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.

RoundsRx

Dashboard

Overview

Recent

Rotations

Quick Reference

Antibiotic Guide Analgesia Guide Sedation Guide Bowel Regimen Electrolyte Replacement Pain Management & Conversions Drug Interactions Anticoag Reversal IV Fluid Guide Inotropes Guide Vasopressors Insulin Guide Code Blue & Rapid Response Procedures Guide ECG Interpretation Lab Interpretation Radiology Quick Ref GCS Pocket Card Admission Orders & I-PASS Landmark Trials

Tools

💎 Clinical Pearls 🧠 Pimp Me Quiz 🧮 Clinical Calculators 📰 What's New 🎓 Intern Survival Guide ✅ Rounding Checklists 🩺 Procedure Guides ⚡ Electrolyte Replacement 💧 IV Fluids Guide 🩸 Transfusion Guide 💓 ECG Pattern Guide 🧪 Lab Interpretation Guide 📱 QR Poster 🔗 Resources 🎙️ Channels & Podcasts 🎮 Medical Games 🏛️ Famous Cases 🎬 Media Library

ℹ️ About

Available offline

CardiologyAcute/Outpatient

Syncope

Transient loss of consciousness from cerebral hypoperfusion. The key question: is this cardiac or benign? Risk-stratify every patient -most syncope is vasovagal, but cardiac syncope kills.

🔍 Overview

Definition & Classification

Syncope = transient loss of consciousness (TLOC) due to global cerebral hypoperfusion, with rapid onset, short duration, and spontaneous complete recovery. NOT seizure, NOT hypoglycemia, NOT stroke.

Classification

Category	Mechanism	Examples	Prognosis
Reflex (neurally mediated)	Inappropriate vasodilation ± bradycardia	Vasovagal, situational (cough, micturition), carotid sinus hypersensitivity	Benign
Orthostatic hypotension	Volume depletion or autonomic failure	Dehydration, hemorrhage, meds (alpha-blockers, diuretics), autonomic neuropathy (DM, Parkinson)	Treat underlying cause
Cardiac -Arrhythmic	Brady or tachy → low CO	Complete heart block, VT, long QT, Brugada, sick sinus, pacemaker malfunction	Dangerous
Cardiac -Structural	Fixed obstruction → low CO	Severe AS, HOCM, massive PE, aortic dissection, cardiac tamponade, atrial myxoma	Dangerous

Key Epidemiology

~40% of people will experience syncope in their lifetime. 1-3% of ED visits.
Reflex syncope accounts for ~60% of cases (most common overall)
Cardiac syncope: ~15% of cases but accounts for majority of syncope-related deaths
Unexplained in ~15-20% even after full workup
1-year mortality: vasovagal ~0%, cardiac syncope ~18-33%

Not all TLOC is syncope. Differential: seizure (postictal state, tongue biting, incontinence), hypoglycemia (glucose < 50), TIA (focal deficits), psychogenic pseudosyncope (eyes closed, prolonged duration).

📋 On Rounds

Pimp Questions

Q: What are the high-risk ECG findings in syncope?

A: Bifascicular block, QTc > 500ms, Brugada pattern (coved ST in V1-V3), pre-excitation (WPW), Mobitz II or complete heart block, sustained or non-sustained VT, sinus pauses > 3 sec, new Q waves suggesting MI. Any of these = admit for monitoring.

Q: What is the San Francisco Syncope Rule (CHESS)?

A: C-HF history, H-Hct < 30%, E-ECG abnormal, S-Shortness of breath, S-Systolic BP < 90. Any positive = high risk (~98% sensitivity). Identifies patients needing admission. Negative SFSR = low risk for 7-day serious outcome.

Q: How do you differentiate syncope from seizure?

A: Syncope: prodrome (lightheaded, warm, diaphoretic), brief LOC (< 30 sec), rapid recovery. Seizure: aura, tonic-clonic activity > 60 sec, tongue biting (lateral), postictal confusion 15-30 min, incontinence. Brief myoclonic jerks CAN occur in syncope (convulsive syncope) -don't be fooled.

Q: When do you admit a patient with syncope?

A: Admit if: abnormal ECG, structural heart disease, exertional syncope, syncope causing significant injury, recurrent syncope, family hx of sudden cardiac death, new neurologic deficits. Low-risk features (young, prodrome, positional trigger, normal ECG, no heart disease) = safe discharge.

Q: What is carotid sinus hypersensitivity?

A: Exaggerated response to carotid sinus stimulation → > 3 sec asystole (cardioinhibitory) or SBP drop > 50 mmHg (vasodepressor) or both (mixed). Common in elderly males. Diagnosed by carotid sinus massage (CSM). Treatment: pacemaker for cardioinhibitory type.

Q: What is the PERC rule's role in syncope?

A: Syncope can be the presenting symptom of PE (up to 17% of PE patients). If you suspect PE, use PERC to rule out (if all 8 criteria negative → no D-dimer needed). If PERC fails → D-dimer or CTPA. Always consider PE in unexplained syncope with tachycardia or hypoxia.

