When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

ECG Guide | 12-Lead Interpretation

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🚨 Emergent -Act Immediately

STEMI

ST-Elevation Myocardial Infarction

Pattern: ST elevation ≥ 1mm in ≥ 2 contiguous leads (≥ 2mm in V1-V3 for men)
Morphology: Concave-up ("tombstone") or convex-up ST elevation with reciprocal ST depression in opposite leads

Localization:
• II, III, aVF → Inferior (RCA)
• V1-V4 → Anterior (LAD)
• I, aVL, V5-V6 → Lateral (LCx)
• V1-V2 depression → Posterior (get V7-V9)
• V3R-V4R elevation → RV infarct (avoid nitrates/volume depletion)

Action: Activate cath lab. ASA 325mg chewed. Heparin. Door-to-balloon < 90 min.

Ventricular Tachycardia (VT)

Wide complex, regular, ≥ 3 consecutive beats

Pattern: Wide QRS (> 120ms), regular, rate 150-250 bpm
Features favoring VT over SVT with aberrancy:
• AV dissociation (P waves marching independently)
• Capture/fusion beats
• Concordance (all precordial QRS same direction)
• Very wide QRS (> 160ms)
• Northwest axis (extreme right axis deviation)

Rule: Wide complex tachycardia = VT until proven otherwise, especially if age > 50 or structural heart disease.

Action: Stable → amiodarone (Cordarone) 150mg IV. Unstable → synchronized cardioversion. Pulseless → defibrillate.

Hyperkalemia

Progressive changes as K⁺ rises

Progression:
• K⁺ 5.5-6.5: Peaked T waves (tall, narrow, symmetric -earliest sign)
• K⁺ 6.5-7.5: Prolonged PR → flattened P waves → widened QRS
• K⁺ 7.5-8.0: Sine wave pattern (QRS merges with T wave)
• K⁺ > 8.0: VF → asystole

Action: Calcium gluconate 1g IV immediately (stabilizes membrane). Then insulin + D50 to shift K⁺. See Hyperkalemia topic for full protocol.

Complete Heart Block (3rd Degree)

No atrial impulses conduct to ventricles

Pattern: P waves and QRS complexes completely independent (AV dissociation). Regular P-P intervals. Regular R-R intervals. But NO relationship between them.

Escape rhythm:
• Junctional escape (narrow QRS, 40-60 bpm) → more stable
• Ventricular escape (wide QRS, 20-40 bpm) → unstable, high risk of asystole

Action: Atropine 1mg IV (may not work if infranodal). Transcutaneous pacing. Cardiology for transvenous pacer. Dopamine or epinephrine drip as bridge.

⚠️ Urgent -Requires Prompt Attention

Wellens Syndrome

Critical LAD stenosis -will STEMI if missed

Pattern: Deep symmetric T-wave inversions (Type A, more common) or biphasic T waves (Type B) in V2-V3 (± V1, V4-V6)

Key: Seen during pain-FREE interval (not during active chest pain). During pain, ST may be elevated.

Critical point: Do NOT stress test -will STEMI on the treadmill. Needs cath.

Action: Admit, anticoagulate, cardiology consult for cath. Medical management until intervention.

Brugada Syndrome

Risk of sudden cardiac death in structurally normal heart

Type 1 (diagnostic): Coved ST elevation ≥ 2mm in V1-V3 with T-wave inversion. "Shark fin" morphology.
Type 2 (suggestive): Saddleback ST elevation in V1-V3. Not diagnostic alone -needs provocation test (ajmaline/procainamide).

Key features: Young male, Asian descent, family history of sudden death, syncope, nocturnal agonal breathing.

Action: EP consult. ICD is the only proven therapy (no drug prevents VF in Brugada). Avoid fever (unmasks pattern), avoid Class I antiarrhythmics.

Prolonged QTc

Risk of Torsades de Pointes

Normal: < 440ms (men), < 460ms (women)
Concerning: > 480ms
Dangerous: > 500ms → high risk for Torsades de Pointes (TdP)

Common offenders: Haloperidol (Haldol), ondansetron (Zofran), fluoroquinolones, azithromycin (Zithromax), methadone, amiodarone (Cordarone), antipsychotics, hypoK, hypoMg

Action: Stop offending drug. Replete K⁺ > 4.0, Mg²⁺ > 2.0. If TdP occurs: IV magnesium 2g bolus + overdrive pacing (↑ HR shortens QT).

PE / Right Heart Strain

Acute right ventricular pressure overload

Classic (but uncommon): S1Q3T3 -deep S in lead I, Q wave + T inversion in lead III. Present in only ~20% of PE.

More common findings:
• Sinus tachycardia (#1 finding -most sensitive)
• Right axis deviation
• T-wave inversions in V1-V4 (RV strain pattern)
• New RBBB or incomplete RBBB
• Atrial fibrillation (new onset)

Remember: A normal ECG does NOT rule out PE. ECG is often normal in PE.

Action: If PE suspected → Wells score → D-dimer or CT-PA. See PE topic.

