta troponin), in the appropriate clinical context.

Testing Protocol (ACC/AHA 2025 / ESC Guidelines):

• Detects 90-100% of AMI at arrival
• Identifies small rises and falls (delta change) that older assays missed
• The 1-hour rapid rule-out algorithm (no abnormal elevation at 0 h or 1 h) has been endorsed by recent guidelines
• Has led to an increase in NSTEMI diagnoses (and corresponding decrease in UA) because smaller levels of necrosis are now detectable

• Troponin peaks at 12-24 hours after symptom onset and gradually decreases
• Elevations persist for up to 14 days (or longer)
• CK-MB is no longer recommended as a primary diagnostic marker for NSTEMI - it lacks cardiac specificity (also present in skeletal muscle)
• BNP/NT-proBNP elevation in ACS without known heart failure suggests large infarction - warrants urgent angiography
• Troponin elevation of any amount is always associated with worse outcomes - more elevation = worse prognosis

Causes of Troponin Elevation That Are NOT NSTEMI (must distinguish):

4. Additional Investigations

5. Risk Stratification Scores

• Age ≥65 years
• Known CAD (stenosis ≥50%)
• ST deviation >0.5 mm on ECG
• ≥2 anginal events in prior 24 hours
• Elevated cardiac markers
• Prior aspirin use (paradoxically indicates higher-risk patients)
• ≥3 CAD risk factors

6. Summary: Diagnostic Criteria for NSTEMI

1. Clinical symptoms consistent with ACS (chest pain/discomfort at rest, or crescendo pattern)
2. No persistent ST-segment elevation on ECG (the absence of STEMI)
3. Troponin above the 99th percentile of the upper reference limit with a dynamic rise and/or fall pattern
4. No alternative explanation for the troponin elevation (e.g., not purely due to PE, sepsis, renal failure alone)