Clinical Examples

Case 1: Vasovagal Syncope

22F fainted while standing in line at DMV. Felt warm, lightheaded, and nauseated beforehand. Witnessed to go limp, regained consciousness in < 30 sec. Normal exam, normal ECG. Dx: Classic vasovagal -prodrome + positional trigger + young + normal ECG. Reassurance and hydration. No workup needed.

Case 2: Cardiac Syncope -Complete Heart Block

78M with h/o CAD found on floor by wife. No prodrome. ECG shows complete heart block with ventricular rate 32. SBP 80. Dx: Cardiac syncope from CHB. Transcutaneous pacing → cardiology for permanent pacemaker. Admit to CCU. No prodrome + abnormal ECG + age = high risk.

Case 3: Orthostatic Syncope

65M on lisinopril, amlodipine, and tamsulosin. Passed out getting up from bed at night. Orthostatics: supine BP 140/80, standing BP 100/60 (drop 40). Dx: Orthostatic hypotension -medication-related (alpha-blocker + antihypertensives). Reduce tamsulosin, hold amlodipine, encourage hydration and compression stockings.

Case 4: Exertional Syncope -HOCM

19M college athlete collapsed during basketball. No prodrome. Exam: harsh crescendo-decrescendo systolic murmur at LLSB that increases with Valsalva. ECG: LVH with deep septal Q waves. Dx: HOCM. Echo confirmed. Restrict from competitive sports. Family screening. Consider ICD if high-risk features. Exertional syncope in young = cardiac until proven otherwise.

Sample Presentation

Mr. Davis is a 74-year-old man with CAD, HTN, and HFrEF (EF 30%) who presents after a witnessed syncopal episode while sitting in a chair. No prodrome. Wife reports he went pale, slumped over, was unresponsive for ~10 seconds, then woke up confused. No seizure activity, no incontinence. ECG shows sinus rhythm with bifascicular block (RBBB + LAFB), QTc 480ms. Orthostatics negative. Troponin negative. BNP elevated at 850.

Key Points: High-risk syncope -no prodrome, structural heart disease (HFrEF), abnormal ECG (bifascicular block). Admit for continuous telemetry monitoring. Consider EP study. Bifascicular block in setting of syncope suggests intermittent complete heart block -may need pacemaker or ICD given EF 30%.

Daily Rounds Checklist

Telemetry review: Any pauses > 3 sec? Any VT runs? Any new arrhythmias?
Orthostatic vitals: Repeat if initially positive or if meds adjusted
ECG changes: Repeat ECG if initial was abnormal or if symptoms recur
Echo results: Structural heart disease? EF? Valvular disease? HOCM?
Medication review: Any QT-prolonging drugs? Antihypertensives? Alpha-blockers?
Recurrence: Any further episodes? Near-syncope? Presyncope?
EP consult: If cardiac etiology suspected -document their recs
Disposition plan: Safe for discharge? Need event monitor? Follow-up arranged?

🧪 Workup

Initial Evaluation (ALL Patients)

Detailed history: Position (supine/standing/exertional), prodrome, witnesses, duration, recovery, medications, family hx of sudden death
Physical exam: Orthostatic vitals (supine → standing, wait 3 min), cardiac auscultation (murmurs), carotid bruits, neurologic exam
12-lead ECG -MANDATORY in every syncope patient. Look for: long QT, Brugada, WPW, heart block, old MI (Q waves), LVH
Orthostatic vitals: SBP drop > 20 mmHg OR DBP drop > 10 mmHg within 3 min of standing = positive

The history + ECG alone will identify the cause in ~50% of syncope patients. Routine labs, CT head, EEG, and carotid ultrasound have extremely low yield and should NOT be ordered unless specifically indicated.

High-Risk ECG Findings

Finding	Suggests	Action
Bifascicular block (RBBB + LAFB or LPFB)	Intermittent complete heart block	Admit, EP consult, likely pacemaker
QTc > 500 ms	Long QT syndrome → torsades de pointes	Admit, telemetry, avoid QT-prolonging drugs
Brugada pattern (coved ST V1-V3)	Brugada syndrome → VF	EP consult, ICD evaluation
Pre-excitation (short PR, delta wave)	WPW → AF with rapid conduction → VF	EP consult for ablation
Mobitz II / CHB	High-grade AV block	Pacing (transcutaneous → permanent)
VT / Non-sustained VT	Ventricular arrhythmia	Admit, EP consult, ICD evaluation
Pathologic Q waves	Prior MI → scar-mediated VT	Echo, EP consult