📋 Important Patterns to Recognize

Atrial Fibrillation

Irregularly irregular -most common sustained arrhythmia

Pattern: No P waves (fibrillatory baseline), irregularly irregular R-R intervals, narrow QRS (unless aberrancy/BBB)

Distinguish from:
• Atrial flutter: Regular, sawtooth P waves (especially II, III, aVF), often 150 bpm (2:1 block)
• MAT: ≥ 3 different P-wave morphologies, irregular, associated with COPD/hypoxia

Action: Rate control (metoprolol (Lopressor) or diltiazem (Cardizem)). CHA₂DS₂-VASc for anticoagulation. See Afib topic.

Pericarditis

Diffuse ST elevation -NOT a STEMI

Pattern: Diffuse concave-up ST elevation in nearly ALL leads + PR depression (especially II) + ST depression in aVR

Distinguish from STEMI:
• Pericarditis: diffuse (many territories), NO reciprocal changes, PR depression, concave-up
• STEMI: localized (one territory), reciprocal changes present, often convex-up

Key: PR depression in lead II is nearly pathognomonic for pericarditis.

Action: NSAIDs + colchicine (Colcrys). Echo to rule out effusion/tamponade. Do NOT give thrombolytics (not a STEMI!).

Heart Blocks (1st, 2nd degree)

AV conduction delays

1st degree: Prolonged PR > 200ms. Every P conducts. Usually benign -no treatment.

2nd degree Type I (Wenckebach): Progressive PR prolongation → dropped beat → cycle repeats. Usually nodal. Often benign.

2nd degree Type II (Mobitz II): Constant PR interval with sudden dropped QRS (no warning). Infranodal. High risk of progressing to complete heart block. Needs pacemaker.

Key rule: Wenckebach = watch. Mobitz II = pacer.

Bundle Branch Blocks

QRS > 120ms -which bundle is blocked?

RBBB: rsR' ("bunny ears") in V1-V2, wide S in I/V6. Mnemonic: "MaRRoW" -V1 has R (tall R'), V6 has W (wide S).

LBBB: Broad notched R in I/V6, deep QS or rS in V1. Mnemonic: "WiLLiaM" -V1 has W (QS), V6 has M (notched R).

Clinical significance:
• RBBB: Can be normal. New RBBB in ACS/PE → concerning.
• LBBB: Almost always pathological. New LBBB + chest pain → treat as STEMI equivalent (Sgarbossa criteria). Old LBBB makes STEMI diagnosis difficult.

Sgarbossa criteria (STEMI in LBBB): Concordant ST elevation ≥ 1mm (5 pts), concordant ST depression ≥ 1mm in V1-V3 (3 pts), discordant ST elevation ≥ 5mm (2 pts). ≥ 3 pts → STEMI.

Digoxin Effect vs Toxicity

Know the difference -one is expected, one is dangerous

Digoxin effect (therapeutic): "Salvador Dali moustache" -downsloping ST depression with scooped/sagging morphology. Shortened QT. This is expected and NOT toxic.

Digoxin toxicity:
• Virtually ANY arrhythmia (classic: regularised Afib, bidirectional VT, accelerated junctional rhythm, PAT with block)
• Nausea, vomiting, visual disturbances (yellow halos)
• Risk factors: hypoK, hypoMg, renal failure, advanced age

Action for toxicity: Hold digoxin. Check level + K⁺ + Mg²⁺. Digoxin-specific antibody (Digibind/DigiFab) if hemodynamically unstable, life-threatening arrhythmia, or K⁺ > 5.0.

Hypothermia (Osborn/J Waves)

Pathognomonic for hypothermia

Pattern: Positive deflection at the J-point (junction of QRS and ST segment). Amplitude increases as temperature drops.

Other findings: Bradycardia, prolonged intervals (PR, QRS, QT), atrial fibrillation, muscle tremor artifact (shivering)

Key: At core temp < 28°C → high risk of VF. Osborn waves resolve with rewarming. NOT an indication for antiarrhythmics.

Action: Rewarm. See Hypothermia topic. "No one is dead until warm and dead."

📐 Quick Reference -Intervals & Axes

Parameter	Normal	Abnormal	Think...
Heart Rate	60-100 bpm	< 60 = bradycardia, > 100 = tachycardia	300 / (# large boxes between R-R)
PR Interval	120-200 ms	> 200 = 1st degree AV block. Short PR = WPW or junctional	3-5 small boxes
QRS Duration	< 120 ms	> 120 = BBB, ventricular rhythm, hyperK, or pre-excitation	< 3 small boxes
QTc	< 440 (M) / < 460 (F)	> 500 = high Torsades risk	QTc = QT / √RR. Use calc.
Axis	-30° to +90°	Left axis: -30° to -90° (LVH, LAFB). Right axis: +90° to +180° (RVH, PE, LPFB)	Lead I and aVF both upright = normal

ECG Systematic Approach: Rate → Rhythm → Axis → Intervals (PR, QRS, QT) → ST segment/T waves → Compare to prior. Never skip steps -pattern recognition fails when you're tired. Systematic review catches what your eyes miss.