Selective Testing

Echocardiogram: If cardiac murmur, abnormal ECG, exertional syncope, or known heart disease
Continuous monitoring: Holter (24-48h) if daily symptoms; event monitor (2-4 weeks) if weekly; implantable loop recorder (ILR) for recurrent unexplained syncope ISSUE-3, 2012
Tilt table test: Recurrent syncope suspected vasovagal but diagnosis unclear. Sensitivity 26-80%.
EP study: Suspected arrhythmic syncope with non-diagnostic non-invasive workup, structural heart disease
Labs: Only if clinically indicated -CBC (anemia/bleeding), BMP (dehydration), troponin (ACS), BNP (HF), glucose, pregnancy test

Risk Stratification Scores

Score	Criteria	Use
San Francisco Syncope Rule (CHESS)	CHF hx, Hct < 30, ECG abnormal, SOB, SBP < 90	Any positive = high risk. ~98% sensitivity for 7-day serious outcome STePS, 2006
Canadian Syncope Risk Score	Predisposition to vasovagal, heart disease, elevated troponin, abnormal QRS axis, QTc > 480, ED diagnosis, SBP < 90	Validated prediction of 30-day serious adverse events. Score -3 to +11. CSRS, 2016
ROSE Rule	BNP ≥ 300, bradycardia ≤ 50, rectal exam with fecal occult blood, anemia, chest pain, ECG Q-wave, saturation ≤ 94% on RA	Predicts 1-month serious outcome. Any positive = high risk. ROSE, 2010

🚨 Management

Admission Criteria

Admit if ANY of these present: Abnormal ECG, structural heart disease (EF < 35%, severe AS, HOCM), exertional syncope, syncope while supine, family hx of sudden cardiac death < 50, significant injury from syncope, recurrent syncope, new neurologic deficits, suspected PE/ACS.

Cardiac Syncope -Arrhythmic

Bradycardia (sinus node dysfunction, heart block): Permanent pacemaker. Atropine or transcutaneous pacing as bridge.
VT with structural heart disease: ICD implantation. Antiarrhythmics (amiodarone, sotalol) as adjunct. EP study for VT ablation.
Long QT: Avoid QT-prolonging drugs (www.crediblemeds.org). Beta-blockers (nadolol) first-line. ICD if cardiac arrest survivor or recurrent syncope on beta-blockers.
Brugada: ICD for cardiac arrest survivors or spontaneous type 1 with syncope. Avoid fever (triggers arrhythmia). Isoproterenol for VT storm.
WPW: Catheter ablation of accessory pathway (curative in > 95%). Avoid AV nodal blockers (digoxin, verapamil, beta-blockers) in AF with WPW.

Cardiac Syncope -Structural

Severe AS with syncope: Urgent AVR (surgical or TAVR). No medical temporizing.
HOCM: Avoid dehydration, Valsalva, heavy exertion. Beta-blockers or verapamil. ICD if high-risk (family hx SCD, massive LVH > 30mm, unexplained syncope, NSVT). Myectomy or alcohol septal ablation for refractory symptoms.
PE: Anticoagulation. Thrombolytics if massive PE with hemodynamic compromise.

Reflex (Vasovagal) Syncope

First-line: Education, reassurance, trigger avoidance, increase salt & fluid intake (2-3L/day), physical counterpressure maneuvers (leg crossing, hand grip, squatting) PC-Trial, 2006
Second-line: Midodrine (ProAmatine) 5-10mg TID (alpha-1 agonist, raises BP). Fludrocortisone 0.1-0.2mg daily (volume expansion).
Tilt training: Progressive standing exercises. Evidence is mixed.
Pacemaker: Only for recurrent vasovagal with documented prolonged asystole (> 3 sec) on ILR. Dual-chamber pacing with rate-drop response. ISSUE-3, 2012

Orthostatic Syncope

Medication review: Reduce/stop offending agents (diuretics, alpha-blockers, vasodilators, TCAs)
Non-pharmacologic: Compression stockings (30-40 mmHg), abdominal binder, rise slowly, elevate HOB, increase salt & fluids
Pharmacologic: Midodrine 5-10mg TID or droxidopa (Northera) for neurogenic OH

Safe for discharge: Young patient (< 50), clear vasovagal trigger, no cardiac history, normal ECG, normal exam, no exertional component, no family hx of SCD. Counsel on prodrome recognition, hydration, and counterpressure maneuvers.

⚡ Summary

Summary

Definition

Transient LOC from global cerebral hypoperfusion. Rapid onset, short duration, spontaneous recovery.

Most Common

Vasovagal (~60%). Prodrome of warmth, nausea, diaphoresis. Positional trigger. Benign.

Most Dangerous

Cardiac syncope (~15%). No prodrome, exertional, abnormal ECG, structural heart disease. 18-33% 1-year mortality.

Key Test

12-lead ECG -mandatory for ALL syncope patients. History + ECG identifies cause in ~50%.

Admit If

Abnormal ECG, structural heart disease, exertional, supine syncope, hx SCD in family, significant injury, suspected PE/ACS.

Pearl

Routine CT head, EEG, carotid US have near-zero yield. Don't shotgun -use the history and ECG.

📄 One Pager

One-Pager

Syncope

Risk Stratification & Workup